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 15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infants and children with symptomatic human immunodeficiency virus (HIV) infection frequently develop neurologic disease with symptoms and signs of acquired microcephaly, developmental delays, encephalopathy, pyramidal tract signs, and less often, movement disorders and ataxia. However, clinical courses vary and, based upon progression of neurologic findings, we have classified them into 2 broad categories; progressive (loss of previously acquired language and cognitive skills) and plateau (failure to acquire additional developmental skills). We have used immunocytochemistry to localize HIV within the brains of neurologically involved children with AIDS. Interestingly, the brains of those children with a progressive neurologic course showed readily detectable HIV antigen, while those with a plateau course showed little or no detectable HIV. These findings suggest that in children with symptomatic HIV infection, the progressive neurologic deterioration is due to continued presence of HIV within deep white matter and gray matter, while the plateau neurologic course is due to HIV induced damage followed by either limited penetration of virus into the central nervous system, or clearance of virus below detectable limits.
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PMID:Human immunodeficiency virus within the brains of children with AIDS. 230 89

The clinical significance of myelopathy associated with HIV infection is poorly understood. Recently, a prospective electrophysiological follow-up study of spinal-evoked potentials in HIV-seropositive men without AIDS revealed a 32% prolongation of the latency from the gluteal crease to the 12th thoracic vertebra (T12) following tibial nerve stimulation at the ankle performed after an interval of 2 years. In AIDS patients this transmission delay did not increase further. Instead, the latency prolongation took place proximal to T12. We assume that myelopathy is an integral part of HIV infection that it is asymptomatic in the early disease phase, spreads from the lumbar part the spinal cord in a rostral direction and leads to the development of leg weakness and ataxia during the later stages of the disease.
AIDS 1990 Jun
PMID:Myelopathy and HIV infection. 238 22

Motor weakness and ataxia of lower limbs and abnormalities of somatosensory evoked potentials occur in many patients with the acquired immunodeficiency syndrome (AIDS). We studied 15 human immunodeficiency virus-seropositive subjects without AIDS and found no clinical neurological abnormalities. The mean latency of the brainstem auditory evoked potential (peak V) was increased, suggesting a central defect. Despite normal peripheral nerve conduction along the tibial nerve, the mean latency of the spinal cord potential of the twelfth thoracic vertebra was increased compared with normal, possibly indicating an incipient conduction defect at or near the spinal root ganglion or lumbar spinal cord.
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PMID:Clinical and electrophysiological studies of human immunodeficiency virus-seropositive men without AIDS. 283 33

The case of a 29-year-old former parenteral drug abuser who presented with a 3rd nerve palsy and contralateral ataxia is reported. The patient was found to have a positive HLTV-III titer and acquired immune deficiency syndrome was diagnosed. Computed tomography demonstrated two ring-enhancing lesions in the brain which were presumed to be due to Toxoplasma gondii.
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PMID:Third nerve palsy as a presenting sign of acquired immune deficiency syndrome. 295 2

A survey of the literature of neurological manifestations associated with the acquired immune deficiency syndrome (AIDS) shows a broad disease spectrum affecting approximately one third of the patients in large hospital series. The complications include focal cerebral lesions caused by abscesses, lymphomas, leucoencephalopathy or infarcts as well as encephalitis, meningitis and myelitis. Most opportunistic infections of the central nervous system presumably are caused by toxoplasma gondii, cytomegalovirus and cryptococcus neoformans. One tenth of all patients have neurological disease as their initial symptom of AIDS. The diagnosis should always be considered in patients at risk and in males with an unusual neurological history or with a peculiar CT scan of the brain. Besides the opportunistic complications of AIDS, LAV/HTLV-III itself probably attacks the nervous system and gives rise to concomitant lesions of the long tracts of the spinal cord with ataxia, paresis and spasticity and to subacute encephalopathy and peripheral nerve abnormalities as well.
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PMID:Neurological complications and concomitants of AIDS. 303 38

In a cross-sectional population study of Danish patients with AIDS 16 of 23 had clinical signs of neurological disease with muscle weakness or ataxia of the lower limbs as the dominant manifestation. Tibial and median nerve conduction was mildly slowed in a few patients and 15 had widening of cerebral ventricles at CT. However, all had prolonged latency of cortical evoked response following tibial nerve stimulation mainly due to slowing through the spinal cord. The prolongation of the latency of the evoked cortical responses was most pronounced in patients with lower limb ataxia and/or paresis. It is concluded that affection of the long tracts of the spinal cord are closely associated with the human immunodeficiency virus infection.
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PMID:Myelopathy in AIDS. A clinical and electrophysiological study of 23 Danish patients. 335 13

