Electroconvulsive Therapy

Introduction
ECT is a form of brain stimulation in which
induction of a seizure occurs when an applied
electrical stimulus creates an electrical field .
The treatment has evolved into a relatively
painless procedure with proven effectiveness.
The rapid response most patients have to
ECTsometimes as fast as after the first or
second treatmentmakes it incredibly
valuable.

Scope
History
Mechanism of action
Indications
Electrode Placement, Stimulus Waveform, and
Dosing.
Anesthesia
Interactions
Adverse Events
Future Direction
History
1938
Cerletti and Bini
Seizures in a catatonic patient
1940
A. E. Bennett develops curare
1951
Introduction of succinylcholine.
History
1958
First controlled study of unilateral
ECT
1970
D'Elia develops electrode positioning
for right unilateral ECT
1976
Constant current Brief-pulse ECT
device developed.
History
1988
Clinical trials of ECT versus lithium.
2000
High-dose right unilateral electrode placement is
associated with fewer adverse cognitive effects.
Lisanby and colleagues - Magnetic stimulation.
2008
Ultrabrief right unilateral ECT is shown to be equivalent to
brief-pulse.
Mechanism of action
Gene Expression Brain structure
Neurotransmitters Endocrine
Psychological
Psychological theories
Several studies have compared standard ECT with
"sham" or placebo ECT.
Those patients who had standard ECT were more
likely to recover, and more quickly than those
who had the placebo treatment.
A number of the patients having "sham"
treatment recovered too.
Previous psychological theories based on fear,
regression and selective memory loss, have been
now discounted in favor of neurobiological
theories.
Changes in brain structure, function
and neural connectivity
ECT causes an increase in bilateral
hippocampal volume (Nordanskog et al,
2010).
Increase and reduce in anterior cingulate
prefrontal cortex rCBF or rCMR.
Regions critical to the efficacy of the
treatment include- Brodmann's area 25, the
anterior cingulum, and the thalamus.

