Transcript athens-2005-sw1-zervas - World Psychiatric Association

COGNITION AND ECT
Iannis M. Zervas, M.D.
Athens University Medical School
ECT effects on cognition
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Memory
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Other
ECT effects on memory
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Apparent
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Real
Apparent effects-positive
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Memory improvement (!)
Inaccurate psychologically but
crucial from a psychiatric viewpoint
Apparent effects-negative
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Residual psychopathology
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Drug effects
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New psychosis
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Unmasking of dementia
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Subjective complaints
(depression)
(psych, anesthesia, other)
(young, new onset)
(old)
(various motives)
Real effects
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Disorientation
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Anterograde amnesia
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Retrograde amnesia
Retrograde
remote
recent
ECT
Anterograde
Time course
of memory disturbance
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Acute
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Subacute
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Long-term
ECT effects on non-memory cognition
Acute phase ( 0-7 hours)
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General intelligence
Perceptual function
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Attention
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*No change can be attributed to ECT
no change*
no change*
-left side inattention
-reduced speed in
vigilance tasks
ECT effects on non-memory cognition
Subacute phase (7-72 hours)
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Intelligence
Language
no change or improved
verbal fluency
may be affected
Perceptual/Visuospatial
Motor function
Higher cognitive/ frontal
no change
no change
no change
ECT effects on non-memory cognition
Middle subacute period (72 hrs -1 wk)
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Intelligence
Language
Perceptual
Attention/frontal
improvement MMSE
improvement (rel. to depression)
improvement
no change (better in reaction time)
ECT effects on non-memory cognition
Late subacute phase (1 wk -7 mo)
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Intelligence
Language
Perceptual
Motor
Attention/frontal
improved (or no change due to ECT)
no change (due to ECT)
improved (normalized depr. changes)
improved ( trend)
improved mental shifts
no change in vigilance
Memory disturbance
Acute phase
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Postictal
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Interictal
Acute memory disturbance
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Postictal
Acute memory disturbance
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Interictal
Subacute memory disturbance
Memory effects
Large inter-individual variability in:
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Severity
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Persistence (Reversibility)
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Subjective tolerance / discomfort
Factors affecting severity
Number of treatments
 Frequency
 Stimulus intensity
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Electrode placement
Waveform
 Oxygenation
 Medications
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Factors affecting persistence
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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)
Attempts to ameliorate
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Non-pharmacological methods ( schedule,
oxygen, electrode placement, etc)
Various pharmacological methods
ECT memory disturbance
Pharmacological attempts
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ACTH
dexamethasone
naloxone
vasopressin
T4
TRH
physostigmine
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caffeine
Ca++ channel blockers
piracetam
pramiracetam
inositol
ergoloid mesylates
herbal preparations
Memory systems involved in ECT
with related brain structures
Short-term
memory or
immediate
Verbal
Visual
Neocortex
Long-term Declarative
memory
Learning
Medial temporal Lobe
Retrieval
Diencephalon
Priming
Striatum/cerebellum
Procedural
Neocortex
NonDeclarative
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 memory
Remote 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
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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 of
Medial Temporal Lobe (MTL)Dysfunction
in ECT memory disturbance
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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
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Most profound physiological effects of ECT
found in PFC -reductions in CB,
-reductions in metabolic rate,
-EEG slow wave activity
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Retrograde amnesia greater for public events
( PFC) not autobiographical (hippocampus)
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Tests of frontal lobe function can co-vary with
tests of retrograde amnesia
SUMMARY
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ECT affects selectively memory
parameters
There is large inter-individual variability
Memory disturbance is not related to
clinical effects on depression
SUMMARY
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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
CONCLUSION
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One should keep in mind that for most
patients memory improves
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Cost-benefit analysis for the patient
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Simple measures can contain disturbance
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Memory parameters should be monitored
systematically - best to acknowledge and
support / educate patient and family