a comprehensive presentation on ECT

1. Chair person:Dr Hari krishna
Assistant professor
Dept of psychiatry
Presenter:Dr V Swarajya Lakshmi
1st
year PG
ELECTRO CONVULSIVE
THERAPY
DR V.SWARAYJYALAKSHMI
PSYCHIATRY PG

2. FOR EXTREME DISEASES , EXTREME
METHODS OF CURE…ARE MOST
SUITABLE
---------- HIPPOCRATES
400BC

3. SCHEME OF PRESENTATION
 History
 Electrical induction of seizures
 Devices
 Mechanism of action
 Indications
 Contraindications
 Technique of ECT
 Adverse effects of ECT
 Attitude towards ECT
 Conclusion
 References

4. INTRODUCTION
 It is the only somatic form of treatment of the
pre-psychopharmacology era still in use
 Despite its proven safety, ECT remains
controversial and is clouded more by emotional
issues than scientific reality.
 Electroconvulsive therapy (ECT), is a well
established, psychiatric treatment in which
seizures are electrically induced in anesthetized
patients for therapeutic effect

5. HISTORY
 The traditional literature on the history of the
medical uses of electricity, began with the Roman
use of electric fish to treat headaches
 Paracelsus, the 16th-century Swiss physician
and alchemist, gave camphor by mouth to
produce convulsions to cure lunacy.
 1934: Meduna begins the modern era of
convulsive therapy using intramuscular injection
of camphor for catatonic schizophrenia. Camphor
is soon replaced with pentylenetetrazol

6. Ugo Cerletti and Lucino Bini
 Experimented on animals to investigate epilepsy and found
that electricity is more efficient in inducing seizures..
 1938
 Cerletti and Bini applied electroshock to first human patient.
 Very successful
 Extremely schizophrenic man is able to live normally with
this new therapy.
 1930s & 1940s
 ECT becomes a very popular treatment.
 Accepted readily because of no better alternatives
 1950s
 Arrival of Thorazine
 Medication was started for treating schizophrenia
 ECT becomes 2nd
choice/last resort

7.  1951: Introduction of succinylcholine.
 1958: First controlled study of unilateral ECT.
 1960: Attenuation of seizure expression with an
anticonvulsant agent (lidocaine) reduces the efficacy of
ECT. The hypothesis that seizure activity is necessary and
sufficient for efficacy is upheld.
 1960s: Randomized clinical trials of the efficacy of ECT
versus medications in the treatment of depression yield
response rates that are significantly higher with ECT.
 1970: The most common electrode positioning for right
unilateral ECT developed.
 1976: A constant current, brief pulse ECT device, the
prototype for modern devices, is developed.

8.  1985 :The National Institutes of Health and National
Institute of Mental Health Consensus Conference on ECT
endorses a role for the use of ECT and advocates research
and national standards of practice.
 1988 Randomized, controlled clinical trials of ECT versus
lithium demonstrate them to be equally effective in mania.
 Current Day
 has regained popularity
Technological advancement  decreased risk

9. ELECTRICAL INDUCTION OF
SEIZURES
Factors in the Generation and Measurement of Electrical
Stimulation for ECT
 ECT is a form of brain stimulation in which induction of a
seizure occurs when an applied electrical stimulus creates
an electrical field with flow of current in the excitable
tissue of the brain sufficient to depolarize cell membranes
of neurons synchronously.
 The generation and behaviour of the electrical stimulus
can be conceptualized in terms of Ohm's law:
V (voltage) = I (current) × R (resistance).
 Voltage is the electromotor force (measured in volts)
causing current to flow; current is the rate of flow of
electrons (in amperes); and resistance is the relative ability
to pass current

10.  ECT devices function on alternating current.
 Biological tissues are nonferrous and thus have low
inductive properties.
 Capacitance (F) is the ability to store charge (in farads).
Neural tissue has relatively low capacitance (10-12
to 10-10
F),
and the electrode–skin interface (estimated 0.4 µF) is the
source of a relatively greater contribution to this term.
 A variety of stimulus waveforms has also been used to
deliver the stimulus,
 sine wave,
 rectified partial sine wave,
 brief-pulse square wave,
 ultrabrief-pulse square wave.

11.  These different waveforms are not of equal efficiency in
depolarizing neural tissue
 The slow rise of a sine wave results in accommodation and
increases in the threshold for neuronal firing. This
observation has led to a preference for brief-pulse
waveforms that “instantly” achieve peak intensity.
 Once the electrical stimulus is generated, current is
distributed inversely to the resistance of the tissue
compartments traversed.
 There are three major components: Scalp , skull , and brain
tissue .
 Because current flow is greatest across the lowest
resistance, it has been estimated that 80 percent of current
is shunted through the scalp.

