Memory Processing

 

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

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

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