Memory Processing

 

Memory, an essential part of life and independence, is primarily stored in the cerebral cortex. The inferior temporal cortex stores visual memory; whereas, the frontal cortex stores associations. New declarative memories, involving facts and events, are formed in the hippocampus and related structures in the medial temporal lobe (memory). The entorhinal cortex supplies the majority of the information that is sent to the hippocampus (Carson, 2004, 416). Some researchers believe that the hippocampus is similar to a temporary holding cell and memories slowly seep into the permanent storage area of the cerebral cortex. This process could be compared to an inbox; once the inbox is full, items are archived into a different area. On the other hand, the majority of researchers believe that the hippocampus does not store information, but instead is needed to help create new memories (memory). Carson agrees with the latter, and that the hippocampus inputs information from the sensory and motor cortex, processes the information, modifies the memories, and links them together in ways that can be more easily remembered (Carson, 2004, 416).

The amygdala plays a vital role in memories of an emotional nature. Someone with amygdala damage may be able to remember details of an event, but will forget emotional information (memory). The right prefrontal and bilateral hippocampal gyrus, which surrounds the hippocampus, is associated with visual (picture) memory; while word associations are connected to the left prefrontal and left hippocampus gyrus. The left hemisphere of our brains is responsible for encoding memories, and the right hemisphere is in charge of retrieving memories. Medial temporal and midline diencephalic processing, composed of the thalamus and hypothalamus, control the consolidation of memories; which, as a result, enables long-term memory processes to occur (neuro). Bilateral anterior lesions on the thalamus can cause permanent amnesia, while posterior lesions do not normally cause a noteworthy problem. The severity of anterior thalamus damage can affect both hippocamal and perirhinal pathways (because of the location); and in turn, disrupt the “transmittal” of memory from one area to another. For example, one well known case involves a man that has had amnesia since 1960 due to a brain injury. The patient’s verbal memory was destroyed, but he has no problem with other cognitive functions. Even as far back as 1988, researchers were able to produce evidence that lesions in the dorsomedial nuclei and the hippocampal tracts cause a memory disorder. The location and extent of the lesions determined the severity of the memory deficit. Accordingly, left-sided lesions produce verbal memory loss, while right-sided lesions produce memory loss of a visual nature (Ringholz, 2000).

The caudate nucleus, located in the lateral ventricle of the brain, regulates the organization and priority of information sent to the frontal lobes. Individuals with Huntingdon Disease often have many memory difficulties due to damage of the connection between this region and the frontal lobes. Unlike patients with Alzheimer’s disease, patients with HD cannot learn or recall motor memories; so, their speech is often slurred, stuttering is common, and body movements are also uncontrollable. They can recall memories, but not find the right words to express them. Also, they can remember experiences when given choices to pick from and benefit from cues- exactly the opposite of patients with Alzheimer’s disease. Without organization, memories only matter so much. Memory problems in HD can be compared to reading a book where the pages or words in a sentence are all out of order. Everything is there, but it still does not make any sense. Even though these individuals can understand what someone is saying, response time is extremely slow due to the brain’s “search mechanism” being damaged. Actions that were almost “unconscious” at one point, such as driving or walking, will now become very difficult because intense concentration will be required (Stanford). Memory, unlike many of the brain’s functions, is something that most people (especially students) think of from time to time. Not being able to recall someone’s name or an important piece of information can be very embarrassing or frustrating, to say the least. Damage to areas such as the hippocampus, amygdala, thalamus, and caudate nucleus can cause memory problems. Memory is so complex that memory loss is actually “specialized”. Some people may have trouble with short-term memory, while other people have trouble with long-term memory. The organization of memories or even creating new memories may be impossible. My memory is not “the best”, but I feel fortunate that I can at least put sentences together, remember what I ate last, and recall vital information. Without these traits, life would be much more difficult and confusing. References: Cognitive Symptoms X1. (2004). HOPES. Retrieved February 15, 2006 from http://www.stanford.edu/group/hopes/diagnsis/cognitiv/x1.html Long, C.J. (n.d.). Memory. Retrieved February 12, 2006 from http://neuro.psyc.memphis.edu/NeuroPsyc/np-ugp-memory.htm Myers, Catherine. (2005). Memory. Memory Loss and the Brain. Retrieved February 12, 2006 from http://www.memorylossonline.com/glossary/memory.html Ringholz, George. (2000). Summary and Discussion: Patient #44. Baylor Neurology Case of the Month. Retrieved February 15, 2006 from http://www.bcm.edu/neurology/challeng/pat44/summary.html.

Animal Research: Positives and Negatives

 

Animal research is a controversial issue. One can not deny that there are many benefits, but also some drawbacks associated with this research. Animal research has accomplished many significant findings, including, but not limited to: modes of adaptation to change, cures for many diseases, and coping with psychological disorders and drug addiction. Studies even help further the animal kingdom by keeping animal populations from going extinct.

Even so, animal activists and the much of the general public would happily comment on the disadvantages of this type of research. The most common concern is the ethical dilemma in researching animals, which often includes operating and eventually putting these creatures to sleep. Psychologists use techniques such as administering anesthesia, pain medication, and antibiotics along with keeping animals in clean conditions to give these creatures the most humane treatment possible during research. Another concern is that animal laboratories are very expensive and difficult to maintain.

Scientists did not begin experimenting with animals, but in my opinion, the end is no where to be seen. I can not see a time when animal research will not be needed. Computers only function from data that humans input; we still have to get that data from some source. Even plants and tissues, which have purpose in some experiments, can not help in the behavioral field of study. Animals must be used to save lives.

Neurotransmitters with an emphasis on opioids

 

The major types of neurotransmitters in the brain are dopamine, norepinephrine, and serotonin, which are catecholamines; glutamate, GABA, and glycine, which are amino acids; peptide neurotransmitters called opioids; a nucleoside called adenosine; a soluble gas called nitric oxide; and acetylcholine, the primary neurotransmitter .

Catecholamines, a subcategory of monoamines, increase or decrease the activities of certain brain functions. Norepinephrine, dopamine, and serotonin make up the catecholamine chemical family. Dopamine helps us to learn, move, and keep our attention on something. Norepinephrine (what we commonly call adrenalin or epinephrine) produces excitatory behavioral effects. Serotonin regulates mood, sleep, pain, and arousal, among other things (Carlson, 2004, 116-122).
Amino acids are used for protein synthesis. The three most common amino acid neurotransmitters are glutamate, gamma-aminobutyric acid (GABA), and glycine. Glutamate is believed to be the first neurotransmitter, on top of being the principal neurotransmitter in the brain and spinal cord. It modifies the threshold of excitation. GABA is produced from glutamic acid and is an inhibitory neurotransmitter in the brain. Glycine serves as an inhibitory neurotransmitter in the lower area of the brain and the spinal cord (Carlson, 2004, 123-126).

Adenosine, a combination of ribose and adenine, is a nucleoside compound. When cells are short on fuel, it is released. This release activates receptors of blood vessels causing them to dilate and increasing blood flow. Nitric oxide receives the most attention out of all the soluble gases and is used as a messenger in many parts of the body. The primary neurotransmitter secreted by axons of the central nervous system, acetylcholine, is responsible for all muscular movement (Carlson, 2004, 113-128).

Finally, I am going to discuss the effect of opioids, a popular peptide. Peptides consist of two or more amino acids that are linked together. Three types of opioid peptides exist (enkephalins, endorphins, and dynorphins). All three reside in the pituitary and adrenal glands, but they are released into circulation and can be found in many organs.
Opioid peptides modify the actions of other neurotransmitters in the central nervous system (CNS). They make the neurons more difficult to excite and can provide pain relief and euphoria along with various behaviors. Opioids are very distinctive because they regulate major neurotransmitters including acetylcholine, dopamine, norepinephrine, serotonin, and gamma aminobutyric acid (Froehlich, 1997).

Alcohol can activate opioids, which explains some people’s disposition to alcohol addiction. These peptides yield the same effects as morphine and heroin (hence the similar name of opioid and opiate). Mediating pain perception, emotional responses, and cardiovascular or respiratory functions are only a few of the functions opioids alter. To produce the aforementioned effects, opioids bind to receptors on the cell surface. Once this is accomplished, the biochemical effects occur. Alterations to the endogenous opioids can enhance the conditions of obesity, depression, diabetes, and epilepsy, along with alcoholism (as previously mentioned) (Froehlich, 1997).

References:
Carlson, Neil R. (2004). Neurotransmitters and Neuromodulators. In Physiology of Behavior, 8, 112-130.
Froehlich, Janice. (1997). Opioid Peptides [Electronic version]. Alcohol Health & Research World, 21, 132-135.

Neuroanatomical Structure: Solitary Tract

 

The solitary tract is “a slender compact bundle of primary sensory fibers that accompany the vagus, glossopharyngeal, and facial nerves and convey information from stretch receptors and chemoreceptors in the walls of the cardiovascular, respiratory, and intestinal tracts and impulses generated by the receptor cells of the taste buds in the tongue” (answers). In simpler terms, this structure is a group of fibers that interact with three cranial nerves responsible for controlling sensations and motor functions. Together, they send information from receptors in the walls of the heart, lung, or intestines that respond when tissues stretch or chemicals react; taste bud receptors also transmit signals in this way.

When researching the aforementioned formation, one will find the most information on the nucleus of the solitary tract, or NST for short. The NST is a cell column that is located in the back part of the medulla oblongata (the structure that controls respiration and circulation). It serves as the sensory nucleus of the brainstem and obtains fibers that send impulses to a nerve center in the brain. These axons that conduct nerve impulses come from the vagus, glossopharyngeal, and facial nerves (as discussed above) by way of the solitary tract (medical-dictionary).

Though not as widely discussed or understood as other neuroanatomical structures, the NSF plays an important role in living organisms. Serving as a “hub” for messages is an essential function of this nucleus. Once taste information is received from cranial nerves, the NSF passes the message to the thalamus. The thalamus then does its job of relaying the message to the cerebral cortex, an area responsible for higher brain function. The limbic system, which contains the hypothalamus(1) and amygdala(2), controls many involuntary functions and is an additional recipient of the information (faculty).

Extensive research has been done on how neurotransmitters interact with the NFS. Glutamate, an excitatory amino acid, is believed to be one of the neurotransmitters that enables communication between the vagal nerve and the NSF. Noradrenergic neurons located in the NSF exist to release norepinephrine(3) in the amygdala and are excited by the amino acid. This excitatory action may very well be the means by which signals sent by the vagus nerve adjust methods of storing new experiences in memory. Experiments have been conducted on rats to prove this point. When NTS neurons were activated with glutamate, memory associations were much stronger; in this case, the association was between drinking water and footshock (Miyashita 2002). The bed nucleus of the stria terminalis (BST)(4)also receives taste information and sends this info to the NFS. Neurons of the NFS that were responsive to sucrose, NaCl, citric acid, and quinine hydrochloride were also affected by BST (Smith, Ye, Li, 2005).

Damage to the NFS can appear in lesions. Unsurprisingly, experiments suggest that rats with lesions on the nucleus can not taste, though scientists can not prove this fact. The rats may in fact be able to taste, but no longer experience pleasure through eating. Whether the rats can in deed taste or not, few can survive with large lesions of the NST. Little evidence has been discovered connecting ingestive behavior to the NFS, yet it is suggested that this structure may play a part in the process, and that the lesions can be disruptive to the every-day process (Shimura 1997).

A study conducted on individuals who died due to acute heart failure caused by ischemia (restriction in blood supply) produced noteworthy findings. Lesions were discovered on the patients’ NFS. This report will seem strange if one only thinks of the NFS as a hub for taste stimuli. One must bear in mind that the nucleus of the solitary tract also functions as one of the nuclei in the medulla responsible for monitoring of respiratory and cardiovascular functions, even though it is not elaborated on in this discussion. All other medullary and pontine nuclei were lesion-free. This suggests that the neurons of the NSF have a special vulnerability. Also, it is believed that these lesions may prevent the patients from recovering by stopping independent cardiac and respiratory functions, even when life-saving procedures are administered (stroke).
In conclusion, the solitary tract is a complicated, but important neuroanatomical structure of our brain. More experiments are sure to follow and hopefully one day we will have a better understanding of how the solitary tract functions. Until then, just be thankful every time you taste that juicy steak or an ice cold drink.

Footnotes:

1.
The part of the brain that lies below the thalamus, forming the major portion of the ventral region of the diencephalon and functioning to regulate bodily temperature, certain metabolic processes, and other autonomic activities (answer).

2.An almond-shaped mass of gray matter in the anterior portion of the temporal lobe. Also called amygdaloid nucleus (answer).

3. A substance, C8H11NO3, both a hormone and neurotransmitter, secreted by the adrenal medulla and the nerve endings of the sympathetic nervous system to cause vasoconstriction and increases in heart rate, blood pressure, and the sugar level of the blood (answer).

4. The Stria Terminalis is a forebrain structure that participates in anxiety and stress responses (answer).

References:

1. http://faculty.washington.edu/chudler/tasty.html

2. http://medical-dictionary.thefreedictionary.com/nucleus+of+solitary+tract. (2004).

3. http://stroke.ahajournals.org/cgi/content/full/31/5/1187. (2000).

4. http://www.answers.com/. 2006.

5. Miyashita, T. & Williams, C. (2002) Glutamtergic Transmission in the Nucleus of the Solitary Tract Modulates Memory Through Influences on Amygdala Noradrenergic Systems[Electronic Version]. Behavioral Neuroscience, Vol. 116, Issue 1.

6. Shimura, T, Grigson, P., & Norgren, R. (1997) Brainstem Lesions and Gustatory Function: I. The Role of the Nucleus of the Solitary Tract During a Brief Intake Test in Rats[Electronic version]. Behavioral Neuroscrience, Vol. 111, Issue 1.

7. Smith, D., Ye, M., & Li, C. (2005) Medullary Taste Reponses are Modulated by the Bed Nucleus of the Stria Terminalis[Electronic version]. Chemical Senses. 421-424.

Correlation between Psychostimulants, Dopamine, & Amphetamine; Sexual behavior

An experiment was conducted at the University of British Columbia to examine the correlation of psychostimulants, dopamine, and sexual behavior. The hypothesis that “behavioral sensitization caused by repeated psychostimulant administration can ‘cross-sensitize’ to a natural behavior, such as sex, and that increased NAC[nucleus accumbens] DA[dopamine] release may contribute to the facilitation of appetitive and consummatory aspects of this behavior” was supported by results of the study (Fiorino 1999). Simply put, giving an organism a drug (like cocaine) over a period of time can cause the drug to have a stronger affect then it originally did, as referred to in the previous sentence as behavioral sensitization. Scientists set out to prove that behavioral sensitivity due to repetitive drug use can influence the sensitivity of other behaviors, and that increased dopamine release in the nucleus accumbens can account for an increase in the desire for gratification by way of sexual intercourse.

The researchers used several of the techniques discussed in Physiology of Behavior to prove their hypothesis. Male and female rats were kept in separate plastic cages when they were not being observed. The ovaries of the female rats were removed, and they were given estradil benzoate (the most powerful hormone secreted by the ovaries) and progesterone (produced by the body to prepare for implantation) (Fiorino 1999).

Stereotaxic surgery, which is most often used for lesion production, was performed on the male rats. In this case, the surgery was done so that the scientists could insert microdialysis probe guide cannulas into the NAC. The cannulas, or small metal tubes, function by carrying a solution into a certain area of the brain (in this case the NAC) so that it can collect molecules from the extracellular fluid; after the molecules are collected, the fluid comes out through another tube. The cannulas were secured to the skull with dental acrylic and jeweler’s screws, and a wire “training post” was cemented to the top of the skull behind the cannula (Carlson & Fiorino, 2004, 1999).

Chambers were used to join the male and female rates together. For twenty consecutive days, the male rats were placed into its appropriate chamber and attached to a liquid swivel by way of a steel coil that was secured to his training post. The rats waited half an hour before D-amphetamine sulfate or the saline control was administered, and two hours more after the injection was given. This way, the rats were able to get accustomed to the probe and their surroundings before testing began. Samples were taken by microdialysis every ten minutes during this two-hour period (Fiorino 1999).

All the male rats were sexually inexperienced, whereas the female rats were not. On the twenty-first day, the female and male rats were joined for sixty minutes, while interaction was allowed for thirty. Sexual behavior was videotaped and recorded by computers. Many statistics were available, including, but not limited to, ejaculation frequency and latency, mount frequency, and intromission (insertion) frequency. Microdialysis was used to determine the amount and alterations of dopamine in the NAC (Fiorino 1999).

After the test was completed, the mice were given a fatal dose of chloral hydrate and underwent perfusion via saline and formalin injection (used to harden the brain). The brains were sliced and sections were stained with cresyl violet to determine if the probes were placed in NAC. Only the mice with correct placement of the probes were included in the study (Fiorino 1999).

Stereotaxic surgery was used to pinpoint the correct area of the brain for probe insertion. Histological methods (such as fixation, sectioning, and staining) were used to ensure the results were valid by verifying what area of the brain was tested. Microdialysis was used to view the extracellular changes, along with video and computer monitoring of physical activity. All these techniques were used to ensure the validity of the test, to make the relationship between psychological and physical functions clear, and to have a deeper understanding then the naked eye can provide (Carlson & Fiorino, 2004, 1999).

In conclusion, the results confirmed that the male rats who were given D-amphetamine displayed a much higher dopamine increase during the first thirty minutes of female-exposure opposed to the control group. They also had an increased number of mounts, ejaculations, and intromissions. A higher dopamine increase occurred for two-hours after drug injection opposed to normal readings, and a noteworthy increase occurred between the first and tenth injection. Scientists can conclude from this study that using a drug over a period of time can cause an increase in the amount of dopamine release, which in turn raises an organism’s sexual drive and triggers behavioral sensitivity (Fiorino 1999). .

References:
1. Carlson, Neil R. (2004). Neurotransmitters and Neuromodulators. In Physiology of Behavior, 8, 112-130.
2. Fiorino, D. & Phillips, A. (1999). Facilitation of Sexual Behavior and Enhanced Dopamine Efflux in the Nucleus Accumbens of Male Rats after D-Amphetamine-Induced Behavioral Sensitization [electronic media]. The Journal of Neuroscience, 19(1), 456-463.

Concordance Study of Bipolar I Disorder in Twins

 

Studying the concordance, which is the similarity of certain characteristics, in twins is a popular method of determining the role of genetic effects in mental disorders (Carlson 2004). Consistent results in studies of twins with bipolar I disorder have supported the hypothesis that genetic factors are great contributors to mental disorders. Accordingly, a similar study was done using a population-based twin sample in which personal interviews were conducted to formulate diagnoses. This study was approved by the Ministry of Social Affairs and Health, along with the Ethics Committee of the National Public Health Institute (Kieseppä, Partonen, Haukka, Kaprio, & Lönnqvist 2004).

All Finish same-sex twins born between 1940 and 1957 were screened for a diagnosis of bipolar I disorder, either through surveys or in the National Hospital Discharge Register. Thirty-eight pairs were identified and invited to participate via mailed invitations; 68% (or 26 pairs) accepted. Participants had to be diagnosed with either bipolar I or the bipolar type of schizoaffective disorder; individuals with bipolar II disorders did not qualify. Five individuals included in the test were deceased (three due to suicide, one due to alcoholic withdrawal and acute mania, and one unknown); forensic examinations along with medical records and information from the opposite twin were utilized All available medical records were obtained prior to personal interviews. Clinical and demographic characteristics of participants in the study and outside of the study were compared using Fisher’s exact test, the chi-square test, Student’s t test, and the Mann-Whitney rank sum test. These tests helped to affirm that there was a representative population sample of twins (Kieseppä, et al. 2004).

Seven of the 26 pairs were monozygotic (identical) and 19 were dizygotic (fraternal). These statistics are also comparable with the national percentages. The study found that the concordance for bipolar I disorder in monozygotic twins was 43%, while only 6% for dizygotic twins. Once the participants with schizoaffective disorder were included, the percentage of concordant monozygotic twins went up to 50%, where as the dizygotic twins went down to 5%. Three-fourths of identical twins experienced concordance for the broad affective disorder spectrum, along with 11% of dizygotic twins. Zygosity testing was performed by means of autopsy tissue samples, microsatellite markers (used in routine paternity tests), and questionnaires on resemblance and confusability during childhood. Interviewers were unaware of the results while testing; the tests were done only after the final diagnoses. Concordance rates were then recalculated to include zygosity results. Two of six (33%) monozygotic twins and one of thirteen (8%) dizygotic twins were concordant for bipolar I disorder; whereas the concordance rates for bipolar I disorder plus schizoaffective disorder and bipolar type were three of seven (43%) and one of fourteen (7%), respectively (Kieseppä, et al. 2004).

Different models were used to account for other factors that could play a part in bipolar I concordance of twins. The E model, which was based strictly on specific environmental factors, was rejected by the chi-square test. The CE model used both common and specific environmental factors; even though it could not be completely rejected, it fit much worse than the ACE and AE models. The AE model, which was the best fit, included both genetic and specific environmental factors. Environmental risk factors, including problems during pregnancy and delivery and childhood infections, were also ascertained from birth clinics, maternity clinics, and child welfare clinics. No significant differences in concordant or discordant pairs of twins were noted (Kieseppä, et al. 2004).

In summary, the results from this study supported past studies. Bipolar I disorder is slightly concordant in fraternal twins, and extremely concordant in identical twins. Concordance rates rise even farther when twin pairs consisting of one individual having bipolar I disorder and another having a disorder in the broad affective spectrum are included. Environmental factors do seem to a play a part in the concordance discussed above, but can not be the only cause. Problems during pregnancy or birth do not appear to have a significant influence on bipolar I concordance in twins. Though this study was small, it included a significant representation of the entire population and used evidence to support the hypothesis that genetics play a role in mental disorders, especially bipolar I disorder.
References:
1. Carlson, Neil R. (2004). Methods and Strategies of Research. In Physiology of Behavior, 8, 160.
2. Kieseppä, T., Partonen, T., Haukka, J., Kaprio, J. & Lönnqvist, J. (2004). High Concordance of Bipolar I Disorder in a Nationwide Sample of Twins [Electronic version]. The American Journal of Psychiatry, Vol. 161, Iss. 10, 1814-1821.

Vision: Binocular Vision

 

Have you ever thought about the fact that you see out of two different places, but only see one picture? Unless one has vision problems, being able to generate one large image out of two separate eyes is something we humans take for granted. Binocular function is the “ability of the eyes to coordinate their activity so that we can merge the visual fields of both eyes into one distinct image. The most commonly observed aspects of binocular functions include convergence (the ability of the two eyes to team and focus on the same object), and accommodations (the ability of the eyes to shift their focus from near point to far point or vice versa). Each eye can have normal acuity (20/20 vision) but unless the eyes team, visual functions are impaired” (McPeck, n.d.).

The majority of neurons in the striate cortex, “an area of the brain that receives visual impulses, contains a conspicuous band of myelinated fibers, and is located mostly in the walls and along the edges of the calcarine sulcus of the occipital lobe” (Merriam-Webster, 2002), are binocular. These binocular neurons have response patterns that seem to contribute to depth perception. Neurons are able to respond to visual stimulation that occurs in either eye, though the response is stronger when each eye views an image in a separate location. Neurons respond to retinal disparity, which causes images to be produced on different parts of the retina of each eye, so that each eye sees a scene differently and the variation of object distance can be noticed (Carlson, 2004). This “single perception of a slightly different image from each eye, resulting in depth perception” is called stereopsis (Answers, 2006).

