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A case is reported in which catatonia and autonomic abnormalities occurred in a patient on long-term fluphenazine decanoate following overdose with an oral anorectic agent containing phenylpropanolamine and caffeine. The catatonic symptoms showed a rapid and complete resolution following intramuscular benztropine. A possible mechanism to explain the catatonic symptoms is discussed.
We performed a factor analysis on research data from 55 consecutive hospitalized psychiatric patients who showed one or more of eight catatonic motor features. Two factors were extracted, accounting for 32% of the variance. Factor 1 (mutism, negativism, stupor) corresponded to the clinical syndrome of negativistic stupor and was unrelated to diagnosis, sex, age at onset, family history, or treatment response. Factor 2 (mutism, stereotypy, catalepsy, automatic obedience) corresponded to the classical description of catatonia, was associated with a research diagnosis of mania, and tended (p less than 0.10) to predict a favorable treatment response. We suggest that the two factors may reflect different forms of cerebral dysfunction which, in the case of Factor 2, may provide clues as to the nature of the morbid process in mania. Republication is now in progress in a different sample.
A patient with schizophrenia for many years presented after an attempted suicide, a severe drug-induced catatonia. In these circumstances, an hereditary coproporphyria was discovered. Clinical and pathophysiological interrelationships between the two syndromes are discussed.
Similar clinical and biological features in lethal catatonia (LC) and neuroleptic malignant syndrome (NMS) suggest a relationship between both affections and common physiopathologic mechanisms. Pharmacological effects of several drugs--dopaminergic agonists, benzodiazepines, carbamazepine--suggest an impairment of several systems of neurotransmitters. We report the case of a young woman with infantile psychosis who developed catatonic syndrome worsened by neuroleptic treatment, arising the problem of the chronology of both affections. The evolution with treatment may partially explain the physiopathology. A 18-year old woman with an history of infantile psychosis, experienced insomnia, anorexia, paradoxical agitation developed after affective traumatism (mother's hospitalization). Chlorazepate (150 mg) remained inefficient and hospitalization was necessary. The patient was dumb, prostate in bed. She presented negativism, rigidity of the four limbs, catalepsia and hyperpyrexia (38.5 degrees C). Hepatic transaminases were increased (SGOT: 71 UI/l; N < 30). After cumulated dose of levomepromazine (100 mg) profuse sudation, thermic and cardiovascular instability, alteration of consciousness, major rigidity of limbs appeared. (Blood) hepatic transaminases and muscular enzymes increased. Bacteriological samples, cerebrospinal fluid analysis, CT-scan and EEG were normal. Within 48 hours after rehydratation and bromocriptine (30 mg per day) alteration of consciousness and autonomic disorders decreased but hyperpyrexia (38 degrees C) persisted. Biological parameters were normalized 10 days later. Negativism and psychomotor inertia remained. Lorazepam (3 mg per day) failed to be clinically beneficial. On carbamazepine (600 mg per day) she started speaking and moving spontaneously. Catalepsia disappeared but rigidity and anorexia persisted. Electroconvulsivotherapy (ECT) was necessary. After 2 shocks she started standing up, walking, taking food and speaking fluently.(ABSTRACT TRUNCATED AT 250 WORDS)
The most recent medical literature has emphasized the notion that catatonia is a syndrome rather than a disease and, on this basis it is associated with a wide variety of medical, neurological and psychiatric conditions. The authors report on five cases of catatonic patients with a favorable response to Lorazepam and analyze the possible mechanisms of action of this Benzodiazepine in catatonic syndrome.
Lethal catatonia (LC) is a life-threatening neuropsychiatric syndrome associated with a host of psychiatric, neurologic and medical conditions. The clinical picture is characterised by fragmented psychotic symptoms, catatonic phenomena particularly alternating stupor and agitation, altered consciousness, hyperthermia and other autonomic disturbances. A case of LC in a 19-year-old Chinese woman showing a dramatic response to lorazepam and bromocriptine is described and a brief overview of the contemporary literature is provided.
They are rare but dangerous complications in the course of acute psychotic diseases. A differential diagnose between these units, based on clinical symptoms, is impossible. Moreover the literature of the last years reveals, that the Malignant Neuroleptic Syndrome and Lethal Catatonia are identical complications in functional psychoses. This is also supported by the evidence of therapeutical consequences. In each case neuroleptics appear generally inadequate, and the interruption of neuroleptic medication is necessary, otherwise they would aggravate the disorder. An efficient supplementary treatment is the ECT.
The zinc transporter gene SLC30A4, located on chromosome 15q15-q21, has previously been reported to show altered expression patterns in post mortem analysis of the brains of schizophrenic patients. As a positional candidate we investigated SLC30A4 in the chromosome 15q15-linked schizophrenic phenotype periodic catatonia (MIM 605419), by means of a systematic mutation screening in affected individuals from exceptionally large pedigrees with perfect co-segregation of a chromosomal segment between marker D15S1042 and D15S659 in all affected individuals. The mutation scan revealed no genetic variants within the coding and the putative promoter region of SLC30A4 and, thus, excludes a genetic association of SLC30A4 with catatonic schizophrenia.
