Indications and Treatment Guidelines of ECT discussed

1. Topic Discussion
Electroconvulsive Therapy
Indiacations and Treatment Guidelines

2. INTRODUCTION
● Electroconvulsive therapy is biological therapy where
seizure is induced under medical supervision by
passing electric current across brain.

3. History
In the early twentieth century, with the success of malarial
fever therapy for general paresis, interest in biological
therapies for psychiatric illnesses increased.
In 1927 Dr.Manfred Sakel initiated insulin coma therapy for
schizophrenia patients after noting the beneficial effects of
insulin coma therapy in drug addicts and soon became a
popular.

4. Histrory
●The Hungarian neuropsychiatrist Ladislas von Meduna
hypothesized that there might be a biological antagonism between
convulsions and schizophrenia.
●Used injections of camphor liniment to induce seizures in patients
with schizophrenia, many of whom responded dramatically.
●Other chemicals, such as Pentylenetetrazol, were also used to
induce seizures.

5. Histrory
●In 1938, Italian physicians Cerletti & Bini applied
electricity to animals to induce therapeutic seizures.
●The idea to apply electric shock therapy to humans
came to cerletti when he saw pigs being shocked into
a coma before being slaughtered.
●First patient had catatonia and he improved.
●Safer than chemically induced seizures.

6. Major Advances in ECT Since
1938
●The introduction of modern anesthesia including
neuromuscular blocking agents.
●The development of the brief pulse wave machine which
allowed for careful energy dosing and determination of seizure
threshold.
●The advances in lead placement which maintained efficacy and
reduced side-effects
●The appreciation that seizure morphology is important not
seizure duration as a determinant of efficacy.

7. UNMODIFIED ECT
● ECT without anaesthesia.
● Previously with sine wave .
Associated with more complication
● Pain, fractures of the spine, broken teeth, tongue bite, severe cognitive
deficits.

8. MODIFIED ECT
Waveform of stimulus (Sine vs Pulse)
Older sine wave devices allow
the setting of stimulus voltage,
the current in the circuit is
decided by varying
interelectrode impedence.
Despite constant voltage but
uniform current is not ensured
even within the same pt.across
session.
The modern devices evaluate
the interelectrode impedence
and dynamically adjust the
voltage to ensure a constant
current throughout the stimulus
application

9. MODIFIED ECT
Waveform of stimulus(Sine vs Pulse)
Brief pulse ECT produces lesser cognitive dysfunction than sine
wave ECT as indicated by :
less postictal confusion
less postictal EEG suppression
Less memory problems

10. MODIFIED ECT
Electrode placement
ELECTRODE
BILATERAL UNILATERAL
TEMPORAL FRONTAL RIGHT LEFT

11. ●Goldman (1949)
●U/L >less cognitive impair.
>less post ECT confusion
MODIFIED ECT
Electrode placement: UNILATERAL

12. Even many years after introduction of unilateral ECT still
bitemporal ECT is preferred due to its effectiveness.
Electrode placement: BITEMPORAL vs UNILATERAL
MODIFIED ECT

13. Bifrontal ECT better effect on major depression than bitemporal
or unilateral.
MODIFIED ECT
Electrode placement: BIFRONTAL ECT

14. Number of treatments
● Though there is no general consensus up to how many ECTs can be
given according to Max Fink
● Catatonia- 4-6
● Depression- 6-8
● Schizophrenia- 8-12 may up to 20
● Mania- up to 20

15. Number of treatments
● If no clinical improvement at all is seen after six properly given
bilateral ECT, then the course should be stopped.
● In patients who have shown slight or temporary improvement with
early treatments, it may be worth continuing up to 12 bilateral ECT
before making decision to stop.

