Assessing Treatment Efficacy: Brief vs. Ultra brief Pulse Widths in Bitemporal Modified Electroconvulsive Therapy

Background: Electroconvulsive therapy (ECT) has been a cornerstone in managing severe psychiatric illnesses. However, concerns about its cognitive side effects have led to evolving techniques aimed at minimizing cognitive impairments. Specifically, the use of ultra-brief pulse width (0.5 ms) compared to brief pulse width (1.5 ms) in bitemporal modified ECT (MECT) offers a promising avenue for cognitive preservation. Aims and Objectives: To compare the cognitive outcomes associated with brief and ultra-brief pulse widths in bitemporal MECT. Materials and Methods: This prospective, randomized comparative study was conducted at a rural tertiary care hospital in Northern India. Sixty-six patients aged 18–60 years, diagnosed with schizophrenia, schizoaffective disorder, bipolar disorder, or severe depression, were randomly assigned to receive either brief or ultra-brief pulse MECT. Cognitive functions were assessed using standardized tools, including the Hindi mental status examination and Battery for ECT-related cognitive deficits. Pre- and post-treatment evaluations were compared to determine changes in cognitive performance. Results: Both groups exhibited some level of cognitive change following treatment. However, patients receiving ultra-brief pulse MECT demonstrated significantly better preservation of cognitive functions, notably in memory retention, attention, and executive functioning (P<0.05). Domains such as verbal learning, processing speed, and short-term recall were notably less affected in the ultra-brief group compared to the brief pulse group. Conclusion: Ultra brief pulse width in bitemporal MECT appears to offer a cognitive advantage over brief pulse width, suggesting it may be the preferred choice when cognitive preservation is a clinical priority.

BackgroundThere are limited studies on the prevalence of misdiagnosis as well as detection rates of severe psychiatric disorders in specialized and non-specialized healthcare settings. To the best of our knowledge, this is the first study to determine the prevalence of misdiagnosis and detection rates of severe psychiatric disorders including schizophrenia, schizoaffective, bipolar, and depressive disorders in a specialized psychiatric setting.MethodIn this cross-sectional study, a random sample of 309 patients with severe psychiatric disorders was selected by systematic sampling technique. Severe psychiatric disorders were assessed using the Structured Clinical Interview for DSM-IV (SCID). The potential determinates of misdiagnosis were explored using univariable and multivariable logistic regression models, adjusting for the potential confounding factors.ResultThis study revealed that more than a third of patients with severe psychiatric disorders were misdiagnosed (39.16%). The commonly misdiagnosed disorder was found to be a schizoaffective disorder (75%) followed by major depressive disorder (54.72%), schizophrenia (23.71%), and bipolar disorder (17.78%). Among the patients detected with the interview by SCID criteria, the highest level of the correct diagnosis was recorded in the medical record for schizophrenia (76.29%) followed by bipolar (72.22%), depressive (42.40%), and schizoaffective (25%) disorders with detection rate (sensitivity) of 0.76 (95% CI 0.69–0.84), 0.42 (95% CI 0.32–0.53), 0.72 (95% CI 0.60–0.84), and 0.25 (95% CI 0.09–0.41), respectively for schizophrenia, depressive, bipolar, and schizoaffective disorders. Patients with bipolar disorder were more likely to be misdiagnosed as having schizophrenia (60%), whereas schizophrenic patients were more likely to be misdiagnosed as having bipolar disorder (56.25%) and patients with depressive disorders were more likely to be misdiagnosed as having schizophrenia (54.72%). Having a diagnosis of schizoaffective and depressive disorders, as well as suicidal ideation, was found to be significant predictors of misdiagnosis.ConclusionThis study showed that roughly four out of ten patients with severe psychiatric disorders had been misdiagnosed in a specialized psychiatric setting in Ethiopia. The highest rate of misdiagnosis was observed for schizoaffective disorder (3 out of 4), followed by major depressive disorder (1 out of 2), schizophrenia (1 out of 4), and bipolar disorders (1 in 5). The detection rates were highest for schizophrenia, followed by bipolar, depressive, and schizoaffective disorders. Having a diagnosis of schizoaffective and depressive disorders as well as suicidal ideation was found to be significant predictors of misdiagnosis.

Transdiagnostic effectiveness and safety of clozapine in individuals with psychotic, affective, and personality disorders: nationwide and meta-analytic comparisons with other antipsychotics.

The aim of the present study was to compare blood serum kynurenic acid (KYNA) concentrations measured before ECT and after 1, 6 and 12 electroconvulsive treatment (ECT) sessions in patients with diagnoses of recurrent depressive disorder (RDD), depression in bipolar disorder (DBD) and schizoaffective disorder (SAD). The study group comprised of 50 patients with ICD-10 diagnoses of RDD, DBD and SAD. Blood serum KYNA concentrations were determined and clinical assessment was performed using the MADRS and the GAF scale. Significant differences were found in blood serum KYNA levels between RDD, DBD and SAD patients treated with electroconvulsive therapy and healthy controls: 1) KYNA concentrations in DBD patients measured before ECT and after 12 ECT sessions were significantly lower than in the control group; 2) KYNA concentrations in the serum of RDD patients measured before ECT and after one and 12 ECT sessions were significantly lower than in the control group, while those measured after 6 ECT session did not differ significantly from KYNA concentrations in healthy controls; 3) higher pre-treatment blood serum concentrations of KYNA in DBD patients correlated with a higher number of illness phases and poorer general functioning before treatment; 4) significant relationships were found between higher blood serum concentrations of KYNA in RDD patients after 1 ECT session and male gender, and between higher KYNA concentrations after 6 ECT sessions and increased depression and poorer functioning before treatment in those patients. Results show that KYNA concentrations in all diagnostic groups were lower before ECT (not statistically significant for the SAD group) and that there were no significant changes in those concentrations (compared with the baseline) during ECT.