Changes in brain structure, function
and neural connectivity
Medial temporal lobe -anterograde amnesia
Prefrontal cortex -retrograde amnesia.
There is evidence that ECT alters the function
and the structure of important brain areas,
especially the fronto-temporal circuits.
Neuroplasticity
Promotes synaptic plasticity in hippocampus.
Including
Mossy fiber sprouting
Alterations in cytoskeletal structure
Increased connectivity in perforant pathways
Promotion of neurogenesis.
Suppression of apoptosis.
Neurotransmitter mechanisms
Variable data on the effects on serotonergic
systems - increased density of 5-HT2
receptors.
Increased dopaminergic functioning - D1- and
D3-receptor function.
GABA-ergic Inhibition may be restored as a
result of upregulation of immediate
modulation of ion channel function.
Neurotransmitter mechanisms
Pre-treatment low glutamate concentrations
in dorsolateral prefrontal cortex and anterior
cingulate cortex, normalised after ECT or
predicted treatment response.
Adverse cognitive effects of ECT could be
mediated through indiscriminate activation of
glutamate receptors in the hippocampus.
Neurotransmitter mechanisms
Increases brain and cerebrospinal
neuropeptide Y concentrations.
Studies of oxytocin and vasopressin; and
measures related to growth and thyroid
hormones have yielded mixed results.
Endocrine effects
Normalises HPA axis dysfunction, including
restoring dexamethasone suppression of
cortisol.
ECT treatment is also associated with surges in
plasma catecholamines and other hormones,
which are important in its cardiovascular
effects.
Indications
Historically, ECT was a first-line treatment for
the major psychiatric syndromes.
Resistance to medications has become the
most common clinical indication.
Indications
Is fast symptom relief crucial?
Have several pharmacotherapies been
ineffective?
Are drugs intolerable?
Past response?
Past treatment failure?
Risk of the side effects of ECT?
Indications
Major Depression
Effective for all subtypes, including unipolarand
bipolar depression, melancholia, and psychotic
depression.
Mania; Mixed States and Rapid Cycling
Reserved for patients resistant or intolerant to
medication, including those with mixed states or
rapid cycling, or who have severe symptoms.
Indications
Schizophrenia - ECT may be useful for
treatment-resistant patients and those who
easily relapse on monotherapy.
Extrapyramidal symptoms induced by
neuroleptics are reversible by ECT.
May protect against the development of
tardive dyskinesia.
Indications
Catatonia resistant to benzodiazepines, ECT
maybe used.
Neuroleptic malignant syndrome can be
treated with ECT and outcomes are
comparable to pharmacotherapy.
Antiparkinsons and Anticonvusant.
Conditions with poor response
Acute response in OCD, but patients soon
relapsed, and ECT is not recommended for
this disorder.
Double depression and dysthymia.
The withdrawal delirium can be treated with
ECT.
Comorbidity with personality disorders.
NICE guidelines
Rapid and short-term improvement of severe
symptoms of - severe depressive illness,
catatonia, prolonged or severe manic episode.
Does not allow the general use of ECT in the
management of schizophrenia.
ECT is not recommended as a maintenance
therapy in depressive illness .
Pretreatment Evaluation
Establishing the indication and target
symptoms- careful diagnosis, and
consideration of other clinical factors
contributing to the recommendation for ECT.
Past treatment with ECT ? Pharmacological
treatments?
Pre-treatment cognitive evaluation.
General medical condition.
Pretreatment Evaluation
General medical evaluation for anaesthetic
fitness. Including past history with
anaesthesia.
CBS, Electrolytes, ECG, CXR, TFT a complete
metabolic panel, brief dental exam , Plasma
pseudocholinesterase.
Spinal x-rays and brain imaging if indicated.
Electrode Placement,Stimulus
Waveform, and Dosing
Adequate seizure duration seems to be necessary
in addition to seizure elicitation.
Studies since the 1980shas demonstrated that,
depending on the combination of electrode
placement and stimulus dose, seizures could vary
in eliciting clinical response from 20 to 70percent.
Clinical effects of electrode placement and dose
suggests that the antidepressant effects depend
on the anatomic specificity and the effects of
current density.
Electrode Placement
Electrode placement Bilateral Right Unilateral

Handedness??

Right hemisphere involved
insustaining depressed
mood regardless of
Handedness.
Speed of response a
priority.

Failure of unilateral ECT.

Previous good response to
bilateral ECT without
significant memory
problems

Where determination of
cerebral dominance is
difficult.

More short- and long-term
adverse cognitive effects
delirium.
Speed of response less
important.

Previous good response to
unilateral ECT.

Where minimising memory
impairment is critical (e.g.
evidence of cognitive
impairment, outpatient
treatment).
StimulusWaveform
Neuronal depolarization is in the range of 0.1 to
0.2 ms.
Sine waves Wide pulse 8.33 ms
Brief pulse 0.5 -2.0 ms
Ultra brief pulse 0.3ms RUL, at six times
the seizure threshold, = efficacy to RUL and BL
ECT using brief pulse widths with lesser acute,
subacute and longterm impairment.

Seizure Threshold and Dosing
The degree to which the electrical stimulus
exceeds the seizure threshold, affects the
efficacy of right unilateral ECT, the speed of
clinical response regardless of electrode
placement, and the cognitive side effects
produced.
Seizure Threshold and Dosing
Empirical titration - The first electrical stimulus
is set low enough that a seizure results in only
a minority of patients.
Restimulations at intervals of 20 to 60 seconds
are given using progressively greater amounts
of charge until a seizure is produced.
The most precise method of stimulus
determination.
Seizure Threshold and Dosing
Formula-based dosing - uses factors known to
influence seizure threshold.
Age, electrode placement, stimulus pulse width,
gender, and concomitant medications, including
anaesthetics, to estimate adequate stimulus intensity.
Seizure threshold is higher in men than women, with
bilateral electrode placement than with unilateral
electrode placement.
Limited success obtaining precision in seizure
threshold approximation.