12.  The skull provides the greatest component of resistance
 Differences in scalp and skull anatomy are thought to be a
major source of the wide variation among individuals in
the electrical dose required to elicit a generalized seizure
or seizure threshold.
 Another influence on current shunting is interelectrode
distance:
 The closer electrodes are placed on the skull, the more
shunting occurs
 It is thought that right unilateral placements can result in
the creation of a virtual electrode occurring in the area
between the two electrodes and, hence, in reduced amounts
of electrical dose required for seizure elicitation

13.  This increased shunting may also result in lower current
density in brain tissue.
 Expressing the quantity of the electrical stimulus delivered
as energy is measured in joules
 Evidence indicates that current density in neural tissue is
the critical factor responsible for seizure production and
the subsequent neurobiological effects of the electrical
stimulation.
 The various elements of the brain have differing electrical
properties and vary markedly in excitability,
 Myelinated axons being most excitable and neuronal cell
bodies and dendrites least.
 Tissue response also varies with distance from electrical
source—in this case, the stimulating electrode

14. DEVICES USED TO DELIVER ECT
 Constant-current, constant-voltage, and constant-energy
devices have been in use, most modern instruments are
constant-current devices
 The range of constant current is on the order of 0.5 to 1 A
in these devices.
 Dose is manipulated by varying the time of exposure to a
fixed current (total charge).
 With brief-pulse devices—the most commonly used
constant-current devices—frequency of pulses, pulse width,
and duration of pulse train are parameters that can be
used to vary the stimulus dose.

15. MECHANISMS OF ACTION
Despite much research the precise mechanism of
action of Electroconvulsive therapy is still not
known. Most theories about the mode of action of
electroconvulsive therapy focus on its efficacy with
depressed patient and includes the following.
 Anticonvulsant effects
Because of the efficacy of anticonvulsant medications in
mania, there is also speculation that the anticonvulsant
effects of ECT contribute to its efficacy in mania.
Mixed GABAergic activity,
Up regulation of adenosine receptors
Blocking of anticonvulsant effects with opiate antagonists.

16. Biochemical Actions :
Neurotransmitter and Peptidergic systems.
 Both electroconvulsive stimulation and
antidepressants down regulate β-adrenergic receptors
 Antidepressants typically down regulate 5-
hydroxytryptamine receptors (5-HT2), whereas ECT
leads to increased density of 5-HT2 receptors (in
rodents) and decreased binding (in primates).
 Serotonergic transmission may be enhanced by both
antidepressants and ECT, the mechanisms appear
distinct.
 Increased dopaminergic functioning following
electroconvulsive stimulation, particularly D1- and
D3-receptor function.

17. Neurophysiology
 Increases in global cerebral blood flow and
cerebral metabolic rate occur along with
increased BBB permeability
 In the postictal period there is functional
suppression, with decreases in CBF and CMR, as
well as varying degrees of bioelectric suppression
on EEG.
 Changes are also topographically distributed.
 These reductions have been correlated with
treatment outcome.

18.  The reductions in CBF in specific prefrontal
regions is related to the efficacy of ECT,
 Responders are more likely to exhibit postictal
suppression and develop slow wave activity on
EEG than non responders.
 The prefrontal cortex, on the right, the anterior
cingulum, and associated subcortical areas,
including the right medial thalamus, brainstem,
and midbrain tegmentum, are involved.
 Involvement of the medial temporal lobe in
anterograde amnesia and prefrontal cortex
involvement in retrograde amnesia.

19. Neuroplasticity:
 Structural changes in the brain associated with
psychiatric syndromes and response to treatment.
 This has been particularly so for microscopic changes
associated with electroconvulsive stimulation, as well
as antidepressant and other medications.
Neurotranmiter theory
Suggests that ECT release hypothalamic or pituitary
hormones or both which results in antidepressant
effects.
Electroconvulsive therapy release prolactin, thyroid
stimulating hormone, adenocorticotropic hormone,
but the specific hormone, responsible for the
therapeutic effect are not known.

20.  Brain damage theory.
Shock damages the brain, causing memory loss and
disorientation that creates an illusion that problems
are gone, and euphoria, which is a frequently
observed result of brain injury. Both are temporary
 Neuro endocrine theory:
Hypothesis that ECT stimulates diencephalic
structures, esp. hypothalamus
Measures: cortisol, DST, oxytocin, vasopressin, GH,
thyroid hormones
Results: increase in neuropeptides during seizure
No consistent evidence that acute/sub acute changes
in neuroendocrine functions affect efficacy

21. Psychological Theories
Psychological theories that had been put forward to
explain the effects of ECT
Regression Hypothesis: A number of authors
regarded ECT as producing regression of behaviour to
infantile or even prenatal levels.The regression was
thought of as being psychologically induced by the
stress involved in the treatment situation or
physically induced by convulsion.
Fear Hypothesis: The central tenet to this hypothesis
was the fact that fear induced by the treatment,
rather than the actual effects of convulsion which was
the effective agent.

