No abstract available.
Stroke*

To consider current concepts of epilepsy further, the brief review begins with a discussion of what is epilepsy, discribes multifactorial nature of epileptic disorders, and ends with a presentation of current classifications. A combination of the standard antiepielptic drugs(AEDs) may be necessary to treat intractable seizures, but no studies have been done to indicate an optimal combination. The new AEDs provide alternative choices, but questions remain about the optimal timing and manner of administration. AEDs selection must individualized, no drug of choice can be named for all patients.
Anticonvulsants* ; Classification ; Epilepsy* ; Humans ; Seizures

The knowledge about nutritional, toxic, and metabolic causes of dementia is particularly important, because they may be reversible. Central pontine myelinolysis(CPM) is one of these causes. CPM is a well known but rare metabolic disease of unknown etiology linked to overly aggressive correction of hyponatremia. We report a 74-year-old woman who developed disorientation, memory disturbance, and behavioral problem following intensive care unit management for pneumonia. Mini-mental status examination-Korean version(MMSE-K) study revealed severe cognitive dysfunction. Brain magnetic resonance imaging showed changes consistent with CPM and extrapontine myelinolysis. After supportive care, patient's clinical status was significantly improved. We suggest that a metabolic problem such as CPM should be considered in the diagnosis of acute or subacute cognitive deterioration in elderly patients.
Aged ; Brain ; Dementia ; Diagnosis ; Female ; Humans ; Hyponatremia ; Intensive Care Units ; Magnetic Resonance Imaging ; Memory ; Metabolic Diseases ; Myelinolysis, Central Pontine* ; Pneumonia ; Problem Behavior

Current treatment strategies for levodopa-induced psychosis in advanced Parkinson's disease have had limited success. Reduction or discontinuation of levodopa and coadministration with dopamine-blocking neuroleptics may attenuate the psychotic symptoms, but these strategies are associated with worsening of parkinsonian symptoms. Administration of 5-HT3 receptor antagonist ; ondansetron, a newer strategy to attenuate psychosis of Parkinson' disease without motor deterioration was introduced. A 41-year-old young-onset male, who was diagnosed as Parkinson's disease 7 years ago, was treated with levodopa therapy, and had levodopa-induced psychosis(delusion, hallucination, paranoid, insomnia). After trial of ondansetron, he showed improvement in the Brief Psychiatric Rating Scale(from 21 points to 9 points) in spite of increasing the dosage of levodopa. With ondansetron, we could increase the dosage of levodopa without psychotic complications(esp, hallucination), and he showed improvement in the motor fluctuation.
Adult ; Antipsychotic Agents ; Hallucinations ; Humans ; Levodopa ; Male ; Ondansetron ; Parkinson Disease ; Psychotic Disorders* ; Receptors, Serotonin, 5-HT3

BACKGROUND AND PURPOSE: Neurotrophic factors has been a subject of interest in the research of Parkinson's disease. In this experiment, intrastriatal 6-Hydroxydopamine(6-OHDA) injection was used to observe the effect of dopaminergic deafferentiation on the neurotrophic factor mRNA expression in the rat brain. METHODS: Male Sprague Dawley rats (250~300 gm) were treated to produce specific unilateral dopaminergic deafferentiation via injection of 6-OHDA at the right striatum without effect on the noradrenergic system. Treatment group (N=20) received same volume of vitamin C at the same site. The rats were sacrificed 3 hours, 12 hours, 24 hours, 3 days, 1 week, 2 weeks, 3 weeks, 4 weeks, after injection. The expression of nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), tyrosine hydroxylase (TH), and enkephalin (ENK) mRNA were observed by in situ hybridization histochemistry in the hippocampus, striatum and substantia nigra. RESULTS: The expression of BDNF mRNA was increased in the cerebral cortex, dentate gyrus, and hippocampus. In the cerebral cortex, the increase of expression was peaked at 12 hours after 6-OHDA injection and confined to injection side. In the dentate gyrus, the expression was significantly increased in the injection side at 12 hours after injection, after that increased expression was observed in both side. The expression of NGF mRNA was increased in the dentate gyrus and cerebral cortex of lesion side at 3 hours and 12 hours after 6-OHDA injection. However, the expression of NT-3 mRNA was not changed. The expression of TH mRNA was gradually decreased in the substantia nigra compacta of injection side from 1 week to 4 weeks after 6-OHDA injection. The expression of enkephalin mRNA was increased from 24 hours, peaked at 1week, and returned to basal level at 4 weeks after injection in the injection side. CONCLUSION: From this results, it may suggest that the expression of neurotrophic factors in the cerebral cortex, dentate gyrus and hippocampus are closely related with the degeneration of dopaminergic neurons, not with the degeneration of noradrenergic neurons.
Adrenergic Neurons ; Animals ; Ascorbic Acid ; Brain* ; Brain-Derived Neurotrophic Factor ; Cerebral Cortex ; Dentate Gyrus ; Dopaminergic Neurons ; Enkephalins ; Hippocampus ; Humans ; In Situ Hybridization ; Male ; Nerve Growth Factor ; Nerve Growth Factors* ; Oxidopamine* ; Parkinson Disease ; Rats* ; Rats, Sprague-Dawley ; RNA, Messenger ; Substantia Nigra ; Tyrosine 3-Monooxygenase

