Folia psychiatrica et neurologica japonica最新文献

In order to examine 5HT metabolism in the hypothalamo-pituitary (HP) system of chronic schizophrenic patients taking haloperidol for a short or long period, chronological changes of blood 5HT, PRL and HGH were measured after an oral loading dose of L-5hydroxytryptophan (L-5HTP), a precursor of 5HT. The subjects consisted of 8 male patients with chronic schizophrenia, who were divided into the following two groups. The 1st group--4 patients taking haloperidol (5.6 mg/day) for 8 months on an average (short-term treatment). The 2nd group--4 patients taking haloperidol (4.8 mg/day) for 7.5 years on an average (long-term treatment). The control group was made up of 9 healthy male volunteers. As a result, the basal level of blood 5HT in the 1st group was significantly higher than that in the control group. The blood 5HT levels in the 1st and 2nd groups showed an equally remarkable increase as compared with the control group. The basal level of plasma PRL in the 2nd group was significantly lowe than that in the control group. Moreover, in the 2nd group, an increase in the plasma PRL level after the loading was suppressed, but it showed less suppression in the 1st group. There was no significant difference in the basal HGH levels among the control, 1st and 2nd groups. After the loading, an increase in the plasma HGH was suppressed in the 2nd group, but the suppression was less in the 1st group.(ABSTRACT TRUNCATED AT 250 WORDS)

Three cases with the occurrence of asterixis during the administration of L-dopa were reported. Liver and metabolic functions were normal in all the patients. Upon the appearance of asterixis no other involuntary movements probably resulting from an excess administration of L-dopa were observed. Asterixis occurred accompanied by clinical symptoms such as hallucination and a mild clouding of consciousness by insomnia. Because of its reversal with drug withdrawal, asterixis seemed to be L-dopa-related. The biochemical basis of asterixis is not known but may involve the dopaminergic or serotonergic system.

Nine cases of neuro-Behcet's disease were investigated clinicopathologically. Pathological pictures of the central nervous system were characterized as follows: the site of predilection was the brain stem, followed by the spinal cord, cerebrum and cerebellum. The pathognomonic changes were recurrent inflammations around small vessels, causing a softening of the tissue. Lesions were composed of a perivascular infiltration of lymphocytes, histiocytes and microglias and, moreover, diapedesis, degenerated nerve cells and oligodendroglias, glial nodule, breakdown of myelin and axon, fatty granule cells and glio-mesenchymal proliferation were present occasionally. Electron microscopic studies on the neurons revealed no evidence of viral particles except for some accumulations of electron dense bodies.

Antibody titers to the Epstein-Barr virus (EBV) in the serum and cerebrospinal fluid (CSF) were determined in 57 cases of acute or subacute neurological diseases. As a result, sera from 11 cases (7 Bell's palsy, 2 encephalitis and 2 acute cerebellar ataxia) were found to be positive for antibodies to early antigen. Seven of these 11 cases either seroconverted for IgG antibodies to viral capsid antigen (VCA) or were proven positive for anti-VCA-IgM antibodies in the serum. While 4 were found positive for IgG antibodies to VCA in CSF, 3 tested by the anti-complement immunofluorescence method were all negative for EBV-associated nuclear antigen (EBNA) in CSF. Three of the 11 cases were considered to be of a primary infection with EBV because of a negative serologic test for antibodies to EBNA initially; a reinfection with the virus or a reactivation of the latent infection was suspected in some of the remaining cases.

The effect of chronic administration of chlorpromazine (CPZ) on the striatal synaptic vesicles was quantitatively investigated with an electron microscope. Six rats, three controls and three experimentals, which received 20 mg/kg b.wt. of CPZ daily for 15 months, were sacrificed and a total of 300 axo-dendritic spine synapses (50 synapses per animal) were randomly taken and divided into three zones with a width of 160-467 nm on electron micrographs (final magnification 60,000). The first zone was adjacent to the presynaptic membrane in the region of the synaptic cleft. The second and third were farther away from the first zone. In these zones we measured the vesicle density, vesicle size and vesicle elongation ratio (the shortest diameter/the longest diameter) with the following results: In both the CPZ-administered rats and the controls the vesicle number per unit area of axoplasm (vesicle density) was smaller in Zone III than in Zones I and II, while those in the latter two zones did not differ from each other. However, there was no significant difference in the vesicle number in any zone between the control and experimental animals. The vesicles in every zone were significantly larger in the CPZ-administered animals than in the controls. There were no conclusive findings on the vesicle elongation ratio (vesicle shape).

A polysomnography was performed on nine rabbits with electrodes chronically implanted at the sensorimotor and visual corticies and hippocampus. The physiological sleep of the rabbits was divided into three stages: awake (W), slow wave sleep (SWS) and REM sleep (REM). For autocorrelation and power spectrum analyses, a transitional zone (T) from W to SWS was added to the fundamental three stages. No essential differences between the mean frequencies of the cortical and hippocampal EEGs were seen. The mean frequencies of hippocampal EEG were as follows: 6.4 in W, 5.4 and 2.4 in T, 2.2 in SWS and 7.3 Hz in REM. The mean peak frequency of hippocampal EEG during REM was significantly higher than that during W.

The lumbar cerebrospinal fluid (CSF) gamma-aminobutyric acid (GABA) levels were measured in 27 patients with epilepsy, another three epileptic patients with status epilepticus and three epileptic patients with chronic cerebellar ataxia. The mean lumbar CSF GABA levels of the 27 patients with epilepsy were not significantly different from those of normal controls. Six of these 27 patients who had daily partial complex and partial motor seizures showed significantly low CSF GABA levels as did the six other patients, three each with status epilepticus and chronic cerebellar ataxia. These findings suggest that some epileptic patients have impaired brain GABAergic neurons.