22.  Punishment Hypothesis: As per this hypothesis
patients regarded the treatment as a form of
punishment. Acceptance of punishment allow the
patient to assuage his conscience, fear and anxiety
becoming unnecessary once retribution has taken
place.
 The psychoanalytic theories were criticized because of
their heavy reliance on treatment situation other
than the convulsion itself, thus ignoring the
consistent finding that the convulsion is the effective
agent.
 ECT was also thought to work as a placebo

23. INDICATIONS
Diagnoses for which ECT may be indicated
 Major depression, both unipolar and bipolar
 Psychotic depression in particular
 Mania, including mixed episodes
 Schizophrenia with
Acute exacerbation
Catatonic subtype
 Schizoaffective disorder

24.  Clinical indication
Primary use
Rapid definitive response required on medical or
psychiatric grounds
Risks of alternative treatments outweigh benefits
Past history of poor response to psychotropics or
good response to ECT
Patient preference
Secondary use
Failure to respond to pharmacotherapy in the
current episode
Intolerance of pharmacotherapy in the current
episode
Rapid definitive response necessitated by
deterioration of the patient's condition

25. DEPRESSION AND ECT
 The most common indication for ECT is major
depressive disorder,
ECT is the fastest and most effective available therapy.
 ECT should be considered for use
In patients who have failed medication trials,
Have not tolerated medications,
Have severe psychotic symptoms,
Are acutely suicidal or homicidal,
Have marked symptoms of agitation or stupor.
Controlled studies have shown that up to 70 percent of
patients who fail to respond to antidepressant
medications may respond positively to ECT.

26. Electroconvulsive therapy is effective in
 Depression in both major depressive disorder
and bipolar I disorder.
 Delusional or psychotic depression has been
considered particularly responsive to ECT;
 Major depressive disorder with melancholic
features is likely respond to ECT.
 Depressed patients less likely to respond to ECT
include those with somatization disorder

27. MANIA AND ECT
 ECT is at least equal to lithium in the treatment
of acute manic episodes.
 The relative rapidity of the ECT response
indicates its usefulness for patients whose manic
behaviour has produced dangerous levels of
exhaustion.
 ECT should not be used for a patient who is
receiving lithium, because lithium can lower the
seizure threshold and cause a prolonged seizure.

28. SCHIZOPHRENIA AND ECT
ECT is an effective treatment for the symptoms of
acute schizophrenia
ECT is not for those of chronic schizophrenia.
Patients with schizophrenia who have marked
 Positive symptoms,
 Catatonia,
 Affective symptoms
are considered most likely to respond to ECT.
In such patients, the efficacy of ECT is about
equal to that of antipsychotics, but improvement
may occur faster.

29. OTHER INDICATIONS
 ECT is also reportedly useful to treat
Episodic psychoses,
Atypical psychoses,
Obsessive-compulsive disorder,
Delirium
 Medical conditions as
Neuroleptic malignant syndrome,
Hypopituitarism,
Intractable seizure disorders,
The on-off phenomenon of Parkinson's disease.

30.  ECT may also be the treatment of choice for
depressed suicidal pregnant women who require
treatment and cannot take medication;
 For geriatric and medically ill patients who
cannot take antidepressant drugs safely;
 For severely depressed and suicidal children and
adolescents who may be less likely to respond to
antidepressant drugs than are adults.
 ECT is not effective in somatization disorder
(unless accompanied by depression), personality
disorders, and anxiety disorders.

31. CONTRA INDICATIONS
 Electroconvulsive therapy has no absolute
contraindications.
 Pregnancy is not a contraindication for ECT,
and fetal monitoring is generally considered
unnecessary unless the pregnancy is high risk or
complicated.
Relative contraindications
 Patients with space-occupying CNS lesions are at
increased risk for crebral edema and brain herniation
after ECT.
If the lesion is small, however, pre treatment with
dexamethasone is given, and hypertension is
controlled during the seizure.
 Patients who have increased intracerebral pressure
or are at risk for cerebral bleeding are at risk during
ECT because of the increased cerebral blood flow
during the seizure.

32.  This risk can be lessened, by control of the
patient's blood pressure during the treatment.
 Patients with recent myocardial infarctions are
another high-risk group,
Risk is greatly diminished 2 weeks after MI and
is even further reduced after 3 months
 Patients with hypertension should be stabilized
on their antihypertensive medications before
ECT is administered.

33. TECHNIQUE OF
ELECTROCONVULSIVE THERAPY
It is unique among psychiatric treatments:
A significant medical intervention requiring
general anesthesia and entailing risks, however,
small, of morbidity and mortality.
The psychiatrist administering ECT requires
 An intimate knowledge of the physiology and
biochemistry of induced seizures,
 An understanding of the pharmacology of
anaesthetic agents,
 Familiarity with the physical properties of the
electrical stimulus used,
 The confidence and skill to lead a treatment team
in the event of a medical emergency.

34. TRAINING
A reasonable training program for psychiatric residents
should be provided in the first year of training ,
 Which includes 3 hours of lecture and discussion on
history, clinical indications, treatment response, side
effects, precautions and contraindications, medical
physiology, cognitive effects, EEG effects, the physical
properties of the electrical stimulus, and the
comparative and combined effects of psychotropic
drugs.
 To gain practical experience, the psychiatric resident
should personally administer at least 30 to 40
treatments under the direct supervision of a faculty
member
 This will usually require a 1-or 2-month rotation on
an ECT service.

