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Query: UMLS:C0018991 (hemiplegia)
 3,997 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Because little was known about the prevalence of neurological complications of human immunodeficiency virus type 1 (HIV-1) infection in Africa, we conducted a cross-sectional study among consecutive admissions to the internal medicine wards of Mama Yemo Hospital in Kinshasa, Zaire. Of the 196 patients studied, 104 (53%) were HIV-1 seropositive, of whom 50 (48%) had stage 3 and 49 (47%) had stage 4 HIV-1 infection according to the provisional WHO staging criteria for HIV infection. Neuropsychiatric abnormalities were present in 43 (41%) of 104 HIV-1-seropositive patients. Of the HIV-1-seropositive patients, 9 (8.7%; 95% confidence interval, 4-16%) were diagnosed as having possible HIV-1-associated dementia complex, 1 (1%) as having possible HIV-1 myelopathy, and 3 (2.7%) as having possible HIV-1-associated minor cognitive/motor disorder. Definitive diagnoses could not be made because there were no facilities for neuroimaging and neuropathology. Meningitis caused by cryptococcus was diagnosed in six (5.6%) and by Mycobacterium avium in two (2%) of the HIV-1 seropositive patients. Acute onset hemiplegia, believed to be due to stroke, was present in four (4%) of the HIV-1-seropositive patients. The prevalence of other central nervous system opportunistic infections and mass lesions, especially toxoplasmic encephalitis, could not be assessed. In this population of Zairian inpatients, the prevalence of neurological complications of HIV-1 infection was similar to that observed in industrialized countries among patients with advanced HIV disease.
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PMID:Neurological complications of HIV-1-seropositive internal medicine inpatients in Kinshasa, Zaire. 131 94

We reported 9 cases of primary Sjogren syndrome (SS) who were complicated with nervous system involvement. All were women. Age between 24 to 58 years old. Their clinical symptoms of the nervous system varied widely, 7 of them manifested with the involvement of central nervous system, the main features were in case 1 bouts of seizures, case 2 multi-level damage of the brain and spinal cord which was similar to multiple sclerosis, case 3 recurrent hemiplegia caused by cerebral thrombosis then fatal vascular hemorrhage, case 4 sudden hemiplegia, case 5 persistent psychological disturbance, case 6 cranial neuropathy of V and VII, case 9 multi-focal symptoms of ataxia, myelopathy and transient blindness. 5 of the 9, case 3, 6-9 all appeared with the symptoms of peripheral neuropathy, case 7 also complicated with carpal tunnel syndrome. 4 of the 9 cases also complicated with renal tubular acidosis and/or chronic active hepatitis and/or fibrosing alveolitis and/or thrombocytopenic purpura and/or myositis. No differences of the positivity of autoantibodies was observed between those with or without nervous system involvement.
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PMID:[The manifestations of the nervous system in primary Sjogren syndrome]. 158 41

Six cases of myelopathy following anterior operations for removal of disc and fusion of the cervical spine are briefly summarized. Preexisting myelopathy or stenosis of the spinal canal may predispose to this complication. Paralysis may be immediate or delayed for hours. The amount of neural dysfunction is variable, and may fluctuate. Some cases are clearly due to intraoperative trauma caused, for instance, by dowel impaction or by use of the osteotome or drill; some are clearly due to clot. Other more arcane occurrences may be caused by edema, treated with hyperosmotic agents and steroids; or vascular disorder, treated with steroids and a deliberate increase in blood pressure and volume in a manner comparable to the treatment of postangiography or postcraniotomy hemiplegia. In some cases, rough instrumentation in the intervertebral foramen may be implicated. Some cases may be aggravated or induced by manipulation of the neck during intubation or change of position for operation. The risks are calculated as less than 2 per thousand but should be explained to the patient or the patient's family in obtaining consent for operation, since it would appear that even the most careful operation may be followed by this complication.
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PMID:Spinal cord malfunction after anterior cervical discectomy. 725 24

