Screwed-up Medical Misfortunes

A little bit of this, and a little bit of that, will a whole lot of medical “stuff” added in!

  • a

Archive for the ‘Disorders’ Category

Stereotypic Movement Disorder [childhood disorder]

Posted by Administrator on November 30, 2006

Many childhood disorders, especially those of a psychiatric form are controversial in nature.  For one, medicating children is a sensitive topic, which some adults highly disagree with.  In addition, no one wants their child to suffer the stereotypes of having a mental disorder and some may even deny their child has a problem. Studies may even be less conclusive because of the limited amount of years in childhood compared to adulthood. 

Stereotypic movement disorder, which consists of seemingly compulsive, repetitive, and nonfunctional behavior, is thought to occur in 2 to 3 percent of children and adolescents (Sadock, 2003).  While most children show some type of repetitive movements in early childhood, children with this disorder have behaviors that interfere with normal functioning or that cause self-inflicted bodily injury (2003). Stein & Christenson (1998) report this disorder is often overlooked and unseen in most psychiatric literature because it occurs most frequently in children with mental retardation; however, this disorder can occur in children of normal intelligence.

 

Because this diagnosis is often overlooked, it is rarely made (AACAP, 1999).  Stereotyped behaviors are seen frequently in other childhood disorders such as autism, but currently a comorbid diagnosis of both autism and stereotypic movement disorder cannot be made.  There is ongoing controversy over whether these stereotypic movements constitute the addition of an extra diagnosis (1999). In addition, the diagnosis criteria can be interrupted in a manner of ways. Freeman (2006) states one of the main diagnostic problems to occur is “The pattern itself can look indistinguishable from autistic stereotypies, but is much more prolonged than tics. Comorbidty (other disorders) are common, including tics, just to confuse everyone.”  Unfortunately, this disorder is likely under-diagnosed, while other similar disorders may be over-diagnosed.

 

To make matters even more difficult, in Stereotypic Movement Disorder there is a fine line between normal and irregular behavior.  Nail biting for instance, can be considered a symptom; but only when it is severe (Sadock, 2003). Other children exhibit behaviors such as head banging for a period of time, but the problem disappears as the child grows older.  Should they be diagnosed with this disorder? How long should you wait before the diagnosis should be made?  Though the DSM criteria lists “the behavior persists for 4 weeks or longer” (Sadock, 2003), when should body rocking or picking at the skin be considered a real danger? 

All of these aforementioned issues make the diagnostic process for Stereotypic Movement Disorder even more difficult.  Though the vast majority of the population has heard of disorders such as autism or schizophrenia, this disorder is widely unknown in individuals outside of the medical profession.  Further research and publications need to be put into place to raise awareness, and the next version of the DSM may benefit from clarification of this diagnosis.

 

References:

American
Academy of Child and Adolescent Psychiatry (AACAP).  (1999). Practice Parameters for The Assessment and Treatment of Children Adolescents, and Adults With Autism And Other Persuasive Developmental Disorders. Retrieved November 29, 2006 from http://www.aacap.org/galleries/PracticeParameters/Autism.pdf

Freeman, Roger.  (2006). Stereotypic Movement Disorder can be confused with tics and TS. Retrieved November 29, 2006 from http://www.tourette-confusion.blogspot.com/

 

Sadock, Benjamin & Sadock, Virginia. (2003). Kaplan & Sadock’s Synopsis of Psychiatry: Behavioral Sciences, Clinical Psychiatry (9th ed.). Philadelphia: Lippincott Williams & Wilkins.

 

Stein, Dan & Christenson, Gary. (1998). Stereotypic movement disorder: A neglected problem.  Psychiatric Annals, vol. 28, p. 304. 

 

 

 

Posted in Stereotypic Movement Disorder | 4 Comments »

Disorganized or Residual Schizophrenia

Posted by Administrator on November 23, 2006

The presentation of an individual with disorganized schizophrenia compared to one with residual schizophrenia will likely be quite opposite. A patient with disorganized schizophrenia will probably appear unkempt and display an inappropriate, silly, and childlike behavior (Sadock, 2003). They may laugh at the most serious of statements, as well as grinning and grimacing frequently. However, the extreme happiness may develop into extreme rage very quickly. The emotional liability of these patients is high. Before sedated or restrained, these patients may seem very anxious because of their constant activity, which normally consists of meaningless and often repetitive movements. Their speech will also come across in the same fashion. Though fairly spontaneous, it is normally unintelligible and may include rhyming and clanging. The break with reality is generally intense; and delusions and hallucinations may also accompany (2003).

On the other hand, someone with residual schizophrenia may seem to be withdrawn and show little emotions about anything (Sadock, 2003). They may appear very passive and even depressed because of their lack of initiative in speech or behavior. Speech is normally understandable, unlike in disorganized schizophrenia. However, one may link completely unrelated thoughts together or use nonverbal communication when possible. These patients usually have strange mannerisms or ways of thinking. They may wear eccentric clothing or have peculiar philosophies. Positive symptoms are very mild or infrequent. While delusions and hallucinations can occur, these are not prominent (2003).

While individuals with the paranoid schizophrenic subtype normally have a better prognosis, there is little variation on prognosis by subtype alone. If this was the first hospitalization for each patient, I would start by explaining the general prognosis for schizophrenia. I would inform them that only ten to twenty percent have a favorable outcome, but that the disorder does not always run a debilitating course (Sadock, 2003). In addition, I would tell them it is likely that their family member will have to be readmitted to the hospital within the next two years even with treatment.

