Takehisa Takano

Continuation electroconvulsive therapy for relapse prevention in middle‐aged and elderly patients with intractable catatonic schizophrenia

Abstract  The authors have previously studied the short‐term effect of the first acute electroconvulsive therapy (ECT) course (phase 1 study) on intractable catatonic schizophrenia and the 1‐year relapse rate after response to the acute ECT (phase 2 study) in middle‐aged and elderly patients. Results indicated that, although acute ECT has an excellent short‐term effect, the 1‐year relapse rate after response to acute ECT is high despite the use of continuation neuroleptics. In the present prospective study the effect was explored of continuation ECT with neuroleptics on the prevention of relapse after response to a second acute ECT course in the relapsed participants of the phase 2 study. The present study included seven consecutive patients >45 years of age with catatonic schizophrenia (Diagnostic and Statistical Manual of Mental Disorders (4th edn; DSM‐IV) who relapsed (despite the use of neuroleptics) within 1 year after response to the first acute ECT course, and then responded to the second acute ECT course. The patients were given continuation ECT combined with neuroleptics; four ECT sessions at weekly intervals, then four ECT sessions every 2 weeks, then three ECT sessions every 4 weeks. Clinical symptoms were evaluated by means of the Brief Psychiatric Rating Scale (BPRS) weekly for 48 weeks or until relapse. Relapse was defined as a BPRS score of at least 37 for 3 consecutive days. Three out of the seven patients (42.9%) had a sustained response to ECT during the 1‐year follow‐up period. In the seven patients the probability of relapse within 1 year under treatment with neuroleptics alone (phase 2 study) was statistically higher than that under continuation ECT combined with neuroleptics (present study). No statistical differences were seen between the phase 2 study and the present study in the severity of psychiatric symptoms, global social function, the number of acute ECT sessions or the dosage of neuroleptics. No patient experienced a severe cognitive or physical adverse effect resulting from continuation ECT. Continuation ECT with neuroleptics is an efficacious and safe treatment for maintaining a response in middle‐aged and elderly patients with intractable catatonic schizophrenia who have relapsed after a positive response to acute ECT despite the use of continuation neuroleptics.

Safety of electroconvulsive therapy in psychiatric patients shortly after the occurrence of pulmonary embolism.

We encountered 2 patients with a psychiatric disorder (depression in one and catatonia in one) accompanied by motor inhibition that was complicated by pulmonary embolism (PE). In both cases, the psychiatric disorder was safely resolved with electroconvulsive therapy (ECT) during anticoagulant therapy. The 2 cases direct our attention to at least 3 important points regarding safe administration of ECT shortly after the occurrence of PE, that is, careful evaluation of cardiac function and residual deep vein thrombosis before the start of an ECT course, adjustment of anticoagulants, and prevention of recurrent deep vein thrombosis and PE by methods in addition to anticoagulant therapy (fluid infusion, use of support hose, and timely ECT).

Adjusting the frequency of continuation and maintenance electroconvulsive therapy to prevent relapse of catatonic schizophrenia in middle-aged and elderly patients who are relapse-prone

Abstract  The purpose of the present paper was to study the effect of continuation electroconvulsive therapy (ECT) on the prevention of relapse in middle‐aged and elderly patients with intractable catatonic schizophrenia. It was found that continuation ECT is efficacious to sustain remission for patients who suffer relapse after response to acute ECT despite continuation neuroleptics. However, three patients suffered relapse during continuation ECT, therefore the effect of adjusting the frequency of continuation ECT and maintenance ECT was investigated in these patients with catatonic schizophrenia who relapsed during continuation ECT. These patients with DSM‐IV catatonic schizophrenia who relapsed during continuation ECT were treated with more frequent continuation ECT and subsequent maintenance ECT after response to acute ECT. The patients’ Brief Psychiatric Rating Scale (BPRS) scores were prospectively evaluated until relapse. Patients were considered to be relapsers if they had a BPRS score ≥37 for 3 consecutive days. The three patients with catatonic schizophrenia who relapsed during continuation ECT were treated successfully with more frequent continuation ECT and subsequent maintenance ECT. No patient experienced a severe adverse effect from continuation or maintenance ECT. More frequent continuation ECT and maintenance ECT deserves consideration in middle‐aged and elderly patients with intractable catatonic schizophrenia who suffer relapse during continuation ECT. Large‐scale systematic studies are warranted to investigate the optimum use of continuation and maintenance ECT in patients with catatonic schizophrenia.

