|Year : 2017 | Volume
| Issue : 2 | Page : 83-98
Electroconvulsive therapy in the elderly: Anesthetic considerations and Psychotropic interactions
Harsh Garekar, Sandeep Grover
Department of Psychiatry, Postgraduate Institute of Medical Education and Research, Chandigarh, India
|Date of Web Publication||29-Dec-2017|
Department of Psychiatry, Postgraduate Institute of Medical Education and Research, Chandigarh - 160 012
Source of Support: None, Conflict of Interest: None
Electroconvulsive therapy (ECT) has been found to be a rapid and effective treatment strategy for psychiatric and neurological conditions in the elderly, but the administration of ECT in the elderly can be challenging due to a high risk of adverse events. The increased risk can be attributed to a declined physiological reserve, the presence of physical comorbidities, and the use of multiple drugs, which interact with the electrical stimulus and the anesthetic medications used during the ECT procedure. The selection of appropriate induction agents and muscle relaxants should be guided by patient's clinical status and the psychotropic drugs being used. Modifications in the doses of psychotropic drugs also need to be carried out before ECT to reduce cardiovascular and neurological side effects. Modification in the conduct of anesthesia can also aid in augmenting seizures and in preventing common side effects of ECT. A vital step in preventing adverse events in the elderly is carrying out a thorough pre.ECT evaluation. Despite these challenges, ECT can be carried out safely in elderly patients with severe comorbidities, provided clinical ECT, and anesthetic parameters are adequately optimized.
Keywords: Adverse effects, anesthesia, elderly, electroconvulsive therapy
|How to cite this article:|
Garekar H, Grover S. Electroconvulsive therapy in the elderly: Anesthetic considerations and Psychotropic interactions. J Geriatr Ment Health 2017;4:83-98
|How to cite this URL:|
Garekar H, Grover S. Electroconvulsive therapy in the elderly: Anesthetic considerations and Psychotropic interactions. J Geriatr Ment Health [serial online] 2017 [cited 2018 Apr 22];4:83-98. Available from: http://www.jgmh.org/text.asp?2017/4/2/83/221899
| Introduction|| |
Electroconvulsive therapy (ECT) is a brain stimulation technique, which was introduced in 1938 as a modification to chemical induction of seizures and soon gained widespread popularity in psychiatric practice for the treatment of severe mental illnesses. With the advent of pharmacotherapy in 1950s and later with the rise of anti-psychiatry movement, the use of ECT became less acceptable. However, over the past few decades, ECT has been established as a highly effective treatment for management of major depression (both bipolar and unipolar), catatonia, schizophrenia, and several other treatment-resistant psychiatric disorders. Its use has been popularized again due to the ineffectiveness of pharmacotherapy in resistant cases and also due to the refinement in techniques of ECT, such as the use of brief and ultra-brief pulse waves, unilateral electrode placements, frontal electrode placement, and the use of anesthetics before ECT (which came to be known as modified ECT). The use of anesthetics agents has not only led to a reduction in traumatic injuries but also has led to reduced psychological trauma for the patient and the family, making ECT a more safe and acceptable procedure. In developing countries including India, unmodified ECT continues to be delivered due to lack of anesthetic resources. However, with the imminent government mandate to abolish unmodified ECT, psychiatric centers, even in remote areas would have to improve facilities to offer modified ECT in the future.
When it comes to mental illness, a large body of research has shown both quantitative and qualitative differences in the effects of mental illness on the elderly, when compared to the normal adult population. Nearly 15% of the population above 60 years of age suffer from a mental disorder, with unipolar depression occurring in 7% of the elderly population. Depression in the elderly is also associated with more functional decline, increased hospitalization and premature death due to suicide, and other causes. Recent studies have suggested that more than 50% of older adults with depression fail to respond to initial treatment with the first-line pharmacotherapy. It is also known that elderly patients are more prone to the side effects of psychotropic medications when compared to the adult population. In such a scenario, ECT becomes a vital clinical strategy for the treatment of elderly mental disorders. ECT has been found to be a safe and effective treatment for older patients when administered in an optimal manner., The adverse effect of ECT on cognitive functions, such as memory, remains the greatest concern for psychiatrists and patients. However, in the elderly population, the cardiovascular complications are the biggest problem rather than the neurocognitive impairments, which are frequently reversible., This can be attributed to several factors including the physiological changes associated with aging, the presence of physical comorbidities, and the altered metabolism of anesthetic drugs.
In such changing political and clinical scenarios, where modified ECTs will become a rule and the increasing burden of mental illness in the growing elderly population, both the psychiatrist and the anesthetist must have a comprehensive knowledge about the anesthetic practices used during the ECT and their effect on aging. For the anesthetist, ECT in the elderly entails the challenge of using general anesthesia in a population who frequently suffer from severe cardiac and systemic diseases. For the psychiatrist, it is vital to have an understanding about the medications used in anesthesia and their interaction with prescribed drugs, risk of ECT-related complications increase with use of higher number of medications. Furthermore, a number of psychotropic and anesthetic drugs influence seizure variables and consequently the efficacy of ECT. Hence, an informed modification of psychotropic medications, anesthetic procedure, and ECT technique is vital in increasing the effectiveness and reducing the risks associated with ECT in the elderly. The current review intends to discuss the physiological effects of aging and its implications for using modified ECT in the elderly.
| Physiological Changes With Aging and Their Impact on Electroconvulsive Therapy Procedure|| |
With aging drug absorption, distribution, metabolism, and elimination undergo substantial change. In addition, changes are seen in the functioning and physiological reserve of various bodily systems. Understanding of these changes is of paramount importance while administrating ECT among elderly.
ECT results in an increased parasympathetic outflow during and after the administration of electrical stimulus and this is followed by a surge in sympathetic outflow. This leads to an initial parasympathetic flow induced bradycardia lasting for 10–15 s followed by transient tachycardia and hypertension lasting 5 min or longer. Bradycardia or asystole can sometimes persist when the parasympathetic discharge is not counteracted by a sympathetic surge due to a subconvulsive stimulation. During the sympathetic surge, there is a transient increase in systolic blood pressure by 30%–40%, and 20% or more increase in heart rate (HR), both of which results in a 2–4-fold increase in the rate pressure product, which is an indicator of myocardial oxygen consumption. Several mechanisms have been postulated to be the cause of these changes, such as stimulation of the sympathetic neurons, norepinephrine release from the medullae, and myotonic reflexes. However, no association has been found between these cardiocirculatory changes with the duration of the seizure. Geriatric patients have decreased beta-adrenergic responsiveness and are at an increased risk of conduction abnormalities and bradyarrythmias. When compared to young adults, patients more than 50 years of age show a similar significant increase in blood pressure and HR, but the return to baseline is longer, taking 1 h after shock, as compared to 25 min in young adults.
These findings suggest an increased risk of adverse cardiovascular events such as myocardial infarction, arrhythmias, and hemorrhage, especially in older patients. However, the incidence of major complications in elderly patients with preexisting cardiac risk factors has not been found to differ significantly from a similar nonrisk group., A study involving 35 patients with median age of 77 and suffering from heart failure (median left ventricular ejection fraction ~ 30%), who underwent 513 ECT sessions reported no major complications. Only three patients suffered from temporary, nonlife-threatening cardiac arrhythmias. Based on these findings, ECT can be carried out in congestive heart failure, provided treatment for heart failure has been optimized before ECT. Routine use of antihypertensives to attenuate the hypertensive peak and tachycardia has not been recommended but can be used in high-risk cases, preferably using a short-acting beta-blockers such as esmolol. Anticholinergic medications are used to prevent bradycardia immediately after electrical stimulation. Intravenous (IV) atropine (0.4–0.8 mg) is effective in preventing bradycardia. Higher doses of atropine should be avoided, as it can increase the risk of post-ECT delirium in the elderly. Glycopyrrolate (0.2–0.4 mg) is also effective in preventing bradycardia with the added advantage of less tachycardia after seizure.
Most of the effects on the respiratory system are related to anesthetic procedures rather than to ECT itself. Aging is associated with reduction in chest wall compliance, decline in forced expiratory volume 1, and a decrease in respiratory muscle strength making it more vulnerable to ventilatory failure during high demand states. Due to these changes, compared to younger subjects, the elderly patients have been shown to have a higher incidence of aspiration pneumonia associated with ECT. Episodes of bronchospasms, laryngospasms, and hypoxic episodes have also been reported. Hence, the patients with acute problems such as unstable chronic obstructive lung disease, respiratory tract infections, obesity, and preexisting airway problems should be adequately monitored during and after ECT, but intubation has not been found to be necessary in most cases.
Oxygen desaturation following ECT is a rather common occurrence. Desaturation has been related to a number of different patient- and procedure-related factors. An important approach to minimize desaturation is to ventilate with oxygen-enriched mixture during the convulsions. Desaturation has also been related to patient BMI and seizure duration. Therefore, it is advisable to limit the seizure duration to the minimum.
Advancing age is associated with a progressive reduction in glomerular filtration rate and renal blood flow. These changes show wide inter-individual variability. In addition, other cardiovascular variables such as reduced cardiac output and systemic hypertension also reduce renal filtration and perfusion. ECT itself does not lead to any significant electrolyte abnormalities, but preexisting renal failure can be associated with electrolyte imbalances such as hyperkalemia, altered fluid volume status, and pH changes. All these factors can increase the risk of adverse cardiovascular events during ECT. Successful ECT has been carried out in patients with chronic renal failure and on dialysis, with specific precautions being taken to select anesthetics, which do not have a renal clearance and do not elevate serum potassium such as succinylcholine., Due to the risk of hyperkalemia, baseline pre-ECT and post-ECT potassium levels are recommended in patients with chronic kidney disease.
