Electroconvulsive Therapy-Resistant Catatonia: Case Report and Literature Review.

BACKGROUND: Untreated catatonia is associated with serious medical complications that can necessitate urgent medical attention. Lorazepam and electroconvulsive therapy (ECT) are effective for catatonia across various psychiatric or medical diagnoses. In rare cases, ECT fails to achieve full response in catatonic symptoms, particularly in patients with chronic catatonia or primary psychotic disorder. Evidence on treating catatonia that does not respond to ECT is lacking. OBJECTIVE: Conduct a literature review on treatment of ECT-resistant catatonia which is defined as that reported lack of full response to ECT treatments. We present a case of a 52-year-old male with schizophrenia where catatonia did not respond to lorazepam and robust ECT but resolved after memantine titration. METHODS: A literature review was performed using Medline/PubMed with the following keywords: treatment-resistant, catatonia, electroconvulsive therapy. References in eligible articles and most recent systematic reviews on catatonia treatment were reviewed. RESULTS: Seventeen patients in 12 case reports were identified where the treatment of catatonia was described after failed ECT trials. Most had chronic catatonia and a diagnosis of schizophrenia. ECT parameters and ictal outcome measures were not consistently reported. Treatment modalities for ECT-resistant catatonia included amantadine, memantine, lorazepam augmentation to ECT, and antiepileptic and antipsychotic medications such as aripiprazole and clozapine. CONCLUSIONS: The literature review and new case suggest reconsideration of catatonia diagnosis, optimizing ECT treatments, cautious use of antipsychotics, consideration of lorazepam augmentation to ECT treatments, and/or use of N-methyl-D-aspartate receptor antagonists.

Benzodiazepines for catatonia in people with schizophrenia or other serious mental illnesses.

BACKGROUND: Catatonia is a debilitating disorder of movement and volition associated with schizophrenia and some other mental illnesses. People with catatonia are more likely to require hospitalisation and highly supervised care than those without the disorder. They also have an increased risk of secondary complications such as pneumonia, malnutrition and dehydration. The mainstay of treatment has been drug therapies and electroconvulsive therapy. OBJECTIVES: To compare the effects of benzodiazepines with other drugs, placebo or electroconvulsive therapy for catatonia in people with schizophrenia or other similar serious mental illnesses (SMIs). SEARCH METHODS: We updated our previous search (28 February 2007) by searching the Cochrane Schizophrenia Group's Study-Based Register of Trials (9 November 2016; 6 February 2019). This register is compiled by systematic searches of major resources (including CENTRAL, MEDLINE, Embase, AMED, BIOSIS, CINAHL, PsycINFO, PubMed, and registries of clinical trials) and their monthly updates, handsearches, grey literature, and conference proceedings, with no language, date, document type, or publication status limitations for inclusion of records into the register. We also manually searched reference lists from studies selected by the search. SELECTION CRITERIA: All controlled clinical trials that randomised people who have schizophrenia or other similar SMI and experiencing catatonia to receive benzodiazepines or another relevant treatment. We included studies that met our inclusion criteria and reported usable data. We excluded those not meeting our inclusion criteria or those not reporting usable data. We contacted authors when we required further information; and if we received no response, we put those studies aside as 'awaiting assessment'. DATA COLLECTION AND ANALYSIS: Review authors extracted data independently. For dichotomous data we calculated relative risks (RR) and their 95% confidence intervals (CI) on an intention-to-treat basis using a fixed-effect model. We completed a 'Risk of bias' assessment for the included study and generated a 'Summary of findings' table using GRADE. MAIN RESULTS: The searches found 130 citations, from which we could identify 22 possibly relevant studies. From these, we could only include one study. This study had a relatively small sample size of 17 participants who received lorazepam or oxazepam and were drug free for one week before the trial started. The only usable data reported by this study were clinically important change in symptoms of catatonia measured as 50% improvement on the Visual Analogue Scale (VAS). There was no difference in the numbers of participants showing a clinically important change in their catatonic symptoms (RR 0.95, 95% CI 0.42 to 2.16; participants = 17; studies = 1; very low quality evidence).No data were reported for other important outcomes of hospital stay, clinically important change in satisfaction with care, global state, adverse effects or general functioningWe did find a few studies meeting our inclusion criteria but they reported no usable data. We had to exclude these. Although poorly reported, these studies do illustrate that relevant studies have been undertaken - they are not impossible to design and conduct. AUTHORS' CONCLUSIONS: Analysis of the results from this review, which was a head-to-head comparison of two benzodiazepine monotherapies, does not show a clear difference in effect. No data were available for benzodiazepines compared to placebo or standard care. The lack of usable data and very low quality of data available makes it impossible to draw firm conclusions and further studies with a high-quality methodology and reporting are required in order to determine more definitively the outcomes associated with benzodiazepine use in the clinical management of catatonia in persons with schizophrenia and other SMI.