Epileptic Seizures Superimposed on Catatonic Stupor

Summary:  Purpose: Some patients with nonconvulsive status epilepticus are known to exhibit catatonic stupor. Thus it is necessary to rule out ictal catatonia by electroencephalography in patients with catatonic stupor. However, few reports are available on epileptic seizures superimposed on catatonic stupor.

A case of catatonia resembling frontotemporal dementia and resolved with electroconvulsive therapy

We describe a case of catatonia in a 51-year-old man in whom the catatonic symptoms could not be distinguished from symptoms of frontotemporal dementia (FTD) until they were resolved with electroconvulsive therapy (ECT). When it is difficult to distinguish between catatonia and FTD in patients with frontal dysfunction associated with frontal lobe atrophy, we believe that sequential administration of benzodiazepines and ECT is important for therapeutic diagnosis because the risk of missing a diagnosis of catatonia outweighs the risks associated with administration of benzodiazepines and/or ECT.

Catatonic stupor during the course of Parkinson's disease resolved with electroconvulsive therapy

Catatonia is a syndrome of mutism, immobility, rigidity, negativism, posturing, stereotypy, and impulsiveness usually accompanied by affective or psychotic symptoms (hallucinations and delusions).1,2 Catatonia can be seen not only in patients with a psychiatric disorder but also in patients with neurological diseases.1–4 We present a patient with Parkinson’s disease (PD) complicated by catatonia that resolved with electroconvulsive therapy (ECT). The patient was a 62-year-old woman. At age 57, she noticed stiffness in the right upper and lower limbs and postural tremor. Her illness was diagnosed as idiopathic PD at a neurology clinic. Dopamine agonist and levodopa were prescribed. Motor fluctuations developed, with Hoehn and Yahr stage 1 in the on state and stage 5 in the off state. The Unified Parkinson’s Disease Rating Scale (UPDRS) score was 35/168 in the on state. At age 62, she experienced sudden cenesthopathy and felt that her genital area burned with fever. She began to pour water over herself. She became incoherent and agitated and was admitted to the local neurology service. At that time, she was taking L-dopa (600 mg/day), cabergoline (4 mg/day), selegiline (10 mg/day), and zonisamide (100 mg/day). The attending physician believed the condition to be an anti-Parkinson druginduced psychosis and quetiapine (50 mg/day) was administered. The L-dopa was then reduced by half, and the other anti-Parkinson drugs were gradually stopped. Four days after the start of quetiapine, akinesia, mutism, severe rigidity, staring, stereotyped movements, and negativisms developed. At times, she climbed over the bed rail and pulled out her gastric tube. After several days, her temperature increased to 38.1°C with an elevation in creatine phosphokinase kinase (CPK; up to 1,074 IU/L). The attending physician believed the condition to be neuroleptic malignant syndrome (NMS). The UPDRS score was 144/168. The full dose of L-dopa was reinstated after an interval of 1 week, and intravenous dantrolene (40 mg/day) was begun. The high fever and CPK elevation resolved after 2 weeks, but akinesia, mutism, severe rigidity, staring, negativism, visual hallucinations, emotional liability, incoherence, and delusions of guilt persisted. After 1 month in this state, the patient was transferred to our hospital. Full blood tests and magnetic resonance imaging scans of the brain revealed no abnormalities except hypoproteinemia. We diagnosed her symptoms as catatonic stupor and recommended ECT. After 12 ECT sessions, the patient’s catatonic and the other psychiatric symptoms were almost completely resolved. Rehabilitation was required because of severe contractures. The patient suffered total amnesia for this episode beginning with the sudden cenesthopathy. Paroxetine (40 mg/ day) was given to prevent relapse. Two weeks after the ECT course, parkinsonian symptoms including cogwheel rigidity, bradyphrenia, and tremor, re-emerged, but responded to L-dopa (350 mg/day) and pramipexole (up to 4.5 mg/day). Six months after ECT, her UPDRS score was 39/168 in the onstate and the Mini-Mental State Examination score was 30/30. The psychiatric symptoms have remained in remission for 1.5 year. The PD patient described herein suffered abrupt onset of psychosis and marked exacerbation of parkinsonian symptoms that resolved with ECT. We considered the neuropsychiatric symptoms observed in this case as catatonia. Besides catatonia, there are two other possible explanations for the symptoms in this case. The first is rapid PD progression.5 However, the symptoms were reversible. In addition, the patient exhibited not only parkinsonian motor symptoms but also hallucinations, delusions, affective symptoms, and negativisms. Thus, the likelihood of rapid progression of PD is low. The second explanation is NMS or dopaminergic withdrawal. Shortly after the start of quetiapine and withdrawal of the L-dopa, severe rigidity, CPK elevation, and fever occurred. These symptoms may indeed indicate NMS or pre-NMS during PD.6,7 The symptoms of NMS and malignant catatonia are indistinguishable.8,9 Both are characterized by progressive hyperthermia, autonomic dysfunction, clouding of consciousness, in addition to the rigidity.1,2,8 In our case, there was no clear line between NMS and malignant catatonia. However, early recognition of catatonia is advantageous in terms of treatment, because ECT is well established as the most efficacious treatment for catatonia.1,2,8 In cases of malignant catatonia, ECT is lifesaving1,2,8 and the efficacy of ECT for catatonia is greater than that of recommended treatment (dantrolene, dopamine agonist) for NMS.2,10 In addition, there has been recent discussion of NMS as a drug-induced form of malignant catatonia included in the larger catatonic syndrome.2 To our knowledge, there are no reports of catatonia during the course of PD. Early recognition of catatonia during the course of PD is important for timely administration of ECT.

