Review Article

Anaesthesia for electroconvulsive therapy: An

overview with an update on its role in potentiating
electroconvulsive therapy

Address for correspondence: Pavan Kumar Kadiyala, Lakshmi Deepthi Kadiyala1

Dr. Pavan Kumar Kadiyala, Department of Psychiatry, Siddhartha Medical College, Vijayawada, Andhra Pradesh, 1Department of
Siddhartha Medical College, Anaesthesia, JJM Medical College, Davanagere, Karnataka, India
Vijayawada ‑ 522 008,
Andhra Pradesh, India.
E‑mail: drkadiyala2@[Link] ABSTRACT

Despite advances in pharmacotherapy, electroconvulsive therapy (ECT) remains a mainstay

treatment option in psychiatry since its introduction in 1930s. It can be used primarily in severe
illnesses when there is an urgent need for treatment or secondarily after failure or intolerance
to pharmacotherapy. The ‘unmodified’ technique of ECT was practised initially, with a high
Access this article online incidence of musculoskeletal complications. Several modifications including general anaesthesia
Website: [Link] and muscle relaxation are used to increase the safety and patient acceptability of ECT. Various
anaesthetic techniques including medications are considered to provide adequate therapeutic
DOI: 10.4103/ija.IJA_132_17
seizure, simultaneously controlling seizure‑induced haemodynamic changes and side effects.
Quick response code
A brief review of literature on choice of these anaesthetic techniques is discussed. This article
is intended to reinforce the knowledge of clinicians, who may have limited exposure to ECT
procedure. Importance is given to the recent updates on the role of induction agents in potentiating
therapeutic response to ECT in psychiatric disorders.

Key words: Anaesthesia, electroconvulsive therapy, synergistic effect

INTRODUCTION contraindications to ECT, some medical conditions

are known to increase the risk due to the significant
Electroconvulsive therapy (ECT), introduced by cardiovascular and cerebrovascular changes
Cerlitti and Bini in 1937, is the induction of a associated with ECT. The cardiovascular effects result
generalised seizure by electrical stimulation of one from autonomic nervous system (ANS) activation
or both cerebral hemispheres. It has become a highly during ECT procedure. This leads to an initial 10–15 s
sophisticated and precise procedure with passage of of parasympathetic discharge resulting in bradycardia
time. Initially, ‘unmodified’ technique was practised and occasional asystole (the tonic phase). This is
in which patients were conscious and without followed by a pronounced sympathetic response of
muscle relaxation. This resulted in musculoskeletal hypertension, tachycardia and other arrhythmias
complications in as many as 40% patients. Beginning peaking 1 min after ECT stimulation and generally
in the 1950s and 1960s, however, several refinements resolving within 5–10 min thereafter (the clonic phase).
including anaesthetic medications and muscle There is increased cerebral metabolic rate (CMR)
relaxants were introduced to increase the safety and which results in a marked increase in cerebral
patient acceptability.[1‑3]
This is an open access article distributed under the terms of the Creative
Commons Attribution‑NonCommercial‑ShareAlike 3.0 License, which allows
Initially, ECT was used to treat several types of others to remix, tweak, and build upon the work non‑commercially, as long as the
author is credited and the new creations are licensed under the identical terms.
psychiatric disorders and to calm disruptive inpatients
in psychiatric wards, regardless of their diagnosis. In For reprints contact: reprints@[Link]

recent years, its use is restricted primarily to severe

How to cite this article: Kadiyala PK, Kadiyala LD. Anaesthesia
mental illnesses when there is an urgent need for for electroconvulsive therapy: An overview with an update on its
treatment or secondarily after failure or intolerance role in potentiating electroconvulsive therapy. Indian J Anaesth
to pharmacotherapy. Although there are no absolute 2017;61:373-80.