Resurgence of catatonia following tapering or stoppage of lorazepam - A case series and implications.

The resurgence of catatonia following tapering of lorazepam is a common clinical phenomenon. However, there is limited evidence on the relationship between tapering method of lorazepam and resurgence of catatonic state. We report seven (0.6%) such patients who were found to have resurgence of catatonia. The mean age is 35.7 years; five of them had schizophrenia and other psychotic spectrum disorders. Five of them had resurgence within one week of stoppage, and three of them had multiple resurgences and required maintenance treatment with lorazepam. So gradual tapering and maintenance treatment with lorazepam might be effective in preventing resurgence of catatonia.

Relapses and recurrences of catatonia: 30-case analysis and literature review.

OBJECTIVE: Relieving catatonia helps identify the underlying etiology and its treatment. However, catatonia may reemerge after some time, but there are few data on the relapses and recurrences of catatonia. We aimed to investigate the characteristics of patients with relapses or recurrences of catatonia as well as the efficacy of the lorazepam-diazepam protocol on them. METHODS: Patients with catatonia who had more than one episode of catatonia and were treated with the lorazepam-diazepam protocol were identified. Their medical charts were reviewed, and interview was conducted. RESULTS: Thirty patients were identified. Nineteen (63.3%) were diagnosed with schizophrenia, five (16.7%) with major depressive disorder, two (6.7%) with bipolar disorder, and four (13.3%) with general medical conditions. In the 68 relapses and relapses the lorazepam-diazepam protocol was used, full response was reported in 54 (79.4%) of them. Twelve of 19 (63.2%) patients with schizophrenia were treated with clozapine. Twenty (66.7%) out of 30 patients were maintained on oral lorazepam by the time of discharge. Literature review showed similar prevalence of schizophrenia in patients with more than one episode of catatonia, and a wide variety of treatment options. CONCLUSION: The lorazepam-diazepam protocol was mostly effective in managing relapses and recurrences of catatonia. Maintenance clozapine and oral lorazepam were beneficial in a significant number of patients.

[Catatonia and neuroleptic malignant syndrome in view of a psychopathological and pathophysiological overlap: a brief review]. / Katatónia és neuroleptikus malignus szindróma a pszichopatológiai és patofiziológiai átfedések tükrében: rövid összefoglaló tanulmány.

Catatonia was first described in the 19th century as a syndrome with motor, affective and behavioral symptoms. During the 20th century it was rather regarded as a rare motoric manifestation of schizophrenia and that classification has almost resulted in the disappearance of catatonia among patients outside of the schizophrenia spectrum. With the introduction of neuroleptics, the incidence of catatonic schizophrenia also declined which was attributed to effective treatment. Simultaneously, neuroleptic malignant syndrome was described, which shows many similarities with catatonia. Recently, several researchers suggested a common origin of the two disorders. In this paper we review case reports of the last five years, in which both neuroleptic malignant syndrome and catatonia had emerged as a diagnosis. Additionally, based on the relevant literature, we propose a common hypothetical pathomechanism with therapeutic implications for the two syndromes. Besides underlining the difficulties of differential diagnosis, the reviewed cases demonstrate a transition between the two illnesses. The similarities and the possible shifts may suggest a neuropathological and pathophysiological overlap in the background of the two syndromes. Electroconvulsive therapy and benzodiazepines seem to be an effective treatment in both syndromes. These two treatment approaches can be highly valuable in clinical practice, especially if one considers the difficulties of differential diagnosis.

Catatonic schizophrenia: therapeutic challenges and potentially a new role for electroconvulsive therapy?