Seizure Threshold and Dosing
Fixed dosing - same dose of electrical stimulus
is applied to all patients receiving ECT.
For low-threshold patients, fixed dosing
enhances the possibility of increased adverse
cognitive side effects.
Only appropriate for patients with such
serious medical conditions that even one
subconvulsive stimulus must be avoided.
Treatment Procedures
Performed in a specific
treatment area that
meets standards for the
performance of day
surgery.
Capacity to manage
medical emergencies and
to recover.
The staffing commonly
consists of a psychiatrist
privileged to administer
ECT, ananesthetist, and
one or more nursing
personnel.
Treatment Procedures
Physiological monitoring is instituted and
continued until the patient is adequately
recovered - Cardiac monitoring and pulse
oximetry.
Monitoring of seizure activity can involve
observing both motor and EEG seizure
duration.
Treatment Procedures
Motor seizure duration Cuff method.
A blood pressure cuff is applied to the forearm
or just above the ankle and inflated to a level
above the anticipated maximum systolic
pressure to prevent anaesthetics from affecting
muscle contraction in the distal limb.
Motor movements resulting from seizure
induction can then be directly observed.
Treatment Procedures
Respiratorysupport - Provided using 100% O2
via mask and administered under positive
pressure.
Discontinued when there is return of
spontaneous respiration.
Preoxygenation earlier in respiratory
impairment.
ET intubation in rare circumstances.
Anaesthetic medications
Anticholinergic medications such as atropine
and glycopyrrolate are used to
Dry secretions .
Decrease the vagally mediated Bradycardia.

Contraindicated when they might provoke
preexisting arrhythmias or threaten cardiac
compensation.
Anaesthetic medications
Methohexital, a shortacting barbiturate.
Thiopental has been associated with a higher
incidence of postictal arrhythmias compared to
methohexital.
Propofol reduces hemodynamic changes
accompanying ECT and produces a rapid, smooth
recovery.
Etomidate and ketamine have been reserved for
situations in which seizure elicitation is difficult.
Anaesthetic medications
Muscle relaxant - Succinylcholine, a
depolarizing agent with rapid onset and brief
duration.
Use of succinylcholine contraindicated in
pseudocholinesterase deficiency, non
depolarizing agents can be used.
Treatment Procedures
The duration of the stimulus is only a Few
seconds.
The duration of the seizure is commonly less than
1 minute.
Seizures of less than 15 seconds can occur close
to the seizure threshold and are considered
abortive.
Seizures longer than 3 minutes, are considered
prolonged and should be controlled using
anticonvulsants.
Treatment Procedures
Pre-ECT checks Identity, Fasting (for 8hrs),
Emptied bowel and bladder, Dentures
jewellery and restrictive clothing removed,
Consent form signed, medication history.
Anaesthetic administration- IV access>
monitoring>Ventilate>Muscle relaxant>
Anaesthetic>Insert bite block to protect
tongue.

Administration of ECT
Electrodes to scalp
Adequate contact between the electrodes and
the scalp prior to treatment.
Dose Administered.
Monitoring length of seizure
Recording dose, seizure duration, and any
problems on ECT record (and ensure anaesthetic
administration also recorded).
Transfering patient to recovery.

Recovery
Adequate airway.
Monitoring of the patient's pulse and blood
pressure until stable.
Continuous nursing presence and observation
until the patient is fully oriented.
IV access until able to leave recovery.

