ECT

Electroconvulsive therapy
History
There have been several accounts of camphor convulsive
therapies from the late 1700s to the mid-1800s.

1500- seizures induced by administering camphor from

mouth to treat psychiatric illness.

1785- first published report of use of seizure induction to

treat mania, using camphor.
1934- The Hungarian neuropsychiatrist Ladislas von
Meduna made the observation that,
- brains of epileptics had greater than normal numbers of
glial cells
- schizophrenics had fewer
and he hypothesized that there might be a biological
antagonism between convulsions and schizophrenia.
The first catatonic psychotic patient was successfully
treated using intramuscular injections of camphor in oil to
produce therapeutic seizures.
1938-Lucio Bini and Ugo Cerletti were interested in the use
of electricity to induce seizures, and, after a series of
animal experiments, the first ECT course was administered
to a delusional and incoherent patient, who improved with
one treatment and remitted after 11 treatments.

1940- first use of ECT in US and curare developed for use

as a muscle relaxant at ECT.

1960,70,80s- various RCTs comparing ECT and

medications for depression concluding high response to
ECT.
1987- H.A Sackheim reports that dosage above the seizure
threshold and right u/l electrode placement and seizure for
sufficient duration, is effective.

2000- controlled trials show that rt electrode placement

associated with less cognitive side effects.

2001- for relapse prevention post ECT- TCA(nortriptyline) and

Lithium found effective.

The Nobel Laureate Paul Greengard has suggested that the

term electrocortical therapy might be used to replace the
current term electroconvulsive therapy.
Electrophysiology
• Neurons maintain a resting potential across
the plasma membrane.

• When action potential is generated normal

brain activity is desynchronised.

• A convulsion or seizure occurs when a large

percentage of neurons fire in unison.
• In ECT, seizures are triggered in normal
neurons by application through the scalp of
pulses of current,
under conditions that are carefully controlled
to create a seizure of a particular duration
over the entire brain.
• The qualities of the electricity used can be
described by Ohm's law: E =IR, or I= E/R,
- E is voltage
- I is current and
- R is resistance
• The intensity or dose of electricity is measured
in terms of charge (milliampere-seconds or
millicoulombs) or energy (watt-seconds or
joules).

I=Qt

R=V/I or I=V/R
• The skull has a high impedance; the brain has
a low impedance.

• Because scalp tissues are much better

conductors of electricity than bone, only
about 20% of the applied charge actually
enters the skull to excite neurons.
Neurobiology
1. Changes in brain monoamine pathways found in
rodents after ECT (e.g. downregulation of noradrenaline
β- adrenoceptors)
2. ECT and antidepressants increase the expression of
dopamine D2 receptors in the nucleus accumbens,
which could be associated with improvements in
motivational behaviour.
3. Thought to interact with glutamatergic pathways.
4. Electrical seizures in animals result in changes in
neurotropins such as BDNF.

5. Increase in neurogenesis in the hippocampus.

(altered hippocampal function is thought to play a role in
the amnestic side effects of ECT.)
Mechanism of action
• The induction of a bilateral generalized seizure is necessary
for the beneficial effect.

Clinicians have generally been convinced that the patient does

not improve unless a convulsion is produced during the ECT
procedure.
Modern ECT machines deliver brief pulses of electrical current
that enable a seizure to be induced
Both electrode placement and electrical dosage have profound
effects on the therapeutic efficacy of ECT.
The amount by which the applied electrical dose exceeds the
seizure threshold of the individual patient is an important
determinant of both- Efficacy and Cognitive side effects of ECT.
• During the course of ECT –

- the interictal EEG is generally slower and of

greater amplitude than usual,
- returns to pretreatment appearance 1 month
to 1 year.
• After the generalized seizure

- EEG shows about 60 to 90 sec of postictal

suppression.
- appearance of high-voltage delta and theta
waves
- return to pre-seizure appearance in about 30
minutes.
• PET studies –