Resolution of SPECT-determined anterior cerebral hypoperfusion correlated with maintenance ECT-derived improvement in residual symptoms in a case of late-life psychotic depression.

A 70-year-old widow with recurrent psychotic depression was successfully treated with maintenance electroconvulsive therapy (ECT) for 4 years up to the present. Anterior cerebral hypoperfusion visualized by single photon emission computerized tomography (SPECT) before ECT persisted (second SPECT study 14 days after the last ECT session) despite a response to the first course of acute ECT. Only mild symptoms remained. Relapse occurred 2 weeks after the post-ECT SPECT study. The hypoperfusion improved after response to a second course of acute ECT (per SPECT 5 days after the last ECT session), and perfusion was normalized after 2-year maintenance ECT (per SPECT 14 days after the last ECT session). The normalization coincided with improvement in depressive symptoms remaining after the second course of acute ECT. We speculate that the effectiveness of maintenance ECT might have been in part the result of the improvement in residual symptoms and that resolution of the persistent anterior hypoperfusion, which might underlie medical refractoriness, illness chronicity, and relapse tendency in late-life depression, might have been associated with the improvement in residual symptoms achieved by maintenance ECT.

Should we convert demand mode to fixed mode when electroconvulsive therapy is administered to patients with pacemakers

To the Editor: Electroconvulsive therapy (ECT) is reported to be safely administered to psychiatric patients with cardiac pacemakers. In the past years, the pacemaker is recommended to be converted from demand mode to fixed mode operation in the ECT session. Recently, however, the need for such a conversion has not been emphasized. We describe a depressive patient with a demand pacemaker to whom ECTwas safely administered without converting to fixed mode. We will discuss whether we should convert demand mode to fixed mode or not. The patient was a 72-year-old woman. At age 47 years, she had depression that was resolved by antidepressants. At age 72 years, the depression recurred. An acute ECT resolved the depression. A 6-month continuation of ECT followed. She began to exhibit severe bradycardia during the continuation period of ECT. Acardiovascular internist diagnosed sicksinus syndrome. A pacemaker was implanted (Nexus I Plus, SR model 1934; Intermedics, Saint Paul, Minn). VVI mode that paces and senses only in ventricle, and is inhibited by intrinsic ventricular beats was chosen. The basic rate was set at 60 pulses per minute. After the implantation, 99% of all heartbeats were paced heartbeats. Continuation ECT was resumed. In ECT sessions, we do not convert VVI mode to VOO (fixed ventricular pacing without sensing or inhibition abilities) mode, the magnet was prepared for the unlikely event of pacemaker inhibition and symptomatic bradycardia, and the patient was insulated from the ground. An engineer checked the operation of the pacemaker before and after each ECT session. Atropine sulfate (0.5 mg), thiopental (200 mg), succinylcholine (80 mg), and nicardipine (0.5 mg) were used. Monthly continuation of ECT (a total of 3 sessions) was successfully administered without any complications. During each ECT session, pulse rate remained constantly above 60 beats per minute, and all detected heartbeats were spontaneous heartbeats (paced heartbeats; 0%). We believe that VVI mode pacemaker should not be converted to VOO pacing during an ECT session. It is true that temporal conversion of demand mode to fixed mode was recommended because demand pacemakers were occasionally inhibited by muscle contraction during ECT sessions, resulting in severe bradycardia. Nowadays, however, muscle relaxant (eg, suxamethonium) is always administered inan ECT session. With the exception of 1 case in which a demand pacemaker stopped discharging, likely due to inhibition by suxamethoniuminduced muscle fasciculations; all reported ECT procedures with suxamethonium have been safely administered to the patients with demand cardiac pacemakers. For this reason, we need not be so worried about pacemaker inhibition caused by muscle contraction. Instead we must be wary of the considerable risk of temporal conversion to fixed mode. Ventricular fibrillation is one of the most serious complications of fixed mode pacemakers. Ventricular fibrillation was caused by BR-on-T[ phenomenon due to paced beat interrupting the T wave of the normal sinus rhythm. The phenomenon with fixed mode pacemakers might be more likely to occur at ECT session because the seizure induced by ECT makes the intrinsic heart rate faster. Therefore, we should not convert demand mode to fixed mode, contrary to the risk of ventricular fibrillation.

