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Neuropsysiology of amnesia

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neuropsycology of amnesia

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Neuropsysiology of amnesia

  1. 1. Neuropsychology of amnesia Dr Rohini N Kathavate
  2. 2. Forms of memory: Larry Squire’s memory taxonomy
  3. 3. Forgetting • There is currently no theory that explains why we forget • Forgetting seems to follow rather strict rules, but even these have not been fully explored • It is postulated that very well rehearsed knowledge will never be forgotten (Harry Barrick’s ‘permastore’)
  4. 4. Before looking at the anatomy and clinical aspects of amnesia • We will review a connectionist model of amnesia • It will not be necessary to review the technical aspects of this model • The model may help you to get an overall idea of what amnesia is
  5. 5. We will focus on some important characteristics • Anterograde amnesia (AA) – Implicit memory preserved • Retrograde amnesia (RA) – Ribot gradients • Pattern of correlations between AA and RA – No perfect correlation between AA and RA
  6. 6. The French neurologist Ribot discovered more than 100 years ago that in retrograde amnesia one tends to loose recent memories Memory loss gradients in RA are called Ribot gradients
  7. 7. x retrograde amnesia anterograde amnesia lesion presentpast 0 20 40 60 80 100 Amnesie patient Normal forgetting
  8. 8. An example of retrograde amnesia patient data 0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 75-'8465-'7455-'6445-'5435-'44 Controls (n=16) Korsakoff's (n=6) Alzheimer's (n=8) Kopelman (1989) News events test
  9. 9. Neuroanatomy of amnesia • Hippocampus • Adjacent areas such as entorhinal cortex and parahippocampal cortex • Basal forebrain nuclei • Diencephalon
  10. 10. The TraceLink model is an abstraction of these areas Link system (hippocampus) Trace system (neocortex) Modulatory system (basal forbrain)
  11. 11. The position of the hippocampus in the brain
  12. 12. There are two hippocampi in the brain!
  13. 13. Connections to and from the hippocampus
  14. 14. Anatomy of the hippocampus
  15. 15. Hippocampus Entorhinal cortex 7a 36 TF TH 46 7b 3aP-IP-BV1M 3b Visual areas Somato- sensory and motor areas To and from sensory organs, via subcortical pathways Hippocampus Entorhinal cortex Unimodal and polymodal association areas (frontal, temporal, and parietal lobes) Parahippocampal cortex Perirhinal cortex (b)(a) Hippocampus has an excellent overview of the entire cortex
  16. 16. Diencephalon: dorsomedial nucleus and the mammillary bodies
  17. 17. Connectionist modelling • Based on an abstraction of the brain • Many simple processors (‘neurons’) • Exchange of simple signals over connections (‘axons and dendrites’) • Strength (‘synapse’) of the connections determines functioning of the network • Such neural networks can be taught a certain range of behaviors
  18. 18. Trace-Link model: structure
  19. 19. System 1: Trace system • Function: Substrate for bulk storage of memories, ‘association machine’ • Corresponds roughly to neocortex
  20. 20. System 2: Link system • Function: Initial ‘scaffold’ for episodes • Corresponds roughly to hippocampus and certain temporal and perhaps frontal areas
  21. 21. System 3: Modulatory system • Function: Control of plasticity • Involves at least parts of the hippocampus, amygdala, fornix, and certain nuclei in the basal forebrain and in the brain stem
  22. 22. Stages in episodic learning
  23. 23. Retrograde amnesia • Primary cause: loss of links • Ribot gradients • Shrinkage
  24. 24. Anterograde amnesia • Primary cause: loss of modulatory system • Secondary cause: loss of links • Preserved implicit memory
  25. 25. Semantic dementia • The term was adopted recently to describe a new form of dementia, notably by Julie Snowden et al. (1989, 1994) and by John Hodges et al. (1992, 1994) • Semantic dementia is almost a mirror-image of amnesia
  26. 26. Neuropsychology of semantic dementia • Progressive loss of semantic knowledge • Word-finding problems • Comprehension difficulties • No problems with new learning • Lesions mainly located in the infero-lateral temporal cortex but (early in the disease) with sparing of the hippocampus
  27. 27. Semantic dementia in TraceLink • Primary cause: loss of trace-trace connections • Stage-3 (and 4) memories cannot be formed: no consolidation • The preservation of new memories will be dependent on constant rehearsal
  28. 28. Severe loss of trace connections Stage-2 learning proceeds as normal Stage 3 learning strongly impaired Non-rehearsed memories will be lost No consolidation in semantic dementia
  29. 29. Clinical presentation of amnesia • Age • Degenerative disorders • Vascular disease • Anoxia • Korsakoff (vitamin B deficiency)
  30. 30. Clinical presentation of amnesia (con’d) • Focal brain damage • Closed-head injury • Transient global amnesia (TGA) • Electroconvulsive therapy • Psychogenic (functional) amnesia
  31. 31. Rehabilitation of amnesia • There is no known treatment • Compensation will, thus, help the patient best: – ‘memory book’ – electronic agenda • Errorless learning is pioneered by Alan Baddeley and Barbara Wilson
  32. 32. Comments • Very few people now believe that the amygdala plays a role in episodic memory • Most neurologists now accept the existence of focal retrograde amnesia (Kapur, 1993) • Animal studies (rats, primates) show clear evidence of Ribot gradients in the range 30 to 100 days

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