35. THE ECT UNIT
The ECT unit is an integral functioning part of the
psychiatric inpatient service and ought to be located
nearby, not a remote area of the hospital.
Physical Requirements
Electroconvulsive therapy should be given in
 Pleasant,
 Well-lit surroundings,
 Air-conditioned in summer and heated in winter,
 With ample room for staff and equipment
 With waiting and recovery areas designed to
maximize privacy and minimize the apprehension

36.  The treatment room should be large enough to
accommodate a patient on a stretcher, all of the
equipment , and for 4 to 8 people.
 A telephone is needed for calling the patients'
units and in the event that emergency assistance
is required.
 The room should have 2 doors:
One for patient entry, the other leading to a
recovery area.

37. Recommended equipment is as follows:
 ECT instrument and cart, preferably with
integral EEG and ECG monitor
 6 rolling stretchers
 Defibrillator and cart
 Oxygen tank with valve, flow meter, and positive
pressure bag
 Tracheal suction pump and cart
 Refrigerator with lock
 Wheeled intravenous pole and stand
 Lockable cabinet for medication and supplies

38.  Medication cart
 Emergency medication tray (not lockable) containing
 atropine (20-mL vial, 0.4 mg/mL)
 diazepam (2-mL ampules, 5 mg/mL)
 diphenhydramine (30-mL vial, 50 mg/mL)
 epinephrine (1-mL ampules, 1 mg/mL)
 lidocaine (50-mL vial, 20 mg/mL)
 methylprednisolone (125-mg vial, 62.5 mg/mL)
 esmolol (10-mL vial, 10 mg/mL)
 Laryngoscope with three sizes of blades and
assorted cuffed endotracheal tubes
 The recovery area should be large enough to hold
at least 3 stretchers, separated from each other
by curtains or screens, and have its own tracheal
suction apparatus, portable positive pressure
ventilation device and intravenous pole.

39. STAFFING REQUIREMENTS
To maximize safety and efficiency,
ECT should be given by a team consisting of
 Psychiatrist,
 A registered nurse,
 An anaesthetic specialist,
 Licensed practical nurse or nursing assistant.
 In hospitals with residency training programs, a
resident should be assigned to assist,
any additional nursing staff who accompany their
patients to the ECT unit and remain to observe
in the recovery room

40. THE PRE THERAPY WORKUP
As for any procedure conducted under general
anaesthesia, a medical history and physical
examination are prerequisite.
No laboratory tests are specific to ECT;
 Routine examinations of the blood and urine
 Chest film,
 ECG
Simply to screen for medical conditions that may
complicate the procedure
 A dental examination to assess the state of
patients' dentition is advisable for elderly
patients and patients who have had inadequate
dental care

41.  Pseudocholinesterase testing.
Pseudocholinesterase is the enzyme responsible for
degrading succinylcholine, the muscle relaxant used.
The absence of this enzyme is transmitted as a rare
genetic abnormality affecting fewer than 1 in 3000
and is responsible, for the complication of prolonged
apnea after ECT.
 Concomitant therapy with lithium,
 Certain antibiotics,
 Aminoglycosides,
 Magnesium salts,
 Procainamide,
 Quinidine
May also prolong post-ECT apnea by enhancing the
neuromuscular blockade induced by succinylcholine.

42. MEDICAL CONSULTATION
 The mean age of patients receiving ECT has
increased in recent years,due to increased longevity,
the greater risk for depressive illness in later life.
 More high-risk patients are thus receiving ECT.
Medical consultation in their management will often
be sought.
 The consultation process is not just a clearance for
ECT;
Rather ,needs the consultant's opinion on
 The nature and severity of the medical disorder in
question,
 Its amenability to medical management,
 The degree of risk imposed by a grand mal seizure
induced under controlled conditions of anaesthesia,
muscle relaxation, and oxygenation.

43. CONSENT
 Except for rare instances of judicially ordered
treatment or treatment given in a genuine emergency
to preserve life patients may not receive involuntary
ECT any more ,
The essential elements of informed consent always
include:
 A full explanation of the procedure in layman's terms
 A presentation of the risks and potential benefits of
the treatment offered, and about alternative
available therapies
 A statement that the patient may withdraw his
consent at any time and for any reason
 An educational videotape is useful both to orient
patients and their families to the procedures for ECT
 Unambiguously document the information that has
been presented to the patient when obtaining
informed consent

44. CONCOMITANT MEDICATIONS
 Patients' ongoing medications should be assessed for
1. Possible interactions with the induction of a seizure,
2. For effects both positive and negative on the seizure
threshold,
3. For drug interactions with the medications used
during ECT.
 The use of tricyclic and tetracyclic drugs,
monoamine oxidase inhibitors, and antipsychotics is
generally considered acceptable.
 Benzodiazepines ___ withdrawn
because of anticonvulsant activity;
 Lithium ____ withdrawn because
increased postictal delirium,
can prolong seizure activity;

45.  Clozapine and Bupropion __withdrawn because
the development of late-appearing seizures.
 Lidocaine _____not administered as it markedly
increases the seizure threshold;
 Theophylline ___contraindicated as it increases
the duration of seizures.
 Reserpine ____ contraindicated as it is
associated with compromise of the
respiratory and cardiovascular systems
during ECT.

