Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018991 (hemiplegia)
 3,997 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 31-year-old veterinarian developed seizures, left hemiparesis, loss of memory, and behavioral disorders 5 months after intensive antirabies vaccination, the longest incubation period yet recorded. Computed tomographic scan revealed a right frontal contrastenhanced mass that extended to the left frontal lobe through the corpus callosum. Brain biopsy showed foci of primary demyelination largely confined to the white matter. The lesions were characteristic of the demyelinating encephalomyelitis that follows treatment with certain vaccines against rabies. The hemiplegia improved, but seizures, memory impairment, and abnormal behavior persisted.
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PMID:Delayed onset of post-rabies vaccination encephalitis. 613 53

A 70 year-old-man with recurrent herpetic keratitis had a meningo-encephalitis with transient left hemiplegia and disorders of consciousness. EEG disclosed periodic slow waves on the right temporal region. Isotope and CT scans showed focal abnormalities in the same region. Antibodies to herpes simplex virus were demonstrated by complement fixation in serum and specific antiherpes IgG and IgM by immunofluorescence assay in serum and CSF. A year later the patient had a status epilepticus. CT scan showed a large right temporal hypodense area. CSF was abnormal with pleiocytosis, increased protein and IgG levels. High titers of antiherpes IgG persisted in serum and CSF. Neuropsychological tests did not demonstrate any memory impairment. The occurrence of persistent inflammation after herpes simplex encephalitis is discussed. The unusual benign course without antiviral therapy, may be related to the reactivation of a latent infection with an efficient immunological response. The unilateral temporal necrosis may explain the absence of amnestic sequelae.
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PMID:[Acute necrotizing herpetic encephalitis with a spontaneously improving clinical course]. 669 26

We report the surgical morbidity and mortality and the results of statistical analysis based on the long-term outcome (average 50.1 months) of 69 patients with unruptured cerebral aneurysms. These patients harbored a total of 76 unruptured cerebral aneurysms, 72 larger than 3 mm in diameter. All the latter were surgically treated. There was no operative mortality. Operative morbidity occurred in 5 patients (7.2%), including hemiplegia in 2 from obliteration of perforator vessels, transient memory impairment in 2 due to brain retraction, and transient oculomotor nerve palsy in 1 patient resulting from an unknown etiology. During the observation period, 53 patients (76.8%) had a good or fair outcome, 11 (15.9%) had a poor outcome, and 5 (7.3%) died from causes unrelated to the aneurysms, such as pneumonia, gastrointestinal bleeding, and heart failure. The 5-year survival rate was 94%. Statistical analysis of the long-term outcome of all patients showed no significantly important factor influencing long-term morbidity. Prophylactic surgery of aneurysm is recommended for low-risk patients who may develop eventual rupture of an aneurysm, but perforator vessels around the aneurysm should be preserved, clips should be properly placed, and brain retraction should be minimized.
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PMID:Long-term outcome of surgically treated unruptured cerebral aneurysms. 798 92

Brain injury sequelae were observed in 24 patients who had sustained diffuse brain injury. According to their ability to lead social life, the severity was classified into 6 levels; vegetative, severe, moderate, mild, fair, and good. The severity levels statistically correlated with the length of the initial unconsciousness (Spearman's correlation coefficient r = 0.929, n = 24, p < 0.01), with posttraumatic amnesia (r = 0.827, n = 8, p < 0.05), with ventricular enlargement (r = 0.808, n = 24, p < 0.01) and with the presence of hemiplegia (r = 0.740, n = 24, p < 0.01). Children and young adults showed a tendency to improve to milder levels. Mild head injury patients who sustained concussion of less than 6 hours in duration also showed minimal sequelae such as mild ventricular dilatation and difficulty in recent memory. This memory impairment had often been ascribed to the so-called postconcussional syndrome. The threshold for occurrence of diffuse brain injury sequelae was estimated as concussion lasting 15-30 minutes or post-traumatic amnesia of a few days in duration in adults and about a week in children. Superficially localized brain contusion was frequently observed and was not correlated with the severity level, hemiplegia or post-concussional syndrome.
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PMID:[Clinical assessment of diffuse brain injury sequelae: with respect to so-called post-traumatic disorder]. 807 29

Subarachnoid hemorrhage (SAH) results in significant nerve dysfunction, such as hemiplegia, mood disorders, cognitive and memory impairment. Currently, no clear measures can reduce brain nerve damage. The study of brain nerve protection after SAH is of great significance. We aim to evaluate the protective effects and the possible mechanism of methazolamide in C57BL/6J SAH animal model in vivo and in blood-induced primary cortical neuron (PCNs) cellular model of SAH in vitro. We demonstrate that methazolamide accelerates the recovery of neurological damage, effectively relieves cerebral edema, and improves cognitive function in SAH mice as well as offers neuroprotection in blood- or hemoglobin-treated PCNs and partially restores normal neuronal morphology. In addition, western blot analyses show obviously decreased expression of active caspase-3 in methazolamide-treated SAH mice comparing with vehicle-treated SAH animals. Furthermore, methazolamide effectively inhibits ROS production in PCNs induced by blood exposure or hemoglobin insult. However, methazolamide has no protective effects in morality, fluctuation of cerebral blood flow, SAH grade, and cerebral vasospasm of SAH mice. Given methazolamide, a potent carbonic anhydrase inhibitor, can penetrate the blood-brain barrier and has been used in clinic in the treatment of ocular conditions, it provides potential as a novel therapy for SAH.
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PMID:Methazolamide improves neurological behavior by inhibition of neuron apoptosis in subarachnoid hemorrhage mice. 2773 52