© 2017 Indian Journal of Anaesthesia | Published by Wolters Kluwer ‑ Medknow 373

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 Kadiyala and Kadiyala: Anaesthesia for ECT

blood flow (CBF) and intracranial pressure (ICP). that increase the morbidity (lithium) or decrease the
Furthermore, there is increased intraocular and efficacy (benzodiazepines, anticonvulsants) of ECT
intragastric pressure. Short‑term memory loss is also should be appraised.[1‑5]
common.[1‑3]
Oxygenation
The anaesthetic requirements for ECT include Many patients became hypoxic and cyanotic with loss
control of these haemodynamic changes and related of sphincter control with the practice of unmodified
complications, together with the primary requirements ECT. The introduction of modified ECT with muscle
of amnesia and muscle relaxation. Although these are relaxation results in reduced oxygen requirement.
essential, the level of anaesthesia should not be so Despite this, however, cerebral oxygen consumption
deep as to overly suppress the seizure activity which increases almost 200% during the seizure. It is,
is the goal of the treatment. The clinician must be well therefore, a standard recommendation that the lungs
versed on the anaesthetic management of patients should be ventilated with 100% oxygen at a rate of
undergoing ECT. This article is a narrative overview of 15–20 breaths/min, beginning approximately 1 min
existing literature intended to reinforce the knowledge before the induction, continued until the resumption
of clinicians, who may have limited exposure to ECT of spontaneous breathing. Hyperventilation may
procedure. Relevant information was extracted from prolong the seizure.[2,6]
searches of computerised databases, hand searches
and authoritative texts from inception through INDUCTION AGENTS
18th February 2017, and the search was limited to
the English language. Recent updates on the role of Induction agents provide amnesia for the brief
induction agents in potentiating therapeutic response period of electrical stimulation and the action of the
to ECT in the treatment of psychiatric disorders are muscle‑relaxing agent. A variety of induction agents
discussed in detail. may be used depending on clinical characteristics of
the patient. An ideal induction agent should have a
ADMINISTRATION OF ANAESTHESIA short half‑life with rapid onset and recovery, maintain
haemodynamic stability and have no interference with
Pre‑medication seizure duration or seizure threshold.[1,2,4]
Anticholinergic agents such as glycopyrrolate and
atropine are often given to antagonize the initial Availability and preference of induction agent
parasympathetic discharge. Glycopyrrolate (0.01 mg/kg) Sodium pentothal (2–4 mg/kg) was the first induction
is preferred and administered either intramuscularly agent used because of its availability at that time.
at least 3 min prior the scheduled procedure or Methohexital (0.5–1.0 mg/kg), a newer barbiturate,
intravenously just before injecting the induction became more popular after its development. It
agent. It may decrease the likelihood and severity of remained the most widely used general anaesthetic
bradycardia or asystole and the risk of aspiration due for ECT for many decades and is considered the
to vagal effects of ECT. Routine use of anticholinergics, ‘gold standard’. However, it’s unlicensed status
however, has been criticised as unnecessary. They may in the United Kingdom and problems with its
be particularly useful in patients who are receiving supply present practical difficulties to those who
sympathetic blocking agents, such as beta‑blockers or to wish to use it.[1,2,7] Ketamine (1.5–2 mg/kg) and
whom a seizure threshold has not yet been established etomidate (0.15–0.6 mg/kg) might seem preferable to
(i.e., for those undergoing their first ECT session). Beta other agents in the light of their lack of anticonvulsant
blockers such as esmolol (1 mg/kg) and labetalol (0.3 mg/ properties, however, other aspects such as drug’s safety
kg) can be used to attenuate the sympathetic response require consideration.[8] Ketamine‑propofol mixture
of surge in systolic pressure and heart rate. However, (“ketofol”) and ketofol‑dexmedetomidine combination
they should be considered after a detailed evaluation of (ketofol‑dex mixture) can be used as alternative
each patient’s cardiovascular risk. Esmolol has a lesser induction agents, which overcome disadvantages of
effect on seizure duration than labetalol. Calcium individual agents.[9,10]
channel blockers and alpha 2 agonists can also be used.
Clonidine and dexmedetomidine (1 mcg/kg over 10 min Sevoflurane (5%–8% for induction, followed by
before induction of anaesthesia) control blood pressure 1–2 minimal alveolar concentration [MAC] is the only
without affecting seizure duration. Medications inhalational agent in widespread use for induction in

