Electroconvulsive Therapy: An

Update
Robert Ostroff, M.D.
Yale Psychiatric Hospital
ECT Center
 What Happens?
 Electrical Stimulation
 Centrally mediated vagal discharge –
bradycardia/asystole
 Grand mal convulsion (20-40 sec)
 Peripherally mediated vagal discharge - bradycardia
 Fall in blood pressure
 Tachycardia
 Rise in blood pressure, CSF pressure
 Minor arrhythmias: increased parasympathetic tone
- atrial arrhythmias. increased sympathetic tone -
pvc, svt
 HISTORY
 Chemically induced seizures used as treatment for
schizophrenia in 1930’s
 Ugo Cerletti developed experimental model for epilepsy
 Adapted first ect apparatus inducing seizures in animals
 First human treatment in 1938. Patient had total of eleven
treatments without adverse effects
 1960’s advent of modern anesthesia including
neuromuscular blockers
 Late 1970’s - development of pulse wave machines
Major Advances in ECT Since 1938

 The introduction of modern anesthesia including

neuromuscular blocking agents
 The development of the pulse wave machine
which allowed for careful energy dosing and
determination of seizure threshold
 The advances in lead placement which maintained
efficacy and reduced side-effects
 The appreciation of the importance of seizure
morphology not seizure duration as a determinant
of efficacy
 Treatment Responsive
Disorders
 Major Depressive Illness with psychotic features
 Bipolar, depressed
 Bipolar, manic
 Schizoaffective Disorder
 Schizophrenia - acute onset, confusion
 Catatonia
 Parkinson’s Disease (bradykinesia, tremor,
rigidity, gait disturbance, postural instability)
 Depressive Illness
 10% of all Americans in any given year
 1 in 3 seek treatment
 50% correctly diagnosed
 18,000 deaths per year
 Mortality 6 per 10,000
 Only advanced coronary artery disease results in
more days spent in bed
 Only arthritis causes more chronic pain
 Economics of Depression
 Total cost $44 billion annually
 Only 28% is cost of treatment
 Lost productivity $12.1 billion
 Lost work days $11.7 billion
 Mortality from suicide $7.5 billion
 Pharmaceuticals $1.175 billion
 Mortality Rate
 Coronary Artery Bypass - 1%
 Depression .06%
 ECT .006%
 Predictors of Response
Positive Negative
 Previous history of  Chronicity
response  Reactive
 Psychomotor  Somatic complaints
retardation  Unstable relationships
 Delusions  Denial
 Positive family hx  Axis II
 Autonomous to
circumstance
 Natural History of Depression
 Bipolar  Bipolar
 80% spontaneous  88% response to ect
remission at 6 months  Unipolar
 Unipolar  80% response to ect
 46% spontaneous  36% mortality at 31
remission at 31 months, half suicide,
months half medical
 Risk Factors
Cardiovascular