- During seizures, cerebral blood flow, use of

glucose and oxygen and permeability of the
blood brain barrier increase.
- After the seizure, blood flow and glucose
metabolism are decreased, most markedly in
the frontal lobes.
• Neurochemical research –
- has focused on changes in neurotransmitter
receptors and changes in second-messenger
systems.
• Virtually every neurotransmitter system is
affected by ECT
- downregulation of postsynaptic β-adrenergic
receptors (same effect with antidepressants).
- increased expressions of D2 receptors in
nucleus accumbens (improve motivational
behavior).
• In second-messenger systems
- affect the coupling of G-proteins to receptors
- the activity of adenylyl cyclase and
phospholipase C
- the regulation of calcium entry into neurons.
structural changes in the brain (animals) –
• Synaptic plasticity in hippocampus, including –
- mossy fiber sprouting
- alterations in cytoskeletal structure
- increased connectivity in perforant pathways
- promotion of neurogenesis
- suppression of apoptosis have been observed.
 Mortality of ECT
The death rate attributable to ECT has been
estimated to be less than 1 per 70,000
treatments.
This is similar to that seen with general
anaesthesia for minor surgical conditions.
The risks are related to the anaesthetic
procedure, and are greatest in patients with
cardiovascular disease.
Death occurs- usually due to
- ventricular fibrillation
- myocardial infarction
Indications
• NICE guidelines(2003):- recommended
- ECT is used only to achieve rapid and
short-term improvement of severe symptoms
after an adequate trial of other treatment
options have proven ineffective
or
- when the condition is considered to be
potentially life threatening in individuals with-
1. Severe depressive illness
2. Catatonia
3. A prolonged or severe mania
NICE guidelines(2009)- modified to add:-
- Consider ECT for acute treatment of severe
depression that is life-threatening and when a rapid
response is required, or when other treatments have
failed.
- Do not use ECT routinely for people with moderate
depression but consider it if their depression has not
responded to multiple drug treatments and
psychological treatment.
• In major depressive disorder
- for both MDD and bipolar 1 disorder

- fastest and most effective

- considered as 2 or 3 line treatment of

depressive illness that is not responsive to
antidepressants.
• Considered for use in patients –

- who have failed medication trials

- have not tolerated medications
- severe or psychotic symptoms
- acutely suicidal or homicidal
- marked symptoms of agitation or stupor.
• Delusional or psychotic depression
- considered as first-line treatment.

• MDD with melancholic features more likely to

respond to ECT.
- less likely to respond with somatization
disorder.
• Elderly patients respond more slowly than
young patients.

• ECT does not provide prophylaxis unless it is

administered on a long-term maintenance
basis.
• In a manic episode –

- ECT is atleast equal to lithium in treatment of

acute manic episode.
- useful for patients whose manic behavior has
produced dangerous levels of exhaustion.
• ECT should not be used with lithium, because
lithium can lower the seizure threshold and
cause a prolonged seizure.
• In schizophrenia –
- patients who have marked positive
symptoms, catatonia or affective symptoms
are considered more likely to respond to ECT.

- 4th line option for treatment resistant

patients, after 2 antipsychotics and clozapine.

- not used for chronic schizophrenia.

 Other indications
• Episodic and Atypical psychoses
• OCD
• Delirium

• Medical conditions –
- NMS, hypopituitarism

- intractable seizure disorder

- on-off phenomenon of Parkinson’s disease.

• Depressed suicidal pregnant woman.
• Geriatric and medically ill patients who can
not take antidepressants drugs safely.
• Severely depressed and suicidal children.