Patients With Refractory Bipolar Depression May Benefit From ECT

Few treatments have been met with more criticism and hostility than electroconvulsive therapy (ECT). For decades, ECT was the subject for intense controversy and opposition, chiefly by civil rights groups, but also some psychologists and social workers were against the treatment due to the idea that mental symptoms should not be treated with biological methods. Despite this public and professional opposition, ECT is widely accepted by psychiatrists in Scandinavia and in many other countries as indispensable in the treatment for severe depression and other severe psychiatric disorders such as delirious conditions, catatonia, and malignant neuroleptic syndrome on the grounds that it is effective, safe, and gives better and quicker results than antidepressant drugs, 1 and, finally, side-effects are usually minor. However, the inevitable, transient, cognitive side-effects occurring after a series of ECT have played a major role for the image of ECT, and for decades, studies have been made to diminish ECT-induced memory impairment—to an extent so that treatment modifications have been recommended which sacrifice therapeutic effect for milder side-effects. Since the 1960s, placing electrodes over the non-dominant hemisphere (right unilateral ECT, RUL-ECT) has in many studies shown that this modification induces less memory impairment than the conventional bitemporal electrode (BT-ECT) placement, but a larger number of treatment sessions are necessary to obtain clinical remission. If the current in RUL-ECT is delivered with higher energy levels, 8–12x the seizure threshold (ST), which is the minimum current that elicits a seizure—the therapeutic effect increases, but at the same time, the cognitive advantage disappears. The efforts to optimize ECT using different electrode placements have for decades alone focused on the memory aspect, as have many attempts to minimize the cognitive side-effects using alternating current stimulation with a pulse width of 0.1–0.3 ms. This is much lower than the conventional 1.0–5.0 ms pulse width used in many Scandinavian and American studies. A serious disadvantage of stimulation with ultra brief pulse width is that it often generates submaximal seizures with impaired antidepressive effect, and thus, the reduction in memory impairment will be at the cost of therapeutic effect. Data from the studies by the Consortium for Research in ECT (CORE)—the most comprehensive ECT studies to date—in the present issue of this journal 2 throw light on some of the controversial issues regarding ECT—in particular the memory problem. The CORE review underlines ECT's speed of action whereby suicidality is diminished—a highly important element when treating severe depression. Patients with symptoms of melancholic depression (having vegetative symptoms) responded dramatically to BT-ECT with a remission rate of up to 84%, and for those harboring delusions or being hallucinated, the remission rate was over 95%—a rate hardly surpassed by any treatment in the whole of medicine. Although our knowledge of the mechanism of ECT is far from complete, it is evident that elicitation of generalized seizures is a prerequisite for therapeutic effect 3, 4 both in melancholic/psychotic depression and in delirious conditions and catatonia. Elicitation of generalized seizures is best obtained using BT-ECT as has been shown in several neurophysiological studies. The effect of RUL-ECT in patients with the same illness characteristics as those from the BT-ECT of the CORE group was studied by researchers from Columbia University (CUC) 5. The remission rate in the CUC study was 55%, in the CORE study 86%. These different rates may well be ascribed to the different electrode placement, pointing to BT-ECT superiority. The idea that it is the intensity of the electrical stimulation that drives the severity of the cognitive side-effects of ECT has inspired to identifying at the first ECT session the seizure threshold (ST)—and giving the patients low doses of electricity just above this threshold to minimize cognitive impairment. In the CORE study, the vast majority of patients showed no rise of ST over time, and the widely applied determination of ST thus does not seem clinically justified 2. After successful ECT, the risk of relapse within a year is over 80% making continued stabilizing treatment necessary. The CORE studies further demonstrated that the use of continuation ECT at increasing intervals was equal to a combination of lithium and nortriptyline with respect to relapse prevention during a 6-month period, a finding of great value for many patients who do not tolerate an adequate drug regime. Again, the most debated issue regarding ECT is the memory impairment. The transient memory disturbance is a side-effect of ECT, which does not contribute to the antidepressive effect. The subjective experience of memory impairment following a course of ECT is sometimes described by patients as being long-lasting, in exceptional cases permanent, but this experience stands in contrast to measurements of objective memory loss. Thus, a recent meta-analysis of 2981 patients treated with ECT found that the cognitive side-effects mainly comprised the first 3 days after the treatment and that all cognitive functions improved compared with pretreatment conditions irrespective of stimulus parameters 6. The solid findings from the CORE studies substantiate the superiority of ECT in the therapy of severe (melancholic/psychotic) depression, where it should be considered first-line treatment, and not a last resort intervention as suggested in many treatment algorithms. Other clear indications for ECT where there are no comparable alternatives comprise delirious mania, catatonic stupor, postpartum psychosis cycloid psychosis lethal catatonia, and neuroleptic malignant syndrome 7. Using BT-ECT favors therapeutic effect over a transient cognitive advantage, and in choosing treatment parameters, this should be borne in mind when treating critically ill patients.