16. PRE ECT PREPARATION
●Baseline blood investigation
●ECG cardiogenic risk factor
●Fundus examination
●Other SPECIFIC
●Consent

17. Day before ECT
● Fasting at least 6 hours before
● Review over ongoing MEDICATION
● Stop if permitted- anticonvulsants
benzodiazepines
lithium
theophylline
adrenergic blockers

18. ON ECT TABLE
●Preoxygenation -- 100 % O 2
●EEG leads placement
●IV anesthetics – Thiopentone Na
3-5 mg/kgbw
●Anticholinergic – Atropine
0.6 mg / kgbw
●Muscle relaxants – Succinylcholine
0.75 – 1mg / kgbw
●Oxygenation
●Electrode placement

19. SEIZURE MONITORING
Visual Monitoring
EEG monitoring is not mandatory, but recommended where possible.
The ICTAL EEG has following sequential component:-

20. Comparison of Motor (Visual) & EEG monitoring
Motor seizure duration is 30% shorter than EEG seizure
(Abrahams,1993,Nimhans guideline)
Seizure duration Motor seizure EEG seizure
INADEQUATE LESS THAN 15 SEC. LESS THAN 25 SEC.
ADEQUATE LESS THAN 90 SEC. 25-119 SEC.
PROLONGED MORE THAN 90 SEC. MORE THAN 120 SEC.

21. EEG MONITORING
 PHASE 1:1-3 seconds high
frequency low amplitude
 PHASE 2:10-20 Seconds
hypersynchronus polyspikes
10Hz,
 PHASE 3:20-40 Seconds spike
and wave rhythm 3Hz.
 POST ICTAL SUPPRETION

22. Vitals
ECG: considered mandatory during ECT procedure,
particularly where Atropine is not used routinely,
which helps in recognising vagal induced bradycardia.
Oxygen saturation.
OTHER PHYSIOLOGICAL
MONITORING

23. Postictal care
●Transfer to a recovery room under observation of trained staff
until awakening
●Maintain adequate airway until return of spontaneous
respiration
●Forced ventilation may be used

24. SIDE EFFECTS & COMPLICATION
● Missed seizures:
no seizures within 20 sec
● Inadequate seizures:
less than 25 sec in duration
●Prolonged seizures :
Royal college of psych. -- > 90 sec motor seizure or 120 sec EEG
seizure
APA task force -- > 180 sec
Should be terminated by IV Diazepam 10 mg
IV Thiopentone 100-200 mg

25. SIDE EFFECT AND COMPLICATION
• Missed/inadequate seizure
• Prolonged seizure
These are dependent on the
seizure threshold.
The threshold is lower in
a)manic, b)during the first ECT
session. Lithium,
antipsychotics,
Theophylline lowers the
seizure threshold.
BZD, anticonvulsant mood
stabilizers elevate the
threshold.

26. SIDE EFFECT AND COMPLICATION
• Status epileptics
• Memory impairment- Retrograde and anterograde amnesia.
• Treatment emergent delirium:-i/v diazepam or haloperidol.

27. Side effect & complications
 Cardiac S/E
 Other S/E:-a) Headache, nausea, bodyache.
b) Prolonged apnoea: due to deficiency of
pseodocholinesterase.
c) Fracture
d) ECT emergent Mania.

28. ECT Responsive Disorders
●Major depression
psychotic
●Mania including mixed
●Schizophrenia acute exacerbation
●Schizoaffective disorder
●Catatonia
●Parkinson’s disease
●NMS
●Intractable seizure disorder
●Severe delirium

29. ● Guidelines for the use of ECT were developed by the Royal
College of Psychiatrists in 1995 and are currently undergoing
revision.
● Currently ECT is used in UK clinical practice as a treatment option
for individuals with
 Depressive illness
 Catatonia and
 Mania
 Schizophrenia
Guidelines

30. NICE Guidelines
It is recommended that electroconvulsive therapy (ECT) is used only
to achieve rapid and short-term improvement of severe symptoms
after an adequate trial of other treatment options has proven
ineffective and/or when the condition is considered to be potentially
life-threatening, in individuals with:
● Catatonia
● A prolonged or severe manic episode.
(Nice Guidelines)

31. Current trends in ECT indications
The 1990 APA task force recommendation:
A. Primary use of ECT
1. Need for rapid response
2. Risk with other treatments outweigh ECT risk
3. H/o poor medication response
4. H/o good ECT response
5. Pt preference

32. Contraindications
There are no absolute contraindications to ECT.

33. Risk Factors
Cardiovascular /CNS / Others
• Coronary ischemia
• Hypertension
• CHF
• Arrhythmia
• Recent MI
• Aneurysm
• Cardiac pacemaker
• Aortic stenosis
• Increased ICT
• Cerebral Hemorrhage
• Tumor
• Dementia
• Hydrocephalus
• AV malformation
• Multiple sclerosis
• Seizure Disorder

34. Mortality Rate
• Risk of death is 1 in 10,000
• Coronary Artery Bypass - 1%

35. Mechanism of Action
●Exact mechanism of action has remained unclear.
●Neuro-physiological theory & Neuro-chemical theory are the most
accepted theories.

