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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.

We describe a case of monozygotic (MZ) male twins (14.6 years old) who suffered from a severe form of catatonic schizophrenia. On admission, the principal symptoms of the brothers were stupor, mutism, catatonic posturing, rigidity, negativism, and refusal of food and liquids. They were treated with electroconvulsive therapy (ECT) with no effect (twin A) and almost no effect (twin B). Both twins improved with initiation of olanzapine therapy. Twin B showed a marked improvement by week 2 on a dose of 10 mg daily (qd). Improvement in twin A was seen by week 4 on a dose of 15 mg qd. Twin B was discharged after 8 weeks and twin A after 11 weeks of olanzapine treatment. This appears to be the first report on concordant positive responses to olanzapine in MZ twins with catatonic schizophrenia, as well as, the first report on concordant resistance to ECT.

The association between neuroleptic treatment and the negative symptom dimension (ND) was evaluated in 1528 schizophrenia patients. In patients receiving more than 820 mg chlorpromazine (CPZ), those with catatonic-type disorder had significantly (p<0.05) higher ND scores than those in any of the other diagnostic subtypes. Even in patients receiving 450 mg CPZ or more, catatonic patients had significantly (p=0.046) higher ND scores than other patients. Patients with catatonic schizophrenia are highly vulnerable to negative symptoms related to neuroleptic drugs, probably because of a defect in their dopaminergic neuronal pathways.

Catatonia is a rare but difficult-to-treat disorder. Here, we report on the case of a schizophrenic patient who developed several episodes of severe catatonia after suffering from adequately treated Lyme disease with encephalitis. The catatonic stupor was not responsive to typical neuroleptics and benzodiazepines. After the medication was changed to risperidone, there was a dramatic and persistent improvement of the patient's condition. Two relapses during the follow-up period over five years were caused by dose reductions. Risperidone might be a promising drug in the treatment of acute catatonia and in preventing further episodes.

Thirty-five patients suffering from schizophrenia, as diagnosed by the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, were preselected from 7 clinical trials according to a priori criteria of catatonic signs and symptoms based on 3 Positive and Negative Syndrome Scale (PANSS) items: scores for PANSS item 19 (mannerism and posturing) and either item 4 (excitement) or item 21 (motor retardation) had to exceed or equal 4 at baseline. This particular patient population represents a severely psychotic sample: mean +/- SD PANSS total scores at baseline were 129.26 +/- 19.76. After I week of olanzapine treatment, mean PANSS total score was decreased significantly (-13.14; p < .001), as was mean PANSS total score after 6 weeks of olanzapine treatment (-45.16; p < .001); additionally, the positive subscale, negative subscale, and mood scores improved significantly. A significant improvement in the catatonic signs and symptoms composite score was also observed at week 6 (-4.96; p < .001). The mean +/- SD daily dose of olanzapine was 18.00 +/- 2.89 mg after 6 weeks of treatment. The present data analysis suggests the efficacy of olanzapine in the treatment of severely ill schizophrenic patients with nonspecified catatonic signs and symptoms.

This case report documents the response of a young, first-episode, neuroleptic naive male with severe catatonic schizophrenia to the novel antipsychotic, risperidone. Initial assessments included the Positive and Negative Syndrome Scales, Global Assessment of Function and the Extrapyramidal Symptom Rating Scale. These were repeated at discharge from hospital and during a 3.5 year outpatient follow-up. Neuroimaging (computed tomography, magnetic resonance imaging and single photon emission tomography) along with electroencephalogram and laboratory examinations were completed. Response to risperidone was prompt, dramatic and sustained over the follow-up period. Possible neurochemical brain mechanisms resulting in catatonia and the role of serotonin/dopamine antagonists such as risperidone are discussed. No other literature on the effect of risperidone in the treatment of severe catatonic schizophrenia in a first-episode patient has been reported.

Lethal catatonia and the malignant neuroleptic syndrome represent two potentially fatal disorders that require different therapeutic regimens. Clinical differentiation is considered difficult because of a number of similarities with respect to mode of onset, signs and symptoms, and outcome. Recent observations emphasizing similarities between the two disorders, however, suggest that catatonia and the malignant neuroleptic syndrome may not represent separate diagnostic entities. Instead, the malignant neuroleptic syndrome has been hypothesized to be a neuroleptic-aggravated form of catatonia. In the present paper, we report the case of a 22-year-old male who developed different forms of malignant neuroleptic syndromes subsequent to a catatonic episode and overlapping it. In addition, the course was complicated by the occurrence of heterotopic calcification within skeletal muscles. The clinical value of diagnostic criteria that help distinguish catatonia from neuroleptic malignant syndrome and their therapeutic consequences are discussed.

The present paper discusses appearance and course of neuroleptic induced hypothermia of a 36 years old woman suffering from periodic catatonia and a 38 years old seriously mentally handicapped man. Analysis of clinical studies and pharmacological tests with animals about body temperature changes caused by neuroleptics yields that these may lead to hypothermia as well as hyperthermia, depending on individual disposition and dose, which is mainly a result of their effect through dopaminergic neurons of the hypothalamus, which controls thermoregulation, and of their influence on vasomotoric mechanisms of vessels of the skin. Though hyperthermic changes are more hazardous and occur more frequently hypothermia by neuroleptic agents is clinically relevant as shown by the summarizing presentation of previously released case reports: hypothermia is found at neuroleptic medicated healthy volunteers and at psychiatric patients with or without physical illness, at which hypothyreosis and impair of the brain seem to represent special risks.

Four schizophrenic patients are reported in whom the acute development of dystonic muscle spasms, usually involving gaze deviation, was accompanied by the exacerbation or appearance of psychotic symptoms. In all cases the relationship between the neurological and psychiatric phenomena was close, and sometimes the presentation was bizarre or dramatic. The similarity of these states to the complex neuropsychiatric disturbances seen in post-encephalitic Parkinsonism is emphasised.

Fifty chronic schizophrenics with severe residual psychopathology were followed up over a 5-year period. All of them had continuously received neuroleptics for many years before and throughout the period of investigation. In 60% (n = 30) of the patients positive symptoms which were unchanged in quality and severity were present throughout the period of investigation. In 28% (n = 14) of the patients marked positive symptoms persisted from the very beginning up to 1990 (in every case more than 20 years). Applying Leonhard's classification it was obvious that syndromes are roughly unchanged with respect to the preneuroleptic era. In these patients neuroleptics seemed to have only unspecific suppressing effects on affectivity. It is supposed that in schizophrenia which leads to severe residual psychopathology, Leonhard's classification is superior to the positive-negative distinction and is a promising concept for future research in etiology and therapy.

A Japanese family consisting of a mother and her two daughters, all experienced NMS on therapeutic or subtherapeutic doses of neuroleptics. The mother and the elder daughter had past histories of severe neuroleptic-induced extrapyramidal symptoms. The predisposition to this syndrome may be genetically transmitted. We suggest that neuroleptic treatment should be introduced with extreme caution to a patient with a family history of NMS.

Reinstitution of antipsychotic medication is problematic in patients with a history of neuroleptic malignant syndrome (NMS). In this case, a patient with a history of probable neuroleptic malignant syndrome caused by administration, as single agents, of haloperidol, molindone, and lithium was later treated successfully with the novel antipsychotic clozapine. The propensity of various antipsychotic agents to cause NMS is discussed.