Treatment Patterns for Schizoaffective Disorder and Schizophrenia Among Medicaid Patients

This study compared background characteristics, pharmacologic treatment, and service use of adults treated for schizoaffective disorder and adults treated for schizophrenia. Medicaid claims data from two states were analyzed with a focus on adults treated for schizoaffective disorder or schizophrenia. Patient groups were compared regarding demographic characteristics, pharmacologic treatment, and health service use during 180 days before and after a claim for either schizophrenia or schizoaffective disorder. A larger proportion of patients were treated for schizophrenia (N=38,760; 70.1%) than for schizoaffective disorder (N=16,570; 29.9%). During the 180 days before the index diagnosis claim, significantly more patients with schizoaffective disorder than those with schizophrenia were treated for depressive disorder (19.6% versus 11.4%, p<.001), bipolar disorder (14.8% versus 5.8%, p<.001), substance use disorder (11.8% versus 9.7%, p<.001), and anxiety disorder (6.9% versus 5.3%, p<.001). After the index claim, a similar proportion of both diagnostic groups were treated with antipsychotic medications (schizoaffective disorder, 87.3%; schizophrenia, 87.0%), although patients with schizoaffective disorder were significantly more likely than patients with schizophrenia to receive antidepressants (61.7% versus 44.0%, p<.001), mood stabilizers (55.2% versus 34.4%, p<.001), and anxiolytics (43.2% versus 35.1%, p<.001). Patients with schizoaffective disorder were also significantly more likely than patients with schizophrenia to receive psychotherapy (23.4% versus 13.0%, p<.001) and inpatient mental health care (9.4% versus 6.2%, p<.001), although the latter was not significant after the analysis controlled for background characteristics. Schizoaffective disorder is commonly diagnosed among Medicaid beneficiaries. These patients often receive complex pharmacologic regimens, and many also receive treatment for mood disorders. Differences in service use patterns between schizoaffective disorder and schizophrenia argue for separate consideration of their health care needs.

Background: Depression is a disorder of concern that affects globally and has become the second leading cause of disability-adjusted life years. The disorder is characterized by persistent sad mood, loss of interest in previous pleasurable activities, reduced energy level, suicidal thoughts, and cognitive disturbances. Electroconvulsive therapy (ECT) is a rapid and effective treatment for severe depression. However, there was stigma toward the application of modified ECT (MECT), the major among them is diminished cognitive particularly memory disturbance. Studies claim that memory disturbances are transient and short-lived. Hence, the current study’s aim is to assess the cognitive status of severe depression patients before and after ECT. Materials and Methods: It is a hospital-based longitudinal analytical study conducted in the psychiatry inpatient department. Ninety-two patients fulfilling the criteria for depression as per DSM-5 were taken into the study after inclusion and exclusion criteria and informed consent. The symptoms of depression are assessed using the Hamilton Depression Rating Scale (HAM-D) and cognitive functions are assessed with Addenbrooke’s Cognitive Examination Scale - Revised (ACE-R). The scale is administered before ECT, post-ECT on day 3, 1 month, and 3 months, respectively. Results: The mean age was 34 years. The majority belonged to the age group of 20–30 years (50%) and were educated up to high school (35%). Before ECT, the mean ACE-R score was 79.39. On day 3 after ECT, the mean score was 78.97. One month after ECT, the mean score was 82.82. Three months after ECT, the mean score was 85.15. The ACE-R scores started to increase at 1 month and at 3 months after ECT, which was statistically significant ( P &lt; 0.05). Before ECT, the mean HAM-D score was 24.41. On day 3 after ECT, the mean HAM-D score was 14.84. One month after ECT, the mean HAM D score was 9.06. Three months after ECT, the mean HAM-D score was 4.43. The decline in HAM-D score from baseline to 3 months after ECT (24.41–4.43) was statistically significant ( P &lt; 0.05). Conclusion: The cognitive impairments due to MECT occur only in the immediate phase following MECT. The impairments are transient and short-lived and improvement in cognition occurs over time.

Polygenic Risk Scores and Genetics in Psychiatry.

COMPARISON OF THE SPEED OF REMISSION BETWEEN BILATERAL AND RIGHT UNILATERAL ECT IN A COHORT OF GERIATRIC PSYCHIATRY PATIENTS

Background and Aim: With the advent of pharmacological agents, there were many changes in prescription patterns for modified electroconvulsive therapy (MECT) over time across the globe. This study aims to evaluate the main indications and prescription patterns of MECT in a tertiary care center. Materials and Methods: A retrospective medical record review was done in a tertiary care hospital after the institutional ethics committee approval, accessing the MECT records of 310 patients who underwent the procedure during the 5-year study period using a semi-structured pro forma. Results: In our file review, we found that the most common diagnosis, for which MECT was prescribed, was schizophrenia 146 cases (47%), and the common indication was augmentation of therapy/to speed up the rate of improvement. Depressive disorder was the primary diagnosis in 81 (26%) cases followed by mania in 46 (15%) cases. Among the major symptomatology which led to the primary use of MECT, suicidality accounted for 72 (23.2%) cases and catatonia in 34 (11%) cases. The mean number of MECTs during the course was 6.4 (2.5) in bipolar disorder, and in schizophrenia, it was 6.3 (2.3). A response rate of 85% was observed. Patient acceptability of MECT was good as only seven (2.3%) patients withdrew consent after initiation of treatment. Conclusion: Most common diagnosis, for which MECT was prescribed, was schizophrenia followed by depression. MECT was most commonly used as an augmentation strategy; however, in case of depression, it was used as first line of management. Response rate to MECT and acceptability were good in majority.