In order for an individual to have sharp binocular vision with stereopsis, he or she must have the correct genetics and proper maturity of the binocular system between birth and age four. Though the first few years are critical, most vision aspects are fully developed by six months of age in humans. One study involving a cat’s visual experience illustrates the abovementioned statement. In one part of the experiment, one eye was either patched for several weeks or blurred with a contact lens. The responses of the cells in the visual cortex were then recorded. Before the eye was covered, 80% of the cells were binocular and 20% were monocular. Afterwards, all of the cells became monocular; cells that would once respond to the input from either eye would only respond to input from one eye. This outcome only occurred when the test was done early in life; older cats experienced little change in their binocular vision (Cooper, 2000).

The layout of the face was not just designed with beauty in mind. Our eyes are spaced approximately two inches apart; whereas a horse’s eyes are closer to the side of the head. Horses have a 35 degree wider field of vision than humans. Why would humans be designed to have a smaller field of vision than some animals? The answer is this: it is essential for animals to be able to spot an approaching predator, so they need to see as much area at once as possible. Humans (along with most carnivores and omnivores), on the other hand, need the ability to make accurate judgments about distance and movement. To do this, our field of vision of both eyes must overlap so we can utilize binocular vision (Sight, 2005).

Several visual ailments can arise when damage or improper development of the binocular system occurs. For instance, poor vision in an otherwise healthy eye can be the result of the brain favoring one eye over the other. This normal begins in infancy or childhood and is known as Amblyopia. Wandering eyes or significant differences in refractive error (such as farsightedness or nearsightedness) between the two eyes are major causes of this disorder. Diplopia, commonly known as “double vision”, is a very troubling problem relating to binocular damage. Eye patches were the only cure at one time, but now other methods are in use (pages). Squinting, which may sound like a small annoyance, actually prevents binocular vision because it impairs an individual from using both eyes to look at the same point. Also known as strabismus (or turned eye), squinting can be caused by various things including, but not limited to: cataracts, brain damage, or immobility of a muscle in the eye. Many times, all of these visual disturbances are connected. For instance, when binocular vision is disturbed, Diplopia follows. Infants with Diplopia will squint so they can see one image in one eye (suppressing the vision in the other eye). This is turn causes Amblyopia (Sayer, 2002).

As you can see, binocular functioning plays an essential role in human vision. Without it we would not be able to tell how far away objects were or be able to focus both eyes on one object. Strabismus, Amblyopia, and Diplopia are serious problems that can occur from damage or underdevelopment of the binocular system.
References:

1. Answers Corporation.(2006). Retrieved January 22, 2006, from http://www.answers.com.

2. Carlson, Neil R. (2004). Vision. In Physiology of Behavior, 8, 182-183.

3. Cooper, Jeffrey. (2000). Development of Vision (Critical Periods). Retrieved January 22, 2006, from http://www.strabismus.org/critical_period_Hubel.html.

4. McPeck, Christopher. (n.d.). Retrieved January 22, 2006 from http://pages.prodigy.net/unohu/binocular.htm.

5. Merriam-Webster, Inc. (2003). Retrieved January 22, 2006 from http://www.intelihealth.com/IH/ihtIH/WSIHW000/9276/9276.html.

6. Sayer, Grant. (2002, July 25). Binocular Vision Problems. Retrieved January 22, 2006, from http://www.hon.ch/Library/Theme/VisionFaq/section6.html-.

7. Sight and the Mammal Eye. (2005, Nov 20). Retrieved January 22, 2006 from http://www.earthlife.net/mammals/vision.html.

Non Visual Senses: Vestibular System and Motion Sickness

 

The vestibular system, which consists of the semicircular canals and otolith organs, is located in the inner ear. For the most part, people are unfamiliar with the term “vestibular”, but almost certainly have heard of motion sickness. Have you ever gotten sick from riding in the car or even playing an intense racing game? If you have, then your vestibular system is in operation. The majority of individuals experience some motion sickness in their lifetime, while a small number of persons have either none at all or are highly susceptible (Lacker, 2004.).

When studying biological events, one must reflect on how many different involuntary bodily functions we humans take advantage of every day. The benefits the vestibular system provides are of no exception. Not surprisingly, the vestibular system senses gravity, along with straight and curved movement, which helps to regulate balance. The ears and eyes must work together for us to accomplish simple tasks. For instance, once the vestibular system is damaged, driving or even walking will be difficult or impossible. This condition is called oscillopsia and occurs when your eye muscles do not receive signals to adjust to movement. The vestibulo-oscular reflex, a term for the eye and ear coordination aforementioned, is so responsive that it senses the minute activity made by the head each time we breathe in or out. The brain then sends instructions to our eye muscles to keep focused rather than shifting with motion. Even our heartbeat causes enough movement to impede our vision if the vestibular system is not functioning. Symptoms similar to motion sickness will occur; dizziness and nausea can arise from the simple task of trying to focus one’s eyes (Bauman, 2003). The vestibular system not only works in conjunction with the ocular system, but also alongside the proprioceptive system. This system identifies the activity or location of the body or a limb by reacting to stimuli developing within the individual (Answers, 2006). The vestibular system works with the muscles, thus constant muscle adjustments are possible to help retain balance when shifting positions. (Bauman, 2003).

The vestibular, ocular, and proprioceptive systems are very important for achieving normality in every-day life, but living without one of the three (though challenging) is doable. On the other hand, if only one of the three systems is functioning, maintaining balance is impossible. Once the vestibular system is dead, it no longer transmits signals to the brain; in contrast, if it is merely damaged, it still sends signals- just the wrong ones. Consequently, the side effects of vestibular damage are worse in the initial weeks. Slowly the brain begins to depend on ocular and proprioceptive input more, while vestibular input is almost disregarded. If only one side is injured, nystagmus develops. Nystagmus is an unpleasant condition where frequent eye jerking produces vertigo, nausea, vomiting, and visual problems (Bauman, 2003).

Astonishingly, vestibular damage can also cause memory problems. Though this may sound far-fetched, here is the reason: a once-automatic reflex, balance, now requires great concentration. The area of the brain once reserved for memory and thought processing must now focus on balance control. Fatigue will often emerge in an individual from the constant requirement to concentrate on keeping one’s balance. Imagine what would happen if we had to remember to breathe! Even if it were possible, the exhaustion we would experience would be too much to handle. Muscular aches and pains may also arise. One must constantly stiffen his or her muscles to maintain his or her balance. Trying to keep the head absolutely still can bring about headaches, as well as a sore neck. As it is plain to see, living without a properly functioning vestibular system can be more than worrisome- it can be downright painful (Bauman, 2003).

Now that the basic functioning of the vestibular system is somewhat clearer, the concept of motion sickness will be easier to understand. Motion sickness was originally used to define sickness caused by unusual movement, such as sea, train, or swing sickness. Presently, the term motion sickness is used to describe any movement, or perception of movement, that causes an uneasy feeling. Physical movement is not required for an individual to experience motion sickness. For example, I myself have had a horrible bout of motion sickness brought on by playing a video game that was in first person view. My eyes were sending messages to my brain that I was going down a steep hill, yet my vestibular system did not sense any movement. My stomach had a “lurching” feeling, then nausea and dizziness set in; some people even experience vomiting, headache, and drowsiness. Though damage to the vestibular system can be severe, motion sickness is not one of the symptoms. On the contrary, partial damage will cause an individual to be less likely to experience motion sickness; complete loss of vestibular function eliminates motion sickness. Prescription and over-the-counter drugs are available to combat motion sickness, though little is known about how they work (Bauman, 2003). Dramamine, an over-the-counter drug, is believed to work either by “acting on the balance mechanisms in the ear or on the part of the brain that controls vomiting” (Dramamine, 2001).

While motion sickness may not be pleasant, I personally would much rather feel a little nauseas from time to time then to have a malfunctioning vestibular system. I can not imagine the difficulty of maintaining constant concentration just to walk or keep my head still. In my opinion, vestibular damage would cause life to be much less enjoyable, at the very least. Every time you ride in a vehicle and feel a little queasy, be thankful that your vestibular system is functioning properly and that your uneasiness will soon disappear!

References:

1. Answers Corporation. (2006). Retrieved January 28, 2006 from http://www.answers.com.

2. Bauman, Neil. (2003). Protect Your Balance System—Or Else. Retrieved January 22, 2006 from http://www.hearinglosshelp.com/BalanceSystem.htm.

3. Dramamine-CMI. (2001). Retrieved January 28, 2006 from http://www.appco.com.au/appguide/drug.asp?drug_id=00072429&t=cmi.

4. Lackner, James. (2004). Motion sickness. Retrieved January 22, 2006 from
http://www.graybiel.brandeis.edu/publications/PDF/191_ms_encns.pdf.

Motor Cortex and its 4 primary tracts

 

The motor cortex, located in the cerebral cortex, is the starting point for electrochemical transmissions that travel from the nerve centers to the muscles. The primary motor cortex is positioned on the precentral gyrus. The precentral gyrus is a bulging ridge that is on the back area of the frontal lobe (the biggest part of each cerebral cortex). It is bound by the central sulcus (located between the frontal and parietal lobes) and the precentral sulcus, which is in front of and parallel to the central sulcus. The primary motor cortex is located just in front of the central sulcus (Carlson).

The organization of the primary motor cortex is somatotopic. This means that the layout of the motor cortex corresponds to different body parts. The supplementary motor cortex and the premotor cortex lie adjacent to the primary motor cortex. Both are involved in arranging movements, which they carry out by interacting with the primary motor cortex. Moving, or even envisioning movement, stimulates these areas. The two auxiliary motor cortexes obtain signals from sections of the parietal and temporal cortex, informing them of what is happening and where it is occurring. For example, the cortex involved in vision is separated into two streams, dorsal and visual. The ventral stream helps answer the “what” of vision- perceiving and recognizing objects- and ends in the temporal cortex; while the dorsal steam helps answer the “where” of vision- perception of location- and ends in the parietal cortex. The parietal lobes also help answer the “how” of vision by organizing visually guided movements. This somatotopic arrangement allows different areas of the brain to control different body parts (Carlson, 2004).

The lateral group is principally involved in the management of independent limb movements; its primary job is controlling the action of the hands and fingers. When the right and left hand move in different manners at the same time, or one moves while the other stays motionless, independent limb movement is taking place (Carlson, 2004).

The corticospinal tract, which is part of the lateral group, is one of the four principal motor tracts and has two sections- lateral and ventral. It is composed of axons that come to an end in the gray matter of the spinal cord. Most of the cells that control these axons are in the primary motor cortex, but axons are also sent through the corticospinal pathway by neurons in the parietal and temporal lobes. The majority of axons in the lateral (side) corticospinal tract are formed in the areas of the primary and auxiliary motor cortexes that control the distal sections of body parts; for instance, the fingers, arms, feet, and toes. Once joined with motor neurons in the spinal cord, synapses are formed. Muscles of the distal limbs are controlled by these motor neurons. Alternatively, axons of the ventral (middle) corticospinal tract form in the upper leg areas of the primary motor cortex and descend to the proper area of the spinal cord. They then divide and propel terminal buttons into both sides of the gray matter. As a result, motor neurons are regulated and can move the muscles of the torso and upper legs (Carlson, 2004).

Another member of the lateral group, the rubrospinal tract, is the second principal motor tract. This tract starts in the red nucleus of the midbrain and obtains its key indicators from the motor cortex through the cerebellum and the corticorubral tract (which controls the movement of the face, neck, tongue, and some eye muscles). The rubrospinal tract’s axons end on motor neurons in the spinal tract; these neurons are responsible for controlling the forelimb and hindlimb muscle movement (Carlson, 2004).

The third principal motor tract, the vestibulospinal tract, is part of the ventromedial group. This group gets information from the areas of the primary motor cortex that control movement of the trunk, along with muscles close to the body (Carlson 2004). The vestibulospinal tract plays a vital role in maintaining posture, along with controlling adjustments of the head and muscles involved in balance (n.a., 2002).

Lastly, the reticulospinal tract, also a part of the ventromedial group, has many cell bodies located in nuclei of the brain stem and midbrain. The neurons control essential automatic functions, such as respiration, sneezing, coughing, and muscle tonus (a state of partial muscle contraction). Additionally, they also control voluntary actions controlled by the neocortex; walking is one example (Carlson, 2004).

In conclusion, the motor cortex controls movement in the body through different motor tracts. The four primary tracts include the corticospinal, rubrospinal, vestibulospinal, and reticulospinal tract. The corticospinal and rubrospinal tracts are in the lateral group which controls independent limb movements. The corticospinal tract controls the distal sections of body parts, along with the muscles of the torso and upper legs; while the rubrospinal tract controls the forelimb and hindlimb muscles. The vestibulospinal and reticulospinal tracts are in the ventromedial group which controls movement of the torso and muscles close to the body. The vestibulospinal tract controls posture, head adjustments, and balance; while the reticulospinal tract controls many automatic functions and voluntary neocortex functions.
Reference:

1. Brain Picture. Retrieved January 28, 2006 from http://www.emc.maricopa.edu/faculty/farabee/BIOBK/cerebrum_1.gif.

2. Carlson, Neil R. (2004). Control of Movement. In Physiology of Behavior, 8, 254-259.

3. N.a. (2002). Retrieved January 29, 2006 from http://sprojects.mmi.mcgill.ca/cns/histo/systems/motor/main.htm.

Narcoleptic symptoms in Parkinson’s Patients

 

Narcolepsy is a chronic sleeping disorder that is more than disruptive, it can be deadly. Patients with this disorder experience excessive daytime sleepiness, or EDS, and are prone to fall asleep at inappropriate moments. Most individuals have bouts of daytime sleepiness when their normal sleep routine is interrupted, or they do not put aside the recommended eight-hours a day; but individuals with narcolepsy have these bouts of EDS no matter how much sleep they get. Narcolepsy has been misdiagnosed because it is often mistaken for other disorders, such as depression. Statistics show that this disorder affects at least 200,000 people in the US, and most are not diagnosed until fifteen years after the initial onset of symptoms (Green & Stillman, 1998).

To have a better understanding of sleeping disorders, one must know the mechanism of sleep. When an individual is awake, he or she shows either alpha or beta brain activity. Alpha activity can be characterized as a state in which a person is not excited or avidly thinking, and includes normal, medium- frequency brain waves of 8-12Hz. Beta activity consists of erratic low-amplitude waves of 13-30 Hz, and normally occurs when someone is alert and in an active thinking process. When an individual becomes drowsy, they enter stage one sleep where some theta activity is displayed; this stage lasts for around ten minutes and can be described as a “prerequisite” to sleep. Stage two sleep still consists of theta activity, but also includes sleep spindles and K complexes. Sleep spindles are short busts of waves occurring two to five times a minute during stages one to four; while K complexes only occur during stage two and are sharp waveforms that can be triggered by noises. Fifteen minutes later, stage three sleep begins, along with delta activity. An hour and a half after falling asleep (or forty-five minutes after stage four), REM sleep begins. Stage four sleep is referred to as Rapid Eye Movement sleep because our eyes move back and forth. During stage four, dreams are likely to take place. Though dreams can occur in other stages, narrative dreams normally are distinctive of REM sleep. For the remainder of the night, individuals have twenty to thirty minutes intervals of REM sleep, and then fifty to sixty minute intervals of non-REM sleep (Carlson, 2004, 276-279).

A study was conducted in the Department of Psychiatry and Neurology at the Karl Franzens University Hospital in Graz, Austria to determine the correlation of sleep attacks in patients taking dopamine agonists for Parkinson’s disease. Dopamine agonists are drugs that combine with a receptor or cell to produce a physiologic reaction similar to that of dopamine (Answers, 2005). Rather than conducting a face to face study, researchers reviewed articles published between July 1999 and May 2001 that discussed narcoleptic-like attacks in patients with Parkinson’s disease. Twenty different publications were selected to include a total of 124 patients that had both attended movement disorder clinics and had sleep ailments; this amounted to nearly seven percent of patients taking dopamine agonists. It should be noted that two-thirds of these patients were men, and dosage amounts varied. Patients had diverse durations of treatment and were included whether or not former symptoms of sleepiness had occurred. Two types of sleep events were found: those without warning and those with drowsiness indicators before the attack. Unsurprisingly, researchers concluded that population based studies were needed to formulate a strategy for the avoidance and treatment of sleep disorders in patients taking dopamine agonists for Parkinson’s disease (Homann, et al., 2002).

Though further research is needed about the aforementioned topic, significant findings were produced. Heated debates have arisen, but this study supports the theory that sleep attacks, not just normal drowsiness, are present in Parkinson’s patients who take dopamine agonists. For example, seventeen of these patients fell asleep at the wheel from a sudden sleep attack, which resulted in ten car accidents. Pramipexole and Ropinirole, two dopamine agonists, were initially believed to be the cause; but now all dopamine drugs are possible factors. Additional non-driving attacks were reported, with twenty patients having recurrent sleep events (Homann, et al., 2002).

Because of the controversy involved and the belief that sleep attacks in Parkinson’s patients are too infrequent to be named as a significant problem, no principal treatment has been found. Twenty-five of the included patients either stopped taking dopamine agonists or reduced their dosage; twenty-two of these patients stopped having sleep attacks and three had reduced attacks. Three patients switched dopamine agonists; one patient’s attacks recurred, while the other two went into remission. Other patients had success with changing their medication schedule to correspond with the time they needed to be awake. Also, common narcoleptic treatments were administered. For example, the stimulant modifil worked as a successful treatment in one patient. Another patient found pulling over to take a nap when experiencing sleepiness while driving would keep him from having sleep attacks (Homann, et al., 2002).

Dopamine-like drugs have been known to cause normal drowsiness, but this is the first study that has addressed bouts of overwhelming sleep attacks. Personally, I found this surprising because it is alleged that up to thirty percent of Parkinson’s patients taking dopamine agonists have sleep attacks. Of course, publication bias in this study might have led to an overestimate. It does seem that males and individuals with damage to the autonomic nervous system might be at a higher risk. Also, health authorities of the United States, Canada, and Europe have acknowledged the danger of Pramipexole and Ropinirole and asked the makers to warn users not to drive or participate in similar activities (Homann, et al., 2002).I found this study interesting because in our textbook, Physiology of Behavior, irregularity of the hypocretin system was said to be the cause of narcolepsy. Dopamine is a neurotransmitter, much like hypocretin (Carlson, 2004, 282). The loss of functioning in Parkinson’s patients is due to a decrease in dopamine; therefore, dopamine agonists are given to supplement that lost. I would be inclined to think that the disruption of the dopamine system is what causes the sleep attacks if it were not for the fact that symptoms seem to disappear once the agonist is ceased. In addition, L-DOPA, another agonist that is used to compensate for dopamine loss, often causes involuntary movements and a worsening of symptoms in Parkinson’s disease (265). Schizophrenia is thought to be brought about by too much dopamine, and dopamine agonists can cause an onset of this disorder in some individuals (519). In addition, if one searches on http://www.google.com for “dopamine and sleep”, a plethora of articles will come up. This supports the findings that dopamine agonists are linked to sleep attacks in some fashion. Carlson also mentions the relationship between REM sleep behavior and Parkinson’s disease (283). It is suggested that dopamine agonists are responsible for this correlation (Gagnon, Montplaisir & Bedard, 2002). The theory that dopamine agonists are to blame for sleep attacks in patients with Parkinson’s disease presents a different point of view than the textbook for a possible cause of narcoleptic-like symptoms.

References:

1. Answers Corporation. (2006). Retrieved February 02, 2006, from http://www.answers.com

2. Carlson, Neil R. (2004). Physiology of Behavior, 8.

3. Gagnon J., Montplaisir J., & Bedard M. (2002). Rapid-eye-movement sleep disorders in Parkinson's disease [Electronic version]. Rev Neurol (Paris), 158, 135-152.

4. Green, P. & Stillman, M. (1998). Narcolepsy [Electronic version]. Archives of Family Medicine, 7, 472-478.

5. Homann, C., Wenzel, K., Suppan, K., Ivanic, G., Kriechbaum, N., Crevenna, R., et al. (2002). Sleep attacks in patients taking dopamine agonists: review. BMJ Publishing Group Ltd. Retrieved February 02, 2006, from http://bmj.bmjjournals.com/cgi/content/full/324/7352/1483

Phineas Gage and the Orbitofrontal Cortex

 

The day of September 13, 1848 marked the beginning of research involving the relationship between the prefrontal lobe and human behavior. Phineas Gage, a railroad foreman, was unearthing rock when a thick piece of iron smashed through the left side of his face. It entered below the cheekbone and came out through his skull. People were shocked when the blow did not kill him, and even more amazed that he was able to speak within a few minutes. Dr. John Martin Harlow, the attending physician, observed the changes in Gage’s personality for the next thirteen years until Gage died from a series of epileptic seizures, and also convinced his family to allow his skull to be exhumed five years later. Before the accident, Gage was known as a competent and adept employee; after the accident, he was rude, impulsive, profane, and negligent. His rational thinking and emotional processing was so impaired that he lost his job. Harlow’s reports, though not readily accepted, were confirmed for the most part by an experiment on monkeys in 1878; thus the analysis of the prefrontal lobes began (Larner & Leach, 2002).

The prefrontal lobe is responsible for formulating plans and strategies, along with a person’s “personality” (Carson, 2004, 84). The orbitofrontal cortex (OFC), part of prefrontal lobes, is located at the base of the frontal lobes right about the eyes. This cortex makes up an important part of who we are by regulating our emotions. The OFC receives input from the dorsomedial thalamus and the temporal cortex (both linked to memory); the ventral tegmental area (associated with the reward system); the olfactory system; and the amygdala, which is tied to anger. It then sends signals to the branches of the limbic system (responsible for moods and emotions) including: the cingulate cortex, the hippocampal formation, the temporal cortex, the lateral hypothalamus, and the amygdala; along with other areas of the frontal lobe. The inputs consist of environmental information, and the outputs regulate one’s behavior and physiological responses, essentially emotion. These inputs and outputs help establish the OFC as an interface between brain mechanisms, such as automatic learned and unlearned emotional reactions, along with complex behaviors (351-352).

Studying primates’ brains and behaviors is a good way to learn about the OFC; unfortunately, rodents’ orbitofrontal cortexes are too small to get significant information from. Some researchers consider the OFC the secondary taste cortex because it receives stimuli from the primary taste cortex in primates. Taste can act as a primary reinforcer; therefore, the OFC taste neurons are controlled by hunger. For instance, a monkey will eat until it is full. Once full, the OFC neurons no longer respond; whereas, the neurons of the primary taste cortex are regulated by the identity of taste, not the reward value. Therefore, the reward value of taste is represented in the OFC. One area of the OFC responds to sweet tastes (those with glucose), while another is activated by the taste of salt. This concept goes for pleasant touch, nice smells, and also foul smells; each works in a different area of OFC. Fatty foods give off a pleasant sensation because the brain knows these foods will probably contain high calories and essential fatty acids. There are even OFC neurons that respond to textures and temperature of food (Rolls, 2004).

It has been shown that smells activate neurons in the OFC of monkeys and in the ventral front region of humans. Thirty-five percent of these neurons are influenced by taste association, while the other sixty-five percent are completely dependent on the odor itself. Just as in taste, the OFC neuron activity decreases when monkeys are full, and the value of odor is represented in this cortex. In addition, the inferior temporal cortex sends visual inputs directly to the OFC. Individuals react differently to items or images depending on their reward association. For example, OFC face-responsive neurons convey signals to one by sending different responses for dissimilar faces and expressions. This is also a method of reinforcement; an area of the OFC responds to face expression by signifying behavior should change. Somatosensory inputs (touch, pain, etc.) are sent from the postcentral gyrus; and the amygdala transmits signals to the caudal (“tail end”) of the OFC. The more pleasure and pain there is, the more OFC activity occurs. Patients with damage to the ventral part of the frontal lobe may feel pain, but report that it does not feel very bad (Rolls, 2004).