Aging is associated with progressive decline in liver function after the fifth decade of life and further decrease occurs after the age of 70 years. The liver and splanchnic blood flow are reduced along with decrease in albumin production. Hence, drugs metabolized by cytochrome P450 system need to be adjusted accordingly. There are no studies directly analyzing the effects of ECT on the liver function, but there are several case reports where ECT has been successfully carried out in patients with decompensated liver disease using reasonable pre-ECT work-up including coagulation profile and platelet function, endoscopic assessment, pretreatment with beta-blockade, and antihypertensive measures.,
Central nervous system
The induction of generalized motor seizure and an acute cardiovascular response, as part of ECT procedure results in a marked increase in the cerebral blood flow and intracranial pressure. Taking these into consideration, the presence of cerebral aneurysms and arteriovenous malformations are considered as relative contraindications for ECT. Besides this, other relative contraindications for use of ECT include increased intracerebral pressure, any space-occupying cerebral lesions, recent intracerebral hemorrhage, the presence of pheochromocytoma, and recent myocardial infarction. Since increased cerebral blood flow is partly due to systemic hypertension, antihypertensive drugs can prevent this cerebral hemodynamic alteration. However, the effect on vertebral and systemic blood pressure is different for different drugs. Beta-blockers and nitrates suppress both vertebral and systemic blood pressure, while calcium channel blockers suppress only systemic hypertension. Cognitive adverse effects are common in the elderly, particularly in patients with preexisting dementia. Other central nervous system complications include disorientation, impaired attention, memory problems, prolonged seizures, or status epilepticus.
| Induction Agents and Elderly|| |
Selecting an appropriate anesthetic agent and determining the correct dose of these agents are a crucial step in ECT, as these can have a potent impact on the induction and duration of seizure. Many anesthetic drugs also have anticonvulsant properties; hence, higher than required doses can decrease the seizure duration. The various agents that can be used for induction includes thiopentone, methohexital, propofol, ketamine, etomidate, and sevoflurane. [Table 1] shows comparison of these agents in the context of elderly patients.
|Table 1: Dose adjustment, advantages, and disadvantages of commonly used induction agents for electroconvulsive therapy|
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Methohexitalis generally considered the “gold standard” general anesthetic for ECT. The dose of methohexital required to induce general anesthesia for most patients is 1.0 mg/kg. It is a rapidly acting barbiturate, with maximal blood concentrations achieved within 30 s after IV administration. The levels then fall as the drug is redistributed to tissues, yielding duration of action of 4–7 min with a single dose. Clearance of methohexital is influenced by changes in hepatic blood flow. It is estimated that the total liver blood flow is reduced by 40%–45% of elderly patients, partly due to reduced cardiac output. In addition, the elimination of half-life is also prolonged in the elderly due to increase in its volume of distribution. Since methohexital dosage is based on lean body mass, elderly patients may, therefore, require dosage <1 mg/kg of body weight. Methohexital compares favorably with other IV anesthetic agents (propofol, thiopental, and etomidate) with respect to its minimal effect on duration of seizure activity., With respect to the speed of recovery of cognitive function after ECT, there is no significant difference between methohexital, propofol, and etomidate. Hence, methohexital remains the drug of choice for anesthesia during ECT, unless specific contraindications exist for its use such as acute porphyrias. Despite being the gold standard for ECT against which other drugs are compared, over the past decade, there has been a shortage of methohexital both in India and abroad, leading to the current scenario where it has fallen out of favor with new anesthetists.
Thiopental is an ultra-short-acting barbiturate, used in a dose of 1.5–5 mg/kg body weight, producing a smooth onset of hypnosis, and a rapid recovery due to redistribution. It is known that the dose required for induction of anesthesia decreases with increasing age. This is due to a change in the initial distribution volume of thiopental, which decreases exponentially with age. However, pharmacodynamic modeling suggests that the brain sensitivity to thiopental does not change with age., The decrease in the required dose of thiopental can vary from 25%–35% to 50%–67% over the age range of 20–80 years., Thiopental, like other barbiturates causes a reduction in the cerebral blood flow and decreases intracranial hypertension; hence, it is a preferred drug for induction in patients with ischemic brain injury and neurosurgical situations with high intracranial pressure. Thiopental has significant effects on the cardiovascular system, characterized by reduction in the mean arterial pressure (MAP) and cardiac output. These cardiovascular effects are, however, comparable to other commonly used anesthetics in ECT such as propofol and etomidate. Motor seizure duration has been found to be longer with thiopental as compared to propofol or midazolam. In another study, which compared thiopental to propofol and etomidate, showed that patients in the thiopental group received lower electrical dosage and also had the longest seizure duration. However, recovery from thiopental has been found to be slower when compared to propofol, methohexital, and etomidate.
Propofol is a short-acting general anesthetic administered as a 1%–2% of aqueous emulsion. A smooth induction of anesthesia in an adult follows a dose of 1–2.5 mg/kg. However, for elderly a dose of 1.0 mg/kg of propofol is sufficient to provide adequate depth of anesthesia in elderly patients. Propofol causes a significant fall in blood pressure when compared to other induction drugs. The fall in blood pressure occurs secondary to systemic vasodilatation and is dose-dependent. The hypotensive side effects can be prevented in the elderly by a slower administration of a reduced dose titrated to effect rather than bolus of a preselected dose. When compared to other drugs, specifically thiopental and midazolam, propofol is superior with respect to shorter time to induction and also quicker recovery. Compared to methohexital, propofol is associated with more moderate increase in blood pressure and shorter duration of seizure. There is some evidence to suggest that when compared to methohexital, propofol is associated with better cognitive functioning after anesthesia., Propofol can be particularly useful for patients with preexisting cardiac ailments which require attenuated hemodynamic response during ECT procedure. Propofol can also be a useful alternative to methohexital for the treatment of patients who have long seizures.
Ketamine is a dissociative drug with hypnotic, analgesic, and local anesthetic properties. Its use in ECT has been limited due to its effects on blood pressure and hallucinogenic properties. Due to centrally mediated sympathetic response, administration of ketamine is usually associated with tachycardia, increased systemic and pulmonary artery blood pressure, and increased cardiac output. In addition, ketamine is also known to have direct myocardial depressant effect. These properties make it unfavorable for use in patients with cardiac disease. There are limited data on modification of ketamine dose in older people. Therefore, as in the general population, an induction dose of 2 mg/kg for racemic ketamine is recommended. In general, use of ketamine is not recommended in older people because of the associated cardiovascular effects and the increased risk of postoperative delirium. Recent findings suggesting that ketamine may have antidepressant properties have revived interest in its use in ECT in depressed patients. However, several clinical trials have failed to show any accelerated antidepressant effect., When compared to methohexital, ketamine did not show any added benefit in quality or speed of post-ECT recovery, but it was associated with longer motor seizures.
Etomidate is a hypnotic through its inhibitory effects on gamma-aminobutyric acid (GABA) and depression of the reticular activating system. Etomidate is well known for its cardiostable properties, producing a minimal reduction in cardiac output, and blood pressure. Therefore, etomidate can be a suitable agent in patients with compromised cardiac function or coronary artery disease. Etomidate is metabolized through the liver microsomal enzymes to inactive metabolites. In the elderly, the diminished hepatic clearance along with reduced volume of distribution results in higher than expected plasma concentrations. Therefore, the standard doses of induction of 0.3–0.4 mg/kg IV should be reduced to 0.2 mg/kg. Etomidate remains less popular due to its adverse effects such as pain on injection site, high rates of postoperative thrombophlebitis, and postprocedure nausea and vomiting. Etomidate has also been associated with increased incidence of myoclonus, which can pose a problem in the clinical assessment of seizure. Etomidate also suppresses cortisol and aldosterone secretion; a single induction dose blocks stress-induced cortisol production for up to 24 h in the elderly patients. For these reasons, it has been advised that etomidate should only be used for short-lasting anesthesia and should be avoided in patients with preexisting endocrine abnormalities., When compared to other agents such as propofol and methohexital, etomidate produces longest durations of motor, and electroencephalogram seizures. This property is specifically useful in patients who become refractory to seizures during the course of ECT therapy. In a study describing four cases of elderly seizure resistant cases whose seizure duration fell below 25 s during the course of ECT-induced with methohexital, substitution of etomidate for methohexital led to increase in the seizure duration by 245% and successful completion of treatment.
Sevoflurane is a nonirritant inhalational anesthetic agent that produces a fast and quick induction and has been found to be an acceptable alternative to IV anesthetics. IV anesthetics are preferred over inhaled anesthetics due to their obvious ease of use and availability, but there are certain situations where inhaled anesthetics can have a distinct advantage. These include patients who are agitated, when an IV line cannot be accessed and the patients with difficult airway management. Another important indication of inhaled anesthetics is in the last trimester of pregnancy. Anesthesia during ECT can be induced with 7%–8% of sevoflurane and then maintained by 2%–4% of mixture in normal adults. Aging is associated with a progressive decline in the mean alveolar concentration and ventilation. Combined with the neurophysiological changes in the brain leading to increased sensitivity, the anesthetic requirement of sevoflurane, in an 80-year-old can be 60%–75% of that required in a young adult. There is limited literature comparing the efficacy of sevoflurane with other agents, however, a study comparing sevoflurane with methohexital, showed that sevoflurane is associated with 25%–30% of shorter seizure duration. Use of sevoflurane is associated with side effects such as hypotension and depression of respiratory and cardiac function in a dose-dependent manner.
| Muscle Relaxants and Elderly|| |
The use of muscle relaxants or neuromuscular blocking agents (NMBAs) during ECT has led to a complete elimination of the violent tonic-clonic convulsions and hence, a reduction in traumatic injuries such as vertebral compression fractures and limb fractures. Various available agents include succinylcholine, mivacurium, atracurium, cisatracurium, and vecuronium. [Table 2] shows a comparison of these agents from the perspective of use of these agents in elderly.
|Table 2: Dose adjustment, advantages, and disadvantages of commonly used muscle relaxants for electroconvulsive therapy|
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Succinylcholine or suxamethonium was the first used synthetic alternative to curare in 1951, and still remains the most popular muscle relaxant in ECT. It is a depolarizing neuromuscular blocker recommended in doses of 0.5–1 mg/kg., It has a fast onset of action and produces a rapid recovery. Succinylcholine is metabolized by plasma cholinesterase and deficiency of cholinesterase due to any inherited or acquired condition can cause a significant prolongation of neuromuscular blockade, leading to prolonged apnea, and paralysis. The levels of plasma cholinesterase are also reduced in the frail elderly patients, which can result in a longer duration of action of succinylcholine in such population.
In the elderly population, despite a low cardiac status and reduction in the volume of distribution, the dose requirement does not appear to change. Succinylcholine use is associated with a serious side effect of hyperkalemia, which is related to its properties of muscle fasciculation and cholinergic activation. This side effect is particularly more common in elderly patients who have experienced prolonged immobilization. The risk of succinylcholine-induced hyperkalemia is also increased in certain other pathologic states such as meningitis, renal failure, catatonia, and in patients at risk of neuroleptic malignant syndrome and malignant hyperthermia.,, Another important side effect of succinylcholine use is bradycardia., Bradycardia occurring during the induction phase of ECT can be prevented by replacing succinylcholine with another muscle relaxant such as mivacurium.,,
When compared to succinylcholine, nondepolarizing NMBAs such as mivacurium do not lead to side effects related to muscle fasciculation such as hyperkalemia and are, therefore, considered a safer alternative to succinylcholine in patients at risk of malignant hyperthermia and neuroleptic malignant syndrome. However, it is hydrolyzed by the same metabolizing enzyme of pseudocholinesterase (butyrylcholinesterase), and can, therefore, cause prolonged apnea and paralysis in predisposed individuals. Due to the reduced cholinesterase activity in elderly, mivacurium can also cause prolonged recovery in elderly patients. Mivacurium has been used safely in elderly patients who are vulnerable to other side effects of succinylcholine such as cardiac arrhythmias. While muscle relaxation can be achieved with doses ranging from 0.12–0.2 mg/kg, only doses at the higher range of 0.20 mg/kg have been found to effectively minimize the motor responses to ECT. Mivacurium is associated with occasional hypotension due to histamine release, which is dose-dependent.