After the general prognosis is described, I would then look at some of the other factors affecting the patient. If the patient is extremely young, has a family history of schizophrenia or perinatal trauma, a prior history of violence, or primarily negative symptoms (as seen in the residual type), then the outlook is probably going to be poor. I would then inform them that having the support or a family, friends, or spouse will improve the prognosis. On the other hand, if the patient is older, has a sudden onset, a positive social history, affective symptoms, or positive symptoms then I would say the prognosis is going to be brighter.

Reference:

Sadock, Benjamin & Sadock, Virginia. (2003). Kaplan & Sadock’s Synopsis of Psychiatry: Behavioral Sciences, Clinical Psychiatry (9th ed.). Philadelphia: Lippincott Williams & Wilkins.

Posted in Schizophrenia | 1 Comment »

Schizophreniform vs. Schizoaffective Disorder

Posted by Administrator on November 23, 2006

Schizophreniform and schizoaffective disorders share many of the same characteristics, but the main difference is that schizophreniform disorder is characterized by primary symptoms of schizophrenia, while schizoaffective disorder has to include both schizophrenic and mood disorder characteristics. In schizophreniform disorder, either no major affective episodes have occurred during the active phase of symptoms, or their total duration has been brief (Bhalla, 2006), compared to schizoaffective disorder where the affective symptoms must have occurred for a significant part of the disorder normally at a minimum of 15-20% (Sadock, 2003).

For an individual to be diagnosed with schizophreniform disorder, the symptoms of psychosis, those affecting speech and behavior, and the negative symptoms will last at a minimum of one month. To be diagnosed with schizoaffective disorder, a patient only has to have psychosis for 2 weeks without symptoms of a mood disorder (Sadock, 2003).

Both disorders have a prognosis somewhere between schizophrenia and mood disorders (Sadock, 2003). While schizophreniform disorder has an equal distribution among the sexes, schizoaffective disorder is more predominant in women. The age of onset, in early adulthood, is comparable in both disorders (2003). Schizoaffective disorder is thought to be around 2.5 to 4 times as prevalent as schizophreniform disorder, 0.2% to .05-.08%. Perhaps this is because the majority of schizophreniform cases evolve into schizophrenia before consultation?

Individuals with schizophreniform disorder can have the same symptoms as those with schizophrenia, but the symptoms must only last between one to six months. However, the onset in schizophreniform disorder is usually more rapid than that of schizophrenia. Unfortunately, sixty to eighty percent of patients with schizophreniform disorder progress to full blown schizophrenia (Sadock, 2003), while this does not seem to be the case in schizoaffective disorder.

While there is much disagreement about whether schizophreniform and schizoaffective disorders should have two different sets of criteria, the different methods of treatment support the idea that these disorders are separate occurrences. In schizophreniform disorder, the mainstay of treatment is an atypical psychotic for a period of three to six months (Sadock, 2003). In schizoaffective disorder, a combination of anti-depressant and anti-psychotic for the depressed subtype, or a combination of mood stabilizer and antipsychotic is utilized for the manic subtype (Brannon, 2005). This coincides with the criteria that schizophreniform is composed of primarily schizophrenic symptoms, while schizoaffective disorder is composed of both schizophrenic and mood disorder symptoms.

If someone presented with his or her first episode of symptoms that resolved within six months, the diagnosis would still be based on the symptoms themselves. Schizophrenia is automatically ruled out because of the short length of time, but either schizophreniform or schizoaffective diagnoses could be made. Though it would be easy to jump to the conclusion that the patient was experiencing schizophreniform disorder, someone with schizoaffective disorder could be in remission. In the patient has an equal, or significant, proportion of mood symptoms occurring along with the schizophrenic criteria, then a diagnosis of schizoaffective disorder would be warranted. Otherwise, the diagnosis would be schizophreniform disorder.

References:

Bhalla, Ravinder. (2006). Schizophreniform Disorder. Retrieved November 15, 2006 from http://www.emedicine.com/med/topic3350.htm

Brannon, Guy E. (2005). Schizoaffective Disorder. Retrieved November 15, 2006 from http://www.emedicine.com/med/topic3514.htm

Sadock, Benjamin & Sadock, Virginia. (2003). Kaplan & Sadock’s Synopsis of Psychiatry: Behavioral Sciences, Clinical Psychiatry (9th ed.). Philadelphia: Lippincott Williams & Wilkins.

Posted in Schizoaffective Disorder, Schizophrenia, Schizophreniform Disorder | Leave a Comment »

ADHD Diagnosis Controversy

Posted by Administrator on November 23, 2006

While the majority of clinicians and health agencies recognize ADHD as a real disorder, there is a great deal of ongoing controversy within the general public. A Frontline television program entitled “Medicating Kids” showcased some of these controversial views (Gaviria, 2001). One interviewee, Fred Baughman, has been a child neurologist for 36 years and is an active opponent of the ADHD diagnosis. Baughman says while the American Psychiatric Association views ADHD as a neurobiologic disorder, the psychiatry field has never “validated ADHD as a biologic entity” (2001). He also declares that these children are all normal and it is the parents and teachers who do not want to accept the responsibility for being unable to control the child. Russell Barker, a professor of psychiatry and neurology at the University of Massachusetts and another interviewee, continues with the discussion of parent responsibility (2001). Barker states:

But there’s also concern because ADHD is a disorder that appears to violate a very deeply held assumption that laypeople have about children’s behavior. All of us were brought up believing, almost unconsciously, that children’s misbehavior is largely due to the way they’re raised by their parents and the way they’re educated by their teachers. If you wind up with a child who is out of control and disruptive and not obeying, that that has to be a problem with child rearing. … Well, along comes this disorder that produces tremendous disruption in children’s behavior, but it has nothing to do with learning, and it isn’t the result of bad parenting. And therefore it violates these very deeply held ideas about bad children and their misbehavior (Gaviria, 2001).

