Role of ECT in psychiatry

1. Presenter : Dr. Kaushik Nandi

2. Overview
 Historical overview
 Indications
 Contraindications
 Adverse Effects
 ECT Stimulus
 ECT Procedure
 Mechanisms of action
 Effectiveness
 Special Populations
 References

3. Historical overview of convulsive therapies
 The roots of Convulsive therapy can be
found in 1500s when Paracelsus gave
Camphor to patients by mouth to induce
seizures and cure psychiatric ailments.
 In 1758, the first report was published
which mentioned the use of camphor for
the treatment of mania by inducing
seizures.

4.  Another breakthrough was achieved in 1927 by a young
Polish neurophysiologist and neuropsychiatrist named
Manfred J. Sakel.
• Sakel discovered accidentally, by
causing convulsions with an overdose
of insulin, that the treatment was
efficient with patients afflicted with
psychosis, particularly schizophrenia

5.  In 1930 he began to perfect, what was to become
the "Sakel's Technique" for treating schizophrenics.
 According to his findings, more than 70 % of his patients
improved after Insulin shock therapy.

6.  In 1934, Hungarian Neuropsychiatrist,
Ladislas Meduna treated a patient of
catatonic schizophrenia by inducing
seizure with intra-muscular injection of
Camphor oil.
 He observed greater glial cells in
epileptics & schizophrenics have lesser
glial cells, hence he tried to increase glial
cell concentration with induced seizures

7.  Later camphor was replaced by
Pentamethylenetetrazol (Metrazol)
 In 1937, the Italian neuropsychiatrists
Ugo Cerletti and Lucio Bini began to
induce seizures experimentally with
electricity

8.  They found that seizures could be more
easily induced and regulated with
electricity than with pharmacological
agents, thereby decreasing the number of
missed or recurrent seizures
 On May 15, 1938, a seizure was
successfully elicited with electricity in a
39-year-old delirious manic man.

9.  After 10 to 20 ECT shocks in alternate days, the
improvement in most of the patients were startling.
 Significant improvements in the technique of ECT have
been made since then, including the use of muscle
relaxants, such as succinylcholine, the anesthesia of
patients with short-acting agents, pre-oxygenation of the
brain, the use of EEG seizure monitoring and better
devices and shock waveforms.

10.  Despite these advances, the popularity of ECT greatly
decreased in the 1960s and 1970s, due to the use of more
effective neuroleptics and as a result of a strong anti-ECT
movement.
 However, ECT gained evidence again in the last 15 years,
due to it's efficacy.
 It is the only somatic therapy from the 30's that remains in
widespread use today.

11. Carrie Fisher (Princess Leia) was treated with ECT for BPAD

12. Indications of ECT
1. Major depression, both unipolar and bipolar and
Psychotic depression
2. Mania
3. Schizophrenia with acute exacerbation; Catatonic
subtype, particularly
4. Schizoaffective disorder
5. High suicidal risk
6. Others: Parkinson disease, Neuroleptic malignant
disorder, Intractable Seizures

13. Primary Use
 Rapid definitive response required on medical or
psychiatric grounds
 Risks of alternative treatments outweighs benefits
 Past history of poor response to psychotropics or good
response to ECT
 Patient preference

14. 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
patient’s condition

15. Contraindications
 ECT has no absolute contraindications.
Medical conditions associated with increased risk:
 Space-occupying intracerebral lesion (tumor, hematoma,
etc.)
 Other condition causing increased intracranial pressure
 Recent myocardial infarction
 Recent intracerebral hemorrhage

16.  Unstable vascular aneurysm or malformation
 Pheochromocytoma
 High anesthesia risk (American Society of
Anesthesiologists [ASA] class 4 or 5)
Mortality Rate
 Extremely low, estimated at 2–10 per 100,000 patients
(0.0001%) - same ratio as for the induction of brief
general anesthesia

17. Cognitive Changes
 Cognitive changes are often the most notable and most
distressing side effects
Factors that may increase cognitive side effects

18. Postictal Disorientation:
 All patients experience some transient postictal
disorientation, lasting from a few minutes to a few hours,
following awakening from the ECT treatment.
 Having received general anesthesia likely contributes to
this disorientation

19. Interictal Confusion:
 Occasionally, postictal confusion may not fully disappear
and, when severe, may develop into an interictal
confusional state or delirium.
 Uncommon
 Rapidly disappears over a period of days following the
conclusion of treatments