• ECT is not effective in somatization disorder,

personality disorders and anxiety disorders.
Relative Contraindications
Any medical illnesses that increase the risk of
anaesthetic procedure by an unacceptable
amount—
respiratory infections
serious heart disease
serious pyrexial illness.
Diseases that are likely to be made worse by the
changes in blood pressure and cardiac rhythm
(that occur in a fit).
recent myocardial infarction
cardiac failure
cerebral or aortic aneurysm
deep vein thrombosis
raised intracranial pressure.
Patients who have sickle-cell trait, care is needed
to ensure that oxygen tension does not fall.
Extra care is also required with diabetic patients
who take insulin.
Clinical guidelines
• ECT is a practical procedure that must be
learned by apprenticeship as well as by
reading.
• Patients and their families are often
apprehensive about ECT.
- clinician must explain both beneficial and
adverse effects and alternative treatment
approaches.
• ECT should be given in pleasant safe
surroundings.
• Patients should not have to wait where they can
see or hear treatment being given to others.
• There should be waiting and recovery areas
separate from the room in which treatment is
given.
• Adequate emergency equipment should be
available
- a sucker,
- endotracheal tubes,
- adequate supplies of oxygen,
- facilities to carry out full resuscitation.
The nursing and medical staff who give ECT should
receive special training and accreditation.
• The informed consent process should be
documented in patients’ medical record and
include –
- a discussion of the disorder
- its natural course
- option of receiving no treatment.
• Involuntary ECT -
- for patients who urgently need treatment and
- who have a legally appointed guardian.
 Pre-treatment evaluation
• Include –
- the records of any previous ECTs, examined
for evidence of delayed recovery from the
relaxant
- Standard physical, neurological and
preanesthesia examinations and a complete
medical history.

- lab investigations – blood and urine

chemistries.
- X-ray chest and ECG
- dental examination
- X-ray of spine if needed
- CT, MRI – if suspicion of seizure disorder or
space-occupying lesion.
Premedications, Anaesthetics,
Muscle relaxants
• NPO for 6 hrs before treatment.

• Oral examination Just before procedure – to

check dentures and other foreign objects.

• IV line should be established.

• A white block is inserted in the mouth – to
protect teeth and tongue during seizure.

• 100% oxygen is administered @ 5L a min

during the procedure until spontaneous
respiration returns.
• Muscarinic Anticholinergic drugs

administered before ECT

- to minimize oral and respiratory secretions
- to block bradycardias and asystoles.
• Not routinely used.

- Indicated for patients taking β- adrenergic

receptor antagonists and those with
ventricular ectopic beats.
• Atropine is commonly used
- administered at 0.3 to 0.6 mg IM or SC 30 to
60 min before the anaesthetic or
- 0.4 to 1.0 mg IV 2-3 min before the
anaesthetic.
• Glycopyrrolate can be used (0.2 to 0.4 mg IM,
IV or SC)
- less likely to cross BBB
- less cognitive dysfunction and nausea

• But less cardio protective than atropine.

Anaesthesia –

• General anaesthesia is required .

- depth of anaesthesia should be as light as

possible
1. to minimise adverse effects
2. to avoid elevation of seizure threshold
associated with use of anaesthetics.
- methohexital (0.75 to 1 mg/kg IV bolus)- m/c
● Short action, lower association with post ictal
arrythmias

- thiopental (2 to 3 mg/kg IV

- etomidate (0.15 to 0.3 mg/kg IV)-

● Does not increase seizure threshold, used in elderly.

- propofol (0.5 to 3.5 mg/kg IV)-

• Less useful because of anticonvulsant properties.

- ketamine (6 to 10 mg/kg IM)

Muscle relaxants –

• After the onset of anaesthetic effect, usually

within a minute, a muscle relaxant is
administered to minimize the risk of bone
fractures and other injuries resulting from
motor activity during seizure.
• Succinylcholine (ultra-fast acting depolarizing
blocking agent)
- usually administered in a dose of 0.5 to 1
mg/kg as an IV bolus or drip.
- actions are marked by muscle fasciculations,
which move in rostrocaudal progression.
• In some patients tubocurarine (3mg IV) is
administered
- to prevent myoclonus and increase in
potassium and muscle enzymes (in cardiac and
musculoskeletal disease).
• To monitor the duration of convulsions,
- a BP cuff may be inflated at the ankle to a
pressure in excess of the systolic pressure
before infusion of muscle relaxant to allow
observation of seizure activity in the foot
muscles.
• If patient had a history of
pseudocholinesterase(metabolism of succinyl
choline) deficiency,