This statement by Barker provides a valid explanation for the continuous controversy over whether ADHD is, in fact, a real disorder. In opposition to Baughman’s opinion, Barker states that ADHD is a valid condition; and if other mental disorders such as Schizophrenia, Bipolar Disorder, etc. required proof, there would be no such thing as psychiatry (2001).

Peter Jensen, the head of child psychiatry for the National Institute of Mental Health, attributes much of this controversy to the fact that “there isn’t good consensus about the best way to draw the boundaries between ADHD and other syndromes” (Gaviria, 2001).
Another article also states that critics of the diagnosis argue that the criterion is vague enough to allow most children to be diagnosed with this disorder (Answers, 2006). For example, psychiatrist Simon Sobo M.D. disputes that the symptoms of ADHD depict children when they are uninterested and unconnected to a task (2006).

There are many other reasons for the controversy surrounding the ADHD diagnosis. Some individuals conclude that teachers consider any child who cannot be controlled in the classroom to have ADHD, while others go on to say that these stimulants given to children diagnosed with ADHD have an affect on anyone (Answers, 2006). Regardless, the psychiatry field supports the diagnosis of ADHD. The aforementioned concerns may be valid and too many children may receive the diagnosis of ADHD. However, there is overwhelming evidence some individuals are affected with ADHD, and that the diagnosis is real.

References:

Answers Corporation. (2006). Controversy about ADHD. Retrieved November 22, 2006 from http://www.answers.com/topic/controversy-about-adhd

Gaviria, Marcela. (2001, April 10). Medicating Kids [Television broadcast]. Boston, MA: Frontline of WGBH.

National Institute of Mental Health (NIMI). (2006). Attention Deficit Hyperactivity Disorder. Retrieved November 22, 2006 from http://www.nimh.nih.gov/publicat/adhd.cfm#intro

Posted in ADD/ADHD | 27 Comments »

ADHD Diagnosis Difficulties

Posted by Administrator on November 23, 2006

 

As most all children have periods of restlessness, impulsivity, and daydream from time to time, diagnosing ADHD can be difficult (NIMH, 2006).  Symptoms vary so much in different situations, which can make this diagnostic process even harder, especially when the primary symptom in inattentiveness. However, whenever these behaviors start affecting school performance or relationships with other children, for example, ADHD may be suspected. Due to this difficulty, the diagnostic process requires behavior that is inappropriate for the child’s age, and as aforementioned, have at least 2 areas of life affected by these behaviors (2006).  If either schoolwork or family life is the only thing affected, then a child should not be diagnosed with ADHD. In addition, clinicians should check to make sure these behaviors are not situational.  For example, a child may begin to show inattentiveness if a family member dies or his or her parents are divorced.  Medical problems should also be considered such as petit mal or temporal lobe seizures, hearing problems, or a different type of learning disability (2006).

 

National Institute of Mental Health (NIMI). (2006). Attention Deficit Hyperactivity Disorder.  Retrieved November 22, 2006 from http://www.nimh.nih.gov/publicat/adhd.cfm#intro

Posted in ADD/ADHD | Leave a Comment »

ADHD Subtypes

Posted by Administrator on November 23, 2006

There are three recognized subtypes of ADHD:  hyperactive-impulsive type (does not show noteworthy inattention), predominately inattentive type (does not show noteworthy hyperactive-impuslive behavior), and the combined type (displays both inattentive and hyperactive-impulsive symptoms) (NIMH, 2006). Children with the hyperactivity-impulsivity type seem to be in constant motion, whether it be with talking, fidgeting, touching everything, etc. Impulsive children may utter inappropriate comments, be unable to wait their turn, and require immediate attention (2006).   Children with the inattentive type may get bored very easily, causing them to skip from one activity to another, become distracted by sounds or other irrelevant things, make careless mistakes, or forget things needed to complete a certain task.  These children, suffering from the inattentive type, are often overlooked because they may be very quite, get along sufficiently with other children, and appear to only be daydreaming (2006). 

National Institute of Mental Health (NIMI). (2006). Attention Deficit Hyperactivity Disorder.  Retrieved November 22, 2006 from http://www.nimh.nih.gov/publicat/adhd.cfm#intro

Posted in ADD/ADHD | Leave a Comment »

ADHD Overview

Posted by Administrator on November 23, 2006

 

 

ADHD, or Attention-Deficit Hyperactivity Disorder, affects approximately 3 to 5 percent of children (NIMH, 2006).  Inattention, hyperactivity, and impulsivity are the three primary symptoms of the disorder, which can appear over many months. Various situations may cause an exacerbation of different symptoms (2006).  Teachers are often the first individuals to recognize a child’s symptoms, because a parent may think all children go through “phases” such as this. For a child to be diagnosed with ADHD, their symptoms must appear before the age of 7, consist for at least 6 months, and create a handicap in two areas of the child’s life (such as in the schoolroom and in social situations) (2006). 