20.  The ECT team at NIMHANS has developed and validated
a short and sensitive battery (Battery For ECT Related
Cognitive Deficits – B4ECT-ReCoDe) for a quick
assessment of cognitive deficits associated with ECT in
the Indian setting

21. Cardiovascular Complications
 They are the main cause of mortality and serious
morbidity with ECT, although most such complications
are minor.
 During the seizure and acute postictal period, both the
sympathetic and parasympathetic autonomic systems are
sequentially stimulated.
 Activation of the parasympathetic system causes a
transient reduction in cardiac rate

22.  Activation of the sympathetic system increases heart rate,
blood pressure, and myocardial oxygen consumption.
 These changes occasionally giving rise to transient
arrhythmias and, in susceptible individuals, transient
ischemic changes.
 During parasympathetic stimulation, cardiac arrhythmias,
such as bradycardia, premature ventricular contractions, or
sinus arrest, may be seen.

23.  The risks of cardiac arrhythmias, ischemia, and
hypertension are greatly diminished by the use of
oxygenation before and during the seizure, and these risks
can be lowered further in susceptible patients by
pretreatment with appropriate medications.
 Stress on the heart during ECT equivalent to
climbing up about 2 floors.

24. Other Adverse Effects
 General somatic complaints (e.g., headaches, nausea,
muscle soreness) are usually minor but are frequent
side effects of ECT.
 Lasting up to several hours, but occasionally longer.
 A soft bite block or other such device is used to
prevent injury to the tongue or teeth

25. ECT Stimulus
 Generation & behaviour of
electrical stimulus has been
conceptualized by Ohm’s law:
 V (voltage) = I (current) × R
(resistance)

26. 1. Waveform of the stimulus:
 Earlier ECT machines delivered current in the form of
sine waves.
 The slow rising and trailing edges of the sine wave do not
produce efficient cerebral stimulation.
 This delivers substantial amounts of electrical stimulation
below seizure threshold and continues stimulation even
while the neuronal tissue is in post-depolarization
refractory period.

27.  This may increase the cognitive adverse effects without
enhancing the benefits.
 Hence, the sine wave has been modified to eliminate the
rising and trailing edges, retaining only the peaks in the
form of ‘rectangular’ pulses

28.  Stimulus is given in the form of brief pulses (0.5ms) with
no stimulus in between the pulses.
 Intermittent stimulation using pulses is more efficient as it
allows the tissue to recover from post-depolarization
refractory period.
 Brief pulse ECT is able to induce seizures with
substantially less charge and energy compared to sine
wave.

29.  Pulse width – 0.5-2ms: brief pulse
<0.5ms: ultra-brief
 Stimulus duration - total period for which the stimulus
train is applied
Sine wave – less than 1s
Pulse wave – 0.5 – 8s
 In the brief pulse ECT, the actual duration of stimulus will
be even lesser if the inter-train interval (where stimulus
is not provided) is excluded.

30. Frequency - number of cycles per second (Hz)
 In the transformer-based sine wave stimuli, this is always
the line frequency (50Hz or 60 Hz)
 Brief pulse – pulses per second (PPS)
Directionality & Polarity : Stimulus in ECT is
bidirectional, alternating current

31. Pulse amplitude:
 The amplitude of the delivered current is an important
determinant of the volume of nervous tissue that is
directly stimulated by the ECT.
 Modern ECT uses a constant current of around 800-
900mA

32. Charge:
 Total amount of electrons traversing the inter-electrode
tissue
 It is the product of current and actual duration of stimulus
in milli-Coulomb (mC)
 Charge = current (in Amperes) × pulse width (in
milliseconds) × pulse frequency × length of train (in
seconds)

33. 2. STIMULUS INTENSITY
 Determines treatment efficacy & cognitive adverse
effects; measured as charge in mC
 Stimulus threshold should be supra-threshold to be
efficacious
 Bilateral ECT – 1.5 to 2.5 times threshold
 Unilateral ECT – 2.5 to 6 times threshold

34. 3. ELECTRODE PLACEMENT
Unilateral ECT
 Stimulus is provided to only one hemisphere (usually
right) to minimize cognitive dysfunction
 Electrode 1: Fronto-temporal site i.e., 1 inch above the
midpoint of an imaginary line linking the outer canthus
and the external auditory meatus
 Electrode 2: 1 inch lateral to the vertex position, on the
same side (usually right)

35. Bilateral ECT
 Bifrontal placement - electrodes are placed 5 cm vertically
above the outer canthus of each eye along an imaginary
vertical line perpendicular to a line connecting the pupils
 Bitemporal placement - electrodes are placed on the
frontotemporal sites, one on each side