More than 100 years ago Kraepelin proposed a very practical and persuasive solution to a long-standing problem in clinical psychiatry. He proposed to reduce heterogeneity by splitting the perplexing variety of psychopathological signs and symptoms, of patterns of deviant behavior and experiences, of short- and long-term course and outcome of functional disturbances into two major groups: schizophrenia (dementia praecox) and affective disorders (manic-depressive illness) (1). In this way, he created the so-called ‘Kraepelinian dichotomy’, which turned out to be clinically useful for subsequent decades. However, he himself got skeptical subsequently (2) if this simplistic solution really worked in practice as the number of ‘cases in-between’ were too numerous. About 70 years ago, the concept of schizoaffective disorders emerged from difficulties in practicing Kraepelin's dichotomy by separating schizophrenia and affective disorders. In 1933, Kasanin first coined this term (3). Although originally related to ‘reactive psychoses’ in the Scandinavian tradition (4), the term became transformed to indicate the intraindividual co-occurrence of both severe affective as well as severe psychotic syndromes, which did not fit in either of Kraepelin's categories. The widespread use of this term reflected the clinical need to consider border-cases separately. Many clinicians are probably motivated to use this category because of implications on the course of illness. However, qualitative inter-class differences cannot be detected: the most recent outcome study (5) saw a less poor outcome in schizoaffective disorders compared with schizophrenia, but it was difficult to distinguish schizoaffective and mood disorders with psychotic symptoms; a progressively worsening intermediate course was reported for both diagnostic groups. Thus, a dimensional view of schizoaffective outcome is recommended. In contrast to its clinical popularity, research investigations in this diagnostic category – although operational definitions became available – remained relatively rare as it becomes evident from a PubMed search (search terms in titles: schizoaffective disorder = 230 citations; schizophrenia = 13.297; bipolar disorder = 2.355; during a 10-year period 1995–2005). If this category became a research topic at all, it was a border-category of schizophrenia and/or affective disorders. Thus, the biological basis and the nature of this category ‘in-between’ remained obscure. Several reasons might account for this fact. An unequivocal definition of schizoaffective disorder was never attained. For example, the concepts of ICD-10 and DSM-IV strongly differ by the criterion of simultaneity or temporal contiguity. The available diagnostic definitions include so complex criteria that the reliability is relatively low (6). Thus, it does not come as a surprise that most cases with a schizoaffective episode change this diagnosis in subsequent episodes (7). Furthermore, both most widely used diagnostic manuals propose criteria which are fully different from the clinical conventions. This is now demonstrated by a careful diagnostic re-evaluation of a representative Danish in-patient sample (n = 59) with the diagnosis of schizoaffective disorder by Vollmer-Larsen et al. (8): not a single patient fulfilled either the DSM-IV or the ICD-10 criteria (full criteria) for schizoaffective disorder. The vast majority of cases were allocated either to schizophrenia or to affective disorders (ICD-10), both by the rater of the clinical records or by an automatic OPCRIT algorithm. This observation is important because the basic assumption for proposing the diagnostic entity of schizoaffective disorders is losing its validity. At the starting point for this diagnostic category ‘in-between’ schizophrenia and bipolar affective disorders were assumed to be due to two distinct disease processes. Doubts in this unproven hypothesis emerged already in the 1970s. Thus, the relationship between depression and schizophrenia has been studied in a variety of contexts in the past. For example, it was recognized that (i) postpsychotic depression was a common phenomenon, and (ii) postpsychotic depression was often preceded by depression, already at the beginning of the psychotic episode but overseen by the clinician [e.g. (9)]. Very recently, a most carefully conducted retrospective epidemiological study reported depressive symptoms and syndromes to be very common precursors of the first negative and psychotic symptoms in subjects developing schizophrenia later-on (10); it was convincingly concluded that depression presents an integral part or even the basic fundament of schizophrenia (10). In this perspective, schizoaffective disorders cannot be considered as a distinct disease entity between the two extremes of Kraepelin's dichotomy. This conclusion also goes together with recent family studies. In a huge case-register in Denmark schizoaffective disorders did not ‘breed true’, and a family history of schizoaffective disorders did not only increase the risk for schizoaffective disorder, but also for schizophrenia and affective disorder by a similar magnitude (11). An increasing number of family and twin studies report that intrafamilial cosegregation and concordance of schizophrenia and affective disorders are more common than expected by chance and point at shared genetic basis (12). Thus, on a clinical level the overlap between the syndromes of schizophrenia and affective disorders are too broad to be captured by the intermediate diagnosis of schizoaffective disorders. It might be argued that clinical phenomenology is too unspecific to clearly differentiate disease processes on a pathophysiological or molecular level. Can the prototypes schizophrenia and affective disorders be clearly distinguished on a neurobiological basis? Yet, they cannot! (13). Multiple neuropathological, biochemical and genetic communalities between schizophrenia and affective disorders (especially bipolar) were also recently detected, which add to the symptomatic overlap. Recently, common susceptibility genes such as NRG1, G72/G30 or DISC1 were detected to impact on schizophrenia, affective disorders as well as schizoaffective disorders (14). In addition to these communalities, both disorders also reveal diagnosis-specific etiological factors (as the susceptibility gene DTNBP1 for schizophrenia). Taken together, there is growing evidence that a substantial proportion of etiological factors is shared between schizophrenia and bipolar disorder; the contribution of these common determinants is particularly strong in the symptomatic interface, especially in schizoaffective disorders. In this perspective, schizoaffective disorders reflect a quantitative variation in the common etiological and pathophysiological underground of schizophrenia and affective disorders. In summary, the historical starting point of the concept of schizoaffective disorders is not valid any more. The diagnosis ‘schizoaffective disorder’ has not yet been unequivocally defined after more than 70 years, the available concurrent diagnostic definitions are not reliable. The most recommended diagnostic definitions in ICD-10 and DSM-IV even lack face validity because they do not fit with clinical conventions. Do we need this category any more? Is it more appropriate to broaden the concepts of schizophrenia and bipolar disorder even more and concede that etiological communalities might come up as symptomatic overlaps? Or is it even more appropriate to discard categorical diagnostic concepts and substitute them by dimensions: a psychotic, a manic and a depressive one, which allow graduations and overlaps? Currently, these questions are open to discussion. The task forces for new versions of the DSM- and ICD-diagnostic systems and manuals have to consider these recent insights and developments. They would be badly advised if they would just continue the historical and current concepts of schizoaffective disorders into the future.