National Institute of Mental Health (NIMI). (2006). Attention Deficit Hyperactivity Disorder.  Retrieved November 22, 2006 from http://www.nimh.nih.gov/publicat/adhd.cfm#intro

Posted in ADD/ADHD | 3 Comments »

Family and Friends of Individuals with Bipolar Disorder

Posted by Administrator on October 29, 2006

Family and friends may be able to provide more accurate information about the patient’s mental condition than the patient themselves.  While they may not know what the patient is feeling, they can give an account of the patient’s behavior from day to day.  In addition, co-workers, instructors, and individuals who frequently come into contact with the individual may provide significant details pertaining to his or her condition. 

If it is confirmed that a patient has family members with a mental disorder, especially immediate family members with bipolar disorder, than the chances of inheritance are great.  Sometimes a genetic link may be the most significant clue of a full-blown or impending case of bipolar disorder.  If a patient has a parent with bipolar disorder and presents with symptoms of depression, then special attention should be given. Bipolar I disorder often begins with depression, so even if mania has not yet arisen, the individual should be carefully monitored for signs of extremely elevated or irritable moods.

 

Bipolar disorder is a difficult disorder to both diagnosis and to live with.  Family members are often affected as much as the patient.  Children with a bipolar parent may live in constant fear of their parent’s extreme mood swings and bear the major blunt of the disorder.  Many times a child may feel it is his or her fault when a parent is depressed or that he or she did something to cause the parent to become angry.  Spouses have it no easier.  The destructive behavior manic patients often engage in may have serious consequences, not just for themselves, but to their relationship as well.  A manic individual may desire sexual intercourse constantly or engage in dangerous sexual practices.  A family may go bankrupt due to a manic induced spending spree. A manic individual may be extremely volatile and have violent outbursts over the most insignificant things. 

 

When a patient comes off of a manic high, the situation is no better.  Depression is almost inevitable, and the consequences of their manic episodes often arise, causing an even deeper form of depression.  Considering how frequent suicide is in patients with bipolar disorder, families may live in a constant state of worry.  If an individual does commit suicide, family members often blame themselves as well.  Family members of individuals with bipolar disorder often experience mental disorders, even when there is no genetic link. The stress and anxiety of trying to take care of, and live with, a bipolar individual is great.  A clinician should not only assess a patient with bipolar disorder, but the family members as well.    

Posted in Bipolar Disorder | Leave a Comment »

Description of Bipolar Disorder

Posted by Administrator on October 29, 2006

Bipolar disorder, which was once termed manic-depressive disorder, is a mood disorder that affects around one percent of the population.  Unlike major depressive disorder, the prevalence of bipolar disorder is the same in men and women.  However, men are more likely to suffer from manic episodes and women from depressed episodes.  When women do experience mania, they are more liable to experience mixed episodes and rapid-cycling. Five to fifteen percent of individuals with bipolar disorder experience rapid-cycling, or having four or more manic episodes in a year (Sadock, 2003).

Two irregular mental states, depression and mania, are the hallmarks of the syndrome. A mixed episode, which meets the criteria for mania and major depression, may also occur.  The symptoms of depression displayed in bipolar disorder are consistent with that of major depressive disorder, including a depressed mood, weight loss or decreased appetite, fatigue, insomnia or hypersomnia, feelings of worthlessness or guilt, psychomotor agitation or retardation, a diminished ability to think, recurrent thoughts of death, and diminished pleasure in activities (Sadock, 2003).

 

Mania is defined as an abnormally elevated, irritable, or expansive mood lasting for a period of a week or longer (if untreated, three months on average) that causes marked impaired functioning. The normal onset is rapid- a few hours or days, but the state may evolve over a few weeks (Sadock, 2003). Symptoms include distractibility, a flight of ideas, a decreased need for sleep, increased talkativeness, inflated self-esteem, an increase in goal-directed activity or psychomotor agitation, and an excessive involvement in possibly detrimental, pleasurable activities (2003).  In severe cases of mania, psychotic features may be present, including delusions or hallucinations.  Patients with mania, especially those with psychotic features, may need hospitalization to keep from harming themselves or others. 

Patients with hypomania, a less severe form of mania, experience similar symptoms to those with mania, but do not have impaired functioning.  Episodes only have to last for four days or more rather than a week, hospitalization is not necessary, and psychotic features are not present (Sadock, 2003).  Even so, symptoms are noticeable by others and individuals in a hypomanic state have an unmistakable heightened level of functioning.

 

There are two main categories of bipolar disorder, Bipolar I and Bipolar II disorder.  To be diagnosed as having Bipolar I, a patient must have experienced at least one manic mood and one episode of major depression or a mixed episode. Bipolar I normally commences with depression; and the earlier the onset, the poorer the prognosis (Sadock, 2003).  Fortunately, around seven percent of individuals with Bipolar I disorder do not have a recurrence of symptoms. However, around a third of patients have persistent symptoms and social decline (2003). The criteria for Bipolar II disorder consists of at least one major depressive episode and hypomanic episode, without any periods of mania or mixed episodes.  Unlike Bipolar I disorder which may have permanent remittance however infrequent, Bipolar II disorder is a chronic, long-term disease. 