As it is clear to see, the OFC takes care of many important functions by combining sensory observations and the reward system, among other things. As a result, when this area of the brain is damaged, many behavioral abnormalities will arise. Inappropriate behavior and emotional changes are imminent, as seen in the Phineas Gage case. Patients will become more impulsive, along with performing worse with stimulus-reinforcement associations. They typically show greater unprovoked emotions of anger and less unwarranted happiness. Also, their sense of time is impaired. In my opinion, the impulsive nature they display may partially be attributed to their belief that time is moving faster (Berline, Rolls, & Kischka, 2004). Misinterpretations of others’ moods, lack of initiative, and unconcern or underestimation of the gravity of a situation are all side effects that hinder patients’ relationships and every day lives. Frontal lobe damage can cause patients to be unable to plan or correct certain behaviors, though they can verbally express the right course of action (Rolls, 2004). Individuals that have lesions on their dorsolateral prefrontal cortex display problems with spatial working memory, unlike people with damage to the OFC (Berline, et al., 2004).

The ability to respond to social reinforcers and the reward system are an essential part of any primate’s life. Not knowing how to respond to facial expressions on someone can be hazardous. What an OFC patient might consider to be a joking expression may be anything but that. Some patients also have problems with voice recognition, but both face and voice recognition problems do not always occur together. “Bilateral surgically circumscribed (but not usually unilateral) lesions of the human orbitofrontal cortex produce deficits in a probabilistic version of a visual discrimination reversal task with monetary reward (Rolls, 2004). For instance, when a person is gambling and receives money, the medial OFC is activated; when a person loses money, the lateral OFC is activated. In a person with normal OFC activity, a person will have better control when gambling because his or her OFC alerts the individual to be aware of the dangers of losing. Someone with damage to this cortex may not have any apprehensions when betting and any bad feelings when losing (Rolls, 2004). Believe it or not, even bladder control is related to the OFC. Patients with bladder control problems show little activity in this area when their bladders are full, compared to individuals with normal activity (Swyers, 2006).

Many patients with mental disorders have abnormal activity in their OFC. Unsurprisingly, research has revealed that patients with bipolar disorder, which has characteristics of extreme mood swings, have abnormalities in several brain areas that control emotion. The amygdala and hippocampus are smaller in both children and adults, which suggests that even though symptoms may not progress until a later time, brain changes are an early feature in this disorder. Frontal areas of the brain, such as the OFC and anterior cingulate also show abnormalities. These irregularities may be caused by a gene known as BDNF, which produces a factor involved in the development of brain structures. When bipolar patients were depressed, the activity in the OFC was extremely high; when the patients were manic, the activity was very low. This occurrence makes sense because patients with OFC damage are impulsive and easily agitated, much like manic bipolar patients; whereas, people that had an overly active OFC would most likely be overly emotional (Bipolar 2003). Another great reference site for this phenomenon is located at http://www.neurotransmitter.net/bipolarpfc.html; it reports many studies dealing with the aforementioned topic. In post traumatic stress disorder, the amygdala and associated areas are activated by traumatic stimuli. The OFC is less capable of inhibiting the activation; and the activation of the amygdala, along with neurotransmitter and endocrine activity, produce many of the symptoms in PTSD (Excerpt, 2005). Patients with obsessive compulsive disorder show heightened activity in the OFC and anterior cingulate gyrus. The hyperactivity of these areas cause excessive signals to be sent to the basal ganglia; which in turn, causes patients to report a feeling that something is wrong (Gladding, 1999).

In conclusion, the orbitofrontal cortex and frontal lobes play a vital part in regulating our emotions and behaviors. Though unfortunate, the accident that Phineas Gage was involved in provided an important building block for research of this brain area. Many disorders show abnormal orbitofrontal activity, and further research is sure to explore this fascinating structure.
References:

1. Berlin, H.A., Rolls, E.T., Kischka, U. (2004). Impulsivity, time perception, emotion and reinforcement sensitivity in patients with orbitofrontal cortex lesions [electronic source]. Oxford Journals, 127, 1108-1126.

2. Bipolar Disorder and the Brain. (2003). Society for Neuroscience. Retrieved February 5, 2006, from http://apu.sfn.org/content/Publications/BrainBriefings/bipolar_disorder.htm

3. Excerpt from Posttraumatic Stress Disorder. (2005). Emedicine. Retrieved February 7, 2006, from http://www.emedicine.com/med/byname/posttraumatic-stress-disorder.htm

4. Carlson, Neil R. (2004). Physiology of Behavior, 8.

5. Gladding, Becky. (1999). Neurobiology for Obsessive-Compulsive Disorder (OCD). Westwood Institute for Anxiety Disorders. Retrieved February 7, 2006, from http://www.hope4ocd.com/research/schwartz1299.html

6. Larner, AJ & Leach, JP. (2002). Phineas Gage and the beginnings of neuropsychology [Electronic Source]. History of Neurology & Neuroscience. ACNR, Vol. 2, No. 3, 26.

7. Rolls, Edmund. (2004). Convergence of Sensory Systems in the Orbitofrontal Cortex in Primates and Brain Design for Emotion [Electronic Version]. The Anatomical Record Part A, 281A, 1212-1225.

8. Swyers, Jim. (2006). Overactive Bladder Related To Orbitofrontal Cortex Activity. Retrieved February 7, 2006 from http://www.medicalnewstoday.com/medicalnews.php?newsid=36593

Sexual Intercourse, Emotions, and the Frontal Lobes

 

When initially posed the question of whether or not sexual intercourse in humans could take place without emotional processing, I assumed the answer was yes. How can prostitutes have sexual relationships with many people everyday and have emotional feelings also? What about porn stars or swingers? Before this discussion, I would not have hesitated in saying that these individuals do not have emotional ties while having intercourse (at least not all intercourse), but my view has significantly changed.

Erections and ejaculation are controlled by spinal reflexes. Even men that have spinal damage (where the spine is disconnected from the brain) can reach an erection and become fathers; though they could not have an orgasm, or be conscious of the fact that they were erect without visual or verbal confirmation (Carson, 2004, 331). Extensive research has led me to the conclusion that only in rare cases, such as the example just mentioned above, or in the case of an unconscious rape victim, can an individual be a participant in sexual intercourse without an emotional response. Even holding this opinion, I can not intelligently state that human sexual intercourse could take place without emotional processing. At least one partner would have to exhibit an emotional response to the physical process.

 

A plethora of hormones and brain areas interact to control sexual functions. Testosterone, estradiol, androgen, and progesterone are hormones involved in sexual functioning. One hormone, oxytocin is released in both males and females during orgasm, to facilitate contractions of muscles in the sexual organs. The medial preoptic area, the sexually dimorphic nucleus, the medial amygdala, and areas of the limbic system, along with various other areas of the brain, play a role in sexual functions. Most areas of the brain involved in sexual processing are larger in males than in females. Studies have shown that these areas in male transsexuals are around the same size as females, and that the areas in male homosexuals are significantly smaller as well. Also, in a study with male rats, it was found that maternal stress reduces the size of the sexually dimorphic nucleus, and that these males had more feminine characteristics. Researchers of a twin study reported that if one identical male twin was homosexual, the other twin had a 52% chance of being concordant, while fraternal twins only had a 22% chance; in females the percentages were 48 and 16, respectively. The previous findings support the theory that sexual preference has a genetic basis, rather than sustaining the idea that they “chose to be” that way (Carlson, 2004, 309-340).

When studying the biological areas responsible for sexual functioning, it is almost impossible to miss the fact that most of these areas also control emotional functioning. For example, studies have shown that amydgala activity increased in humans when watching an erotic film, opposed to a normal video (348). In one study, men were asked to respond naturally when watching an erotic film. The men were sexually aroused; and consequently, their amydgala, hypothalamus, and other areas of the limbic system showed increased activity. When asked to detach themselves from the video and not become aroused, the men were able to do so. In this case, rather than having increased activity in the limbic system, the activity occurred in the prefrontal cortex (354). This supports the theory that emotional responses can increase or suppress sexual responses.

Though physical symptoms can cause sexual impotency, a lot of problems are psychological. For example, individuals with schizoid personality disorder are found to be emotionally cold and detached. They have a detachment from social relationships and find difficulty in taking pleasure in few, if any, activities. Thus, they rarely show interest in having sexual intercourse with another individual (Stroup, 2002). The basis for this stems from the fear of having an intimate relationship with someone. Most adults with schizoid fears have an underlying attachment disorder due to an insufficient mother-infant relationship (Alperin, 2001). Generally, sexual dysfunction is caused by a response to something else and does not lie completely in the genitals. Stress, relationships, and learning are all contributing factors. Sexual responses can start in the body, mind, or emotions; but three break points can occur to inhibit the response. First of all, inappropriate stimulation or pain can cause a negative response. Secondly, anxiety, pressure, self-consciousness, or any other negative emotions can reduce sexual stimuli. Lastly, sometimes one’s mind is too busy to become relaxed enough for arousal to take place. All of these situations are common, and will have a diminishing affect on sexual enjoyment. Even premature ejaculation could be called an “emotional disorder,” because it can be treated by helping a man to learn how to control his feelings and response time. Accordingly, compulsive sexual behavior, more often than not, can be controlled by behavior modification therapy (Ramage, 1998).

Multiple Sclerosis is thought to be an autoimmune disease of the central nervous system. The name comes from the effects of the disease- myelin is lost in multiple areas, leaving sclerosis (scar tissue) in its place. In regular human brains, myelin protects nerve fibers and allows them to function correctly. In patients with Multiple Sclerosis, the electrical impulses of the nerves are disrupted, which causes many symptoms. Regular exacerbations occur in 85% of people with this disease, and are essentially “flare-ups”, or severe declines in neurological functions. One study, in the Archives of Neurology, discussed research of the occurrence of acquired sexual paraphilia (extreme abnormal sexual behavior) in patients with M.S. Sexual dysfunction, which includes erectile and ejaculatory dysfunction in men, poor lubrication and the inability to reach orgasm in women, and diminished libido in both sexes, is typical in patients with M.S. Patients in this study showed quite the opposite symptoms, including hypersexual behavior and paraphilias. All were found to have various focal brain lesions. One man in the study displayed inappropriate sexual activity during an exacerbation, consisting of an irresistible desire to touch women’s breasts. Neuroimaging was used to discover lesions in the right sides of the midbrain and hypothalamus, stretching into the right sides of the substantia nigra, the red nucleus, and the internal capsule. Significant evidence was presented that acquired sexual paraphilic behavior in patients with M.S. results from inflammatory demyelination that involves the septal and hypothalamic regions of the basal forebrain (Frohman, Frohman, & Moreault, 2002). This study supports the theory that when areas of the brain responsible for emotional processing are damaged, abnormal sexual responses will occur.

In conclusion, there is a thin line between emotions and sexual stimuli in humans. For most animals, intercourse is a primal instinct used to further their species by reproduction and is impossible outside of the ovulation period. In contrast, human intercourse is not only important to further our species, but also to tie a physical act with the need for emotional intimacy with a partner. Psychological disorders, more often than not, have an effect on sexual enjoyment. Many areas of the brain, chiefly sections of the limbic system, play an important part in the emotional and physical aspects of sexual intimacy. Emotions are a vital part of normal sexual processes, and to separate the two functions is not only rare, it is nearly impossible.

References:

1. Alperin, Richard. (2001). Barriers to Intimacy: An Object Relations Perspective [electronic version]. Psychoanalytic Psychology, Vol. 18, Issue 1.

2. Carlson, Neil R. (2004). Reproductive Behavior & Emotion. Physiology of Behavior, 8, 309-372 .

3. Frohman, E., Frohman, T., & Moreault, A. (2002). Acquired Sexual Paraphilia in Patients With Multiple Sclerosis [electronic version]. Archives of Neurology, Vol. 59, No. 6, 1006-1010.

4. Ramage, Margaret. (1998). Management of sexual problems [electronic version]. ABC of Sexual Health, 317, 1509-1512.

5. Stroup. (2002). Personality Disorders. Neurobiology of Psychiatry: Syllabus & notes. Retrieved February 11, 2006 from www.med.unc.edu.

Memory Structures

 

Memory, an essential part of life and independence, is primarily stored in the cerebral cortex. The inferior temporal cortex stores visual memory; whereas, the frontal cortex stores associations. New declarative memories, involving facts and events, are formed in the hippocampus and related structures in the medial temporal lobe (Myers, 2005). The entorhinal cortex supplies the majority of the information that is sent to the hippocampus (Carson, 2004). Some researchers believe that the hippocampus is similar to a temporary holding cell and memories slowly seep into the permanent storage area of the cerebral cortex. This process could be compared to an inbox; once the inbox is full, items are archived into a different area. On the other hand, the majority of researchers believe that the hippocampus does not store information, but instead is needed to help create new memories (Myers, 2005). Carson agrees with the latter, and that the hippocampus inputs information from the sensory and motor cortex, processes the information, modifies the memories, and links them together in ways that can be more easily remembered (Carson, 2004).

The amygdala plays a vital role in memories of an emotional nature. Someone with amygdala damage may be able to remember details of an event, but will forget emotional information (memory). The right prefrontal and bilateral hippocampal gyrus, which surrounds the hippocampus, is associated with visual (picture) memory; while word associations are connected to the left prefrontal and left hippocampus gyrus. The left hemisphere of our brains is responsible for encoding memories, and the right hemisphere is in charge of retrieving memories. Medial temporal and midline diencephalic processing, composed of the thalamus and hypothalamus, control the consolidation of memories; which, as a result, enables long-term memory processes to occur (Long, n.d.). Bilateral anterior lesions on the thalamus can cause permanent amnesia, while posterior lesions do not normally cause a noteworthy problem. The severity of anterior thalamus damage can affect both hippocamal and perirhinal pathways (because of the location); and in turn, disrupt the “transmittal” of memory from one area to another. For example, one well known case involves a man that has had amnesia since 1960 due to a brain injury. The patient’s verbal memory was destroyed, but he has no problem with other cognitive functions. Even as far back as 1988, researchers were able to produce evidence that lesions in the dorsomedial nuclei and the hippocampal tracts cause a memory disorder. The location and extent of the lesions determined the severity of the memory deficit. Accordingly, left-sided lesions produce verbal memory loss, while right-sided lesions produce memory loss of a visual nature (Ringholz, 2000).

The caudate nucleus, located in the lateral ventricle of the brain, regulates the organization and priority of information sent to the frontal lobes. Individuals with Huntingdon Disease often have many memory difficulties due to damage of the connection between this region and the frontal lobes. Unlike patients with Alzheimer’s disease, patients with HD cannot learn or recall motor memories, so their speech is often slurred; stuttering is common; and body movements are also uncontrollable. They can recall memories, but not find the right words to express them. Also, they can remember experiences when given choices to pick from and benefit from cues- exactly the opposite of patients with Alzheimer’s disease. Without organization, memories only matter so much. Memory problems in HD can be compared to reading a book where the pages or words in a sentence are all out of order. Everything is there, but it still does not make any sense. Even though these individuals can understand what someone is saying, response time is extremely slow due to the brain’s “search mechanism” being damaged. Actions that were almost “unconscious” at one point, such as driving or walking, will now become very difficult because intense concentration will be required (Cognitive, 2004).

Memory, unlike many of the brain’s functions, is something that most people (especially students) think of from time to time. Not being able to recall someone’s name or an important piece of information can be very embarrassing or frustrating, to say the least. Damage to areas such as the hippocampus, amygdala, thalamus, and caudate nucleus can cause memory problems. Memory is so complex that memory loss is actually “specialized”. Some people may have trouble with short-term memory, while other people have trouble with long-term memory. The organization of memories or even creating new memories may be impossible. My memory is not “the best”, but I feel fortunate that I can at least put sentences together, remember what I ate last, and recall vital information. Without these traits, life would be much more difficult and confusing.
References:

Carlson, Neil R. (2004). Learning and Memory: Basic Mechanisms. Physiology of Behavior, 8, 411-450.

Cognitive Symptoms X1. (2004). HOPES. Retrieved February 15, 2006 from http://www.stanford.edu/group/hopes/diagnsis/cognitiv/x1.html

Long, C.J. (n.d.). Memory. Retrieved February 12, 2006 from http://neuro.psyc.memphis.edu/NeuroPsyc/np-ugp-memory.htm

Myers, Catherine. (2005). Memory. Memory Loss and the Brain. Retrieved February 12, 2006 from http://www.memorylossonline.com/glossary/memory.html

Ringholz, George. (2000). Summary and Discussion: Patient #44. Baylor Neurology Case of the Month. Retrieved February 15, 2006 from http://www.bcm.edu/neurology/challeng/pat44/summary.html.

Mind or Memory Transfer: Is it a Possibility?

Mind transfer has been a popular fictional theme of many movies, but the more technology progresses, the closer this theme gets to becoming a reality. Because of the fact that so many natural chemicals already function to enhance, sustain, or transfer memory in the human brain, the concept of actual mind transfer is not new. Scientists have been researching the possibilities for over a century now. In 1908, Charles Guthrie, an American scientist, “made” a two-headed dog by removing the head from another dog’s body and connecting blood vessels. Though the additional head had gone without oxygen for too long to properly function, it did exhibit basic reflexes such as blinking. Forty-three years later, Vladimir Demikhov attempted to duplicate the experiment more rapidly, so that damage would not occur in the additional brain. Believe it or not, it worked; but the additional head was quite aggravated and bit the other head’s ear off. Another problem also existed: the immune system rejected the new tissue, and the dogs would die. By the 1960s, this problem was also solved with immunosuppressant drugs, still currently used in human organ transplants (Weir, 2004). Furthermore, in 1962 Psychologist James McConnell discovered evidence supporting the theory that untrained flatworms could acquire knowledge through the consumption of trained worms. Other experiments have led researchers to believe that memory can be transferred by injecting brain extract from one animal (rats or mice) to another (Chemical, 1968).

The subject of mind (or memory) transfer is very controversial for many reasons. First of all, scientists have had trouble reproducing results from other studies. For example, in 1969 Paul Pietsch and Carl W. Schneider performed a study involving brain transplantation of salamanders in hopes of supporting previous indications that suggest memory transfer is possible. They inserted brains from trained salamanders into the coelomic (body) cavities of untrained larvae. Even though some increased performance was displayed in the transplant animals, no evidence of memory transfer was found. The salamanders had to be trained in order for the enhanced performance to take place. This does not meet the criteria of “true” memory transfer, which would consist of automatic knowledge without training (Pietsch & Schneider, 1969). Even after these disappointing results were publicized, Pietsch and Schneider, along with other scientists, did not discard the idea. By 1970 “head transplants,” or White’s preferred terminology “full body transplants,” had been successfully conducted on primates. Fourteen years later, Dr. Robert White felt the techniques he used in these operations were advanced enough for human subjects (Weir & Human, 2004, 1988).

The second obstacle is trying to transfer someone’s mind without the actual brain. For starters, the brain already moves memories and information on a continual basis. As far as we know, it is not a static set of neurons that can be replaced with an alien set of data. Synaptic connections actually evolve to fit a set of experiences. Even if we were able to transfer someone’s brain into a robot’s body, the limitations of that brain would still be there. The process of transferring memories is even more problematic. Because of the brain’s constant and high-speed activity, building a static model of one’s brain would not be adequate. Also, memories are not as simplistic as a video tape. They are an individual’s personal outlook on past experiences. No matter what the situation, the same question asked by an interviewer almost always results in a plethora of unique answers. Sure, the same concept might be there, but the way a person remembers the situation is different. By applying this way of thinking to the notion of memory transfer, one can see the potential dilemma. Even if a piece of “memory” is transferred into someone’s head, that person’s perception of the recollection might be completely unique. Also, gaining instant knowledge could trigger a type of overload to the brain (prohibiting vital functions), drastically change an individual’s personality, and cause numerous other problems. The question of whether or not an individual will still be the same “person” is debatable; but in my personal opinion, doubtful (Phillips, 2000). Finally, some of the most gifted individuals including, but not limited to: Woolf, Beethoven, Tolstoy, Van Gogh, Newton, Michelangelo, Churchill, and even Abraham Lincoln, suffered from mental illness. Would this instant knowledge also bring about “craziness”?

The only way the aforementioned question could be brought to any kind of supported conclusion is through experimentation; everything else is nothing but speculation and personal opinion. Hence, the third (and most challenging) obstacle arises: ethics. Ethical dilemmas are prevalent in many every-day medical procedures. The more knowledge humans gain, the more open most people are to new ideas. Nevertheless, cloning of any living organism or even using stem cells in the umbilical cord blood later in life are highly-debated topics. Even if we were able to transfer memories from one human to another, experimentation must take place on humans to perfect the technique. This would be dangerous, and have serious moral considerations, even if individuals willingly agreed.

If one discards the moral issues and complications involved in memory (or mind) transfer, there are several techniques that could be utilized. Taking multiple over-lapping holograms of memories and placing them on a single molecule, which is then inserted in the brain, is called hologramic theory. This concept came from evidence that even organisms without brains (such as bacteria, etc.) store memories on molecules (Pietsch & Schneider, 1969). Another idea is to form an MRI image of an “open skull,” while magnetically and electrically recording movement by movement neuron pulses. A program would then be made, “fine-tuned”, and copied to brain tissue. An alternative would be to connect the corpus callosum to computer cables and upload/download information (Phillips, 2000). Serial sectioning, or slicing, freezing, and scanning layers of the brain, is yet another idea. The scans could be combined later on, and uploaded to an artificial brain or a human’s brain by combining other techniques (Burton, 1999). If cell-sized machines could be transplanted in one’s brain, artificial neurons could possibly be formed and inserted into the brain in place, or in addition, of/to the neurons already there (Jacques, 2005). Various alterations on these theories exist, and I am sure as research progresses, knowledge and thoughts will only increase.

As you can see, transferring memory or the “mind” has many complications and moral issues with it. I personally believe that one day it will indeed be possible. The further technology grows the closer we become. Many theories have already been publicized and similar research has been done for over a century. What will this emerging technology do to the human race as we know it, if it is finalized? It is hard to imagine all the positive possibilities, along with all the dreadful outcomes that could occur. Who knows, a future clone of mine could remember writing this discussion…Almost scary, isn’t it?

References:

Burton, Brent. (1999). Automated 3D Reconstruction of Neuronal Structures from Serial Sections. Retrieved February 18, 2006 from http:// research.cs.tamu.edu/bnl/pubs/burton_thesis.pdf

Chemical Transfer of Fear [electronic version]. (1968, April 19). Time Magazine, Vol. 91, No. 16.

Human Head Transplants. (1988, Sept.). New Zealand Anti-Vivisection Society. Mobilise, 22.Retrieved February 18, from http://www.nzavs.org.nz/mobilise/22/print/6.html

Jacques, Robert. (2005). Scientists Fret over nanotech breakthrough. Retrieved February 18, 2006 from http://www.vnunet.com/vnunet/news/2137318/scientists-fret-nanotech-breakthrough

Pietsch, P. & Schneider, C. W. (1969). Brain transplantation in salamanders: an approach to memory transfer [electronic version]. Brain Research, 14, 707-715.

Weir, Kirsten. (2004, Dec. 3). Getting a head: who will volunteer for the first head transplant? Current Science. Retrieved February 18, 2006 from http://www.findarticles.com/p/articles/mi_m0BFU/is_7_90/ai_n8589469

Phillips, Winfred. (2000). Chapter 4: The Mechanism of Mind Transfer. In The Extraordinary Future. Retrieved February 18, from http://www.mind.ilstu.edu/published/Phillips/PhillipsCh4.html

Theoretical Orientation: Carl Roger

 

When doing research on different psychological theorists, some of the ideas (especially older ones) were shocking to me. I have read several books on insane asylums. I do not mean psychiatric hospitals; I mean asylums of decades ago. Scientists once believed that anything from nearly drowning patients to pulling out all of their teeth could cure individuals with psychiatric illnesses. I am sure that to most people these theories probably sound bizarre, but before psychology was an accepted field of medicine, they were every day occurrences.