Of 70 autopsied patients with the acquired immune deficiency syndrome (AIDS), 46 suffered progressive dementia that was frequently accompanied by motor and behavioral dysfunction. Impaired memory and concentration with psychomotor slowing represented the most common early presentation of this disorder, but in nearly one half of the patients either motor or behavioral changes predominated. Early motor deficits commonly included ataxia, leg weakness, tremor, and loss of fine-motor coordination, while behavioral disturbances were manifested most commonly as apathy or withdrawal, but occasionally as a frank organic psychosis. The course of the disease was steadily progressive in most patients, and at times was punctuated by an abrupt acceleration. However, in 20% of patients a more protracted indolent course was observed. In the most advanced stage of this disease, patients exhibited a stereotyped picture of severe dementia, mutism, incontinence, paraplegia, and in some cases, myoclonus. The high incidence and unique clinical presentation of this AIDS dementia complex is consistent with the emerging concept that this complication is due to direct brain infection by the retrovirus that causes AIDS.
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PMID:The AIDS dementia complex: I. Clinical features. 372 8

Twenty of 89 consecutive patients with the acquired immunodeficiency syndrome (AIDS) in whom autopsies were performed over a 3 1/2-year period had a vacuolar myelopathy that was most severe in the lateral and posterior columns of the thoracic cord. Light and electron microscopy showed that vacuoles were surrounded by a thin myelin sheath and appeared to arise from swelling within myelin sheaths. Signs and symptoms referable to the spinal-cord lesions, including paraparesis, often accompanied by spasticity or ataxia (or both), were present in all five patients with marked pathological changes, in five of seven patients with moderate changes, and in two of eight patients with mild changes. Fourteen patients were demented. The clinical presentation was sufficiently distinctive to provide a guide for antemortem diagnosis. Possible causes of the vacuolar changes include uncharacterized viral infection or a metabolic derangement related to selective nutritional deficiency.
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PMID:Vacuolar myelopathy pathologically resembling subacute combined degeneration in patients with the acquired immunodeficiency syndrome. 397 73

The authors' primary purpose was to identify home healthcare needs of adults (N = 244) living with HIV disease/AIDS. The study followed a retrospective chart review of a stratified random sample of cases discharged during 1991 from a certified home health agency (CHHA) in New York City. Frequently observed signs and symptoms included dyspnea, weakness, fatigue/lethargy, pain, ataxia, cough, skin lesions, and memory deficit. Additional problems identified included inadequate nutrition, issues related to compliance with prescribed medications, inadequate in-home support systems, inadequate facilities/utilities in the home, financial concerns and lifestyles that included drug/alcohol abuse and tobacco use. The results suggest that the health care needs of people living with HIV disease/AIDS in the home care setting are multifaceted and extend beyond the clinical manifestations of HIV disease.
J Assoc Nurses AIDS Care
PMID:Home healthcare needs of adults living with HIV disease/AIDS in New York City. 803 11

Wernicke's encephalopathy (WE) is a neuropsychiatric disorder caused by thiamine (vitamin B1)-deficiency. WE is most commonly seen among patients with alcohol abuse, and thiamine deficiency is here caused by several factors, among others inadequate diet, insufficient gastrointestinal absorption and enzymatic abnormalities. The syndrome, however, is also seen among non-alcoholic, undernourished patients, e.g. certain patients with cancer or AIDS. The diagnosis WE has traditionally been given when the triad of confusion, ataxia and ophthalmoplegia was present. However, it should be recognised, that these three symptoms are not always present at the same time, partly because the mental symptoms often dominate and cloud, possible ocular abnormalities and ataxia. The syndrome is, according to the author's opinion, still underdiagnosed. The treatment of WE, consisting of large doses of intravenous thiamine, is effective and safe, and therefore it is important to be aware of WE among risk-patients, especially among patients with alcohol abuse, and to institute treatment with intravenous thiamine at the slightest suspicion.
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PMID:[Wernicke's encephalopathy]. 863 25


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