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COGNITION AND ECT

COGNITION AND ECT. Iannis M. Zervas, M.D. Athens University Medical School. ECT effects on cognition. Memory Other. ECT effects on memory. Apparent Real. Apparent effects -positive. Memory i mprovement (!) Inaccurate psychologically but crucial from a psychiatric viewpoint.

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COGNITION AND ECT

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  1. COGNITION AND ECT Iannis M. Zervas, M.D. Athens University Medical School

  2. ECT effects on cognition • Memory • Other

  3. ECT effects on memory • Apparent • Real

  4. Apparent effects-positive Memory improvement (!) Inaccurate psychologically but crucial from a psychiatric viewpoint

  5. Apparent effects-negative • Residual psychopathology (depression) • Drug effects (psych, anesthesia, other) • New psychosis (young, new onset) • Unmasking of dementia (old) • Subjective complaints (various motives)

  6. Real effects • Disorientation • Anterograde amnesia • Retrograde amnesia

  7. ECT Retrograde Anterograde remote recent

  8. Time course of memory disturbance • Acute • Subacute • Long-term

  9. ECT effects on non-memory cognitionAcute phase ( 0-7 hours) • General intelligence no change* • Perceptual function no change* • Attention -left side inattention -reduced speed in vigilance tasks *No change can be attributed to ECT

  10. ECT effects on non-memory cognitionSubacute phase (7-72 hours) • Intelligence no change or improved • Language verbal fluency may be affected • Perceptual/Visuospatial no change Motor function no change • Higher cognitive/ frontal no change

  11. ECT effects on non-memory cognitionMiddle subacute period (72 hrs -1 wk) • Intelligence improvement MMSE • Language improvement (rel. to depression) • Perceptual improvement • Attention/frontal no change (better in reaction time)

  12. ECT effects on non-memory cognitionLate subacute phase (1 wk -7 mo) • Intelligence improved (or no change due to ECT) • Language no change (due to ECT) • Perceptual improved (normalized depr. changes) • Motor improved ( trend) • Attention/frontal improved mental shifts no change in vigilance

  13. Memory disturbance Acute phase • Postictal • Interictal

  14. Acute memory disturbance • Postictal

  15. Acute memory disturbance • Interictal

  16. Subacute memory disturbance

  17. Memory effects Large inter-individual variability in: • Severity • Persistence (Reversibility) • Subjective tolerance / discomfort

  18. Factors affecting severity • Number of treatments • Frequency • Stimulus intensity • Electrode placement • Waveform • Oxygenation • Medications

  19. Factors affecting persistence • Prolonged post-ictal disorientation • Pre-ECT cognitive impairment • Probably age, neurological illness (e.g. Parkinson’s disease) • other obvious factors never studied ( i.e. substance abuse, medications, cardiac output status, etc)

  20. Attempts to ameliorate • Non-pharmacological methods ( schedule, oxygen, electrode placement, etc) • Various pharmacological methods

  21. ACTH dexamethasone naloxone vasopressin T4 TRH physostigmine caffeine Ca++ channel blockers piracetam pramiracetam inositol ergoloid mesylates herbal preparations ECT memory disturbancePharmacological attempts

  22. Memory systems involved in ECT with related brain structures

  23. Immediate / short-term memory (working memory) • Prefrontal cortex involved; Medial temporal lobe lesions spare this subtype • Dysfunctions after course of ECT (patients learn OK but forget fast) • Returns to baseline after a few weeks • Old patients more sensitive plus difficulty to learn new material. In 6 months no difference with younger.

  24. Declarative memory*New learning (anterograde amnesia) • Transitory difficulties in retaining new information and in recognizing or retrieving information learned some time previously • Increases with increasing number of treatments • Not associated with global cognitive dysfunction • Recovers within a few weeks after ECT *conscious recollection of facts and events, autobiographical or public

  25. Declarative memoryRemote memory (Retrograde amnesia) • Deficits in recall of autobiographical facts and events learned before ECT • Temporal gradient ( more so for events within the year prior to ECT) • Worse with bilateral • Worse with sinewave treatments • Reversible by 3 -6 months

  26. Non-declarative memory* No change includes • procedural learning ( neostriatum) • classical conditioning ( amygdala, cerebellum) • perceptual priming (cortical areas) Implicit memory** No change *non-conscious recollection of performance **non-conscious ability to learn spatial and temporal data

  27. Neurobiological correlates • Transient disruption of mechanisms for consolidation, retention, maintenance • Disruption of LTP related to persistence of stimuli, specificity /plasticity, associative organization • Possibly causes massive long-term induction of potentiation and saturates synaptic strengths obstructing formation of new memories • Time course of memory disturbance coincides with LTP disruption • Related to mesial temporal lobe; less affected by bifrontal treatments

  28. Neurochemical correlates • ECT inhibits activity of central cholinergic system= decrease in cholinergic transmission • Excessive release of excitatory amino acids and activation of their receptors • Ketamine ( NMDA antagonist) may be better alternative for anesthesia

  29. In support ofMedial Temporal Lobe (MTL)Dysfunction in ECT memory disturbance • role of MTL in memory • low seizure threshold in hippocampus • LTP disruption (ECS)is a hippocampal process • theta activity in left frontal and temporal sites associated with greater retrograde amnesia for autobiographical information

  30. In support of involvement of Prefrontal Cortex (PFC)in ECT memory dysfunction • Most profound physiological effects of ECT found in PFC-reductions in CB, -reductions in metabolic rate, -EEG slow wave activity • Retrograde amnesia greater for public events ( PFC) not autobiographical (hippocampus) • Tests of frontal lobe function can co-vary with tests of retrograde amnesia

  31. SUMMARY • ECT affects selectively memory parameters • There is large inter-individual variability • Memory disturbance is not related to clinical effects on depression

  32. SUMMARY • Memory disturbance is in general reversible • In some cases some retrograde amnesia for sporadic events (public mainly) may persist • Both mesial temporal lobe and prefrontal cortex (lowest seizure threshold in brain) have been implicated in memory trouble

  33. CONCLUSION • One should keep in mind that for most patients memory improves • Cost-benefit analysis for the patient • Simple measures can contain disturbance • Memory parameters should be monitored systematically - best to acknowledge and support / educate patient and family

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