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Brain stimulation therapies 

Brain stimulation therapies
Brain stimulation therapies

Daniel W. O’Connor

and Chris Plakiotis

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Electroconvulsive therapy, transcranial magnetic stimulation, and deep brain stimulation all entail the delivery of electrical energy, either episodically or continuously, to the brain with the object of relieving mental or neurological symptoms. This chapter discusses their indications, application, effectiveness, and safety with respect to depression and other psychiatric conditions. Because the latter two treatments are relatively novel, the bulk of this chapter is devoted to electroconvulsive therapy.

Electroconvulsive Therapy

Electroconvulsive therapy (ECT) is an effective treatment of severe depression, mania, catatonia, and some cases of schizophrenia. It is important, therefore, that old age psychiatrists have a good understanding of its uses, benefits, and risks. Most researchers have failed to distinguish between older and younger patients in their reports and so much of the evidence presented in this chapter is generic in nature and readers must apply the information as best they can to their own practice.

ECT’s mechanisms of action are still poorly understood. It induces the release of prolactin, oxytocin, and other hormones related to the hypothalamic-pituitary axis; it boosts cerebral blood flow and metabolism, particularly in frontal and anterior temporal areas; and it stimulates neurogenesis in animal models (McCormick et al., 2007; Bolwig, 2011). Contrary to expectation, ECT has no proven, consistent links with changes in the production, reuptake, and metabolism of the neurotransmitters serotonin and noradrenaline, which explains perhaps its benefits in patients resistant to pharmacotherapy (Grover et al., 2005).

Patterns of use

ECT declined in use in most countries from the 1970s onwards, due to the advent of effective antidepressant and antipsychotic medications and to its depiction in popular media as a tool to control aberrant behaviour. Few countries or regions publish complete datasets, but, judging from the number of research publications, ECT and other brain stimulation therapies are in the ascendancy.

ECT is prescribed more to older people than younger ones in Australia (Plakiotis et al., 2012), Denmark (Munk-Olsen et al., 2006), the US (Olfson et al., 1998), and probably most other countries. In Victoria, Australia, where data from all public and private hospitals are collated systematically, applications rose steeply with age until 85 years (Plakiotis et al., 2012) (Fig. 14.1). Likely reasons include an age-related intolerance of antidepressant and antipsychotic medications coupled with an increase with age in depressive psychomotor retardation and psychosis, both of which predict a good response to ECT. It might also reflect a view by psychiatrists that severely depressed old people benefit more from medically oriented therapies. It is conceivable, therefore, that treatment patterns will change yet again now that medications are safer and the role of psychotherapy is expanding.

Fig. 14.1 ECT application rates per 100,000 for age- and sex-specific populations in 2007, Victoria, Australia (Reproduced with permission from Plakiotis, C., George, K. and O’Connor, D.W. (2012). Has ECT utilisation remained stable over time? A decade of ECT service provision in Victoria, Australia. Australian and New Zealand Journal of Psychiatry. © Wiley 2012).

Fig. 14.1
ECT application rates per 100,000 for age- and sex-specific populations in 2007, Victoria, Australia (Reproduced with permission from Plakiotis, C., George, K. and O’Connor, D.W. (2012). Has ECT utilisation remained stable over time? A decade of ECT service provision in Victoria, Australia. Australian and New Zealand Journal of Psychiatry. © Wiley 2012).

Does ECT work?


A series of randomized controlled trials in the 1970s and 1980s established that real ECT was superior to sham ‘treatments’ that entailed an anaesthetic but no electrical stimulation. In a meta-analysis of these studies, depressed patients given real ECT progressed faster and scored 9.7 fewer points on the 64-point Hamilton Depression Rating Scale (HDRS) 2–4 weeks later (UK ECT Review Group, 2003).

ECT also proved superior to a range of older and newer antidepressants over periods of 3–12 weeks in all but two of the13 studies summarized by the UK ECT Review Group (2003). This difference in response translated to 5.2 fewer points on the HDRS. In one of the largest trials, 66% of patients given ECT had no or few symptoms after 4 weeks compared with 42% of those on imipramine 200 mg daily (Medical Research Council, 1965).

ECT can certainly work quickly and effectively when administered by skilled clinicians to carefully selected patients. In a large, prospective North American study of suprathreshold bilateral ECT, 75% of patients had remitted after seven sessions as shown by scores of 10 or less on the HDRS (Husain et al., 2004). The same might not apply, though, when patients with complex, chronic conditions are treated in mainstream facilities using suboptimal methods. As an example, in a survey of hospitals in New York state where treatment practices varied widely, HDRS scores fell below 10 points in only 47% of all cases. To make matters worse, 40% of accrued improvement was lost within 10 days and relapse rates ranged from 46% to 79% across sites (Prudic et al., 2004).

There have been remarkably few prospective controlled studies of ECT in older people. When O’Leary et al. (1994) extracted data from a larger study regarding its 35 aged subjects, their scores on the HDRS fell 31.7 points on average after six real ECTs versus 10.3 with sham ones. Bilateral ECT worked a little better and faster than unilateral treatment. Similarly, Flint and Rifat (1998) found in an open, nonrandom trial that 88% of aged patients with depressive psychoses responded positively to ECT within 6 weeks compared with 25% of those treated with adequate doses of nortriptyline and perphenazine. HDRS scores fell to 10 or less 3 weeks sooner with ECT than medication.

Most other reports describe series of depressed psychogeriatric in-patients. In the four largest series, outcomes were mostly positive. Benbow (1987) discharged 52% of patients as ‘well’ and another 28% as ‘improved’, while Godber et al. (1987) found that 74% of patients made a ‘full recovery’ or were ‘much improved’. In a report by Tew et al. (1999), 41% of their ‘oldest-old’ patients made a complete recovery, as did 39% of those described by Brodaty et al. (2000).

Response predictors

Older patients responded better to ECT than younger ones in some studies (Wilkinson et al., 1993; O’Connor et al., 2001) but not in others (Hickie et al., 1996; Birkenhäger et al., 2010). Outcome correlates better with depressive psychosis and melancholia, especially as reflected by objective signs of psychomotor agitation and retardation, than with age per se. Depressed patients with psychotic symptoms scored 5.9 points less on average on the HDRS than nonpsychotic patients after treatment by Mulsant et al. (1991) and 8% fewer points after treatment by Petrides et al. (2001). The combination of psychotic symptoms with observable psychomotor change has even stronger predictive capacity. Deluded-retarded cases in one placebo-controlled trial lost 34.7 points on the HDRS in contrast to 16.2 in the retarded, nondeluded group and 10.7 in the nonretarded, nondeluded group (Buchan et al., 1992).

Certain factors reduce, but do not preclude, the likelihood of responding to ECT. These include chronicity and resistance to antidepressant medications (Dombrovski et al., 2005); subcortical hyperintensities (Steffens et al.,, 2001); medial temporal lobe atrophy (Oudega et al., 2011); and personality disorder (Black et al., 1988).

Dementia and other organic mental disorders

Two-thirds of the British old age psychiatrists surveyed by Benbow (1991) agreed that ECT was ‘often or sometimes’ appropriate when depression overlaid on dementia failed to respond to antidepressant medication. Published reports are favourable with improvement rates, however defined, of up to 80% in cases of depression comorbid with Alzheimer’s disease, vascular dementia, Lewy body dementia, and frontotemporal dementia (Price and McAllister, 1989; Rao and Lyketsos, 2000; Rasmussen et al., 2003). These reports take the form of small, retrospective case series that are subject to bias: positive reports are more likely to be published than negative ones. To counter this, Nelson and Rosenberg (1991) compared 21 consecutive patients with dementia and comorbid major depression with 84 similarly aged nondemented ones. The dementia group derived almost as much benefit from ECT. While confusion post-ECT was more common and correlated with the degree of dementia, mini-mental state examination (MMSE) scores actually improved on average by 1.6 points. Confusion complicated ECT in half the cases described by Rao and Lyketsos (2000) but it lasted only a few days and treatments continued uneventfully. Few reports provide follow-up data, though in one, relapse rates were high (Rasmussen et al., 2003). With respect to mania in dementia, McDonald and Thompson (2001) described two patients who responded well to ECT in the short term but required ongoing treatment to hold symptoms at bay.

ECT is not a standard treatment of the disturbed behaviours like screaming and aggression that arise in mid- to late-stage dementia, except where patients have comorbid depression and fail to respond to antidepressant medication. Notwithstanding this, there are detailed reports of patients who were not obviously depressed but benefited greatly from ECT (Carlyle et al., 1991; Holmberg et al., 1996; Grant and Mohan, 2001; Bang et al., 2008; Sutor and Rasmussen, 2008). Their disturbed behaviours, which posed serious risk to themselves and others, resolved quickly, but about half required maintenance treatments.

ECT can also be delivered safely and effectively to patients with mental disorders secondary to stroke (Currier et al., 1992), Huntington’s disease (Ranen et al., 1994), head injury (Kant et al., 1999), and intellectual disability (van Waarde et al., 2001), though relapse rates tend to be high.

Schizophrenia, mania, and catatonia

All major clinical guidelines accept acute schizophrenia, schizoaffective disorder, mania, and catatonia as possible indications for ECT (American Psychiatric Association, 2001; Royal College of Psychiatrists, 2005; Royal Australian and New Zealand College of Psychiatrists, 2007).

The use of ECT in acute schizophrenia plummeted once antipsychotic medications became available in the 1950s. ECT works a little faster than antipsychotics and is just as effective in reducing psychotic symptoms (Abraham and Kulhara, 1987), but medications are simpler to administer on a long-term basis and are preferred by most patients. Despite recent advances, there remain patients who do not respond to medications, cannot tolerate them, or require urgent intervention to prevent self-injury. Naturalistic studies suggest, but do not prove, that half or more of those who failed to benefit from standard medications improved substantially once ECT was added. ECT responders had fewer negative symptoms and had been unwell for shorter periods than nonresponders (Chanpattana and Andrade, 2006). Old age need not be a barrier to recovery. Kramer (1999) described five women aged 58–74 years whose florid schizophrenia or schizoaffective disorders improved dramatically with ECT. Against this, all of six aged patients with late-onset schizophrenia reported by Figiel et al. (1992) became confused after ECT and none showed symptomatic improvement.

In cases of mania, ECT performs as well or better than standard pharmacotherapy (Loo et al., 2011; Versiani et al., 2011). There is little information regarding older patients specifically, but clinical experience suggests that those who cannot tolerate antipsychotic or mood stabilizing medications, or are so manic that they look to be delirious, respond best to ECT. Only small numbers of treatments may be required, even in life-threatening cases of ‘delirious mania’ (Karmacharya et al., 2008).