36. Electrode Placements
Bitemporal Right unilateral /
d’Elia
Bifrontal /
Letemendia

37. Selective Preferences Of Electrode Placement
Unilateral ECT
• Concern about potential cognitive side-effects (children,
elderly, brain damaged)
• Instrument limitations (e.g., sine wave stimulus)
Bilateral ECT
• Mania or schizo-affective disorder
• Patient has not satisfactorily responded to UL ECT
(usually after 6 ECTs)
• When more urgent response is essential (suicidal, starving
etc)

38. 4. FREQUENCY OF TREATMENTS
 ECT is generally administered twice or thrice a week
 However, it is recommended that the patient be evaluated
both for therapeutic and adverse effects
5. NUMBER OF SESSIONS
 Decided based on the degree and rate of clinical
improvement and adverse effects
 A typical course of ECT for depression consists of 6 to 12
sessions

39.  Continuation ECT - begins after the index course, lasts
up to 6 months, and is designed to prevent relapse of the
episode
 Maintenance ECT - to prevent further episodes for
longer periods
 Frequency of ECT is slowly tapered off to once a month

40. ECT Procedure
 Administration of ECT without a muscle relaxant is
known as unmodified ECT.
 In modified ECT, anesthesia, muscle relaxant, and the
seizure-eliciting electrical stimulus are administered in the
same order.
 Use of a muscle relaxant prevents musculoskeletal injuries
resulting from peripheral seizures

41. Preparation of patient:
 Avoid solid food for at least 6 hours before treatment.
 Moderate amounts of clear fluids can be taken till 2 hours
 Oral medications should be taken 2 hours before treatment
 Pass urine to prevent bladder rupture during ECT.
 Dentures, jewellery, hair clips, contact lenses and hearing
aids should be removed.
 Hair should be dry and clean.

42. Modification Procedures:
 Short acting barbiturates are commonly used as induction
agents. E.g: Thiopentone (3-5 mg/kg)
 Succinylcholine (0.5-1 mg/kg) is the preferred muscle
relaxant due to its rapid onset, short duration of action,
and rapid recovery.
 Patient is allowed to breathe 100% oxygen through face
mask for 3 minutes at 15 -20 breaths per minute

43.  Atropine (0.6 mg) given along with intravenous anesthetic
helps in preventing vagal effects of electrical stimulation
on heart
 Seizure Monitoring:
1. Cuff method
2. EEG monitoring

44.  Cuff method:
Technique
 Place the BP cuff (preferably between knee and ankle). If
unilateral ECT is used cuff should be attached to the right
side (ipsilateral) to confirm generalization of seizures.
 Just prior to the injection of succinylcholine inflate the
cuff to a pressure 50 - 80 mm Hg above systolic blood
pressure.

45.  Observe that fasciculation after succinylcholine injection,
which appear in other parts of the body do not appear in
the isolated limb.
 Apply the stimulus and note the time.
 At the start of tonic phase of seizure release the cuff.
 Record the total duration of tonic and clonic phases till the
last clonic movement

46. EEG monitoring:
 Although not mandatory, it has distinct advantages and is
recommended where possible as it is the most direct
measure of cerebral activity available.
 The length of the convulsions measured by direct
visualization is approximately 70% that of EEG seizures

47. Schematic of various phases of a typical ECT seizure.

48. Motor and EEG ictal responses during ECT
Stage Motor response EEG response
Onset- epileptic recruiting
rhythm
- 10 Hz waves with increasing
amplitude
Tonic phase- polyspikes Tonic muscular
contractions
Bursts of high amplitude
spike discharges lasting 10-
15 seconds
Tonic –clonic phase –
polyspike and slow wave
complexes
Regular myoclonic
contractions
Polyspikes intermixed with
slow waves
Post- ictal cortical extinction Post-ictal sleep Isoelectric or flat EEG
Recovery Gradual regaining of
consciousness
Resumption of delta, then
theta & then alpha activity

49. Determination of Seizure Adequacy
 Achievement of an adequate seizure duration has been
assumed to be both necessary and sufficient to ensure
therapeutic adequacy of ECT treatment
 20- second motor response and/or
 25-second EEG response

50. Other Physiological Monitoring:
 Vital signs such as Blood pressure and Pulse should be
recorded before and after ECT.
 ECG monitoring is considered mandatory during ECT
procedure.
 Pulse oximetry

51.  Missed seizure, inadequate and prolonged seizures are
known phenomena during ECT.
 These are dependent on the seizure threshold.
 The threshold is lower in a) young subjects, b) manic
patients, and c) during the first ECT session.
 Conversely, benzodiazepines, carbamazepine and
thiopentone elevate the threshold.