 Coronary ischemia
 Hypertension
 CHF
 Arrhythmia
 Recent MI
 Aneurysm
 Cardiac pacemaker
 Risk Factors
 There are no absolute contraindications to
ECT
 Risk/Benefit ratio is the important factor
 Ineffectively treated depression has a high
mortality rate. This should be weighed
when considering any treatment for the
disorder including ECT
 Risk Factors
CNS
 Cerebral Infarction
 Cerebral Hemorrhage
 Tumor
 Dementia
 Hydrocephalus
 AV malformation
 Multiple sclerosis
 Seizure Disorder
 Risk Factors
Other
 Theophylline
 Increased intracranial pressure
 Aortic Stenosis
 Digitalis toxicity
 Technique
Pretreatment
 Benzodiazepines inhibit seizures and may increase
confusion
 Discontinue psychotropics unless truly necessary
– especially D/C anticonvulsants
 Tricyclics/MAOs make BP and pulse rate less
predictable. Do not augment treatment
 Lithium may cause increase OBS. Prolongs
neuromuscular blockade
 Can use neuroleptics
 Pretreatment
Workup
 EKG
 Chest x-ray if indicated <75
 CBC, lytes, BUN, creatnine, Ca, Phos,
TFTs, LFTs, UA
 EEG if clinically indicated
 CT if clinically indicated
 Anesthesia
 Methohexital .75-1.0 mg/kg
 Succinylcholine l75-1.0 mg/kg
 Atropine or glycopyrolate are optional - indicated
for bradycardia
 Pre-stimulis hyperventilation very important
 Hypertension after seizure can be controlled with
atenolol
 Monitor oxygenation,BP,EKG
 Cardiac monitoring is essential
 Stimulus
 Low as possible to induce generalized seizure
 Electrode placement important
 Bilateral probably more efficacious than unilateral
 Present practice is to use as low a dose of energy as
possible to cross seizure threshold
 Second bilateral treatment set at 50% above threshold/
second unilateral treatment set at 3.5-5x seizure threshold
 Sine wave and pulse wave equally effective. Brief pulse
wave induces seizures with less energy. Less disruptive to
cognition. Because of this sine wave machines are no
longer approved by FDA.
Pulse and sine wave comparison. Energy = area under curve
 Seizure Characteristics
 Target 30-40seconds
 Less than 20 sec may be less effective
 Can increase with caffeine
 Total seizure time probably not significant
 Ave number for successful trial = 7-8
 Multiple ECT during same treatment session has
no advantage
 Seizure morphology – particularly postictal
suppression most important characteristic
 Cognitive Impairments
 Retrograde - for events nearest time of
treatment
 Anterorade: up to 6 months post-treatment
in some studies
 Greatest with bilateral
 Greatest with sine wave
 Interictal delirium
– greatest in elderly
– reduced by decreasing freq, and unilateral rx
 Cardiac complications
 Hypertension, abrupt rate transitions can
result in arrhythmias
 Cardiac modified ect
– pretreatment with atropine or glycopyrolate
(should almost always be used for first
treatment when seizure threshold is established)
– pretreatment with labetalol and/or nifedipine
 Post-treatment Confusion.
Determinants
 Electrode placement
 Stimulus dose
 Length of seizure
 Adequacy of oxygenation
 Age of patient
 History of substance abuse-regardless of
remission time
 Emergence Delirium
 Occurs immediately post-anesthesia
 Patient potentially a risk to self and others
 Risks
– size
– SA hx
 Treatment
– Prolonging sedation -methohexital, midazalam
– Crucial to maintain iv line
– Physical management/reassurance
 Mechanism of Action
 100 theories (Kety -1974)
 Increase in GABA in CNS following ECS
 Evidence of Up-regulation of specific mu-
opiate binding sites in ECS
 Generalized seizure to diencephalon is
essential
 Postictal prolactin rise correlates with
efficacy
 Research Issues
 Mechanism of action - hormonal vs. receptor sensitivity
assays
 Cardiovascular response
 Headaches
 Parkinson’s disease
 Markers of hypothalamic seizure activity
 ECT destabilize mood disorders
 Memory
– Ketamine – potent NMDA antagonist may reduce cognitive
side effects
 Emergence delirium
 Memory
 ECS increases LTP in rats
 NMDA antagonists block the formation of
LTP in ECS
 Ketamine is a potent NMDA antagonist
 Ketamine plus bifrontal placements have
prevented recurrence of ECT-induced
encephalopathy
Orange/yellow areas show
increased bloodflow during
bilateral ECT
Bilateral ECT Right Unilat.
ECT

Blumenfeld, Ostroff, et al, 2000

Bilateral R Unilateral
ECT Red is area of greatest
ECT
SPM
Results Blumenfeld, Ostroff, et al., 2002
blood flow
Bifrontal
ECT
SPM
Results Blumenfeld, Ostroff, et al.,
 Bilateral
Bilateral

Right Delia
Right
Delia

EEG evidence for differences in seizure morphology depending on

lead placement. The bilateral treatment yields a symmetrical seizure
compared to the asymmetrical seizure induced by right nondominant
lead placement.
 Blood flow in Bifrontal vs Bilateral ECT

Yellow shows area where blood flow is higher with BF ECT,

blue shows area where blood flow higher with BL leads
Bigeminy during ECT administration
 The following four slides show a typical
two lead EEG during an ECT treatment

Recruitment

Tonic phase of seizure

Clonic phase of seizure
End of Motor
Seizure
Postictal Suppression
EKG Artifact