Panic attack associated with flumazenil at electroconvulsive therapy session.

Benzodiazepines should be discontinued before the course of electroconvulsive therapy (ECT) due to their anticonvulsant effect which may diminish the efficacy of ECT. However, some ECT patients need benzodiazepines due to severe anxiety, agitation, or insomnia. In such cases, flumazenil, a benzodiazepine antagonist, is available for clinical use to reverse the action of benzodizapines at ECT session. We described a benzodiazepine-dependent ECT patient who experienced a panic attack precipitated by flumazenil immediately after an ECT session. The patient was a 46-year-old woman. At age 28, she labored under delusions of persecution and auditory hallucinations. Paranoid schizophrenia was diagnosed. At age 43, her psychotic symptoms exacerbated, and she was administered a psychiatric hospital. The psychotic symptoms did not respond to a sufficient dose of neuroleptics. At age 45, the patient was transferred to Tohoku University Hospital for administration of ECT. She exhibited excitement and auditory hallucination and made a suicide attempt. A course of acute ECT was given. Atropine (0.5 mg), thiopental (150 mg), succinylcholine (60 mg), and nicardipine (0.5 mg) were used. She had been prescribed nitrazepam (10 mg/d) for more than 2 years. Nitrazepam could not be stopped due to excitement and insomnia. Thus, flumazenil (0.3 mg) was intravenously administered just before electric stimulation during ECT sessions. Twenty acute ECT sessions partially relieved the psychotic symptoms. She needed weekly continuation ECT to prevent exacerbation of psychosis. However, she experienced relapse 1 month after response to the first acute ECT course. The second course of acute ECT was given and partially relieved the psychotic symptoms; weekly continuation of ECT followed. Flumazenil (0.3Y0.5 mg) continued to be intravenously administered to achieve therapeutic seizure at each ECT session. Four months after the response to the second acute ECT course, she experienced a panic attack that included fear of dying, sensation of choking, and hyperventilation just after awakening from anesthesia for ECT. Breathing into a paper bag did not relieve the panic attack. Intramuscular injection of diazepam (10mg) slowly relieved the panic attack. However, she experienced anticipatory anxiety and fear to ECT after the ECT session. At the next ECT session, she exhibited a further panic attack, which was quickly relieved by intravenous administration of midazolam (8 mg). From then on, midazolam (10 mg) was intravenously administered immediately after completion of seizure in each ECT session. There have been no further panic attacks or apparent side effects (eg, delay of awakening and respiratory depression) in a total of 30 subsequent ECT sessions with combination flumazenil with midazolam. In the present case, we believe that the panic attack just after ECT session may have been precipitated by the administration of flumazenil. Panic attack is one of the most typical benzodiazepine withdrawal symptoms. Some studies reported panic attack precipitated by flumazenil in even low-dose benzodiazepine users without history of panic attack. As to ECT, there is 1 report of appearance of breakthrough anxiety after administration of flumazenil. The present case was a longterm benzodiazepine user and had no previous history of panic disorder. In addition, there has been no panic attack since the occurrence of the 2 described panic attacks. Taking these findings into consideration, although new onset of idiopathic panic disorder cannot be ruled out completely, it is possible that the panic attack is precipitated by administration of flumazenil. Care should be taken for panic attack associated with flumizenil at ECT session. Kazumasa Suzuki, MD

Acute embolic stroke in a patient with atrial fibrillation after electroconvulsive therapy

Although patients with atrial fibrillation (AF) have an increased risk of embolic stroke, some clinicians hesitate to provide anticoagulation therapy for these patients during electroconvulsive therapy (ECT), which is widely applied for the treatment of intractable depression, bipolar disorder, and catatonic schizophrenia, because of potential intracerebral hemorrhage. We report on a 77-year-old female depressive patient with AF treated with aspirin but not on anticoagulation therapy because of poor compliance who developed embolic stroke 1 day after the last ECT. The CHADS2 score of this patient was 2 and included the age and hypertension. The present case suggests that anticoagulation therapy should be considered for patients with obvious risks of embolic stroke when they are subjected to ECT.