I find Carl Roger’s theory of personality to have the most relevance in conjunction with my career goals in the field of psychology and helping others in general. Roger’s theory, often called “person-centered”, is a humanistic personality theory that evolved from his work as a clinical psychologist. Rogers believes humans have a tendency to develop attributes that will enhance themselves and move them closer to autonomy, the process of formulating one’s own morals and personal law. He thinks that this tendency can be suppressed, but not destroyed. I agree with this part of his theory to an extent. I do believe that most individuals form their own set of morals. Even many serial killers have their limit. For example, child rapists are normally not welcome in jail. They may be surrounded by criminals, but most people do not take kindly to child abuse. On the other hand, I do believe there are individuals that are so deranged or mentally ill, that they have no morals or guilt what-so-ever (Pescitelli, Analysis 1996).

The second part of Roger’s theory involves something he calls the “phenomenal field”. This field is composed of all the experiences (conscious and subconscious) the individual has undergone and is what we base our “self” picture on, or more simply put, who we are. He believes that along with the self-awareness aspect is the “need for positive regard from others” and “the need for positive self-regard”. “Conditions of worth” are formed when parents base love on a child’s action (conditional love) and can be very damaging (Pescitelli, Analysis 1996)

The reason why I chose the “person-centered” theory is because of Roger’s therapy concept. He believes that a therapist should not disagree or point out contradictions; instead, he or she should free a person by removing obstacles so the person can become independent and self-directed. The therapist has to “have unconditional positive regard for the client as well as show emphatic understanding”. The therapist must be genuine, but he or she is not expected to be perfect. He or she should accept his client’s personal self-worth regardless of his feelings, condition, or situation he or she is in (Pescitelli, Rogerian 1996).

Though I do not agree with everything about Roger’s theory, I think that, for the most part, it is a great guide to structure a psychology career around. Carl Roger was known to be a gifted clinical psychologist. He took a huge step by recording his sessions so others could study and learn from them. I strive to have the emphatic understanding he did and to have genuine respect for my future clients.

1. Pescitelli, Dagmar. (1996). An Analysis of Carl Rogers’ Theory of Personality in Personality & Consciousness. Retrieved January 16, 2006, from http://panda.ca/?cat=carl_rogers&page=rogerian_theory

2. Pescitelli, Dagmar. (1996). Rogerian Therapy. Retrieved January 16, 2006, from http://panda.ca/?cat=carl_rogers&page=rogerian_theory

Applying the Taxonomy in Practical Discussions

 

Using the basic tenets illustrated in Bloom’s Taxonomy is essential for being a productive critical thinker. First, one must have a general knowledge of the information he or she is researching. If one does not know what different terminology means, how will one understand the subject matter? Also, being aware of past theories and studies of the topic is vital when striving to form a valid hypothesis from new information obtained.
Bloom describes knowledge as remembering previously learned information. Recalling statistics, lists, and views are only a few examples of obtaining sufficient knowledge. One must be able to understand the information he or she gathers. What good is memorizing results for past studies if no insight is gained from them? If one can explain past theories or studies in a way that others can understand, then he or she most likely has a proficient comprehension of the subject matter (Bloom, 1956).

Without application of the knowledge learned, obtaining a plethora of information will serve no purpose. One must use the previously learned information to solve new problems, preferably in new situations where results will be easily illustrated. For example, repeating a past study that already has a solid conclusion in the exact manner as before will most likely do little good. Unless some aspect is altered or the first experiment was publicized incorrectly, the results will be the same. Also, using an inanimate object to study human behavior would not provide accurate, if any, results (Bloom, 1956).

After the new study is done, the results must be analyzed in the proper manner. Past generalizations should be compared, along with possible motives and causes. Diagrams, correlations, or illustrations should be utilized in processing the information. As mentioned above, information that is not put to use is futile. Once the researcher comes to an educated conclusion, the experiment results must be put to use in some manner. Why do animal research studies on cancer, only to find a cure and not utilize it in treatment?
Even once this information is applied to practical situations, it should be evaluated. The FDA does not allow a new medication to be placed on the market without thorough testing, application, and follow-up. Most medications undergo years of evaluation before being released (Bloom, 1956).

All of the following steps aforementioned are equally important in the critical thinking process and should be utilized when doing research. The first step I use in writing a paper (or posting) is to relate the discussion question to current knowledge I have. Even if I am not familiar all aspects of the question, I try to link the main topic to something I am familiar with. For example, in one class I was asked to discuss the motor cortex and its 4 tracts. I knew little about the motor cortex, but was aware it was part of the brain in the cerebral cortex; this led me to the conclusion that it most likely controlled movement in the body. Once researching the issue, many terms were difficult to understand. I looked up anything that was confusing in the dictionary or other sources, sometimes looking up words in, not only the first definition, but also subsequent definitions. Looking up definitions helps me to comprehend the information, as well as have proficient knowledge of the terminology. After collecting the information I need, I compared different studies and tried to make an easy to understand explanation. Afterwards, I will use others’ evaluation of my paper to decide whether my conclusion was informative or lacking. If the paper was enlightening, I will use that information in further discussions and experiences.
Reference:

Bloom, Benjamin. (1956). Major Categories in the Taxonomy of Educational Objectives. Retrieved January 30, 2005 from (http://faculty.washington.edu/krumme/guides/bloom.html)

Understanding Attachment Disorders in Children

(Click above to see the story behind the picture) 

An article entitled Understanding Attachment Disorders in Children was published by the Center for Family Development. This article explains the reasons why the attachment system in an infant-mother relationship is as important as feeding and reproduction in human survival. For instance, a baby’s self-worth comes from the attention his mother bestows on him. If the mother does not respond to his or her cries, the child will feel he or she is unworthy of attention. I found this article interesting and of importance because it helps to explain the problems children encounter when not given the proper attention as an infant, as well as ways to counter the problems once they exist (Center, 2005).

First, to understand attachment disorders, one must understand the concept of attachment bonds and affectional bonds. Affectional bonds consist of five basic tenets. Bonds must be persistent and involve a specific person who has no substitute. The relationship must be emotionally significant; and the individual who develops the affectional bond must want to stay in contact with the other person, incurring sadness when unwilling separated. Normally an individual has many affectional bonds. A sixth condition is required for a true attachment bond to be formed; an individual seeks security and comfort in the relationship. Babies usually have more than one attachment bond, but have a single preferred attachment. For example, when a mother responds to her baby’s cries, a strong affectional bond develops between the pair. This is said to be the building block for a child’s relationships later in life. Young babies will cry, reach for, or cling to their mother when hungry, tired, frightened, or lonely. Toddlers normally see their mother as a secure “place”. They tend to wander off to explore, but often look back for eye contact or call out to hear their mother’s voice. By the time a child is four, they are normally alright with separation, as long as it is agreed upon (Center, 2005).

Second, patterns of attachment must be understood. The way a mother responds to a child’s needs for help, attention, or protection determines the quality of the child’s attachment. As mentioned above, a true attachment bond involves security. If safety is acquired, the bond will be secure; otherwise, it is insecure. The most used research method for measuring attachment, a procedure called Strange Situation, was utilized in this study. The child is taken away from the mother, given to a stranger briefly, and then reunited; with the child’s reaction being the deciding factor to classify the attachment as secure, avoidant, resistant, or disorganized/disoriented. Children that have a secure attachment actively seek contact with their mother, along with being distressed on separation or displaying less comfort with a stranger. The reunion of a securely attached child is a happy one and many times the child will not let go of the mother. Children with avoidant attachment will often ignore their mother when reunited and many times find more comfort in a stranger’s arms. Resistant children have mixed reactions. At first they may want contact, but then push their mother away or run away from her. Unlike avoidant children, they do not prefer strangers and stay angry at the stranger, along with the mother. Disorganized or disoriented behavior normally stems from a child finding their attachment frightening. They may try to avoid or resist their mother; or they may be confused or frightened by her. Many times mothers with disorganized or disoriented children fight violently with their partner, mistreat their child, or abuse alcohol (Center, 2005).

Now that an understanding of how attachment works has been created and different patterns have been identified, one should be able to understand attachment disorders. Reactive attachment disorder, as stated in the DSM-IV, is composed of emotional withdrawal, emotional promiscuity, and/or indiscriminate behavior and could be labeled as a “non-attachment disorder”. Most often children with this disorder have not had one main attachment to depend on, so they do not know how to become attached even as adults with children of their own. If they have emotional promiscuity, they try to use their bodies to gain affection; whereas indiscriminate behavior might consist of latching on to a complete stranger as an attachment. Children with disordered attachment have a main attachment figure in their life, but do not have a normal relationship with them. Negative feelings about the relationship are expressed by the child through indirect means. For example, a child may comfort the mother instead of the other way around or do something that is extremely dangerous to his or her own well-being (Center, 2005).

Lastly, once attachment and associative disorders are understood, treatment must be administered. Cradling is one of the principal techniques for babies. This involves physically containing the child while making eye contact to build an emotional bond. If successful, the openness to attachment will transfer from the caregiver to the mother. Some therapists even encourage the older children to wear diapers and use bottles. This technique is based on the theory that attachment is a process that is developed from infancy to adulthood, and in order for a secure attachment to be established, children should regress back to that time. I do not know if I personally agree with this, but I could see some children needing the same comfort an individual should have as an infant. Dyadic Developmental Psychotherapy has been proven to be an affective treatment method for teenagers with trauma-attachment disorders. Infant-parent psychotherapy is another method that focuses on healing a parent’s emotional conflicts in relation to the child’s well-being (Center, 2005).

In conclusion, this article was well-written and helped me to better understanding attachment. By understanding the way attachment is formed, different patterns can be analyzed. Once patterns are analyzed, disorders can be understood. Treatment can then be fashioned through synthesis and should be evaluated for effectiveness. Using this technique to restore attachments in children with both non-attachment disorders and disordered attachments will give them a better chance to form successful relationships later on in life.

References:

Center for Family Development. (2005). Understanding Attachment Disorders in Children. Retrieved January 05, 2006 from http://www.center4familydevelop.com/understandingad.htm

*This can be located at:

Historical Role of Psychologists

<———Click on Me for More Pics of Freud

Defining the role of psychologists in history can be looked at as very simple or very challenging. Psychology in general has played a role in almost every aspect of our lives. From philosophy to geography, from sports to biology, even to the army, the workings of a psychologist are not far behind.

Years ago psychology was not a stand-alone discipline. It played a part in similar studies such as philosophy and even geography. For example, Anaximander, a Greek philosopher, organized a world map in 580 B.C. The world picture of the open universe replaced the closed view of the celestial vault (geocities). Plato stated that the brain is the mechanism of mental processes (387 BC), but was rebutted by Aristotle who stated the heart is the mechanism (335 BC) (allpsych).

It was not until 1821 that Rudolphi Burdach defined physiology as including the study of psychological matter; even so, psychology has played a huge role in the discovery of biology and physical wellness long before it was announced. As early as 1020, Avicenna formed the theory that three ventricles of the brain perform five functions: common sense, imagination, cogitation, estimation, and memory. Vesalius, a Belgian physiologist, started dissecting cadavers in 1543 and by 1616 English physiologist William Harvey was able to explain how the blood circulates. The total separation of body and soul was described in Passions of the Soul by Rene Descartes, the first modern philosopher. In 1774 Luigi Galvani used animal research to test stimulation of a frog’s muscles through electric pulse. An anatomy of the brain was displayed in the book Recherches sur le System Nerveux (1809) by Gall and Spurzheim. By the year 1848, French neurologist Jean-Baptiste Bouillard had come to the conclusion that speech disturbances come from damage to the left frontal lobe and dared to bet 500 francs that he was correct. Thirty-eight years later the British Medical Association listened as Victor Horsley told of a successful surgery for epilepsy. The list goes on, but as one can see, psychologists have played a huge role in the human physiology field (geocities).

In 1883 America began to accept the concept of psychology. John Hopkins University established the first American psychological laboratory. Psychology even intertwined with sports in 1894 when Philippe Tessie published an article about the psychological aspects of bicycle racing. The study of inheritance of human mental characteristics was publicized in 1904 by Karl Pearson. Psychology was even used in the application of legal problems four years later. By 1927 German officer candidates were not even allowed to join the army until a psychology examination had been conducted. Guess who made questionnaires a popular form of acquiring information? You guessed it, a psychologist- Francis Galton, the founder of differential psychology (geocities).

Psychology history can not be mentioned without introducing a few well-known individuals. Sigmund Freud is definitely one of these people. He introduced the concept of psychoanalysis in 1900. In 1913 John B. Watson begins the behaviorism movement (Pereira). Twenty-four years later the book Personality: A Psychological Interpretation by Gordon W. Allport helped to establish personality as a field of academic study. The fight or flight phenomenon was introduced by Walter B. Common in 1932. Finally, Abraham Maslow helped found humanistic psychology and the famous hierarchy of needs (allpsych).

As portrayed above, psychology was, and still is, an important part of our every day life. Human society would not exist without the brain; therefore, the mind will forever be a subject of interest and study.

References:
1. http://www.geocities.com/Athens/Delphi/6061/en_linha.htm
2. Pereira, Marcos. A Timeline of psychological ideas. http://library.thinkquest.org/C005870/history/index.php?id=timeline
3. http://allpsych.com/timeline.html

The”Two-Brain” Theory: Lateralization in the Separate Hemispheres

 

The human brain is asymmetrical in function, but is symmetrical in most structural aspects. Lateralization of the human brain is normally used to describe the asymmetrical functionality of the brain. Though the two sides of the body and brain are virtually mirror images of each other, the functionality of the two sides is partially unique, at the very least. For example, ninety percent of people are “right-handed”. The coordination in their right hand is far superior to the coordination in their left hand. Consequently, one arm or hand is almost always stronger than the other.

As far as the two hemispheres in the brain go, there is little similarity outside of structure; though the mind does strive for symmetry in some aspects. Individuals with obsessive compulsive disorder often have a fixation on things being symmetrical; for example, they will only walk on left-squares of the pavement or must have pictures on the wall perfectly aligned with one another. When this pattern is broken, the patient will experience severe anxiety (Hugdahl, 2005). Because the two hemispheres are functionally lateralized, nerve fibers in the corpus callosum serve as a method of communication between the two sides. Lesions in, or disconnection of, the nerve fibers can cause a person to behave as if he or she has “two separate consciousnesses”. Without this nerve connection, one side of the brain will not know what the other side is doing; hence, the “two-brain” theory was formulated (Cardoso, 1998).

It has been common knowledge for many years that the hemispheres of the brain are responsible for the functionality of the opposite sides of the body. It was not until a later date that scientists had an in-depth knowledge of the specialized functions unique to either the left or the right hemisphere. For instance, the left hemisphere is involved in language and rational tasks, while the right hemisphere is responsible for spatial relations and emotional responses (Cardoso & Hugdahl, 1998, 2005). By 1864, French neurologist Paul Broca discovered that when an individual has a lesion in the middle frontal gyrus of the left hemisphere, he or she will no longer be able to verbally communicate, but can understand when spoken to. This disorder is known as “Broca’s [expressive] aphasia.” Wernicke’s [impressive] aphasia, on the other hand, occurs when a lesion is in the left upper posterior area of the temporal lobe. The patient will have the ability to speak, but can not understand verbal dialogue (Hugdahl, 2005).

The study of epileptics has shed much light on brain lateralization, thanks to the initial research of Robert Sperry (Cardoso, 1998). In 1960-1970, Sperry conducted simple experiments on patients who had undergone surgery for epilepsy. By severing the corpus callosum, seizures can no longer spread from one side of the brain to the other (Hugdahl, 2005). The results of his study were so significant, that he received a noble prize for his efforts (Cardoso, 1998). Sperry placed individuals in front of a screen that had words projected on the left and right sides. He instructed the patients to focus their sight on a central point of the screen, so that any projection on the left would be interrupted by the right hemisphere (due to the ‘x’ shaped crossing of fibers from the eyes to the visual cortex). Amazingly, the patients would report they saw nothing when words were on the left side of the screen; whereas, when words were on the right side of the screen, they not only saw, but could also correctly identify them. Even in the first instance, the patients were able to pick up an item (placed outside their field of view) which corresponded to the words on the screen while using their left hand. How could someone be unable to see a word with their left eye, but be able to pick up the corresponding item with their left hand? The answer stems from the fact that the left hemisphere is responsible for verbal functions. Because the person saw the words with their left eye, the information was sent to be processed in the right hemisphere and then forwarded to the left-hand; since the information did not go through the left hemisphere, the person was not able to verbally express what they saw (Hugdahl, 2005).

Another intriguing finding, which adds to the “two-brain” controversy, is the asymmetry in structure and function of the two sides of the planum temporale. This structure, located in the upper posterior plane of the temporal lobes, is 30-35% larger in the left hemisphere than in the right. The left area of the planum temporale has broader spaced columns and more heavily myelinated axons, which indicate better connectivity per neuron and increased transmission speed, respectively. What makes this structure more intriguing is the fact that it is asymmetric in primates and humans only. Some researchers could hypothesize that humans and primates developed the essential structures for verbal processes, but that something went wrong in the primate’s evolutionary path. On the contrary, individuals opposed to the aforementioned theory could conclude that because chimpanzees do not communicate verbally, but have an asymmetric planum temporale, structure differences do not correlate with language functions (Hugdahl, 2005).

I have trouble making a solid stance on either side of the spectrum; my personal opinion is somewhat in the middle. On one hand, it seems as if the two sides of the brain are just that- two sides in one brain. Many studies have supported the conclusion that both sides are responsible for individual specialized functions. As commonly seen in stroke victims, when one side of the brain is damaged, many crucial human processes are no longer functional, as well as physical operations in an entire side of the body. Alternatively, language studies performed on individuals that had a complete hemispherectomy (or the removal of one hemisphere) differ greatly in children and adults. Even though adults seem to suffer from aphasia after a hemispherectomy, children under five years of age rarely suffer from this disorder. This could imply that language lateralization, though somewhat noticeable in children, does not have a profound effect until after puberty (Krashen, 2002); and that we are born with two separate brains that are capable of functioning independent from one another. Do the two parts of the brain “grow” to become dependent on one another as a person ages? As I stated previously, I am torn between both concepts. If one theory is ever agreed upon universally, I will be very shocked. There are very valid arguments in both cases and even though I might not be in complete agreement with either one, I know without a doubt I want to keep both of my hemispheres in tact!

References:

1. Cardoso, Silvia. (1998). What is Mind? Brain & Mind, No. 4. Retrieved February 20, 2006 from http://www.cerebromente.org.br/n04/editori4_i.htm

2. Hugdahl, Kenneth. (2005). Symmetry and asymmetry in the human brain [Electronic Source]. European Review, Vol. 13, No. 2, 119-133.

3. Krashen, Stephen. (2002). The Neurological Correlates of Language Acquisition: Current Research. In Second Language Acquisition and Second Language Learning, 72-82. Retrieved February 22, 2006 from http://www.sdkrashen.com/SL_Acquisition_and_Learning/076.html

Mental Help Net Website

Mental Help Net is a wonderful source of information for any psychologist or individual interested in psychological disorders. First of all, information about various disorders can be found, including, but not limited to: affective, conversion, childhood, dissociative, eating, impulse, and personality disorders. The news section on this website has well over two hundred different article categories about recent studies, and the majority of these categories have multiple links within them. This adds up to a plethora of information! Psychiatrists and psychologists alike can use this website to find out about break through treatments. Even social workers, school counselors, professors, or individuals in the forensic psychology fields can find important information here pertaining to their career. The large variety of resources provided makes this site even more useful to the common individual as well. One can find book reviews, advice columns, self-help groups, psychological tests, and phone numbers to all the pertinent foundations. In addition, links to different mental health communities are available. A job-seeker can search for positions in the health field, find out about license information, and how to continue their education. Someone wishing to promote their business can advertise on this site. This website has won multiple awards, and it is not hard to realize why. Over 325,000 unique visitors are reported to visit every month. This site is very well laid out, and a great tool for anyone that is interested in the mental health field.

Mental Help Net. (2006). Center Site, LLC. Retrieved February 23, 2006 from http://www.mentalhelp.net/poc/view_index.php?idx=about

Autism and DLD Lateralization

 

Lateralization of the two hemispheres is an important process in human brain development. Even so, it is hypothesized that excessive asymmetry can affect higher-order association mechanisms, such as those responsible for language processing. Similarities of asymmetry in autism and developmental language disorder (DLD) provide supporting evidence that above normal lateralization can affect average functioning in these individuals. This discussion will focus on a study conducted to examine the similarities and differences of brain matter and lateralization in children with autism and DLD compared to control groups. It should be noted that this is the first comprehensive whole-brain survey of volume lateralization in DLD and high-functioning autism (Herbert, Ziegler, Deutsch, O'Brien, Kennedy, Filipek, et al., 2005).

Disorder Summary and Hypothesis

Autism and DLD are disorders that materialize early in life and involve language impairment. Previous studies have shown evidence of large brain volume (primarily white matter) in children with autism. In addition, even though most DLD studies have leaned toward examination of language regions in the brain, entire brain analyses have exposed an increase in full brain volume as well. Researchers hypothesized that cortical components of neural systems with superior interconnectivity are more liable to be affected by large areas of white matter, and that these two disorders should exhibit volume asymmetry in the higher-order association cortex. Regions of the association cortex correlating to language functions were one distinct area of study, being that asymmetry reversal in children with autism has been noted in the language-associated cortex (Herbert, et al., 2005).

Subjects

The subjects of the study included 46 boys between 5 and 12 years of age whose primary language was English. Fifteen candidates were autistic, 15 had DLD, and 15 were controls. To make the study more evenly balanced, the three groups had an almost equal percentage of right-handed children (around 28 % a piece) and of left-handed children (around 6% a piece). Individuals with autism and DLD had performance IQs of 80 or above, but normal children were chosen on factors such as normal school performance, neurological exams, and development; and lack of seizures, head injuries, brain lesions, hearing or sensorimotor impairments, anticonvulsant medications, etc. opposed to IQ. This is one downfall of the study, but because the similarities of results in the autism and DLD groups (whose IQs were not dissimilar), and the fact that the control group displayed normal development and school performance, the results of the study should not be particularly biased (Herbert, et al., 2005).

Techniques

MRIs were conducted on participants and data was analyzed on Sun Microsystems workstations. Neuroanatomical segmentation was used to divide the brain into grey matter and white matter. The neocortical (dorsal region of the cerebral cortex) ribbon was parcellated (divided) into 48 primarily gyral-based sections (elevated areas) per hemisphere, also known as PUs. Sulcal patterns (grooves) were identified and labeled in multiplaner views to allow for markers to be tracked three-dimensionally. Anatomical markers for other anterior-posterior divisions of large gyral areas were also tracked. Volumes (amount of space occupied) were formulated by adding the voxels (quantity of 3D data) in each cortical PU (Herbert, et al., 2005).

Asymmetry analyses included examination of total brain volume, segmented divisions, lobes of the cerebral cortex, and individual PUs of the cerebral cortex. General linear models with multiple variables (multivariate) for correlated data were used to test for differences in asymmetry in the three groups. PUs were categorized according to their functional nature. For example, forty PUs were classified in the following groups: primary sensory and motor cortexes, unmoral association cortex, and higher-order association cortex. Subtypes of PUs were also identified, such as the planum temporale, inferior frontal gyrus, and the insula, to name a few (Herbert, et al., 2005).