To read the symptoms of bipolar disorder is one thing; to experience them is a totally different situation.  Imagine being on a roller coaster. When the coaster is sitting still, the patient is stable, but may very well have an impending sense of dread for what is about to happen. Then the roller coaster starts climbing the hill.  One could equate this to the evolution of a manic episode.  Sleep starts to diminish and the mood starts to elevate.  The “rider” no longer has a sense of dread because he or she gets excited, elevated, and feels as if he or she can do anything. Then the ride truly begins.  Thoughts start flowing rapidly and the individual wants everyone to feel what he or she is feeling and has a desperate “need” to talk to anyone who will listen.  Things are truly wonderful and the world is a nice place to live.  However, once the ride goes on for a while, things begin to get confusing.  Everything seems to be rapidly flying past, but things start to make less and less sense.  Words don’t come out as fluently and this sense of elevation starts to become a source of extreme irritation. Everything starts to become exasperating.  Then the ride slowly comes to a stop.  The sense of elevation suddenly ends and the excitement is over.  After such a ride and being able to accomplish so much, what is left?  Every day life seems boring and thoughts are still muddled. The individual no longer wants to be around anyone because he or she has nothing to say.  Words don’t come out right anymore, and no one can understand what they are feeling. The only thing left is death because he or she no longer has anything left to give.  Of course, this is only a simplistic analogy of some of the symptoms patients experience when bipolar, but hopefully it provides a little insight into the disorder.

Posted in Bipolar Disorder | 2 Comments »

Anxiety Symptoms in Hypothyroidism

Posted by Administrator on October 19, 2006

Hypothyroidism, one of the most common endocrinological conditions associated with anxiety (Hall, 2002), is a state in which the body does not produce enough of the thyroid hormone (EndocrineWeb.com, 2005). One of the most common causes of hypothyroidism is autoimmune thyroiditis, also known as Hashimoto’s thyroiditis, which is an inflammation of the thyroid gland caused by an individual’s own immune system.  This inflammation will damage or destroy cells, leaving them incapable of producing an adequate amount of hormones (2005).  However, there are other causes, for i.e. individuals that do not produce enough hormones due to a problem with the pituitary gland (2005).

The main diagnostic tool for hypothyroidism is a blood test; if the thyroid hormone (TH) level is below normal range, then a patient most likely has hypothyroidism (EndocrineWeb.com, 2005).  Normally, an individual will have a high thyroid stimulating hormone (TSH) level along with a low TH level because the pituitary gland is trying to overcompensate for the lack of TH created (2005).

There is a wide range of severities within hypothyroidism, and the severity of symptoms does not always correlate with the severity of the disorder (EndocrineWeb.com, 2005). Some common physical symptoms are fatigue and lethargy, diminished libido, headaches, weakness, cold intolerance, and dry skin; physical signs include thin, course hair, pallor, brittle nails, and a slowed pulse (Hall, 2002).  Once the disease progresses, vision and hearing deficiencies, weight gain, inability to sweat, muscle cramps, and several other symptoms often arise.

Psychiatric symptoms, such as anxiety, are often the first indicators of hypothyroidism (Hall & Lowrance, 2002, & 2006).  Anxiety disorders occur in approximately 30-40% of patients with emerging acute hypothyroidism (Hall, 2002).  Severe anxiety attacks, panic attacks, and “free floating anxiety”, or a continuous feeling of being on edge, are all common anxiety reactions when hypothyroidism is developing (Lowrance, 2006). 

Hall (2002) reports the rapidly changing hormone levels in hypothyroidism is a key factor in the development of anxiety symptoms.  Patients with myxedema, a condition caused by hypothyroidism which involves blunting of the intellect and senses, thickening skin, and labored speech, present with progressive anxiety accompanied with generalized anxiety (2002).  Delusions, hallucinations, paranoia, and extreme restlessness mixed with lethargy are all common in individuals with myxedema.  Patients with more gradual drops in hormone levels still present with anxiety symptoms, but normally have a type of “chronic anxiety”. 

Lowrance (2006) reports in Hashimoto’s Disease that anxiety symptoms can be attributed not only to the abnormal thyroid levels, but also to the autoimmune disease process.  Anti-thyroid-peroxidase and anti-thyoglobulin, two anti-thyroid antibodies, can cause depression and anxiety symptoms even before hormone levels are out of the normal range (2006).  Lowrance states, “Researchers describe the anxiety symptoms from autoimmune hypothyroidism, as being caused by the gland’s attempts to ‘sputter back to life’ as it begins to fail and in attempt to fight off the autoimmune attack.  The actual medical term for this is ‘Hashitoxicosis’ and patients will have it to varying degrees but usually…causes significant anxiety symptoms.” 

When psychiatric clinicians are initially analyzing a patient, medical conditions must be considered before a diagnosis is made.  Some subtle differences may alert a clinician of the differences between psychologically caused and medically caused anxiety disorders.  For instance, medically induced anxiety disorders often show instability in the duration and severity of panic attacks or anxiety (Hall, 2002).  In addition, patients with anxiety disorders that form prior to the age of eighteen or after the age of 25 and who have a negative personal and family history of anxiety should be closely analyzed for an underlying medical condition (2002).  Hall reports that anywhere from 10-40% of medical patients with anxiety disorders are thought to have an organic etiology for their symptoms. 

