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Memory and the brain
Sub-Topics
How Memory Works
Forgetting and Amnesia

Linked
HelpLinked Module: AmnesiaLink : How Memory Works
Researcher
Researcher Module: Brenda Milner, an Eminent Neuropsychologist
History
History Module:  The Modern Era of Memory Research

If an individual displays a particular behavioural deficit after a certain structure in the brain has been destroyed, that does not necessarily mean that this structure was the source or “centre” of that behaviour. All it means is that the lesion has destroyed a circuit whose integrity was necessary for that behaviour.

When the destruction of the hippocampus causes amnesiac syndrome, we can deduce that the hippocampus is definitely part of the circuit that allows memorization.

LESIONS THAT CAUSE AMNESIA

Amnesiac syndrome is probably the most disabling form of memory disturbance. It is characterized by ongoing forgetting of any new information (anterograde amnesia) and by retrograde amnesia of varying severity.

This was exactly the type of deficit that affected the famous patient H.M. After the inner portions of his two temporal lobes were surgically removed to treat his epilepsy, H.M. was unable to encode new information in his long-term memory. He no longer suffered from epilepsy, but without his hippocampi, everything in his memory vanished after a few minutes.

The literature now records some 50 well documented cases of amnesiac syndrome following the destruction of both hippocampi (as the result of a stroke, for example). And just like H.M., though these other patients suffered from severe anterograde amnesia, their general knowledge and their memories of episodes from long ago in their lives were generally not affected by their lesions.

These cases led scientists to conclude that the hippocampus and the neighbouring regions of the cortex did not seem to be involved in storing information, but only in encoding it.

The hypothesis was therefore formulated that information might be stored in other areas of the brain, and in the rest of the temporal cortex in particular. This hypothesis was supported by other cases where patients had suffered damage to their entire temporal lobes, but the region of the hippocampus had been preserved. These patients suffered from a syndrome exactly the opposite of H.M.’s: they remembered things that they had learned recently better than they did their childhoods.

Current theories on the brain structures involved in memory therefore postulate that the hippocampus and the temporal cortex play distinct but complementary roles in acquiring and storing information.

But they are not the only structures that do so, because other amnesiac syndromes involving other regions of the brain also exist.

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