Results

No significant dissimilarities in asymmetry were noted for any of the three groups when solely comparing total hemispheric volume. Even so, noteworthy differences in asymmetry between the groups were displayed when the hemispheres were segmented. Surprisingly, these increased morphological (structural) asymmetries were actually found in the control groups. These findings might lead one to believe that children with autism or DLD actually have greater lateralization in the brain, but asymmetry in cortical PUs was much higher in boys with autism and DLD opposed to control groups. Cortical volume was the largest in the autism group (41.7%), followed by the DLD group (32.6%), and the smallest in the control group (20.1%). The greatest right-asymmetrical volume was once again the most considerable in the autism group, followed by the DLD group, and then the control group. As far as the left-asymmetrical cerebral cortex goes, the DLD group had the highest volume reduction, followed by the autism group and control group, respectively. A highly noteworthy result of this study was the significant difference in asymmetry of the language-related cortical areas, which is the basis of asymmetry in the unimodal association cortex PU. While this has many implications, results of various studies have not consistently linked asymmetry in language regions to diagnosis. Atypical lateralization was discovered in many other PUs of the brain, with the autism and DLD group consistently showing greater asymmetry compared to the control group (Herbert, et al., 2005).

Discussion

The founders of this study hypothesized that the asymmetrical aspects of the brain in patients with autism and DLD are not the direct cause for language and functional disorders, but more of an underlying basis for the real root of the problem- the lack of connectivity between the hemispheres. Both groups have noted increased brain volume, but also corpus collossi that either grows slowly or decreases in size. Due to the fact the corpus collosum serves as the primary transportation mechanism between the hemispheres, this proportional abnormality may in fact result in interhemispheric constraints of information transfer. A collosal transfer insufficiency has already been recognized in cases of DLD. This deficiency increases the chance for greater functional lateralization and anatomical asymmetry. Perhaps the reason that both autistic and DLD children have language deficits, but do not have routine regional anatomical abnormalities is due to the fact that volume and white matter are links to underlying processing anomalies. The volume and white matter grow postnatally, and the increase is greatest in areas that myelinate later in life. This gradual growth increases the asymmetry and amplifies it over time. The arrangement of the nerve-cell bodies in the language regions of the cerebral cortex (cytoarchitecural organization) also appears to be associated with asymmetries in cortical processing deficits (Herbert, et al., 2005).

Conclusion

Asymmetry and rightward cerebral cortical lateralization has been discovered in autism and DLD. Researchers found supporting evidence that volume increases in white matter of the brain may be an underlying factor for the lack of interhemispheric connectivity leading to dysfunction in higher-order association areas, such as those involved in language processing. Some processes may be affected more so than others, as demonstrated in normal functionality of certain areas in individuals with autism and DLD (Herbert, et al., 2005). This study adds to examples in the text of individuals who have had their corpus collosum severed. Once the interhemispheric connectivity was broken, individuals often suffer from communication deficiencies. Also, Carlson notes that most verbal deficiencies occur when the left side of the brain is damaged (2004). The rightward lateralization in patients with autism and DLD may contribute to the language problems in these disorders (Herbert, et al., 2005). The posterior areas of the cerebral hemispheres are chiefly responsible for our having something to say, as stated in the text (Carlson, 2004). In this study, the DLD group had the greatest volume reduction in the left-asymmetrical areas of the cerebral cortex, which could also add to the language deficits in this disorder (Herbert, et al., 2005). The study described in this discussion contributes to our text by adding supporting evidence of the effects lateralization can have on language disorders.
References:

1. Carlson, Neil R. (2004). Human Communication. Physiology of Behavior, 8, 481-514.

2. Herbert, M., Ziegler, C., Deutsch, L., O'Brien, D., Kennedy, P., Filipek, A, et al. (2005). Brain asymmetries in autism and developmental language disorder: a nested whole-brain analysis. Brain, Vol. 128, No. 1, Pgs. 213-226.

What causes the receptor neurons to actually fire……..

There are two different types of sensory receptor cells, or hair cells, that fire. The first type of hair cell is cup-shaped and surrounded by an afferent terminal that forms a nerve group. The second type is clyndrical and is innervated by boutons, enlargements at the axon end that form synapses. Excitatory amino acids serve as neurotransmitters at the receptor cells (afferent fiber synapses). Both types of hair cells obtain synapses from the vestibular efferent fibers, which contain the neurotransmitters acetylcholine and calcitonin gene (a peptide). These efferent fibers regulate the sensitivity of the receptor and are activated by arousing or facial stimulations (Dickman, 2005).

The hair cells lie in the crista, a saddle shaped ridge in the ampulla (dilated region of canal). The first type of hair cells are concentrated in the middle of the crista, while the second type are more periphery in nature. The cupula, a gelatinous structure, emerges from the crista, covers the stereocillia, and attaches to the roof and walls of the ampulla. Here it forms a fluid-tight separation with the same density of the fluid in the membrane or endolymph. When the head is rotated, the endolymph is displaced, which causes the cupula to be pushed to one side. Accordingly, the stereocilia and kinocilium (microscopic hair-like processes that aid in moving cell) are thrust in the same direction. The otolith organs use the macula to hold the receptor cells; this structure is akin to the crista. The otolith stereocilia extend into the otolith membrane, which is covered by otoconia, calcium carbonated crystals. The crystals are about three times as dense the endolymph; therefore, they are not replaced by normal movement of the endolymph. Instead, head movements produce displacements of the otoconia, which in turn bend the stereocilia (Dickman, 2005).

The depolarization and hyperpolarization of the vestibular hair cells rely on the K+ character of endolymph and the K- character of the perilymph that stays immersed in the bottom of the hair cells. When the sterocilia is pushed toward the kinocilium, the potassium channels open. The K+ then flows into the cell by way of the endolymph and depolarizes the cell membrane. Once depolarized, the calcium gated channels at the base open, allowing Ca++ to enter. The Ca++ influx causes neurotransmitters to be released into the synaptic clefts; afferent fibers then depolarize and increase their rate of firing. Once the stimulus is over, the stereocilia and kinocilium return to their normal position, most calcium channels close, and potassium channels open. The K+ flows outward and returns the hair cell membrane to its resting potential (Dickman, 2005).

When the stereocilia is pushed away from the kinocilium, the potassium channels in the bottom areas of the hair cells open; K+ flows out of the cell into the interstitial space, resulting in hyperpolarization. This decreases the rate of neurotransmitter release, as well as the rate of firing of the afferent fibers. Most afferent fibers fire even when at rest. Consequently, some calcium channels stay open and constantly release neurotransmitters. As aforementioned, opposite deflections between the stereocilia and kinocilium cause opposing effects. The positioning of the hair cells play an essential role in controlling the direction of movement (Dickman, 2005).

References:

Dickman, David. (2005). Vestibular System Primer. Retrieved January 30, 2006 from http://vestibular.wustl.edu/vestibular.html.

Synaptic Transmissions and Drug Effects

 

Most individuals have taken one drug or another for different reasons. Most drugs are used to produce “healing” effects, while others are used for recreational purposes. To understand how drugs actually work, their affect on synaptic transmissions must be understood. Synapses are connections created with other neurons; the presynaptic terminal of one cell comes into contact with the postsynaptic terminal of another. The presynaptic terminal is part of the cell where a wave of activity is sent to the synapse junction, whereas a postsynaptic terminal is the area in which activity is carried away from a synapse. Dendrites are short fibers that resemble tree branches and stem from the cell body. They function almost like antennas by receiving information that is sent to the cell. Terminal buttons are small knobs at the end of axons (fibers that carry information away from the cell) which release neurotransmitters (Introductory, 2006).

Normally, information is received by the dendrites and sent through the cell body (soma) to the end of the axon, where the terminal button resides and the synaptic terminal is formed. The terminal button then releases neurotransmitters which travel to the presynaptic membrane and through the junction, or synaptic cleft, to the postsynaptic junction (made of a soma or dendrite), where they can bind with receptor sites. Once the neurotransmitters bind with the side of the synapse, the receiving cell is either excited (more likely to fire) or inhibited (less likely to fire). An action potential occurs when the cell is excited enough. When a cell sends information from an axon in one cell to the dendrite of another, an axodendritic synapse is formed (Introductory, 2006). Some dendrite membranes contain autoreceptors. When these autoreceptors become active, the dendrites and terminal buttons release neurotransmitters, which stimulate the same dendrites’ autoreceptors. Once stimulated, hyperpolarizations (changes in membrane potential) will be produced and neural firing will decline. This process keeps the neurons from becoming overly active (Carlson, 2004, 110).

Drugs can function as antagonists, whose function is to block synaptic transmissions; or as agonists, which promote synaptic transmissions. These two actions can occur in a number of ways. First, the transport molecules of synaptic vesicles can become blocked when molecules of a drug bind to an area on the transporter and inactivate it. Neurotransmitters are housed in synaptic vesicles, and they normally are released when their proteins come into contact with calcium. Because these sites are inactivated, the neurotransmitters never release; which causes an antagonist effect. In addition, some drugs can prevent the release of neurotransmitters from the terminal button by deactivating proteins, while others can bind with proteins to trigger the release of neurotransmitters. The first drug serves as an antagonist, and the second as an agonist. Direct antagonist or agonists work by binding with postsynaptic receptors. Direct antagonists prevent neurotransmitters from opening the ion channel, while direct agonists mimic neurotransmitters. These agonists attach to a site where neurotransmitters normally join and open the ion channels. Once the channels are open, ion flows through and produces postsynaptic potentials. Indirect agonists and antagonists produce the same results as direct agonists and antagonists; the only difference is that they are noncompetitive, meaning they attach to receptors with multiple binding sites. Some drugs selectively block presynaptic receptors. These drugs work as agonists by increasing the amount of neurotransmitters released; the opposite is true for antagonist drugs in this category- they lessen the amount of neurotransmitters released. A number of cells have presynaptic heteroreceptors. These heteroreceptors function by causing a domino affect; when one terminal button is activated, its activation then stimulates another terminal button. Drugs that inhibit heteroreceptors are antagonists, opposed to stimulators who are agonists. The dendrite autoreceptors, mentioned above, can also be affected when drugs bind to the autoreceptors. Antagonists activate these receptors, and agonists deactivate them. Certain enzymes destroy neurotransmitters; when molecules of a drug bind to these, an agonist reaction occurs because the enzymes can no longer block neurotransmitters. The same thing goes for reuptake agonists. When these agonists bind to the molecules responsible for transportation of reuptake, neurotransmitter effects are prolonged and receptors are stimulated. As you can see, drugs can affect synaptic transmissions in a variety of ways (Carlson, 2004, 573-599).

Most people have heard of an individual developing a tolerance to a drug. This is very common when someone takes a substance for a long period of time. The brain tries to compensate for the strange chemical reaction by producing opposite affects. Once this occurs, someone will have less sensitivity to a drug, and it will take more each time to produce the same reaction. Drugs such as cocaine can be very addictive, even though one does not build a tolerance to them. When dopamine is released, an individual will experience a pleasant sensation. This alone can cause someone to become addicted to a substance. A less common occurrence is that of sensitization. Over time and possibly even after one use, an individual can take less of a drug to cause a reaction or experience larger effects from the drug (Carlson, 2004, 573-599). Drugs such as amphetamine, morphine, and nicotine can result in long-lasting hyperactivity of dopaminergic and noradrenergic nerve terminals, or actually alter reactivity of certain nerve terminals. The alteration in nerve terminals may account for many characteristics of addiction and also sensitization (Vanderschuren, Schoffelmeer, Mulder, & Vries, 1999).

Synapse transmissions are responsible for brain and body functioning. Companies come out with new pharmaceuticals every day. Drugs can work by either activating or blocking certain synaptic transmissions. When these transmissions are activated, an agonist reaction occurs. When blocked, an antagonist reaction occurs. When people use drugs for an extended period of time, they will normally form a tolerance to the drug. Though less common, some drugs can actually cause sensitization, or a stronger reaction when taken repeatedly. Medications are an important part of modern medicine, but their use should be controlled or abnormal synaptic responses can occur.

**Note: There are two types of synapses- electrical and chemical, but this discussion focuses on chemical synapses.

References:

1. Carlson, Neil R. (2004). Psychopharmacology & Drug Abuse. In Physiology of Behavior, 8, 110 & 573-599.

2. Introductory Biological Psychology Tutorials. (2006). Athabasca University. Retrieved February 25, 2006 from http://psych.athabascau.ca/html/Psych289/Biotutorials/1/part1.html.

3. Vanderschuren, L., Schoffelmeer, A., Mulder, A. & Vries, T. (1999). Lack of Cross-Sensitization of the Locomotor Effects of Morphine in Amphetamine-Treated Rats [electronic version]. Neuropsychopharmacology, 21, 550-559.

Addiction and Opiates with a focus on Methadone

 

Opiates can be categorized as narcotics containing opium or natural hormones that produce similar effects. The use of illegal opiates can result in a variety of adverse reactions. The most common result is that of addiction. There are two main types of addiction, physical and psychological. By and large the two are closely related, but it is possible to have one without the other. The psychological need or desire for a drug is most commonly referred to as addiction, while the physical need for a drug is primarily due to the user forming a tolerance for the drug. When a tolerance is reached, the abuser must consume more and more of a drug to get the same feeling they had initially (Carlson, 2004).

Individuals abuse substances for many different reasons, but the majority of people take an illegal drug more than once due to positive reinforcement. By remembering the pleasant feeling the drug produced, the user is likely to desire that sensation again. Many people believe true addiction is caused by the unpleasant physiological responses that occur when someone attempts to stop taking a drug. For example, addicts who use heroin exhibit tolerance and withdrawal symptoms when they abstain from taking the drug. Heroin disturbs normal homeostatic mechanisms in the brain and, in turn, the brain produces opposite chemicals to compensate for the imbalance. Once the drug use is decreased or stopped, the brain continues to overcompensate for the prior drug effects. Being how the drugs are no longer providing opposite reactions of the brain’s overcompensating mechanisms, a balance fails to occur and withdrawal symptoms follow (Carlson, 2004).

When someone has a relapse, the primary cause is psychological, but physiological mechanisms play an important part in this process. After months or years of being drug-free, an individual may crave a drug because of the pleasant physiological effects that occur while using the substance. This supports the idea that psychological factors may play a role in physiological factors. During a relapse, the mesolimbic system of dopaminergic neurons is activated; without this system, relapse will no longer occur. Drug addiction causes long-term changes in the brain, specifically activation of the orbitofrontal cortex and anterior cingulated, while taking or craving a substance. Studies have found that addicts have lower activity than controls in the aforementioned areas while abstaining from a drug. Stress induced relapses also include both types of features. Psychologically, many individuals have relapses because they want to forget about their current situation, while physically the corticotropin-releasing hormone can trigger a drug craving when the individual feels stressed (Carlson, 2004).

Drugs that are highly addictive are normally fast-acting. For instance, heroin and morphine are both opiates that produce the same effect, but heroin effects occur much more rapidly (Carlson, 2004). For this same reason, Clonazepam has become more readily prescribed for anxiety disorders opposed to Xanax and Valium. It has a slower release time; therefore, it is not as addictive. This reason corresponds with psychological features. The body has the same physical “symptoms” with both heroin and morphine or Clonazepam and Xanax, but the positive reinforcement is greater in the fast-acting drugs.

When opiates stimulate receptors, a variety of effects occur. For instance, opiate receptors located in the periaqueductal (midbrain) grey matter account for analgesic effects. Hypothermia can be caused by opiate receptors in the preoptic area; whereas sedation occurs when receptors in the mesencephalic reticular formation (composed of parts of the brain stem in the midbrain) is activated. There are three primary opiate receptors known as mu, delta, and kappa. Mu and delta receptors play a part in reinforcement, while the kappa receptors produce unpleasant effects. Studies have shown without the mu receptor, morphine may not produce analgesic, reinforcing, or withdrawal symptoms. Kappa receptor agonists reduce the release of dopamine in the nucleus accumbens, much like in the opiate withdrawal process. Even though most studies have found that activation of the mesolimbic system for the purpose of releasing dopamine is essential in the drug reinforcement process, studies conducted on opiate use indicate that the release of dopamine is not necessary to reinforce behaviors in this drugs of this type (Carlson, 2004).

An interesting study conducted by the Department of Pharmacology and Experimental Therapeutics of the Louisiana State University Medical Center tested the effects of several drugs used in opiate treatment. One drug of interest is methadone, the most commonly used pharmaceutical in opiate dependence therapy. Methadone has the behavioral effects of opiates, such as heroin and morphine, but has a longer lasting duration. It actually accumulates with repeated use. Methadone is popular because of its previously mentioned long duration, as well as its oral availability and ability to prevent withdrawal. Drugs used in opiate treatment focus on regulating mu opiate receptors, though their pharmacologies are different; methadone is a narcotic. Some treatments use naltrexone, which works as an antagonist on mu receptors when narcotics are administered. Because of this, users can not get “high” by using other narcotics, even though drugs such as marijuana will produce behavioral results. Methadone utilizes mu receptor agonists to mimic effects of the addictive drug, and its molecules primarily bind to mu sites. In this study, methadone produced reversed naltrexone lever responses seen in other opiates such as alfentanil and nalbuphine. Previous studies have shown that this response is particular to the mu sites as opposed to kappa, delta, or nonopiates. It has been indicated in long-term methadone therapy that cross-tolerance of other mu agonists will develop (Brandt, Cabansag, & France, 1997). This study is important in illustrating how opiate treatments use agonists or antagonists to modulate opiate receptors.

Addiction has many psychological and physical correlates. Psychological correlates are based on the concept of positive reinforcement, while physical correlates are based on a drug’s response to opiate receptors. Drugs used to combat opiate addiction may be of different pharmacologies, but the basic mechanism is the same- the regulation of opiate receptors. Hopefully, further research of specific opiate receptors will bring about more effective treatments for drug addiction.
References:

1. Brandt, M., Cabansag, S., & France, C. (1997). Discriminative Stimulus Effects of l–Acetylmethadol (LAAM), Buprenorphine and Methadone in Morphine-Treated Rhesus Monkeys [electronic version]. The Journal of Pharmacology and Experimental Therapeutics, Vol. 282, Issue 2, 574-584.

2. Carlson, Neil R. (2004). Drug Abuse. In Physiology of Behavior, 8, 573-600.

Methadone Info

 

Methadone is an opioid agonist and works by “filling up” the opiate receptors. We naturally have a certain amount of opioid receptors in the brain and narcotics work by filling up a certain percentage of the receptors to produce that “high” feeling or reduce pain. The larger the percentage, the larger the effect. Methadone helps in the treatment of opiate addiction (most often painkillers and heroin) because taking other narcotics actually decreases the effects of methadone. For example, some drugs increase opiate receptors. When this is done, the methadone takes up a smaller percentage of receptors, and the effects are not nearly as strong. Methadone users will say that cocaine “eats up” their methadone, and will request a higher dose to feel the same effect. Unfortunately, this is normally the case in methadone overdoses (Woods, 1997). Methadone is a highly controlled substance (you normally have to go a specific pain/detox center to receive it) and is usually administered in the clinic daily until a person becomes addicted to the substance (so they won’t sell it on the street). Eventually though, they will let the patient take their doses home on the weekend and sometimes during the week. If a person has several doses of methadone available and shoots up heroin, for instance, they will feel as if they need more methadone (because they won’t be able to feel its effects any more), and possibly OD.

Methadone is used because of its long lasting effects and the blockage of other drugs I just spoke about. Excess methadone “stores up” in the liver and blood stream, so it usually works for around 24 hours. There is much controversy with this drug though. To be honest, even though it has benefits, I do not agree with this particular treatment program. For one thing, methadone is addictive (just like heroin) even though it doesn’t cause potential health problems that illegal drugs do. In addition, the withdrawal period from methadone can be much worse than heroin. The symptoms may not be as severe, but whereas someone could physically detox from heroin in less than two weeks, it could take over a month for methadone. Even though methadone clinics are fairly common, detox “help” for this substance are not. Patients must get down to an almost inexistent dose of methadone on their own before they can be hospitalized, and then it is a very painful and trying experience. Unfortunately, the majority of methadone users either never get off the drug, or they combine other drugs to get more of a high. Unlike heroin or morphine which would decrease the effects of methadone, benzodiazepines (anti-anxiety drugs) such as valium, clonazepam, or xanax increase the effects of methadone.

Reference:

Woods, Joycelyn. (August 1997). Narcotic Blockade [electronic version]. Methadone Today, Vol. II, Issue 8.

Consciousness

 

I would have to agree with the opinion that both sides of the brain are conscious. I have trouble understanding how only one side of the brain, the hemisphere that controls verbal communication, could be completely responsible for our self-awareness. What about mute individuals? They have no verbal communication, but can express themselves in many other ways, while conveying the same message you or I could. Also, only a handful of animals use verbal communication. Are they the only non-humans that have consciousness? Speaking is a wonderful tool we humans use to communicate, but by all means not the only one. In my personal opinion, it is more of a convenience then a necessity.

Monist Vs. Dualist

If I were just looking at the definitions for monism and dualism, I would probably find myself leaning toward the popular view of monism. After actually reading about what these views entail, I would say I was a dualist. I agree with Amy Bankovic and her discussion topic (u01d1 Consciousness, Jan. 4, 2006). It is very hard for me to believe in any kind of higher-being and also call myself a monist. I think there are many unexplainable events in life, whether they are fate or “out of body” experiences. Though I have never seen ghosts and would not call myself a believer of extraterrestrial existence, I do believe that many things in life can not be defined. For instance, take love, willpower, or happiness and try to explain what “causes” those feelings. You can not specify a physical body function for feelings. What makes one personal happy or gives him or her the willpower to go on might make another person miserable. In summary, I do consider myself a dualist.

Animal Research Rebuttal

I do agree with the point that we need to work on eradicating animal research, but I still feel strongly that unless a law is made, it will never be completely stopped. I think doing so would be detrimental to the human society. You mentioned that polio has virtually disappeared, but do you know why? You got it, animal research. In the 1940s, scientists injected the polio virus into mice and monkeys to replicate the virus. By the 1950’s, the polio vaccine had been administered. Over two million cases of polio have been prevented because of animal research. You can find information about this on the Research Defense Society’s website (http://www.rds-online.org.uk/pages/page.asp?i_ToolbarID=3&i_PageID=42, 2006).

Don’t get me wrong, I love animals and hate to see anything suffer. Think about it though- human testing still goes on. Please note: human testing is done on a volunteer basis, so the ethical dilemma is not comparable to that in animal testing, but it is still needed. While we should have a goal to eliminate as much animal testing as possible, new problems are always going to arise; therefore, I believe animal research is always going to be needed.

Perception

 

I do agree with the opinion that "a mind will see what you want it to see". I think that this point relates to so many things in life. Some people can not see the bad in people, while others can not see the good. Both people are looking at the same thing, but perceive it differently. This applies equally for the mental and physical world. Pain, beauty, and length of life are all based on both physical and mental factors. For example, even though people have many reasons for living a long life, they say individuals who have a strong will to live can conquer many illnesses modern medician cannot.

Animal Research Ethics

I agree with you that animal research is acceptable as long as it is for good purposes. When it comes to saving millions of lives (or even a handful to be honest), I think that it is correct decision to make. However, animal testing that is administered to formulate items such as shampoo or mascara that are serving no purpose other than making us look good is morally wrong in my opinion. The positives need to out way the negative.

Opioids and alchoholism

 

I have read various studies regarding opioids and alchoholism. Scientists know that there is certainly a relationship between the two, but still have much more research to do on the matter. If you go to the website http://www.medicalnewstoday.com/medicalnews.php?newsid=17819, you will find an entire article about the topic entitled Genetic difference at opiate receptor gene affects a person's response to alcohol.

Robert Swift, on the the author makes the following comment:
"The inheritance of alcoholism is complex," said Swift, "and there are certainly more genes, still undiscovered, that are involved in alcoholism. The search for these genes is an active area of investigation and well worth pursuing. Understanding the genetic basis of the response to alcohol and how it may predict risk for the development of alcoholism could be used as a kind of genetic counseling to help individuals at risk. Persons carrying a risk gene, if they are made aware of it, may be able to alter their drinking and reduce their risk of developing alcoholism."