A 36-year-old man with known schizophrenia, presented with increasingly bizarre behaviour. The development of catatonia and subsequent neuroleptic malignant syndrome in itself posed numerous therapeutic challenges. However, following resolution of neuroleptic malignant syndrome, the reintroduction of antipsychotics was not tolerated. This case report proposes a novel use for electroconvulsive therapy as a treatment of mental state, following resolution of neuroleptic malignant syndrome, to facilitate successful reintroduction of antipsychotics.

Neuroleptic malignant syndrome masked by cerebral malaria.

A 38-year-old man with an underlying psychiatric illness presented with altered sensorium and abnormal behaviour. He was febrile at 38°C and weak looking; otherwise no other abnormalities were detected. A blood film conducted for malarial parasite (BFMP) revealed Plasmodium falciparum; hence a diagnosis of cerebral malaria was made. He was treated with antimalarial drugs for 2 days prior to being transferred out to the ward following clinical improvement. He subsequently developed episodes of stupor and refusal of feeding. Following an evaluation by the psychiatrist, a diagnosis of catatonic schizophrenia was made and he was started on oral sulpiride and benhexol. Unfortunately, he developed high-grade fever at 40°C with muscle rigidity and fasciculation. The diagnosis of neuroleptic malignant syndrome (NMS) was clinched and the antipsychotics were discontinued. However he succumbed to NMS several days later due to multiorgan failure.

[Hypothermia under olanzapine treatment: clinical case series and review of current literature]. / Hypothermie unter Olanzapin : Eine Fallserie mit Literaturübersicht.

BACKGROUND: Antipsychotic drugs may lead to hypothermia as well as hyperthermia. Although known for decades and clinically highly relevant, the mechanisms by which antipsychotic drugs alter thermoregulatory processes in the human body are still far from being fully understood. In clinical practice, much attention is paid to antipsychotic drug-induced elevation of body core temperature as observed in the neuroleptic malignant syndrome (NMS). But also hypothermia is a clinically highly relevant adverse reaction to antipsychotic drugs. MATERIAL AND METHODS: Here we report a case series of three patients who developed severe hypothermia after administration of olanzapine. A review of the current literature is given with a focus on risk factors for the development of antipsychotic drug-induced hypothermia and its pathophysiologic mechanisms. RESULTS: A 51-year-old female patient suffering from catatonic schizophrenia, cachectic nutritional condition and hypothyroidism developed severe hypothermia of 30.0°C body core temperature after administration of 30 mg olanzapine per day under comedication with lorazepam and L-thyroxine. A 48-year-old female patient with catatonic schizophrenia showed hypothermia of 31.0°C (rectal measurement) after single-dose administration of olanzapine 10 mg orally and a total of 3 mg lorazepam (1-1-1 mg). The third case report describes a 69-year-old male patient with acute delusional disorder exhibiting hypothermia of 33.0°C (rectal measurement) in combination with a reversible atrioventricular block grade III without any further comedication. CONCLUSION: A review of the current literature reveals that thermoregulatory disturbances as sequelae of antipsychotic drug administration depend on individual disposition as well as various independent risk factors such as environmental temperature, somatic comorbidities, endocrinological abnormalities (e.g. hypothyroidism) and structural damage of the brain. A complex interaction of dopaminergic regulatory mechanisms in the ventral hypothalamus and peripheral vaso- and sudomotor adjustments seems to be causative. Hypothermia following antipsychotic drug administration represents a serious adverse drug reaction and a potentially life-threatening event.

Supplementary motor cortex involvement in reading epilepsy revealed by magnetic source imaging.

Reading epilepsy (RE) is an idiopathic reflex epilepsy syndrome characterized by perioral myoclonic jerks (PMJs) during reading associated with left-dominant frontotemporal spike-wave discharges (SWDs). To better understand the pathophysiology of this syndrome, we studied a 45-year-old patient using magnetic source imaging (MSI). The patient underwent two whole-head magnetoencephalography (MEG) recordings (Elekta Neuromag Oy) within 2 months while reading aloud. Forty-two SWDs associated with PMJs were recorded and averaged with respect to SWDs peak power. Epileptic discharges were then reconstructed using conventional equivalent current dipoles (ECDs) modeling, distributed sources sLORETA modeling, and beamformer approach. These methods identified two brain sources located in the left supplementary motor cortex (SMC) and the left primary sensorimotor face area (PSMFA). The spatiotemporal pattern of the sources was characterized by a cross-talk between these two brain regions, with an initial source in the left SMC. This MSI investigation suggests that RE-PMJs are associated with reading-induced activation of hyperexcitable neurons in the left SMC, followed by secondary propagation to the left PSMFA producing the myoclonus.