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 Kadiyala and Kadiyala: Anaesthesia for ECT

ECT, with comparable effects to intravenous (IV) agents. The durations of EEG and motor seizures are
It is preferred in patients not cooperative for IV access. longest after etomidate and shortest after propofol.
It has the advantage of attenuating uterine contractions Thus, etomidate and also ketamine are effective in
following ECT and is used in the third trimester of patients in whom it has been found to be difficult to
pregnancy.[1,11] Opioids, such as remifentanil in higher produce any seizure activity. Although the seizure
doses, can be used as a sole agent in patients refractory duration of propofol is shortest, this does not
to seizure induction. However, they are not usually alter seizure quality indicators and does not affect
recommended as sole agents and are combined with efficacy. Therefore, it may be useful in the presence
other anaesthetic agents. They offer an advantage of of prolonged seizures. Methohexital produce
attenuating haemodynamic responses to ECT and also dose‑dependent decreases in seizure duration
increase the seizure duration by an induction agent and can be minimised by giving divided doses.
dose‑sparing effect.[7,12] Alternatively, induction agents such as methohexital,
propofol and etomidate are combined with a short
In the current health‑care environment, use of general acting, highly potent opioids, such as alfentanil
anaesthetic techniques with a rapid onset and recovery (10–25 mcg/kg) or remifentanil (1 mcg/kg) but not
is essential to facilitate the discharge of the patients fentanyl, to increase seizure duration.[1,7,14,16] Another
within 1–2 hours after the ECT. Since the half‑life of useful adjunct to augment seizure duration is moderate
propofol is shorter than that of anaesthetic barbiturates hyperventilation (approximately twenty breaths) with
and, with the advantage of minor haemodynamic an end‑tidal carbon dioxide of around 30 mmHg. It
effects, it is universally becoming the induction agent is given immediately after the succinylcholine (SCh)
of choice, in spite of higher cost. It is also considered as is injected and continued (with a break for stimulus
reference agent due to its wider use and advantages over delivery) until the desired seizure duration is
others.[4,8,9] Because of ‘smoother’ anaesthesia experience achieved. It is generally considered safe with an
and relatively greater anticonvulsant action than other advantage of more rapid orientation following the
induction agents, it may be the agent of choice for ECT treatment. However, there is increased chance of
in children and adolescents, many of whom may have prolonged seizures (>120 s) and diminished drive
prolonged seizures early in their treatment course.[12] to breathe postictally, particularly for patients with
chronic obstructive pulmonary disease.[2,4,11,12]
There is no robust evidence to recommend a particular
induction agent for ECT and all currently available SEIZURE THRESHOLD
induction agents are suitable for ECT. They should be
chosen on the basis of their effect on seizure quality, Initiation of ECT routinely involves the estimation
adverse effect profile and emergence time.[13] A careful of the seizure threshold as it varies in different
balance will need to be struck between the clinical individuals. Stimulus should be suprathreshold to
condition of the patient and the induction agent utilised. ensure therapeutic seizure. Most of the patients have
Whichever drug is used, it is preferable to utilise the seizure threshold below specified stimulation levels.
same one throughout a course of ECT and rarely may However, older patients or those on anticonvulsants,
need to be changed during the course of treatment.[4] have higher threshold levels. In addition, the cognitive
side‑effects of ECT are proportional to how much
ACTION ON SEIZURE: DURATION OF SEIZURE the stimulus dose is above threshold. To reduce the
threshold, the medication regime should be modified
ECT seizure duration provides, at best, a moderate or hyperventilation may be considered.[11]
predictor of the efficacy of treatment. It is monitored
by both motor and electroencephalogram (EEG) Induction agents in descending order of seizure
activity as each has its own limitations. The goal is to threshold reducing property are:[1,4,8,12,17‑19]
induce a motor and a central EEG seizure of at least Etomidate > ketamine > methohexital > thiopental >
25 and 40 s respectively.[11] propofol.