- apnea may occur and emergency airway

management is needed.
- atracurium (0.5 to 1 mg/kg IV) or curare can
be used instead of succinylcholine.
Electrode placement
• Historically, bifronto-temporal electrode
placement were used.
- more short and long term adverse cognitive
effects
- more likely to produce delirium.
Newer electrode placement includes –

• Unilateral or bilateral placement

• Overall, bilateral ECT has superior efficacy to
unilateral ECT.

• Bilateral treatment is associated with more

cognitive impairment.
• when right unilateral ECT is dosed about 6
times the seizure threshold,
- its efficacy approaches that of bilateral ECT,
but the associated cognitive disturbance is
also similar.
• For unilateral ECT,
- the first electrode is placed on the non
-dominant side, 3 cm above the midpoint
between the external angle of the orbit and
the external auditory meatus.
• The second electrode is placed at least 10 cm
away from the first one, vertically above the
meatus of the same side.

• A wide separation of the electrodes increases

the efficacy of unilateral ECT.
• For bilateral ECT –
- electrodes are placed on opposite sides of
head, each 3 cm above the midpoint of the
line joining the external angle of the orbit to
the external auditory meatus – just above the
hairline.
Electrical Stimulus
• Sufficiently strong to reach the seizure
threshold (the level of intensity needed to
produce a seizure).
• Given in cycles, and each cycle contains a
positive and a negative wave.

• Old machines use a sine wave - obsolete now

because of the inefficiency of that wave
shape,delivering extra electrical stimulus.
• Modern ECT machines use a brief pulse
waveform that administers the electrical
stimulus usually in 1 to 2 milliseconds at a rate
of 30 to 100 pulses a second.

• Machines that use an ultrabrief pulse (0.5

milliseconds) are not as effective as brief pulse
machines.
 Establishing Seizure Threshold
• A 40 times variability in seizure thresholds
occurs among patients.

• During the course of ECT treatment, a

patient's seizure threshold may increase 25 to
200%.
• 2/3 of the population have seizure thresholds
in range 100-200 millicoulombs.

• Seizure thresholds are higher in men than in

women and increases with age.
• A common technique is to:-
- initiate treatment at an electrical stimulus

that is thought to be below the seizure

threshold for a particular patient.
- then increase this intensity by 100 percent for

unilateral placement and

- 50 percent for bilateral placement,
until the seizure threshold is reached.
 Dose

- a minimally suprathreshold dose

- a moderately suprathreshold dose (1.5 times
the threshold), or
- a high suprathreshold dose (3 times the
threshold).
• Data support the conclusion that -
- high suprathreshold doses are the most
rapidly effective and
- minimal suprathreshold doses are associated
with the fewest and least severe cognitive
adverse effects.
• For fixed dose right unilateral ECT the initial
dose should be set at 400 millicoulombs.

Dose can also be estimated from the fact that ⅔

of people have seizure threshold range of
100-200.
• Psychotropic drugs may alter seizure
threshold and seizure duration.

- most antidepressants and antipsychotics

lower seizure threshold whereas
- BZD, valproate and lamotrigine increases.
• Additional procedures to lower the seizure
threshold include –
- hyperventilation and
- administration of 500 to 2,000 mg IV of
caffeine sodium benzoate 5 to 10 minutes
before the stimulus.
• SSRIs prolonged seizures during ECT.

• Nortriptyline to unmedicated patients

improves efficacy and lessened cognitive
adverse effects.
 Induced Seizures
• A brief muscular contraction, in jaw and facial
muscles is seen concurrently with the flow of
stimulus current, regardless of whether a seizure
occurs.
- First, the muscles of the face begin to twitch and
the mouth drops open.
- Then the upper eyelids, thumbs, and big toes
jerk rhythmically for about half a minute.
Not to confuse these convulsive movements
with muscle twitches due to the depolarization
produced by suxamethonium.
• The first sign of the seizure is often a plantar
extension, which lasts 10 to 20 seconds and
marks the tonic phase.

