cognition and ect
DESCRIPTION
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. - PowerPoint PPT PresentationTRANSCRIPT
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COGNITION AND ECT
Iannis M. Zervas, M.D.Athens University Medical School
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ECT effects on cognitionMemory
Other
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ECT effects on memory
Apparent
Real
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Apparent effects-positiveMemory improvement (!)
Inaccurate psychologically but crucial from a psychiatric viewpoint
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Apparent effects-negativeResidual psychopathology (depression)
Drug effects (psych, anesthesia, other)
New psychosis (young, new onset)
Unmasking of dementia (old)
Subjective complaints (various motives)
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Real effectsDisorientation
Anterograde amnesia
Retrograde amnesia
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ECTAnterogradeRetrograderecentremote
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Time course of memory disturbanceAcute
Subacute
Long-term
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ECT effects on non-memory cognitionAcute phase ( 0-7 hours)
General intelligenceno change*Perceptual functionno change*
Attention-left side inattention-reduced speed in vigilance tasks*No change can be attributed to ECT
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ECT effects on non-memory cognitionSubacute phase (7-72 hours)
Intelligenceno change or improvedLanguage verbal fluency may be affected
Perceptual/Visuospatial no change Motor function no changeHigher cognitive/ frontal no change
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ECT effects on non-memory cognitionMiddle subacute period (72 hrs -1 wk)Intelligence improvement MMSELanguage improvement (rel. to depression)Perceptual improvementAttention/frontal no change (better in reaction time)
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ECT effects on non-memory cognitionLate subacute phase (1 wk -7 mo)Intelligenceimproved (or no change due to ECT)Languageno change (due to ECT)Perceptualimproved (normalized depr. changes)Motorimproved ( trend)Attention/frontalimproved mental shifts no change in vigilance
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Memory disturbance Acute phase
Postictal
Interictal
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Acute memory disturbancePostictal
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Acute memory disturbanceInterictal
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Subacute memory disturbance
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Memory effectsLarge inter-individual variability in:
Severity
Persistence (Reversibility)
Subjective tolerance / discomfort
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Factors affecting severity
Number of treatmentsFrequencyStimulus intensity
Electrode placement
WaveformOxygenationMedications
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Factors affecting persistenceProlonged post-ictal disorientationPre-ECT cognitive impairment
Probably age, neurological illness (e.g. Parkinsons disease)
other obvious factors never studied ( i.e. substance abuse, medications, cardiac output status, etc)
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Attempts to ameliorateNon-pharmacological methods ( schedule, oxygen, electrode placement, etc)
Various pharmacological methods
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ECT memory disturbancePharmacological attemptsACTHdexamethasone naloxonevasopressinT4TRHphysostigminecaffeineCa++ channel blockerspiracetampramiracetaminositolergoloid mesylates herbal preparations
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Memory systems involved in ECT with related brain structures
Short-term memory or immediate
Verbal
Visual
Neocortex
Long-term memory
Declarative
Learning
Retrieval
Medial temporal Lobe
Diencephalon
Non-Declarative
Priming
Procedural
Striatum/cerebellum
Neocortex
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Immediate / short-term memory (working memory)Prefrontal cortex involved; Medial temporal lobe lesions spare this subtypeDysfunctions after course of ECT (patients learn OK but forget fast)Returns to baseline after a few weeksOld patients more sensitive plus difficulty to learn new material. In 6 months no difference with younger.
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Declarative memory* New learning (anterograde amnesia)Transitory difficulties in retaining new information and in recognizing or retrieving information learned some time previouslyIncreases with increasing number of treatmentsNot associated with global cognitive dysfunctionRecovers within a few weeks after ECT*conscious recollection of facts and events, autobiographical or public
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Declarative memoryRemote memory (Retrograde amnesia)
Deficits in recall of autobiographical facts and events learned before ECTTemporal gradient ( more so for events within the year prior to ECT)Worse with bilateral Worse with sinewave treatmentsReversible by 3 -6 months
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Non-declarative memory*
No changeincludes 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
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Neurobiological correlatesTransient disruption of mechanisms for consolidation, retention, maintenanceDisruption 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 memoriesTime course of memory disturbance coincides with LTP disruptionRelated to mesial temporal lobe; less affected by bifrontal treatments
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Neurochemical correlatesECT inhibits activity of central cholinergic system= decrease in cholinergic transmissionExcessive release of excitatory amino acids and activation of their receptorsKetamine ( NMDA antagonist) may be better alternative for anesthesia
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In support ofMedial Temporal Lobe (MTL)Dysfunction in ECT memory disturbance
role of MTL in memorylow seizure threshold in hippocampusLTP disruption (ECS) is a hippocampal process theta activity in left frontal and temporal sites associated with greater retrograde amnesia for autobiographical information
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In support of involvement of Prefrontal Cortex (PFC)in ECT memory dysfunctionMost profound physiological effects of ECT found in PFC -reductions in CB, -reductions in metabolic rate, -EEG slow wave activityRetrograde amnesia greater for public events ( PFC) not autobiographical (hippocampus)
Tests of frontal lobe function can co-vary with tests of retrograde amnesia
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SUMMARYECT affects selectively memory parameters
There is large inter-individual variability
Memory disturbance is not related to clinical effects on depression
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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
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CONCLUSIONOne 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