Lethal catatonia

Mann, Stephan C.; Caroff, Stanley N.; Bleier, Henry R.; Welz, Werner K.R.; Kling, Mitchel A.; Hayashida, Maiko

doi:10.1176/ajp.143.11.1374

Cited by 238 publications

(35 citation statements)

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“…56,66 However, moving with alacrity to ECT in cases of malignant catatonia has also been strongly recommended given the risk of medical complications and fatality from cardiovascular collapse. 67 Two cases of safe and successful ECT after cerebral hypoxia have been described, both for depression in the subacute/chronic phase (Table 3). 66,68 Thus clinicians are left with a meager evidence base on which to formulate the risk-benefit analysis, between offering ECT to the patient with catatonic symptoms after hypoxia given its broad efficacy, versus withholding ECT given potential for worsening.…”

Section: Cerebral Hypoxia and Catatoniamentioning

confidence: 99%

Catatonia After Cerebral Hypoxia: Do the Usual Treatments Apply?

Quinn

Abbott

2014

Psychosomatics

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Introduction Neurologic deterioration occurring days to weeks after a cerebral hypoxic event accompanied by diffuse white matter demyelination is called delayed post-hypoxic leukoencephalopathy (DPHL). Manifestations of DPHL are diverse, and include dementia, gait disturbance, incontinence, pyramidal tract signs, parkinsonism, chorea, mood and thought disorders, akinetic mutism, and rarely catatonia. Methods The authors report a case of malignant catatonia in a patient diagnosed with DPHL that was refractory to electroconvulsive therapy (ECT), and review the literature on catatonia in DHPL. Results The patient was a 56 year-old female with schizoaffective disorder who was admitted with catatonia two weeks after hospitalization for drug overdose and respiratory failure. Her catatonic symptoms did not respond to lorazepam, amantadine, methylphenidate, or ten sessions of bilateral ECT at maximum energy. Repeat magnetic resonance imaging revealed extensive periventricular white matter lesions not present on admission scans, and she was diagnosed with DPHL. Discussion No treatment for DPHL has been proven to be widely effective. Hyperbaric oxygen treatments may reduce the rate of development, and symptom improvement has been reported with stimulants and other psychotropic agents. Review of the literature reveals rare success with GABAergic agents for catatonia after cerebral hypoxia, and no cases successfully treated with ECT. There are seven case reports of neurologic decompensation during ECT treatment after a cerebral hypoxic event. Conclusion Caution is advised when considering ECT for catatonia when delayed sequelae of cerebral hypoxia are on the differential diagnosis, as there is a dearth of evidence to support this treatment approach.

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Section: Cerebral Hypoxia and Catatoniamentioning

confidence: 99%

Catatonia After Cerebral Hypoxia: Do the Usual Treatments Apply?

Quinn

Abbott

2014

Psychosomatics

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“…Excited catatonia, on the other hand, is characterized by severe psychomotor agitation[4], potentially leading to life-threatening complications such as hyperthermia, altered consciousness, and autonomic dysfunction. This so-called “malignant” or “lethal” catatonia can be rapidly fatal if not appropriately treated[5,6]. The relative prevalence and diagnostic significance of catatonic signs differ among studies and patient populations, but there is general agreement that catatonia occurs in 9%-17% of patients with acute psychiatric illnesses[1,2,7] and that retarded catatonia is the more frequently observed subtype[4,8-10].…”

Section: Introductionmentioning

confidence: 99%

Catatonia: Our current understanding of its diagnosis, treatment and pathophysiology