INTRODUCTION Electroconvulsive therapy (ECT) is a clinical procedure where a small dose of electric current is passed through the brain for a brief period to induce seizures for therapeutic purposes in psychiatric (and certain neurological) conditions. Modified ECT is the modern form of ECT where the electrical stimulus is given under general anesthesia and muscle relaxation. This is one of the most effective treatments for many psychiatric conditions. Modern modified ECT is a safe treatment when practiced with adequate knowledge, skills, and expertise. Following the basic standards of ECT practice is necessary for better clinical outcomes including minimal cognitive adversities. This guideline document is aimed at enabling consistent, safe, and effective practice of ECT in patients in applicable psychiatric disorders. METHODS These guidelines are developed as part of the initiative of Clinical Practice Guidelines (CPG) subcommittee of Indian Psychiatric Society. The initial draft guideline was developed by the authors. The information was sourced from key research articles, national/international guidelines on psychiatric care, and ECT. No formal systematic literature search was conducted. The current guideline was prepared to suit the existing Indian mental health care system and legislations. The draft was further presented and discussed in the in-person workshop of CPG-2022. The draft was revised following the discussion in the workshop based on the consensus-based recommendation method. This guideline is not a directive or mandatory instruction but a guidance document for professional practitioners administering ECT. This is not a full and complete review of ECT procedure. But it is intended to improve patient outcomes by facilitating best practice standards by maximizing benefits and minimizing adversities. USE OF ELECTROCONVULSIVE THERAPY Indications Table 1 shows the indications for ECT. Evidence exists for the efficacy of ECT in depressive episodes, manic episodes, and acute exacerbations of psychosis in schizophrenia. Treatment-resistant depression, mania, and schizophrenia, including clozapine-resistant schizophrenia, are well-recognized indications,[1-6] with evidence from comparative trials (comparison across types of ECT or with waitlisted patients). ECT should not be withheld until the failure of several medication/psychotherapy trials in severe depression. Health economics suggest that it is beneficial to consider ECT as a second or third line agent in severe depression. ECT is considered as first-line (primary) treatment for emergency psychiatric conditions across diagnoses. These include high suicidality, catatonia, excitement, aggression, poor oral intake, acute psychotic symptom exacerbations, and severe physical debilitation secondary to psychiatric disorders.[7-13] The rigor of the evidence base is limited for such indications due to ethical and pragmatic considerations in conducting sham-controlled trials in these emergency life-threatening transdiagnostic situations. It may be noted that almost all international standard guidelines suggest ECT as a first-line treatment option for these indications.[8-13]Table 1: Indications of ECTPredictors of response In general, older age, psychotic symptoms, and shorter episode duration are predictors of response to ECT. Melancholic features and greater baseline depressive symptom severity are also associated with better ECT response. Past good response to ECT is considered a good predictor of response for the current episode. Continuation/Maintenance (C/M) ECT should be considered for patients with a history of severe, recurrent episodes who have failed to remain well on medications.[14] ECT is a first-line treatment when rapid and/or definitive response to avert harm to self/others is needed. Acute suicidal risk, agitation, catatonia, and deteriorating physical status secondary to psychiatric conditions are some of such situations. After an acute course of ECT, C/M treatment with pharmacotherapy and/or psychotherapy is needed. All the indications mentioned above have to be individualized and should be based on the clinical needs, patient's preferences, and putative risk of adverse effects. ECT staffing ECT without anesthesia and muscle relaxation is now prohibited under the Mental Health Care Act, 2017. Hence, the staffing shown in Table 2 is advisable for administering modified ECT.Table 2: Staffing for ECTTreatment site and equipment The treatment suite ideally involves three distinct areas, but which are nearby or closely connected:[9,10] a. Waiting/preparation room: should have the following facilities: i. Waiting area for patients and caregivers ii. Space for assessment: for interviewing, examining, verifying the records, and to ensure adequate preparation iii. Sphygmomanometer and stethoscope b. ECT administration room i. ECT apparatus including bite block, electroencephalogram (EEG) monitor, and ECG monitor ii. Anesthetic agents (e.g., thiopentone, propofol, etomidate, ketamine, isoflurane, sevoflurane, etc.) and muscle relaxants (along with succinylcholine, at least one nondepolarizing agent like atracurium or rocuronium should be available) iii. Emergency medication tray to manage uncontrolled hypertension, hypotension, cardiac arrhythmia, cardiopulmonary arrest, anaphylactic shock, prolonged seizure, and status epilepticus. This should include intravenous fluids, epinephrine, dopamine, atropine or glycopyrrolate, cholinesterase inhibitors (neostigmine, physostigmine), anticonvulsants (lorazepam, diazepam, phenytoin), steroids, beta blockers (esmolol, labetalol), alpha-blockers (prazosin, clonidine), vasodilators (nitroglycerin, hydralazine), antiarrhythmics (lidocaine), analgesics (paracetamol), antiemetics (domperidone, metoclopramide), antihistamines (chlorpheniramine, cetirizine), bronchodilators (aminophylline) among others) iv. Vitals monitoring: sphygmomanometer, reflex hammer, oxygen saturation, ECG v. Intubation set: oral and naso-pharyngeal airways vi. Oxygen delivery system with intermittent positive pressure