Why do we study Amnesia and brain damage?

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well, hey.

i know it has been a while since last we spoke, and yes i have longed for the incessant clicking of my fingers on the keys, alas university exams have been controlling my internet usage with no respite. So i figured, since i have completed one and have another in a few days i would write some stuff about why cognitive psychologists study amnesia and brain damage patients. You might wonder; why would they not just study a healthy brain? Well, i guess sometimes it makes sense  to do that. However, when you are trying to decipher the effects of recognition, recall or procedural memory for example, there is only so much a healthy brain can provide.

Let’s take HM as our first example of amnesia and how it helped us in regards to memory. HM was a guy who had a bilateral medial temporal lobotomy. This specific surgery removed large/entire portions of the hippocampi, parahippocampal cortices, amygdalae, as well as a few other surrounding cortices. You are probably wondering why anyone would undertake such an extreme operation, removing such a large portion of the brain. Well, Henry had terrible epilepsy. He gained this epilepsy from a bicycle accident he had at age 9. Between the ages of 9 and 16, Henry had very aggressive seizures. in 1953, at age 27, Henry was referred to a neurosurgeon by the name of Scoville and it was decided, after Scoville localised the problem to the right and left medial temporal lobes, that Henry was to have surgery to remove them and possibly solve his horrid seizures.

The good news: the surgery was a fantastic success! Henry no longer suffered from seizures. Hazzah!

The bad news: Henry now had severe anterograde amnesia. Whoops.

anterograde amnesia is that which does not allow your brain to retain new information. What makes life that much harder for Henry though, is that he also had mild retrograde amnesia (which if you are smart, you would realise means that his brain does not allow the retention of old memories, i know you all got that *high 5*). For many years after this, Henry who went on to be known as HM, was studied for his wonderfully, somewhat ruined brain.

What did we learn from HM? Well, after his surgery although HM’s procedural and working memory were intact, he was unable to commit any new semantic information to his explicit memory. HM’s brain surgery allowed insight into how particular areas of the brain function in regards to memory and memory retention. One example is his capability to complete tasks that require recall from the short term memory and procedural memory but not long term episodic memory. This suggests that maybe recall from these memory systems may be (in part) mediated by different areas in the brain, due to one being affected by the operation and not the other.

whoa, whoa, whoa, i hear you say; what the heck is explicit, episodic, or working memory anyway?

WELL…

Episodic memory – this is the long term memory we have for autobiographical events and their contexts. Think episodes of Firefly (oh Mal :3)

Explicit memory – this is conscious memory that we use memory processes to attain.

Working memory – this is the part of memory that we use for understanding language and immediate conscious perceptions. A guy named Baddelley brought it into theoretical being. It consists of 4 things; a phonological loop (processes verbal data), a central executive (which combines the sketch pad and the loop), an episodic buffer (mediates between working and long term memory) and a visuo-spatial sketchpad (for interpreting visual stimuli).

So if you think about it; HM had no long term memory (mild retrograde amnesia) and definitely no short term memory (anterograde amnesia) so where exactly was he living? Well, you know how people tell you to “live in the moment” more? That is literally what HM was doing.

However, HM was not completely void of function. He had retained a somewhat good short term memory store and would do well in word, phoneme etc tests. So that shows, again, that memory is not all condensed into one specific area of the brain as previously thought. Too, his retrograde amnesia was indeed bad, but it was only the 2 or so years before the surgery that he could not remember. The earlier years, such as that of his childhood, were clear and able to be recalled. This shows that certain long term memories do not rely on the medial temporal lobe as do the ones that are newer.

Psychology uses amnesia and brain damage patients instead of healthy brains as they have so much more to give than a healthy brain. It is in the not knowing of how certain parts work that we realise that perhaps certain memory channels have different pathways and the like. Even in the cases where short term is the lost key and long term is intact there are still a great deal of differences between task completion between participants, showing that depending on when the brain is damaged depends on how well it can repair it self and create new neural pathways.

S xo

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