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The clinical picture of catatonia includes impressive motor phenomena, such as rigidity, dyskinesia, festination, negativism, posturing, catalepsy, stereotypies and mannerisms, along with affective (e. g. aggression, anxiety, anhedonism or emotional lability) and behavioral symptoms (e.g. mutism, autism, excitement, echolalia or echopraxia). In English speaking countries seven catatonia rating scales have been introduced, which are widely used in clinical and scientific practice. In contrast, only one validated catatonia rating scale is available in Germany so far. In this paper, we introduce the German version of the Northoff catatonia rating scale (NCRS-dv). The original English version of the NCRS consists of 40 items describing motor (13 items), affective (12 items) and behavioral (15 items) catatonic symptoms. The NCRS shows high internal reliability (Crombachs alpha = 0.87), high interrater (r = 0.80-0.96) and high intrarater (r = 0.80-0.95) reliability. Factor analysis of the NCRS revealed four domains: affective, hyperactive or excited, hypoactive or retarded and behavior with individual eigenvalues of 8.98, 3.61, 2.98 and 2.82, respectively, which explained 21.5 %, 9.3 %, 7.6 % and 7.2 % of variance, respectively. In conclusion, the NCRS-dv represents a second validated instrument which can be used by German clinicians and scientists for the assessment of catatonic symptoms.

Based on a case study and the classic French concept of "monomania," the development of the psychiatric term "poriomania" is discussed. It is suggested that poriomania should still be regarded as a specific psychopathological symptom that can be part of various syndromes. The fate of monomanias is shown using examples whose traits are followed according to modern operationalized classification systems.

Between September 1st, 1994, and the end of August, 1995, 3% of all inpatients (21 of 731) were treated with electroconvulsive therapy (ECT) at the Department of General Psychiatry at the University Hospital for Psychiatry in Vienna. These patients suffered from psychotic and/or therapy-resistant depression (n = 15), therapy-resistant schizoaffective psychosis (n = 3), and catatonic schizophrenia (n = 3). ECT was administered in short-time anaesthetised and muscle relaxed patients. On average, each patient was treated with ECT on 9 non-consecutive days. As a rule, electrodes were placed unilaterally over the non-dominant hemisphere at the beginning. In four cases electrodes were placed bifronto-temporally. To be considered as effective the seizure had to last for at least 25 s. In shorter seizure duration ECT was repeated up to a maximum of three times in one session. With this procedure a reduction in clinical global impressions of -3.7 points was achieved in ECT-treated patients, who had been considered to be "severely" to "most severely" ill according to CGI before starting ECT. ECT proved to be effective for treating severe depression and catatonic schizophrenia, with only minor and reversible side effects. For establishing a favorable relation between good clinical outcome and remarkable few side effects, the following factors seem to be of importance, in accordance with the literature: (1) application of biphasic short-impulse stimuli in anaesthetised and muscle relaxed patients; (2) measurement of static impedance to avoid high skin impedance and short circuits. (3) at the beginning of each ECT series unilateral electrode placement over the non-dominant hemisphere; (4) ECT three times weekly on non-consecutive days.

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.

Two patients with acute schizophrenic or schizo-affective psychosis were treated with benzodiazepine-monotherapy. In the first patient with paranoid-hallucinatory psychosis, catatonic symptoms disappeared completely after application of Lorazepam. Side effects of neuroleptic medication (neuroleptic turbulences) were the reason for benzodiazepine treatment in the second patient. In neither patients were psychotic symptoms observed during several weeks on benzodiazepine medication. Subsequently, no further neuroleptic treatment was necessary in one patient. Benzodiazepine effects on schizophrenia are probably caused by an activation of inhibitory GABA-ergic neurons. Besides stupor and catatonia, severe side effects of neuroleptic treatment or even contra-indications of neuroleptic medication may be an indication for benzodiazepine treatment in acute schizophrenia.

In a case report the clinical manifestation of negativistic catatonia with its modified symptomatology by first onset in early childhood is presented. The symptomatology consists of negativism, negativistic excitations with (auto)aggressivity and impulsive behaviour. Development of expressive language is lacking or is arrested. Physical development is retarded. These conditions are seldom recognized but diagnosed as organic brain syndrome or more unspecifically as "pervasive developmental disorder" (DSM III-R, ICD 10).