52. Missed seizures:
 When electrical stimulation is not followed by any motor
or EEG seizure activity, it is termed a missed seizure.
 Wait for 20 seconds before restimulation to allow for
delayed onset of seizures.
 Restimulation should occur only after 45 seconds with
higher dosage.

53. Methods of managing missed seizure :
 Change of anesthetic agent to Etomidate or Ketamine
 Vigorous hyperventilation
 Use of EEG monitoring
 Change to bilateral ECT, as the seizure threshold is high
with unilateral ECT
 Reducing the frequency of sessions

54.  Reducing the frequency of sessions (from 3/wk to 2/wk)
can facilitate adequate seizures
 Lower change rate by shortening pulse width or increasing
interpulse intervals by decreasing frequency of stimulus
 Avoiding / reducing the dosage of Anti-epileptics and
Benzodiazepines.

55. Prolonged seizure:
 In most situations, the seizure terminates within 100
seconds.
 The American Psychiatric Association task force defines a
prolonged seizure if seizure duration is beyond 180
seconds.
 Prolonged seizures can be terminated by intravenous
diazepam 10 mg. or thiopentone 100-200mg

56. Mechanisms of action of ECT
Mechanisms of action of ECT have been studied in five
important domains:
1. Neuroplasticity
2. Contribution of EEG correlates
3. Neurophysiology
4. Neurotransmitters
5. Neuroendocrinology

57. Neuroplasticity:
 This happens through remodelling of synapses, generation
of new neurons, proliferation of glial cells, and
improvement in blood supply in specific brain areas.
 Animal studies have more robust findings favouring the
role of ECT in promoting neuroplasticity, particularly in
hippocampus, and recently in the prefrontal cortex and
amygdala also

58.  Serum levels of BDNF, an important neurotrophin
regulating synaptogenesis and neuronal cell growth, have
been found to be increased following ECT.
 One study demonstrated increases in volumes of amygdala
and prefrontal cortex.

59. Contribution of EEG correlates :
Anticonvulsant theory:
 Gradual increase in seizure threshold occurs over the
course of successive ECT sessions.
 The plasma levels of inhibitory neurotransmitter GABA
has been noted to increase following ECT
 Hence, it has been postulated that the clinical
improvements following ECT are not due to seizure per
se, but due to the brain’s efforts to reduce the probability
of occurrence of subsequent seizures

60. Connectivity Resetting :
 This is supported by the finding that ECT leads to
frequency specific modification of theta activity and
reduced blood flow in the Subgenual, ACC, Medial frontal
cortex, and increased blood flow to the Thalamus
 Thus, it is postulated that ECT rectifies the aberrant
modulatory activity of alpha and theta oscillations by the
thalamus.

61.  It stimulates the thalamo-cortical loop, takes over the
thalamic pacemaker function, resets it, and restores the
functional connectivity and control between various brain
areas.

62. Neurophysiology:
 The related hypothesis is called “Reducing
Hyperconnectivity”.
 ECT produces post-ictal states of diffuse slowing of
EEG with high amplitude delta and theta activity.
 This is followed by a period of post-ictal suppression,
which initially lasts for few hours after each ECT
session.

63.  This slowing gradually prolongs over many sessions of
ECT into an inter-ictal suppression
 PET and SPECT studies have also shown decreased blood
flow and glucose metabolism in the frontal lobe, following
ECT.
 Functional MRI studies are few, but they have
corroborated the reduced functional connectivity in frontal
cortex post-ECT.

64.  Overall, it can be assumed that ECT reduces the
“hyperconnectivity” secondary to depression in the frontal
cortex, particularly in the VMPFC, DMPFC, and some
parts of ACC.

65. Neurotransmitters :
 ECT has been found to affect 5-HT, DA, and adrenergic
system. More pronounced on DA than on 5-HT and
adrenaline.
 Increased dopamine release consistently in the striatum,
and inconsistently in the frontal and occipital regions.
 It also causes up-regulation of DRD1 and DRD3 receptors

66.  There is evidence of inhibition of adrenergic α2 auto
receptors by ECT, resulting in increased secretion of
catecholamines.
 ECT increases concentrations of glutamine, (a metabolite
of glutamate) and N-acetyl aspartate, a neuronal marker in
the ACC, PFC, and amygdala. This supports the
neuroplastic hypothesis of ECT.
 ECT also increases GABA levels, particularly in ACC,
PFC, and occipital cortex, thus reinforcing the
anticonvulsant hypothesis.