Atracurium and cisatracurium
Atracurium and its stereoisomer cisatracurium are intermediate-acting NMBAs which are metabolized through Hoffman elimination and ester hydrolysis, because of which there are only minor differences in the pharmacokinetic and pharmacodynamic property of these drugs in various patient populations including the elderly. However, due to a larger volume of distribution at steady state, compared to other neuromuscular blockade agents, recovery may be delayed with atracurium in the elderly., Atracurium and cisatracurium are used during ECT when certain comorbid conditions preclude the use of other muscle relaxants. These conditions include the presence of pseudocholinesterase deficiencies and severe neuromuscular diseases. Full neuromuscular blockade with complete suppression of tonic-clonic convulsions can be achieved at 0.5 mg/kg IV dose. The duration of neuromuscular blockade provided by atracurium at this dose is longer than that required for the ECT procedure, hence, reversal with atropine and edrophonium is required in all cases. Atracurium is associated with several hemodynamic side effects at doses greater than 0.5 mg/kg. Rapid bolus doses result in significant increases in plasma histamine and associated decrease in MAP and increase in HR. To prevent these responses, a slow IV administration and pretreatment with cimetidine and chlorpheniramine have been advised.,,
Vecuronium is an intermediate-acting muscle relaxant, classified as an aminosteroid. Vecuronium does not cause histamine release and has very few cardiovascular side effects. Vecuronium undergoes deacetylation in the liver producing an active metabolite, which can accumulate in patients with renal failure producing prolonged neuromuscular blockade. With an age-related decline in renal and hepatic functions, vecuronium has been found to produce prolonged neuromuscular blockade in elderly patients., Vecuronium has been successfully used to prevent suxamethonium-induced myalgias in patients who experience this distressing side effect. The technique involves pretreatment with 1 mg vecuronium 3 min before suxamethonium use.
| Anesthesia and Psychiatric Drugs|| |
A majority of patients planned to undergo ECT are on psychotropic drugs, which exert a strong effect on the central and peripheral nervous system. Hence, a consideration of their effects and possible interaction with anesthetic agents used during ECT should be understood.
| Antidepressants|| |
The use of tricyclic antidepressants (TCAs) has significantly decreased since the advent of selective serotonin reuptake inhibitors antidepressants (SSRIs), however, these agents continue to have a significant role in treatment of severe and resistant depression. Commonly used TCAs include amitriptyline, imipramine, clomipramine, doxepin, amoxapine, and others. These act not only by augmenting serotonergic and noradrenergic neurotransmission but also possess significant anticholinergic, antihistaminergic, and anti-alpha adrenergic activity. Due to these receptor profiles, TCAs associated with side effects such as postural hypotension, cardiac dysrhythmias, urinary retention, dry mouth, blurred vision, and sedation. Postural hypotension can be a significant problem in the elderly population, which could be increased by anesthetic drugs. TCAs can also potentiate the action of other anticholinergic drugs such as atropine administered during the procedure, increasing the likelihood of post-ECT confusion, and delirium. With regards to ECT, TCAs reduce the seizure threshold in a dose-dependent manner. TCAs are also well known for the cardiovascular side effects. TCAs cause blocking of the reuptake of norepinephrine and serotonin at nerve terminals leading to cardiac arrhythmias and an exaggerated response to indirectly acting vasopressors and sympathetic stimulation [Table 3]. Hence, drugs such as epinephrine, ephedrine, pancuronium, and ketamine should be avoided in patients on long-term TCA therapy. In a study comparing cardiovascular effects of ECT in patients on TCAs versus patients in whom TCA was discontinued for at least 2 weeks, no significant differences were observed. Sudden withdrawal of TCAs can also precipitate a withdrawal syndrome; hence, current guidelines support the continuation of the drug during ECT.,
|Table 3: Interaction of psychotropic medications with electroconvulsive therapy and anesthetic drugs|
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Selective serotonin reuptake inhibitors
SSRIs are the most commonly used class of antidepressants, and because of their selective action on the serotonergic pathway, are considered safer than TCAs. Their influence on seizure threshold is minimal. SSRIs are metabolized by cytochrome P450 system and some drugs such as fluoxetine, paroxetine, and fluvoxamine are potent inhibitors of CYP450 2D6 isoenzyme. As a result, the plasma levels of drugs such as benzodiazepines (BZDs), NMBAs, and barbiturates can rise, in patients taking these drugs for an extended period. Two side effects of SSRIs which can interfere with complications associated with ECT include hyponatremia and anticholinergic side effects.
Hyponatremia can often interfere with ECT by increasing the risk of delirium and cardiac arrhythmias. Although hyponatremia has been noted with nearly all antidepressants, the strongest association has been found with SSRIs such as citalopram, escitalopram, fluoxetine, and paroxetine and the lowest association with drugs such as venlafaxine, duloxetine, and mirtazapine. The incidence with SSRIs has been found to vary from 0.5% to 32% in various studies., Further research has shown that the elderly are at an increased risk for hyponatremia with SSRI use, with the highest risk during the first 2 weeks of therapy. Other risk factors identified include female gender, patients on diuretic therapy, low body weight, and low baseline sodium levels., The impact of hyponatremia in the elderly can be quite severe when compared to the young, often presenting as confusion and delirium. Even mild hyponatremia has been associated with impaired cognition and falls in elderly individuals. Hyponatremia in the elderly can often be multifactorial; hence, a thorough evaluation of the underlying cause should be performed. Correction of hyponatremia and elimination of possible causes should be ensured before starting ECT. In addition, based on the choice of antidepressant and the duration of the therapy, serum sodium levels should be routinely monitored during the course of ECT.
While the adverse effects of TCAs on cardiac conduction have been well established, some of the reports have demonstrated association of SSRIs with arrhythmias, prolonged QTc, and orthostatic hypotension., These cardiac side effects can occasionally interference with ECT [Table 3]. Among SSRIs, citalopram can cause conduction defects in a dose-dependent manner. These can present as sinus bradycardia and tachycardia, supraventricular tachycardia, and QTc prolongation. Fluoxetine use has been associated with atrial fibrillation, bradycardia, and syncope. The use of fluoxetine in the elderly has been associated with increased risk of syncope and orthostatic hypotension. While data on other SSRIs is limited, these findings suggest that SSRIs cannot be assumed to be free of any cardiovascular effects. Therefore, in elderly with preexisting cardiovascular and conduction defects, close monitoring of these potential side effects should be performed with regular electrocardiogram (ECG).
Similar to the TCAs, SSRIs such as paroxetine and to a lesser extent fluvoxamine have relatively high muscarinic acetylcholine receptor affinity, resultant central, and peripheral anticholinergic effects., These central anticholinergic effects not only present as subtle cognitive impairments in memory and attention but can also increase the risk of delirium in the elderly., In elderly patients presenting with post-ECT confusion or delirium, a medication review should be carried out, and careful consideration should be given to stopping, reducing, or substituting medications with anticholinergic effects.
Serotonin–norepinephrine reuptake inhibitors
venlafaxine, duloxetine, and desvenlafaxine are among the most widely used antidepressants today and have efficacy similar to SSRIs. Venlafaxine in combination with ECT has been found to effective and safely tolerated, but few reports have cautioned against the possibility of asystole in patients receiving high dose venlafaxine (>300 mg/day), with propofol used as an anesthetic agent., The use of duloxetine with concomitant ECT has been found safe in few reports, but studies with larger samples are still needed. Unlike the TCAs, venlafaxine and other serotonin–norepinephrine reuptake inhibitors have a reduced propensity to cause anticholinergic effects and cardio toxicity.
| Mood Stabilizers|| |
The use of ECT and lithium in combination is a common clinical practice; however, the safety of combined use remains a topic of debate. Some authors have recommended discontinuing lithium before starting ECT, but prospective study designs have demonstrated the safety of the combined approach., While its use in young individuals with no risk factors has been deemed safe, and in elderly individuals, there remains an increased risk of prolonged apnea and neurological side effects such as prolonged seizure activity and delirium. To reduce the risk of prolonged seizures, it is, therefore, prudent to start with a low electrical dose in patients on lithium. The combined effects of lithium and IV anesthetics have been studied in animal experiments, which have shown increased sleeping times with barbiturates, methohexital, thiopental, and ketamine. Lithium also potentiates the actions of both depolarizing and nondepolarizing muscle relaxants. Therefore, anesthetists must be wary of such abnormal results and titrate anesthetic doses with evaluation of effects.,
Anticonvulsant drugs are commonly used for prophylaxis in bipolar disorders. Similar to lithium, recommendations regarding the concomitant use of anticonvulsant mood stabilizers such as sodium valproate and carbamazepine with ECT remain mixed. Theoretically, the use of anticonvulsants will increase the seizure threshold and thus, reduce the effectiveness of ECT. The American Psychiatric Society in its guidelines for ECT recommends discontinuation of anticonvulsants during ECT. On the other hand, randomized controlled trials have shown that combination treatment is not only safe but also can improve the speed of recovery when patients are maintained on a full dose of anticonvulsants., In the case of use of antiepileptic drugs (AEDs) for epilepsy, it is recommended to continue the same throughout the course of ECT. The dose AEDs may need to be reduced in cases of missed or brief seizures. There are limited studies describing the interaction of anesthetic drugs with valproate. Propofol requirement during ECT is reduced in patients on valproate, possibly due to their synergistic action on GABA receptors. Similarly, the combined use of thiopentone and valproate has been found to increase recovery times. Both valproate and carbamazepine have been found to have pharmacodynamic interactions with neuromuscular blockers. While acutely administered AEDs potentiate the effects of nondepolarizing neuromuscular blockers, chronic AED therapy can cause resistance to such muscle relaxants.,,
| Antipsychotics|| |
Current evidence suggests that use of ECT among patients receiving antipsychotics is safe and the combination of two is an effective treatment strategy for patients with schizophrenia., Both typical and atypical antipsychotics are associated with cardiac side effects that can be of great concern to the anesthetist. Cardiovascular morbidity is higher among patients in antipsychotics and the risk increases 2-fold in elderly patients.,, The increased risk has been explained by the changes produced in the ECG, which includes QT and PR interval prolongation, ST segment depression, and rarely premature ventricular contractions. Among typical or first-generation antipsychotics, high risk of arrhythmias is associated with thioridazine, pimozide, droperidol and to a lesser extent with haloperidol, and chlorpromazine. Among atypical antipsychotics, sertindole has the highest risk followed by ziprasidone and risperidone, with quetiapine, clozapine, and olanzapine having negligible effects. The risk of arrhythmias with antipsychotics is further increased if they are combined with other drugs, which are known to increase the QT interval. Among anesthetic drugs, these include halogenated volatile anesthetics such as sevoflurane and IV anesthetics such as etomidate., Ketamine is also to be avoided due to its sympathomimetic properties. Among muscle relaxants, succinylcholine can prolong QT interval while vecuronium, rocuronium, and atracurium do not. Apart from the serious consequences of arrhythmia and sudden death, antipsychotics are also associated with minor cardiovascular effects such as hypotension and tachycardia. These effects can be, especially prominent in the elderly during anesthesia.