Relationship between Social Rejection and Physical Pain

 

I personally did not come up with anything factual on the relationship between social rejection and physical pain relating to opioids. I did do some research on the subject after reading your post, but found little evidence, though many opinions were readily available on the web. (maybe I didn't search hard enough) Regardless, I know there is a correlation with social and physical pain. Stress can do a number of things to you. Unfortunately, I have learned this first hand. When I get "too" stressed out or extremely upset, I get headaches and many times even vomit. Not a pretty site I know, but the link is still there. On the other hand, I have a high threshold for physical pain, yet a fairly low threshold for "emotional" pain. As I stated before, I honestly believe there is a strong connection between the two, but defining that definition seems to be fairly difficult. How can one thing (meaning a neurotransmitter) regulate two related types of pain in different ways? I am not saying it is impossible by any means, but it seems to be strange considering that opioids either excite or slow down other neurotransmitters.

Amygdala damage

I find it very interesting that damage to the amygdala could cause individuals not to recognize fear or emotions in others. It would make since to me that the person could not experience fear themselves, but you would think they could still see a person's expressions and understand the concept.

ADHD and ADD

 

I was not surprised at all to find genetic factors influence ADHD and ADD. From reading various other studies, it seems that most mental disorders do have genetic ties, though other factors are involved also. Though I have seen some diagnoses for ADHD that I thought were premature, I do not think teachers should be chastised for bringing the subject up, as many individuals do have the disorder. This helps confirm my opinion that mental disorders are hereditary.

Lazy Eye

 

The condition of lazy eye can cause a permanent decrease in vision that can not be corrected with glasses, contacts, or lasik surgery. If detected early (hopefully before the age of two), simple treatments such as eye drops, glasses, or patching can be very effective. The longer you wait, the bigger the chance that a cure will not be possible. Even so, treatment done before the age of seventeen can normally help to increase vision and should be attempted.

Lazy eye is not due to any eye disease and affects three percent of children under the age of six. Normally (but not always) it only affects the vision in one eye. A constant turning of the eye (strabismus) can cause lazy eye, but an eye that only turns part of the time rarely is the cause. Other causes include different vision/prescriptions in each eye or blockage of an eye. If you did not notice the problem yourself, don't feel bad. Parent and child alike are unaware in many cases. Consequently, lazy eye is the number one cause of vision loss in individuals under the age of forty.

**Wearing an eye patch is one of the oldest and simple treatments for lazy eye (along with some other visual disorders). It forces your weak eye to do all the work, which strengthens it, much like any other muscle in the body.**

Reference:
Cooper, J. & Cooper, R. (2005) All About Amblyopia.

Retrieved January 25, 2005 from http://www.strabismus.org/amblyopia_lazy_eye.html.

Color Vision & Evolution

I do believe that our color vision evolved for a purpose; whereas it did not in some animals because they do not need it. When reading about this topic, I think about the early chapters in the book that discuss Darwin and evolution. Supposedly, most of the "features" that we humans have (including walking upright and using our hands for other things, etc.) come from our need of those certain functions.

Though I am not a big fan of Darwin's theory that we evolved from "apes", many of his theories on the reason for why we able to "do what we do" make sense. I saw something on the news a few days ago about a dog with 2 legs. Here comes the amazing part- he had learned to walk upright. I don't mean just take a couple steps….truly walk upright like a human. He had to adapt to the current situation that we was in. He did not have four legs to move on like most animals, so he used the two he had. The owner said he began walking one day when another dog took his bone (or toy) and has been walking ever since.

Luxury of Color Vision

Being able to see color is a luxury that most of us take for granted. Imagine trying to drive at night if you are color blind. If it is raining or snowing heavily, the only way I can stay on the road is to look at the yellow line. I can't even turn into my street (though I know the way by heart) without color; the red reflectors on the side of the road alert me to turn.

Motion Sickness, Heridatory or Not?

 

Knowing how the vestibular system truly functions is intriguing. I experienced motion sickness myself quite severely when I was younger, as did my sister. I always assumed that I just “out-grew it”, but reading studies about the topic has made me realize my vestibular system most likely learned to adjust to the movement. I always wondered why closing my eyes or sitting the front seat helped to alleviate the problem. Now I know this is because motion sickness often comes from your eyes seeing one thing, but your body feeling something else. I still can not ride an intense circular ride at the fair or on a winding road without feeling queasy, but I definitely have been thankful for the improvement. Unfortunately, my mother still has problems riding in a vehicle if she is not driving. This makes me wonder if “motion sickness” is partially hereditary.

Chronic Pain

 

I have experienced this myself, and it is not pleasant at all. I had a shooting pain from my neck down my arm. The first time this occurred, it went away after a month or so. The second time it occurred, a couple years later, it did not go away for over a year. I guess that I am lucky though- many people suffer with this for the rest of their life. I had an MRI done, several nerve tests, along with other procedures. I went through psychical therapy for months to no avail. The last physician I visited eventually put me on prescription pain pills in high doses. This did not completely relieve the pain, but made it manageable until it finally “went away”. He told me that he believed I felt psychical pain, but the root of the problem was in my head. At first, I was offended; but later on I came to the realization that he was probably correct. Once your body feels pain for so long, it seems that your mind expects it. The pain will be mimicked even when the psychical problem is gone.

Bauman and Memory Loss

Bauman spoke on the memory loss problems. You can find more information about him at http://www.hearinglosshelp.com/director.htm. He has dealt with life-long hearing loss himself and wrote many books on the subject. The exact quote is listed below:

Unlikely as it seems, vestibular damage can cause memory problems. Here is why. When you damage your vestibular system, keeping your balance is now largely a conscious effort, not the automatic effortless procedure it once was. Consequently, those areas of your brain that you once just used for thought and memory, now must constantly work on keeping you balanced. As a result, your memory may suffer. You may grope for words when talking. You may easily forget what is being spoken about during a conversation. You may be easily distracted. You may have difficulty comprehending directions or instructions. You may have trouble concentrating and may feel disoriented at times (Bauman 2003).

Here are a few other websites you might want to glance at:
http://brain.oxfordjournals.org/cgi/content/abstract/128/11/2732
http://www.onbalance.com/clinical_info/BalanceControl.aspx
http://thedizzylounge.com/

I am not advocating the above sites, but they do discuss the topic of damage to the vestibular system causing memory problems.

Four Major Motor Tracts

 

I did struggle immensely with trying to decide which tracts were the four major ones. I am very familiar with the side effects of anti-psychotic medications. Even so, I am embarrassed to admit I did not think about them when researching this topic . Anti-psychotic medications are wonderful at helping control mania and delusions, but in increased doses, can cause severe motor loss. If I am not mistaken, I remember reading a few articles pertaining to patients on Risperdal for extended periods of time. Many of them developed slurred speech and “drooled”, even once taken off of the medication. I have actually seen this first hand in someone that did not have a mental disorder and was giving the anti-psychotic Geodon. It was someone close to me and was a very frightening experience; they became like a zombie. It took them her weeks to recover from the medication's effects after she was taken off of it- even though she was on it for less than a month. Thank you for mentioning this correlation. It really helped me make practical sense out of the study of the motor cortex.

Apraxia

 

Apraxia is normally used to describe a disorder where individuals can not follow motor commands, though the reason is not due to a motor deficit or language impariment. The actual "planning" of the task is the problem. If a patient was asked to perform a simple task such as brushing his or her hair, the action he or she actually performed would only slightly resemble the action. Being that people with this disorder have a normal understanding of other things along with a normal motor exam, it makes the disorder hard to understand. There are many types of apraxia; the type previously described is called ideomotor apraxia. Other forms of apraxia can affect the mouth and face, distal limbs, or even the entire body. The term apraxia is often used in many different contexes; for example, constructional apraxia is used to describe an inability to draw complex figures (Blumenfeld, 2001). Ideational apraxia describes a disorder where an individual has problems doing a series of actions, though he or she can accomplish the individual actions successfully. It is still unknown if these disorders are actually related in some way (National, 2000). In conclusion, my understanding of the disorder is that it is not so much that the individual's actions are rigid, but that the patient is unable to perform the action correctly.

References:

1. Blumenfeld, Hal. (2001). Apraxia. Neuroanatomy through Clinical Cases. Retrieved February 2, 2006 from http://www.neuroexam.com/content.php?p=9.
2. National Academy of Neuropsychology. (2000). Apraxia. Behavioral Neuropsychology. Retrieved February 2, 2006 from http://nanonline.org/nandistance/mtbi/ClinNeuro/apraxia.html.

Sleep Terrors, Why does Age Matter?

 

I am certainly not an expert on dreams, but I never thought that dream content changed that much between different ages. I guess I have never seriously contemplated it, but if someone asked me I would have thought dreams had more to do with what is going on in one’s life then someone’s age. I wonder if this has anything to do with the reason children have sleep terrors, whereas adults do not?

Too much sleep..

I believe someone can get too much sleep. I know from personal experience if I sleep for too long I feel horrible in the morning, much like I feel when I don't sleep at all!

NO2

I actually tried to find an explanation for why the NO2 would make you tired, but did not see one. Most people have few sides affects (aside from nausea or stomach problems). I am sure there is some reason though. I have seen this happen myself when I tried to take some diet pills, (for energy) and they made me exhasuted; though they made my co-worker hyper. Strange how the body works sometimes…..

Narcolepsy is Scary

When reading about narcolepsy, I thought about how awfully scary having this disorder would be. Even if you didn't drive, can you imagine being in a strange place around some "not so trustworthy" people? Falling asleep could cause you to be easily robbed, or allow for the possiblity of something far worse. Even cooking could be dangerous. Deep frying a turkey could be disastrous if you left it unattended for a few minutes. I feel so fortunate I do not have this disorder!

Insomnia, Direct or Indirect Disease?

 

I do think that the majority of insomnia cases are caused by other factors, but not every case. Studies have shown that insomnia has a higher concordance rate in identical twins then fraternal twins. In my opinion, this suggests that some genetic factor plays a role. Though an extreme example, fatal familial insomnia certainly is a genetic disorder, in which the thalamus degenerates (Akroush, 1997). Also, sleep apnea is a form of insomnia and has genetic factors along with the environmental stressors. An example of this can be found at http://jap.physiology.org/cgi/content/abstract/99/4/1600 (Patel, 2005). Of course this is just my personal opinion, and I am sure articles can be found stating that genetics do not play a role in insomnia.

References:

1. Akroush, Ann. (1997). Fatal Familial Insomnia. Case Studies in Virtual Genetics 1996-1997. Retrieved February 5, 2006 from http://www-personal.umd.umich.edu/~jcthomas/JCTHOMAS/1997%20Case%20Studies/AAkroush.html

2. Patel, Sanjay. (2005). Shared genetic risk factors for obstructive sleep apnea and obesity [Electronic version]. Journal of Applied Physiology, 99, 1600-1606.

Age and OFC damage

I could be wrong, but I honestly do not think that age (significantly) matters. Reason being, individuals with damage to the obitofrontal cortex have trouble responding to the "reward system". It is not that their memory is damaged, but that they are not able to realize what negative or postive consequences will result from an action. Past experiences (for instance, when I did a, a good thing occured; but when I did b, a bad thing occured) do not seem to "stick" with them. Because of this, I do not think that age would matter that much. Just my opinion, of course.

Attachment Disorders and Sex Drive

I struggled myself with trying to make the correct decision, but I think in the end you came to the correct conclusion. Even though sexually abused individuals may have differing reactions (an overactive sex drive opposed to a diminished sex drive), both are based on emotional responses. The same reasoning goes for individuals with damaged areas of the frontal lobe. The reaction may be different; but more often than not, one symptom will be the individual has an abnormal sex life. You might be interested on researching reactive attachment disorder. Children with this disorder (and adults, for that matter) often try to use sex to gain affection, because they never had an appropriate attachment figure in their life.

Reference:

Center for Family Development. (2005). Understanding Attachment Disorders in Children. Retrieved January 05, 2006 from http://www.center4familydevelop.com/understandingad.htm

 

OFC Research

 

I agree with the fact that future research will no doubt further our knowledge on what areas of the brain control certain emotions. I did want to note that we already have some knowledge relating to this. For instance, the amygdala controls anger. Also, in my post on the orbitofrontal cortex, I even went into detail about how different areas of the OFC control our response to different tastes; for example, one area responds to salt and another to sweets.

Erasing Memories…

I do believe that memory erasable will one day be possible. I actually think it might be somewhat simpler than adding memories. Even hypnosis, medications, or ECT can cause memory loss. The real obstacle, in my opinion, will be trying to isolate certain memories like in the movie you mentioned.

Erasing Memories in Children

Though a noble idea, I think this would also be a bad idea in most cases. What happens if the child later on realizes that everything they remembered was a lie? In a recent movie, “The Island”, clones actually had memories implanted into their brains. The confusion they felt was immense- and they were designed not to have emotion at all. I know the positive aspects are there, but you still have to consider all the predicaments that might occur later on. This goes for any memory removal, replacement, or addition……

Patient wins 2.4 million in a wrongful psychiatry lawsuit

 

The thought of the psychiatrist who implanted false memories in her patients head is extremely fascinating and creepy at the same time. I am glad she won the 2.4 million dollars. I believe she should have won more than that. How horrifying! It just makes you realized how dangerous memory implantation could be. If dishonest army officials (I am not saying the US, just in general) or even murderers were able to place false memories in one’s head, they could have a willing and vengeful army ready to kill on command. Placing false memories of horrible things happening to loved ones (or even yourself) would push many individuals over the edge.

Visual Memory Transplantation

I believe that if memories can be transplanted, the visual part would not be an issue. Different brain structures account for different “versions” of memory. In this case, the right prefrontal and bilateral hippocampal gyrus is responsible (as explained in my last post). I think that the major difficulty would come from the rapid movement of memories from one part of the brain to another and actually finding a successful and safe way to transmit the memories into the correct areas of the brain.

Part II:
I believe that if memories can be transplanted, the visual part would not be an issue. Different brain structures account for different “versions” of memory. In this case, the right prefrontal and bilateral hippocampal gyrus is responsible (as explained in my last post). I think that the major difficulty would come from the rapid movement of memories from one part of the brain to another and actually finding a successful and safe way to transmit the memories into the correct areas of the brain.

Also, though I know what you were getting at with your example of abused women, I do not completely agree with you. Yes, many abused women do start to feel as if the abuse is their fault, but I do not think the problem is as much having false memories as it is a self-confidence issue and a desire to be loved and make the abuser happy. I have seen this first hand and experienced it without the physical aspect. The stress one is under can cause the individual to have problems thinking critically, but normally once the person is separated long enough from the abusive partner, they will realize that what happened was not their fault. Of course, therapy may be needed and many women never recover because they keep falling for abusive men. I could be completely wrong about this, of course; and even if I am not, this type of mind control is similar to the effects false memories could produce.

Transplanting Memories in People

I cannot see much good coming from transplanting memories in people who have not experienced something. Sure, I could name good things, but everything seems to have an even worse consequence tied with it. I am normally all for technology- I received my bachelor’s degree in Computer Information Systems. If this theory becomes a reality though, I think human manipulation has probably gone a little too far for our own good.

Memory Transfer- Amazing and Scary

It is amazing and scary how far technology has come. I was even more surprised that the first "two-headed" dog was formed in 1908. I am very open minded about many things, but I don't think I could even advocate mind/memory transfer. I may not be religous as some, but the possible of being "immortal"-at least in the sense of one's mind never dieing- is something that I think should only occur in the movies.

Personality Traits: In response to an article on “Left-brain thinkers”

 

I can believe some of the personality traits you mentioned could possibly correlate to one hemisphere over the other, such as being verbally inclined or doing well at math. On the other hand, traits such as enjoying classical music, being a dog lover, and being able to think better while sitting down seem a little hard to believe. I would have to see further research to support these conclusions, as well as reasons explaining the “why’ before I could really understand the validity of these statements. Maybe I am just not open minded enough or am not using critical thinking to the best of my ability.

Aphasia

I thought it was interesting that "almost all right-handers and for about 1/2 of left-handers, damage to the left side of the brain causes aphasia." It is amazing how much lateralization can affect brain processes.

(Aphasia is a disorder that results from damage to language centers of the brain. For almost all right-handers and for about 1/2 of left-handers, damage to the left side of the brain causes aphasia. As a result, individuals who were previously able to communicate through speaking, listening, reading and writing become more limited in their ability to do so. The most common cause of aphasia is stroke, but gunshot wounds, blows to the head, other traumatic brain injury, brain tumor, and other sources of brain damage can also cause aphasia.)

Autism Rebuttal

 

It is interesting to discuss the language disorders these individuals have. I also found that the brain matures too quickly (in certain areas). I liked reading the information regarding synaptic transmissions. The researchers of the study I posted had the opposite hypothesis that this disorder most likely does not occur from one or two genes, but rather from many different genes and factors. I enjoy reading opposing views. In my opinion, it just further displays the complexities of psychological disorders in general. Very few of the studies I have read have shown a clear picture of what causes the disorders, though many hypotheses are out there.
Reference:

Herbert, M., Ziegler, C., Deutsch, L., O'Brien, D., Kennedy, P., Filipek, A, et al. (2005). Brain asymmetries in autism and developmental language disorder: a nested whole-brain analysis. Brain, Vol. 128, No. 1, Pgs. 213-226.

Drug Sensitization Resources

I found quite a bit of information on drug sensitization. Here are some resources on the subject. The first reference is pretty simple, the second two are studies (quite complex, though), and the 3rd is a powerpoint presentation.

1. http://www.utexas.edu/research/asrec/dopamine.html
2. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12663081&dopt=Abstract
3. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12000017&dopt=Abstract=opera

 

Agonists and Antagonists

It did seem very complicated at first, but the more I read, the more I realized almost everything has a "positive and negative". Agonists have "positive" results on neurotransmitters (whether directly or indirectly) and antagonists do the opposite.

Speed, Addiction, and Tolerance

 

Addiction may lead certain people to OD, *but* when you need more and more of a drug [physically] to get the same result, you do build up a tolerance. You can think of "addiction" as a psychological effect (such as people wanting a cigarette even though they have not smoked in years) and "tolerance" as a physical addiction. The body needs more of the drug to function "normally" and in tolerance the "mind" wants more of the drug. Your friend probably built up a tolerance to the drug- that is why she took more and more of it. You might want to check out this website regarding speed: http://www.dancesafe.org/documents/druginfo/speed.php. A good example of this (to me) is web addiction. You would be surprised how many resources and help lines are out there for this! Some individuals are actually "addicted" to the web…but of course they haven't built up a physical tolerance for it!

Emotions

I believe that dealing with your emotions is one of the most difficult, but important aspects of a person's life. Most of my life I have let my emotions control me in a negative way. This may be one of the main reasons that I chose the field of psychology. I feel as if I am growing in the fact that I can look at situations in a more objective manner than in the past. I can function much easier in the professional world and with my personal life.

The Constructivist Model for Learning by B.F. Skinner

 

The Constructivist Model for Learning was popularized by B.F. Skinner and is based on the idea that people learn the most by building their own knowledge through reflection. The process of learning is facilitated through cognitive structures that the learner already possesses, which are in constant development. To accept the constructivist model, the individual also has to agree with the methods of learning and pedagogy (preparatory training or instruction) (ncrel).
I chose this model because I feel it represents the way I learn the best. Though we humans can definitely learn new things, I think we have to use, whether consciously or subconsciously, our past and present experiences to be able to fully comprehend what we are studying. Text books use this method repeatedly by giving real-life examples to illustrate the lesson that is presented. It is so much harder to learn if you can’t relate what you are learning to something that you are already familiar with. Another reason I chose the Constructivist Model is because it encourages researching and exploring new ideas along with present knowledge to find the most accurate way of thinking. Also, rather than taking the traditional classroom approach, students following the model are more inclined to use critical thinking to come up with their own solutions opposed to memorizing information.
I plan on using this model as a point of reference for my education, along with my every day life. I’m embarrassed to say that I did not soak up half of the knowledge that I could have gotten from my bachelor’s studies. I went straight from high-school to college, and in turn set a goal to get out as quickly as possible instead of getting as much as possible from the experience (ncrel).

(B.F. Skinner)

Reference site: http://www.ncrel.org/sdrs/areas/issues/content/cntareas/science/sc5model.htm

Mind over Matter

I agree with your statement of "mind over matter". Though growing up in a good home or being financially stable certainly helps, a person’s will is what makes him or her who they really are. I also think that the pharmaceutical side of psychology is very interesting. Having a doctor that is not experienced or superb in prescribing medication, especially psychiatric medication, can be the most destructive incident in a patient’s life.

Accepting Others

Accepting others is an important quality to bring to the field of psychology. If you judge others because their views are different then yours, then you will never be able to look at things in an objective manner which is essential to helping people. Every individual is unique and we all have our strengths and weaknesses.

Technique vs. Compassion

I agree that so many psychiatrists or psychologists focus more on a technique or theory than on attending to an individual's personal needs. Rather than taking the time to get to know you, they want everything to have a textbook label and to follow a certain way of thinking. Study and technique are very important, but compassion plays an essential role in assisting others. We all have our good and bad moments, but people need to focus on the whole person.

Qualifications for a Psychologist in TN

 

The qualifications for a psychologist assistant in Tennessee are as follows:

-You must attend a regionally accredited university.
-A minimum of 1 year of graduate training in psychology is required, including a master’s degree from an accredited school. A degree should be based on a minimum of 33 hours of graduate semester hours not including practicum and field experience. In lieu of a master’s degree, an applicant may be considered for certification id they have completed 33 hours as a matriculated student in a doctoral program in psychology.
-The 33 hours must consist of the following: 3 hours on professional standards and ethics of the APA; 3 hours in Abnormal psychology or psychopathology; 9 hours in basic substantive areas of psychology (3 hours must be in substantive areas); 9 hours relating to application of psychology (must have 3 in cognitive/intellectual testing and 3 in formal personality testing); The remaining 9 hours can consist of substantive or applied course work, or thesis hours.
-You must attend at least 1 on-site supervised practicum in psychological assessment worth 3 hours of credit. (This is in addition to the 33 hours.) It must be a minimum of 300 clock hours with 75 of those hours in individual and group supervision.
-You must submit evidence of good moral character consisting of 3 letters of recommendation from HSP Psychologists.
-You must take a written and oral examination.

Extra qualifications to be a psychologist (in addition to the ones above):
-You must have a doctoral degree from an educational program which is listed in the latest edition of “Designated Doctoral Programs in Psychology” by ASPPB and CNRHSPP or a program designated as a professional psychology program by the APA unless you received your degree prior to 1982.
-If you are going to provide health services you must complete an internship that is at least 1 year and no less than 1900 hours in psychology. It must be approved by the APA or developed/administered by an internship center with membership in the APPIC.
-You must have 1 year of supervised postdoctoral experience (in addition to an internship). It must compose at least 1900 hours and the individual must have a provisional license. (unless the internship in at an approved TN site)

Child’s early development

 

I believe that a child's early development plays a crucial role in the way that he or she learns and interacts later on in life. For example, when infants are left in their crib to cry for extensive periods of time (as it often happens in some foreign countries’ adoption agencies) the child will not be able to form emotional attachments. They do not know how to love because they have never received love.

Ancient Psychology Theories

 

When doing research on different psychological theorists, some of the ideas (especially older ones) were shocking to me. I have read several books on insane asylums. I do not mean psychiatric hospitals; I mean asylums of decades ago. Scientists once believed that anything from nearly drowning patients to pulling out all of their teeth could cure individuals with psychiatric illnesses. I am sure that to most people these theories probably sound bizarre, but before psychology was an accepted field of medicine, they were every day occurrences.

