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Severe imipramine-induced myoclonus in a patient with psychotic bipolar depression, catatonia, and schizencephaly.

Mild myoclonus is reasonably common with various cyclic antidepressants. However, antidepressants rarely cause severe myoclonus, and no risk or predisposing factors have been reported in the literature. We report a case of exceptionally severe myoclonus developing at therapeutic doses and modest serum levels of imipramine. The patient went on to experience dystonia and catatonia. Both of these were in typical settings (after haloperidol and with psychotic bipolar depression, respectively) and responded to typical treatment. On further investigation, the patient was found to have left-sided schizencephaly and a corresponding history of very mild developmental delay. We suggest that the onset of one movement disorder after drug therapy (eg, myoclonus) may predict the development of other movement disorders (e.g., catatonia). We further propose that severe tricyclic-induced myoclonus should prompt the physician to rule out a coexisting structural lesion of the central nervous system.

Adult↗

Malignant catatonia--a continuing reality.

A comprehensive review of the world literature confirms that malignant catatonia continues to occur and is reported and discussed in psychiatric community. It is associated with affective disorders as well as schizophrenia. The pathophysiology is still unclear but most reports suggest a hypodopaminergic state. Its reported mortality has declined from 75-100% in the preneuroleptic era to 31% during the review period (1986-1992). Bomocriptine, dantrolene, and benzodiazepines have been used with success but ECT has been found to be life-saving. The present review supports earlier reports that neuroleptics are frequently lethal in some patients with malignant catatonia.

Adult↗

Catatonia and ECT: Meduna's biological antagonism hypothesis reconsidered.

Catatonia is a motor syndrome with abnormalities in neuroendocrine regulation. Both the motor syndrome and the neuroendocrine abnormalities respond rapidly to electroconvulsive therapy (ECT). This rapid efficacy supports a neuroendocrine hypothesis of the mode of action of ECT and encourages neuroendocrine studies of catatonia.

Amobarbital↗

[Clomipramine in the treatment of catatonia].

The use of intravenous clomipramine gave rise to the remission of catatonia on the third or fourth day of treatment in two patients diagnosed as suffering from affective disorders. Therapeutic effect was maintained on switching to oral clomipramine. Clomipramine could be a therapeutic alternative in the management of catatonia associated with affective disorders.

Adolescent↗

[Malignant catatonia].

INTRODUCTION: Malignant catatonia is thought to be due to a severely decreased central dopaminergic activity of a medical, psychiatric, toxic-pharmacologic or idiopathic origin. CLINICAL CASE: A 24 year-old man presented with a generalized tonic-clonic seizure of focal onset. Within the following 48 hours, he developed agitation and paranoid ideation, which evolved into a severe catatonic syndrome complicated by aspiration pneumonia requiring transfer to Intensive Care Unit (ICU). Complementary tests (CT scan MRI, CSF, blood and urine studies) were negative or could not provide an etiological diagnosis. Initial EEG showed theta and delta waves, originating in the right frontal regions which later generalized. He stayed in ICU for the following three months in a state of catatonic stupor with frequent medical complications. During this time, he was given 27 sessions of electroconvulsive therapy (ECT) that eventually led to a remission of the catatonic syndrome. He was discharged from hospital one month later, fully asymptomatic except for a residuary amnesia, with a final diagnosis of idiopathic malignant catatonia. CONCLUSIONS: The authors have reviewed the management of this syndrome, which can be challenging for the physician because of the wide array of possible etiologies and its potentially lethal nature. A favorable outcome can be expected when ECT is started early, provided the underlying pathological process is treatable and there are no structural lesions in the central nervous system.

Adult↗

[A case of catatonia associated with the ingestion of hydroxyzine].

A twenty-six-year male who presented with a consciousness disturbance induced by the ingestion of an estimated 7g of hydroxyzine. He demonstrated bipolar symptoms which consisted of both stupor and excitement, and both an increase in muscle tension and apnea, however, these symptoms improved after the infusion of diazepam. He was diagnosed to demonstrate catatonia. After treatment composing three days of mechanical ventilation in combination with the administration of sedatives and muscle relaxatants, his symptoms improved. Hydroxyzine is thus considered to be able to induce catatonia and this mechanism of this condition is discussed.

Adult↗

[Multiple forms of monoaminoxidase in the rat brain during experimental catatonia].

Catalytic properties of multiple forms (separated by affinity chromatography) of rats brain mitochondrial monoamine oxidase (MAO, MAO-I, MAO-11 alpha, MAO-11 beta, MAO-111) have been studied in the animals selected for propensity to development of catatonic syndrome considered as an experimental model of the catatonic syndrome occurring in schizophrenia. It was shown that in experimental catatonia (as compared with rats of the corresponding control group) there was a dramatic increase in the brain stem of the rate of oxidative deamination of beta-phenylethylamine catalyzed by MAO-III; there was also a statistically significant (albeit less expressed than in the experiments with beta-phenylethylamine) increase in the rate of deamination of tyramine and a decrease in the rate of deamination of serotonin. In the systems with MAO-II beta we detected statistically significant increase in the rates of deamination of tyramine and beta-phenylethylamine in experimental catatonia as compared with corresponding control. Studies of multiple forms of brain MAO provide more informative data than estimation of "total" MAO activity (without separation of the multiple forms of this enzyme).