In the second paper on the Rating Scale for Psychotic Symptoms (RSPS), distraction symptoms (Subscale 2) and delusions (Subscale 3) are described. Subscale 2 includes distraction symptoms, which arise from one of two mechanisms: the symptom may arise either by loss of attentional focus (LAF) due to a competing channel of information, or by the intrusion of the competing channel into the focus of attention [attentional intrusions (AI)]. The symptom classes resulting from loss of attentional focus (LAF) include motor catatonia, negativism, and thought blocking; the attentional intrusions (AI) symptoms rated include three types of passivity experiences (Schneiderian symptoms): (1) thought insertion, (2) movements or action controlled, and (3) speech controlled by an external force. Subscale 3, consisting of delusions, is organized on the basis of content identification. Nineteen types of delusions are rated. Each item of delusional content is rated along three axes (active elaboration, persistence and active extinction) and complexity, and optionally if primary or mixed (i.e. primary with secondary elaborations). The last section of the paper includes the semi-structured interview (SCI-RSPS) for each of the items, as well as guidelines for practical application of the interview.
Multineuron activity was recorded from the sensorimotor cortex of the right and left hemispheres during immobilization catatonia in rabbits. The first session of immobilization of the animals was followed by changes in spike frequency in 47% of neurons in the sensorimotor cortex of the right hemisphere. Of these, 30% showed decreases in spike frequency and 17% showed increases. Spike frequency in the sensorimotor cortex of the left hemisphere changed in only 18% of cells, of which 13% showed decreases in spike frequency and 5% showed increases. The spike frequency of neighboring (recorded with the same electrode) neurons could change reciprocally. Differences in neuron activity in the two hemispheres were virtually absent after the second session of immobilization (several days after the first)--spike activity changed in 21% of neurons in the right hemisphere and 24% in the left hemisphere. The ratios of the numbers of neurons with increases and decreases in spike activity in "hypnosis" also became identical in the cortex of the right and left hemispheres. A hypothesis is proposed for the involvement of cortical neurons in the organization of "hypnosis-like" states.
Catatonia is a psychomotor syndrome characterized by concurrent emotional, behavioral, and motor anomalies. Pathophysiological mechanisms of psychomotor disturbances may be related to abnormal emotional-motor processing in prefrontal cortical networks. We therefore investigated prefrontal cortical activation and connectivity patterns during emotional-motor stimulation using functional magnetic resonance imaging (FMRI). We investigated 10 akinetic catatonic patients in a postacute state and compared them with 10 noncatatonic postacute psychiatric controls (age-, sex-, diagnosis-, and medication-matched) and 10 healthy controls. Positive and negative pictures from the International Affective Picture System were used for emotional stimulation. FMRI measurements covered the whole frontal lobe, activation signals in various frontal cortical regions were obtained, and functional connectivity between the different prefrontal cortical regions was investigated using structural equation modeling. Catatonic patients showed alterations in the orbitofrontal cortical activation pattern and in functional connectivity to the premotor cortex in negative and positive emotions compared to psychiatric and healthy controls. Catatonic behavioral and affective symptoms correlated significantly with orbitofrontal activity, whereas catatonic motor symptoms were rather related to medial prefrontal activity. It is concluded that catatonic symptoms may be closely related to dysfunction in the orbitofrontal cortex and consequent alteration in the prefrontal cortical network during emotional processing. Because we investigated postacute patients, orbitofrontal cortical alterations may be interpreted as a trait marker predisposing for development of catatonic syndrome in schizophrenic or affective psychosis.
Sudden death from aspiration pneumonitis during acute catatonia is a generally recognized but poorly understood occurrence. The author describes a case in which a schizophrenic patient died following aspiration of gastric contents. In view of findings that suggest that the acidity of gastric contents is related to morbidity following aspiration, he recommends that liquid antacid medication be given routinely to catatonic patients.
A 61-year-old white female patient with known endogenous depression developed acute life-threatening catatonia. Associated cardiac and respiratory insufficiency prevented drug therapy. The patient was successfully treated with ECT.
Lethal catatonia (LC) is a life-threatening syndrome associated with diverse neuropsychiatric or systemic disorders. Neuroleptic agents appear inadequate in treating LC. We report a case of LC successfully treated by electroconvulsive therapy (ECT) that adds to the experience of ECT as a safe and effective treatment for LC occurring in the context of the major psychoses. Anecdotal evidence suggests that ECT is dramatically effective in LC regardless of etiology. The use of ECT in the treatment of neuroleptic malignant syndrome (NMS), viewed here as a subtype of LC, is considered and compared with that of specific drug therapies for NMS.
In a patient with near-lethal catatonia, complications progressed from mild fever and tachycardia to severe hyperthermia, malignant hypertension, and cortical and subcortical dysfunction with increased urine cortisol and catecholamine concentrations, bilateral extensor toe reflexes, decerebrate posturing, and Cheyne-Stokes respirations. Electroconvulsive treatment reversed these changes and prevented almost certain death.
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).
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