Devout Christian Scientists

 

"Devout Christian Scientists do not use medications and usually eschew medical aid. They are opposed to vaccination, immunization, and quarantine for contagious diseases, although official church policy advises members to comply with state laws. A physician or midwife may be used during childbirth. A physician may also be used to set a broken bone if no medication is administered."

Reference:
Barrett, Stephen. (2005, Nov 14). Christian Science, a religion that practices faith healing. Retrieved January 23, 2006, from http://skeptically.org/spiritualism/id15.html.

Principles of Ethical Judgment as Listed in the APA

 

Principles of Ethical Judgment as Listed in the APA
A. Section 3.06: a psychologist should not take on a professional role if personal, scientific, or other interests could impair their objectivity, competence, or effectiveness.
B. Section 3.01: a psychologist should not discriminate against patients
C. Section 2.04: psychological practice must be based on scientific and professional knowledge
D. Section 2.04a: a psychologist should only provide services within the boundaries of their competence based on their education, training, supervised experience, etc
E. Section 9.01: a psychologist must base their opinions on information and techniques to substantiate their findings
F. Section 10.01: a psychologist must inform his or her patient if using a technique or procedure that have not been established, along with any risks or alternative treatments

References
Ethical Principles of Psychologists and Code of Conduct. (2002). Retrieved January 21, 2006 from http://www.apa.org/ethics/code2002.html.

Writing is Essential

 

I think that writing is one of the most important forms of expression. Many people communicate in different ways, some through music, some through art, etc. For me, writing is one of the easiest and best ways to express my true feelings. When I was in high school and going through a horrible depression, I wrote poems constantly. I had a book that I kept just for that purpose. Many times I would skip lunch and write instead. It helped me to release the hurt and pain I was feeling without hurting others in the process. When I wanted to move out of the house once I started college, my father objected and no matter how hard I tried to talk to him, it did not work. He would not listen to me. Guess what I did? Write. I was able to get through to him once I expressed my feelings on paper and he was able to read them without being able to interject his own feelings into the conversation. I said all this to say that I have learned many things about myself through journaling.

When I decided to major in Psychology, I had a very vague idea of what I wanted to do, but no solid plan to get me there. Being in this class and writing about my goals and ambitions have helped me to focus in on what I truly want to accomplish in a future career. I can look at my journal and take from it the reasons I want to go into clinical psychology and the obstacles I am going to face.

I see that I am already growing as a person and how to better control my feelings. Writing something in the heat of the moment and going back to it later on helps me to see my own faults in my personal way of thinking. When we are feeling a strong emotion, many times rational thinking is out of the picture. Writing it down and then reading it later once we are composed helps to see if what we were feeling was a true problem or something that could be put aside. I strongly believe that we have to choose our battles. Many times, I will write a letter to someone and wait until I have cooled off to deliver it. If I still think that is a reasonable position, I will present it. Otherwise, I will let it go.

For me, journaling is an important part of growing as an individual and a professional. I can see the mistakes I have made and learn from them. Writing down my educational and career goals have helped me to focus in on what I really want. Hopefully, I will learn from this experience and look back in years to come and smile (or possibly groan).

Men’s Emotions vs Women’s Emotions

 

It is stated that men were normally more rational and logical, while women were more relational and emotional, but that as they grow older they become more alike. I have never thought about that, but what do you consider the reason to be? In my opinion, I think that life experience has everything to do with it. If you have every noticed, most small children are extremely emotional. Even little boys tend to cling to their mother when they are upset; yet as they grow older, it is not “socially acceptable” for boys to be as emotional. As men grow older, they are not as concerned about what other people think and can more readily share their true emotions. On the contrary, I think that it is more acceptable for girls to be emotional, and as they grow older they grow more “callous”. I know this is a strange example, but I think of it in relation to feet. If someone is disabled and does not walk or an individual always wears shoes, his or her feet are going to be tender; whereas, if someone walks on rocks every day, they will be able to withstand much more pressure. I believe the same goes for many women. We tend to let our feelings intercede into all parts of our life, but eventually we tend to not let things bother us as much. Of course genetics and hormones (testosterone and estrogen) also play a major part in this. Plus, this is just my personal opinion.

Are there other types of treatment offered for attachment and associative disorders besides the ones mentioned?

 There probably are, but other research I have done has shown those methods to be the most popular. Here is a good link to look at in regards to your question: http://www.attachmentdisorder.net/Treatment_Links.htm.

What is the DSM-IV?

This is a classification of the disorder as referred to in the Diagnostic and Statistical Manual of Mental Disorders published by the American Psychiatric Association, the main diagnostic reference of Mental Health professionals in the US.

“There are two presentations of attachment disorders in the ICD-10 and the DSM-IV-TR classification systems. These are (1) inhibited type (or `reactive' according to the ICD-10) and (2) disinhibited type. The inhibited type of attachment disorder refers to a disorder where a child is unable to initiate and respond in a developmentally appropriate way to most social interactions (e.g. having ambivalent responses or being hypervigilant).
A child with a disinhibited type of attachment disorder would show no selection in his or her choice of attachment figures and may include attention-seeking and indiscriminately friendly behaviour (Attachment Disorders, 2003).”

References:

Attachment Disorders. (2003). Retrieved February 9.2006 from
http://www.nelmh.org/page_view.asp?c=15&did=1621&fc=019002

Gurian, Anita. (2002). Depression in Adolescence: Does Gender Matter?. Retrieved February 5, 2006 from http://www.aboutourkids.org/aboutour/articles/dep_gender.html#gender
The Adult Attachment Interview. (n.d.). Retrieved February 9,2006 from http://www.dur.ac.uk/elizabeth.meins/Aai.htm

The Adult Attachment Interview. (n.d.). Retrieved February 9,2006 from http://www.dur.ac.uk/elizabeth.meins/Aai.htm

What other types of research methods are used to measure attachment?

There are many research methods used, but the Adult Attachment Interview is one method used to used for adults with attachment disorders (the adult).

What are the 5 basic tenets of an affectional bond?

 

Here are the five basic tenets: Bonds must be persistent and involve a specific person who has no substitute. The relationship must be emotionally significant; and the individual who develops the affectional bond must want to stay in contact with the other person, incurring sadness when unwillingly separated.
In other words 1) a persistent relationship (not temporary); 2) must involve a significant person, with no substitute for that person; 3) must be emotionally significant; 4) must want to stay in contact; 4) feels sadness when unwillingly separated

Additional Attachment Disorder References

Ainsworth, M. D. S. (1989). Attachments beyond infancy. American Psychologist, 44, 709‑716.

Ainsworth, M. D. S. Blehar, M., Waters, E., & Wall, S. (1978). Patterns of attachment: A psychological study of the strange situation. Hillsdale, NJ: Erlbaum.

American Psychiatric Association (1994).

Diagnostic and statistical manual of mental disorders, fourth edition. Washington. DC: American Psychiatric Association.

Bowlby, J. (1969/1982). Attachment and loss: Vol. 1. Attachment. New York: Basic Books

Bowlby, J. (1973). Attachment and loss: Vol. 2. Separation. New York: Basic Books.

Bowlby, J. (1980) Attachment and loss: Vol. 3. Loss. New York: Basic Books.

Cohn, D. A. (1990). Child‑mother attachment of six‑year olds and social competence at school. Child Development, 61, 152‑162.

Fraiberg, S., Adelson. E., Shapiro, V. (1975). Ghosts in the nursery: A psychoanalytic approach to the problem of impaired infant‑mother relationships. Journal of the American Academy of Child Psychiatry, 14, 387‑422.

Fraberg, S., Lieberman, A. F., Pekarslry, J. H., & Pawl (1981). Treatment sad outcome in an infant psychiatry program: Part Q. Journal of Preventive Psychiatry, 1, 143‑167.

Freud, S. (1940). An outline of psychoanalysis. The complete psychological works of Sigmund Freud Standard Edition, vol. 23. London: The Hogarth Press.

Greenberg, M. T. (1999). Attachment and psychopathology in childhood. In J. Cassidy & P. R. Shaver (Eds.). Handbook of attachment: Theory, research. and clinical applications (pp. 469‑496). NY: The Guilford Press.

Greenspan, S.1. (1997). The growth of the mind and the endangered origins of intelligence. Reading, MA: Perseus Books.

Grossmann, K. E., & Grossmann, K. (1991). Attachment quality as an organizer of emotional and behavioral responses in a longitudinal perspective. In C. M. Parties, J. Stevenson‑Hinde, & P. Marris (Eds.), The place of attachment in human behavior (pp. 60‑76). New York: Basic Books.

Hughes, D. A. (1997). Facilitating developmental attachment: The road to emotional recovery and behavioral change in foster and adopted children. Northvale, NJ: Jason Aronson, Inc.

Keck. G., & Kupecky, R M. (1995). Adopting the hurt child Colorado Springs, CO: Pon Press.

Lieberman, A F. (1993). The Emotional Life of the Toddler. New York: The Free Press.

Lieberman, A. F., and Pawl, J. H. (1988). Clinical applications of attachment theory. In 1. Belsky, & T. Nezworski (Eds), Clinical implications of attachment. Hillsdale, NJ: Eribaum.

Lieberman, A. F., Weston, D. R., & Pawl, J. H. (1991). Preventive intervention and outcomes with anxiously attached dyads. Child Development, 62, 199‑209.

Lieberman, A. F., & Zeanah, C. H. (1995). Disorders of attachment in infancy. Child and adolescent psychiatric clinics of North America, 4, 571‑587.

Lyon-Ruth, K., Connell, D., Zoll, D., & Stahl, J. (1987). Infants at social risk: Relations among infant maltreatment, maternal behavior, and infant attachment behavior. Developmental Psychology, 23, 223-232..

Permission is required to copy articles for use beyond your personal individual use. ©2002, Center For Family Development. All rights reserved.

Lyons‑Ruth, K.. & Jacobvitz, D. (1999). Attachment disorganization: unresolved loss, relational violence, and lapses in behavioral and attentional strategies. In J. Cassidy & P. R. Shaver (Eds.). Handbook of attachment: Theory, research, and clinical applications (pp. 520‑554). NY: The Guilford Press.

Main. M., & Hesse, E. (1990). Parents' unresolved traumatic experiences are related to infant disorganized attachment status: Is frightened and/or frightening parental behavior the linking mechanism? In M. T. Greenberg, D. Cicchetti, & E. M. Cummings (Eds.), Attachment in the preschool years ( pp. 161‑182). Chicago: University of Chicago Press.

Main, M., & Solomon, J. (1990). Procedures for identifying infants as disorganized/disoriented during the Ainsworth Strange Situation. In M. T. Greenberg, D. Cicchetti, & E. M. Cummings (Eds.), Attachment in the preschool years (pp. 121‑160). Chicago: University of Chicago Press.

Marvin, R. S.. & Greenberg, M. T. (1982). Preschoolers' changing conceptions of their mothers: A social‑cognitive study of mother‑child attachment. In D. Forties & M. T. Greenberg (Eds.), New directions for child development: No. 18. Children's planning strategies (pp. 47‑60). San Francisco: Lossey‑Bass.

Schore, A. N. (1994). Affect regulation and tire origin of the self.' The neurobiology of emotional development. Hillsdale, NJ: Erlbaum.

Siegel, D. J. (1999). The developing mind: Toward a neurobiology of interpersonal experience. New York: The Guildford Press.

Sroufe• L. A. 11983). Infant‑caregiver attachment and patterns of adaptation in preschool: The roots of maladaptation and competence. In M. Perlmutter (Ed.), Minnesota symposia on Child Psychology: Vol. 16. Development and policy concerning children with special needs (pp. 41‑83). Hillsdale, NJ: Erlbaum.

Steiner, H., Zeanah. C. H., Stuber, M.. Ash, P., & Angell. R. (1994). The hidden faces of trauma: An update on child psychiatric traumatology. Scientific Proceedings of the Annual Meeting of the American Academy of Child and Adolescent Psychiatry. 3 1.

Turner, P. (199 t ). Relations between attachment, gender, and behavior with peers in the preschool. Child Development, 62, 1475‑1488.

Urban, J., Carlson, E., Egeland, B„ & Sroufe, L. A. (1991). Patterns of individual adaptation across childhood. Development and Psychopathology, 3, 445‑460.

Wanner, U. G.. Grossmann, K., Fremmer‑Bombik, E.. & Suess. G. (1994 t. Attachment patterns at age six in south Germany: Predictability from infancy and implications for preschool behavior. Child Development, 63, 1209‑1222.

Weinfield, N. S.. Sroufe. L. A.. Egeland, B.. & Carlson, E. A.. (1999 ). The nature of individual differences in infant‑caregiver attachment. In J. Cassidy & P. R. Shaver (Eds.). Handbook of attachment: Theory. research, and clinical applications (pp. 68‑88). NY: The Guilford Press.

Work Preferences

I would love to deal with a diverse population. In my opinion, being open to diversity in your personal and professional life is an important part of the growth process. Theoretical orientation should compliment this diversity. The wider variety of theories researched, the greater knowledge one can possess. I would rather have objectivity from a supervisor. Nurture is always encouraging, but knowing what you have done wrong and correcting your mistakes is essential to being a successful psychologist or employee in general. I am not sure if I would move to a new location or not. I think in the future I would be more open to the idea, but seeing that I just moved six months ago, I am not too keen on the idea of moving again at this time. I do not mind working with a team, but I enjoy working by myself. I have always been a loner in a sense and feel like I work well by myself. Even so, working with a group does provide you with support and helpful suggestions from co-workers that you might not have otherwise.

Once a child has an attachment disorder is there a chance the disorder will not go away?

Yes, if therapy is not administered, the individual may always have an attachment disorder. The earlier the child is treated, the better chance they have of learning how to interact with others. The later treated is delayed, the more likely the child will have permanent problems (Thackery, 2003). A child will not “outgrow” an attachment disorder. If the condition is left untreated, it can destroy a child, as well as its family (wpic).

Please refer to my reference page for this post: http://freednerd.wordpress.com/2006/06/04/attachment-disorders-q-a-references/

How does each of the different treatments work?

Well, I briefly mentioned how cradling and using “infant techniques” are performed, but I will elaborate on the other methods.

  Dyadic Developmental Psychotherapy is a family-focused treatment that should be administered by a well-trained, licensed professional. The main objective is to develop healthy, secure, and trusting relationships with caregivers. This method is based on five central principles, which correlate with the causes and courses of the attachment disorder.

The first principal states that therapy must be experiential by creating healing experiences, not just words. This process is used because other methods such as talk therapy, play therapy, and residential treatment are based on the client having a relationship with the therapist, which most children with attachment disorder are not open to. The second principal emphasizes the main objective: therapy must be family-focused. The parents must be able to create a secure and nurturing environment for the child, and must be actively involved in the treatment. Parents either have the child on their lap during the treatment or are watching them through a one-way mirror or monitor. The third principal is focused around the task of addressing the trauma. Re-experiencing the painful emotions must be done in order for the child to change their view of the world. Next, a safe and secure environment must be established, at home and in therapy. The child must be able to tie in home, school, and therapy in conversations. Dyadic Devlopmental Psychotherapy is built around the theory that "Compression-wraps," invasive and intrusive stimulation designed to evoke rage, "re-birthing," and other provocative techniques” are “intrusive and invasive” and “have no place in a reputable treatment program”. The fifth principal states that therapy must be consensual. No physical restraint is used, though cradling is a technique used to create security when agreed upon. Parents and teenagers must sign consent documents, and the first session is based on what the child wants to change in his or her life (Becker-Weidman, 2005).

Infant-parent psychotherapy is focused on helping the parent change their outlook on life, so they can give their child the correct attention and security. The therapeutic relationship is used to change how the parent’s own sense of worth and their expectations of relationships. The therapist view’s the history of the parent’s feelings and interactions with the child in order to liberate the child from misconceptions the parent might have about their own childhood. The parent is taught age-appropriate methods of dealing with their child, to promote realistic expectations of for the child’s understanding. Resources and services are given to the client. Direct intervention is given during sessions with the child and parent. This process helps the parent understand the child’s special needs and weaknesses (Pekarsky, n.d.).

Please refer to my reference page for this post: http://freednerd.wordpress.com/2006/06/04/attachment-disorders-q-a-references/

It is possible for children to form different attachment disorders during different situations due to their environment?

Question:

It is possible for children to form different attachment disorders during different situations due to their environment? For example, a child may respond differently to strangers in their own home as opposed to an unfamiliar place.

Answer:

I am not completely sure that I understand your question, but as I mentioned in number 4, I could not find any evidence that a child can have more than one type of attachment disorder. I personally do not think that it would matter whether a child was in one “physical” environment opposed to another, but more as to the individuals around him or her. Of course, I think the child would feel more secure in a “clean” and “non-threatening” environment, opposed to a crack house, for instance.

Can a child possess more that one attachment disorder?

I have not found any evidence that a child can have more than one type of attachment disorder. I think this is because the different types of disorders are classified by the symptoms caused by the disorder, and disordered attachment consists of multiple reactions to attachment.

Out of the attachment types that were listed (secure, avoidant, resistant, and/or disorganized/disoriented), is one considered worse than the other?

 

Research has shown that there are different severities to attachment disorders. Some children have attachment “issues”, but do not necessarily have a disorder. Children with disorganized attachment are labeled as having the most severe attachment disorder, because they normally combine anxious resistant attachment with post-traumatic stress disorder caused by abuse. Their behavior, and attachment style, is often called chaotic. Treatment is often extremely difficult due to the fact that more than one issue has to be treated- the traumatized attachment and the trauma of abuse. Many of these children are over aroused (known as hyperarousal), which can result in a number of anxiety disorders. These children can not comfort themselves, and do not trust others’ attempts at soothing them (Dicke, 2006). They fear closeness and see themselves unworthy of love and support. They view others as unavailable, frightening, and rejecting. Behavioral issues such as lack of empathy and remorse, selfishness, being controlling, disregarding rules, and refusing to take responsibilities for their actions are common. Children disorganized attachment disorder are much more vulnerable to a plethora of social, moral, and emotional problems; and consequently, are at a much higher risk for abusing their own family, participating in criminal activity, and abusing drugs and alcohol (Attachment Treatment, 2006).

Please refer to my reference page for this post: http://freednerd.wordpress.com/2006/06/04/attachment-disorders-q-a-references/

Can the child form attachment disorders between parents?

Question: 

Can the child form attachment disorders between parents? For example, if the father has the child, is it possible for the child to incur sadness because they want their mother?

Answer:

I believe that a child can certainly incur sadness from missing a parent, but I think that not having a primary attachment figure is the cause of the majority of attachment disorders. Having two supportive parents is always recommended and most likely the “best” situation for a child to be in, but as long as a child knows that they are loved and supported by at least one person, I think the chances for him or her to develop an attachment disorder is low.

The link to criminal behavior in a single-parent home compared to a home with a mother and father is higher; whereas, “the link from single-parent households to attachment disorder is a weaker causal connection with a lower probability (Morse, n.d.).” Another study of preschool-aged children dealing with attachment showed that, “risk factors of single parent status, low socioeconomic status, and gender were not significant predictors.” Even so, it is important to note that a father’s attachment history influences the child’s externalizing behavior; while the mother’s attachment history influences the child’s internalizing behavior (Breazeale, 2001).

Though research supports the theory that single-parent homes do not play a significant role in causing a child to have an attachment disorder, the odds of a child having an attachment disorder in a single-parent is much greater. Reason being, children have a 120% greater chance of experiencing some form of abuse, tend to have weak ties to family and acquaintances, and many times experience constantly changing family configurations (Mintz, 2006).

Please refer to my reference page for this post: http://freednerd.wordpress.com/2006/06/04/attachment-disorders-q-a-references/

Does gender have any affect on attachment?

I could not find any significant evidence that gender plays a role on the odds that a child will have an attachment disorder. I do not think that it does because attachment disorder is not caused by a certain gene (or is hereditary), but by environmental factors.

Also, research has shown that an equal number of male and females suffer depression before adolescence. Ten to fifteen percent of all children have moderate to severe signs of depression; though after the age of thirteen, twice as many females as males suffer with depression (Gurian, 2002). This being said, I do not assume that gender would play a significant role in attachment disorders.

Please refer to my reference page for this post: http://freednerd.wordpress.com/2006/06/04/attachment-disorders-q-a-references/

Attachment Disorders: Q & A References

Attachment Disorder. (2004). Disability Brochure #3. Retrieved February 9, 2006 from http://www.wpic.org/brochures.htm

Attachment Treatment and Training Institute, PLLC. (2006). Attachment Continuum. Retrieved February 5, 2006 from http://attachment.adoption.com/bonding/attachment-continuum.html

Becker-Weidman, Arthur. (2005). Dyadic Developmental Psychotherapy: What it Is and What it Isn't. Retrieved February 9, 2006 from http://www.mental-health-matters.com/articles/article.php?artID=575

Breazeale, Tami. (2001). Literature Review. Retrieved February 5, 2006 from http://www.visi.com/~jlb/thesis/attachment.html
Dicke, John. (2006). Attachment Continuum. Retrieved February 5, 2006 from http://attachment.adoption.com/bonding/attachment-continuum.html
Gurian, Anita. (2002). Depression in Adolescence: Does Gender Matter?. Retrieved February 5, 2006 from http://www.aboutourkids.org/aboutour/articles/dep_gender.html#gender

Mintz, Ann. (2006). Ensuring Our Children’s Safety: How Communities Are Addressing Child Abuse and Neglect [electronic version], Vol. III, No. 2. Retrieved February 5, 2006, from http://72.14.207.104/search?q=cache:y2tP6EQ96zgJ:www.gafcp.org/pubs/rep/ChildMaltreatmentWinter2006Final.doc+attachment+disorder+single+parent+-adoption&hl=en&gl=us&ct=clnk&cd=84&client=opera

Morse, Jennifer. (n.d.). Parents or Prisons. Policy Review. Retrieved February 5, 2006 from http://www.policyreview.org/aug03/morse.html

Pekarsky, Judith. (n.d.). Focuses of work in Infant-Parent Psychotherapy. Retrieved February 9, 2006 from www.healthychild.ucla.edu

Thackery, Ellen. (2003). Reactive attachment disorder of infancy or early childhood. Encyclopedia of Mental Disorders. Retrieved February 9, 2006 from http://health.enotes.com/mental-disorders-encyclopedia/
reactive-attachment-disorder-infancy-early

Delusions in Schizophrenic Patients

Unlike hallucinations (which are completely "imaginary"), I believe that delusions do have some relevance in a schizophrenic's every day occurrences. For instance, while we know someone is trying to help us, a schizophrenic may think someone is doing the exact opposite. I think of it almost as dreams. When we are dreaming, bits and pieces of things we have seen or experienced are often mixed in, but everything seems to be mixed up or have additional features tied in. I think this is how a schizophrenic feels much of the time while awake. Paranoia can be a very scary and almost debilitating feature. It makes forming bonds with people very difficult, etc. Just imagine if your waking state was similar to your dreaming state…it would be a very scary thought!

Positive & Negative Symptoms of Schizophrenia

 

Schizophrenia is a severe mental illness with both positive and negative symptoms. The actual term “schizophrenia” means “split mind”, but schizophrenics do not have multiple personalities. Eugen Bleuler, the man who created the word, intended its use to mean “a break from reality caused by disorganization of the various functions of the mind (Carlson, 2004).” There are many types of schizophrenia including: paranoid, hebephrenic, catatonic, undifferentiated, residual, and simple schizophrenia, to mention a few. All have certain dominant features, but share the same common symptoms (Mental Health, 2005).