Catatonia is now uncommon, but it arises occasionally in schizophrenia, depression, mania, and organic conditions including brain tumour, head trauma, stroke, encephalitis, and metabolic disturbance with any or all of the following signs: mutism, negativism, echolalia, echopraxia, muscle rigidity, posturing, and waxy flexibility. Its severest form, lethal catatonia, is associated with extreme agitation, stupor, fever, sweating, and autonomic instability, leading to dehydration, exhaustion, and death if left untreated. It must be distinguished from neuroleptic malignant syndrome and malignant hyperthermia by means of a reliable medication history. ECT proved effective in 60% of cases after an average of 15 treatments (van Waarde et al., 2010a), though maintenance therapy may be required to prevent relapse (Wilkins et al., 2008).

Other conditions

ECT can improve tremor, rigidity, bradykinesia, and gait in Parkinson’s disease for periods of several weeks but is rarely used for this indication (Kennedy et al., 2003). It is of greater benefit in neuroleptic malignant syndrome, a condition that overlaps in form with catatonia and is precipitated by antipsychotic medication. Patients who fail to respond to supportive therapy, benzodiazepines, and dopamine agonists, or whose lives are in danger, may benefit from a brief course of ECT. Care is required, however, since patients are often medically unstable and require constant monitoring (Troller and Sachdev, 1999).

Relapse and maintenance therapy

Relapse is common in the period following ECT. In a study by Sackeim et al. (2001), patients whose major depression remitted successfully with ECT were randomly assigned to receive placebo, nortriptyline, or a combination of nortriptyline and lithium carbonate. Over the ensuing 24 weeks, 84% of those on no continuing medication had relapsed, compared with 60% in the nortriptyline group and 39% of those on combination therapy. Relapse was more common in patients who had failed to respond to previous pharmacotherapy. In one naturalistic outcome study, relapse rates were higher in cases of psychotic depression (31% versus 22%), comorbid psychiatric disorder (43% versus 27%), and personality disorder (23% versus 14%). Relapse occurred most often within the first 12 weeks of follow-up (Prudic et al., 2004).

It is now standard practice to introduce an antidepressant medication, either alone or together with an antipsychotic or mood stabilizer, during the ECT course or soon afterwards (Haskett and Loo, 2010). Where this is known to be ineffective or unsafe, continuing or maintenance ECT is an option. Continuation therapy (C-ECT) follows directly from an acute course of ECT with the object of preventing relapse. Treatment intervals are typically stretched from weekly to monthly depending on progress. Maintenance ECT (M-ECT) refers somewhat arbitrarily to treatments extending beyond 6 months, and occasionally for years, where the risk of relapse is known to be high (Fink et al., 1996). Intervals between treatments are typically extended until breakthrough symptoms provide clues to the optimal schedule. More recently, Lisanby et al. (2008) devised a treatment algorithm based on patients’ depression rating scores to bring some rigor to this process.

In a retrospective chart review of 58 aged patients with severe, medication-resistant depression or psychosis, hospital readmissions fell by 53% in number and 79% in duration in the 2 years after M-ECT started compared with the previous 2 years (O’Connor et al., 2010a). Within the actual M-ECT treatment period, which varied widely, admissions fell by 90% in number and 97% in duration compared with the same time beforehand. Similar findings emerged in earlier reviews of adult patients (Petrides et al., 2011). M-ECT has also been used to limit relapse in bipolar disorder and schizophrenia (Vanelle et al., 1994; Chanpattana et al., 1999).

The National Institute for Health and Clinical Excellence (2003), in a review of ECT, concluded that maintenance therapy could not be recommended on the grounds that its longer-term benefits and risks had yet to be established. While case reports are subject to publication bias and lack the authority of controlled trials, painstaking clinical histories are still persuasive. M-ECT looks to be safe and there is no evidence of progressive cognitive impairment (Rami et al., 2004), even in a patient who received 430 treatments over an 8-year period (Barnes et al., 1997).

Since M-ECT is usually delivered on an outpatient basis, patients must be cooperative, medically stable, and conversant with practical requirements. Processes must also be in place to conduct physical and mental state checks at predetermined intervals, to gauge the intervals between treatments, and to decide when treatment ends (O’Connor et al., 2010b).



The ideal anaesthetic induction agent ensures rapid, painless unconsciousness, an adequate seizure, and speedy recovery with minimal post-ECT confusion. Methohexital has a rapid onset, short duration of action and no anticonvulsant properties. By contrast, propofol is sometimes painful on injection and raises seizure thresholds, though not to a significant degree in usual doses. Its major advantage is that pulse rate, blood pressure, and heart rhythm are a little more stable (Hooten and Rasmussen, 2008). Other agents include alfentanil, remifentanil, etomidate, ketamine, and sevoflurane. Differences between them with respect to ECT practice are unclear (Hooten and Rasmussen, 2008). Little available information refers specifically to older people.

Muscle relaxants like succinylcholine virtually eliminate the risk of fractures during ECT, though two cases of vertebral compression fractures were reported by Mulsant et al. (1991) in patients known to be osteoporotic. Doses of relaxant can be increased if desired in these situations. There is no uniform view on the routine use of anticholinergics (usually atropine or glycopyrrolate) just prior to treatment to reduce salivation and bradycardia. Most centres now use them selectively, given the increased risks of tachycardia due to unopposed sympathetic activity, myocardial ischaemia, and post-ECT confusion (Mondimore et al., 1983).

Seizure threshold

Tonic-clonic seizures are critical to ECT’s success (Cronholm and Ottoson, 1960) and the electrical charge must therefore exceed seizure threshold to ensure that a convulsion ensues. Thresholds can vary tenfold or more between patients but lie mostly between 20 and 100 millicoulombs (mC)(Sackeim et al., 1987). Increasing age, male gender, and bilateral electrode placement all predict higher initial thresholds (Sackeim et al., 1987; van Waarde and van der Mast, 2010b). Men prescribed bilateral ECT will therefore have higher mean thresholds than women prescribed unilateral ECT.

Electrical charge is not critical in itself. What matters more is that energy levels exceed threshold by a defined amount. Bilateral ECT is effective at, or just above, seizure threshold. Unilateral ECT is not, as shown in a critical study by Sackeim et al. (2000) in which ‘low dose’ unilateral treatment (50% above threshold) was much less effective than ‘high dose’ unilateral treatment (500% above threshold). ‘Moderate dose’ ECT (150% above threshold) occupied an intermediate position. ‘High dose’ unilateral ECT worked almost as well as bilateral ECT (50% above threshold) in lifting depressive symptoms (Figure 14.2).

Fig. 14.2 Hamilton Depression Rating Scale scores for patients treated with high and low energy, unilateral and bilateral ECT (Sackeim et al., 2000).

Fig. 14.2
Hamilton Depression Rating Scale scores for patients treated with high and low energy, unilateral and bilateral ECT (Sackeim et al., 2000).

Stimulus dosing

In former times, the same electrical dose was given to every patient. There is no place for this now: treatments are individualized to maximize efficacy and reduce side effects. There is debate, however, about how best to achieve this. One approach, called stimulus dose titration, entails giving one or more stimulations in the first session to ascertain threshold. One widely used protocol recommends that, for women receiving unilateral ECT, electrical charge is delivered at 32 mC, 48 mC, and then 80 mC until a convulsion is provoked. Once threshold is established, a therapeutic stimulus is delivered at between three times and six times this level, depending on local practice. A ‘multiplier’ of three is recommended by the Royal Australian and New Zealand College of Psychiatrists (2007). Other authorities are less specific (Royal College of Psychiatrists, 1995; American Psychiatric Association, 2001). For bilateral ECT, the ‘multiplier’ is typically one and a half times threshold.

In experienced hands, stimulus titration takes just a few minutes to complete. Inexpert clinicians are less sure-handed, resulting in longer anaesthesia and slower recovery. There is also a risk that repeated subconvulsive stimulations will precipitate cardiac arrhythmias. This certainly happened in the 1940s and 1950s but is rarely seen now (McCall et al., 1994). There is no evidence that subconvulsive stimulation causes more cognitive impairment (Prudic et al., 1994).

Age-based dosing strategies are simpler, faster, and possibly safer for very old, frail patients. According to one formula for unilateral ECT, doses for patients aged 60, 70, and 80 years are about 300 mC, 350 mC, and 400 mC respectively. Doses for bilateral ECT are half these. While not as individualized as stimulation titration, it works well enough in most instances. According to Tiller and Ingram (2006), age-based dosing led to only 2% of their women patients and 7% of men receiving subtherapeutic doses. Against this, doses would have been too high, at seven or more times threshold, for 30% of women and 8% of men. In addition, if treatment is not progressing well, it is harder to take sensible corrective action if threshold is not known. It is advisable therefore to establish threshold, unless there are good reasons not to do so.

Seizure monitoring

Threshold levels tend to rise as treatment progresses, more for bilateral than unilateral ECT, and electrical charge must be increased to keep pace if this happens (Sackeim et al., 1987). It is not practicable to recheck patients’ thresholds week after week. Instead, clinicians make judgements based on EEG monitoring of seizure duration and morphology. This is an imprecise science. ECT machines now produce measures of seizure duration, amplitude, interhemispheric synchronicity, and postseizure electrical suppression, but none of this information can be interpreted exactly.

Greater seizure intensity, regularity and postseizure suppression correlate with better outcomes (Plakiotis and O’Connor, 2011), but what is cause and what is effect is not clear: patients who respond well to ECT may possess this sort of profile from the outset (Nobler et al., 1993; Perera et al., 2004). A good ‘electrical picture’ might therefore predict recovery, not cause it. To complicate matters, older people typically have shorter, weaker, and less synchronous seizures, irrespective of clinical outcome, and their thresholds rise faster as treatment progresses (Nobler et al., 1993). In the absence of clear evidence, it seems reasonable to increase electrical charge by 50 mC at a step if seizures become obviously shorter and weaker. Clinicians will naturally differ to some extent in how they interpret technical parameters (Little et al., 2002).

Treatment variants

Efforts continue to find ways to boost treatment efficacy while minimizing adverse effects. One alternative to the standard bilateral (actually bitemporal) approach is bifrontal ECT in which the electrodes are placed 3–5 cm above the outer angle of both orbits. In a recent trial, bitemporal ECT worked a little faster, but the two placements were otherwise indistinguishable (Kellner et al., 2010).

