COGNITION AND ECTCOGNITION AND ECT
Iannis M. Zervas, M.D.Iannis M. Zervas, M.D.
Athens University Medical SchoolAthens University Medical School
ECT effects on cognitionECT effects on cognition
MemoryMemory
OtherOther
ECT effects on memoryECT effects on memory
Apparent Apparent
RealReal
Apparent effectsApparent effects-positive-positive
Memory iMemory improvement (!)mprovement (!)
Inaccurate psychologically but Inaccurate psychologically but
crucial from a psychiatric crucial from a psychiatric viewpointviewpoint
Apparent effectsApparent effects-negative-negative
Residual psychopathology Residual psychopathology (depression)(depression)
Drug effects Drug effects (psych, anesthesia, other)(psych, anesthesia, other)
New psychosis New psychosis (young, new onset)(young, new onset)
Unmasking of dementia Unmasking of dementia (old)(old)
Subjective complaints Subjective complaints (various motives)(various motives)
Real effectsReal effects
DisorientationDisorientation
Anterograde amnesiaAnterograde amnesia
Retrograde amnesiaRetrograde amnesia
ECT AnterogradeRetrograde
recentremote
Time course Time course of memory disturbanceof memory disturbance
AcuteAcute
SubacuteSubacute
Long-termLong-term
ECT effects on non-memory ECT effects on non-memory cognitioncognition
Acute phase ( 0-7 hours)Acute phase ( 0-7 hours)
General intelligenceGeneral intelligence no change*no change* Perceptual functionPerceptual function no change*no change*
AttentionAttention -left side inattention-left side inattention-reduced -reduced
speed in speed in vigilance vigilance taskstasks
*No change can be attributed to ECT*No change can be attributed to ECT
ECT effects on non-memory ECT effects on non-memory cognitioncognition
Subacute phase (7-72 hours)
IntelligenceIntelligence no change or improvedno change or improved Language Language verbal fluency verbal fluency
may be affectedmay be affected
Perceptual/Visuospatial Perceptual/Visuospatial no change Motor function no change Motor function no changeno change
Higher cognitive/ frontal Higher cognitive/ frontal no changeno change
ECT effects on non-memory cognitionECT effects on non-memory cognitionMiddle subacute period (72 hrs -1 Middle subacute period (72 hrs -1
wk)wk)
IntelligenceIntelligence improvement MMSE improvement MMSE LanguageLanguage improvement improvement (rel. to (rel. to
depression)depression)
Perceptual Perceptual improvement improvement Attention/frontal no change Attention/frontal no change (better in (better in
reaction time)reaction time)
ECT effects on non-memory ECT effects on non-memory cognitioncognition
Late subacute phase (1 wk -7 mo)Late subacute phase (1 wk -7 mo)
IntelligenceIntelligence improved improved (or no change due to ECT)(or no change due to ECT)
LanguageLanguage no change no change (due to ECT)(due to ECT)
PerceptualPerceptual improved improved (normalized depr. changes)(normalized depr. changes)
MotorMotor improved improved ( trend)( trend)
Attention/frontalAttention/frontal improved mental shiftsimproved mental shifts no change in vigilance
Memory disturbance Memory disturbance Acute phaseAcute phase
PostictalPostictal
InterictalInterictal
Acute memory disturbanceAcute memory disturbance
PostictalPostictal
Acute memory disturbanceAcute memory disturbance
InterictalInterictal
Subacute memory Subacute memory disturbancedisturbance
MemoryMemory effects effects
Large inter-individual variability in:Large inter-individual variability in:
SeveritySeverity
Persistence (Persistence (ReversibilityReversibility))
Subjective tolerance / discomfort Subjective tolerance / discomfort
Factors affecting severity Factors affecting severity
Number of treatmentsNumber of treatments FrequencyFrequency Stimulus intensityStimulus intensity
Electrode placementElectrode placement
WaveformWaveform OxygenationOxygenation MedicationsMedications
Factors affecting Factors affecting persistencepersistence
Prolonged post-ictal disorientationProlonged post-ictal disorientation Pre-ECT cognitive impairmentPre-ECT cognitive impairment
Probably ageProbably age, , neurological illness neurological illness (e.g. Parkinson’s dis(e.g. Parkinson’s diseaseease) )
other obvious factors never studied other obvious factors never studied ( i.e. substance abuse, medications, ( i.e. substance abuse, medications,
cardiac output status, etc) cardiac output status, etc)
Attempts to ameliorateAttempts to ameliorate
Non-pharmacologicNon-pharmacologicalal methods methods ( schedule, oxygen, ( schedule, oxygen, electrode electrode placement, placement, etc)etc)
Various pharmacological methodsVarious pharmacological methods
ECT memory disturbanceECT memory disturbancePharmacological attemptsPharmacological attempts
ACTHACTH dexamethasonedexamethasone naloxonenaloxone vasopressinvasopressin T4T4 TRHTRH physostigminephysostigmine
caffeinecaffeine CaCa++ ++ channel channel
blockersblockers piracetampiracetam pramiracetampramiracetam inositolinositol ergoloid mesylates ergoloid mesylates herbal preparationsherbal preparations
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
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.
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
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
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
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
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
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
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
SUMMARYSUMMARY
ECT affects selectively memory ECT affects selectively memory parametersparameters
There is large inter-individual There is large inter-individual variabilityvariability
Memory disturbance is not related to Memory disturbance is not related to clinical effects on depressionclinical effects on depression
SUMMARYSUMMARY Memory disturbance is in general Memory disturbance is in general
reversiblereversible
In some cases some retrograde In some cases some retrograde amnesia for sporadic events (public amnesia for sporadic events (public mainly) may persistmainly) may persist
Both mesial temporal lobe and Both mesial temporal lobe and prefrontal cortex (lowest seizure prefrontal cortex (lowest seizure threshold in brain) have been threshold in brain) have been implicated in memory troubleimplicated in memory trouble
CONCLUSIONCONCLUSION One should keep in mind that for most One should keep in mind that for most
patients memory improves patients memory improves
Cost-benefit analysis for the patient Cost-benefit analysis for the patient
Simple measures can contain Simple measures can contain disturbancedisturbance
Memory parameters should be Memory parameters should be monitored systematically - best to monitored systematically - best to acknowledge and support / educate acknowledge and support / educate patient and family patient and family