When one hears the word positive, he or she most likely thinks of something that is        good or helpful. This is definitely not the case in schizophrenia. The term “positive symptoms” refers to symptoms that are easily recognized by their presence. One        positive symptom, and likely the most prominent of schizophrenia, is thought disorder. Schizophrenics have difficulty in arranging their thoughts in a logical pattern. They       often jump from one topic to another and form irrational conclusions. To a schizophrenic student, the conclusion that he or she received a bad grade because aliens graded his or her paper would make as much sense as the conclusion that he or she did a poor job. While holding a normal conversation, you will often hear one of these individuals  muttering irrelevant words or rhyming words instead of choosing words that actual describe what they are speaking about. Another positive symptom is delusions.    Common delusions might include the following: someone is trying to kill them; they     have supernatural powers; or radars have been placed inside of their head to control them. Hallucinations, which can be caused by drugs such as LSD, occur naturally in schizophrenics. Auditory hallucinations are most common, but some individuals also    have visions. You will often hear patients say they have “voices in their head” instructing them to do something, reprimanding them, or rattling irrelevant phrases. Olfactory hallucinations are also frequent. Many times patients will have the delusion that someone is trying to kill them with poison gas (Carlson, 2004). One of the main positive symptoms of hebephrenic schizophrenia is incongruous mood, or a shallow, inappropriate mood which can consist of constant giggling, smiling, grimaces, or pranks. Catatonic schizophrenics have a positive symptom of increased motor function that is non-related  to stimuli around them. Of course, many people think of catatonic individuals as nonmoving or functioning, and while schizophrenic catatonics do experience long periods of inactivity and stupor, violent outbursts and inappropriate motor activity also occurs (Mental Health, 2005).

The term “negative symptoms” refers to the absence of typical behavior. For instance, schizophrenics will often have severe apathy, or indifference, lack of emotion, or lack of interest about important matters. When speaking about anything emotional, they may speak with a monotone voice. When experiencing positive symptoms, patients may be very talkative, whereas experiencing negative symptoms will cause a patient to say very little. Also, individuals will have difficulty in feeling any type of pleasure. More often than not, these negative characteristics will cause a patient to be withdrawn from others and have little social interaction. It should be noted that these symptoms cannot be due to depression or drug abuse to be classified as true negative symptoms of schizophrenia. Many times these symptoms will be overlooked opposed to positive symptoms that are more apparent. One is more likely to notice if someone is talking to a person who isn’t there opposed to someone being quite or unemotional. Consequently, the social life of     a schizophrenic will often wane considerably when only the positive symptoms of the disorder are noticed treated.

The biological basis for positive and negative symptoms in schizophrenia is as different   as the actual symptoms themselves. There are many different variations on the hypothesis for the biological cause of positive symptoms, but all theories lead back to   one central point: the role of dopamine. Many scientists believe that schizophrenics have hyperactivity of dopaminergic synapses, most likely in the mesolimbic pathway that links the ventral tegmental area (located in the midbrain and rich in dopamine and serotonin)   to the nucleus accumbens and amygdala (parts of the limbic system). What first gave researchers the hypothesis that dopamine was linked to positive symptoms in schizophrenia was the analysis of antipsychotic medication. All of the antipsychotic medications had one thing in common: they blocked dopamine receptors. In comparison, drugs such as cocaine, amphetamine, and methylphenidate worked as dopamine agonists and would produce the positive symptoms. Antipsychotic medications would also relieve the symptoms found in drug users. This pharmaceutical examination brought researchers to the conclusion that increased dopamine production, neurons sensitive to dopamine, or the slow absorption rate could possibly cause the aforementioned positive symptoms. Patients with greater amounts of dopamine have shown greater positive symptoms,   which would support the theory that dopamine is increased in schizophrenics. Other studies have tried to find evidence of an increased number of dopamine receptors, but results have been mixed. It is probably a farfetched idea that this is the primary basis for the disorder. Because drugs that function as agonists reinforce behavior, positive symptoms might be caused by reinforcement of behavior at the wrong moments. For instance, schizophrenics often feel “great” at the beginning of an episode; this euphoric feeling is most likely caused by increased activity of dopaminergic neurons. Other symptoms, such as delusions and hallucinations, are not so wonderful. Presumably,    since dopamine is thought to be an important part of the reinforcement process and dopamine levels are increased when a patient has positive symptoms, the patient may think that these responses are normal and acceptable. The amygdala, which is known    for its correlation with emotional responses, is thought to bring about delusions when overstimulated with dopamine.

The negative symptoms of schizophrenia are thought to be caused by brain  abnormalities. The majority of patients have neurological difficulties, such as unusual   facial expressions and poor eye movement control. Studies have shown that the normal ventricle size of a schizophrenic patient is twice as large as in control groups. CT and MRI scans have also shown loss of brain tissue, which most likely accounts for the enlarged ventricle size. Everyone loses a little brain tissue as they age, but schizophrenics have a more rapid  loss. Also, brain abnormalities are known to exist in the medial temporal  lobes, frontal lobes, lateral temporal lobes, parietal lobe, basal ganglia, thalamus, corpus callosum, and maybe even the cerebellum. Decreased activity of the frontal lobes is   known as hypofrontality. This decline in action, particularly in the dorsolateral prefrontal cortex, may be another cause of the negative symptoms. Although the positive and negative symptoms of schizophrenia are so different, studies have shown they may actually be related. The aforementioned decreased activity may be caused by a decline in dopamine in the prefrontal cortex. This may sound strange since the increase of  dopamine has been known to cause positive symptoms in schizophrenia, but research on certain drugs have helped to shed light on this topic. For instance, schizophrenics usually perform poorly on neurological tests (specifically for prefrontal cortex damage) but when given amphetamine, the blood flow in the dorsolateral prefrontal cortex increases, as well as their performance on the test. In addition, PCP addicts will experience negative symptoms due to a decline in the metabolic activity of the frontal lobes. It has also been found that PCP decreases the amount of dopamine the dorsolateral prefrontal cortex creates, and behavioral impairment directly correlates with this dopamine decrease. Thus, the decreased dopamine production creates the hypofrontality of the frontal lobes, which further creates the negative symptoms of schizophrenia. Some researchers think that the decreased prefrontal activity actually causes hyperactivity in the mesolimbic dopamine pathway. Neurons located in the prefrontal cortex send axons to the ventral tegmental area. The axons then form synapses with neurons that secrete GABA (an inhibitory neurotransmitter) which is transmitted to the nucleus accumbens. When the prefrontal cortex is electrically stimulated, the release of dopamine declines in the nucleus accumbens. In other words, if the opposite is true then the decline of activity in the prefrontal cortex would lead to an increase of dopamine release in the nucleus accumbens. Clozopine, an atypical psychotic, successfully relieves negative and positive symptoms and increases dopamine release in the prefrontal cortex, while decreasing dopamine release in the nucleus accumbens. All these neurological responses point to one hypothesis: a domino effect. Hypoactivity of dopamine in the prefrontal cortex causes hypofrontality, which results in negative symptoms of schizophrenia. Furthermore, the hypofrontality causes an increase of dopamine release in the prefrontal cortex, which accounts for the positive symptoms of schizophrenia (Carlson, 2004). Studies of bipolar disorder, which has many similarities to schizophrenia, have also coincided with this theory. Researchers propose that a dopamine decrease may be responsible for the depression stages, while a dopamine increase may be responsible for the manic stages (Lundbeck, 2005).

In conclusion, schizophrenia can be a debilitating illness with both positive and negative symptoms. While having positive symptoms, a patient may be overly active, but have  very poor and scattered judgment, along with delusions and hallucinations. While having negative symptoms, a patient may lose all sense of pleasure and be overly withdrawn. Both of these symptoms can cause great social difficulties. People often find schizophrenics difficult to be around in the positive stages because of their off the wall ideas, and schizophrenics do not want to be around others when experiencing negative symptoms. Scientists have hypothesized that the negative symptoms are caused by   brain abnormalities and the positive symptoms by hyperactivity of dopamine release. These are thought to be related; the decrease of dopamine in the prefrontal cortex indirectly causes the increase of dopamine in the nucleus accumbens. Further research   on this topic may explain the reasons some disorders share many of the same  symptoms, and also bring forth new methods of treatment.
References:

1. Carlson, Neil R. (2004). Vision. In Physiology of Behavior, 8, 182-183.

2. Health Matters. (2005). Schizophrenia. Retrieved March 5, 2006, from http://www.mental-health-matters.com/disorders/dis_details.php?disID=84

3. The Lundbeck Institute. (2005). Aetiology. In Bipolar Disorder.                          Retrieved March 6, 2006, from http://www.brainexplorer.org/bipolar_disorder/Bipolar_Disorder_Aetiology.shtml

Less Brief Overview of Hepatic Adenomas

 

Hepatic adenoma is a rare benign primary tumor of the liver. Approximately 90% of liver adenomas occur in young women of reproductive age and in these patients it is associated with the use of oral contraceptives. Other patient populations at risk for developing hepatic adenomas include men who use anabolic steroids and infants and children with metabolic disorders including type I glycogen storage (von Gierke’s) disease, type III glycogen storage (Cori’s) disease, tyrosinemia, and familial diabetes mellitus.

Pathologically, adenomas are most often solitary lesions (70-80%) but they can be multifocal. These tumors consist of sheets of normal appearing hepatocytes but lack the normal acinar architecture of the surrounding hepatic parenchyma. The hepatocytes may be rich in fat or glycogen, and Kupffer cells are occasionally present, but bile ducts and portal tracts are absent. These tumors may be partially or completely enclosed by a pseudocapsule derived from the compressed and collapsed hepatic parenchyma. Hepatic adeomas are yellow in color due to their fat content and often contain areas of hemorrhage or infarction. They may also demonstrate focal scar formation which is indicative of remote infarction. They are pedunculated in 10% of cases. Malignant transformation of these benign tumors is rare.

Most patients with hepatic adenoma are asymptomatic and almost invariably have normal liver function tests (unlike in liver adenomatosis) and no elevation of serum tumor markers such as ?-fetoprotein. Large adenomas may cause a sensation of right upper quadrant fullness or discomfort with or without a palpable abdominal mass. However, the classic presentation of hepatic adenoma is spontaneous rupture or hemorrhage leading to acute abdominal pain and possibly progressing to hypotension, shock, and death. Hepatic adenomas have a tendency to undergo spontaneous rupture in 25-50% of cases. In patients with liver adenomatosis hemorrhage can occur in more than 60% of patients.

On T1-weighted MRI images, the signal intensity of adenomas typically varies from hypointense to hyperintense (most often) in comparison to the liver parenchyma. This variation in signal intensity on T1-weighted images reflects the fat content of the tumor. Adenomas can also appear heterogeneous on T1-weighted images due to areas of increased signal intensity resulting from fat and hemorrhage and areas of low signal intensity, corresponding to areas of necrosis, old hemorrhage, or calcification. On T2-weighted images, hepatic adenomas are most often mildly hyperintense to liver parenchyma, although some hypointense and isointense lesions have been reported. The finding of a hyperintense lesion on T2-weighted imaging is not specific for hepatic adenoma and can reflect other hepatic lesions including, hepatocellular carcinoma and metastases. Hepatic adenomas can also be heterogeneous in appearance on T2-weighted imaging, again reflecting areas of hemorrhage and necrosis. A peripheral rim of low signal intensity on T1-weighted images and variable intensity on T2-weighted images can be seen in 17-31% of patients and histologically corresponds to a pseudocapsule.

Dynamic gadolinium enhanced gradient echo MR imaging can be used to demonstrate that most hepatic adenomas have intense enhancement during the early arterial phase and are isointense to liver tissue on delayed imaging. Characteristically, hepatic adenomas have a transient blush immediately after gadolinium administration that fades by 1 minute. Chemical-shift imaging showing homogeneous drop in signal intensity on out-of-phase or fat-suppressed images is a relatively common feature of fat-containing adenomas. However, 40% of hepatocellular carcinoma lesions are known to contain fat and, therefore, the presence of fat does not help differentiate hepatic adenoma from hepatocellular carcinoma. Because adenomas contain hepatocytes, hepatocyte-specific contrast agents can accumulate in these tumors and show contrast enhancement. These hepatocyte-specific agents can be used to help differentiate hepatic adeomas from liver lesions that may not contain hepatocytes, such as metastases and hemangiomas. However, hepatic lesions that do contain hepatocytes such as, focal nodular hyperplasia or hepatocellular carcinoma can not be easily distinguished. Kupffer cell-specific MRI agents such as superparamagnetic iron oxide (SPIO) and ultrasmall superparamagnetic iron oxide (USPIO) generally show no uptake by hepatic adenomas.

Hepatic adenomas secondary to oral contraceptive or steroid use generally regress or completely disappear following withdrawal of the contraceptive therapy or steroid use. However, it is important to distinguish between hepatic adenoma and other benign hepatic lesions, such as focal nodular hyperplasia, because of its propensity to hemorrhage and the possibility of malignant transformation. A confident distinction of hepatic adenoma from other lesions such as, hepatocellular carcinoma, based solely on imaging is not yet clear-cut. Therefore, histological examination is advocated to make a definitive diagnosis..

Hepatic adenomatosis is a separate clinical entity which can be distinguished from isolated hepatic adenoma by the presence of multiple adeomas, usually greater than 10, in patients lacking other known risk factors for adenomas. Although the adenomas in hepatic adenomatosis are histologically similar to isolated hepatic adenomas, they lack association with steroid medication, have almost equal prevalence in men and women, tend to be progressive, symptomatic, are more likely to lead to impaired liver function, and have a higher incidence of hemorrhage and malignant degeneration. Hepatic adenomatosis has to be differentiated from other diseases causing multiple liver lesions including metastatic disease, multifocal hepatocellular carcinoma, focal nodular hyperplasia, and adenomatous hyperplasia.

Surgical resection is generally recommended in patients with solitary symptomatic hepatic adenomas, but may not be possible in patients with hepatic adenomatosis. In patients with hepatic adenomatosis, periodic follow-up is recommended.

Very Brief Hepatic Adenoma Overview

 

Hepatic adenomas are benign solid neoplasms of the liver. They are most commonly seen in young woman, and are typically solitary, although multiple adenomas can also occur. Prior or current use of estrogens (oral contraceptives) is a clear risk factor for development of a liver adenoma, although they can occur even in the absence of oral contraceptive use. Hepatic adenomas carry a significant risk of spontaneous rupture with intraperitoneal bleeding. Further, there is also a risk of malignant transformation to a well-differentiated HCC. Therefore, it is usually recommended that a hepatic adenoma be surgically resected.

PCOS Symptoms

Polycystic ovarian syndrome presents a complex and baffling array of symptoms, consisting of some combination of the following symptoms that vary with each individual:

——>Multiple ovarian cysts

——->Irregular or absent menses

——->Infertility

——->Acne

Obesity or inability to lose weight

Excessive body or facial hair (hirsutism)

—->Insulin resistance and possibly diabetes

—–>Thinning of scalp hair
—–>Velvety, hyperpigmented skin folds (acanthosis nigricans)
—–>High blood pressure
—–>Polycystic ovaries that are 2-5 times larger than healthy ovaries.

Multiple hormone imbalances, commonly including:
Androgens (testosterone)
Cortisol
Estrogens
FSH (follicle stimulating hormone)
Insulin.
LH (luteinizing hormone)
progesterone
Prolactin.
Thyroid hormones.

What Causes Polycystic Ovarian Syndrome?

Polycystic ovarian syndrome presents a complex and baffling array of symptoms,
There is disagreement and uncertainty as to what causes polycystic ovarian disease. Polycystic ovaries and polycystic ovary syndrome have been associated with one or more of these factors:

Genetic predisposition.

Insulin resistance or hyperinsulinism (high blood levels of insulin).

Obesity.

Hyperandrogenism (excessive production of male hormones).

Abnormality of the hypothalamic-pituitary-gonadal axis (organ/hormonal disorder).

Environmental chemical pollution (hormonal disruptors)

Food adulterantion (excitatory amino acids, for example)

Chronic inflammation.

Some of these causal factors may also be consequences of polycystic ovary disease. In other words, we have an amazingly complex network of interacting variables, each of which influences the other. Polycystic ovarian syndrome is not a simple disease with a single cause.
Information retrieved from: http://www.ovarian-cysts-pcos.com/pcos.html

How Common Is PCOS?

 

Polycystic ovary syndrome is the most common hormonal disorder occurring in women during their reproductive years. It’s thought that 4% to 10% of all women have the disorder. However, since many women don’t know they have polycystic ovarian syndrome or some aspect of it, the actual number probably exceeds 10%. Polycystic ovarian syndrome is one of the leading causes of infertility. Symptoms frequently start to show up soon after puberty.
Information retrieved from: http://www.ovarian-cysts-pcos.com/pcos.html

PCOS Definitions

 

"Syndrome" simply means a set of symptoms that occur together, in a pattern.

"Polycystic" means there is an accumulation of incompletely developed follicles (cysts) in the ovaries.

 

 

"Polycystic ovarian syndrome" refers to a health disorder where there may be many cysts in the ovaries, accompanied by a distinctive pattern of symptoms.

"Metabolic" refers to the physical and biochemical processes required for the body to function.

"Polycystic ovary syndrome" is the name given to a metabolic condition in which a woman will have cystic ovaries, along with a certain pattern of other symptoms that reflect imbalances in reproductive and other hormones.

We referred to polycystic ovary syndrome as a “metabolic disorder”. By this we mean that there are numerous factors in basic body processes that have gone awry. Because your body is a unified whole, a problem or dysfunction in one area causes dysfunction in other areas. Polycystic ovary syndrome is a dysfunction that is related in some way to your whole body, not just your ovaries.
Information retrieved from: http://www.ovarian-cysts-pcos.com/pcos.html

Brief Overview of PSOD

 

In each menstrual cycle, follicles grow on the ovaries. Eggs develop within those follicles, one of which will reach maturity faster than the others and be released into the fallopian tubes. This is "ovulation". The remaining follicles will degenerate.

In the case of polycystic ovaries, however, the ovaries are larger than normal, and there are a series of undeveloped follicles that appear in clumps, somewhat like a bunch of grapes. Polycystic ovaries are not especially troublesome and may not even affect your fertility.

However, when the cysts cause a hormonal imbalance, a pattern of symptoms may develop. This pattern of symptoms is called a syndrome. These symptoms are the difference between suffering from polycystic ovary syndrome and from polycystic ovaries.

So you can have polycystic ovaries without having PCOS. However, nearly all women with PCOS will have polycystic ovaries. Polycystic Ovary Syndrome is the name given to a metabolic condition in which a woman will have polycystic ovaries, along with a certain pattern of other symptoms that reflect imbalances in reproductive and other hormones.

We referred to polycystic ovarian syndrome as a “metabolic" disorder. By this we mean that there are numerous factors in basic body processes that have gone awry. Because your body is a unified whole, a problem or dysfunction in one area causes dysfunction in other areas. Polycystic ovarian syndrome is a dysfunction that is related to your whole body, not just your ovaries.
Information retrieved from: http://www.ovarian-cysts-pcos.com/pcos.html

What a month….what a life.

I have never been a fan of blogs…until I found one that really had my intrigued. There is so much going on in my life right now, I thought what the hell…let me write about it.

To be able to sum up my life to this point is impossible, but I will say it has been full of ups and downs. Lately the downs seem to be much more abundant then the ups! The past month has been one of those laughing, crying, just saying “why the flying fuck is this happening kind of times”. You ever have those?

Anyways….I was diagnosed as bipolar around 2 years ago…other than that my “health” had always been pretty decent….around a month ago my partner and I decided we wanted to have a baby..well, this had never happened in the past- but I thought maybe it was the wrong person, wrong time, wrong whatever…well, to make a long story short, I was having all kinds of symptoms and thought hey…maybe I am pregnant..but the tests kept telling me nope. I was pretty certain I was pregnant even though the tests said no and I kept telling myself I wasn’t so I wouldn’t be set up for disappointment.

 

Well, eventually I went to the OBGYN and she said I wasn’t pregnant too. She said one of my ovaries felt bigger then the other and I probably had a cyst….Oh don’t stop reading yet…the fun just starts to begin. She sent me for an ultrasound the next day and the tech said she thought I had polycystic ovarian syndrome (PSOD for short). Obviously, my ovaries were covered in follicles (cysts where the eggs don’t release). The biggest dream I have ever had was to have a child…so needless to say this was a big bummer.

Anyways…..the nurse called me back and said not to worry because “everything looked normal”, but the doctor wanted to set up an appointment to see me a few days later. I thought, what the hell, how is everything normal if the doctor needs me to come back in??

Well, my appointment was scheduled for a few days later, but the doctor couldn’t make it in so they re-scheduled. Things just kept getting better- a few days later I started having sharp shoulder pain and something possessed me to get another pregnany test. Well this time, I got a clear blue digital test and it showed up PREGNANT. I started to really freak out then. I have been reading about everything possible on the internet so maybe I could figure out what was going on and I guess I make myself a little paranoid in the process. Of course I thought the worst- so I went to the ER and they said I had muscle strain. MUSCLE STRAIN….BULLLLLSHIT. I told the doctor, look- I may not be pregnant- but this isn’t muscle strain either. She said uh huh and sent me on my way with a muscle relaxer shot and pills. Needless to say, I was not a happy camper. And it keeps getting better…

 

I went to a family practice doctor a couple of days after that and they did every test in the book-mono, strep, EKG, diabetes, thyroid, etc. Everything showed up normal…Great….but not great because I am still wondering what the hell is wrong with me. But she also scheduled an abdominal catscan.

So…….I had an antagonizing weekend of waiting for my appointment. I went to get the CT scan not knowing I had to drink two big things of liquid that tasted similar to puke. So….I did that, had the catscan, and almost was back home and they called me to come back…but of course they didn’t give me an explanation why…They just said they wanted to do an IV catscan. I thought great….more fun fun fun…

Hours later, the doctor called me and said I had an 8cm mass in my liver. WHAT?!* How in the hell did that get there I was wondering…? Oh, and to make matters so so much better- this problem is normally caused by oral contraceptives (which I have never taken). They think it is a hepatic adenoma. Your chances of getting that without birth control are a mere one in a million. Great odds huh?

Well……I went back to the doctor the next day and scheduled a liver biopsy for Monday. I actually had a day off from going to the doctor (it seemed like paradise) and then my appointment finally came today for my ultrasound results for my wonderful follicly ovaries. Yeah, you guessed it, I have PSOD. It would have been way to easy not to. To make matters even worse (if it could get much worse), I can’t take the medication I need to because my liver may not process it correctly. Sometimes birth control is used…but that REALLY would not be good considering my nice liver mass would probably grow rapidly and rupture. A little internal bleeding is all, but I think I will do without…

Anyways…more entertaining to come….me and my liver mass are going to bed for the night.

BTW…any comments will be more than welcome and greatly appreciated!

Causes for Schizophrenia

 

There is still much speculation on the causes of schizophrenia (as well as most mental disorders), but research has shown genetic and environmental links. In most parts of the world schizophrenia is more prevalent in men; but in China, it is more prevalent in women. This could account for the environmental role of the disorder. Also, certain genes have been linked to schizophrenia. A monozygotic twin of a person with schizophrenia has a 40-50 percent chance of developing the illness. When a parent has schizophrenia, a child has about a 10 percent chance of developing schizophrenia (Healthy Place, 2006). One study even found 16.4% of schizophrenic probands had at least one first-degree relative affected with the disorder (Shimizu,Kurachi,Yamaguchi,Torri, & Isaki, 1987).
References:

Healthy Place Thought Disorders Community. (2006). What Causes Schizophrenia? Retrieved March 08, 2006 from http://www.healthyplace.com/communities/ thought_disorders/schizo/nimh/causes.asp

Shimizu A, Kurachi M, Yamaguchi N, Torii H, & Isaki K. (1987). Morbidity risk of schizophrenia to parents and siblings of schizophrenic patients. Jpn J Psychiatry Neurology, 41,65-70.