In another approach, the standard electrical square wave stimulus is shortened from a pulse width of 0.5–2 milliseconds (ms) to an ultrabrief pulse of 0.3 ms, with the object of depolarizing neurons and stimulating seizures, at lower electrical doses. Unilateral ultrabrief ECT is certainly effective and is associated with significantly fewer cognitive sequelae than standard unilateral ECT (Sackeim et al., 2008), but response is slower and more treatments are required (Loo et al., 2008). Counterintuitively, bilateral ultrabrief stimuli are strikingly less effective than unilateral ultrabrief stimuli (Sackeim et al., 2008).

Some patients have very brief or low-amplitude seizures, and poor clinical outcomes, even at maximal electrical stimulation. Efforts to lengthen and optimize seizures have included hyperoxygenation, pretreatment with oral or intravenous xanthine alkaloids (caffeine, theophylline, aminophylline), and the addition of short-acting opioids (alfentanil, remifentanil) to the induction agent. None of these strategies has been subject to rigorous study and xanthine alkaloids can lead to prolonged seizures, tachycardia, and cardiac arrhythmias (Loo et al., 2010).

With respect to frequency, ECT is traditionally administered three times a week, but twice weekly treatments are just as effective (Charlson et al., 2012), require no more treatments in total, and cause less cognitive impairment (Shapira et al., 1998). Barring life-threatening cases, there is no benefit in administering ECT more often.

Concomitant medications

Benzodiazepines raise seizure thresholds and should therefore be avoided, reduced, or stopped if possible (Pettinati et al., 1990), but modest doses (e.g. lorazepam up to 3 mg daily) have little impact in reality (Boylan et al., 2000) and are permitted in most ECT research trials to lessen anxiety and agitation. Mood stabilizers that are also anticonvulsants (e.g. carbamazepine and valproate) should also be stopped if possible.

Medications with anticholinergic properties have been linked with worsened cognition post-ECT, especially when taken in combination. Mondimore et al. (1983) found that eight of their 12 patients with high serum anticholinergic levels lost two or more points on the MMSE after a single ECT compared with only one of eight patients with lower anticholinergic levels. Tricyclic antidepressants, some antipsychotics, and even lithium carbonate all have discernable anticholinergic activity, as do some analgesics, antihistamines, and antispasmodics (Chew et al., 2008).

Lithium might be hazardous too when combined with ECT, given occasional reports of severe confusion, prolonged seizures, and catatonia, even with ‘normal’ blood levels (Sartorius et al., 2005). By way of confirmation, rates of confusion were higher at 22% in 27 patients given lithium and ECT concurrently, compared with 12% in those whose lithium was stopped just prior to ECT, and 6% in those with no exposure (Penney et al., 1990). Against this, Dolenc and Rasmussen (2005) cite reports in which lithium and ECT were combined safely. Though the risk of serious mishap is slight, lithium should be stopped before starting ECT.


ECT is generally very safe. In the US, there were no deaths related to the 73,440 treatments administered to Veterans Affairs patients in 1999–2010, placing the risk of ECT at the bottom of the range for procedures entailing general anaesthesia (Abrams, 1997; Watts et al., 2011). This is not because treatment is reserved for physically fit patients. The reverse is often the case. ECT is given quite commonly to patients with serious medical comorbidities compounded by dehydration, inanition, and exhaustion secondary to depression or psychosis. It might actually be safer than psychiatric medications in such circumstances. In a chart review by Zielinski et al. (1993), 11 of 21 patients with cardiac disease were forced to discontinue treatment with tricyclic antidepressants because of cardiovascular complications compared with only two of 40 similar patients given ECT. Similarly, rates of cardiovascular and gastrointestinal adverse events were more common in 39 very old medically treated depressives compared with 39 carefully matched patients treated with ECT. Their rates of hypertension, myocardial infarction, and heart failure were virtually identical (Manly et al., 2000). There are risks, however, as the following sections make clear.

Cardiovascular effects

ECT exerts its effect on the heart principally by direct neuronal transmission of impulses from the hypothalamus to the heart via parasympathetic and sympathetic tracts. During and immediately after electrical stimulation, an intense parasympathetic surge flows through the vagal nerve to the heart, resulting in a transient sinus bradycardia, with periods of asystole lasting for 2 s on average but occasionally for 5 s or more (Burd and Kettl, 1998). A sympathetic surge then follows, leading to an average rise in blood pressure of 55 mmHg, and in pulse rate of 37 beats per minute, together with clinically benign premature atrial and ventricular contractions. Rare complications at this time include acute myocardial infarction and ventricular fibrillation (Burd and Kettl, 1998). Pulse rates and blood pressure both rise more during bilateral than unilateral ECT, and more with higher than lower energy levels (Gangadhar et al., 2000). Cardiac function usually returns to normal within 15 min, but ST changes and bursts of bigeminy or trigeminy are a little more common than usual in the following 24 h (Huuhka et al., 2003).

Frequency and severity of adverse events

Aged patients are at higher risk of adverse events. In a report by Burke et al. (1987), 15% of their patients aged 60 years and over experienced a cardiorespiratory complication (mostly changes in blood pressure) compared with 3% of younger patients, and 15% sustained a fall versus none in the younger group. Rates of post-ECT confusion were 18% and 13%, respectively. Altogether, 35% of older patients had a complication, but most were transient and settled spontaneously. Side effects also rose with age in a chart review by Alexopoulos et al. (1984). Cardiovascular complications arose in 19% of their patients aged 65 years and over versus 1% of younger patients, and 14% had neurological complications (mostly confusion) compared with 12%. Apart from an 87-year-old man who died of a myocardial infarction 48 h after his second treatment, most patients went on to complete their course.

Octogenarians were found by Cattan et al. (1990) to have adverse events roughly twice as often as ‘younger old’ patients. Cardiovascular complications and falls were both more frequent in very old patients than younger ones at 36% versus 12%, and 36% versus 14%, respectively. Confusion was the commonest problem, arising in 59% and 45% of the two groups. Outcomes were more benign in the patients aged 75 years and over described by Gormley et al. (1998), of whom 7% suffered prolonged confusion and 4% became manic. All problems resolved within 2 weeks. Similarly, 32% of the patients aged 85 years and over of Tomac et al. (1997) experienced prolonged confusion and 10% fell. One of the 34 patients sustained a fracture between treatments and six died of causes unrelated to ECT within 45 days after the last treatment, attesting to their very high rates of physical comorbidity.

Other uncommon side effects include dental injury, fractures secondary to falls (de Carle and Kohn, 2001), and vertebral compression fractures due to poorly modified seizures (Mulsant et al., 1991). Very rare sequelae include stroke (Bruce et al.,, 2006 and status epilepticus (Srzich and Turbott, 2000). Note that neurological asymmetries are common after ECT but generally resolve within 20 min (Kriss et al., 1978).

Prevention and management

Contraindications to ECT include recent myocardial infarction and stroke, severe valvular heart disease, clinically significant arrhythmias, unstable angina, uncompensated cardiac failure, and cardiac and arterial aneurysms, but these rules are not absolute. Patients who refuse to eat or drink or take essential medications might respond better to ECT than other treatments after a detailed evaluation of their mental and physical health (American Psychiatric Association, 2001; Royal College of Psychiatrists, 2005). ECT has been applied safely and effectively in patients with recent myocardial infarction (Magid et al., 2005), cardiomyopathy (Adabag et al., 2008), aortic aneurysm (Mueller et al., 2009), pulmonary embolism (Suzuki et al., 2008), and cerebral aneurysms and angiomas (Kang and Passmore, 2004).

Examples of the strategies required to minimize risk in medically compromised patients are described by Tess and Smetana (2009). These include pretreatment with atropine or glycopyrrolate to prevent bradycardia (though atropine may worsen post-ECT confusion); pretreatment with betablockers to limit hypertension and tachycardia (though unopposed parasympathetic activity can worsen bradycardia); reductions in anticoagulant therapy for patients with an intracranial mass or aneurysm; and additional muscle relaxation for those with fractures or marked osteoporosis. A careful physical examination, ECG, measures of renal function, and detailed discussions with medical and anaesthetic colleagues are vital. Other laboratory and imaging results add little extra information (Lafferty et al., 2001). Implanted cardiac pacemakers present no special risk (Dolenc et al., 2004).


Objective changes

No evidence has emerged from numerous anatomical and imaging studies that ECT causes altered brain structure, neuronal death, or cerebral atrophy (Devanand et al., 1994; Ende et al., 2000). There is no doubt, however, that ECT can result in objective cognitive disruption. Patients are sometimes confused and disoriented on wakening from anaesthesia. This typically lasts just for a few minutes but extends occasionally for hours and rarely for several days. Risk factors for emergent confusion include bilateral electrode placement (Sackeim et al., 1993); high electrical dose relative to threshold (Sackeim et al., 1993); a sinusoidal waveform (Daniel and Crovitz, 1986); advanced age (Tomac et al., 1997); pre-existing dementia (Rao and Lyketsos, 2000); and concomitant anticholinergic medications (Mondimore et al., 1983).

Most studies show some reduction in the acquisition and retention of new verbal and nonverbal material (anterograde memory) over the course of a treatment cycle. Improvement starts within a few days of treatment completion, more quickly for information acquisition than retention, and continues for up to 6 months. Recall of past events (retrograde memory) is affected too, especially for personal or autobiographical memories, and for recent events more than distant ones (Ingram et al., 2008). Autobiographical memory is difficult to measure in a standardized way and so the nature, extent, and duration of lapses is unclear. Knowledge of events in the days or weeks prior to treatment may never be recovered, however, extending in some cases to a more than a year beforehand (Ingram et al., 2008).

Risk factors for anterograde and retrograde amnesia include bilateral electrode placement (Sackeim et al., 2000), high electrical dose relative to threshold (Sackeim et al.,, 2000), advanced age (Zervas et al., 1993), and limited education (Legendre et al., 2003). Impaired cognition at baseline and prolonged disorientation after treatment also increase the risk of retrograde amnesia (Sobin et al., 1995). Other possible factors include substance abuse, cardiac disease, and neurological disorders (Sackeim, 2000).

Remarkably few studies have focused on old people, despite their higher rates of premorbid cognitive impairment, and most were small and of poor quality. Post-treatment confusion is certainly more common and cognition typically declines as treatment progresses, more for bilateral than unilateral ECT (O’Connor et al., 2010c), but recovery is usually rapid (Russ et al., 1990; Rubin et al., 1993). Published reports may not be fully representative of clinical experience, however, since many severely depressed patients cannot participate in cognitive testing or consent to research. The patients who are most vulnerable to cognitive side effects might therefore be excluded from study (Gardner and O’Connor, 2008).