Some of the antipsychotics also have varying degrees of anticholinergic effects, placing the elderly patients at an increased risk of cognitive impairment and delirium. Among various antipsychotics, clozapine has the highest anticholinergic effect. As a result, a high incidence of delirium has been reported among patients treated with clozapine, with the risk increasing in older patients, and those receiving other central anticholinergic drugs.,, Furthermore, the combination of high-dose clozapine and ECT has been associated with increased incidence of delirium., Taking these into consideration, it is highly recommended that in patients receiving ECT and clozapine, it is important to avoid use of other anticholinergic drugs and carefully monitor patients for delirium. Clozapine also significantly lowers seizure threshold; hence, it is advised to start with a low-dose of electrical stimulation during the first treatment. As post-ECT delirium is a self-limiting condition, it does not necessitate discontinuation of clozapine or ECT; however, recurring or delayed onset or protracted delirium may require supportive management and discontinuation of both ECT and clozapine. Reduction in dose while giving ECT can be used as a strategy to prevent delirium. Clozapine has been safely restarted at the original dose, after resolution of the delirium.
| Benzodiazepines|| |
BZDs due to their anti-convulsive properties increase the seizure threshold and can potentially reduce the effectiveness of ECT. A number of retrospective studies and few controlled trials have shown that while BZDs do not affect the efficacy of bitemporal ECT they can decrease the efficacy of unilateral ECTs.,, In the absence of controlled studies, clinical recommendations advise a cautious approach of avoiding the concomitant use of BZDs and ECT. However, considering that BZDs are one of the most commonly prescribed psychiatric drugs, for patients who have been on moderate- to high-doses for an extended period, a gradual tapering of dose should be initiated to avoid withdrawal symptoms. Other antianxiety agents such as buspirone, zolpidem, and antihistamines can be used during the ECT period. In cases where BZDs are necessary, short-acting agents such as lorazepam should be used. If the BZD dose cannot be tapered and stopped before the administration of ECT, BZD can be continued at a reduced dose during the course of ECT. Furthermore, use of BZDs should be avoided at least 8–12 h before ECT. The use of flumazenil (BZD antagonist) before ECT to reverse the effects of BZD on seizure induction has been studied with positive results but requires further clinical trials.,
| Antiparkinson Drugs|| |
ECT has long been recognized as a safe and effective palliative treatment for late stages of Parkinson's disease and the frequently co-occurring psychiatric disorders such as depression, mania, and psychosis.,,, It has been suggested that the dose of levodopa should be withheld or reduced by half before ECT to prevent cases of post-ECT agitation, psychosis, and/or delirium, as both levodopa and ECT have dopamine-enhancing effects., With respect to anesthetic considerations, antiparkinsonian drugs have a variety of potential interactions with anesthetic drugs. Levodopa can contribute to hypotension through a central mechanism while direct-acting dopamine agonists such as bromocriptine may precipitate hypotension by peripheral vasodilation. Thiopentone has been found to worsen motor symptoms as it decreases dopamine release from the striatum. The use of succinylcholine has been associated with hyperkalemia in few case reports.
Anticholinergic medications are widely used for symptomatic treatment of Parkinson's disease. These medications increase the anticholinergic burden and lead to progressive cognitive decline. Available evidence suggests that patients with Parkinson's disease on anticholinergics have more frequent cognitive decline when compared to those on other antiparkinsonian drugs., However, some of the authors who used ECT in patients with Parkinson's disease observed no differences in neurocognitive functioning between pretreatment and posttreatment evaluations. However, all patients showed transient memory problems within the first 48–72 h after each session.
| Anti-Dementia Drugs|| |
Depression is a frequently occurring morbidity in patients with dementia, but the use of ECT in this patient population has been generally overlooked due to the risk of worsening of cognitive symptoms. There is a scarce literature on both the effectiveness and the cognitive side effects of ECT in patients with dementia. In a study carried out on sixteen patients with dementia that received ECT for agitation and aggression, only one patient failed to show improvement while transient postictal confusion was seen in eight patients. Donepezil, galantamine, and rivastigmine enhances the effects of depolarizing neuromuscular blockers. Prolonged paralysis with suxamethonium has been described in a case report. However, in another study, no increased risk for postoperative complications was seen in patients on cholinesterase inhibitors who received general anesthesia for the hip surgery.
Anti-dementia drugs have been suggested as a possible strategy to prevent cognitive impairments during ECT. A randomized control trial using donepezil showed significant improvement in recovery times in the post-ECT period. In another study, use of galantamine showed slightly better post-ECT cognitive performance. Memantine, an N-methyl-D-aspartate receptor antagonist, also showed positive cognitive results in a study conducted on 38 patients with various mental disorders. While the preliminary results have been promising, the clinical utility of any of these drugs remains inconclusive at present. Hence, larger and long-term studies are necessary to understand the role of these drugs in attenuating cognitive side effects of ECT.
| Principles of Assessment of Elderly Patients for Electroconvulsive Therapy|| |
Pre-ECT assessment should include a thorough history taking and detailed physical examination [Table 4]. Medical history should rule out important medical conditions such as diabetes, hypertension, angina, drug allergies, cerebrovascular accidents, and cardiovascular conditions. The patients must be referred for specialty consultation for evaluation of comorbidities. There are no absolute contraindications for ECT, but some of the relative contraindications include acute respiratory infection, recent myocardial infarction (within 3 months and depending on severity), recent cerebrovascular accident (within 1 month and depending on severity), uncontrolled cardiac failure, raised intracranial pressure/untreated cerebral aneurysm, deep venous thrombosis, unstable major fracture, and untreated pheochromocytoma. ECT can be safely carried out in patients with cardiac pacemakers and implantable defibrillators when accompanied by appropriate cardiac and pacemaker/defibrillator assessment., Routine laboratory investigations such as complete blood counts, renal function tests, electrolytes, liver function tests, and chest X-ray are highly advisable for all elderly patients before starting of ECT. The International normalized ratio should be evaluated in patients taking anticoagulants. Imaging studies such as magnetic resonance imaging of brain may be requested if history and examination suggest pathology. An ECG is recommended for all elderly patients. Dental assessment should be performed in all patients to identify problems such as loose or missing teeth or presence of dentures.,, [Table 5] outlines the pre-ECT assessment and anesthetic precautions necessary in elderly patients with systemic morbidities.
|Table 4: Suggested pre-electroconvulsive therapy evaluation and changes during electroconvulsive therapy procedure in elderly|
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|Table 5: Pre-electroconvulsive therapy considerations and anesthetic precautions in patients with systemic morbidities|
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Assessment of cognitive functions
Baseline cognitive functioning, followed by intermittent monitoring throughout the ECT is recommended by the multiple international organizations and national guidelines., While no consensus exists regarding the types of assessment schedule or battery to be used in these guidelines, mini-mental state examination (MMSE) is the most commonly recommended cognitive screening test. However, some of the studies suggest that MMSE may be insensitive in detecting ECT-related cognitive changes. At a minimum, those aspects of cognitive function should be evaluated which are most likely to be affected by ECT. These include global cognitive function, nonverbal and visuospatial memory, working memory, executive function, and autobiographical memory. The commonly used neuropsychological batteries are listed in [Table 6]. A brief cognitive battery called battery for ECT-related cognitive deficits (B4ECT-ReCoDe) has been developed in India, which can be applied in routine clinical practice. Assessment on this battery are completed over 20–30 min and includes verbal, visual, working and autobiographic memory, sustained attention, psychomotor speed, and subjective memory impairment. The American Psychiatric Association guidelines propose assessment of cognitive function at least 48 h after ECT and the same battery repeated every week or after every two ECT treatments. Further assessment should be conducted at a remote point usually between 2 and 6 months and again at 1 year to assess for permanent cognitive deficits.,
|Table 6: Neuropsychological batteries (include references for all tests)|
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Preelectroconvulsive therapy documentation
Written informed consent should be obtained in all cases. Separate consent should be obtained for both anesthesia procedures and electrical stimulation. The information sheet for ECT must include information on the risks, side effects, and frequency of the treatment. The patient and the family members may be given an information sheet to read about the procedure and must be given a chance to seek clarification. No coercion must be used at the time of seeking consent. If a patient does not have the capacity for informed consent, consent must be obtained from the legal guardian. In the medical records of the patient, indication for the use of ECT, comorbid psychiatric diagnoses, concurrent medical conditions, and current medications must be documented clearly.
| Conduct of Anesthesia|| |
Identity of the patient should be verified with the medical records. Consent should be checked again. Anesthetic and monitoring equipment should be checked to meet acceptable standards. Emergency drugs and equipment should be available in the treatment room. Pre-ECT fasting must be confirmed before anesthetic administration. Prescribed medications should be taken at least 2 h before ECT, with only sips of water. The patient should be advised to empty bladder to avoid incontinence. Monitoring of blood pressure, ECG, pulse oximetry, and end-tidal carbon dioxide must be performed during the procedure. The patient should be preoxygenated with continuous flow oxygen and ventilation is to be continued with facemask until the muscle relaxant is effective. Breathing should be supported with manual ventilation during the seizure and continued till breathing resumes. Careful monitoring after ECT is particularly indicated for elderly patients, as they are at a higher risk for post-ECT delirium and cardiac arrhythmias., Pulse oximetry, ECG, blood pressure monitoring, and oxygen supplementation should continue during the recovery period. Oxygen desaturation is a common occurrence after ECT, but ventilating the lungs during seizure period can significantly reduce its incidence.