[Use of aripiprazole in the treatment of catatonia]. / Az aripiprazol alkalmazása katatóniában.

INTRODUCTION: Successful aripiprazole treatment of catatonia was reported in some recent case reports. METHOD: Review of the literature and three case reports. RESULTS: In the presented cases it was demonstrated that aripiprazole was effective in the treatment of catatonia in patients with schizophrenia, major depression or brief psychotic disorder. CONCLUSION: Besides benzodiazepines and electroconvulsive therapy, aripiprazole might be an alternative treatment for catatonia, however randomized controlled trials are required to prove the effectiveness of aripiprazole in patients with catatonia.

Amenorrhoea - consequence of combined treatment with sulpiride and risperidone in a patient suffering from schizophrenia.

It is well documented that sulpiride causes hormonal adverse events, like amenorrhoea and galactorrhea, due to its mechanism of action. Furthermore, risperidone can produce amenorrhoea and galactorrhea also, due to its mechanism of action, which differs from that of sulpiride. This case report is of a patient that was treated with large doses of sulpiride, but did not develop an adverse event like amenorrhoea. However, when risperidone was introduced into therapy it leads to the onset of amenorrhoea. Gynecologist saw it as the beginning of menopause. General practitioner questioned the existence of an intra-cerebral process that could produce amenorrhoea as well. Therefore, the patient was sent to perform an MRI of the brain, under work diagnosis of pituitary adenoma, which was later ruled out as a cause of the illness. Well experienced psychiatrist linked the loss of menstruation with the adverse event profile of sulpiride and therefore gradually discontinued sulpiride from therapy, while risperidone was left and subsequently menstrual cycle was restored. Good knowledge of adverse events profile of antipsychotic medication used, especially when used in a combination, allows us to correctly question appearance of adverse events, to adequately treat them and lowers the cost of unneeded medical procedures.

Catatonia and its treatment.

Psychiatric diagnoses are currently categorized on a syndromic basis. The syndrome of catatonia, however, remains in a diagnostic limbo, acknowledged predominantly as a subtype of schizophrenia. Yet, catatonia is present in about 10% of acutely ill psychiatry patients, only a minority of whom have schizophrenia. Among those with comorbid affective disorders, who comprise the largest subgroup of catatonic patients, the catatonic signs typically resolve dramatically and completely with benzodiazepine therapy. Those with schizophrenia respond less reliably, suggesting that the underlying processes causing the catatonia may be different in this group. The majority of patients with catatonia have concurrent psychosis. Failure to treat the catatonia before institution of antipsychotic medication may increase the risk of inducing neuroleptic malignant syndrome. At this point of time, the pathobiology of catatonia is unknown; the major reason for considering catatonia as a separate diagnostic entity would be to increase recognition of this eminently treatable neuropsychiatric syndrome.

Catatonia as a risk factor for the development of neuroleptic malignant syndrome: report of a case following treatment with clozapine.

Catatonia is characterized by the predominance of psychomotor abnormalities and shares many clinical, biological and treatment response features with the neuroleptic malignant syndrome (NMS), a rare adverse reaction to psychoactive medications. It has been advocated that the two conditions should be placed along the same spectrum of disorders. A case of a 49-year-old woman, who developed NMS while on low dose clozapine soon after recovering from catatonia, is presented. The potential relationship between catatonia and NMS is discussed in the light of the existing literature, and attention is drawn to the risk for clozapine-induced NMS in catatonic patients.

Benzodiazepines for catatonia in people with schizophrenia and other serious mental illnesses.