Induction agents in the descending order of seizure Many anaesthetics exhibit dose‑dependent
duration after their use are:[1,4,7,14,15] anticonvulsant and/or proconvulsant properties. All
Etomidate > ketamine > methohexital > sevoflurane > agents have been reported to produce EEG excitatory
thiopental > propofol. activity on induction of anaesthesia. The highest

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incidence appears to be with etomidate, followed at risk for or intolerant of decreases in blood pressure.
by methohexital, thiopental and propofol.[1,17] A However, propofol should be considered in patients
systematic review by Hooten and Rasmussen on all who have problematic pre‑existing hypertension
currently available induction agents (except ketamine) during ECT.[20,21] Unlike other anaesthetics, ketamine
reported etomidate as the only induction agent that typically increases blood pressure, heart rate, cardiac
may reduce the seizure threshold.[14] At higher doses, output and myocardial oxygen consumption. Thus,
all agents act as anticonvulsants. At these doses, the it can be used in patients at risk for hypotension
barbiturates (thiopental and methohexital), ketamine during anaesthesia; however, it is not an ideal drug for
and propofol are well established as agents for patients at risk for myocardial ischaemia. Sevoflurane
the treatment of refractory status epilepticus.[17] To produces a concentration‑dependent decrease in
reduce the anticonvulsant effects on seizure expression, arterial blood pressure, without reflex tachycardia.
the anaesthetic‑ECT time interval should be extended Thus, it may be a preferable agent in patients prone
to as long as practically possible to facilitate the to myocardial ischaemia. Etomidate, at induction
production of better quality seizures.[15] Combining doses, typically produces a small increase in heart
opioids such as remifentanil or alfentanil with these rate and little or no decrease in blood pressure. It
agents reduce seizure threshold by an induction agent has little effect on coronary perfusion pressure and
dose‑sparing effect. Remifentanil, for instance, is reduces myocardial oxygen consumption. Thus, of all
the medication recommended in patients who when induction agents, etomidate is best suited to maintain
treated with methohexital remain refractory despite cardiovascular stability in patients with coronary
maximum stimulus.[1] Sevoflurane, similarly, has artery disease, cardiomyopathy, valvular heart disease,
both proconvulsant and anticonvulsant properties at cerebral vascular disease or hypovolemia.[20,21] Opioids
different doses. High concentration of sevoflurane has are known to blunt autonomic responses to noxious
seizure‑provoking activity, particularly in children stimuli. Remifentanil and alfentanil can be combined
and when used in conjunction with hypocapnea.[4,17] with other agents to reduce haemodynamic response
associated with ECT.[7,21]
EFFECTS ON CARDIOVASCULAR FUNCTION
Induction agents in the descending order of ability to
All induction agents used in ECT, except etomidate and increase heart rate:[22,23]
ketamine, blunt the acute haemodynamic response of Ketamine > methohexital > thiopental > etomidate (no
ECT procedure.[1] Etomidate maintains cardiovascular effect) > propofol (decreased heart rate).
stability compared to others and produces minimal
changes in heart rate and cardiac output. Because Induction agents in descending order of ability to
of its reduced cardiovascular depressant properties, decrease blood pressure (MAP):[22,23]
the acute haemodynamic response to ECT become Propofol > thiopental > methohexital > etomidate
more prominent, when compared to barbiturates and (no increase) > ketamine (increased MAP).
propofol.[20] Ketamine, through its sympathomimetic
action, produces tachycardia and hypertension. CARDIAC ARRHYTHMIAS: QT PROLONGATION
However, they are manageable and does not impede
its use.[19] Thus, all induction agents used in ECT can Major depression may alter ANS activity in a patient
be used safely in patients with normal cardiovascular and may increase the risk of arrhythmias and sudden
function. cardiac death. In addition, ECT may cause an acute rise
in QT dispersion, which may predispose to arrhythmias.
The anaesthetic barbiturates produce dose‑dependent All induction agents used for ECT prolong the QT
decreases in mean arterial pressure (MAP), and an interval. Sevoflurane should be avoided in patients at
elevation in heart rate, provided that the baroreceptor risk of QT prolongation. Ketamine is not recommended
reflex is active. Propofol also produces a dose‑dependent because of its sympathomimetic properties. Propofol,
decrease in blood pressure. This decrease is etomidate and thiopental can be used safely.[14,24]
significantly greater than thiopental. It simultaneously
blunts the baroreceptor reflex or is directly vagotonic; CEREBRAL HAEMODYNAMICS
in some patients, this may result in significant
bradycardia and even asystole. Therefore, thiopental Barbiturates, propofol and etomidate reduce CBF,
and propofol should be used with caution in patients ICP and CMR, as measured by cerebral oxygen