46. PRE MEDICATIONS, ANAESTHETICS,
AND MUSCLE RELAXANTS
 Patients should not be given anything orally for 6
hours before treatment.
 Just before the procedure, the patient's mouth should
be checked for dentures and other foreign objects,
 An intravenous (IV) line should be established.
 A bite block is inserted in the mouth just before the
treatment is administered to protect the patient's
teeth and tongue during the seizure.
 Except for the brief interval of electrical stimulation,
100 percent oxygen is administered at a rate of 5 L a
minute during the procedure until spontaneous
respiration returns.
 Emergency equipment for establishing an airway
should be immediately available in case it is needed.

47. ANAESTHESIA
 Un modified ECT:ECT with out muscle relaxant and
anesthesia
 Modified ECT: use of anesthesia as a pre treatment is
modified ECT
First curare was used by A.E Bennet in 1950
The current practice includes use of anesthesia and
muscle relaxant in modified ECT.
In INDIA ,
As early as 1962, Dr. Bagadia used succinylcholine
successfully in modified ECT.
The Union Cabinet on 13 june 2013 cleared the Mental
Health Care Bill,
It bans the electric-convulsive therapy without
anaesthesia .

48. MUSCARINIC ANTICHOLINERGIC
DRUGS
Muscarinic anticholinergic drugs are administered
before ECT to
 Minimize oral and respiratory secretions
 To block bradycardias and asystole.
The most commonly used drug is Atropine, which
can be administered
0.3 to 0.6 mg IM or SC 30 to 60 minutes before
the anaesthetic
0.4 to 1.0 mg IV 2 or 3 minutes before the
anaesthtetic is given.

49. ANAESTHESIA
Administration of ECT requires general anaesthesia
and oxygenation.
The depth of anaesthesia should be as light as possible,
 To minimize adverse effects
 To avoid elevating the seizure threshold associated
with many anaesthetics.
Methohexital (0.75 to 1.0 mg/kg IV bolus) is the most
commonly used anaesthetic because of its shorter
duration of action and lower association with postictal
arrhythmias than thiopental(usual dose 2 to 3 mg/kg
IV),
Four other anaesthetic alternatives are etomidate ,
ketamine , alfentanil , and propofol .

50. MUSCLE RELAXANTS
After the onset of the anesthetic effect,
 A muscle relaxant is administered to minimize the
risk of bone fractures and other injuries resulting
from motor activity during the seizure.
 Succinylcholine, an ultrafast-acting depolarizing
blocking agent, has gained virtually universal
acceptance for the purpose.
 Succinylcholine is usually administered in a dose of
0.5 to 1 mg/kg as an IV bolus or drip.
 Succinylcholine is a depolarizing agent, its action is
marked by the presence of muscle fasciculations,
which move in a rostrocaudal progression.
 The disappearance of these movements in the feet or
the absence of muscle contractions after peripheral
nerve stimulation indicates maximal muscle
relaxation.

51.  If a patient has a known history of
pseudocholinesterase deficiency,
In such a patient, the metabolism of
succinylcholine is disrupted, and prolonged
apnea may necessitate emergency airway
management.
 Then atracurium (Tracrium) (0.5 to 1 mg/kg IV)
or curare can be used instead of succinylcholine.

52. ELECTRODE PLACEMENT
Unilateral : Here the electrodes are placed only on
one side of head , usually the non dominant
hemisphere , right side in the right handed.
Bilateral :This is standard from of electro
convulsive therapy used most commonly. Each
electrode is placed 2.5 – 4 cm above the midpoint
on a line joining the tragus of the ear and the
lateral canthus of the eye.

53.  Electrode placements.
 Position 1: represents the
frontotemporal position, used
for both electrodes, one on
each side of the head, in
conducting bilateral
electroconvulsive therapy .
 For right unilateral ECT, one
electrode is in the right
frontotemporal position, and
the other is just to the right of
the vertex at position 2

54. DIFFERENCES BETWEEN U/L AND
B/L ECT

55. MISCELLANEOUS ELECTRODE
PLACEMENTS
Various modifications of the bitemporal, right
unilateral, and bifrontal placements
 right frontoparietal
 fronto-frontal
 left frontal-right temporal
However, none of these has been demonstrated to
have either greater clinical efficacy or fewer
cognitive side-effects than any of the original
placements.

56. ELECTRICAL STIMULUS
 The electrical stimulus must be sufficiently
strong to reach the seizure threshold .
 The electrical stimulus is given in cycles, and
each cycle contains a positive and a negative
wave.
 Old machines use a sine wave; however, When a
sine wave is delivered, the electrical stimulus in
the sine wave is unnecessary and excessive.
 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.

57.  Establishing a patient's seizure threshold is not
straight forward.
 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 percent.
 A common technique is to initiate treatment at an
electrical stimulus that is thought to be below the
seizure threshold for a particular patient and then to
increase this intensity by 100 percent for unilateral
placement and by 50 percent for bilateral placement
until the seizure threshold is reached.
 Essentially, the data support the conclusion that
doses of three times the threshold are the most
rapidly effective.

59. INDUCED SEIZURES
 A brief muscular contraction, usually strongest in
a patient's jaw and facial muscles, is seen
concurrently with the flow of stimulus current,
regardless of whether a seizure occurs.
 The first behavioral sign of the seizure is often a
plantar extension, which lasts 10 to 20 seconds
and marks the tonic phase.
 This phase is followed by rhythmic i.e., clonic
contractions that decrease in frequency and
finally disappear.

60.  The tonic phase is marked by high-frequency,
sharp EEG activity on which a higher frequency
muscle artifact may be superimposed.
 During the clonic phase, bursts of polyspike
activity occur simultaneously with the muscular
contractions but usually persist for at least a few
seconds after the clonic movements stop.

61. MONITORING SEIZURES
 An objective measure that a bilateral generalized
seizure has occurred after the stimulation.
 Observe either some evidence of tonic-clonic
movements or electrophysiological evidence of
seizure activity from the EEG or electromyogram
.
 Seizures with unilateral ECT are asymmetrical,
with higher ictal EEG amplitudes over the
stimulated hemisphere than over the
nonstimulated hemisphere.
 For a seizure to be effective in the course of ECT,
it should last at least 25 seconds.

62. FAILURE TO INDUCE SEIZURES
 If a particular stimulus fails to cause a seizure of sufficient
duration, up to four attempts at seizure induction can be
tried during a course of treatment.
 The onset of seizure activity is sometimes delayed as long
as 20 to 40 seconds after the stimulus administration.
If a stimulus fails to result in a seizure,
1. The contact between the electrodes and the skin should be
checked,
2. The intensity of the stimulus should be increased by 25 to
100 percent.
 The clinician can also change the anaesthetic agent to
minimize increases in the seizure threshold caused by the
anaesthetic.
 Additional procedures to lower the seizure threshold
include hyperventilation and administration of 500 to
2,000 mg IV caffeine sodium benzoate 5 to 10 minutes
before the stimulus.

63. PROLONGED AND TARDIVE
SEIZURES
Prolonged seizures :seizures lasting more than 180 seconds
 Prolonged seizure and status epilepticus can be terminated
either with additional doses of the barbiturate anaesthetic
agent or with IV diazepam (5 to 10 mg).
 Management of such complications should be accompanied
by intubation, because the oral airway is insufficient to
maintain adequate ventilation over an extended apneic
period.
Tardive seizures: These are 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. Such situations should be managed
clinically as if they were pure epileptic disorders.

64. POSTICTAL CARE
 The goal of the postictal phase is primarily that
of maintaining an adequate airway until the
return of spontaneous respirations and,
eventually, alertness.
 The anesthetic specialist continues forced
ventilation until the patient is breathing on his
own, at which time he is transferred to a recovery
area under the observation of trained staff until
awakening

65. MULTIPLE MONITORED
ELECTROCONVULSIVE THERAPY
 Multiple monitored ECT (MMECT) involves
giving multiple ECT stimuli during a single
session, most commonly two bilateral stimuli
within 2 minutes.
 This approach may be warranted in severely ill
patients and in those at especially high risk from
the anesthetic procedures.
 MMECT is associated with the most frequent
occurrences of serious cognitive adverse effects

66. NUMBER AND SPACING OF
TREATMENTS
 Electroconvulsive therapy treatments are usually
administered two to three times a week;
 Twice-weekly treatments are associated with less
memory impairment than thrice-weekly treatments.
In treatment of
 Major depressive disorder _ 6 to 12 treatments
(although up to 20 sessions are possible);
 Manic episodes _ 8 to 20 treatments;
 Schizophrenia _more than 15 treatments;
 Catatonia and delrium_ as few as 1 to 4 treatments.

67.  Treatment should continue until the patient
achieves the maximal therapeutic response.
 The point of maximal improvement is usually
thought to occur when a patient fails to continue
to improve after two consecutive 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.

68. Continuation ECTs :
 After initial course of 6-12 exposures ECTs are
phased to once in 2 wks or once a month for 6
months.
 Continuation treatment, that is, treatment for 6
months beyond remission of an acute episode of
illness to prevent relapse, is standard practice for
the major syndromes that are somatically treated

69. FAILURE OF ELECTROCONVULSIVE
THERAPY TRIAL
 Patients who fail to improve after a trial of ECT
should again be treated with the pharmacological
agents that failed in the past.
 Many 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
treatments, even if the ECT seemed to be a
therapeutic failure.

70. AMBULATORY THERAPY
This phrase refers to outpatient administration of
the entire course of ECT:
 The patient is never hospitalized.
 ECT is ideally suited to the outpatient setting.
 It is brief, safe, and well tolerated
Ambulatory ECT is only unsuitable for patients
whose illness severity and consequent risk
mandate inpatient observation and care.

71. A BERGONIC CHAIR, A DEVICE "FOR GIVING GENERAL
ELECTRIC TREATMENT FOR PSYCHOLOGICAL
EFFECT, IN PSYCHO-NEUROTIC CASES".
WORLD WAR I ERA.

