The+case+study+of+HM

=**Henry Molaison: A Summary**=

H.M.: Lost the ability to create new explicit memories, which lead to a greater understanding of localization of function over the 50 years he was tested.

At 27 - in an attempt to cure his epilepsy -> surgery removed both his temporal lobes including a structure known as the hippocampus Impact Significance
 * H.M. could no longer transfer memories from primary (short-term) to secondary (long-term) memory.
 * H.M.'s ST memory was normal. He could hold a normal conversation, and his memory span (primary memory capacity) was normal. However, when his attention was distracted, H.M. forgot everything that was in his mind a moment before. This condition is called anterograde amnesia.
 * Anterograde amnesia refers specifically to a loss of memory for events after the traumatic event causing the amnesia.
 * Also lost some of his existing LTM (retrograde amnesia).
 * mainly episodic memory that is lost, the ability to recall memories of events and certain factual information such as faces, dates etc.
 * So called semantic memory is largely unaffected so patients can still use language, and still retain an understanding of ‘how things work.’
 * However his STM remained intact with a normal capacity and duration, limited only by his inability to rehearse.
 * procedural memory not affected - could be taught new skills, which over time would improve with practice even though each time he used these skills, he had no recollection of previously doing so
 * Generated theory showed that
 * ST and LT memory were localized in biologically distinct systems
 * event memory and procedural memory were distinct.
 * the hippocampal circuit (which also involves parts of the temporal lobe and other structures) seems to be crucial for episodic or event memory.
 * though case information was unique to HM, it could be generalized to other patients with similar injuries

Evaluation (1 paragraph)
We must be careful not to jump to cause-effect relationships.
 * It is a fact that HM's hippocampal area was damaged. It is also a fact that his short term and long term memory were severely affected. **However**, keep in mind that he had suffered severe epileptic seizures prior to surgery. How do we know that sustained damage from those seizures were not also connected to memory loss? We don't.
 * Findings from HM's study need to be compared to those of others such as Clive Wearing, before determining the significance of the hippocampus.

However, one strength of this study is that it has provided a basis from which to compare other cases.

Another issue is to do with explaining his loss of memories specific to time and place. A conclusion was drawn (because HM could no longer recount such memories) that these memories are localized to the medial temporal lobe.
 * **However**, researchers later identified (from new scans in 2002 - 3) that changes had taken place in HM's brain, specifically "[|cortical thinning, subcortical atrophy, large amounts of abnormal white matter (Salat et al, 2006)]"
 * What was the connection between such changes and HM's remote memory for autobiographical events? Researchers cannot be sure.
 * **Another possibility** was that remote memories need constant rehearsal for effective retrieval. Perhaps the atrophy was a result of HM's inability to rehearse this information because he could not follow discussions of past events (ie. opportunities for rehearsal).
 * The point is, researchers cannot pinpoint the exact interaction taking place between localization of function and the deficits in HM's memory.

(Source: [|The legacy of patient H.M. for neuroscience)]