Memory Disorders: Anterograde Amnesia

amnesia

In this article introduces memory disorders; specifically anterograde amnesia. Using one of the most famous case studies of amnesia; the case of HM Henry Gustav Molaison (1926-2008).

POST-TRAUMATIC AMNESIA (PTA)
  • Most common form of amnesia
  • Cause: severe head trauma
    • Leads to brain lesions, twisting and tearing of microstructures, bony skull protrusions may scar (especially in temporal lobe)
  • Symptoms: initial unconciousness followed by period of confusion, inability to keep track of on-going activities or where they are
  • Duration: few minutes/hours
  • Recovery: Gradual return to normal although period around trauma may remain lost

memory disorder

LONG-TERM AMNESIA

Extreme head trauma may lead to long-term amnesia; the inability to recall old or encode new memories.

  • Anterograde amnesia: inability to create new memories
  • Retrograde amnesia: inability to recall memories prior to trauma

memory disorder

CASE STUDY: HM

Henry Gustav Molaison(1926-2008)

  • Severe epilepsy from 10 yrs
  • 1953 Experimental removal of medial temporal lobe (MTL)
    • Hippocampus, amygdala and parts of lateral temporal areas
  • Severe anterograde amnesia
  • Some retrograde amnesia
  • Preserved working memory
  • Preserved motor-skill learning
  • Deficit in transfer from WM to LTM
  • Language essentially frozen in the 1950s

“Pure” Amnesia

  • H.M. was widely studied because the precise surgical removal of most of his hippocampus allowed its function to be tested without other confounding impairments.
    • Brain Trauma is typically non-specific e.g. Hypoxia (lack of oxygen) can kill neurons throughout the brain.
  • H.M. was studied by thousands of psychologists/neuroscientists.
  • But, every day of testing was like the first.
  • Never recovered

memory disorders

ANTEROGRADE: NEW/OLD MEMORIES
  • Working memory (WM) is intact
    • Hippocampus (HC) is not critical for WM
  • Difficulty learning new information
    • HC is critical for the formation of new memories
  • Good memory up to brain injury
    • Recall of established LTM does not require HC
  • Personality, intelligence, judgment IQ unaffected
    • Not located in HC
    • Located in frontal lobes (as shown by other cases)

Hippocampus “Gateway” to Permanence

  • Brain legion evidence suggests that the hippocampus is important in the process of “consolidation
    • “Binding” episodes (input from sensory areas)
    • Transfering WM to LTM
    • Strengthening memories by
      • Learning new pathways
      • reusing existing pathways (through retrieval)

memory disorder

Amnesic evidence: Conditioning

Claparade (1911)

  • Neuropsychiatrist shook hands every morning with his amnesic patients.
  • Patients had no explicit recollection of him.
  • One day, hides a pin (US) in his hand patient recalls in shock (UR)
    • Unconditioned stimulus – unconditioned response
  • Next day, patient refuses to shake hands (CS) but cannot say why!
    • Conditioned stimulus – anticipation of shock (CR)

Conditioning does not require explicit memory or the brain regions (HC) necessary for explicit memory.

Amnesic evidence: Procedural Memory

  • H.M’s Existing procedural memories (i.e. Motor and perceptual skills ) intact
  • Can form new procedural memories!

Corkin (1968): Mirror-tracing task

  • Can learn skill and retain for up to 1 year.
  • Even though he has no episodic memory of doing it before!

memory disorder

Amnesic evidence: Priming

Repetition Priming = easier perception due to repetition, e.g. Words recognised faster if presented previously even in the absence of explicit memory!

Graf & Schacter (1985):

  • Study: word list (table, garden, umbrella)
  • Test:
    • Free recall (= poor as no explicit memory)
    • Cued recall: complete word stem with word from study list

umb____ ??

  • word stem completion: complete word stem with first word that comes to mind

gar___??

= Faster on both due to Priming.

Read next: ‘How do we store memories?

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