In the longer term, some cases of dementia must be expected in older age groups because of the established links between depression, on the one hand, and incipient cerebrovascular and Alzheimer’s diseases, on the other. While rates look high at 14% in the patients aged 65+ years who were followed for 3 years by Godber et al. (1987) and 36% in those aged 75+ years followed for 5 years by Brodaty et al. (2000), there is no reason to believe that ECT plays a causative role.

Clinical guidelines highlight the need for cognitive assessment before, during, and after an ECT course but leave the choice of tests to the clinician (American Psychiatric Association, 2001; Royal College of Psychiatrists, 2005). Porter et al. (2008) proposed using the MMSE as a baseline measure and checking reorientation in the recovery room after every treatment. Later, they recommend a brief test of verbal learning after every third treatment together with an abbreviated autobiographical memory questionnaire after every sixth treatment. All these tests can be administered by a trained ECT nurse coordinator.

Cognitive impairment is prevented or minimized by administering unilateral ECT in the first instance, titrating stimulus intensity, prescribing only two treatments each week, and limiting the number of treatments in a course, subject to clinical progress (Prudic, 2008).

Subjective reports

While complaints of poor memory subside as depression remits (McCall et al., 1995; Coleman et al., 1996), between 29% and 88% of patients describe some persistent forgetfulness in coming weeks and months (Brodaty et al., 2001; Rose et al., 2003; Philpot et al., 2004). Gaps in memory of the 6 months before treatment and the 2 months afterwards are common and mostly well tolerated (Freeman et al., 1980). Of more concern to patients are ‘holes’ in past memories and difficulties with remembering faces, names, and lists (Freeman et al., 1980). Risk factors for subjective deficits include bilateral electrode placement and high electrical charge (Squire and Slater, 1983; Coleman et al., 1996).

Mood plays a role too. Patients whose depression persists despite treatment tend to report greater memory difficulties and to perceive ECT more negatively (Freeman and Kendall, 1980; Coleman et al., 1996). This is not surprising: mood correlates strongly with self-rated memory, even in community populations (O’Connor et al., 1990).

Self-perceived cognitive changes, when assessed using standard questionnaires, are only weakly associated with scores on objective tests, perhaps because the questionnaires fail to tap patients’ personal memories. In fact, responses to a single, general question about memory changes correlate quite well with objective performance, suggesting that complaints have real validity (Brakemeier et al., 2011).

Previously, psychiatrists tended to blame complaints on patients’ ongoing psychopathology, their loss of self-efficacy, or excessive concern with normal cognitive changes (Prudic et al., 2000). Others were more circumspect. Freeman et al. (1980) noted that ECT ‘complainers’ were only fractionally more depressed on mood rating scales than ‘noncomplainers’. Following from this, and from the observation that the temporal gradient in complaints fitted better with ECT than depression as causative agent, Sackeim (2000) concluded that ‘attributing these subjective deficits to ongoing psychopathology or natural disease progression would seem disingenuous and defensive’. An account by one patient is especially compelling. Donahue (2000) wrote that ECT (initially unilateral and then bilateral) saved her from suicide. She felt grateful to be alive and would have ECT again if necessary, but whole chunks of her life had been lost—a price she accepted but could not deny.

Ethical issues

For patients with the capacity to consent, ECT should be administered only with their agreement. Consent must be voluntary, based on an adequate explanation of the nature of ECT, its practical implications and side effects, tailored to individual circumstances. Patients bothered by cardiac symptoms, for example, need more detailed information about cardiovascular sequelae. Verbal discussion is best supplemented by an informational brochure that patients and families can digest at leisure, modelled perhaps on the exemplary document prepared by the American Psychiatric Association (2001). Moderately depressed, cognitively intact older patients absorb and retain this sort of information quite adequately (Lapid et al., 2004). A visit to the ECT treatment suite to explain its procedures and equipment can allay patients’ and relatives’ concerns.

Clinicians will naturally advocate for ECT when its use is warranted. There is a fine line, however, between persuasion and coercion. Patients’ apprehension typically settles with appropriate reassurance and factual responses to questions, but doctors and patients sometimes perceive this process differently (McCall, 2006). In a review of 17 reports by Rose et al. (2003), only half the respondents believed they had been given an adequate explanation of ECT and most had limited knowledge of actual procedures. Patients sometimes recounted giving ‘consent’ while heavily sedated or threatened by legal compulsion. These recollections might sometimes be inaccurate, but small numbers of patients are left traumatized as a result. An account by Johnstone (1999) of the perceptions of shame and despair by 20 aggrieved ECT recipients is required reading.

Some of the patients most likely to benefit from ECT are unable to consent by virtue of marked depression or psychosis. Pointers to lack of capacity include: an inability or refusal to speak; a rejection of general nursing and medical care; rapid forgetting of basic information about the nature and consequences of ECT; and marked ambivalence. Treatment can be applied in most jurisdictions on an involuntary basis with review by a court or tribunal. It is important to document the reasons for mandating ECT; the pros and cons of alternative treatments; patients’ mental state and capacity to make informed decisions; and family viewpoints. Except in emergencies, second opinions are encouraged. The limited research conducted to date suggests that nonconsenting patients often rate their outcome as satisfactory (Wheeldon et al., 1999). Patients who accept ECT passively but cannot contribute to the decision-making process are best treated involuntarily to ensure legal oversight and protection (Law-Min and Stephens, 2006).

ECT typically entails a series of treatments over a period of weeks. Mental capacity will often improve as depression or psychosis abate, with the result that noncompetent patients become competent and can participate in the decision to continue with treatment. Conversely, a patient made confused by ECT may lose competence for a period of time. Ethical practice requires a constant monitoring of patients’ mental states, attitudes to ECT, and decisional capacity. Repeated explanations of the reasons for administering ECT and its likely benefits and side effects may be required if patients fail to recall initial discussions.

Attitudes to ECT

Patients’ views

Fear of ECT is widespread. In a survey of 56 Australian hospital visitors, none of whom had received ECT, many agreed that it ablated memory and rendered patients zombies (Kerr et al., 1982). Psychiatrists attribute this fear to misinformation spread by popular movies and certain lobby groups, but, in reality, a dread of electricity is instilled in children from an early age.

Malcolm (1989) detailed the concerns expressed by 100 patients prior to ECT. Their fears included brain damage, memory loss, pain, being seen by strangers while unconscious, having a heart attack, and developing epilepsy. Their knowledge of ECT was rudimentary: only 16% knew that a convulsion was induced and many expected a single treatment. Older people were more stoical: 52% denied fear compared with 30% of younger ones. When the same patients were asked later what aspects most perturbed them, they nominated waiting for treatment, seeing equipment laid out, hearing staff talk in the background, breathing into an anaesthetic mask, and waking up afterwards.

In a retrospective survey, only 6% of 70 British patients rated ECT as much worse than a visit to the dentist (Benbow and Crentsil, 2004). By contrast, 7% of Australian patients said that they dreaded it and another 12% found it frightening (Kerr et al., 1982). Occasionally patients develop an overwhelming horror of ECT, usually after lengthy or repeated courses (Fox, 1993).

Not all patients are negatively disposed. A psychiatrist who received ECT himself described a lifting of mood after the first treatment. Side effects—nausea, stiffness of the jaw, topographic disorientation, and mild memory loss—were a small price to pay in his view (A Practising Psychiatrist, 1965). Another patient, while grateful for treatment, described the stigma and inconvenience of maintenance ECT (Hensley, 2008).

Patients’ views are coloured in part by their mental status. Depression brings with it fears of therapeutic nihilism. As these fears remit with treatment, opinions of ECT may become more positive (Chakrabarti et al., 2010). Favourable views post-ECT correlate with severity of mental disorder and disability pre-ECT, fewer treatment side effects, and a perception of good care while in hospital, but not with legal status (Wheeldon et al., 1999; Philpot et al., 2004; Rosenquist et al., 2006). This suggests that the sickest patients, who stand to derive the greatest benefit from ECT, come to perceive it most favourably.

In an intriguing meta-analysis of 16 published reports, positive views of ECT emerged most commonly from studies conducted shortly after ECT by psychiatrists using brief checklists. Studies conducted by independent investigators some time after admission using open-ended questions were much less encouraging (Rose et al., 2003). This suggests that structured assessments conducted by doctors in medical environments may fail to tap patients’ true perceptions.

Proposed strategies to improve acceptance of ECT include educational videos, use of ECT-experienced volunteers, minimizing time in the waiting room, and reducing exposure to technical paraphernalia (Westreich et al., 1995; Koopowitz et al., 2003; Parvin et al., 2004). The video deployed in one study made no discernable difference to patients’ knowledge, perhaps because they were too depressed to benefit, but it was greatly appreciated by families, whose support is often critical (Westreich et al., 1995).

Families’ views

Little research has been conducted of family members’ attitudes to ECT, both before and after treatment. This is a deficiency, since an informed, supportive family can do much to support patients through their illness and treatment. In the meantime, two compelling accounts have been published of relatives’ battles with sceptical psychiatrists to secure ECT for a father and son respectively whose mental disorders had failed to respond to medications and psychotherapy. Their efforts were rewarded eventually by excellent clinical outcomes (D’Agostino, 1975; A Grateful Parent, 2005).

Practice standards and training

Variations in practice

In New York state, Prudic et al. (2001) were perturbed to find that 17% of 59 mental health facilities administered the same electrical charge to all patients; 8% of facilities failed to monitor seizure duration; and 20% neglected to check patients’ cognitive status. Whether these lapses detracted from patients’ recoveries was unclear, but the authors concluded that ‘the wide variability in how ECT is conducted undoubtedly raises public health concerns’.

In former times, training deficiencies were commonplace. Of 160 junior doctors in England and Wales, 63% had watched an instructional video but only 53% had been supervised by an experienced psychiatrist when giving their first treatment and only 4% were routinely supervised thereafter (Duffett and Lelliott, 1998). Similar findings emerged in New South Wales, Australia, where 20% of doctors were not supervised in their first session by another medical practitioner (Halliday and Johnson, 1995).

Clinical guidelines

Three national professional bodies have since published detailed accounts of ECT’s indications and contraindications; proper assessment and treatment procedures; legal and ethical issues; and training and supervision requirements (American Psychiatric Association, 2001; Royal College of Psychiatrists, 2005; Royal Australian and New Zealand College of Psychiatrists, 2007). The American Psychiatric Association stipulates that trainee psychiatrists should complete at least 10 treatments under direct supervision and then attend regular ECT review meetings. ‘Privileging’ to administer ECT independently requires objective evidence of safe, proficient practice that conforms to local policy. Further education might include attendance at an ECT course, a structured clinical practicum, supervised reading, and participation in quality assurance activities to identify gaps in performance and take corrective action.