The selection of an appropriate induction agent should be guided by patient's clinical status and the seizure characteristics during the course of ECT. While methohexital is considered a gold standard for induction in ECT, due to its minimal effects on seizure duration and quick recovery, its use has declined in recent times due to limited availability. Propofol and thiopentone are now the most commonly used drugs. Propofol offers the advantages of a quick recovery and few cognitive adverse effects but is limited by its property of reducing seizure duration and causing hypotension.
| Vrecommendations for Use of Psychotropics during the Electroconvulsive Therapy Course|| |
The effects of concurrent use of psychotropics with ECT in the elderly are continually being studied. Among antidepressants, TCAs and few SSRIs such as paroxetine have significant anticholinergic action, which may contribute toward post-ECT delirium. The use of SSRIs in the elderly is frequently associated with hyponatremia, which may also present with cognitive changes and confusion. Despite these possible side effects, no change in dosage or stoppage of antidepressants is recommended. The safety of combined use of lithium and ECT remains undetermined. While some authors suggest stopping or lowering the lithium dose to prevent side effects such as prolonged seizures and delirium, current guidelines recommend continuing with the previous dosage but using low first electrical stimulus during ECT. Antipsychotics such as thioridazine, pimozide, and sertindole increase the risk of arrhythmias; hence, they should not be combined with anesthetic drugs, which are known to increase QT intervals such as etomidate, sevoflurane, ketamine, and succinylcholine. Clozapine, because of its anticholinergic properties, can increase the incidence of post-ECT delirium in the elderly patients.
| Missed, Brief, or Prolonged Seizures|| |
Missed or brief seizures have been found to occur more commonly in the elderly population. It is important to consider that missed seizures results from premature termination of stimulus; hence, practitioners should first check ECT equipment such as electrode contacts, cables, and device settings. It is also important to review the anticonvulsant effects of any prescribed medication and the use of high doses of induction agents. In the absence of any such contributing factors, several augmentation strategies can be utilized. While the American Psychological Association (APA) task force report first recommends restimulation at higher intensities, this strategy can increase the risk of cognitive adverse effects in the elderly. Hence, other augmentation strategies such as ventilation with 100% oxygen, hyperventilation of the patient, use of drugs like theophylline, and the use of proconvulsant anesthetics such as etomidate and ketamine can be tried instead.
Inspired oxygen concentration during ECT has been shown to influence seizure duration and increasing the inspired oxygen concentration from 30% to 100% can significantly prolong the seizure duration. APA recommends augmenting seizure duration with hyperventilation-induced hypocapnia. This includes moderate hyperventilation (approximately 20 breaths), just before application of the electrical stimulus, with the end-tidal pressure of carbon dioxide maintained at 30 mmHg. Oral theophylline administered a night before ECT has also been used to increase seizure duration in a safe and effective manner.,
Along with missed or brief seizures, the anesthetist should also be prepared for the possibility of a prolonged seizure, generally defined as lasting for more than 2 min. Management of prolonged seizures includes administration of anticonvulsants such as short-acting BZDs and monitoring for airway blockage and cardio-respiratory instability. The patients with prolonged seizures should undergo a review of their medications and history to determine risk factors. Anesthetic modification for prolonged seizures can include use induction agents such as propofol to increase the seizure threshold.
| Postelectroconvulsive Therapy Delirium|| |
A short-lasting confusional state can usually last for 10–20 min after the seizure, but in 1%–12% of treatments such confusional states can persist for hours and can progress to delirium. While most such episodes are short-lasting and self-limiting, warranting no treatment other than reassurance, in few cases administration of BZDs or haloperidol along with physical restraints to protect the patient from harm, may be necessary. When patients fail to respond to these medications, a few reports have shown promising results with drugs such as dexmedetomidine and donepezil in shortening the duration of delirium., A large number of medications (with or without anticholinergic properties) can predispose toward delirium; hence, a thorough medication review and a reduction in the dose or stoppage of the contributing drug should be performed. A comprehensive neurological assessment with neuroimaging studies should be undertaken in patients with preexisting brain pathology, when delirium fails to resolve or when delirium emerges with successive treatments.
| Conclusion|| |
ECT offers an effective and rapid treatment for elderly mental disorders and it can be administered with relative safety to the elderly patients with severe comorbidities. A careful assessment of all clinical variables must be undertaken to minimize potential risks. Knowledge of the physiological effects of ECT and those of psychotropic and anesthetic drugs is essential to carry out ECT safely. Unfortunately, there is a lack of randomized controlled trials on the therapeutic and adverse effects of psychotropic medications administered along with ECT. Similarly, randomized trials on ECT in the elderly with systemic comorbidities are rare. Current evidence and recommendations rely heavily on observational and retrospective studies. Future research and clinical studies should focus on determining appropriate dose adjustments of psychotropics and anesthetics with ECT. The effects of this combined approach on clinical and seizure parameters should be assessed through standardized measures and instruments. Future research should also focus on establishing pharmacokinetic and pharmacodynamic properties of anesthetics and psychotropics in the presence of systemic comorbidities. Treating psychiatric disorders in the elderly patients is a challenging task, and ECT can be a lifesaving choice if the risks associated are minimized by modifying the ECT regimen to suit the clinical status of the patient.
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| References|| |
Baghai TC, Möller HJ. Electroconvulsive therapy and its different indications. Dialogues Clin Neurosci 2008;10:105-17.
Chanpattana W, Kramer BA, Kunigiri G, Gangadhar BN, Kitphati R, Andrade C. A survey of the practice of electroconvulsive therapy in Asia. J ECT 2010;26:5-10.
Gangadhar BN. Mental health care bill and electroconvulsive therapy: Anesthetic modification. Indian J Psychol Med 2013;35:225-6.
] [Full text]
Blazer DG, Hybels CF, Pieper CF. The association of depression and mortality in elderly persons: A case for multiple, independent pathways. J Gerontol A Biol Sci Med Sci 2001;56:M505-9.
Smagula SF, Butters MA, Anderson SJ, Lenze EJ, Dew MA, Mulsant BH, et al.
Antidepressant Response trajectories and associated clinical prognostic factors among older adults. JAMA Psychiatry 2015;72:1021-8.
Williamson J, Chopin JM. Adverse reactions to prescribed drugs in the elderly: A multicentre investigation. Age Ageing 1980;9:73-80.
Jain G, Kumar V, Chakrabarti S, Grover S. The use of electroconvulsive therapy in the elderly: A study from the psychiatric unit of a North Indian teaching hospital. J ECT 2008;24:122-7.
van Schaik AM, Comijs HC, Sonnenberg CM, Beekman AT, Sienaert P, Stek ML. Efficacy and safety of continuation and maintenance electroconvulsive therapy in depressed elderly patients: A systematic review. Am J Geriatr Psychiatry 2012;20:5-17.
Dybedal GS, Tanum L, Sundet K, Gaarden TL, Bjølseth TM. Cognitive side-effects of electroconvulsive therapy in elderly depressed patients. Clin Neuropsychol 2014;28:1071-90.
Antosik-Wójcinska A, Swiecicki L. The efficacy and safety of ECT in population before and after 60 years of age. Psychiatr Pol 2016;50:1015-26.
Burke WJ, Rubin EH, Zorumski CF, Wetzel RD. The safety of ECT in geriatric psychiatry. J Am Geriatr Soc 1987;35:516-21.
Wells DG, Davies GG. Hemodynamic changes associated with electroconvulsive therapy. Anesth Analg 1987;66:1193-5.
Mulgaokar GD, Dauchot PJ, Duffy JP, Anton AH. Noninvasive assessment of electroconvulsive-induced changes in cardiac function. J Clin Psychiatry 1985;46:479-82.
Fu W, Stool LA, White PF, Husain MM. Acute hemodynamic responses to electroconvulsive therapy are not related to the duration of seizure activity. J Clin Anesth 1997;9:653-7.
Takada JY, Solimene MC, da Luz PL, Grupi CJ, Giorgi DM, Rigonatti SP, et al.
Assessment of the cardiovascular effects of electroconvulsive therapy in individuals older than 50 years. Braz J Med Biol Res 2005;38:1349-57.
Rice EH, Sombrotto LB, Markowitz JC, Leon AC. Cardiovascular morbidity in high-risk patients during ECT. Am J Psychiatry 1994;151:1637-41.
Burd J, Kettl P. Incidence of asystole in electroconvulsive therapy in elderly patients. Am J Geriatr Psychiatry 1998;6:203-11.
Rivera FA, Lapid MI, Sampson S, Mueller PS. Safety of electroconvulsive therapy in patients with a history of heart failure and decreased left ventricular systolic heart function. J ECT 2011;27:207-13.
McCall WV. Antihypertensive medications and ECT. Convuls Ther 1993;9:317-25.
Ding Z, White PF. Anesthesia for electroconvulsive therapy. Anesth Analg 2002;94:1351-64.
Sharma G, Goodwin J. Effect of aging on respiratory system physiology and immunology. Clin Interv Aging 2006;1:253-60.
Alexopoulos GS, Shamoian CJ, Lucas J, Weiser N, Berger H. Medical problems of geriatric psychiatric patients and younger controls during electroconvulsive therapy. J Am Geriatr Soc 1984;32:651-4.
Tecoult E, Nathan N. Morbidity in electroconvulsive therapy. Eur J Anaesthesiol 2001;18:511-8.
Kadar AG, Ing CH, White PF, Wakefield CA, Kramer BA, Clark K. Anesthesia for electroconvulsive therapy in obese patients. Anesth Analg 2002;94:360-1.
Swindells SR, Simpson KH. Oxygen saturation during electroconvulsive therapy. Br J Psychiatry 1987;150:695-7.
Lew JK, Eastley RJ, Hanning CD. Oxygenation during electroconvulsive therapy. A comparison of two anaesthetic techniques. Anaesthesia 1986;41:1092-7.
Surve R, Bansal S, Sriganesh K, Subbakrishna DK, Thirthalli J, Umamaheswara Rao GS. Incidence and risk factors for oxygen desaturation during recovery from modified electroconvulsive therapy: A prospective observational study. J Anaesthesiol Clin Pharmacol 2015;31:99-103.
] [Full text]
Lindeman RD. Overview: Renal physiology and pathophysiology of aging. Am J Kidney Dis 1990;16:275-82.
Williams S, Ostroff R. Chronic renal failure, hemodialysis, and electroconvulsive therapy: A case report. J ECT 2005;21:41-2.
Pearlman C, Carson W, Metz A. Hemodialysis, chronic renal failure, and ECT. Convuls Ther 1988;4:332-3.
Anantharaju A, Feller A, Chedid A. Aging liver: A review. Gerontology 2002;48:343-53.
Blewett AE, Kareem O. ECT in a patient with psychotic retarded depression, metastatic hepatic cancer, and esophageal varices. J ECT 2000;16:291-4.