Animals↗

Catatonia as a manifestation of paraneoplastic encephalopathy.

The psychopathological, electrophysiological, and pathological features of a 58-year-old woman suffering from anaplastic lung carcinoma with paraneoplastic encephalopathy are presented. The predominant behavioral manifestation was a catatonic syndrome that was partially responsive to clonazepam. Although a variety of neurological, psychiatric, and other causes of catatonia have been reported, this is the first reported case of catatonia caused by paraneoplastic encephalopathy.

Brain Diseases↗

Lupus catatonia: a case report.

A 19-year old female with catatonia associated with multi-system involvement with systemic lupus erythematosus is described. There was no evidence of CNS involvement (negative CT scan, normal EEG, normal ice-caloric response, and normal CSF findings). The patient improved on large doses of steroids. It is suggested that cerebral lupus should be considered in the differential diagnosis of catatonia even in the absence of radiological and focal neurological signs when the active disease is present.

Adult↗

A case of catatonia induced by bacterial meningoencephalitis.

A 51-year-old man with renal cell carcinoma developed lethargy, disorientation, and fever; shortly thereafter, he had several episodes of sudden-onset catatonia. He was found to have bacterial meningoencephalitis and frontal lobe EEG abnormalities. Treatment with antibiotic and phenytoin was started, and the catatonic episodes subsided. The authors emphasize the need for a diligent investigation of all possible causes of sudden-onset catatonic syndrome and recommend that bacterial meningoencephalitis be added to the list of differential diagnoses of acute catatonia.

Acute Disease↗

GABAergic, dopaminergic and cholinergic interactions in perphenazine-induced catatonia in rats.

Anticatatonic effects of systemic and intracerebroventricularly administered GABAergic agents (GABA, muscimol piracetam, sod. valproate) were studied in rats against perphenazine-induced catatonia. All GABAergic agents, except piracetam, were found to posses anticatatonic actions as they significantly blocked perphenazine-induced catatonia. When these GABAergic agents were administered simultaneously with anticholinergic (scopolamine) or dopaminergic (bromocriptine) substances there was potentiation of the anticatatonic effect. The protective effect of GABAergic agonists and GABA antagonist and its modification by anticholinergic and dopaminergic agents has been explained on the basis of neurotransmitter interaction.

Animals↗

Intravenous lorazepam in neuroleptic-induced catatonia.

Presented here are four cases of catatonic reactions which were felt to be neuroleptic induced. Intravenous lorazepam was rapidly effective in reversing the catatonia and attendant symptoms. Lorazepam's previous uses and pharmacological profile are discussed. Reviewed briefly are catatonia and its neuroleptic-induced forms. Possible mechanisms responsible for the therapeutic effect of intravenous lorazepam in these cases are then examined.

Adult↗

[So-called pernicious catatonia].

After a review of the literature centered on the possible relationship of acute psychiatric symptomatology and death, more specifically in relation with acute catatonia, the writers examine all cases of schizophrenic patients admitted to the Psychiatric University Hospital of Lausanne (Hôpital de Cery) during the period from 1961 to 1981. The importance of acute catatonia is discussed and compared to other similar syndromes (the porcine stress syndrome, malignant hyperthermia, the neuroleptic "malignant" syndrome).

Acute Disease↗

Catatonia associated with disulfiram therapy.

This is the first report of a catatonic syndrome occurring in a patient receiving disulfiram treatment. A causal relationship is strongly suggested by the mode of onset, the absence of a previous history of catatonia, and the rapid resolution of the syndrome within 72 hours of discontinuance of the disulfiram therapy. Neurophysiological mechanisms which aid in elucidating the role of disulfiram in the etiology of catatonia are discussed. It is important that physicians be alerted to this serious, potentially lethal, complication, as it is readily reversible if the disulfiram is discontinued and appropriate supportive measures are taken. Also, it appears that these patients may be more susceptible to complications with future disulfiram usage and should be strongly counseled to seek alternative therapies for their alcohol problems in the future.

Alcoholism↗

Catatonia associated with glutethimide withdrawal.

Catatonia is a syndrome that is often considered as a subtype of schizophrenia, although studies have shown that it is most often associated with affective disorders. There are also many medical causes of catatonia. A case is presented in which glutethimide withdrawal seems the most likely explanation for catatonic symptoms.

Adult↗

Neuroleptic-induced catatonia: case report.

A case is reported of neuroleptic-induced catatonia that developed after treatment with loxapine succinate, a drug not previously reported to cause catatonia. The syndrome, characterized by marked parkinsonism, episodes of posturing, social withdrawal, and urinary incontinence, persisted during haloperidol treatment and remitted when the drug was discontinued. This syndrome appears to represent severe neuroleptic-induced parkinsonism.

Adolescent↗

[Treatment trials with hemofiltration/hemodialysis in pernicious catatonia].

Two juvenile patients affected for the first time with pernicious catatonia were treated repeatedly with combined hemofiltration and hemodialysis. During the first two or three sessions, the distinct psychopathological improvement only persisted during the session itself and in a lesser degree during the following hours. It was only after further treatments that the therapy effect lasted longer and passed over into a continuous remission tendency. The findings might support a toxin hypothesis (in a broad sense) with respect to the genesis of catatonia and encourage a continuation of the studies.

Adolescent↗