The importance of taking medical conditions into consideration when diagnosing psychiatric patients is great.  If the anxiety disorder is truly organically induced, a patient will not recover psychologically without treatment of the physical disorder. Because emotional symptoms often arise before any physical symptoms in hypothyroidism, both patients and clinicians often make the mistake of attributing the disorder to a mental health problem.  While psychiatric drugs alone cannot cure the psychological symptoms involved during hypothyroidism and may in fact make the situation worse, drugs that treat the hypothyroidism will normally cure the anxiety symptoms, as well as the medical condition.  Lowrance (2006) exclaims, “Remember, thyroid diseases are a major cause and possibly the most common ‘medical cause’ of emotional symptoms!”

The articles presented by EndocrineWeb.com (2005), Hall (2002), and Lowrance (2006) provide both solid explanations and examples for anxiety symptoms presented in hypothyroidism.  Though the exact medical etiology is debatable and may involve a combination of factors, the high correlation of anxiety symptoms in patients with hypothyroidism supports the organic basis of psychological symptoms. Some symptoms of anxiety may be brought upon by the stress of having the disorder; but considering anxiety symptoms often precede any physical symptoms, this seems unlikely to be the sole cause.   

References:

EndocrineWeb.com. (2005). Hypothyroidism. Retrieved October 17, 2006 from http://www.endocrineweb.com/hypo1.html


Hall, Richard. (2002). Anxiety and Endocrine Disease. Retrieved October 17, 2006 from
http://www.drrichardhall.com/anxiety.htm

Lowrance, Jan & Jim. (2006). Anxiety and Depression Symptoms in Thyroid Disease.  BellaOnline.  Retrieved October 17, 2006 from http://www.bellaonline.com/articles/art41515.asp

Posted in Anxiety, Emotions, Hypothyroidism | 20 Comments »

Diabetes Prevention Strategy

Posted by Administrator on September 1, 2006

It is estimated that only ten percent of the original Native American population was alive by the eighteenth century (Sue and Sue, 2003). Much of this was due to disease. After being placed on reservations, the rate of obesity and diabetes rose drastically due to their sedentary lifestyle (Sue and Sue). A counselor can help an individual combat the physical aspects that lead to obesity and diabetes by establishing an informative and positive counseling method with the client. The outline Sue and Sue created for drug and alcohol counseling can be modified to create a successful diabetes prevention strategy.

To begin with, the first step in preventing diabetes is through knowledge. After finding out more information from my client, I would inform my clients what effects non-activity, unhealthy eating, and heavy alcohol use can have on the body. I could provide my clients with free literature from The Diabetes Association, or suggest other reference materials. I would also make my clients aware of the complications of diabetes, such as loss of eyesight, heart disease, or even kidney failure.

After making my clients aware of the causes and dangers of diabetes, I might refer my clients to a dietician if necessary. The clients would then be able to learn what to eat and what not to eat, as well as how much exercise is needed. The dietician could provide healthy tips such as choosing how to say “no” to certain foods, and how to determine how to eat balanced meals. If one is not aware of what foods are healthy and how blood sugar is controlled, he or she will not have the knowledge to make smart food choices.

Changing diet is not easy. I, myself, take a diabetic medication called metformin. Though offering personal opinions and thoughts is often frowned against in the mental health profession, I could share some of the ways I coped with changing my diet. Small tips such as avoiding the candy aisle and finding alternative solutions to unhealthy foods could help the client realize eating a healthy diet can still be enjoyable.

I believe one of the best ways of enforcing diabetes prevention, especially in native populations or other family-centered cultures, would be to bring the whole family into the counseling process. If the entire family is educated, each member can use positive reinforcement (Sue and Sue) to encourage one another. It is much easier for one to stick to a diet plan, or even for a smoker to quit, if the people around that person support him or her.

Making diabetes prevention one aspect of family “togetherness” could be looked on favorably by family-centered individuals. Along with diet, the family could schedule a time each week (or each day, as time permits) to do some kind of physical activity together. A counselor could present this strategy as a time to bond, while strengthening the body and soul.

For clients with a more individual identity, encouraging the buddy system could be productive. Some favorable suggestions would be to join a support group, utilize a health club, or become a member of a sports team. Any kind of positive support is healthy.

Most of all, I would try to emphasize a healthy lifestyle is doable and preventing diabetes is much easier than trying to manage diabetes itself. Providing resources, helping the client or family to set goals, and encouraging a positive social network would be strategies I would employ in a diabetic prevention program.

Sue, D.W. & Sue, D. (2003). Counseling the Culturally Diverse Theory and Practice (4th Ed.). NY: John Wiley & Sons, Inc.

Posted in Diabetes | 1 Comment »

Meet the renaissance dad

Posted by Administrator on July 8, 2006

Here is an interesting article on father involvement….

 Volume 36, No. 11 December 2005  

Meet the renaissance dad

Fathers are more involved in their children’s lives than ever before, and researchers are taking notice.

By Zak Stambor
Monitor Staff

Print version: page 62

Andrew Greengrass changes 21 diapers a week–ballpark. Sometimes more.Despite his demanding job as an attorney-editor for the legal publisher Thomson/West, Greengrass says his first priority is his family.

Outside the office, he devotes his time to cooking–he’ll make nearly anything as long as he has a recipe for it–and caring for his 10-month-old daughter Rebecca.

Weekday mornings Greengrass and his wife take turns changing and dressing Rebecca, then most days he drops her off at day care on his way to work. He picks her up 10 hours later. He telecommutes to work once a week so that he can spend time with Rebecca. And two or three times a week he straps his daughter into a baby backpack and heads to the grocery store to shop for that night’s dinner–be it chicken parmigiana, tacos or chicken marsala. When whipping together the ingredients, he adds the spiciest ones last so that Rebecca can try them.

