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This study examines early antiepileptic treatment with valproic acid for acute cerebral hemorrhage against a placebo group immediately post event to evaluate the outcome of these patients regarding seizures and neurological outcome.
Allocation: Randomized, Control: Placebo Control, Intervention Model: Parallel Assignment, Masking: Double-Blind
Post Cerebral Hemmorrahge
valproic acid, palcebo bid
Wolfson Medical Center
Published on BioPortfolio: 2010-07-15T17:00:00-0400
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A fatty acid with anticonvulsant properties used in the treatment of epilepsy. The mechanisms of its therapeutic actions are not well understood. It may act by increasing GAMMA-AMINOBUTYRIC ACID levels in the brain or by altering the properties of voltage dependent sodium channels.
Bacterial infections of the leptomeninges and subarachnoid space, frequently involving the cerebral cortex, cranial nerves, cerebral blood vessels, spinal cord, and nerve roots. The type of causative organism varies with age and clinical status (e.g., post-operative, immunodeficient, or post-traumatic states). Clinical manifestations include the acute onset of fever, stiff neck, altered mentation, seizures, and focal neurologic deficits. Death may occur within 24 hours of disease onset. Pathologic features include a purulent exudate in the subarachnoid space, and diffuse inflammation of neural and vascular structures. (From Joynt, Clinical Neurology, 1994, Ch24, pp1-5)
Syndromes which feature DYSKINESIAS as a cardinal manifestation of the disease process. Included in this category are degenerative, hereditary, post-infectious, medication-induced, post-inflammatory, and post-traumatic conditions.
Bleeding into one or both CEREBRAL HEMISPHERES including the BASAL GANGLIA and the CEREBRAL CORTEX. It is often associated with HYPERTENSION and CRANIOCEREBRAL TRAUMA.
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