Treatment Course
Twice-weekly treatment is equally effective
compared with thrice weekly treatment, takes
longer to reach efficacy but associated with lesser
cognitive effects.
Average is from 6 to 12 sessions.
Treatment should end when there is remission of
target symptoms or when further improvement
has not occurred over two or three sessions.
MMECT - used only in extremely unusual
circumstances, such as intractable seizures.
Treatment Course
Higher stimulus intensity may be useful later
in a treatment course if response is
inadequate.
Anticonvulsant discontinuation or decreasing
dose should be evaluated, when the patient
has a high seizure threshold.
10 treatments with optimal electrode
placement and dosing should be given before
nonresponse is declared.
Continuation and Maintenance
Evidence is limited, maintenance ECT (e.g.
once a week, or every 2 weeks, for 4 months
or as an outpatient procedure) when a patient
has responded well to ECT, and when drug
treatments have been ineffective prior to ECT.
Collaborative approach can be established
(balancing frequency of ECT against return of
symptoms and side-effects, esp. memory
problems).
Medications and ECT
Esmolol and labetalol are anticonvulsant used
in this setting.
Lidocaine and its analogs can interfere with
seizure induction.
Diuretics, hypoglycemics, including insulin
and long-acting cholinesteraseinhibitors for
glaucoma may interfere with anesthesia
recovery.
Medications and ECT
Theophylline - increase seizure duration, can
result in status epilepticus.
Lithium - result in confusional states,serotonin
syndrome, and prolonged and/or focal
seizures.
-lactam antibiotics proconvulsant
Anticonvulsants
Medications and ECT
Augmenting effect for neuroleptics when
combined with ECT in schizophrenia.
Clozapine and olanzapine have proconvulsant
properties, and quetiapine has anticonvulsant.
Reserpine cannot be combined safely with ECT
.
Medications and ECT
Antidepressants to augment ECT
trial found that nortriptyline and venlafaxine increased the
response rate to ECT by 15 percent.
-Nortriptyline was associated with diminished cognitive effects.
-Venlafaxine was associated with increased adverse cognitive
effects.
TCAs are safe in noncardiac populations and selective
serotonin reuptake inhibitors in most populations.
Series of cases in which asystole occurred at doses of
venlafaxine greater than 225 mg with the concurrent use of
atropine, advisable to limit the dose of venlafaxine if it is
combined with ECT.
The well-known proconvulsant effect of bupropion prompts
caution.
Adverse Effects
The estimated risk of serious complications,
occurring in about 1 in 1,000 patients, is
similar to that of general anaesthesia for
minor medical procedures.
Adverse Effects
Cardiovascular
Parasympathetic Bradycardia, asystole
Sympathetic Output - heart rate, blood
pressure, and,, rate pressure product increase.
Non specific arrhythmias usually non sustained.
Respiratory - associated with anesthesia
procedures
Neurogenically induced laryngospasm
Adverse Effects
Central Nervous System-risk of structural brain
injury along with cardiovascular and
pulmonary complications if the seizure
persists beyond 30 minutes even when
oxygenation is adequate.
Dental and musculoskeletal.
Adverse Effects
Neurocognitive - Functions such as reasoning,
creativity, the ability to form memories
,procedural memory and priming, does not
appear to be affected in an enduring manner.
Disorientation, diminished processing speed,
decreased anterograde and retrograde
memory, and errors in visual-spatial function
and word finding immediately after a
treatment session
Adverse Effects
Retrograde memory improves gradually, but
spotty deficits may persist, with recent memories
for public information more vulnerable than older
memories for personal experiences.
The likelihood of developing adverse cognitive
effects is influenced by Bilateral electrode
placement; inefficient stimulus -sine waveform;
suprathreshold dosing; greater frequency and
number of treatments; largerdoses of anesthesia.
Adverse Effects
Those with baseline neurologicaldisease,
magnetic resonance imaging abnormalities,
and baseline impairments inglobal cognitive
functioning ,older and female patients re
more vulnerable to developing deficits.
N-methyl D-aspartate antagonists ketamine
anaesthesia, and thyroid hormone.
Adverse Effects
Postictal agitation - severe forms require emergent
management with decreased stimulation, medications such
as short-acting benzodiazepines, Haldoperidol and
restraints.
Prophylaxis
Switching electrodeplacement to unilateral,
Increasing the dose of anesthetic agent pre- and post-ECT
Modifying the dose of succinylcholine to prevent
awakening while paralyzed
Regimens to address agitation by the use of neuroleptics.

Headaches and Nausea
Future Direction
Refinements of ECT techniques.
Optimizing dose delivery and location

Better understanding the MOA

Efficacy vs current pharmacotherapy