36. Neuro-Physiological Theory
●Two Hypothesis
Anticonvulsant Hypothesis
Seizure Generalization Hypothesis
- Diencephalon Model
- Pre-frontal Model

37. Anticonvulsant Hypothesis
Over the course of ECT……
Seizure threshold increases,
Seizure duration decreases,
Slow-wave (delta) activity in EEG increases and persists longer- if last for weeks or
months then indicates positive clinical outcome.
Intractable seizure disorder patients show improvement, probably
proposing anticonvulsant mechanism by aborting kindling.

38. The Seizure Generalization
Hypothesis
It proposes that more the ECT-induced seizure activity spreads
throughout the brain, the better is the clinical response.
Diencephalon Model :
For manifestation of full therapeutic effect of ECT, seizure must be
sufficiently generalized to involve diencephalon.
Diencephalic centers implicated in the regulation and modulation of appetitive behaviors, diurnal
rhythms, hormone release and physiological homeo-stasis.
Prefrontal Model :
Observation of an association between clinical ECT response shows..
greater inter-ictal prefrontal slowing is related to higher efficacy.
(Sackeim et al, 1996)

39. Neurochemical Theory
Norepinephrine, Serotonin, Dopamine, GABA, Glutamate
●↑ α1 & ↓ α2 (Vetulani et al, 1983) (Andrade & Sudha, 2000)
●Decrease reuptake and increase release of NE. (Andrade et al, 2001)
●Increase 5HT2a receptors. (Butler et al, 1993; Burnet et al, 1995)
●ECT facilitates dopamine transmission. (Gangadhar et al; 1990)
●Increased D1 & D3 receptor binding in basal ganglia. (Strome et al; 2007)
●Augmentation of GABA receptors (Gray & Green, 1987)
●Increase in Glutamate receptor expression & enhanced induction of BDNF.
(Naylor et al,1996)

40. Blood Brain Barrier and CBF
●ECT increases blood brain barrier permeability and facilitate entry of co-
administered psychotropic medications.
(Devanand et al,1994; Andrade et al,1997; Oby et al; 2006)
● In ECT responders there is increased perfusion in the frontal regions and
decreased perfusion in hyper-perfused area. (Milo et al; 2001)

41. Psychological Theories
Psychoanalytic Theory Non-Psychoanalytic Theory
Brain Damage Theory Amnesia Theory

42. Psycho-analytic Theory
The punishment theory postulates that for depressed and guilty
patients, ECT may provide a mean of fulfilling the ego needs to punish
the id in order to regain the superego approval.
(Miller et al, 1967)

43. Non Psychoanalytic Theory
Brain Damage Theory
Principle : responses on Rorschach’s test were similar in subjects
after ECT or diffuse brain damage.
(Summerskill et al, 1952)
The evidence for structural brain damage due to ECT was grossly
inadequate. (Devanand et al, 1994; Zacharisson et al, 2000)

44. Neuro-endocrine Theory
● Prolactin release peaks after 15-20 min and this is most consistent
neuro endocrine finding. (Markianos et al; 2002)
● Increase in TSH acutely following ECT. Addition of T3 to ECT enhances
the antidepressant response. (Stern et al; 1993)
● Acute increase in oxytocin after ECT & its magnitude correlates with
clinical response. (Riddle et al; 1993)
● CSF levels of other neuro-peptides like endothelin, neurokinin A, and
Neuro-peptide Y (NPY) also rise over a ECT course. (Mathe et al; 1999)

45. Neuro-genesis Theory
ECT results in increase in Neuro-genesis.
- Sprouting of mossy fiber pathways in hippocampus
- Increase in volume of dentate gyrus.
(Bolwig et al; 2007)