FINISH Neurobiology of learning, memory and cognition: memory Flashcards
Retrograde amnesia
Forgetting of events occurring prior to trauma e.g closed head injury/ electroconvulsive shock therapy
Anterograde amnesia
Inability to retain in a permanent form new material: i.e an inability to learn
Causes of amnesia (KAINE)
Anoxia, ischaemia, encephalitis, alcoholism & associated dietary insufficiency (Korsakoff’s syndrome), neurosurgery e.g to relieve epilepsy
Alzheimers disease- regions affected
Amnesia is a prominent component
Neuropathology strikes especially hippocampus & entorhinal cortex (within parahippocampal gyrus) of temporal lobe
Medial temporal lobe amnesia- patient HM
Unilateral lesions to R or L?
Received bilateral resection of his temporal lobes to relieve epilepsy.
Profound, polymodal anterograde amnesia for verbal & non-verbal material. However can hold a conversation, perform mental arithmetic, remember events from more distant past (a few years prior to op)
- severe recognition memory deficit as shown on performance matching to sample
- milder retrograde amnesia
- intact digit & spatial span and short term memory
- preserved IQ.
- sparing of procedural memory: can learn to draw in a mirror even though no recollection of daily sessions of testing.
Unilateral lesion limited to right: generally produce nonverbal memory deficits
Unilateral lesion limited to left: generally produce verbal memory deficits.
Diencephalic amnesia: patient NA, Korsakoff’s
NA: lesion of mediodorsal nucleus of the thalamus. Developed anterograde amnesia
Korsakoff patients have damage to diencephalic structures, including Papez’s circuit. Show anterograde amnesia (NB but also greater degree of retrograde amnesia than HM)
Sparing of procedural memory: learn perceptual skill of mirror reading as rapidly as controls, but are impaired at remembering what words they read. NB contrast Huntington’s Disease: impaired at developing mirror reading skill but perform better on word recognition.
Papez’s circuit
Cortex -> Hippocampus -> via fornix -> Mammillary body -> Thalamus -> Cortex
Damage to the posterior cortex, generally temporal-parietal junction.
Selective deficit in intermediate memory, shown by deficient memory span. However are able to consolidate info into LTM- not anterograde amnesiacs
Often conduction aphasiacs.
May involve a specific type of STM that evolved to allow us to follow conversations?
Agnosias
Higher level sensory deficits
Movement agnosia
Subject cannot ‘see’ movement
Prosopagnosia
Subject cannot recognise faces
Associative agnosia
Type of visual agnosia
Patient cannot recognise, name, or use objects appropriately. But can identify objects by selecting correct drawing, and can draw object accurately
Apperceptive agnosia
Type of visual agnosia
Patient can name an object is appropriate perceptual cues are present but cannot draw object. Also impaired at ‘naming’ object if presented if presented in unusual view.
Declarative vs procedural memory systems
Definitions?
Brain regions implicated?
Squire suggests that pattern of memory loss for anterograde amnesiacs gives evidence for distinction.
Declarative: facts, events. Suggested to have evolved more recently, depend on e.g temporal lone & diencephalon.
Procedural: knowledge gained through performance, Skill, habits, priming, conditioning etc. Brain systems less well defined, may include basal ganglia, cerebellum.