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consumption (cerebral metabolic rate of oxygen steroidogenesis. Single induction doses of etomidate
[CMRO2]). Because they lower cerebral metabolism, may mildly and transiently reduce cortisol levels, but
they have been used for neuroprotection in patients no significant differences in outcome after short‑term
at risk for cerebral ischaemia. Ketamine, however, administration have been found. In addition, it can
increases CBF and ICP with minimal alteration of cause nausea and vomiting resulting in delayed
cerebral metabolism. It is relatively contraindicated recovery. A unique and undesirable effect of ketamine
for patients with increased ICP or those at risk for is its association with psychomimetic emergence
cerebral ischaemia as it may aggravate a “tight” brain. delirium. This can be particularly prominent after
Total IV anaesthesia accomplished by propofol is often rapid awakening from induction doses. Patients can
used for the “tight” brain, including moderate to severe experience vivid dreams, illusions, hallucinations and
brain oedema. Volatile anaesthetics like sevoflurane delusions. The risk is lower in children and in those
also reduce CMRO2 like IV agents. However, their pre‑medicated with benzodiazepines.[20]
effect on cerebral physiology is different from IV
agents as they possess intrinsic cerebral vasodilatory MUSCLE RELAXATION
activity, which is least with sevoflurane. At 1 MAC,
CBF and ICP remain unchanged in patients with Muscle relaxation is used to eliminate musculoskeletal
normal intracranial compliance. In patients with poor injury and aid in airway management. Succinylcholine
intracranial compliance and with MAC >1, sevoflurane (0.5–1.5 mg/kg) remains the relaxant of choice due
dilates the cerebral vasculature, producing increased to its rapid onset and short duration. Atracurium,
CBF and ICP. The increase in ICP may be prevented mivacurium or rocuronium may be acceptable
by hyperventilation as the response to hypocapnia alternatives, although their relatively prolonged
is preserved during sevoflurane anaesthesia. Opioids action will need continued anaesthesia and/or
have relatively little effect on CBF and CMR in the active reversal after treatment. Sevoflurane, the only
normal, unstimulated nervous system.[20,25,26] inhalational induction agent used in ECT, has an
advantage as it produces skeletal muscle relaxation
Induction agents in the descending order of CMRO2 and enhances the effects of neuromuscular blocking
reducing ability:[20,25,26] agents.[3,7,20]
Propofol > sevoflurane > thiopental and methohexital
> etomidate > ketamine. ROLE OF INDUCTION AGENTS IN POTENTIATING
THERAPEUTIC EFFICACY OF ELECTROCONVULSIVE
Induction agents in the descending order of CBF and THERAPY
ICP reducing ability:[20,25,26]
Propofol > thiopental and methohexital > etomidate > In the early days of modified ECT, barbiturates were
ketamine. the only choice for induction, and it did not occur
to psychiatrists to be involved in decision making
EMERGENCE TIME regarding anaesthetic agents. Over time, many
anaesthetic agents have been developed. Furthermore,
Emergence time is the time from drug administration there has been increasing literature regarding the
for general anaesthesia till eye opening or following influence of induction agent on the therapeutic
commands. The differences in emergence time among efficacy of ECT, which led psychiatrists to liaise with
induction agents suitable for ECT are small, and these the anaesthesiologist in making the choice of the
small variations in emergence should not govern drug induction agent.[28]
choice.[14]
Ketamine has intrinsic antidepressant properties
Induction agents in the descending order of emergence as it is an N‑methyl‑D‑aspartate antagonist. [12]
time:[14,27] Many studies assessed whether its antidepressant
Ketamine > etomidate > barbiturates > propofol > effect might be synergistic with ECT and showed
sevoflurane. mixed results. [19,29,30] It may speed the onset of
antidepressant response to ECT but does not result
OTHER EFFECTS in greater efficacy at the end of the ECT course. [27]
This could be due to the potential development of
Etomidate, in a dose‑dependent manner, inhibits tolerance due to the repeated use. Administering
the adrenal enzyme 11‑β‑hydroxylase, important for other induction agent (like thiopental) in alternate
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 Kadiyala and Kadiyala: Anaesthesia for ECT