A detailed checklist prepared by the Royal College of Psychiatrists’ Research Unit (2006) of basic, standard, and ideal policies and procedures covering all aspects of physical facilities, staff training, patient assessment and treatment, consent, and follow-up provides a template for self-appraisal in any ECT service and is highly recommended. A suitable curriculum for psychiatry trainees has been proposed by Dolenc and Philbrick (2007), covering all important areas of theory and clinical application.

Transcranial Magnetic Stimulation

Repetitive transcranial magnetic stimulation (TMS) involves using a pulsed magnetic field to induce local electric current in the cerebral cortex, targeting neural circuits implicated in mood regulation. The brief magnetic pulses are comparable to those used in magnetic resonance imaging and are administered in rapid succession to achieve changes in neurotransmission that persist beyond the stimulus period (Kim et al., 2009; George and Aston-Jones, 2010). During the procedure, patients sit in a specially designed chair with a coil positioned over their scalp. Several brief pulses are administered to determine the minimum amount of power required to produce hand twitching (the ‘motor threshold’), thereby allowing individualized treatment dosing. The coil is then positioned over the left prefrontal cortex for therapeutic stimulation. Treatments typically take 20–40 min on 5 days per week over 4–6 weeks depending on clinical progress. As no sedation is required, normal activities can be resumed immediately afterwards (George and Aston-Jones, 2010).

TMS is contraindicated in patients with nonremovable metal implants in their heads, or within 30 cm of the coil, as heating or movement of these objects due to the magnetic field may result in serious injury or death. Examples of prohibited devices include aneurysm clips or coils, cardiac pacemakers or cardioverter defibrillators, and metallic eye implants. TMS is also contraindicated in patients with a history of seizures or with potentially epileptogenic frontal cortical ischaemia. Subcortical ischaemia is not a contraindication. Its safety in patients with dementia is not established (Jorge and Robinson, 2011).

TMS has proven effectiveness as an antidepressant. In one of two large, multicentre trials, O’Reardon et al. (2007) compared active versus sham TMS in patients with medication-resistant major depression. Active TMS administered daily for a 4- to 6-week period to the left prefrontal cortex was twice as likely as sham TMS to induce remission at 6 weeks. Only 4.5% of patients withdrew from treatment because of adverse events. In the second trial, George et al. (2010) reported that remission was significantly more likely (odds ratio, 4.2) following at least 3 weeks of active high-intensity TMS, in contrast to sham TMS, delivered to the left prefrontal cortex. A significant interaction was found between clinical benefit and the degree of antidepressant treatment resistance. However, overall 6-week remission rates with active TMS were modest in both trials: 17.4% in the former and 14.1% in the latter, using the 24-item HDRS. Age did not significantly predict treatment response in either study.

In a trial of TMS for the treatment of vascular depression in older adults, active treatment proved superior to sham (Jorge et al., 2008), with higher doses resulting in better 3-week response (39.4%) and remission (27.3%) rates, using the 17-item HDRS. Response rates were lower, though, with older age and smaller frontal grey matter volumes, possibly because of ischaemic damage to white matter pathways connecting the left dorsolateral prefrontal and anterior cingulate cortices. Responders and nonresponders did not differ significantly in baseline neuropsychological performance and TMS itself did not give rise to cognitive deficits in this vulnerable population.

Despite its cognitive-sparing properties, the time and expense associated with TMS limits its utility as a first-line psychiatric treatment and its role relative to ECT requires elucidation. Randomized trials favour ECT over TMS in treating depression, showing significantly higher response or remission rates for ECT (58.8% versus 38.0%) (Rasmussen, 2008) and significantly lower Beck Depression Inventory (BDI) suicide subscale scores (0.5 versus 1.2) (Keshtkar et al., 2011).

Suggested areas for future research include optimization of stimulation frequency, intensity, and scheduling; stimulation of cortical sites other than the left prefrontal cortex; combining treatment with pharmacotherapy or psychotherapy; identification of the patients likely to benefit most; and the role of TMS in other conditions including anxiety disorders and psychosis (Kim et al., 2009; Jorge and Robinson, 2011).

Deep Brain Stimulation

Deep brain stimulation (DBS) has generated interest as a psychiatric treatment modality following its success in treating medication-resistant Parkinson’s disease. It involves implanting one or more electrodes into specific brain regions using imaging-guided stereotactic neurosurgery. The electrodes are then connected via subcutaneous extension wires to an implanted pulse generator containing a battery and stimulation computer. A handheld computer interface held close to the generator allows noninvasive setting and adjustment of stimulus parameters including temporary and permanent stimulus deactivation (Holtzheimer and Mayberg, 2011).

The mechanisms of action of DBS are more complex than simply producing a ‘reversible lesion’ (as an alternative to ablative neurosurgery) in stimulated grey matter. Neuronal effects of DBS are both inhibitory and excitatory in nature, depending on the location and mix of cell bodies and white matter fibres in the stimulated field, as well as the stimulus parameters themselves (Holtzheimer and Mayberg, 2011). At a systems level, DBS is presumed to act on cortico-striatal-thalamic-cortical (CSTC) neural circuits implicated in psychiatric conditions such as obsessive-compulsive disorder and depression (Ward et al., 2010).

Studies of DBS for psychiatric disorders are limited in size, but the results look promising. Lakhan and Callaway (2010) recently analysed 16 trials reporting on the efficacy of DBS in treating obsessive-compulsive disorder, treatment-resistant depression, or both. The largest of these for obsessive-compulsive disorder, examining subthalamic nucleus stimulation in 16 patients, showed significantly lower mean symptom scores after active compared to sham treatment (19 versus 28, using the Yale-Brown Obsessive Compulsive Scale) and significantly higher mean global functioning scores (56 versus 43, using the Global Assessment of Functioning Scale) (Mallet et al., 2008). The largest study of DBS for depression, involving 20 patients who received subcallosal cingulate gyrus stimulation, showed 60% response and 35% remission rates, using the 17-item HDRS (Lozano et al., 2008). Other disorders of interest include addiction and Tourette’s syndrome (Holtzheimer and Mayberg, 2011).

DBS is invasive and adverse effects include seizure induction, haemorrhage, superficial infection, and anaesthetic complications. Stimulation itself may generate anxiety and fear. Unlike lesional psychosurgery, however, DBS is potentially reversible, producing minimal tissue destruction and being easily adjusted or switched off. Clarification of optimal stimulus targets, treatment profiles, patient selection criteria, and long-term outcomes are future research directions (Fitzgerald, 2011).


  • ECT is an effective, accepted treatment of depression. It works faster, and may be safer than pharmacotherapy for frail, older patients but relapse rates are high once treatment stops. Continuing pharmacotherapy is mandatory. ECT works best in patients with psychomotor changes and psychotic symptoms.

  • There is a place for ECT in medication-refractory cases of mania, acute schizophrenia, and catatonia.

  • Electrical stimulation must always exceed seizure threshold, more for unilateral than bilateral ECT. Stimulus titration ensures that energy charges are individualized. Alternative strategies include age-based formulae. Fixed dose, high energy treatments are not acceptable.

  • Very old patients have higher rates of cardiovascular complications, confusion, and falls. Twice-weekly ECT is adequate. Benzodiazepines, anticonvulsants, and medications with anticholinergic properties should be stopped if possible.

  • Cognition is often improved by ECT. Complaints of memory loss abate with time, but gaps in memory may persist.

  • Capacity to consent to ECT can change as treatment progresses and explanations may need to be repeated. Educational brochures and videos are encouraged.

  • ECT is perceived negatively by many patients and families and great efforts must be made to address their concerns accurately and to reduce the risk of poor outcomes.

  • Such a complex treatment should never be administered by untrained staff.

  • Few published reports focus just on frail, aged patients. Further research is required to ensure that treatment of this vulnerable group is made as safe and effective as possible.

  • TMS is better tolerated, but less effective, than ECT as a treatment of major depression.

  • DBS requires major surgery and its role is limited to the treatment of very severe, chronic, and disabling psychiatric disorders.

Abraham, K.R. and Kulhara, P. (1987). The efficacy of electroconvulsive therapy in the treatment of schizophrenia: a comparative study. British Journal of Psychiatry, 151, 152–5.Find this resource:

Abrams, R. (1997). The mortality rate with ECT. Convulsive Therapy, 13, 125–7.Find this resource:

Adabag, A.S., Kim, H.G., and Al Aloul, B. (2008). Arrhythmias associated with electroconvulsive therapy in hypertrophic cardiomyopathy. Pacing and Clinical Electrophysiology, 31, 253–6.Find this resource:

A Grateful Parent. (2005). A family member’s experience with ECT. Journal of ECT, 21, 199.Find this resource:

Alexopoulos, G.S., et al. (1984). Medical problems of geriatric psychiatric patients and younger controls during electroconvulsive therapy. Journal of the American Geriatrics Society, 32, 651–4.Find this resource:

American Psychiatric Association (2001). The practice of ECT: recommendations for treatment, training and privileging, 2nd edition. American Psychiatric Association, Washington, DC.Find this resource:

    A Practising Psychiatrist (1965). The experience of electro-convulsive therapy. British Journal of Psychiatry, 111, 365–7.Find this resource:

    Bang, J.B., et al. (2008). ECT treatment for two cases of dementia-related pathological yelling. Journal of ECT, 20, 379–80.Find this resource:

      Barnes, R.C., et al. (1997). Maintenance electroconvulsive therapy and cognitive function. British Journal of Psychiatry, 170, 285–7.Find this resource:

      Benbow, S.M. (1987). The use of electroconvulsive therapy in old age psychiatry. International Journal of Geriatric Psychiatry, 2, 25–30.Find this resource:

      Benbow, S.M. (1991). Old age psychiatrists’ views on the use of ECT. International Journal of Geriatric Psychiatry, 6, 317–22.Find this resource:

      Benbow, S.M. and Crentsil, J. (2004). Subjective experience of electroconvulsive therapy. Psychiatric Bulletin, 28, 289–91.Find this resource:

      Birkenhäger, T.K., et al. (2010). Influence of age on the efficacy of electroconvulsive therapy in major depression: a retrospective study. Journal of Affective Disorders, 126, 257–61.Find this resource:

      Black, D.W., et al. (1988). The importance of Axis II in patients with major depression: a controlled study. Journal of Affective Disorders, 14, 115–22.Find this resource:

      Bolwig, T. (2011). How does electroconvulsive therapy work? Canadian Journal of Psychiatry, 56, 13–18.Find this resource:

      Boylan, L.S., et al. (2000). Determinants of seizure threshold in ECT: benzodiazepine use, anesthetic dosage, and other factors. Journal of ECT, 16, 3–18.Find this resource:

      Brakemeier, E.L., et al. (2011). Self-evaluation of the cognitive effects of electroconvulsive therapy. Journal of ECT, 27, 59–66.Find this resource:

      Brodaty, H., et al. (2000). A prospective follow-up study of ECT outcome in older depressed patients. Journal of Affective Disorders, 60, 101–11.Find this resource:

      Brodaty, H., et al. (2001). ‘Side effects’ of ECT are mainly depressive phenomena and are independent of age. Journal of Affective Disorders, 66, 237–45.Find this resource:

      Bruce, B.B., Henry, M.E., and Greer, D.M. (2006). Ischemic stroke after electroconvulsive therapy. Journal of ECT, 22, 150–2.Find this resource:

      Buchan, H., et al. (1992). Who benefits from electroconvulsive therapy? Combined results of the Leicester and Northwick Park Trials. British Journal of Psychiatry, 160, 355–59.Find this resource:

      Burd, J. and Kettl, P. (1998). Incidence of asystole in electroconvulsive therapy in elderly patients. American Journal of Psychiatry, 6, 203–11.Find this resource:

      Burke, W.J., et al. (1987). The safety of ECT in geriatric psychiatry. Journal of the American Geriatrics Society, 35, 516–21.Find this resource:

      Carlyle, W., Killick, L., and Ancill, R. (1991). ECT: an effective treatment in the screaming demented patient. Journal of the American Geriatrics Society, 39, 637.Find this resource:

        Cattan, R.A., et al. (1990). Electroconvulsive therapy in octogenarians. Journal of the American Geriatrics Society, 38, 753–8.Find this resource:

        Chakrabarti, S., Grover, S., and Rajagopal, R. (2010). Electroconvulsive therapy: a review of knowledge, experience and attitudes of patients concerning the treatment. World Journal of Biological Psychiatry, 11, 525–37.Find this resource:

        Chanpattana, W. and Andrade, C. (2006). ECT for treatment-resistant schizophrenia: a response from the Far East to the UK NICE report. Journal of ECT, 22, 4–12.Find this resource:

        Chanpattana, W., et al. (1999). Continuation ECT in treatment-resistant schizophrenia: a controlled study. Journal of ECT, 15, 178–92.Find this resource:

        Charlson, F., et al. (2012). ECT efficacy and treatment course: a systematic review and meta-analysis of twice vs thrice weekly schedules. Journal of ECT, 138, 1–8.Find this resource:

        Chew, M.L., et al. (2008). Anticholinergic activity of 107 medications commonly used by older adults. Journal of the American Geriatrics Society, 56, 1333–41.Find this resource:

        Coleman, E.A., et al. (1996). Subjective memory complaints prior to and following electroconvulsive therapy. Biological Psychiatry, 39, 346–56.Find this resource:

        Cronholm, B. and Ottoson, J. (1960). Experimental studies of the therapeutic action of electroconvulsive therapy in endogenous depression. Acta Psychiatrica et Neurologica Scandinavica, 35, 69–102.Find this resource:

        Currier, M.B., Murray, G.B., and Welch, C.C. (1992). Electroconvulsive therapy for post-stroke depressed geriatric patients. Journal of Neuropsychiatry and Clinical Neurosciences, 4, 140–4.Find this resource:

        D’Agostino, A.M. (1975). Depression: schism in contemporary psychiatry. American Journal of Psychiatry, 132, 629–32.Find this resource:

        Daniel, W.F. and Crovitz, H.F. (1986). Disorientation during electroconvulsive therapy. Annals of the New York Academy of Sciences, 462, 293–306.Find this resource:

        De Carle, A.J. and Kohn, R. (2001). Risk factors for falling in a psychogeriatric unit. International Journal of Geriatric Psychiatry, 16, 762–7.Find this resource:

        Devanand, D.P., et al. (1994). Does ECT alter brain structure? American Journal of Psychiatry, 151, 957–70.Find this resource:

        Dolenc, T.J. and Philbrick, K.L. (2007). Achieving competency in electroconvulsive therapy: a model curriculum. Academic Psychiatry, 31, 65–7.Find this resource:

        Dolenc, T.J. and Rasmussen, K.G. (2005). The safety of electroconvulsive therapy and lithium in combination: a case series and review of the literature. Journal of ECT, 21, 165–70.Find this resource:

        Dolenc, T.J., et al. (2004). Electroconvulsive therapy in patients with cardiac pacemakers and implantable cardioverter defibrillators. Pacing and Clinical Electrophysiology, 27, 1257–63.Find this resource:

        Dombrovski, A.Y., et al. (2005). Predictors of remission after electroconvulsive therapy in unipolar major depression. Journal of Clinical Psychiatry, 66, 1043–9.Find this resource:

        Donahue, A.B. (2000). Electroconvulsive therapy and memory loss: a personal journey. Journal of ECT, 16, 133–43.Find this resource:

        Duffett, R. and Lelliott, P. (1998). Junior doctors’ training in the theory and the practice of electroconvulsive therapy. Journal of ECT, 14, 127–30.Find this resource:

        Ende, G., et al. (2000). The hippocampus in patients treated with electroconvulsive therapy. Archives of General Psychiatry, 57, 937–43.Find this resource:

        Figiel, G.S., et al. (1992). The treatment of late onset psychoses with electroconvulsive therapy. International Journal of Geriatric Psychiatry, 7, 183–9.Find this resource:

        Fink, M, et al. (1996). Ambulatory electroconvulsive therapy: report of a task force of the Association for Convulsive Therapy. Convulsive Therapy, 12, 42–55.Find this resource:

        Fitzgerald, P.B. (2011). The emerging use of brain stimulation treatments for psychiatric disorders. Australian and New Zealand Journal of Psychiatry, 45, 923–38.Find this resource:

        Flint, A.J. and Rifat, S.L. (1998). The treatment of psychotic depression in later life: a comparison of pharmacotherapy and ECT. International Journal of Geriatric Psychiatry, 13, 23–8.Find this resource:

        Fox, H.A. (1993). Patients’ fear of and objection to electroconvulsive therapy. Hospital and Community Psychiatry, 44, 357–60.Find this resource:

        Freeman, C.P.L. and Kendall, R.E. (1980). ECTI: patients’ experiences and attitudes. British Journal of Psychiatry, 137, 8–16.Find this resource:

        Freeman, C.P.L., Weeks, D., and Kendall, R.E. (1980). ECT: II: patients who complain. British Journal of Psychiatry, 137, 17–25.Find this resource:

        Gangadhar, B.N., et al. (2000). Cardiovascular response during ECT: a cross-over study across stimulus conditions. Journal of ECT, 16, 177–82.Find this resource:

        Gardner, B.K. and O’Connor, D.W. (2008). A review of the cognitive effects of electroconvulsive therapy in older adults. Journal of ECT, 24, 68–80.Find this resource:

        George, M.S. and Aston-Jones, G. (2010). Noninvasive techniques for probing neurocircuitry and treating illness: vagus nerve stimulation (VNS), transcranial magnetic stimulation (TMS) and transcranial direct current stimulation (tDCS). Neuropsychopharmacology, 35, 301–16.Find this resource:

        George, M.S., et al. (2010). Daily left prefrontal transcranial magnetic stimulation therapy for major depressive disorder: a sham-controlled randomized trial. Archives of General Psychiatry, 67, 507–16.Find this resource:

        Godber, C., et al. (1987). Depression in old age: prognosis after ECT. International Journal of Geriatric Psychiatry, 2, 19–24.Find this resource:

        Gormley, N., et al. (1998). The safety and efficacy of electroconvulsive therapy in patients over age 75. International Journal of Geriatric Psychiatry, 13, 871–4.Find this resource:

        Grant, J.E. and Mohan, S.N. (2001). Treatment of agitation and aggression in four demented patients using ECT. Journal of ECT, 17, 205–9.Find this resource:

        Grover, S., Mattoo, S.K., and Gupta, N. (2005). Theories on mechanism of action of electroconvulsive therapy. German Journal of Psychiatry, 8, 70–84.Find this resource:

          Halliday, G. and Johnson, G. (1995). Training to administer electroconvulsive therapy: a survey of attitudes and experiences. Australian and New Zealand Journal of Psychiatry, 29, 133–8.Find this resource:

          Haskett, R.F. and Loo, C. (2010). Adjunctive psychotropic medications during electroconvulsive therapy in the treatment of depression, mania and schizophrenia. Journal of ECT, 26, 196–201.Find this resource:

          Hensley, M.A. (2008). The meaning of electroconvulsive therapy: a patient’s perspective. Journal of ECT, 24, 112–13.Find this resource:

          Hickie, I., et al. (1996). Prediction of ECT response: validation of a refined sign-based (CORE) system for defining melancholia. British Journal of Psychiatry, 169, 68–74.Find this resource:

          Holmberg, S.K., Tariot, P.N., and Challapalli, R. (1996). Efficacy of ECT for agitation in dementia: a case report. American Journal of Geriatric Psychiatry, 4, 330–4.Find this resource:

          Holtzheimer, P.E. and Mayberg, H.S. (2011). Deep brain stimulation for psychiatric disorders. Annual Review of Neuroscience, 34, 289–307.Find this resource:

          Hooten, W.M. and Rasmussen, K.G. (2008). Effects of general anesthetic agents in adults receiving electroconvulsive therapy: a systematic review. Journal of ECT, 24, 208–23.Find this resource:

          Husain, M.M., et al. (2004). Speed of response and remission in major depressive disorder with acute electroconvulsive therapy. Journal of Clinical Psychiatry, 65, 485–91.Find this resource:

          Huuhka, M.J., et al. (2003). Cardiac arrhythmias induced by ECT in elderly psychiatric patients: experience with 48-hour Holter monitoring. Journal of ECT, 19, 22–5.Find this resource:

          Ingram, A., Saling, M.M., and Schweitzer, I. (2008). Cognitive side effects of brief pulse electroconvulsive therapy: a review. Journal of ECT, 24, 3–9.Find this resource:

          Johnstone, L. (1999). Adverse psychological effects of ECT. Journal of Mental Health, 8, 69–85.Find this resource:

          Jorge, R.E. and Robinson, R.G. (2011). Treatment of late-life depression: a role of non-invasive brain stimulation techniques. International Review of Psychiatry, 23, 437–44.Find this resource:

          Jorge, R.E., et al. (2008). Treatment of vascular depression using repetitive transcranial magnetic stimulation. Archives of General Psychiatry, 65, 268–76.Find this resource:

          Kang, N. and Passmore, M.J. (2004). Successful ECT in a patient with an orbital cavernous hemangioma. Journal of ECT, 20, 267–71.Find this resource:

          Kant, R., Coffey, C.E., and Bogyi, A.M. (1999). Safety and efficacy of ECT in patients with head injury: a case series. Journal of Neuropsychiatry and Clinical Neurosciences, 11, 32–7.Find this resource:

          Karmacharya, R., England, M.L., and Öngur, D. (2008). Delirious mania: clinical features and treatment response. Journal of Affective Disorders, 109, 312–6.Find this resource:

          Kellner, C.H., et al. (2010). Bifrontal, bitemporal and right unilateral electrode placement in ECT: randomised trial. British Journal of Psychiatry, 196, 226–34.Find this resource:

          Kennedy, R., Mittal, D., and O’Jile, J. (2003). Electroconvulsive therapy in movement disorders: an update. Journal of Neuropsychiatry and Clinical Neuroscience, 15, 407–21.Find this resource:

          Kerr, R.A., et al. (1982). ECT: misconceptions and attitudes. Australian and New Zealand Journal of Psychiatry, 16, 43–9.Find this resource:

          Keshtkar, M., Ghanizadeh, A., and Firoozabadi, A. (2011). Repetitive transcranial magnetic stimulation versus electroconvulsive therapy for the treatment of major depressive disorder, a randomized controlled clinical trial. Journal of ECT, 27, 310–14.Find this resource:

          Kim, D.R., Pesiridou, A., and O’Reardon, J.P. (2009). Transcranial magnetic stimulation in the treatment of psychiatric disorders. Current Psychiatry Reports, 11, 447–52.Find this resource:

          Koopowitz, L.R., et al. (2003). The subjective experience of patients who received electroconvulsive therapy. Australian and New Zealand Journal of Psychiatry, 37, 49–54.Find this resource:

          Kramer, B.A. (1999). ECT in elderly patients with schizophrenia. American Journal of Geriatric Psychiatry, 7, 171–4.Find this resource:

          Kriss, A., et al. (1978). Neurological asymmetries immediately after unilateral ECT. Journal of Neurology, Neurosurgery and Psychiatry, 41, 1135–44.Find this resource:

          Lafferty, J.E., et al. (2001). Laboratory screening prior to ECT. Journal of ECT, 17, 158–65.Find this resource:

          Lakhan, S.E. and Callaway, E. (2010). Deep brain stimulation for obsessive-compulsive disorder and treatment-resistant depression: systematic review. BMC Research Notes, 3, 60.Find this resource:

          Lapid, M.I., et al. (2004). Decisional capacity of depressed elderly to consent to electroconvulsive therapy. Journal of Geriatric Psychiatry and Neurology, 17, 42–46.Find this resource:

          Law-Min, R. and Stephens, J.P. (2006). Capacity, compliance and electroconvulsive therapy (ECT): the practice of ECT among consultant psychiatrists. Psychiatric Bulletin, 30, 13–5.Find this resource:

          Legendre, S.A., et al. (2003). The influence of cognitive reserve on memory following electroconvulsive therapy. Journal of Neuropsychiatry and Clinical Neurosciences, 15, 333–9.Find this resource:

          Lisanby, S.H., et al. (2008). Toward individualized post- electroconvulsive therapy care: piloting the symptom-titrated, algorithm-based longitudinal ECT (STABLE) intervention. Journal of ECT, 24, 179–82.Find this resource:

          Little, J.D., et al. (2002). Australian and US responses to electroconvulsive therapy dosage selection. Australian and New Zealand Journal of Psychiatry, 36, 629–32.Find this resource:

          Loo, C.K., et al. (2008). A comparison of RUL ultrabrief pulse (0.3 ms) ECT and standard RUL ECT. International Journal of Neuropsychopharmacology, 11, 883–90.Find this resource:

          Loo, C., Simpson, B., and MacPherson, R. (2010). Augmentation strategies in electroconvulsive therapy. Journal of ECT, 26, 202–7.Find this resource:

          Loo, C., et al. (2011). Physical treatments for bipolar disorder: a review of electroconvulsive therapy, stereotactic surgery and other brain stimulation techniques. Journal of Affective Disorders, 132, 1–13.Find this resource:

          Lozano, A.M., et al. (2008). Subcallosal cingulate gyrus deep brain stimulation for treatment-resistant depression. Biological Psychiatry, 64, 461–7.Find this resource:

          Magid, M., et al. (2005). Use of electroconvulsive therapy in a patient 10 days after myocardial infarction. Journal of ECT, 21, 182–5.Find this resource:

          Malcolm, K. (1989). Patients’ perceptions and knowledge of electroconvulsive therapy. Psychiatric Bulletin, 13, 161–5.Find this resource:

          Mallet, L., et al. (2008). Subthalamic nucleus stimulation in severe obsessive-compulsive disorder. New England Journal of Medicine, 359, 2121–34.Find this resource:

          Manly, D.T., Oakley, S.P., and Bloch, R.M. (2000). Electroconvulsive therapy in old-old patients. American Journal of Geriatric Psychiatry, 8, 232–6.Find this resource:

          McCall, W.V. (2006). Refusal versus reluctance. Journal of ECT, 22, 89–90.Find this resource:

          McCall, W.V., Reid, S., and Ford, M. (1994). Electrocardiographic and cardiovascular effects of subconvulsive stimulation during titrated right unilateral ECT. Convulsive Therapy, 10, 25–33.Find this resource:

          McCall, W.V., et alC. (1995). Comparison of the efficacy of titrated, moderate-dose and fixed, high-dose right unilateral ECT in elderly patients. American Journal of Geriatric Psychiatry, 3, 317–24.Find this resource:

          McCormick, L.M., et al. (2007). Metabolic correlates of antidepressant and antipsychotic response in patients with psychotic depression undergoing electroconvulsive therapy. Journal of ECT, 23, 265–73.Find this resource:

          McDonald, W.M. and Thompson, T.R. (2001). Treatment of mania in dementia with electroconvulsive therapy. Psychopharmacology Bulletin, 35, 72–82.Find this resource:

          Medical Research Council (1965). Clinical trial of the treatment of depressive illness. British Medical Journal, 1, 881–6.Find this resource:

          Mondimore, F.M., et al L. (1983). Post-ECT confusional states associated with elevated serum anticholinergic levels. American Journal of Psychiatry, 140, 930–1.Find this resource:

          Mueller, P.S., et al. (2009). Safety of electroconvulsive therapy in patients with unrepaired abdominal aortic aneurysm. Journal of ECT, 25, 165–8.Find this resource:

          Mulsant, B.H., et al. (1991). A prospective naturalistic study of electroconvulsive therapy in late-life depression. Journal of Geriatric Psychiatry and Neurology, 4, 3–13.Find this resource:

          Munk-Olsen, T., et al. (2006). Electroconvulsive therapy: predictors and trends in utilization from 1976 to 2000. Journal of ECT, 22, 127–32.Find this resource:

          National Institute for Health and Clinical Excellence. (2003). Guidance on the use of electroconvulsive therapy. NICE, London.Find this resource:

            Nelson, J.P. and Rosenberg, D.R. (1991). ECT treatment of demented elderly patients with major depression: a retrospective study of efficacy and safety. Convulsive Therapy, 7, 157–65.Find this resource:

              Nobler, M.S., et al. (1993). EEG manifestations during ECT: effects of electrode placement and stimulus intensity. Biological Psychiatry, 34, 321–30.Find this resource:

              O’Connor, D.W., Pollitt, P.A., and Roth, M. (1990). Coexisting depression and dementia in a community survey of the elderly. International Psychogeriatrics, 2, 45–53.Find this resource:

              O’Connor, D.W., et al. (2010a). The effectiveness of continuation-maintenance ECT in reducing depressed older patients’ hospital re-admissions. Journal of Affective Disorders, 120, 62–6.Find this resource:

              O’Connor, D.W., et al. (2010b). Continuation-maintenance electroconvulsive therapy: quality standards in 3 Australian aged psychiatry services. Journal of ECT, 26, 95–7.Find this resource:

              O’Connor, D.W., et al. (2010c). Cognition in elderly patients receiving unilateral and bilateral electroconvulsive therapy: a prospective, naturalistic comparison. Journal of Affective Disorders, 124, 235–40.Find this resource:

              O’Connor, M.K., et al. (2001). The influence of age on the response of major depression to electroconvulsive therapy. American Journal of Geriatric Psychiatry, 9, 382–90.Find this resource:

              O’Leary, D., et al. (1994). The effectiveness of real versus simulated electroconvulsive therapy in depressed elderly patients. International Journal of Geriatric Psychiatry, 9, 567–71.Find this resource:

              Olfson, M., et al. (1998). Use of ECT for the inpatient treatment of recurrent major depression. American Journal of Psychiatry, 155, 22–9.Find this resource:

              O’Reardon, J.P., et al. (2007). Efficacy and safety of transcranial magnetic stimulation in the acute treatment of major depression: a multisite randomized controlled trial. Biological Psychiatry, 62, 1208–16.Find this resource:

              Oudega, M.L., et al. (2011). White matter hyperintensities, medial lobe atrophy, cortical atrophy, and response to electroconvulsive therapy in severely depressed elderly patients. Journal of Clinical Psychiatry, 72, 104–12.Find this resource:

              Parvin, M.H., Swartz, C., and LaMontagne, B. (2004). Patient education by electroconvulsive therapy-experienced volunteer. Journal of ECT, 20, 127–9.Find this resource:

              Penney, J.F., et al. (1990). Concurrent and close temporal administration of lithium and ECT. Convulsive Therapy, 6, 139–45.Find this resource:

              Perera, T.D., et al. (2004). Seizure expression during electroconvulsive therapy: relationships with clinical outcome and cognitive side effects. Neuropsychopharmacology, 29, 813–25.Find this resource:

              Petrides, G., et al. (2001). ECT remission rates in psychotic versus nonpsychotic depressed patients: a report from CORE. Journal of ECT, 17, 244–53.Find this resource:

              Petrides, G., Tobias, K.G., and Kellner, C.H. (2011). Continuation and maintenance electroconvulsive therapy for mood disorders: review of the literature. Neuropsychobiology, 64, 129–40.Find this resource:

              Pettinati, H.M., et al. (1990). Evidence for less improvement in patients taking benzodiazepines during unilateral ECT. American Journal of Psychiatry, 147, 1029–35.Find this resource:

              Philpot, M., et al. (2004). Eliciting users’ views of ECT in two mental health trusts with a user-designed questionnaire. Journal of Mental Health, 13, 403–13.Find this resource:

              Plakiotis, C. and O’Connor, D.W. (2011). Ictal electroencephalographic measures in electroconvulsive therapy practice. Current Psychiatry Reviews, 7, 265–80.Find this resource:

              Plakiotis, C., George, K., and O’Connor, D.W. (2012). Has electroconvulsive therapy utilisation remained stable over time? A decade of ECT service provision in Victoria, Australia. Australian and New Zealand Journal of Psychiatry, 46 (4), 522–31.Find this resource:

              Porter, R.J., Douglas, K., and Knight, R.G. (2008). Monitoring of cognitive effects during a course of electroconvulsive therapy: recommendations for clinical practice. Journal of ECT, 24, 25–34.Find this resource:

              Price, T.R.P. and McAllister, T.W. (1989). Safety and efficacy of ECT in depressed patients with dementia: a review of clinical experience. Convulsive Therapy, 5, 61–74.Find this resource:

              Prudic, J. (2008). Strategies to minimise cognitive side effects with ECT: aspects of ECT technique. Journal of ECT, 24, 46–51.Find this resource:

              Prudic, J., et al. (1994). Acute cognitive effects of subconvulsive electrical stimulation. Convulsive Therapy, 10, 4–24.Find this resource:

              Prudic, J., Peyser, S., and Sackeim, H.A. (2000). Subjective memory complaints: a review of patient self-assessment of memory after electroconvulsive therapy. Journal of ECT, 16, 121–32.Find this resource:

              Prudic, J., Olfson, M., and Sackeim, H.A. (2001). Electro-convulsive therapy practices in the community. Psychological Medicine, 31, 929–34.Find this resource:

              Prudic, J., et al. (2004). Effectiveness of electroconvulsive therapy in community settings. Biological Psychiatry, 55, 301–12.Find this resource:

              Rami, L., et al. (2004). Cognitive status of psychiatric patients under maintenance electroconvulsive therapy: a one-year longitudinal study. Journal of Neuropsychiatry and Clinical Neurosciences, 16, 465–71.Find this resource:

              Ranen, N.G., Peyser, C.E., and Folstein, S.E. (1994). ECT as a treatment of depression in Huntington’s disease. Journal of Neuropsychiatry and Clinical Neurosciences, 6, 154–9.Find this resource:

              Rao, V. and Lyketsos, C.G. (2000). The benefits and risks of ECT for patients with primary dementia who also suffer from depression. International Journal of Geriatric Psychiatry, 15, 729–35.Find this resource:

              Rasmussen, K.G. (2008). Electroconvulsive therapy versus transcranial magnetic stimulation for major depression: a review with recommendations for future research. Acta Neuropsychiatrica, 20, 291–4.Find this resource:

              Rasmussen, K.G., et al. (2003). Electroconvulsive therapy for patients with major depression and probable Lewy body dementia. Journal of ECT, 19, 103–9.Find this resource:

              Rose, D., et al. (2003). Patients’ perspectives on electroconvulsive therapy: systematic review. British Medical Journal, 326, 1363.Find this resource:

              Rosenquist, P.B., et al V. (2006). What predicts patients’ expressed likelihood of choosing electroconvulsive therapy as a future treatment option. Journal of ECT, 22, 33–7.Find this resource:

              Royal Australian and New Zealand College of Psychiatrists (2007). Electroconvulsive therapy: clinical memorandum 12. Royal Australian and New Zealand College of Psychiatrists, Melbourne.Find this resource:

                Royal College of Psychiatrists (2005). The ECT handbook, 2nd edition, ed. A.I.F. Scott. Royal College of Psychiatrists, London.Find this resource:

                  Royal College of Psychiatrists’ Research Unit (2006). The ECT Accreditation Service (ECTAS): standards for the administration of ECT. Royal College of Psychiatrists, London.Find this resource:

                    Rubin, E.H., et al. (1993). The nature and time course of cognitive side effects during electroconvulsive therapy in the elderly. Journal of Geriatric Psychiatry and Neurology, 6, 78–83.Find this resource:

                    Russ, M.J., et al. (1990). Cognitive effects of ECT in the elderly: preliminary findings. International Journal of Geriatric Psychiatry, 5, 115–18.Find this resource:

                    Sackeim, H.A. (2000). Memory and ECT: from polarisation to reconciliation. Journal of ECT, 16, 87–96.Find this resource:

                    Sackeim, H., et al. (1987). Seizure threshold in electroconvulsive therapy: effects of sex, age, electrode placement, and number of treatments. Archives of General Psychiatry, 44, 355–60.Find this resource:

                    Sackeim, H.A., et al. (1993). Effects of stimulus intensity and electrode placement on the efficacy and cognitive effects of electroconvulsive therapy. New England Journal of Medicine, 328, 839–46.Find this resource:

                    Sackeim, H.A., et al. (2000). A prospective, randomized, double-blind comparison of bilateral and right unilateral electroconvulsive therapy at different stimulus intensities. Archives of General Psychiatry, 57, 425–34.Find this resource:

                    Sackeim, H.A., et al. (2001). Continuation pharmacotherapy in the prevention of relapse following electroconvulsive therapy: a randomized controlled trial. JAMA, 285, 1299–307.Find this resource:

                    Sackeim, H.A., et al. (2008). Effects of the pulse width and electrode placement on the efficacy and cognitive effects of electroconvulsive therapy. Brain Stimulation, 1, 71–83.Find this resource:

                    Sartorius, A., Wolf, J., and Henn, F.A. (2005). Lithium and ECT—concurrent use still demands attention: three case reports. World Journal of Biological Psychiatry, 6, 121–4.Find this resource:

                    Shapira, B., et al. (1998). Cost and benefit in the choice of ECT schedule: twice versus three times weekly ECT. British Journal of Psychiatry, 172, 44–8.Find this resource:

                    Sobin, C., et al. (1995). Predictors of retrograde amnesia following ECT. American Journal of Psychiatry, 152, 995–1001.Find this resource:

                    Squire, L.R. and Slater, P.C. (1983). Electroconvulsive therapy and complaints of memory dysfunction: a prospective three-year follow-up study. British Journal of Psychiatry, 142, 1–8.Find this resource:

                    Srzich, A. and Turbott, J. (2000). Nonconvulsive generalised status epilepticus following electroconvulsive therapy. Australian and New Zealand Journal of Psychiatry, 34, 334–6.Find this resource:

                    Steffens, D.C., et al. (2001). Severity of subcortical gray matter hyperintensity predicts ECT response in geriatric depression. Journal of ECT, 17, 45–9.Find this resource:

                    Sutor, B. and Rasmussen, K.G. (2008). Electroconvulsive therapy for agitation in Alzheimer’s disease: a case series. Journal of ECT, 24, 239–41.Find this resource:

                    Suzuki, K., et al. (2008). Safety of electroconvulsive therapy in psychiatric patients shortly after the occurrence of pulmonary embolism. Journal of ECT, 24, 286–8.Find this resource:

                    Tess, A.V. and Smetana, G.W. (2009). Medical evaluation of patients undergoing electroconvulsive therapy. New England Journal of Medicine, 360, 1437–44.Find this resource:

                    Tew, J.D., et al. (1999). Acute efficacy of ECT in the treatment of major depression in the old-old. American Journal of Psychiatry, 156, 1865–70.Find this resource:

                    Tiller, J.W.G. and Ingram, N. (2006). Seizure threshold determination for electroconvulsive therapy: stimulus dose titration versus age-based estimations. Australian and New Zealand Journal of Psychiatry, 40, 188–92.Find this resource:

                    Tomac, T.A., et al. (1997). Safety and efficacy of electroconvulsive therapy in patients over age 85. American Journal of Geriatric Psychiatry, 5, 126–30.Find this resource:

                    Troller, J.N. and Sachdev, P.S. (1999). Electroconvulsive treatment of neuroleptic malignant syndrome: a review and report of cases. Australian and New Zealand Journal of Psychiatry, 33, 650–9.Find this resource:

                    UK ECT Review Group. (2003). Efficacy and safety of electroconvulsive therapy in depressive disorders: a systematic review and meta-analysis. Lancet, 361, 799–808.Find this resource:

                    Van Waarde, J.A., Stolker, J.J., and van der Mast, R.C. (2001). ECT in mental retardation: a review. Journal of ECT, 17, 236–43.Find this resource:

                    Van Waarde, J.A., et al. (2010a). Electroconvulsive therapy for catatonia: treatment characteristics and outcomes in 27 patients. Journal of ECT, 26, 248–52.Find this resource:

                    Van Waarde, J.A. and van der Mast, R.C. (2010b). Seizure thresholds in elderly patients treated with electroconvulsive therapy for major depressive disorder: a review. Current Psychiatry Reviews, 6, 184–90.Find this resource:

                    Vanelle, J.-M., et al. (1994). Maintenance ECT in intractable manic-depressive disorders. Convulsive Therapy, 10, 195–205.Find this resource:

                    Versiani, M., Cheniaux, E., and Landeira-Fernandez, J. (2011). Efficacy and safety of electroconvulsive therapy in the treatment of bipolar disorder: a systematic review. Journal of ECT, 27, 153–64.Find this resource:

                    Ward, H.E., Hwynn, N., and Okun, M.S. (2010). Update on deep brain stimulation for neuropsychiatric disorders. Neurobiology of Disease, 38, 346–53.Find this resource:

                    Watts, B.V., et al. (2011). An examination of mortality and other adverse events related to electroconvulsive therapy using a national adverse event report system. Journal of ECT, 27, 105–8.Find this resource:

                    Westreich, L., et al. (1995). Patient knowledge about electroconvulsive therapy: effect of an informational video. Convulsive Therapy, 11, 32–7.Find this resource:

                    Wheeldon, T.J., et al. (1999). The views and outcomes of consenting and non-consenting patients receiving ECT. Psychological Medicine, 29, 221–3.Find this resource:

                    Wilkins, K.M., Ostroff, R., and Tampi, R.R. (2008). Efficacy of electroconvulsive therapy in the treatment of nondepressed elderly patients: a review of the literature. Journal of Geriatric Psychiatry and Neurology, 21, 3–11.Find this resource:

                    Wilkinson, A.M., Anderson, D.N., and Peters, S. (1993). Age and the effects of ECT. International Journal of Geriatric Psychiatry, 8, 401–6.Find this resource:

                    Zervas, I.M., et al. (1993). Age-dependent effects of electroconvulsive therapy on memory. Convulsive Therapy, 9, 39–42.Find this resource:

                    Zielinski, R.J., et al. (1993). Cardiovascular complications of ECT in depressed patients with cardiac disease. American Journal of Psychiatry, 150, 904–9.Find this resource: