This document provides an overview of electroconvulsive therapy (ECT), including its history, mechanisms, procedures, indications, and controversies. It discusses how ECT was developed from early seizure therapies and first applied using electricity in the 1930s. It also describes how ECT works, involving inducing seizures through electrical stimulation of the brain, and summarizes some of the leading theories about its therapeutic mechanisms. The document outlines the typical ECT procedure and treatment course, including electrical parameter settings and monitoring techniques used. It notes some potential side effects and provides guidelines on patient selection and risk-benefit assessment for ECT.

1. All sections to appear here
ELECTROCONVULSIVE
THERAPY

2. Presented by
Dr. Anusa AM
2ndYear MD PG
Madurai Medical College
Prepared by
Prof. Rooban T,
Oral & Maxillofacial Pathologist

3.  History
 Basics
 Theories
 Mechanism of ECT
 Procedure
 Indication and Contraindications
 Issues and regulation of ECT

4.  OldTreatments
 Theory of BiologicalAntagonism
 Insulin ShockTherapy
 Electrically induced seizures

5.  Hippocrates: Cure of insane patient
following malaria-induced seizures.
 Galen and Scribonius Largus in Rome
-Electric rays to treat headaches
& other disorders
 Placed across the brow of a suffering
patient or had patient stand on
several live rays

6.  Swiss physician “Paracelsus” in 1500 s,
induced seizures with oral camphor to treat
psychiatric illness.

7.  In 18th Century - Roess claimed
improvement in mental
patients after inoculation
 1917 - JuliusWagner von
Jauregg – Mental Diseases &
Fever – 1927 NOBEL Prize

8.  Manfred Sakel, a
Viennese physician in
1920s.
 Administered in
patients to induce a
hypoglycemic state.

9.  Hungarian physician
Meduna in 1934 - an
inherent biological
antagonism between
schizophrenia and
epilepsy.
 Beneficial effects of
seizures induced by
camphor in catatonic
patient.

10.  In 1937, Italian physicians Cerletti & Bini
applied electricity to head to induce
therapeutic seizures.
 First patient had catatonia and he improved.
 Safer than chemically induced seizures.
 Widespread acceptance through out Europe
and USA.

14. Ugo Cerletti
Lucio Bini

15.  Early period complications l-bone fractures & patient
discomfort.
 Use of Curare, as muscle relaxant, by Bennett in 1940
allowed complete paralysis of patient during seizure.
 Development of brief general anaesthesia in 1950s
replaced Curare

16.  Not sure!!!
 Massive release of neurotransmitter?
 Alteration in seizure threshold?

17.  Ohm’s Law; Current (I) =Voltage (E) / Resistance (R )
 E = I *R for DC & AC :Voltage = I X Impedance ‘Z’
 Z or impedance
 Capacitance
 Inductance
 Resistance

18.  In ECT= 100-500 milliCoulombs; AC only
 Brain - low impedance (resistance), skull very high
 Seizure involves propagation of action potentials in a
large percentage of neurons.

19.  Neurotransmitter levels all ↑ in CSF after seizure
 ↓ regulation of β-adrenergic receptors.
 During seizure- PET studies show an ↑
 BBB permeability
 Cerebral blood flow
 Metabolism.
 After seizure, blood flow and metabolism is ↓
especially in the frontal lobes. Research shows
this correlated w/ response.

20.  PsychologicalTheories
 PsychoanalyticTheories
 Non-PsychoanalyticTheories
 The Brain DamageTheory
 The AmnesticTheory
 NeurophysiologicalTheories
 AnticonvulsantTheory
 AntideliriumTheory
 NeurogenesisTheory

21.  BiochemicalTheories
 NeurochemicalTheory
 NeuroendocrineTheory
 Neuropeptides

23.  Electrical stimulus delivered via a variety of waveforms.
 Waveform is “shape” of the stimulus as a function of
time
 Cycles of negative and positive current flow, is referred
as frequency of the stimulus - Hz
 2 forms
 Sine wave currents - continuous stream of electricity -
alternating directions & continuously undulating
 Brief pulse waveform is bidirectional and consists of a series of
instantaneously rising and falling rectangular pulses of
current, with adjacent wave with period of inactivity

24.  Duration of each pulse is referred to as Pulse
width, in milliseconds
 Pulse frequency, is defined in terms of pulse pairs
per second, actual number of pulses per second is
twice frequency.
 Duration is defined as length of entire series of
pulses delivered, and is measured in seconds.
 Peak current, which is maximum intensity of each
pulse, measured from the zero baseline, in
amperes.

