Causes of Anterograde Amnesia:
- Alzheimer's disease (also short term memory deficits and confusion)
- Korsakoff's psychosis (RA too, maybe reflecting gradual onset, confabulation)
- Herpes encephalitis
- Anoxia/ ischaemia (can result in very selective AA)*
- Injuries or tumours to limbic system and/or diencephalon (i.e. thalamus & hypothalamus)
- Surgeries for epilepsy involving temporal lobe(s)
- Degenerative brain diseases (e.g. schizophrenia, advanced multiple sclerosis, Huntington's disease)
>>The case of H.M. (Milner et al., 1968)
-Generalised epileptic seizures
-Bilateral medial temporal lobe resection
-Severe AA
-Above average IQ
-Normal on perceptual tests
-Good memory for events prior to surgery and early life history
-While at the research centre, HM repeatedly asked where he was and how he came to be there.
-Compared with a few other cases with restricted limbic and/or temporal lobe damage: they all have reasonable IQ, intact STM, but very poor LTM for new material, and intact perceptual/motor learning
The Claparede Effect: When Claparede went up to a patient with a pin in his hand when they shook their hands, the pin would hurt her. Everyday Claparede greets the lady and she could not recognise him at all time, however, when he offered to shake, she hesitated, recognising a threat despite her memory has been severely damaged.
The nature of the deficit:
1. Selective effect on LTM, but STM or WM intact.>Normal working memory on digit span-usually 7+3 digits
>Extended digit span-multiple repetitions of same digit string can increase the span, usually up to 20
>HM could not recall any string in excess of his normal ST span, even after 25 repetitions of the same string
2. Global-impairments across different modalities and materials
>Various tests conducted on patients to assess their learning and memory (e.g. free recall, cued recall, recognition...)
>Amnesia seen for information presented in different modalities (e.g. visual, auditory and olfactory)
3. Selective-only impairments in remembering new facts and events
>HM is unable to report any personal or public events since time of surgery
>Impaired on list-based tasks (e.g. paired associate learning)
4. Selective-amnesia spares learning and expression of skilled performance
>Amnesics' performance in repetition priming (e.g. picture fragment completion, word stem completion) improved by experience
>Amnesics showed savings in mirror tracing task (reproducing outline with only visual information from mirror)
>Amnesics get fast and accurate with multiple presentations in mirror-image reading task
**Spared skilled and performance but have little or not memory for learning experience, little recall/recognition of test materials, little or no insight into skills acquired (typically unaware that performance has improved)
5. Information that can be learned is inflexible and can only be expressed in limited contexts
>Performance has to be measured in exactly the same way to show savings
>Facilitation does not carry over to other tasks or test contexts
Hypotheses arising from the human clinical literature based on preserved abilities in cases otherwise severely amnesic:
=>Ryle (1949)-A number follow the distinction from philosophy between knowing how and knowing that.
=>Squire (1992)-Procedural vs declarative memory
=>Tulving (1972)-Semantic vs episodic memory
Two(or more) memory systems?
~Wider circuitry, not just hippocampus, involved in declarative or episodic processing
~Relatively pure amnesia also results from damage to mamillary body
Studies of AA confirm the distinction between long-term and working memory & implicit and explicit learning.
Learning and memory affected in amnesia seem to require hippocampus and/or related structures.
But the hippocampus cannot be the storage site for LTM, neocortex?
Intrusions errors evidence suggests material is in memory somewhere but appropriate retrieval is problematic. Lost/reduced encoding specificity?
没有评论:
发表评论