67. Neuroendocrinology:
 Neuroendocrine-diencephalic theory of depression
hypothesized that the HPA axis is disturbed producing a
state of hypercortisolemia and abnormal DST
 ACTH, cortisol and prolactin levels increased soon after a
session of ECT and came down to normal level within few
hours.
 Normalisation of DST has been correlated with clinical
response

68. Major depressive disorder
 ECT was found to be 20 to 40% more effective than
medications
 Response to ECT in antidepressant non-responders is
around 50 to 70 %
Effectiveness of ECT

69.  Comparison of ECT versus antidepressants (MAOI &
TCA) - a significant superior effect of ECT noted
- Gangadhar BN et al (1982), Pagnin D et al
 An RCT found ECT to be superior to paroxetine in
medication-resistant major depression, in terms of both
degree and speed of response
- Folkerts HW et al
 Equal efficacy in unipolar & bipolar depression –
- Narayanaswamy JC et al

70.  ECT is an effective short-term treatment for depression,
and is probably more effective than drug therapy. Bilateral
ECT is moderately more effective than unilateral ECT,
and high dose ECT is more effective than low dose
- UK ECT Review Group.

71. Mania:
 Second-line treatment (CANMAT, APA), third-line
(NICE)
 Response rates 75-80%; Increased responsiveness in rapid
cyclers & mixed affective states
 Controlled retrospective comparisons have found ECT to
be equivalent to lithium, & at least as efficacious as
typical neuroleptics

72. Schizophrenia:
 Indicated in treatment-resistant patients and those who
relapse on monotherapy
 Combination treatment is more effective than ECT alone,
& more effective than medications alone
 Equivalent to pharmacotherapy in management of NMS;
superior in that it treats underlying condition where
neuroleptics cannot be used

73.  Response to ECT among a group of adolescents was
around 76%. The main diagnosis was schizophrenia &
MDD
- Grover et al, 2013
 Another study on children with a predominant diagnosis
of catatonia showed ECT was efficacious in 77.3%
patients
– Jacob et al, 2014

74. Delirium tremens:
 ECT is an effective method of suppressing the symptoms
of delirium associated with alcohol withdrawal
 In all cases, one treatment produced a period of sedation
followed by a clearing of the sensorium and termination of
hallucinations within 24 hours.
-William H. C. Dudley, Jr. and J. G. Williams

75. ECT in Special Populations
Elderly population:
ECT is particularly useful in the elderly
 Medication intolerance is common
 Drug interactions are common
 Cognitive side effects are more common
 Response to ECT is better in the elderly
 Seizure threshold is greater ⇒ It may be difficult to get
adequate seizures

76. Pregnancy:
 Use of psychotropics is associated with problems in first
and last trimester
 Untreated psychiatric disorders may have adverse effect
on the baby
 ECT is effective
 Many guidelines on mood disorders advocate use of ECT
as first line treatment for major depression and mania in
first trimester

77.  APA Taskforce on ECT: “low risk and high efficacy in
the management of specific disorders in all three
trimesters of pregnancy”

78. Children and adolescents:
 ECT should be used with extreme caution (and very rarely
as a first-line treatment) in young people because of the
lack of evidence from randomised controlled trials
 Seizure threshold is low
 Propensity for prolonged seizures
 Two consultants need to independently opinion about the
need for ECT

79. Relapse after ECT
 51.1% of patients (depression) relapsed by 12 months
following successful initial treatment with ECT, with the
majority (37.7%) relapsing within the first 6 months
-Ana Jelovac et al
 C-ECT and continuation pharmacotherapy may be more
effective than either alone for preventing relapse.
-Nagy A. Youssef et al

80. References:
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Kumar CN et al. ECT Administration manual. 2nd ed. Bangalore:
NIMHANS; 2013
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Affective Disorders 63 (2001) 1–15
 UK ECT Review Group. Efficacy and safety of electroconvulsive therapy in
depressive disorders: a systematic review and meta-analysis. Lancet. 2003
Mar 8;361(9360):799-808
 Gangadhar BN, Viswanath B, Keshavan M, Sundar AS. Hnadbook of
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electroconvulsive therapy for major depression: a meta-analysis.
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84. THANK YOU