Rasmussen¹,

Mazurek²,

Rosebush³

2016

WJP

217

168

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Catatonia is a psychomotor syndrome that has been reported to occur in more than 10% of patients with acute psychiatric illnesses. Two subtypes of the syndrome have been identified. Catatonia of the retarded type is characterized by immobility, mutism, staring, rigidity, and a host of other clinical signs. Excited catatonia is a less common presentation in which patients develop prolonged periods of psychomotor agitation. Once thought to be a subtype of schizophrenia, catatonia is now recognized to occur with a broad spectrum of medical and psychiatric illnesses, particularly affective disorders. In many cases, the catatonia must be treated before any underlying conditions can be accurately diagnosed. Most patients with the syndrome respond rapidly to low-dose benzodiazepines, but electroconvulsive therapy is occasionally required. Patients with longstanding catatonia or a diagnosis of schizophrenia may be less likely to respond. The pathobiology of catatonia is poorly understood, although abnormalities in gamma-aminobutyric acid and glutamate signaling have been suggested as causative factors. Because catatonia is common, highly treatable, and associated with significant morbidity and mortality if left untreated, physicians should maintain a high level of suspicion for this complex clinical syndrome. Since 1989, we have systematically assessed patients presenting to our psychiatry service with signs of retarded catatonia. In this paper, we present a review of the current literature on catatonia along with findings from the 220 cases we have assessed and treated.

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“…[3] Malignant catatonia is characterized by excitement, altered mental status (altered level of consciousness), hyperthermia and autonomic instability as well as catatonic symptoms. [4,5] In contrast, neuroleptic malignant syndrome (NMS) associated with the use of antipsychotic medications is considered to be a variant of malignant catatonia. [4–7] The diversity of symptoms often leads to a delay in diagnosis.…”

Section: Introductionmentioning

confidence: 99%

“…[4,5] In contrast, neuroleptic malignant syndrome (NMS) associated with the use of antipsychotic medications is considered to be a variant of malignant catatonia. [4–7] The diversity of symptoms often leads to a delay in diagnosis. The mortality rate associated with malignant catatonia has declined but remains high (10%–20%).…”

Section: Introductionmentioning

confidence: 99%

Response to benzodiazepines and the clinical course in malignant catatonia associated with schizophrenia

Ohi¹,

Kuwata

Shimada³

et al. 2017

Medicine

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Background:Malignant catatonia (MC) is a disorder consisting of catatonic symptoms, hyperthermia, autonomic instability, and altered mental status. Neuroleptic malignant syndrome (NMS) caused by antipsychotics is considered a variant of MC. Benzodiazepine (BZD) medications are safe and effective treatments providing rapid relief from MC. This case study reports a detailed clinical course of a case of MC associated with schizophrenia initially diagnosed as NMS that responded successfully to BZDs but not to dantrolene.Case presentation:A 53-year-old man with schizophrenia was admitted to the psychiatric hospital because of excitement, monologue, muscle rigidity, and insomnia. In the 3 days before admission, the patient had discontinued his medications after his family member's death. He presented with hyperthermia, tachycardia, hypertension, excessive sweating, and an elevated serum creatine phosphokinase (CPK) level. On the basis of these features, he was suspected to have NMS. The patient was treated with dantrolene for 7 days without improvement despite having a normalized serum CPK level. The patient was transferred to our university hospital for an in-depth examination and treatment of his physical status. Infection and pulmonary embolism were excluded as possible causes. To treat his excitement and auditory hallucination, an intravenous drip (IVD) of haloperidol was initiated, but this treatment increased the patient's catatonic and psychotic symptoms, although his serum CPK level had remained within a normal range. As a result, the treatment was changed to diazepam. After an IVD of diazepam, the patient's symptoms rapidly improved, and the IVD was subsequently replaced with oral administration of lorazepam. Eventually, the patient was diagnosed with MC associated with schizophrenia. BZD therapy was dramatically effective.Conclusion:Catatonia, MNS, and MC may be due to a common brain pathophysiology and these conditions may be in a spectrum, although uncertainty in the boundaries among conditions, and the BZD treatment may be useful. Most importantly, catatonia has not been described as a subtype of schizophrenia on the basis of the Diagnostic and Statistical Manual of Mental Disorders (DSM)-5 criteria, and the medications for catatonia and schizophrenia are different. Antipsychotics are not effective in relieving catatonia, or they may induce NMS, whereas BZDs are effective for treating both MC and NMS.

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Lethal catatonia

Cited by 238 publications

References 0 publications

Catatonia After Cerebral Hypoxia: Do the Usual Treatments Apply?

Catatonia After Cerebral Hypoxia: Do the Usual Treatments Apply?

Catatonia: Our current understanding of its diagnosis, treatment and pathophysiology

Response to benzodiazepines and the clinical course in malignant catatonia associated with schizophrenia

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