72. BEAUTIFUL MIND

73. ECT ROOM GHMC

74. ECT MACHINE IN GHMC

75. ADVERSE EFFECTS OF ECT
 ECT is generally low risk and one of the safest
procedures performed under general anesthesia.
 The estimated risk of serious complications,
occurring in about 1 in 1,000 patients
 Death rate about 1 in 10,000 patients in modern
populations undergoing ECT.

76. NEUROLOGICAL PHENOMENA
Transient neurologic abnormalities,
 aphasias,
 apraxias, and
 agnosias, which were considered normal rather than
complications, during the immediate postictal phase
following bitemporal ECT
 Asymmetrical motor responses observed during the
induced seizure usually consisted of more intense
clonic movements of the musculature contralateral to
the stimulated hemisphere, despite the induction of a
generalized, bilateral seizure.
 Following the seizure, and before recovery of
consciousness, upper limb reflexes ipsilateral to the
treated hemisphere generally return first.

77.  Limb strength tested after the return of
consciousness revealed upper limb weakness in
80% of the observations, with a gradual return to
normal over the ensuing 15 minutes.
 Motor and visual inattention, corresponding
tactile inattention on contralateral to the treated
side also occurred.
 All patients receiving left-sided ECT showed
signs of dysphasia immediately afterward.
 Anosognosia was profound and striking after
right-unilateral ECT, even after patients had
become fully alert and cooperative.

78. EMERGENT DYSKINESIAS
Dyskinetic movements take several forms,
 The most ubiquitous of which are the typical
postictal chewing and lip-smacking automatisms
observed during the postictal phase and which
characterized as mild bilateral oro bucco lingual
dyskinetic movements lasting 1 to 3 min.
 ECT-emergent dyskinesias reported in patients with
Parkinson's disease who continued to receive
levodopa during ECT; the dyskinesias disappeared
with a reduction in the dose of levodopa.
 ECT-emergent dyskinesias are due to ECT-induced
increases in post synaptic dopamine receptor
sensitivity.

79. PROLONGED APNEA
 There is no antidote for succinylcholine and no
specific treatment to reverse prolonged apnea.
 Assisted respiration is continued as long as it takes
the patient's own limited pseudo cholinesterase
activity to metabolize the succinylcholine (usually 30
to 60 minutes).
 Intubation is not required as long as good pulmonary
exchange documented by oximetry is achieved by face
mask.
 If apnea may be prolonged for more than an hour,
administration of a unit of typed and cross-matched
fresh whole blood or plasma to supply an exogenous
source of pseudo cholinesterase .

80. EMERGENCE DELIRIUM
About 10% of patients develop a self-limited delirium or
acute confusional state during the immediate
postictal phase, characterized by all of the following
clinical features occurring in concert:
 Restless agitation
 Disorientation
 Clouded consciousness
 Repetitive stereotyped movements
 Impaired comprehension
 Failure to respond to commands
 Subsequent amnesia for the episode
It is readily terminated by intravenous benzodiazepines
or barbiturates

81. CARDIOVASCULAR SYSTEM:
ECT results in parasympathetic outflow during and
immediately after ECT
 Sinus bradycardia and even asystole can occur
 Patients older than 50 years of age,
supraventricular ectopic beats are common but clinically
insignificant.
 In vulnerable patients, vagally related arrhythmias can
occur, such as
atrial, junctional, and nodal rhythms,atrial flutter and
atrial fibrillation.
Following parasympathetic stimulation, sympathetic output
increases,
 As a consequence, heart rate, blood pressure, increase.
These increases peak immediately postictally and drop off
within minutes to pre-ECT values.

82. RESPIRATORY SYSTEM
Adverse events related to pulmonary functions are a
leading cause of morbidity and mortality associated
with ECT.
Most of the effects are associated with Anesthesia
 Patients with underlying pulmonary disease,
exacerbation of asthma or COPD is possible.
 Excess secretions leads to aspiration pneumonitis.
 Rarely negative-pressure pulmonary edema due to
inspiration against an obstructed airway or
mechanical irritation precipitating laryngospasm;
 Another rarely observed complication is prolonged
apnea resulting from slow metabolism of
succinylcholine due to pseudocholinesterase
deficiency.

83. DENTAL
 Due to direct stimulation of jaw muscles during
delivery of the electrical stimulus,
patients bite down , strongly, and unstable teeth
may be broken or dislodged completely
Bite the tongue leading to bleeding
 The approach to this complication is routine
prophylactic screening, and may necessitate
dental consultation and procedures prior to ECT.
 If teeth are injured during treatment, care must
be taken to remove any broken fragments before
respiration resumes, when they may obstruct the
patient's airway.

84. MUSCULOSKELETAL
 More common in the modern era and, often an
adverse effect of depolarizing agents, is myalgia.
 These muscle pains are a consequence of the
fasciculations produced during depolarization
and are most prominent after the first treatment
 Patients with temporo mandibular joint problems
may experience an exacerbation of pain resulting
from the unmodified contraction of jaw muscles
during stimulus delivery. Spasm can also be
induced.