Ozdemir O, Aydin A, Tapanci Z, Atilla E. Electroconvulsive therapy in a patient with a liver transplant. J Neuropsychiatry Clin Neurosci 2014;26:E57.
Saito S, Miyoshi S, Yoshikawa D, Shimada H, Morita T, Kitani Y. Regional cerebral oxygen saturation during electroconvulsive therapy: Monitoring by near-infrared spectrophotometry. Anesth Analg 1996;83:726-30.
Richard J. Handbook of ECT. Am J Psychiatry 1999;156:1459-60.
Avramov MN, Husain MM, White PF. The comparative effects of methohexital, propofol, and etomidate for electroconvulsive therapy. Anesth Analg 1995;81:596-602.
Bryson EO, Aloysi AS, Popeo DM, Bodian CA, Pasculli RM, Briggs MC, et al.
Methohexital and succinylcholine dosing for electroconvulsive therapy (ECT): Actual versus ideal. J ECT 2012;28:e29-30.
Martone CH, Nagelhout J, Wolf SM. Methohexital: A practical review for outpatient dental anesthesia. Anesth Prog 1991;38:195-9.
Ghoneim MM, Chiang CK, Schoenwald RD, Lilburn JK, Dhanaraj J. The pharmacokinetics of methohexital in young and elderly subjects. Acta Anaesthesiol Scand 1985;29:480-2.
Lihua P, Su M, Ke W, Ziemann-Gimmel P. Different regimens of intravenous sedatives or hypnotics for electroconvulsive therapy (ECT) in adult patients with depression. Cochrane Database Syst Rev 2014;4:CD009763.
Hooten WM, Rasmussen KG Jr. Effects of general anesthetic agents in adults receiving electroconvulsive therapy: A systematic review. J ECT 2008;24:208-23.
Eranti SV, Mogg AJ, Pluck GC, Landau S, McLoughlin DM. Methohexitone, propofol and etomidate in electroconvulsive therapy for depression: A naturalistic comparison study. J Affect Disord 2009;113:165-71.
Homer TD, Stanski DR. The effect of increasing age on thiopental disposition and anesthetic requirement. Anesthesiology 1985;62:714-24.
Christensen JH, Andreasen F, Jansen JA. Influence of age and sex on the pharmacokinetics of thiopentone. Br J Anaesth 1981;53:1189-95.
Hizli Sayar G, Eryilmaz G, Semieoglu S, Ozten E, Gögcegöz Gül I. Influence of valproate on the required dose of propofol for anesthesia during electroconvulsive therapy of bipolar affective disorder patients. Neuropsychiatr Dis Treat 2014;10:433-8.
Russo H, Bressolle F. Pharmacodynamics and pharmacokinetics of thiopental. Clin Pharmacokinet 1998;35:95-134.
Rosa MA, Rosa MO, Marcolin MA, Fregni F. Cardiovascular effects of anesthesia in ECT: A randomized, double-blind comparison of etomidate, propofol, and thiopental. J ECT 2007;23:6-8.
Shah PJ, Dubey KP, Watti C, Lalwani J. Effectiveness of thiopentone, propofol and midazolam as an ideal intravenous anaesthetic agent for modified electroconvulsive therapy: A comparative study. Indian J Anaesth 2010;54:296-301.
] [Full text]
Zahavi GS, Dannon P. Comparison of anesthetics in electroconvulsive therapy: An effective treatment with the use of propofol, etomidate, and thiopental. Neuropsychiatr Dis Treat 2014;10:383-9.
Rosa MA, Rosa MO, Belegarde IM, Bueno CR, Fregni F. Recovery after ECT: Comparison of propofol, etomidate and thiopental. Rev Bras Psiquiatr 2008;30:149-51.
Hascilowicz T, Hamaguchi T, Nakata S, Yamamoto Y, Kiyama S, Uezono S. How much propofol should be given to the elderly for induction of anaesthesia? A prospective study based on change of bispectral index (BIS) values: 18AP1-5. Eur J Anaesthesiol 2011;28:222.
Chan VW, Chung FF. Propofol infusion for induction and maintenance of anesthesia in elderly patients: Recovery and hemodynamic profiles. J Clin Anesth 1996;8:317-23.
Geretsegger C, Nickel M, Judendorfer B, Rochowanski E, Novak E, Aichhorn W. Propofol and methohexital as anesthetic agents for electroconvulsive therapy: A randomized, double-blind comparison of electroconvulsive therapy seizure quality, therapeutic efficacy, and cognitive performance. J ECT 2007;23:239-43.
Geretsegger C, Rochowanski E, Kartnig C, Unterrainer AF. Propofol and methohexital as anesthetic agents for electroconvulsive therapy (ECT): A comparison of seizure-quality measures and vital signs. J ECT 1998;14:28-35.
Bailine SH, Petrides G, Doft M, Lui G. Indications for the use of propofol in electroconvulsive therapy. J ECT 2003;19:129-32.
Maneglia R, Cousin MT. A comparison between propofol and ketamine for anaesthesia in the elderly. Haemodynamic effects during induction and maintenance. Anaesthesia 1988;43 Suppl:109-11.
Rybakowski JK, Bodnar A, Krzywotulski M, Chlopocka-Wozniak M, Michalak M, Rosada-Kurasinska J, et al.
Ketamine anesthesia, efficacy of electroconvulsive therapy, and cognitive functions in treatment-resistant depression. J ECT 2016;32:164-8.
Abdallah CG, Fasula M, Kelmendi B, Sanacora G, Ostroff R. Rapid antidepressant effect of ketamine in the electroconvulsive therapy setting. J ECT 2012;28:157-61.
Rasmussen KG, Kung S, Lapid MI, Oesterle TS, Geske JR, Nuttall GA, et al.
A randomized comparison of ketamine versus methohexital anesthesia in electroconvulsive therapy. Psychiatry Res 2014;215:362-5.
Arden JR, Holley FO, Stanski DR. Increased sensitivity to etomidate in the elderly: Initial distribution versus altered brain response. Anesthesiology 1986;65:19-27.
Holdcroft A, Morgan M, Whitwam JG, Lumley J. Effect of dose and premedication on induction complications with etomidate. Br J Anaesth 1976;48:199-205.
Hartle AJ, Peel PH. Etomidate puts patients at risk of adrenal crisis. BMJ 2012;345:e7444.
Allolio B, Stuttmann R, Leonhard U, Fischer H, Winkelmann W. Adrenocortical suppression by a single induction dose of etomidate. Klin Wochenschr 1984;62:1014-7.
Preziosi P, Vacca M. Adrenocortical suppression and other endocrine effects of etomidate. Life Sci 1988;42:477-89.
Ilivicky H, Caroff SN, Simone AF. Etomidate during ECT for elderly seizure-resistant patients. Am J Psychiatry 1995;152:957-8.
Toprak HI, Gedik E, Begeç Z, Oztürk E, Kaya B, Ersoy MO. Sevoflurane as an alternative anaesthetic for electroconvulsive therapy. J ECT 2005;21:108-10.
Rasmussen KG, Spackman TN, Hooten WM. The clinical utility of inhalational anesthesia with sevoflurane in electroconvulsive therapy. J ECT 2005;21:239-42.
Muravchik S. Pharmacological Changes of Aging. 53rd
ASA Annual Meeting Refresher Course Lectures #19; 2002. p. 1-7.
Calarge CA, Crowe RR, Gergis SD, Arndt S, From RP. The comparative effects of sevoflurane and methohexital for electroconvulsive therapy. J ECT 2003;19:221-5.
Murali N, Saravanan ES, Ramesh VJ, Gangadhar BN, Jananakiramiah N, Kumar SS, et al.
An intrasubject comparison of two doses of succinylcholine in modified electroconvulsive therapy. Anesth Analg 1999;89:1301-4.
Konarzewski WH, Milosavljevic D, Robinson M, Banham W, Beales F. Suxamethonium dosage in electroconvulsive therapy. Anaesthesia 1988;43:474-6.
Zhou W, Lv S. Delayed recovery from paralysis associated with plasma cholinesterase deficiency. Springerplus 2016;5:1887.
Hubbard RE, O'Mahony MS, Calver BL, Woodhouse KW. Plasma esterases and inflammation in ageing and frailty. Eur J Clin Pharmacol 2008;64:895-900.
Barnett SR. Manual of Geriatric Anesthesia. New York: Springer-Verlag; 2013.
Strayer RJ. Succinylcholine, rocuronium, and hyperkalemia. Am J Emerg Med 2016;34:1705-6.
Martyn JA, Richtsfeld M. Succinylcholine-induced hyperkalemia in acquired pathologic states: Etiologic factors and molecular mechanisms. Anesthesiology 2006;104:158-69.
Cooper RC, Baumann PL, McDonald WM. An unexpected hyperkalemic response to succinylcholine during electroconvulsive therapy for catatonic schizophrenia. Anesthesiology 1999;91:574-5.
Claudius C, Garvey LH, Viby-Mogensen J. The undesirable effects of neuromuscular blocking drugs. Anaesthesia 2009;64 Suppl 1:10-21.
Muñoz-Martínez T, Garrido-Santos I, Arévalo-Cerón R, Rojas-Viguera L, Cantera-Fernández T, Pérez-González R, et al.
Contraindications to succinylcholine in the Intensive Care Unit. A prevalence study. Med Intensiva 2015;39:90-6.
Birkenhäger TK, Pluijms EM, Groenland TH, van den Broek WW. Severe bradycardia after anesthesia before electroconvulsive therapy. J ECT 2010;26:53-4.
Tang WK, Ungvari GS. Asystole during electroconvulsive therapy: A case report. Aust N
Z J Psychiatry 2001;35:382-5.
Arias L, O'Brien JJ, Kimball JN. Electroconvulsive therapy- and succinylcholine-related asystole. J ECT 2009;25:144.
Kelly D, Brull SJ. Neuroleptic malignant syndrome and mivacurium: A safe alternative to succinylcholine? Can J Anaesth 1994;41:845-9.
Fox MH, Hunt PC. Prolonged neuromuscular block associated with mivacurium. Br J Anaesth 1995;74:237-8.
ØStergaard D, Viby-Mogensen J, Pedersen NA, Holm H, Skovgaard LT. Pharmacokinetics and pharmacodynamics of mivacurium in young adult and elderly patients. Acta Anaesthesiol Scand 2002;46:684-91.
Janis K, Hess J, Fabian JA, Gillis M. Substitution of mivacurium for succinylcholine for ECT in elderly patients. Can J Anaesth 1995;42:612-3.
Fredman B, Smith I, d'Etienne J, White PF. Use of muscle relaxants for electroconvulsive therapy: How much is enough? Anesth Analg 1994;78:195-6.