BACKGROUND: Catatonia is a debilitating disorder of movement and volition associated with schizophrenia and some other mental disorders. People in a catatonic state have increased risk of secondary complications such as pneumonia, malnutrition and dehydration. The mainstay of treatment has been drug therapies and electroconvulsive therapy. OBJECTIVES: To compare the effects of benzodiazepines with other drugs, placebo or electroconvulsive therapy for people with catatonia. SEARCH STRATEGY: We searched the Cochrane Schizophrenia Group Trials Register (March 2007) and manually searched reference lists from the selected studies. SELECTION CRITERIA: All relevant randomised controlled clinical trials. DATA COLLECTION AND ANALYSIS: We (RCG, GW) extracted data independently. For dichotomous data we would have calculated relative risks (RR) and their 95% confidence intervals (CI) on an intention-to-treat basis using a fixed-effect model. MAIN RESULTS: No studies could be included. We did find studies reporting no usable data that we had to exclude or assign to those awaiting assessment. These studies, although poorly reported, do illustrate that relevant studies have been undertaken, and are not impossible. AUTHORS' CONCLUSIONS: Studies have been justified and undertaken in the past. This justification remains as relevant as ever. Further studies with a high-quality methodology and reporting are required and it may be for countries where catatonia is seen often to take a lead in this area.

Tardive seizure and antibiotics: case reports and review of the literature.

Tardive seizure is a serious adverse reaction of electroconvulsive therapy (ECT). However, it was rarely reported in ECT sessions for psychiatric patients who needed concurrent antibiotic treatments. We present 2 cases of patients with schizophrenia who manifested a catatonic syndrome and were indicated for ECT, along with antibiotic therapies for infectious diseases with piperacillin and cefotiam, respectively. The beta-lactam antibiotics are reported to induce convulsions caused by the suppression of inhibitory GABAergic functions. In addition, there is a report on prolonged ECT seizure related to ciprofloxacin, which has an epileptogenic property with a similar action to beta-lactam antibiotics. Thus, tardive seizures in our cases are thought to be related to piperacillin and cefotiam.

Catatonic syndrome: importance of detection and treatment with lorazepam.

BACKGROUND: A resurgence of interest has led to renewed attempts to clarify the concept and treatment of catatonia. METHOD: A large prospective study was conducted to estimate the incidence of catatonic syndrome in 138 consecutive psychiatric patients admitted to a general hospital in India, to demarcate the common symptom presentations and its response to intravenous benzodiazepines. Patients were screened using the Bush Francis Catatonia Screening Instrument. Patients with two or more signs on the Instrument were subsequently administered intravenous lorazepam and their response was rated on the Bush Francis Catatonia Rating Scale. RESULTS: Catatonic syndrome was found in 11% of patients with a wide variety of diagnoses, especially schizophrenia. Mutism (87.5% incidence) was the most common symptom. A significant proportion (93%) of these patients showed a marked immediate response to lorazepam, with 75% showing sustained improvement. CONCLUSIONS: Catatonic syndrome is common, often undiagnosed, and quickly responsive to treatment, irrespective of the diagnosis. It needs to be identified and actively treated with benzodiazepines to minimize distress, and facilitate diagnosis and treatment. Most patients also need additional treatment for the underlying psychiatric condition.

Review of adjunctive glutamate antagonist therapy in the treatment of catatonic syndromes.

Catatonia is a common neuropsychiatric syndrome which may arise from GABA-A hypoactivity, dopamine (D2) hypoactivity,and possibly glutamate NMDA hyperactivity. Amantadine and memantine have been reported as effective treatments for catatonia in selected cases, and probably mediate the presence of catatonic signs and symptoms through complex pathways involving glutamate antagonism. The authors identified 25 cases of catatonia treated with either agent. This article provides indirect evidence that glutamate antagonists may improve catatonic signs in some patients who fail to respond to established treatment, including lorazepam or electroconvulsive therapy. Further study of glutamate antagonists in the treatment of catatonia is needed.

Topiramate effect in catatonia: a case series.

The authors describe four cases of catatonia in which topiramate treatment was used. Commonly effective therapies, including benzodiazepines and divalproex, were proven refractory. In all four cases, subjects experienced complete remission of catatonic symptoms and tolerated treatment well. In one case, all psychotropic medications were discontinued because the patient became delirious. The delirium resolved after discovery and treatment of a urinary tract infection. Catatonic agitation relapsed when topiramate was withdrawn but remitted again when topiramate and lorazepam therapy was restored. In two cases, continued topiramate therapy was accompanied by sustained remission. These case reports present a novel approach to the treatment of catatonia.