treatment sessions with ketamine may prevent the to highlight the superiority of any anaesthetic agent
development of tolerance. [31] The enhancement of with regards to response rate at the end of treatment.
efficacy early in the course by ketamine, may be These results also show that seizure duration, as
particularly advantageous in two situations: (a) a single factor, may not explain the superiority of
in right unilateral ultra‑brief ECT where the one anaesthetic agent over other. Furthermore, it
onset of antidepressant effect is slower, (b) highlighted that ketamine administration cannot be
in cases of high suicide risk or high clinical recommended to date as an anaesthetic of choice
severity (e.g., catatonia), when a very rapid for ECT for depression, alone or in combination.
response is required. [15,27] Anaesthetic agents should be chosen on the basis of
adverse event profile and emergence, along with effect
Propofol or barbiturates do not have any intrinsic of these medications on seizure duration.[34]
antidepressant properties, however, they are quite
comparable to ketamine in ultimate antidepressant There are no specific studies on the influence of
efficacy of ECT, though ketamine produces a quicker induction agents on ECT when used for mania or
response. Furthermore, combining propofol with psychosis. Switch from depression to mania can
ketamine (ketofol) retains the early antidepressant happen in bipolar patients with ketamine’s use in ECT.
property of latter, while reducing the adverse However, as manic switches may also be a side‑effect
effects. This suggests that propofol combined with of ECT treatment, further studies are needed.[34]
ketamine anaesthesia might be the technique of Ketamine can induce psychotic symptoms, however,
first‑choice in patients with depressive disorders practitioners have used it without encountering such
undergoing ECT.[28,32] Adding dexmedetomidine to this problems.[12] Although barbiturates can be used for the
combination (ketofol‑dex) has added anti‑depressive treatment of catatonia, no studies compared them with
effect following first ECT session, but not at the end. other induction agents in ECT for catatonia. Transient
However, ketofol‑dex combination has advantages cognitive deficits are common after ECT which are
in the form of increased seizure duration, lower often a reason for terminating a course of ECT before
incidence of agitation, more patient satisfaction and remission is achieved. Ketamine was shown to be
acceptable decrease in heart rate and blood pressure preferable to thiopental, methohexital and etomidate
when compared to ketofol and without any significant in this aspect.[8]
side effects.[10]
Neuroleptic malignant syndrome (NMS) is a
Etomidate may improve major depressive disorder serious side‑effect produced by some antipsychotic
more than sodium thiopental.[28] However, depression drugs with some clinical similarities to malignant
is associated with stress‑related hypothalamic hyperthermia (MH). Although evidence is lacking to
pituitary adrenal axis dysregulation, and there is support NMS and MH having a similar pathophysiology,
concern regarding the consequences of etomidate’s caution is advised when administering general
unwanted suppression of adrenal function on anaesthesia to patients with NMS. Agents such as
depression, particularly on the course of illness.[8] sevoflurane, suxamethonium (SCh) or their combination,
However, the findings of Wang et al. in 2011, through known to trigger MH should be avoided, though the
measurements of serial cortisol levels at various time administration of SCh to patients receiving ECT for NMS
points during ECT, found no worrisome reductions is safe. Therefore, in patients with a history of NMS, a
with etomidate.[28,33] There is no literature regarding more promising method of muscle relaxation is to use
the outcomes of depression with sevoflurane or with rocuronium‑sugammadex as an alternative to SCh.[16]
the combination of induction agents with opioids or
hyperventilation.[28] CONCLUSION