85. NEUROCOGNITIVE
 Cognitive side effects are a major limitation to the use of
ECT, With ECT, these effects have been best described for
depressed populations.
 The first factor in the development of adverse cognitive
side effects is the time point in treatment, which influences
not only severity, but also the type of effect observed.
 The phenomena are made more difficult to discriminate
because depression itself is accompanied by impairments
in attention, concentration, and learning.
 Post-ECT, with remission of depression, attention and
concentration are improved.
 Functions such as reasoning, creativity, and the ability to
form memories are not affected

86.  Non declarative memory, that is, procedural memory
and priming, does not appear to be affected .
 Disorientation, diminished processing speed,
decreased anterograde and retrograde memory, and
errors in visual-spatial function and word finding are
greatest immediately after a treatment session.
These effects diminish fairly quickly once the treatment
course ends.
 Except for retrograde memory impairment, other
cognitive effects generally return to pre-ECT baseline
or even improve over baseline with right unilateral
ECT.

87.  Diminished processing speed persists when sine wave
ECT has been administered.
 Retrograde memory improves more gradually, but
spotty deficits may persist, with recent memories for
public information more vulnerable than older
memories for personal experiences.
 In a community setting, 12.4 percent of patients
manifested marked and persistent retrograde
amnesia, defined as deterioration in autobiographical
memory of at least two standard deviations from pre-
ECT baseline at 6 months post-ECT.

88. The likelihood of developing adverse cognitive effects is
influenced by technical factors in the treatment:
 Bilateral electrode placement;
 Inefficient stimulus waveforms, including brief pulse,
but most particularly sine waveform;
 Markedly suprathreshold dosing;
 Greater frequency and number of treatments;
 Larger doses of anesthesia are more likely to result
in deficits during the acute and subacute courses of
treatment.
Bilateral electrode placement is associated with greater
likelihood of persistent retrograde memory deficits
long term.

89. Patient characteristics and clinical factors also
affect the severity of adverse cognitive effects.
 Those with baseline neurological disease,
 MRI abnormalities,
 Baseline impairments in global cognitive
functioning,
 Older and female patients
are more vulnerable to developing deficits.
The concurrent use of certain medications such as
lithium or medications with anticholinergic
effects also increases the risk of adverse cognitive
effects.

90. PREDICTION OF POST-ECT
COGNITIVE IMPAIRMENT
 Pretreatment global cognitive status assessed
via Mini-Mental State Examination and postictal
orientation recovery time, were both significantly
associated with retrograde amnesia for
autobiographical memories.
 These findings suggest that the Mini-Mental
State Examination might be used as a screening
test to guide the selection of ECT treatment
parameters demonstrated to affect cognition.

91. MANAGEMENT OF MEMORY
IMPAIRMENT
No specific treatment is available to reduce the extent
or duration of the memory impairment of ECT
 Use Breif Pulse wave instead of sine wave
 2 times weekly than 3 weekly
 Unilateral or BiFrontal instead of Bi Temporal ECT
 Increasing efficacy by changing stimulus parameters
There are no well-established pharmacological
approaches to attenuating adverse cognitive effects,
although there is interest in using N-methyl D-
aspartate antagonists, such as ketamine anesthesia,
and thyroid hormone.

92. OTHER ADVERSE EFFECTS
 Postictal agitation
 Headaches
 Nausea occasionally occur postictally
 Mania and Organic Euphoria
Years ago, described the emergence of organic
psychotic states during the course of bitemporal
ECT; additional ECTs would typically attenuate
the syndrome
 Post ECT confusion

93. PATIENT & PUBLIC ATTITUDES
 In view of the fact that most of the several hundred
patients interviewed in the studies had rather positive
views about ECT and did not find the treatment especially
frightening, upsetting, painful, or unpleasant.
Misinterpretation of ECT in Media
 Films, and several other media , created indelible images
of the apparent brutality of ECT and the callousness of
those who administer it, inculcating negative feelings
towards ECT and even refusal of ECT among its potential
recipients
 The nature of ECT had been completely transformed by
modern anaesthesia techniques decades before that films
in which ECTs were portrayed
 Public surveys among those who have not received ECT
and are not about to, have generally revealed an
unexpectedly overall positive attitude toward the
treatment

94. CONCLUSION
 ECT is practiced fairly commonly to this day.
 ECT is much safer than before due to the precision in
administering electric currents offered by modern-day
technology, which minimizes sides effects.
 Complications, such as memory loss, still arise in patients
who are treated with ECT, and this causes many people to
oppose it.
 ECT has the highest success rate of any other treatment
for Major Depressive Disorder and is a plausible option for
individuals suffering from severe forms of this illness.
Indian experience:
81.7% psychiatrists use ECT.
Of pts treated with ECT 48.4% had depression .
13% had mania.
Response rate 79% for depression, 65.5% for mania.
Mostly comonly used is B/L ECT.

95. REFERENCES
 Electro convulsive therapy – ABRAMS
 Comprehensive text book of psychiatry
 Synopsis of psychiatry
 Internet sources