ventilation capabilities through a mask as well as endotracheal tubes vii. Suction apparatus, iv infusion set, syringes with needles, cotton and gauze pads, hand gloves. viii. Defibrillator ix. Portable cots/beds, disposable containers c. Recovery room: should have all items iii to ix listed above Informed consent (Supplements 1–4) Written informed consent has to be taken before initiating ECT based on principles of shared decision-making. Consent should be taken following due procedures in accordance with the highest ethical standards and applicable laws/regulations. Written information material may be provided to the patient and caregivers, and adequate time should be provided for reverting with any clarifications. Information should be provided regarding the anticipated benefits and possible short-term and long-term adverse effects of modified ECT, including possible risks with both anesthesia and ECT, in the given individual. Discussion on the type of ECT, modification procedure, electrode placement, and expected outcomes should be included in this process. Unless the patient disagrees, it is recommended to make caregivers a part of the consenting process. If a patient does not have the capacity to consent, the same needs to be documented. The advance directives, if any, have to be examined and, in accordance with that, consent may be obtained from the nominated representative. In the case of minors, oral/verbal assent (as per the age) should be obtained along with written informed consent from parents/nominated representative; the decision about initiating ECT has to be taken only after concurrence by two independent psychiatrists or a psychiatrist + a physician, and due permission from the mental health review board as per the law. As and when a patient regains the capacity to consent or attains 18 years of age, his/her consent has to be obtained for continuing ECT sessions then onwards.[15,16] Consent has to be obtained again before initiating C/M ECT, as the clinical condition, purpose (consolidation/relapse prevention), and character of treatment (frequency of ECT sessions and end-point) would have changed. Pre-ECT evaluation (Supplement 5): This should be performed as close to the ECT course as possible. Psychiatric and physical evaluation Psychiatric evaluation is needed to ascertain indications. Rating scales can be used to determine these indications systematically and measure the changes during the ECT course. If the patient has received ECT in the past, details of the electrode placement and electrical parameters in earlier ECTs, level of achieved response, and associated cognitive deficits would guide the current course of ECT. It is important to evaluate the psychotropic medications that can potentially interfere with anesthesia and ECT. For instance, anticonvulsants increase seizure threshold; antipsychotics like chlorpromazine and clozapine are known to be pro-convulsants; lithium can increase the risk of postictal delirium; tricyclic antidepressants are known to increase the risk of cardiac adverse events during ECT/anesthesia. Physical examination is needed to identify any relative contra-indications and prevent complications [Table 3]. It should mandatorily involve fundoscopic examination along with other systemic examinations. Dental evaluation for loose or missing teeth, cardiovascular examination for arrhythmias, assessment for neurological comorbidities, and pulmonary clinical evaluation are mandatory.Table 3: Clinical conditions requiring caution while administering ECTPreanesthetic evaluation is recommended to plan for an anesthetic agent and a muscle relaxant. Also, suitable investigations or interventions can be planned in the presence of medical conditions associated with a substantial risk for general anesthesia-related complications. Liaison with other specialist physicians if deemed is necessary by the psychiatrist/anesthetist. Baseline cognitive screen Monitoring of cognitive adverse effects would be necessary for patients receiving ECT. Baseline knowledge of cognitive abilities is crucial in attributing the changes in cognitive abilities with ECT. Hindi Mental Status Examination and Mini Mental Status Examination are simple tools for monitoring, but are not sensitive to subtle cognitive changes associated with ECT. Montreal cognitive assessment battery (MoCA) and brief ECT cognitive screen are assessment tools used internationally. "Battery for ECT-Related Cognitive Deficits" (B4ECT RECODE) is a tool validated in the Indian population and is recommended to be used during the initiation and course of ECT.[10] Investigations For general anesthesia: hemoglobin levels, blood sugar, electrolytes, blood urea, and serum creatinine would facilitate the detection of common risk-enhancing medical comorbidities but are not mandatory. Similarly, X-ray, electrocardiography, echocardiogram, and other tests would be indicated based on physical evaluation and associated medical comorbidities TREATMENT PROCEDURE ECT is mandatorily used as a modified procedure, as per the law in India. The modification involves using muscle relaxants to reduce the neuromuscular injuries and using anesthetic agents to induce sedation and amnesia for the procedure involving muscle relaxation and electrical stimulation. a. Anesthesia Preparation before anesthesia [Figure 1, Table 4 and Supplement 6]The procedure may be anxiety provoking. So, reassure patients while initiating the procedure including while securing iv access and placing the mask for oxygenation.An ideal anesthetic agent for ECT would be rapidly inducing and short acting (early emergence from effects of anesthesia), has a good amnesic effect and stable systemic/cerebral hemodynamics during ECT, and would not have any effects on seizure threshold. Tables 5 and 6 provide information helpful in selecting anesthetic agents.