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The Neural Basis Of Amnesia Lec 3 Notes

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The Neural Basis of Amnesia Problems with human data:

Lesions are rarely localised to a single structure  making it difficult to be precise about the exact pathology characteristic of amnesia (Aggleton &
Pearce, 2001) Functional imaging can provide insight into which brain regions are active or inactive during healthy controls or amnesic patients during an episodic memory task BUT- cannot establish cause and effect from this  further evidence from precise lesion studies is needed to substantiate the claims. The literature regarding amnesia, especially in rarer disorders, is based on evidence from single case studies due to a lack of sufficient cases available to researchers. Patients may have a mix of problems e.g. Clive Wearing - preserved semantic, intact STM but impaired LTM + confabulation  unlikely to have damage limited to one area

Animal models of amnesia:

Provides an opportunity to overcome some of these issues and has been necessary to further develop our understanding of the neural bases of amnesia Allows precise lesion, genetic and molecular techniques to be carried out that cannot be ethically applied to humans (Dere, 2006) Allows for the controlled conduction of experiments to assess the neurobiological basis of human memory dysfunction (Winters, 2010)

DMTS - Delayed Match to Sample Test
 One way of assessing episodic like memory (ELM) is the delayed non match (DMNS) and delayed match to sample (DMTS) task.
 An animal is first presented with a sample stimulus and after a retention delay, the sample object is presented alongside a novel stimulus.
 The subject is required to seek out the novel (DNMTS) or sample (DMS) stimulus in order to obtain a reward (Winters et al., 2010).
 Monkeys are typically good at this amnesia sensitive task  however lesions to the hippocampal formation, parrahippocampal cortex and perirhinal cortex, crucial neural structures implicated in human amnesia, result in severe impairments (Zola-Morgan et al., 1993).
 Zola-Morgan et al (1993)  lesioning several different combinations of areas in the monkey
- They demonstrated that their H++ lesion which includes the hippocampal formation, perirhinal cortex, - but sparing the amygdala produces the greatest memory deficit in the amnesia sensitive task of DMTS
 Hippocampus + surrounding cortex plays an important role in performing DMTS in monkeys
 Amygdala plays little or no role

 Hippocampus + surrounding cortex has become known as the medial temporal lobe memory system (MTLMS)

Support for the amygdala playing little or no role Bechara et al (1995)  Double dissociation of conditioning + declarative knowledge relative to the amygdala + the hippocampus o

o o o

Patient with selective bilateral damage to amygdala = impaired at conditioning autonomic (SCR's) responses to visual/auditory stimuli - but did acquire the declarative facts about which visual/auditory stimuli were paired with the unconditioned stimulus Patient with selective bilateral damage to the hippocampus failed to acquire the facts but did acquire the conditioning Patient with bilateral damage to both amygdala + hippocampal formation acquired neither the facts nor the conditioning Demonstrates a double dissociation of conditioning + declarative knowledge relative to the human amygdala + hippocampus

Squire's MTLMS (MEDIAL TEMPORAL LOBE MEMORY SYSTEM): (Squire, Stark & Clarke, 2004)
 MTLS includes system of anatomically related structures that are essential for declarative memory (conscious - facts + events) - makes a memory system
 Consists of the hippocampal region + the adjacent perirhinal + entorhinal
+ parahippocampal cortices
 Three pieces of evidence that the MTLMS contributes to declarative memory 1) Patients with damage limited to hippocampal region have a moderately severe memory impairment - less severe than those found in patients with larger lesions inc MT cortex (Corkin, 1997) 2) Systematic comparisons of monkeys with MTL lesions - monkeys with limited hippocampal lesions = moderately impaired but monkeys with lesions that inc hippo region + adjacent cortex = more severe memory impairment (Zola-Morgan et al, 1994) 3) Impairment is multimodal - memory affected regardless of sensory modality info is presented in  consistent with the fact that structures of the MTL = convergent zones of cortical processing + receive input from all sensory modalities Can model all types of amnesia through the use of animals:

DMTS = AA memory Spared abilities (motor + cognitive skills)  Zola-Morgan & Squire (1984)
- Monkeys with conjoint lesions to the hippocampus + amygdala (modelling HM)

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