Brain neurotransmitter changes in three patients who had a fatal hyperthermia syndrome

Article Abstract:

Fatal hyperthermia syndrome, also called neuroleptic malignant syndrome, refers to a range of symptoms, both mental and physical. Severe motor function disturbances often occur, resulting in either inhibition or agitation. Inhibition may cause a catatonic stupor condition; a state of catatonia prior to death is characteristic of this disease. Other symptoms that have been observed in these patients include dramatic circulatory disturbances leading to a total breakdown of the nervous system causing sweating, irregular heart beat, and extremely high fever (hyperthermia). Some believe that this condition is an adverse reaction to psychotropic drugs. The actual pathophysiology of this condition is unknown, but there is some evidence which suggests that the brain dopamine system is involved. To further investigate this, the brains of three patients who died from fatal hyperthermia syndrome were examined at autopsy. In all three patients, a significant decrease in noradrenaline in the hypothalamus was found. In two patients, a severe brain choline acetyltransferase deficiency, accompanied by nucleus basalis cell loss, was detected; the third patient had mild to moderate brain choline acetyltransferase loss. All the patients had received neuroleptic drugs; striatal dopamine metabolite/dopamine ratio was below normal in two patients and normal in the third; after short-term neuroleptic therapy, these concentrations would be expected to be elevated. This suggests the possibility of the involvement of dopamine system malfunction in the development of fatal hyperthermia syndrome. One or more of these brain neurotransmitter abnormalities may predispose individuals to this condition. (Consumer Summary produced by Reliance Medical Information, Inc.)

Abnormalities, Cholinergic mechanisms, Neurotransmitters, Neuroleptic malignant syndrome

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Autoantibodies to brain lipids in schizophrenia

Article Abstract:

Although the cause of schizophrenia is still unknown, some have hypothesized that the disorder is a result of a viral infection which creates an autoimmune response within the patient. Thus far, the evidence to support this theory is inconclusive. Efforts have been made to detect and identify an antibody against brain tissues in schizophrenics. Some studies have suggested that immunoglobulin G antibody against brain lipids may be involved. This study has investigated the serum level of antibodies against specific brain lipids in 38 schizophrenic patients and in 22 normal controls. It was thought that schizophrenics would have higher levels of antibodies against these lipids than normal control subjects. Blood samples of the subjects were taken and tested using an ELISA (enzyme-linked immunosorbent assay) technique to measure antibody levels. No significant differences were found between the antibody levels in the two groups; the data did not substantiate the results of the early studies. The results are discussed with suggested interpretations of the data. It was pointed out that testing for other brain antigens might reveal different results; only two types were measured in this experiment. Limitations of the study which may have influenced the results are also discussed. (Consumer Summary produced by Reliance Medical Information, Inc.)

Research, Measurement, Autoantibodies, Lipids, Schizophrenia, Brain chemistry

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Clozapine-induced stuttering: epileptic brain activity?

Article Abstract:

A case of stuttering associated with clozapine is reported, in which the stuttering was followed by a generalized epileptic seizure, and recovery occurred after antiepileptic treatment.

Case studies, Complications and side effects, Epilepsy, Stuttering, Clozapine

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