Kisor DF, Schmith VD. Clinical pharmacokinetics of cisatracurium besilate. Clin Pharmacokinet 1999;36:27-40.
Kitts JB, Fisher DM, Canfell PC, Spellman MJ, Caldwell JE, Heier T, et al
. Pharmacokinetics and pharmacodynamics of atracurium in the elderly. Anesthesiology 1990;72:272-5.
Parker CJ, Hunter JM, Snowdon SL. Effect of age, gender and anaesthetic technique on the pharmacodynamics of atracurium. Br J Anaesth 1993;70:38-41.
Hicks FG. ECT modified by Atracurium. Convuls Ther 1987;3:54-59.
Lui PW, Ma JY, Chan KK. Modification of tonic-clonic convulsions by atracurium in multiple-monitored electroconvulsive therapy. J Clin Anesth 1993;5:16-21.
Scott RP, Savarese JJ, Basta SJ, Sunder N, Ali HH, Gargarian M, et al.
Atracurium: Clinical strategies for preventing histamine release and attenuating the haemodynamic response. Br J Anaesth 1985;57:550-3.
Hughes R. Local reactions and histamine release by atracurium. Anaesthesia 1985;40:593-5.
Fukushima K, Aoki T, Nagashima H. Plasma histamine release following the intravenous administration of atracurium in man. Masui 1989;38:190-4.
Appiah-Ankam J, Hunter JM. Pharmacology of neuromuscular blocking drugs. Continuing education in anaesthesia. Crit Care Pain 2004;4:2-7.
McCarthy G, Elliott P, Mirakhur RK, Cooper R, Sharpe TD, Clarke RS. Onset and duration of action of vecuronium in the elderly: Comparison with adults. Acta Anaesthesiol Scand 1992;36:383-6.
Lien CA, Matteo RS, Ornstein E, Schwartz AE, Diaz J. Distribution, elimination, and action of vecuronium in the elderly. Anesth Analg 1991;73:39-42.
Herriot PM, Cowain T, McLeod D. Use of vecuronium to prevent suxamethonium-induced myalgia after ECT. Br J Psychiatry 1996;168:653-4.
Tundo A, de Filippis R, Proietti L. Pharmacologic approaches to treatment resistant depression: Evidences and personal experience. World J Psychiatry 2015;5:330-41.
Attri JP, Bala N, Chatrath V. Psychiatric patient and anaesthesia. Indian J Anaesth 2012;56:8-13.
] [Full text]
Pisani F, Oteri G, Costa C, Di Raimondo G, Di Perri R. Effects of psychotropic drugs on seizure threshold. Drug Saf 2002;25:91-110.
Nezafati MH, Vojdanparast M, Nezafati P. Antidepressants and cardiovascular adverse events: A narrative review. ARYA Atheroscler 2015;11:295-304.
Waite J, Easton A. The ECT Handbook. London (GB): Royal College of Psychiatrists; 2013.
Garner EM, Kelly MW, Thompson DF. Tricyclic antidepressant withdrawal syndrome. Ann Pharmacother 1993;27:1068-72.
Bajwa SJ, Jindal R, Kaur J, Singh A. Psychiatric diseases: Need for an increased awareness among the anesthesiologists. J Anaesthesiol Clin Pharmacol 2011;27:440-6.
] [Full text]
Leth-Møller KB, Hansen AH, Torstensson M, Andersen SE, Ødum L, Gislasson G, et al.
Antidepressants and the risk of hyponatremia: A Danish register-based population study. BMJ Open 2016;6:e011200.
Viramontes TS, Truong H, Linnebur SA. Antidepressant-induced hyponatremia in older adults. Consult Pharm 2016;31:139-50.
Liu BA, Mittmann N, Knowles SR, Shear NH. Hyponatremia and the syndrome of inappropriate secretion of antidiuretic hormone associated with the use of selective serotonin reuptake inhibitors: A review of spontaneous reports. CMAJ 1996;155:519-27.
Jacob S, Spinler SA. Hyponatremia associated with selective serotonin-reuptake inhibitors in older adults. Ann Pharmacother 2006;40:1618-22.
Gunathilake R, Oldmeadow C, McEvoy M, Kelly B, Inder K, Schofield P, et al.
Mild hyponatremia is associated with impaired cognition and falls in community-dwelling older persons. J Am Geriatr Soc 2013;61:1838-9.
Pacher P, Kecskeméti V. Cardiovascular effects of selective serotonin reuptake inhibitor antidepressants. Orv Hetil 2004;145:425-31.
Wenzel-Seifert K, Wittmann M, Haen E. Torsade de pointes episodes under treatment with selective serotonin reuptake inhibitors. Pharmacopsychiatry 2010;43:279-81.
Cooke MJ, Waring WS. Citalopram and cardiac toxicity. Eur J Clin Pharmacol 2013;69:755-60.
Pacher P, Ungvari Z, Kecskemeti V, Furst S. Review of cardiovascular effects of fluoxetine, a selective serotonin reuptake inhibitor, compared to tricyclic antidepressants. Curr Med Chem 1998;5:381-90.
Cherin P, Colvez A, Deville de Periere G, Sereni D. Risk of syncope in the elderly and consumption of drugs: A case-control study. J Clin Epidemiol 1997;50:313-20.
Sanchez C, Reines EH, Montgomery SA. A comparative review of escitalopram, paroxetine, and sertraline: Are they all alike? Int Clin Psychopharmacol 2014;29:185-96.
Fujishiro J, Imanishi T, Onozawa K, Tsushima M. Comparison of the anticholinergic effects of the serotonergic antidepressants, paroxetine, fluvoxamine and clomipramine. Eur J Pharmacol 2002;454:183-8.
Han L, Agostini JV, Allore HG. Cumulative anticholinergic exposure is associated with poor memory and executive function in older men. J Am Geriatr Soc 2008;56:2203-10.
Tune LE. Serum anticholinergic activity levels and delirium in the elderly. Semin Clin Neuropsychiatry 2000;5:149-53.
Llorca PM, Fernandez JL. Escitalopram in the treatment of major depressive disorder: Clinical efficacy, tolerability and cost-effectiveness vs. venlafaxine extended-release formulation. Int J Clin Pract 2007;61:702-10.
Gonzalez-Pinto A, Gutierrez M, Gonzalez N, Elizagarate E, Perez de Heredia JL, Mico JA. Efficacy and safety of venlafaxine-ECT combination in treatment-resistant depression. J Neuropsychiatry Clin Neurosci 2002;14:206-9.
Agelink MM, Zeit T, Klieser E. Prolonged bradycardia complicates antidepressive treatment with venlafaxine and ECT. Br J Psychiatry 1998;173:441.
Eraslan D, Genc Y, Odabasioglu G, Ergun BM, Ozturk O. Safety of electroconvulsive therapy-duloxetine combination. J ECT 2011;27:e51-2.
el-Mallakh RS. Complications of concurrent lithium and electroconvulsive therapy: A review of clinical material and theoretical considerations. Biol Psychiatry 1988;23:595-601.
Thirthalli J, Harish T, Gangadhar BN. A prospective comparative study of interaction between lithium and modified electroconvulsive therapy. World J Biol Psychiatry 2011;12:149-55.
Volpe FM, Tavares AR Jr. Lithium plus ECT for mania in 90 cases: Safety issues. J Neuropsychiatry Clin Neurosci 2012;24:E33.
Mukherjee S. Combined ECT and lithium therapy. J ECT 1993;9:274-84.
Leone CW. Anesthetic management of lithium-treated patients. Anesth Prog 1984;31:138-40.
Hill GE, Wong KC, Hodges MR. Lithium carbonate and neuromuscular blocking agents. Anesthesiology 1977;46:122-6.
American Psychiatric Association. The Practice of Electroconvulsive Therapy Recommendations for Treatment, Training and Privileging. A Task Force Report of the American Psychiatric Association. Washington, DC: American Psychiatric Association; 2001.
Jahangard L, Haghighi M, Bigdelou G, Bajoghli H, Brand S. Comparing efficacy of ECT with and without concurrent sodium valproate therapy in manic patients. J ECT 2012;28:118-23.
Rakesh G, Thirthalli J, Kumar CN, Muralidharan K, Phutane VH, Gangadhar BN. Concomitant anticonvulsants with bitemporal electroconvulsive therapy: A randomized controlled trial with clinical and neurobiological application. J ECT 2017;33:16-21.
Aguilera L, Calvo R, Garcia RC. Interaction between thiopentone and sodium valproate. An in vitro
and in vivo
study. Br J Anaesth 1986;58:1380-3.
Soriano SG, Martyn JA. Antiepileptic-induced resistance to neuromuscular blockers: Mechanisms and clinical significance. Clin Pharmacokinet 2004;43:71-81.
Richard A, Girard F, Girard DC, Boudreault D, Chouinard P, Moumdjian R, et al.
Cisatracurium-induced neuromuscular blockade is affected by chronic phenytoin or carbamazepine treatment in neurosurgical patients. Anesth Analg 2005;100:538-44.
Koenig HM, Hoffman WE. The effect of anticonvulsant therapy on two doses of rocuronium-induced neuromuscular blockade. J Neurosurg Anesthesiol 1999;11:86-9.
Braga RJ, Petrides G. The combined use of electroconvulsive therapy and antipsychotics in patients with schizophrenia. J ECT 2005;21:75-83.
Painuly N, Chakrabarti S. Combined use of electroconvulsive therapy and antipsychotics in schizophrenia: The Indian evidence. A review and a meta-analysis. J ECT 2006;22:59-66.
Ray WA, Meredith S, Thapa PB, Meador KG, Hall K, Murray KT. Antipsychotics and the risk of sudden cardiac death. Arch Gen Psychiatry 2001;58:1161-7.
Kuehn BM. FDA warns antipsychotic drugs may be risky for elderly. JAMA 2005;293:2462.
Setoguchi S, Wang PS, Alan Brookhart M, Canning CF, Kaci L, Schneeweiss S. Potential causes of higher mortality in elderly users of conventional and atypical antipsychotic medications. J Am Geriatr Soc 2008;56:1644-50.
Gury C, Canceil O, Iaria P. Antipsychotic drugs and cardiovascular safety: Current studies of prolonged QT interval and risk of ventricular arrhythmia. Encephale 2000;26:62-72.
Hanci V, Aydin M, Yurtlu BS, Ayoglu H, Okyay RD, Tas E, et al.
Anesthesia induction with sevoflurane and propofol: Evaluation of P-wave dispersion, QT and corrected QT intervals. Kaohsiung J Med Sci 2010;26:470-7.
Erdil F, Demirbilek S, Begec Z, Ozturk E, Ersoy MO. Effects of propofol or etomidate on QT interval during electroconvulsive therapy. J ECT 2009;25:174-7.