25. Sine-wave form
Brief pulse

28.  Current : is the number of
electrons per second flowing
through a circuit
 Voltage: force that drives the
flow of electrons during the
stimulus
 Impedence: measure of the
obstacle to the current (220 ohms)
Causes of high
impedance
Causes of low
impedance
Scalp tissue Stimulus electrodes are
too close together
Poor contact of
electrodes with
scalp
Low impedance pathway
(sweat,conducting gel)
Small electrodes Large electrodes
Poor preparation
of scalp(hair,
insufficient gel)
skull defect
Faulty connection
of electrodes
Too little pressure
over electrodes

29. Function of
 Charge
 Energy

30.  Charge
 currrent in a single pulse X number of
pulses
Peak current X pulse width
2(frequency) X duration

31.  Energy
 Voltage X Current over the entire stimulation

32.  The total amount of electricity necessary
to induce a seizure
 Markedly suprathreshold
 Barely suprathreshold
 Moderately suprathreshold

34.  Based on clinical outcome rather than
seizure duration
 Greater intensity > greater efficacy > speedy
recovery > increased cognitive side effects

35.  Dose titration method
 Pre selected dose
 Fixed dose paradigm
 Calculated dose paradigm

37. Dose titration method Preselected dose
method
Merits •Moderate suprathreshold
calculation
Demerits • Restimulation
•Variable rise in seizure
threshold over the
treatment course
•Very rough
estimate of stimulus
intensity

38. ECS
Neuronal
Growth
and
Protective

41.  Evaluation – Pretreatment
 Consent – Informed,Written
 Preparation of patient – from the night
before

42.  A complete psychiatric history
 Pre-existing medical conditions and ongoing
treatments
 Appropriate modifications of ECT procedure.
 Risk-benefit comparison of all viable treatment
options.
 Informed consent
 Anesthetic evaluation

44.  Bilateral
 Right unilateral
 Bifrontal

46.  Patient’s motor response
 Blood pressure
 Pulse rate
 Electroencephalographic (EEG)
 Electromyographic (EMG) data
 Oxygen saturation.

47.  Purpose: to induce a generalized grand
mal type of seizure.
 not an all-or-nothing phenomenon.
 Seizures-
 the ictal motor response (convulsion)
 monitoring ictal EEG activity

48.  extension of the neck
 flexion of the ankle
 clenching of the jaw.
 A gradual, sustained tonic contraction
represents the first phase of the ictal
motor response
 Clonic phase

50. Ictal routine EEG monitoring
 Reflects activity of organ that is actually generating seizure
(i.e., brain)
 EEG seizure activity is typically 10–20 seconds longer (and
occasionally much longer) than motor activity
 Motor response may not always be observable, or in some
cases no motor response may occur during the seizure
 Prolonged seizures may be detectable only by EEG

54. Treatment Course

55. Malignant Catatonia•Delirious Mania
•Neuroleptic Malignant Syndrome
•Malignant Catatonia

56. • Recent intracranial hemorrhage
• Recent thromboembolic stroke
• Intracranial lesion (tumor or infection)
causing mass effect
• Recent myocardial infarction, particularly if
sequelae are present
• Unstable angina or decompensating heart
failure
• Unstable vertebral fracture

57.  Cognitive changes
 Postictal disorientation
 Interictal confusion
 Memory impairment
 Transient cardiovascular alterations
 General somatic complaints

59.  2-10 per 100,000 patients (0.0001%)

62. Seizure augmentation
 Hyperventilation
 Caffeine
 Changing the anaesthetic agent
▪ Barbiturates ->Ketamine

64.  Index ECT
 Frequency
▪ Multiple monitored ECT
 Number

65.  Pharmacotherapy
 Continuation ECT
 Maintenance ECT
 Pharmacotherapy + ECT

72. REFERENCE
1. Clinical Manual of Electroconvulsive Therapy-Mehul V. Mankad, M.D.;
John L. Beyer, M.D, .Richard D. Weiner, M.D., Ph.D.; Andrew D. Krystal,
M.D
2. The ECT Handbook-Allan I. F. Scott
3. Brain Stimulation Therapies for Clinicians-Edmund S. Higgins, M.D.;
Mark S. George, M.D.
4. Baghai TC, Moller H. Electroconvulsive therapy and its different
indications. Dialogues Clin Neurosci. 2008;10:105-117.
5. SCott AIF. College guidelines on electroconvulsive therapy: an update for
Prescribers. Adv Psy Treat 2005;11:150-56.
6. Gangadhar N, Phutane VH, Thirthalli J. Research on electroconvulsive
therapy in India: An overview.Indian J Psychiatry 2010;52:S362-5.
7. Andrade C, Shah N, Tharyan P, Reddy MS, Thirunavukarasu M,
Kallivayalil RA, et al. Position statement and guidelines on unmodified
electroconvulsive therapy. Indian J Psychiatry 2012;54:119-33.
8. Read J, Bentall R. The effectiveness of electroconvulsive therapy: A
literature review. Epidemiologia e Psichiatria Sociale 2010;19:333-48.
9. Grover S, Mattoo SK, Gupta N. Theories of Mechanism of Action of
Electroconvulsive Therapy. German J Psychiatry 2005; 8: 70-84