[17]A combination of propofol and ketamine called ketofol can be used to balance seizure duration and hemodynamic effects. Adjunctive short-acting opiates (remifentanyl, alfentanil, fentanyl) or dexmedetomidine have dose-sparing effects and can be used, but they need more evidence of their exact role in ECT. The differential effects of anesthetic agents are dependent on their dose, and this needs to be considered while choosing the anesthetic agent.Muscle relaxation is an important component of modified ECT. Ideal muscle relaxants should have the ability to avoid musculoskeletal injury without affecting cerebral seizure activity and provide rapid recovery without residual paralysis. Succinylcholine (0.3–1 mg/kg) is a preferred muscle relaxant due to its rapid onset and recovery. Nondepolarizing muscle relaxants may be considered in certain conditions. These include peudocholinesterase deficiency, recent organophosphorus poisoning, severe, widespread burns, hypercalcemia, severe neuromuscular disease or injury (e.g., quadriplegia, amyotrophic lateral sclerosis, muscular dystrophy), history of malignant hyperthermia in the patient or his/her family. In a patient with suspected/known history of a recent (4 weeks) suicide attempt and referred to ECT, a high suspicion of organophosphorous poisoning should be considered. There are reports of prolonged apnea even after 4 weeks of poisoning. Clinicians may consider the assessment of pseudocholinesterase level when in doubt or may use of nondepolarizing agents in such cases.Pseudocholinesterase level can be assessed in patients with high suspicion (e.g., patients belonging to Arya Vysya community, an earlier history of prolonged apnea). Routine determination of pseudocholinesterase level is not recommended. Routine prophylactic use of anticholinergics (atropine/glycopyrrolate), beta-blockers, calcium channel blockers, nitrates, hydralazine, and ganglionic blockers for cardiovascular stability is not recommended. Wherever used, the rationale for using such an agent should be noted. b. ECT Dosing The protocol of ECT varies considerably and choice on the protocols should be based on individual needs of a given patient. The rapidity of needed response, effectiveness, and potential cognitive adverse effects of the protocols should guide the choice. Rather than any set of protocols, it is important to have knowledge of each parameter in the protocol, and personalization of protocol can be done based on clinical situations.[18,19] i. Electrical Parameters A brief or ultrabrief pulse is strongly recommended and should be administered with a constant current device. Sinewave ECT and constant voltage systems are not recommended in the modern practice of ECT due to safety concerns. Electrical charge is generally considered as a linear measure and chief parameter of dosing. But this approach is faulty, and the combination of electric current intensity, pulse width, pulse frequency and train duration (number of pulses) along with electrode placement (stimulation site), frequency of sessions and duration of session should be carefully considered in choosing a protocol. Electrical current intensity: Historically, 500–1000 mA has been used in the practice of ECT. Most devices come with a default current of 800–900 mA. The current intensity is known to linearly correlate with tolerability, cognitive as well as seizure quality but is generally kept constant and not modified during dose incrementation. Recently, low amplitude (200–400 mA) has been explored as part of individualized low-amplitude seizure therapy.[20] Its clinical utility is yet to be understood. Pulse width: ECT is classified as brief pulse (0.5–2 ms) and ultrabrief pulse (0.2–0.4 ms). Pulse width is likely to have a linear effect on cognitive adverse effects with broader widths being associated with worse cognitive effects. Ultrabrief pulse of 0.3 ms has been shown to have a cognitive advantage over brief pulses with right unilateral placement in depressive disorders. But the antidepressant efficacy may be compromised with it. A lower range of brief pulse (0.5–1 ms) may be considered optimal to obtain a rapid clinical effect. But when cognitive effects are of major concern, a stimulus with ultra-brief pulse width may be chosen.[21] Pulse frequency: The number of biphasic pulses every second is the electrical parameter that is inverse of the interpulse interval. It is an important electrical parameter that generally ranges from 20 to 240 pulses/s (10–120 Hz, i.e., bidirectional pulse pair per second). Stimuli with lower frequencies are generally more efficient, i.e., a seizure can be elicited at a lesser charge with lower frequency than with higher frequency when all other parameters are kept constant. Many ECT devices in the default increment method involve an increase in frequency. ECT clinicians should be aware of this aspect while using a default way of increasing stimulus charges to address the issue of high seizure threshold. Train duration: This is the most commonly modified parameter to set the dose. Generally, the pulse duration is limited by the devices. Most devices have a range of 0.2–8 s, but certain devices come with the highest limit of up to 16 s. No limit has been examined/recommended on the highest duration. An increase in charge is achieved by increasing train duration till the upper limit of the device is reached. The number of pulses: It is directly a factor of train duration and will also be influenced by pulse frequency. The number of pulses may intuitively suggest a direct correlation with seizure. But as "crowding of pulses" is inefficient in eliciting seizure, the number of pulses by itself may not be a good indicator for setting electrical parameters. Directionality: The default ECT parameter widely applied is bidirectional current. There are preliminary trials of unidirectional current – anodal at one site and cathodal at the other. But the evidence is limited to suggest the clinical utility of unidirectional current. Patterned doses: Bursts of pulses are provided similar to theta bursts in transcranial magnetic stimulation. The available evidence is for continuous pulses with similar intervals, which is supported by most commercially available devices. Currently, patterned