No abstract available.

No abstract available.

No abstract available.
Brain Stem* ; Evoked Potentials* ; Hallucinations* ; Humans

No abstract available.
Follow-Up Studies* ; Poisoning* ; Sodium*

There had been few reports of arachnoid cyst accompanying psychiaric disturbance and no report treated with low-dose resperidone administration. We report a patient, developed first-transient psychotic episode considered to be provoked by an arachnoid cyst, responsive to risperidone, which was found in the middle cranial fossa as follows. A 57-year-old man was admitted by suddenly developed headache, auditory hallucination, delusion of persecution and, an arachnoid cyst in the anteromedial aspect of middle cranial fossa was found on MRI after admission. The psychotic episode was first to him and he was also negative to other clinical evaluation including endocrine abnormality, his psychotic symptom was suspected to be induced by arachnoid cyst and was well controlled to low-dose risperidone administration. He left hospital free from psychotic symptoms on 14 hospital days.
Arachnoid* ; Cranial Fossa, Middle ; Delusions ; Hallucinations ; Headache ; Humans ; Magnetic Resonance Imaging ; Middle Aged ; Psychotic Disorders* ; Risperidone*

No abstract available.
Atrophy* ; Brain*

No abstract available.
Electroconvulsive Therapy* ; Prolactin*

OBJECTIVES: The purpose of this study was to investigate the effects of methysergide(serotonin receptor antagonist) on serum growth hormone response after electroconvulsive therapy(ECT). METHODS: We studied the changes of the serum growth hormone levels of the day before ECT(No ECT), ECT without methysergide pretreatment(ECT alone), and ECT with methysergide pretreatment(M+ECT) by radioimmunoassay method in 14 psychiatric patients. ECT was induced by the application of 110 volts for a period 0.3-1.0 second, using bitemporal electrodes. RESULTS: 1) Serum growth hormone levels at 15, 30, and 60 minutes after ECT were significantly increased in the ECT alone group than in the No ECT group(p<0.05). 2) Serum growth hormone levels at 15, 30, and 60 minites after ECT were significantly decreased in the M+ECT group than in the ECT alone group(p<0.05). CONCLUSION: These results suggest that the response of growth hormone after ECT seems to be mediated by the activation of serotonergic system.
Electroconvulsive Therapy* ; Electrodes ; Growth Hormone* ; Humans ; Methysergide* ; Radioimmunoassay

OBJECTIVE: Schizophrenia is known to have high genetic influences. Recently, the main focus of etiologic study in schizophrenia has been concentrated on molecular genetic approach including polymorphism analysis. This study was designed to investigate the relationship between schizophrenia and immunologic influences by analyzing polymorphism of TNFB that is involved in interaction between immunologic system and CNS. METHOD: 146 schizophrenic patients diagnosed by DSM-IV criteria were included and data of 206 normal population from the Catholic Hemopoietic Stem Cell Information Bank(Seoul, Korea) were used as a control group in this study. DNA was extracted from whole blood, thereafter amplified by polymerase chain reaction, and digested by NcoI. We obtained and assessd RFLP of two alleles, TNFB1 which has a NcoI restriction site generating 555bp and 185bp fragments, and TNFB2 which lacks the NcoI restriction site. All data were analyzed by K 2 test. RESULTS: There were no significant differences in frequency of TNFB1/1, TNFB1/2, and TNFB2/2 between the schizophrenic patient and the control group. Alleric frequencies of TNFB1 and TNFB2 were significantly different between schizophrenic patient and control group. CONCLULSION: We found the possible association between alleles of TNFB and schizophrenia in this study. To clarify the influences of TNFB on schizophrenia, further systematic studies should be conducted.
Alleles ; Diagnostic and Statistical Manual of Mental Disorders ; DNA ; Humans ; Molecular Biology ; Necrosis* ; Polymerase Chain Reaction ; Polymorphism, Restriction Fragment Length* ; Schizophrenia* ; Stem Cells

OBJECTIVE: Immediate early gene (IEG), c-fos is known to encode a 62 kDa nuclear protein (Fos) which has a critical role in the stimulus response process of many cells. c-fos can be activated in the central nervous system by a variety of physiological and pharmacological treatment. Recently evidences has been reported suggesting that glucocorticoid hormones, which are released from adrenal cortex in response to stress, may regulate IEG expression. We observed whether immobilization stress or corticosterone altered the induction of c-fos by haloperidol in the nucleus accumbens, lateral striatum, and prefrontal cortex. METHODS: Twenty-four healthy Wistar rats of male sex, weighing 300-450 g, were divided into 6 groups according to injection agents [vehicle (1 mg/kg), haloperidol (1 mg/kg), corticosterone (1 mg/kg), immobilization stress, haloperidol (1 mg/kg) and corticosterone (1 mg/kg), haloperidol (1 mg/kg) and immobilization stress] respectively. Fos-immunoreactivity was measured by counting of Fos-positive neurons in the nucleus accumbens, lateral striatum, and prefrontal cortex. RESULTS: (1) The number of Fos-positive neurons in the nucleus accumbens was significantly decreased in the haloperidol plus immobilization stress group and haloperidol plus corticosterone group compared with that in the haloperidol group (p<0.05). (2) The number of Fos-positive nurons in the lateral striatum was significantly decreased in the haloperidol plus corticosterone group compared with that in the haloperidol group, but the number of Fos-positive neurons in the lateral striatum was not significantly different between the haloperidol plus immobilization stress group and the haloperidol group (p<0.05). (3) The number of Fos-positive neurons in the prefrontal cortex was significantly increased in the haloperidol plus immobilization stress group and haloperidol plus corticosterone group compared with that in the haloperidol group (p<0.05). CONCLUSION: These results suggest that regulatory process exerted by corticosterone may alter the antipsychotic effect of haloperidol.
Adrenal Cortex ; Animals ; Antipsychotic Agents ; Brain* ; Central Nervous System ; Corticosterone* ; Haloperidol ; Humans ; Immobilization* ; Male ; Neurons ; Nuclear Proteins ; Nucleus Accumbens ; Prefrontal Cortex ; Rats* ; Rats, Wistar