Andrew’s involvement with his daughter reflects a trend for fathers to take a more active parenting role than in years past, says Michael Lamb, PhD, a Cambridge University social and developmental psychology professor. Lamb and his colleagues point to psychological research across ethnic groups suggesting that fathers’ affection and their increased family involvement help promote children’s social and emotional development. In turn, researchers are hoping to change the way therapists and the court system view fathers.

The shift in fathers’ roles began, Lamb says, around the time when more women entered the work force. Between 1948 and 2001, the percentage of working-age women employed or looking for work nearly doubled–from less than 33 percent to more than 60 percent–according to the Employment Policy Foundation’s Center for Work and Family Balance.

As a result, fathers like Greengrass have assumed roles that were formerly mainly the province of mothers, Lamb says.

“Formerly, fathers did not tend to be too involved with their children early on,” he says. “Their relationships were broadly based only later in their children’s lives. Now they’ve become significant child-care providers from early in their children’s lives.”

Father love

The cultural shift’s effects are just beginning to be explored through psychological research, says psychologist Ronald Rohner, PhD, director of the Center for the Study of Parental Acceptance and Rejection at the University of Connecticut.

“Even being a single dad myself, I’ve been knocked in the head a few times because I didn’t fully appreciate the importance of father’s roles,” he says. “By limiting our research by looking to children’s mothers to understand the youngsters’ development, we were only getting half the story.”

In a 2001 article in the Review of General Psychology (Vol. 5, No. 4, pages 382–405), Rohner and social worker Robert Veneziano, PhD, examined more than 90 articles published between 1933 and 2001 that explored the influence of fathers’ warmth and affection, or “father love,” on children. They found only 27 articles published between 1933 and 1980 related to the topic. But since the 1980s, nearly three articles each year have been published on the topic, many of which suggest that the influence of father love on children’s development is as great as the influence of a mother’s love.

“We’ve seen a realignment of roles within the vast majority of families,” he says. “Men are expected to be loving and supporting fathers rather than just a pocketbook.”

Rohner’s research suggests that father love helps children develop a sense of their place in the world, which helps their social, emotional and cognitive development and functioning. Moreover, he’s found that children who receive more father love are less likely to struggle with behavioral or substance abuse problems.

Lamb adds that father love provides an important template for meaningful relationships later in a child’s life.

“[Children] need to experience a sense of emotional security within their relationships with their parents or caregivers in order to learn how to relate to others,” he says.

Lamb rejects previous research that suggested that, to develop a sense of “manhood” and to understand social relationships, boys need a traditionally masculine father who primarily concerns himself with what goes on outside the home, rather than domestic details.

Instead, he says that fathers’ and mothers’ roles, and their impact, are more similar than different.

“What’s important is that children experience nurturing, warmth and sensitivity, and that someone is investing the time and energy in the child,” he says.

Spanning demographics, income levels

Most men, regardless of income level or demographics, share such a desire to be a nurturing father, says Jeffrey Shears, PhD, a professor of African-American studies and social work at Colorado State University.

“Across demographics, fathers are no longer content just shaking their children’s hands before they go off to work, like Ward Cleaver,” Shears says. “Fathers want to, and are, assuming caregiving roles.”

In an upcoming article in Families in Society, Shears and his colleagues found little variation between Hispanic, black and white fathers’ notions of their own caregiving, regardless of their children’s gender, how many children they had and whether they were in a relationship with the children’s mother.

In another study currently under review, Shears and his colleagues asked 485 fathers how often they engaged in 33 child-related activities, such as playing ball games or changing diapers.

Shears found cultural variations in fathers’ caregiving practices that counter several negative stereotypes. For instance, he found that black men are more likely to physically care for, feed and prepare meals for their infants than either white or Hispanic fathers.

That variation leads Shears to suggest that researchers should change the way they measure fathers’ involvement–from measuring the frequency and types of activities fathers engage in to focusing on how they interact with their children.

“Part of the perception that black men are not being there for their children is that we weren’t measuring what it is that they’re doing,” he says.

Likewise, psychologist Ross Parke, PhD, director of the Center for Family Studies at the University of California, Riverside, has found that some Mexican-American households are more egalitarian in terms of child care than previously thought, countering previous research that had suggested a pervasive hierarchical structure in Latino families, with an in-charge father who has limited interaction with his children.

“We’ve found that the stereotypes associated with Mexican-American families are simply not true,” he says. “If anything, Mexican-American fathers are more involved with their children and more supportive of their children.”

Parke and Shears suggest that researchers broaden how they define father participation in child-rearing.

“There is not simply one role of fathers,” he says. “There’s a lot of variation out there.”

Shears points to the range of child-care tasks men like Greengrass perform, from cooking dinner to changing diapers.

Clinical and court implications

Rohner also suggests that even if fathers are less actively involved–for example assuming a lesser role in a joint-custody situation–they still significantly affect their children. And that impact should be reflected in both therapy and the courtroom, he says.

“In clinical settings we have a tendency to…assume that problems that arise from childhood have something to do with something that mom did,” he says. “But we need to take a look at dad too.”

William DeFranc, PhD, a Harvard Medical School psychologist at Children’s Hospital Boston and a public school psychological consultant, agrees. He suggests that clinicians need to recognize that fathers’ presence is essential to understanding family dynamics.