pulses cannot be recommended for routine clinical application. ii. Electrode placement The electrodes are placed in different ways [Figure 2]:[22-25] 1. Bilateral: Bitemporal: Classical method. One electrode is placed in the frontotemporal region (one above the line the and placed on above on an line to the line two Clinical trials have shown that is if not more effective than placement, but with lesser cognitive effects in patients with mania, as well as schizophrenia. right placement of electrodes with the on the region and right on frontotemporal is Evidence from systematic is for this One electrode is placed on the right frontotemporal region and electrode 1 right to of of two one two and other This is shown to have lesser cognitive but the dose when provided as an ultrabrief pulse for that of as right unilateral on the This is to be to the right This placement can be when and is needed more than It is also considered in the right brain The evidence for the efficacy of unilateral ECT is available only for depression. The evidence of unilateral ECT is for other common indications or iii. of ECT ECT is discussed in of charge A higher charge is associated with better efficacy and higher cognitive adverse effects. But as discussed the charge is not a linear measure but a combination of electrical parameters [Figure 3]. Table Preparation for ECT of of anesthesia agents in choosing for and of anesthetic agents used during 1: of 2: ECT electrode 3: Electrical charge intensity pulse width pulse frequency train duration. The dose for optimal efficacy through ECT sessions is considered with to the seizure threshold; efficacy is also dependent on pulse width and electrode charge seizure is recommended in ECT with brief pulse ECT width of 1 ms or evidence a of a higher charge seizure when a lower range of ms) is used with ECT. There is evidence that a seizure is with ultrabrief ms) ECT, with the evidence available for right unilateral ECT, in depression. For right unilateral ECT with brief pulse width, electrical charge is to be considered the seizure threshold. Ultrabrief at 0.3 ms) is to be effective and may not be advisable with the existing the dose increment has to for a current pulse and pulse Hence, the dose should also be a of train duration. But most of the standard devices have a of train duration at in default and they increase pulse frequency to increase the duration. Most have used these default and this guideline should be with are needed to ascertain this This will be the recommended method in The session can be in the dose needed for seizure can be used as guidance for the dose of may be with higher in and with may be in sessions can be provided at as discussed on the and of the different are There is a need to be in using the as medications and anesthetic agents may the seizure threshold. The stimulus should have the same pulse width, pulse and electrode from which the was high This a high dose, commonly the for all the The use of a high should be only for patients with medical conditions in which of is a Dosing from A high dose will be administered at the The and would be In the are to at the dose a similar This be a better to the high it is c. and and i. ECT procedure [Figure of ECT method is recommended for seizures by the in the right unilateral from muscle a direct measure of seizure activity and is recommended from at least two and to the is only a channel is a channel is can have due to muscle and other Hence, should be used to seizure quality seizure should be given more than any duration. A good quality seizure, even of shorter has been to be in of of seizure and of seizure to adequate seizure is to be of clinical or quality seizure involves different is a seizure during after the the stimulation. This will be by will which will A will the with the of and The should be even in the presence of method of and of the in the case of unilateral electrode is preferred in modified ECTs, as it of from the of ECT stimulus till the of the in any part of the in the be considered for seizure duration. quality seizure involves the of seizure activity in quality seizure will have [Figure 1: involving with increasing 2: high amplitude bursts at to 3: with for to the – a line is The onset of this the of The is recovery from to theta to of is better in patients than in of If is or seizure even after 20 of of electrical then may be by increasing the stimulus dose. onset seizure should be If the seizure is of low quality or the seizure is to one of the or to the region at higher may be after s. may be till the patient of relaxant. Generally, to can be If of or dose, can be from the It may be noted that reduce the quality of If the seizures are brief (e.g., and if the patient is the expected clinical response, then with a higher dose need not be on the same after adequate seizure, called the ECT is not recommended. in of unilateral ECT, would not be necessary on the of This be considered only conditions like malignant or In the case of a prolonged seizure than can be if a seizure s. and should be closely till the complete of seizure. A seizure may be using or the anesthetic agent used for If the patient is on or or may be considered. to anesthetic agents may also be considered. lateral and in the ECT suite should under the care of an till is the patient can be to the recovery ii. Monitoring in the recovery room Monitoring of the should be pulse blood and oxygen ECG should be in patients of cardiac should be for arrhythmia, seizure, and should be until the patient regains full during the procedure should be musculoskeletal injuries and should be assessed for recovery to baseline or baseline before the patient from the recovery iii. the course of ECT The number of should not be but should be based on the needs of individual in of clinical and cognitive and other adverse effects should be at least a during the course of ECT. ECT may be at any time if complete clinical is If clinical is not a of ECT sessions should be provided in acute before

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