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 42-year-old man developed necrosis of the brainstem 10 months following fast neutron irradiation of a recurrent adenocystic carcinoma of the right submandibular salivary gland. The neoplasm had been diagnosed 15 years earlier. Neck dissection and several local excisions failed to control local extension, so that 7000 rad 4.8 MeV x-rays were administered. The right mandible and part of the tongue and palate were resected for recurrence and chemotherapy and transfer factor were given. Because of cranial neuropathy and erosion of the skull base, fast neutron radiation (2.080 rads) was administered five and one-half years after the x-ray therapy, but to a nonoverlapping field. Ten months later, rapidly progressive symptoms and signs of multiple cranial nerve palsies on the right side and left hemihypesthesia and hemiplegia appeared. Clinical manifestations of brainstem necrosis lasted 4 months. Postmortem examination demonstrated radionecrosis of pons and upper medulla, predominantly on the right side. This case illustrates the efficacy of neutron radiation in eradicating local carcinoma and also the serious complications of this therapeutic modality.
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PMID:Delayed radiation necrosis of brainstem related to fast neutron beam irradiation: case report and literature review. 22 99

A 37-year-old woman was admitted to Osaka Neurological Institute after the sudden onset of left hemiplegia, hemihypesthesia, and ipsilateral hemianopia on February 4, 1992. Computed tomography (CT) disclosed the presence of hemorrhage in the right thalamus extending to the ipsilateral internal capsule. Cerebral angiography after CT scanning disclosed the presence of a cerebral arteriovenous malformation (AVM) fed by copsulothalamic and lateral geniculate body arteries originating from the right anterior choroidal artery. She was operated on with removal of the AVM using a right orbito-fronto-malar approach (OFM approach), which did not require transection of the cerebral parenchyma. The anterior choroidal artery could be followed distally from its origin and small feeding branches originating from the parent artery were easily identified, and the cerebral base could be examined in greater detail than with the conventional frontotemporal approach. The nidus could be excised in its entirety without difficulty. Postoperative angiography confirmed total excision of the AVM. She was transferred to another hospital for rehabilitation on April 13, 1992. Motor strength on the left side had improved to 3/5 by that time. The OFM approach appears to be potentially useful for the resection of inferolateral thalamic AVMs, because it does not require corticotomy and feeding branches can be identified and dealt with prior to other surgical manipulations.
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PMID:Total excision of a thalamic arteriovenous malformation using an orbito-fronto-malar approach: case report. 797 23

Patients with carotid cerebrovascular disorder can be categorized as having either right hemiplegia with various degrees of aphasia, left hemiplegia with hemihypesthesia, or homonymous hemianopsia, or the triad of left hemiplegia, hemihypesthesia and homonymous hemianopsia. The purpose of this study was to compare the functional performance of patients with each type of carotid cerebrovascular disorder before and 1 year after comprehensive rehabilitation aimed at improving communication and/or functional skills. Performance was measured using both the Barthel Index and Williams Drawing Test. On average, patients with the triad of neurologic deficits started and finished with poorer functional performance than the other patients. However, the average gain in functional scores over time was similar for all groups.
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PMID:The triad of left hemiplegia, hemihypesthesia, and homonymous hemianopsia: implications for rehabilitation. 809 Dec 55

A 59-year-old male patient presented in 1991 with left-sided hemiplegia and hemihypesthesia and left homonymous hemianopsia, which had developed for the preceding 12 months. The cerebrospinal fluid (CSF) level of protein was mildly elevated, oligoclonal IgG band was initially negative, but finally positive and myelin basic protein was absent. Magnetic resonance imaging and X-ray computed tomography (CT) of the brain revealed a unilateral demarcated lesion extending around the posterior horn and triagular part of the right lateral ventricle, apparently capped by remarkably gadolinium enhancement at its front, which had no mass effect, and several small isolated plaques were also observed in other areas of the brain. All lesions appeared as high intensity areas on T2 weighted images and hypodense areas on CT. The JC virus hemagglutination-inhibition antibody titers were 1:32 in serum and 1:8 in CSF; the antibody titer ratio and index both suggested an intrathecal antibody production. Pathological examination of brain biopsy specimen taken from the large lesion demonstrated profound demyelination with preservation of axons, a large number of macrophages and spotted perivascular lymphocyte cuffings. Based on this experience, we discussed the features in this case which differentiated it from multiple sclerosis, leukodystrophy and typical progressive multifocal leukoencephalopathy (PML). Diffuse-disseminated sclerosis or transitional sclerosis was most likely so far as the clinical picture, imaging and histology were concerned. However, we implicated the possible involvement of JC virus infection to the etio-pathogenesis of the demyelinating lesions in view of the intrathecal JC virus antibody production in CSF observed in this case.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A unilateral large demyelinating lesion in the cerebral white matter with slowly progressive hemiplegia and intrathecal JC virus antibody production]. 839 19

We describe a patient with successive attacks (40 to 90 minutes) of cluster-like headache associated with aphasia, and contralateral hemihypesthesia and hemiplegia. The condition can best be described as cluster-like headache aura status.
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PMID:Cluster-like headache aura status. 1566 19

We describe a patient with successive attacks (40 to 90 minutes) of cluster-like headache associated with aphasia, and contralateral hemihypesthesia and hemiplegia. The condition can best be described as cluster-like headache aura status.
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PMID:Manual therapies in the management of tension-type headache. 1570 27

We report a 47-year-old woman with progressive multifocal leukoencephalopathy (PML). She was a carrier of HTLV-I virus, and developed subacute right hemiparesis and marked motor aphasia. She had a malignant lymphoma in the left neck and basal cell carcinoma in the right inguinal region. Three months after the onset, she became unable to walk because of the right leg weakness or to speak because of motor aphasia. Magnetic resonance imaging (MRI) revealed multifocal T2-high lesions in the white matter of the left frontal lobe, and a brain biopsy revealed demyelinating pathology. A biopsy of the left parotid gland revealed a diffuse pleomorphic type large B cell lymphoma. Although anti-HTLV-I antibody was positive in the serum and cerebrospinal fluid (CSF), no adult T-cell leukemia (ATL) cells were found in the blood or CSF. The patient was then admitted to our hospital. Neurological examinations revealed severe motor aphasia, mild sensory aphasia/cognitive impairment, right hemiplegia, mild right hemihypesthesia, limb-kinetic apraxia in the left hand, idiomotor apraxia, agraphia, perseveration, marked spasticity and brisk tendon reflex in four extremities, and positive bilateral pathological reflexes. MRI showed multifocal T2-high lesions mainly in the cerebral white matter, predominantly in the left hemisphere, and partly in the cerebral cortex. No gadolinium enhancement was found. In addition, 99mTcECD-SPECT showed a broad decrease in cerebral blood flow (CBF) in the cortex. Anti-HTLV-I antibody was positive but anti-HIV antibody was negative in serum. ATL cells were found in 1-3% of the peripheral white blood cells after admission. CSF examination revealed that the cell count (1/microl), protein level (24 mg/dl), and IgG index (0.4) were all normal. However, the myelin basic protein level (321 pg/ml; normal < 102) was increased, JC virus DNA was detected by PCR, and anti-HTLV-I antibody (x 8) was detected in CSF. The regulatory region of the JC virus DNA in the CSF was partly deleted; immunostaining with anti-JC virus protein antibodies revealed the existence of JC virus in biopsied brain specimens, and these findings were consistent with PML. Her symptoms such as motor aphasia, cognitive dysfunction and left hemiparesis were subacutely progressive, and she developed akinetic mutism two weeks after admission. Since the efficacy of cytosine arabinoside for PML has been reported, she was administered 80 mg/day of the drug for five days. After treatment, her communication function was mildly improved but the efficacy was transient. Since it has been reported that HTLV-I, as well as HIV, activates the JC virus promoter and its proliferation, the latent infection of HTLV-I in the central nervous system (CNS) in this case might have stimulated the JC virus proliferation, promoting lesion extension over the cerebral cortex. There have been only a few reports of broad decreases in CBF by SPECT in PML patients. Further MRI and SPECT studies on PML patients are therefore necessary to evaluate the significance of HTLV-I in promoting the JC virus infiltration into the CNS.
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PMID:[A case of progressive multifocal leukoencephalopathy presenting white matter MRI lesions extending over the cerebral cortex and a marked decrease in cerebral blood flow on SPECT, and associated with HTLV-I infection]. 1602 67