In tonic phase high-frequency, sharp EEG

activity is seen.
• This phase is followed by rhythmic (i.e clonic)
contractions that decrease in frequency and finally
disappear.

• During the clonic phase -

- bursts of polyspike activity occur simultaneously
with the muscular contractions.
• There is no direct correlation between treatment
outcome and duration of seizure activity,but
• For a seizure to be effective it should last at least
25 seconds(20-50sec).
 Recovery phase

After the seizure:-

● The lungs are oxygenated thoroughly with an
airway in place.
● The patient remains in the care of the
anaesthetist and under close nursing
observation until breathing resumes and
consciousness is restored.
● During recovery, the patient should be turned
on to their side and cared for in the usual way
for any patient recovering from an anaesthetic
after a minor surgical procedure.
● A qualified nurse should be in attendance to
supervise the patient and reassure them.
● The psychiatrist makes a note of the date, type
of electrode placement, drugs used, and amount
of current, together with a brief description of
the fit and any problems that have arisen.

When the patient is awake and orientated, they

should rest for an hour or so on their bed or in a
chair.
 Monitoring Seizures
- Observe for tonic-clonic movements.

- electrophysiological evidence of seizure from

the EEG- high frequency spike waves followed
by slower spike and wave complexes with a
frequency of around 3 Hz

- electromyogram (EMG).
- Isolating one forearm from the effects of the
muscle relaxant.
This can be done by blowing up a blood pressure
cuff to above systolic pressure before the
relaxant is injected.
The pressure is maintained during the period in
which the seizure occurs and then released.
Seizure activity can then be observed in the
muscles of the isolated part of the arm.
• Seizures with unilateral ECT are asymmetrical,
with higher ictal EEG amplitudes over stimulated
hemisphere than nonstimulated hemisphere.
 Failure to Induce Seizures
• Up to 4 attempts should be made.

• Sometimes the onset is delayed as long as 20

to 40 sec after the stimulus administration.
• Contact between the electrodes and the skin
should be checked

• The intensity of the stimulus should be

increased by 25 to 100%.

• Change the anaesthetic agent to minimize

increase in the seizure threshold.
 Prolonged and Tardive Seizures
• Prolonged seizures (seizures > 180 sec) and
status epilepticus can be terminated either
with additional doses of the barbiturates or
with IV diazepam (5 to 10 mg).

- intubation may be needed.

• Tardive seizures-
- additional seizures appearing some time after
the ECT treatment
- may develop in patients with pre-existing
seizure disorders.
• Rarely, ECT precipitates the development of an
epileptic disorder in patients.

• Managed clinically as if they were pure

epileptic disorders.
 Number and Spacing of Treatments
• ECT treatments are usually administered 2-3
times a week.
- twice-weekly treatments are associated with
less memory impairment than thrice-weekly
treatments.
• The course of treatment –
- MDD can take 6 to 12 treatments (up to 20
sessions)
- manic episodes - 8 to 20 treatments
- schizophrenia more than 15 treatments
- catatonia and delirium can take as few as 1 to
4 treatments.
• If a patient is not improving after 6 to 10
sessions –
- bilateral placement and high-density
treatment (three times the seizure threshold)
should be attempted before ECT is
abandoned.
Multiple-Monitored Electroconvulsive
Therapy (MMECT)
• Involves giving multiple ECT stimuli during a
single session,
- most commonly 2 bilateral stimuli within 2
minutes.

• Warranted in severely ill patients and in those

at high risk from the anaesthetic procedures.
• MMECT is associated with the most frequent
occurrences of serious cognitive adverse
effects.
 Maintenance Treatment
• A short-term course of ECT induces a
remission in symptoms but does not, prevent
a relapse.