A recent meta‑analysis on the role of IV induction Anaesthesia not only enables the ECT procedure but
agents in ECT for major depression showed that after may also have a significant influence on its clinical
excluding trials responsible for heterogeneity, the efficacy and tolerability through the impact on
depression scores after the ECT course were lower electrophysiological variables and seizure parameters.
with methohexital compared to propofol, and lower Psychiatrists used to be in charge of administration
with propofol compared to thiopental. However, it and recovery from ECT, many years ago. Nowadays,
concluded based on overall data, that it was not possible the procedure is performed in an ECT administration

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room where an anaesthesiologist is in charge of general anaesthesia: A systematic review and critical commentary on
efficacy, cognitive, safety and seizure outcomes. World J Biol
anaesthesia and a psychiatrist administers ECT. Thus, Psychiatry 2016:1-21. Available from: [Link]
anaesthesiologists and psychiatrists must be aware of [Link]/pubmed/27892759. [Last accessed on 2016 Nov 28].
not only the physiological responses to ECT and how 16. Kadoi Y. Selection of anesthetics and muscle relaxants for
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Financial support and sponsorship 17. Perks A, Cheema S, Mohanraj R. Anaesthesia and epilepsy. Br
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Nil. 18. Lee TA, Byrne RW, Sturaitis MK. Anesthetic considerations
in cortical mapping and awake surgery. In: Byrne RW, editor.
Conflicts of interest Functional Mapping of the Cerebral Cortex: Safe Surgery in
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19. Kellner CH, Bryson EO. Ketamine Anesthesia for
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Announcement

CALENDAR OF EVENTS OF ISA 2017

The cut off dates to receive applications / nominations for various Awards / competitions 2017 is as below. Hard copy with all supportive documents to
be sent by Regd. Post with soft copy (Masking names etc.) of the same by E Mail to secretaryisanhq@[Link]. The masked soft copy will be circulated
among judges. Only ISA members are eligible to apply for any Awards / competitions. The details of Awards can be had from Hon. Secretary & also
posted in [Link]

Cut Off Date Name of Award / Competition Application to be sent to

30 June 2017 Bhopal Award for Academic Excellence Hon. Secretary, ISA
30 June 2017 Late Prof. Dr. A .P. Singhal Life Time Hon. Secretary, ISA
Achievement Award
30 June 2017 Rukmini Pandit Award Hon. Secretary, ISA
30 June 2017 Dr. Y. G. Bhoj Raj Award Award Hon. Secretary, ISA
30 Sept. 2017 Kop’s Award Chairperson, Scientific Committee ISACON 2017
copy to Hon. Secretary, ISA
30 Sept. 2017 ISACON Jaipur Award Chairperson, Scientific Committee ISACON 2017
copy to Hon. Secretary, ISA
30 Sept. 2017 Prof. Dr. Venkata Rao Oration 2017 Hon. Secretary, ISA
30 Sept. 2017 Ish Narani Best poster Award Chairperson, Scientific Committee ISACON 2017
30 Sept. 2017 ISA Goldcon Quiz Chairperson, Scientific Committee ISACON 2017
10 Nov. 2017 Late Dr. T. N. Jha Memorial Award Hon. Secretary, ISA, copy to Chairperson
& Dr. K. P. Chansoriya Travel Grant Scientific Committee of ISACON 2017
20 Oct. 2017 Awards (01 Oct 2016 to 30 Sept 2017) Hon. Secretary, ISA
(Report your monthly activity online every month after logging in using Secretary’s log in ID)
1. Best City Branch
2. Best Metro Branch
3. Best State Chapter
4. Public Awareness – Individual
5. Public Awareness – City / Metro
6. Public Awareness - State
7. Ether Day (WAD) 2017 City & State
8. Membership drive
9. Proficiency Awards
Send hard copy (where ever applicable) to
Dr. Venkatagiri K.M.
Hon Secretary, ISA National
“Ashwathi”’ Opp. Ayyappa temple,
Nullippady, Kasaragod 671 121.
secretaryisanhq@[Link] / 9388030395.

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