Depression and hallucination are the two main psychiatric symptoms in parkinsonian patients. Depressive features in Parkinson patients are very close to those of endogenous depression, except for a relative lack of anxiety, irritability, suicidal ideations, delusions and circadian rhythm. Pharmacotherapy with antidepressants is most reliable in the treatment of parkinsonian depressives, although levodopa or other antiparkinsonian drugs may relieve a depression. Hallucinatory complications of long-term antiparkinsonian treatment appear in two types of symptoms: (1) hallucinosis type – vivid visual hallucination and illusion with clear consciousness and well-preserved orientation, and (2) delirium type – less vivid visual hallucination and illusion with disturbed orientation and confusion. Antipsychotic drugs and 'drug holiday' are recommended for the management of hallucinations as side effects of antiparkinsonian drugs.
Spongy state and degeneration of the white matter in the 6-aminonicotinamide intoxicated rats were studied neuropathologically and electromicroscopically. Young albino rats, four weeks of age, received 0.1% of 6-aminonicotinamide solution intraperitoneally as a single dose of 10 mg/Kg of body weight. Four hours after the administration, paralysis of the hind limbs occurred in the rats. Neuropathological investigations revealed a characteristic spongy and degenerative change of white matter as well as gray matter of the central nervous system. Corpus callosum, cerebellar cortex, and optic nerves showed edematous and spongy degeneration in the early stage of the experiment. Ultrastructural changes of myelin sheath were initially seen in the vicinity of severely damaged oligodendrocytes. The vacuoles in the myelin, i.e. intramyelinic vacuoles, were formed by splitting between the innermost myelin lamellae and axon. Axons remained usually unchanged in the early stage. The pathogenesis of ultrastructural changes of the white matter in the 6-aminonicotinamide intoxication was discussed.
Abstract: The relationship between the quantitative EEG variables and plasma levels after the administration of diazepam (DZ) or N‐desmethyldiazepam (synthesized NDDZ) was evaluated by simultaneously measuring the power spectra for EEG with two biological markers and plasma concentrations. After a single DZ administration, the EEG change corresponding to sedation appeared rapidly and showed a short duration. A close relationship was found between these effects and changes in the DZ plasma concentrations. DZ and synthesized NDDZ had the same pharmacodynamic characteristics, but the main metabolic product of DZ (metabolite NDDZ) showed a different pharmacokinetic profile. A multiple administration of DZ or synthesized NDDZ caused some reduction in sedation at the steady‐state. These results led to the conclusions that a single administration of DZ causes sedation of a short duration, and the main metabolic product of DZ (metabolite NDDZ) does not seem to contribute to sedation. In addition, the reduction in the pharmacological effect after continuous treatment with DZ depends not on autoinduction or interference, but on acute tolerance or adaptation.
