PSY 335 Memory and Amnesia

1. PSY 335Memory and Amnesia Memory Disorders

2. Influences on Memory • Alcohol – Bits & Pieces • Stress -- Kolb & Whishaw Seg 32 (CD 2) • Diabetes – Kolb & Whishaw Ch 13 Seg 6 (CD 3)

3. Kinds of Memory Disorders • Organic – having a physical cause • Functional – having a psychological cause • Dys (as a prefix) means difficulty or limited ability to perform. • A (as a prefix) means complete inability or lack of a function.

4. Alcohol & Memory • Alcoholic amnesia – alcohol prevents consolidation so nothing is remembered and no memory can be recovered. • Alcoholic blackout – state-dependent memory, so recall is possible if one is back in the same state. • Because many crimes are committed while drunk, memory failure is frequently blamed on alcohol.

5. Sleep & Memory • New sleep studies suggest a "memory life-cycle” with three stages - stabilization, consolidation, and re-consolidation. • Initial stabilization takes up to 6 hours. • Sleep needed for consolidation, deep non-REM • Alcohol disrupts consolidation • Sleep deprivation produces effects similar to aging. • Procedural memory and recognition memory are most strongly affected.

6. Sources of Organic Dysfunction • Accident • Car accidents and other injuries (e.g., N.A.) • War • Disease • Encephalitis (viral) – inflammation of the lining of the brain, causing swelling. • Stroke • Alzheimer’s disease • Korsakov’s syndrome (prolonged alcoholism)

7. Alzheimer’s Disease • A fatal degenerative disease caused by cell failure – neurofibrillary tangles and plaques that interfere with cell function. • All areas of the brain are eventually affected, but frontal lobes and memory go first. • Confusions and memory problems do not resemble normal aging, amnesia or other memory problems.

9. Classification of Disorders • See Parkin, Ch 5, for tests used to assess memory problems. • Disorders classified by type of symptom: • Generalizing – confusion, fuzziness, mental slowing. • Localizing – few generalizing symptoms but impairment of specific functions. • Clusters of symptoms are a syndrome. • Concern about symptoms is a symptom itself.

10. Frontal Lobe Deficits • Confabulation – production of a false memory. • Momentary confabulation – responses that could be correct. • Fantastic confabulation – responses clearly fictional. • Source amnesia – fact is remembered but not the source. • Memory of temporal order.

11. Frontal Lobe Deficits (Cont.) • Impaired recall – more “ugly stepsisters,” no categorization. • Metamemory is impaired, including FOK judgments and monitoring of search. • False recognization: • Increased false alarms • Increased intrusions

12. Frontal Lobe Deficits (Cont.) • Faulty encoding and poor representation may be a cause of poorly focused search. • Information is needed to guide search. • The left frontal lobe guides encoding. • The right frontal lobe guides retrieval.

13. Frontal Lobe Deficits (Cont.) • Emotional deficits: • Cognitive apathy, lack of motivation • Flattened affect • Impaired awareness of memory loss: • Inaccurate assessment of performance • Lack of distress • If confabulations are believed by others, no feedback on normalcy.

14. Alien Hand (Anarchic Hand) Syndrome – a Frontal Lobe Deficit

15. Peter Sellars in “Dr. Strangelove: or How I learned to story worrying and love the bomb”

16. Damage to the Parietal Association Cortex • Confusion about directions, inability to use words describing spatial relations: • Under, up, down • Inability to name body parts or point to parts of the body. • Capgras syndrome (rt. Posterior parietal) inability to recognize close family members • Sometimes animals or even furniture • Invasion of the body snatchers

17. Reading & Writing Disorders • Alexia – inability to read • Agraphia – inability to write • Caused by damage to the left angular gyrus which integrates information from the sensory modalities.

18. Pure Word Deafness • A person can hear and speak, read and write normally but cannot understand speech. • Occurs with bilateral destruction of the auditory cortex or disconnection from Wernicke’s area. • Because Wernicke’s area is not damaged, speech produced is OK.

19. Perceptual Deficits • Aphasia – involves inability to name something. • Agnosia – involves inability to recognize something. • Visual agnosias – inability to combine individual visual impressions into complete patterns.

20. Types of Visual Agnosias • Object agnosia – inability to recognize common objects. • Prosopagnosia – inability to recognize faces. • Color agnosias: • Achromatopsia (cortical color blindness) • Color anomia – inability to name colors. • Color agnosia – inability to recognize colors

21. Other Agnosias • Amusia – tone deafness, melody deafness, disorders of rhythm, measure, tempo. • Astereoagnosia – inability to recognize the nature of an object by touch. • Asomatoagnosia – knowledge of one’s own body. • Indifference to illness, asymbolia for pain

22. Pure Anomia • Loss of memory of words (anomic aphasia) • Cannot name pictures of common objects • Difficulty reading and writing • Produced by damage to either Broca’s or Wernicke’s area (fluent anomia). • Use circumlocutions to get around missing words.

23. Broca’s Aphasia • Broca’s area may contain memories of the movements needed to produce speech. • Produces three deficits: • Anomia – word-finding difficulty • Agrammatism – loss of grammatical construction • Difficulty with articulation • Slow, laborious, nonfluent speech without function words with with content words.

24. Conduction Aphasia • Disruption of verbal short term memory due to damage to the subcortical axons that connect Broca & Wernicke’s areas. • Results in poor repetition – only meaningful words can be repeated (through other means). • Non-words cannot be repeated (blaynge).

25. Amnesic Syndrome • Short term memory is intact (unimpaired) • Anterograde amnesia present affecting both recognition and recall tasks. • Retrograde amnesia present, but extent varies. • Semantic memory largely intact but can be affected by antero & retro amnesias. • Procedural memory is intact.

27. Causes of Amnesic Syndrome • Damage to: • Hippocampus • Temporal cortex • Diencephalon (especially mamillary bodies) • Herpes simplex encephalitis • Korsakoff’s syndrome (thiamine deficiency plus chronic alcoholism) • Direct injury (H.M., N.A.)

28. Anterograde Amnesia • No new declarative information can be added to long-term memory • Events from the present are quickly forgotten • Usually accompanied by retrograde amnesia. • Performance on IQ tests is unimpaired because it relies on info learned in past.

29. Retrograde Amnesia • Declarative information from the past is forgotten. • Information is forgotten in a temporal gradient (based on time): • Ribot’s law – newer information forgotten first. • Both semantic and episodic information show this gradient. • Difficult to test due to differences in life experiences, impairment varies.

30. Focal Retrograde Amnesia • Loss of remote memory unaccompanied by anterograde amnesia. • May occur when the temporal cortex is damaged but not the hippocampus. • Cases reported without head injury and with loss of procedural memory are probably malingering (faking).

31. Evidence for Implicit Memory • Alzheimer’s patients show impaired priming. • Huntington’s Chorea patients show normal priming but impaired procedural memory. • Procedural memory and priming are spared by amnesia.