• Post-ECT maintenance treatment should

always be considered.
• Indications for maintenance ECT treatments
can include –
- rapid relapse after initial ECT
- severe symptoms
- psychotic symptoms
- the inability to tolerate medications
• Maintenance therapy is generally
pharmacological,

- but maintenance ECT treatments (weekly,

biweekly or monthly) have been reported to
be effective relapse prevention treatments,
although data from large studies are lacking.
A RCT of 200 patients found post-ECT prophylaxis
with a combination of lithium and nortriptyline as
effective as maintenance ECT in sustaining remission
in the 6 months following a successful course of
treatment.

A few patients respond well to ECT but continually

relapse even when maintained on multiple drug
therapy. In these circumstances, some practitioners
give maintenance ECT at a reduced frequency (e.g.
fortnightly or monthly).
 Failure of Electroconvulsive Therapy
Trial
• Reports indicate that –
- patients who had previously failed to improve
while taking an antidepressant drug do
improve while taking the same drug after
receiving a course of ECT, even if the ECT
seemed to be a therapeutic failure.
 Adverse effects
General adverse effects –
• Nausea & Vomiting- antiemetics at time of ECT.
• Headache – 26-85% patients- NSAIDS or
Ketorolac(i.v) if severe.
-pretreatment with ketorolac and postseizure
management with
acetaminophen-propoxyphene- to manage more
intractable headache.
• Myalgia
• Compression fracture of thoracic vertebral
bodies, fractures of long bones, dislocations –
rare with modified ECT.
Adverse effects due to muscle relaxants –

• Prolonged apnoea
• Malignant hyperthermia
• Hyperkalemia
• Muscle soreness- NSAIDS
Seizure related effects –

• Prolonged seizures
• tardive seizures
• Todd phenomena (aphasia, hemiparesis, or
visual loss- lasting for few hours).
Postictal confusional states-

• Predisposing factors –
- old age
- comorbid brain disease (Parkinson's disease)
- concurrent lithium use
- pre-treatment anxiety
- inadequate anaesthesia dose
Cardiac effects –
• Commonest cause of morbidity and mortality

• Asystole
- due to stimulation of vagal nuclei.

• Raised BP
- can reach >200mg because of sympathetic surge.
• ECG abnormalities –
- ventricular ectopics, T-wave inversion and ST
depression.

• MI –
- ECT is best avoided within 3 months of MI (may
suffer reinfarction).

• Cardiomyopathy
Respiratory adverse effects –

• Aspiration leading to pneumonitis

• Neurogenic pulmonary oedema
• Pulmonary embolism
Neurologic adverse effects –

• Cognitive impairment –
- transient and self limiting
- deficits in attention and immediate memory
- orientation may be impaired
- postictal confusion and delirium in severe
forms
Memory loss- Amnesia

ECT is not normally followed by -persisting

anterograde memory disorder, or problems with
working memory and executive function
There is usually memory loss:-
- shortly before the treatment (retrograde
amnesia)
- impaired retention of information acquired soon
after the treatment (anterograde amnesia).
• Characteristics of ECT induced amnesia –

- anterograde and retrograde amnesia both

cumulate across the ECT course ie increase
with number of ECTs.

- both exhibit a temporal gradient.

These effects depend on:-
- electrode placement (unilateral versus
bilateral)
- electrical dose
but electrode placement appears to be the
more important factor.
• Anterograde amnesia attenuates days to
weeks after ECT, substantially complete within
a month.

• Retrograde amnesia slowly attenuates weeks

to months
- many patients experience long lasting, patchy
memory deficit.
Long- term effects of ECT on memory is-
The loss of memories for personal remote events
(retrograde amnesia for remote events) or
Autobiographical memory loss.
• Pregnancy complications –
- maternal complications –
- gastric reflux, uterine contractions, vaginal
bleeding, premature labour.

• Fetal complications –
- bradycardia, neonatal death, congenital
anomalies.