Fazio G, Vernuccio F, Grutta G, Re GL. Drugs to be avoided in patients with long QT syndrome: Focus on the anaesthesiological management. World J Cardiol 2013;5:87-93.
Buckley NA, Sanders P. Cardiovascular adverse effects of antipsychotic drugs. Drug Saf 2000;23:215-28.
Stahl SM. Essential Psychopharmacology. 4th
ed. New York: Cambridge University Press; 2013.
Tracy JI, Monaco CA, Abraham G, Josiassen RC, Pollock BG. Relation of serum anticholinergicity to cognitive status in schizophrenia patients taking clozapine or risperidone. J Clin Psychiatry 1998;59:184-8.
Centorrino F, Albert MJ, Drago-Ferrante G, Koukopoulos AE, Berry JM, Baldessarini RJ. Delirium during clozapine treatment: Incidence and associated risk factors. Pharmacopsychiatry 2003;36:156-60.
Shankar BR. Clozapine-induced delirium. J Neuropsychiatry Clin Neurosci 2008;20:239-40.
Szymanski S, Jody D, Leipzig R, Masiar S, Lieberman J. Anticholinergic delirium caused by retreatment with clozapine. Am J Psychiatry 1991;148:1752.
Manjunatha N, Ram Kumar GS, Vidyendaran R, Muralidharan K, John JP. Delayed onset, protracted delirium and aspiration pneumonitis associated with a combination of clozapine and electroconvulsive therapy. Indian J Psychol Med 2011;33:80-2.
] [Full text]
Kumar S, Goswami U, Behera D, Khastgir U. ECT and Clozapine combination producing delirium: A case report. Indian J Psychiatry 2003;45:193.
Gálvez V, Loo CK, Alonzo A, Cerrillo E, Menchón JM, Crespo JM, et al.
Do benzodiazepines moderate the effectiveness of bitemporal electroconvulsive therapy in major depression? J Affect Disord 2013;150:686-90.
Jha A, Stein G. Decreased efficacy of combined benzodiazepines and unilateral ECT in treatment of depression. Acta Psychiatr Scand 1996;94:101-4.
Krystal AD, Watts BV, Weiner RD, Moore S, Steffens DC, Lindahl V. The use of flumazenil in the anxious and benzodiazepine-dependent ECT patient. J ECT 1998;14:5-14.
Doering EB, Ball WA. Flumazenil before electroconvulsive therapy: Outstanding issues. Anesthesiology 1995;83:642-3.
Yi J, Torres J, Azner Y, Vaidya P, Schiavi A, Reti IM. Flumazenil pretreatment in benzodiazepine-free patients: A novel method for managing declining ECT seizure quality. J ECT 2012;28:185-9.
Pintor LP, Valldeoriola F, Fernández-Egea E, Sánchez R, Rami L, Tolosa E, et al.
Use of electroconvulsive therapy in Parkinson disease with residual axial symptoms partially unresponsive to L-dopa: A pilot study. J ECT 2012;28:87-91.
Avila A, Sastre F, Cardona X, Maho P, Bello J, Sancho I. Electroconvulsive therapy in Parkinson disease. Description of three cases. Neurologia 1997;12:313-6.
Atre-Vaidya N, Jampala VC. Electroconvulsive therapy in parkinsonism with affective disorder. Br J Psychiatry 1988;152:55-8.
Popeo D, Kellner CH. ECT for Parkinson's disease. Med Hypotheses 2009;73:468-9.
Nymeyer L, Grossberg GT. Delirium in a 75-year-old woman receiving ECT and levodopa. Convuls Ther 1997;13:114-6.
Shaikh SI, Verma H. Parkinson's disease and anaesthesia. Indian J Anaesth 2011;55:228-34.
] [Full text]
Muravchick S, Smith DS. Parkinsonian symptoms during emergence from general anesthesia. Anesthesiology 1995;82:305-7.
Gravlee GP. Succinylcholine-induced hyperkalemia in a patient with Parkinson's disease. Anesth Analg 1980;59:444-6.
Katzenschlager R, Sampaio C, Costa J, Lees A. Anticholinergics for symptomatic management of Parkinson's disease. Cochrane Database Syst Rev 2003;CD003735.
Yarnall A, Rochester L, Burn DJ. The interplay of cholinergic function, attention, and falls in Parkinson's disease. Mov Disord 2011;26:2496-503.
Ujkaj M, Davidoff DA, Seiner SJ, Ellison JM, Harper DG, Forester BP. Safety and efficacy of electroconvulsive therapy for the treatment of agitation and aggression in patients with dementia. Am J Geriatr Psychiatry 2012;20:61-72.
Baruah J, Easby J, Kessell G. Effects of acetylcholinesterase inhibitor therapy for Alzheimer's disease on neuromuscular block. Br J Anaesth 2008;100:420.
Seitz DP, Gill SS, Gruneir A, Austin PC, Anderson G, Reimer CL, et al.
Effects of cholinesterase inhibitors on postoperative outcomes of older adults with dementia undergoing hip fracture surgery. Am J Geriatr Psychiatry 2011;19:803-13.
Pigot M, Andrade C, Loo C. Pharmacological attenuation of electroconvulsive therapy – Induced cognitive deficits: Theoretical background and clinical findings. J ECT 2008;24:57-67.
Prakash J, Kotwal A, Prabhu H. Therapeutic and prophylactic utility of the memory-enhancing drug donepezil hydrochloride on cognition of patients undergoing electroconvulsive therapy: A randomized controlled trial. J ECT 2006;22:163-8.
Matthews JD, Blais M, Park L, Welch C, Baity M, Murakami J, et al.
The impact of galantamine on cognition and mood during electroconvulsive therapy: A pilot study. J Psychiatr Res 2008;42:526-31.
Alizadeh NS, Maroufi A, Jamshidi M, Hassanzadeh K, Gharibi F, Ghaderi E. Effect of memantine on cognitive performance in patients under electroconvulsive therapy: A double-blind randomized clinical trial. Clin Neuropharmacol 2015;38:236-40.
Dolenc TJ, Barnes RD, Hayes DL, Rasmussen KG. Electroconvulsive therapy in patients with cardiac pacemakers and implantable cardioverter defibrillators. Pacing Clin Electrophysiol 2004;27:1257-63.
MacPherson RD, Loo CK, Barrett N. Electroconvulsive therapy in patients with cardiac pacemakers. Anaesth Intensive Care 2006;34:470-4.
Saito S, Kadoi Y, Nara T, Sudo M, Obata H, Morita T, et al.
The comparative effects of propofol versus thiopental on middle cerebral artery blood flow velocity during electroconvulsive therapy. Anesth Analg 2000;91:1531-6.
Robertson H, Pryor R. Memory and cognitive effects of ECT: Informing and assessing patients. Adv Psychiatr Treat 2006;12:228-37.
Teng EL, Chui HC. The modified mini-mental state (3MS) examination. J Clin Psychiatry 1987;48:314-8.
Manna CG, Alterescu K, Borod JC, Bender HA. Benton visual retention test. In: Encyclopedia of Clinical Neuropsychology. New York: Springer; 2011. p. 392-4.
Brannigan GG. Bender Visual-Motor Gestalt Test. New York: John Wiley and Sons, Inc.; 2003.
Brown L, Sherbenou RJ, Johnsen SK. Test of Nonverbal Intelligence: TONI. Austin, TX: PRO-ED; 1982.
Wechsler D. WAIS-IV administration and scoring manual. San Antonio, TX: Psychological Corporation, 2008.
Prigatano GP. Wechsler memory scale: A selective review of the literature. J Clin Psychol 1978;34:816-32.
Nyhus E, Barceló F. The wisconsin card sorting test and the cognitive assessment of prefrontal executive functions: A critical update. Brain Cogn 2009;71:437-51.
Reitan RM. Validity of the trail making test as an indicator of organic brain damage. Percept Mot Skills 1958;8:271-6.
Keith Berg W, Byrd D. The tower of London spatial problem-solving task: Enhancing clinical and research implementation. J Clin Exp Neuropsychol 2002;24:586-604.
Sackeim HA. Autobiographical memory and electroconvulsive therapy: Do not throw out the baby. J ECT 2014;30:177-86.
Kopelman MD. The autobiographical memory interview (AMI) in organic and psychogenic amnesia. Memory 1994;2:211-35.
Viswanath B, Harihara SN, Nahar A, Phutane VH, Taksal A, Thirthalli J, et al.
Battery for ECT related cognitive deficits (B4ECT-ReCoDe): Development and validation. Asian J Psychiatr 2013;6:243-8.
Porter RJ, Douglas K, Knight RG. Monitoring of cognitive effects during a course of electroconvulsive therapy: Recommendations for clinical practice. J ECT 2008;24:25-34.
Huuhka MJ, Seinelä L, Reinikainen P, Leinonen EV. Cardiac arrhythmias induced by ECT in elderly psychiatric patients: Experience with 48-hour Holter monitoring. J ECT 2003;19:22-5.
Tomac TA, Rummans TA, Pileggi TS, Li H. Safety and efficacy of electroconvulsive therapy in patients over age 85. Am J Geriatr Psychiatry 1997;5:126-30.
Pettinati HM, Nilsen SM. Increased incidence of missed seizures during ECT in the elderly male. Convuls Ther 1987;3:26-30.
Rasanen J, Martin DJ, Downs JB, Hodges MR. Oxygen supplementation during electroconvulsive therapy. Br J Anaesth 1988;61:593-7.
Sawayama E, Takahashi M, Inoue A, Nakajima K, Kano A, Sawayama T, et al.
Moderate hyperventilation prolongs electroencephalogram seizure duration of the first electroconvulsive therapy. J ECT 2008;24:195-8.
Stern L, Dannon PN, Hirschmann S, Schriber S, Amytal D, Dolberg OT, et al.
Aminophylline increases seizure length during electroconvulsive therapy. J ECT 1999;15:252-7.
Rasmussen KG, Zorumski CF. Electroconvulsive therapy in patients taking theophylline. J Clin Psychiatry 1993;54:427-31.
Whittaker R, Scott A, Gardner M. The prevalence of prolonged cerebral seizures at the first treatment in a course of electroconvulsive therapy. J ECT 2007;23:11-3.
Fink M. Post-ECT delirium. Convuls Ther 1993;9:326-30.
Cohen MB, Stewart JT. Treatment of post-electroconvulsive therapy agitation with dexmedetomidine. J ECT 2013;29:e23-4.
Logan CJ, Stewart JT. Treatment of post-electroconvulsive therapy delirium and agitation with donepezil. J ECT 2007;23:28-9.
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6]