Recently protective and supportive functions of neurotrophic factors on dopaminergic neurons have been reported. In this study, in situ hybridization histochemistry with "S-labeled oligonucleotide probes for brain-derived factor (BDNF) and neurotrophin-3 (NT-3) mRNAs was performed to determine the effect of unilateral deafferentation of midbrain dopaminergic cells with 6-hydroxydopam'me (6-OHDA) on the expression of niRNAs of the above neurotrophic factors in the hippocampal areas. The deafferentation of midbrain dopaminergic cells induced changes of expression of BDNF mRNAs and NT-3 mRNAs. Although the reduction of NT-3 MRNA is limited to dentate gyrus of the lesion side, the induction of BDNF MRNA was observed in the lesion side firstly and then showed in the contralateral side conseqently. These results support the suggestion that these neurotrophic factors may protect or support dopaminergic neurons. In addition, these data propose the possibility that neurotrophic factors may be related with degenerative diseases such as Parkinson's disease.
Brain-Derived Neurotrophic Factor ; Dentate Gyrus ; Dopaminergic Neurons ; In Situ Hybridization ; Mesencephalon ; Nerve Growth Factors* ; Oligonucleotide Probes ; Parkinson Disease ; RNA, Messenger*

BACKGROUNDS: The inflammatory reaction after cerebral ischemia involving adhesion molecules aggravates neurologic deficit. This study aimed to study the change of plasma level of the adhesion molecules after acute cerebral ischemia. METHODS: Nineteen patients with acute cerebral infarction and ten control subjects without a history of cerebrovascular disease were included in this study. The patient groups were subgrouped into large artery atherosclerosis and small artery occlusion groups according to TOAST classification. Plasma levels of sP-selectin, sE-selectin, sICAM-1 and sVCAM-1 were measured within 24 hours and in 6 to 8 days after acute ischemic infarction. RESULTS: The plasma level of sP-selectin was elevated in acute stroke patients within 24 hours and in 6 to 8 days after stroke onset compared with control group(p<0.05). But plasma levels of sE-selectin, sICAM-1 and sVCAM-1 were not different from those of control group. The plasma level of sP-selectin was significantly elevated in large artery artherosclerosis group compared with control group. CONCLUSION: This study suggest that P-selectin actively involves in inflammatory process after acute ischemic stroke, especially associated with atherosclerosis.
Arteries ; Atherosclerosis ; Brain Ischemia ; Cerebral Infarction ; Classification ; Humans ; Infarction ; Neurologic Manifestations ; P-Selectin ; Plasma* ; Stroke*

BACKGROUND AND PURPOSE: Valproic acid (2-propylpentanoic acid) which enhances GABA synthesis and blocks it's degradation has been useful treatment of migraine and may activate GABA receptors to modulate trigeminal nociceptive neurons innervating the meninges. But the mechanism and action of sodium valproate in headache is not clear. To investigate the mechanism of valproic acid action in headache model, we compared the change of dural plasma protein extravasation in both substance-P neurogenic inflammation rats with valproic acid pretreatment and without valproic acid pretreatment. METHOD: Sprague-Dawely rats were pretreated with valproate 30 minutes prior to substance-P administration in order to test the effects of sodium valproate on dural plasma protein extravasation by detecting the amount of extravasated Evans blue in the dura matter. To examine the abilities of either bicuculine (GABAA antagonist) and phaclofen (GABAB antagonist) to reverse the effect of valproate, they were administered 5 min before valproate administration. After then we also test the effect of muscimol (GABAA agonist) and bicuculine (GABAA antagonist) in substance-P induced neurogenic inflammation rats. RESULTS: Intraperitoneal injection of sodium valproate and muscimol reduced dural plasma protein extravasation after intravenous substance-P administration. The GABAA antagonist bicuculine completely reversed the effect of valproate and muscimol on plasma extravasation following substance-P administration, whereas the GABAB receptor antagonist, phaclofen, did not. CONCLUSION: We concluded that the attenuation of dural plasma protein extravasation by valproate and muscimol is mediated by via GABAA receptors within the meninges. Agonists and modulators at the GABAA receptor may become useful for the development of selective therapeutic agents for migraine headache.
Animals ; Evans Blue ; gamma-Aminobutyric Acid ; Headache* ; Injections, Intraperitoneal ; Meninges ; Migraine Disorders ; Muscimol ; Neurogenic Inflammation ; Nociceptors ; Plasma ; Rats* ; Receptors, GABA ; Sodium* ; Valproic Acid*

No abstract available.
Contraceptives, Oral* ; Female ; Humans

No abstract available.
Blood Platelets* ; Monoamine Oxidase* ; Selegiline*