#10620 - Functional Deficits Underlying Amnesia. Lec 2docx - Neuropsychology of Memory

Functional Deficits Underlying Amnesia

Historical attempts to understand amnesia

• Lashley (1929)

• Wanted to search for the “engram” of memory physical representation of memory in the brain / single biological locus of memory

• He researched this by looking at the measurement of behaviour before + after specific, carefully quantified , induced brain damage in rats

• He trained rats to perform specific tasks – for food rewards -then lesioned specific areas of the rats cortex – either before or after training

• Cortical lesions had specific effects on the acquisition + retention of knowledge - but the location of the rats cortical damage had no effect on the rats performance on the maze

• This led Lashley to conclude that memories are not localised - rather they are widely distributed across cortex

• Developed a theory of ‘Mass Action’ rate, efficacy + accuracy of learning depends upon the amount of cortex available - deterioration of performance on the task is determined by the amount of tissue removed rather than its location

• Also developed idea of ‘Equipotentiality’ one part of the cortex can take over the function of another part within a functional area of the brain - any tissue within that area can perform the function - therefore to destroy a function – all tissue in that area must be destroyed.

• Penfield (1954)

• While conducting surgery to remove specific types of temporal loci which were causing epilepsy – noticed that stimulation of the temporal lobe induced vivid memory representations in patients

Can Penfield’s results be otherwise explained?

• Only small minority of patients (7%) stimulated in the temporal lobe gave memory like responses

• These memories had a dream like quality to them – inaccessible, fantasy like – are they really memories?

• Some memories appeared to be false

• Memory experience was not tied to the location of stimuli - sometimes got memories when stimulated different locations

• The effects may have been a result of electrical discharges spreading to other brain sites

Case R.B. (Zola-Morgan, Squire & Amaral, 1986)

• Early evidence suggested memory impairment could be localised to the medial temporal lobe (Glees & Griffith, 1952)

• Formal testing of H.M + 9 other patients - Scoville & Milner (1957) – led to the view that damage to the hippocampus was responsible for the amnesia

• Memory impairment was observed whenever the hippocampus + hippocampal gyrus were damaged bilaterally

• Patient whose resection included the amygdala + uncus - + sparing the hippocampus was not amnesic

• The severity of deficits correlated with the extent of hippocampal damage – directly proportional (Milner, 1972)

• Case R.B.

• Suffered an ischematic episode during heart surgery – severe temporary loss of BP – blood oxygen doesn’t reach certain areas of the brain

• Given battery of neuropsychological tests (paired associate, word pairs, WMS, diagram recall, Rey-Osterreith) severe impairment on tests of verbal + non-verbal memory function => severe AA

• Given RA tests – public events, famous faces, TV programmes, autobiographical recall had little or no loss of memory from before damage

• No signs of sig cognitive impairment bar his memory

• Post mortem analysis extensive + fairly selective damage to the CA1 region of the hippocampus – no cell loss was detectable in any other field of the hippocampal formation other than CA1

• Also were unilateral lesions to basal ganglia + somatosensory cortex (not associated with memory before) – must consider the possibility that impairment came from combo of this and CA1.

• Memory impairment following limited damage is stable + long lasting – persisted for more than 4yrs after injury

• Consistent with findings that experimentally induced ischemia in rats damages the CA1 region of the hippocampus + results in long-lasting deficits in new learning ability (Davis et al., 1986)

• Findings support the idea that declarative memory is impairment + that the hippocampus is an essential component of this damaged neural system – procedural memory is independent of this system.

• Circumscribed bilateral lesion to the CA1 field of the hippocampus is sufficient to induce amnesia

Many types of amnesia:

• Encephalitis – clive wearing

• Surgical removals – H.M

• Anoxia (depleted O2 levels) – R.B.

• Alcohol abuse (thiamine deficiency) Korsakoff syndrome – P.Z.

• Accidents e.g. fencing iron – N.A.

• Degenerative disorders

• Strokes

Squire (1982) – Two different types of amnesia

• Amnesic patients damage falls roughly into 2 areas

1. Diencephalic region (thalamus) – N.A., Korsakovs, P.Z

2. Medial temporal region – e.g. HM, RB, Clive Wearing.

• Suggested that recent studies of forgetting provide strong evidence that there are two forms of amnesia that are fundamentally different – diencephalic + bitemporal

• Idea first advanced by Lhermitte & Signoret (1972)

• Patients viewed 120 coloured slides

• Retention assessed by yes/no recognition procedure at 3 diff intervals after learning (1m,1day,7days) -40new slides + 40 original slides presented at each interval (amnesics given longer to look @ slides)

• Findings support the idea that diencephalic amnesia (Korsakoff + N.A) is characterised by a normal rate of forgetting

• Bitemporal amnesia (H.M + ECT patients) characterised by rapid forgetting

What are the cognitive processes disrupted in amnesia?

Encoding failure to encode info in a suitable way for long term retention

Storage failure to retain info over a delay

Retrieval failure to access existing memory

ENCODING

• Cermack (1979) – used Craick &Lockhart (1972) levels of processing theory

• Hyp = amnesics fail to spontaneously encode info deeply

• Shown cartoons (funny or neutral) – given 3 tasks...