Seventy-three horses with cervical stenotic myelopathy underwent cervical vertebral interbody fusion (n = 63) or dorsal laminectomy (n = 10). Neurologic function improved in 77% of horses, and 46% of horses achieved athletic function (racing, race training, or pleasure riding) after cervical vertebral interbody fusion for static and dynamic spinal cord compressive lesions. Neurologic status improved in 4 of 10 horses after dorsal decompression for static compressive spinal cord lesions. The duration of clinical signs prior to surgical intervention was shorter for horses that achieved athletic function or improved by at least 2 neurologic grades than for horses that did not improve in neurologic status or improved 1 neurologic grade after cervical vertebral interbody fusion. The number of cervical spinal cord compressive lesions and age of horses did not affect the long-term surgical outcome of cervical vertebral interbody fusion. Seroma formation, implant failure, right laryngeal hemiplegia, and colitis were nonfatal complications associated with cervical vertebral interbody fusion. Dorsal laminectomy and cervical vertebral interbody fusion of static compressive lesions of the caudal cervical vertebral column were associated with fatal postoperative complications, including vertebral body fracture, spinal cord edema, and implant failure.
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PMID:Surgical treatment of cervical stenotic myelopathy in horses: 73 cases (1983-1992). 840 41

Records of 108 patients with lupus erythematosus beginning in childhood (1953-1990) were reviewed; 25 had recorded neurologic findings. This is the largest group of childhood lupus erythematosus patients with neurologic disease that has been reported. The average age of children at the time of diagnosis of lupus was 154 months. There were 22 girls and 3 boys in the group. All patients met at least four of the 1982 American Rheumatism Association criteria for the classification of systemic lupus erythematosus. Average age at onset of neurologic difficulties was 168 months. In 4 patients, the neurologic symptoms preceded the diagnosis: 1 month (spastic diplegia), 1 month (bilateral weakness and spasticity), 24 months (chorea), and 26 months (chorea), respectively. Four patients had neurologic symptoms coincident with the diagnosis of lupus erythematosus. In those patients whose symptoms followed the diagnosis of lupus erythematosus, the average elapsed time until symptoms appeared was 33 months; the single lowest and highest outliers were discounted. Most frequent findings were headache (16/25) and behavioral aberrations (10/25). All behavioral manifestations were depression except in 1 patient. Other prevalent findings included hemichorea or chorea (7/25), cerebrovascular accident with hemiplegia or diplegia (7/25), seizures (5/25), visual loss (3/25), and cranial neuropathy (2/25). Vertigo and myelopathy occurred in 1 patient each. All patients were treated primarily with corticosteroids and azathioprine; in the presence of active disease, the drug dosages were increased with significant improvement in neurologic symptoms. Resolution usually occurred from days to months; most improved in a few days to a few weeks; 3-4 months was the longest period until symptoms subsided.
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PMID:Neurologic characteristics of childhood lupus erythematosus. 855 56

Spontaneous cervical epidural hematomas are uncommon lesions that usually produce permanent neurological deficit unless there is early surgical decompression. They are now well-recognized by scan X and especially by sagittal MRI of the spine. We describe 2 patients, a 24 year-old man and a 79 year-old woman with no previous history of trauma who were admitted in emergency for a sudden weakness of limbs, respectively a tetraplegia and a right hemiplegia. Both patients complained of inaugural and acute neck pain. Motor deficit completely resolved in few hours and MRI of the spine showed on T1 a signal isointense, extending respectively from C3 to C6 and C5 to C7, consistent with an hematoma. Laboratory data and angiography were normal. Surgery was recused. Neck pain lasted about a week. Follow-up MRI, in one case, was normal two months later. Cervical epidural hematomas revealed by transient neurological findings that completely and permanently resolved are exceptional. They could mimic ischemic myelopathy and should be considered in the differential diagnosis of other painful vascular conditions like symptomatic vertebral dissection to avoid inappropriate anticoagulation. Conservative management in these cases may be proposed if spontaneous neurological resolution is confirmed by MRI.
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PMID:[Transient neurological manifestations disclosing spontaneous acute cervical epidural hematoma]. 929 66

We present an atypical case of adult moyamoya disease whose clinical onset consisted of ischemic symptoms of the brain stem. She initially presented with left hemisensory disturbance caused by a pontine lesion, followed by a myelopathy of the upper cervical spinal cord. Eight months later, she presented with left hemiplegia and disturbed consciousness. Magnetic resonance angiography showed significant narrowing of both horizontal portions of the middle cerebral arteries (M1). Conventional angiography revealed bilateral occlusion of the internal carotid arteries. Her anterior circulation was supplied from the vertebro-basilar system through Moyamoya vessels and leptomeningeal collaterals. The intracranial steal phenomenon was thought to be the reason for the preceding events in the brain stem and upper cervical spinal cord. In addition, transcranial color-coded duplex sonography (TCCS) showed identical findings to conventional angiography with antegrade flow in the proximal M1 and retrograde flow in the distal M1. Thus, TCCS was useful for diagnosing the M1 occlusion in this case of Moyamoya disease.
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PMID:An atypical case of adult Moyamoya disease with initial onset of brain stem ischemia. 960 Jun 84

Pediatric human immunodeficiency virus type 1 (HIV-1) infection is endemic throughout southern Africa. Neurologic complications are described in 20% to 60% of published series, mostly related to HIV-1 encephalopathy. With increasing HIV prevalence, more atypical cases are presenting. We present, as illustrative cases, seven children (three girls) with unusual neurologic sequelae as a consequence of HIV-1 infection. The median age at presentation was 33 months (range 7 months-6 years). Five of the seven children were developmentally normal before presentation. They presented with progressive multifocal leukoencephalopathy, myelopathy, intractable seizures, acute vasculitis and blindness, hemiplegia, peripheral neuropathy, and paraspinal lymphoma. Neuroimaging of the brain was performed in five patients, of whom one had basal ganglia calcification. All children had poor outcome with incomplete recovery or continued deterioration. In conclusion, children with HIV-1 infection who survive beyond the first year of life can present with a wide variety of neurologic complications. A similar spectrum of neurologic manifestations is likely to occur in other sub-Saharan African countries, characterized by high HIV prevalence. The case histories demonstrate that the neurologic features of pediatric HIV infection do not easily fit into a simplified classification system.
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PMID:Specific neurologic complications of human immunodeficiency virus type 1 (HIV-1) infection in children. 1697 Aug 87

MLL gene rearrangement is common in both adult and childhood acute myeloid leukaemia (AML), and its role in oncogenesis has been investigated. While over 50 translocated-partner genes have been identified so far, few studies have detailed the molecular mechanism of partial tandem duplication (PTD) of the MLL gene. The prognostic impact and contribution to leukaemogenesis of MLL-PTD, especially in childhood cases, remain unknown. We have established a novel cell line containing MLL-PTD derived from an 11-year-old patient with AML and designated as KOPM-88. KOPM-88 cells exhibited certain characteristics associated with the myeloid lineage including abundant primary granules in the cytoplasm and the expression of myeloperoxidase. The cell growth of KOPM-88 was cytokine independent but was accelerated by granulocyte colony-stimulating factor and granulocyte-macrophage colony-stimulating factor. MLL-PTD of exon 2 to exon 6 and exon 2 to exon 8 was revealed using Southern blotting, fluorescence in situ hybridisation, and reverse transcription polymerase chain reaction/DNA sequencing. Furthermore, non-obese diabetic/severe combined immunodeficient mice inoculated with KOPM-88 cells exhibited leukaemic infiltrations in the bone marrow and hemiparalysis because of compression myelopathy. This is the first report of an in vivo animal model exhibiting the systemic involvement of childhood AML containing MLL-PTD. KOPM-88 cells and our murine model may be useful for investigating the pathogenesis of childhood AML associated with MLL gene rearrangement.
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PMID:Establishment of a novel childhood acute myeloid leukaemia cell line, KOPM-88, containing partial tandem duplication of the MLL gene and an in vivo model for childhood acute myeloid leukaemia using NOD/SCID mice. 1740 61

We report on the case of a 36-year-old Hispanic woman with a spinal cord infarct, who was subsequently diagnosed with methylmalonic aciduria and homocystinuria, cblC type (cblC). Mutation analysis revealed c.271dupA and c.482G > A mutations in the MMACHC gene. The patient had a past medical history significant for joint hypermobility, arthritis, bilateral cataracts, unilateral hearing loss, anemia, frequent urinary tract infections, and mental illness. There was no significant past history of mental retardation, failure to thrive, or seizure disorder as reported in classic cases of cblC. Prior to the thrombotic incident, the patient experienced increased paresthesia in the lower extremities, myelopathy, and impaired gait. Given her previous psychiatric history, she was misdiagnosed with malingering until hemiplegia and incontinence became apparent. The authors would like to emphasize the recognition of a neuropsychiatric presentation in late onset cblC. Ten other reported late onset cases with similar presentations are also reviewed.
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PMID:Late-onset combined homocystinuria and methylmalonic aciduria (cblC) and neuropsychiatric disturbance. 1785 53


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