For instance, during a recent intake interview, DeFranc met with a mother and child about the child’s separation anxiety. The mother told DeFranc that the child threw tantrums when the mother left her at preschool in the morning. However, after talking with the woman’s husband, DeFranc found that the mother was also having a hard time letting go of her first born.

“It’s important to get both sides,” he says. “We need to know how a child acts across different settings.”

In the court system, Rohner says family court judges are often not aware of the important role many fathers play in their children’s lives, despite numerous studies’ findings that suggest benefits of joint custody (see page 60).

For example, a 2002 meta-analysis in the Journal of Family Psychology (Vol. 16, No. 1, pages 91–102) by psychologist Robert Bauserman, PhD, of Maryland’s Department of Health and Mental Hygiene, found that children in joint-custody settings have fewer behavioral and emotional problems, higher self-esteem, better family relations and better school performance than children in sole parental custody.

When judges order one-size-fits-all custody arrangements, fathers who want to be actively involved in their children’s lives are often not allowed to be, Rohner suggests.

When loving fathers are cut out of their children’s lives, everyone suffers, he says.

“Fathers can have a tremendous influence on their children,” he explains. “And they need to realize that their children need to feel their love.”

Posted in Attachment Disorders, Family Ties, Misc | Leave a Comment »

Hospitalizations for Personality Disorders

Posted by Administrator on June 25, 2006

Posted in Disorders | Leave a Comment »

Concordance Study of Bipolar I Disorder in Twins

Posted by Administrator on June 4, 2006

 

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.

Posted in Bipolar Disorder | 1 Comment »

Narcoleptic symptoms in Parkinson’s Patients

Posted by Administrator on June 4, 2006

 

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

Posted in Narcolepsy, Parkinson's Disease | 3 Comments »

Understanding Attachment Disorders in Children

Posted by Administrator on June 4, 2006

Abandoned Child

(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:

Posted in Attachment Disorders | 8 Comments »

Autism and DLD Lateralization

Posted by Administrator on June 4, 2006

 

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.

Posted in Autism, Brain Lateralization, Frontal Lobes | Leave a Comment »

ADHD and ADD

Posted by Administrator on June 4, 2006

 

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.

Posted in ADD/ADHD | 3 Comments »

Apraxia

Posted by Administrator on June 4, 2006

 

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.

Posted in Apraxia | Leave a Comment »

Sleep Terrors, Why does Age Matter?

Posted by Administrator on June 4, 2006

 

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?

Posted in Sleep Disorders | 1 Comment »

Too much sleep..

Posted by Administrator on June 4, 2006

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!

Posted in Sleep Disorders | Leave a Comment »

Narcolepsy is Scary

Posted by Administrator on June 4, 2006

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!

Posted in Narcolepsy, Sleep Disorders | 7 Comments »

Insomnia, Direct or Indirect Disease?

Posted by Administrator on June 4, 2006

 

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.

Posted in Sleep Disorders | Leave a Comment »

Attachment Disorders and Sex Drive

Posted by Administrator on June 4, 2006

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

 

Posted in Attachment Disorders, Sex | Leave a Comment »

Aphasia

Posted by Administrator on June 4, 2006

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.)

Posted in Aphasia | Leave a Comment »

Autism Rebuttal

Posted by Administrator on June 4, 2006

 

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.

Posted in Autism | 1 Comment »

Child’s early development

Posted by Administrator on June 4, 2006

 

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.

Posted in Attachment Disorders | Leave a Comment »

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

Posted by Administrator on June 4, 2006

 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.

Posted in Attachment Disorders | Leave a Comment »

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

Posted by Administrator on June 4, 2006

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

Posted in Attachment Disorders | Leave a Comment »

What are the 5 basic tenets of an affectional bond?

Posted by Administrator on June 4, 2006

 

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

Posted in Attachment Disorders | Leave a Comment »

Additional Attachment Disorder References

Posted by Administrator on June 4, 2006

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.

Posted in Attachment Disorders | 3 Comments »

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

Posted by Administrator on June 4, 2006

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/

Posted in Attachment Disorders | Leave a Comment »

How does each of the different treatments work?

Posted by Administrator on June 4, 2006

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/

Posted in Attachment Disorders | 2 Comments »

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

Posted by Administrator on June 4, 2006

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.

Posted in Attachment Disorders | Leave a Comment »

Can a child possess more that one attachment disorder?

Posted by Administrator on June 4, 2006

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.

Posted in Attachment Disorders | Leave a Comment »

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

Posted by Administrator on June 4, 2006

 

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/

Posted in Attachment Disorders | 1 Comment »

Can the child form attachment disorders between parents?

Posted by Administrator on June 4, 2006

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/

Posted in Attachment Disorders | Leave a Comment »

Does gender have any affect on attachment?

Posted by Administrator on June 4, 2006

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/

Posted in Attachment Disorders | Leave a Comment »

Attachment Disorders: Q & A References

Posted by Administrator on June 4, 2006

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

Posted in Attachment Disorders | 1 Comment »

Delusions in Schizophrenic Patients

Posted by Administrator on June 4, 2006

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!

Posted in Schizophrenia | 2 Comments »

Positive & Negative Symptoms of Schizophrenia

Posted by Administrator on June 4, 2006

 

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

Posted in Frontal Lobes, Schizophrenia | Leave a Comment »

Causes for Schizophrenia

Posted by Administrator on June 4, 2006

 

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.

Posted in Schizophrenia | 2 Comments »