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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The most common type of peripheral neuropathy associated with human immunodeficiency virus (HIV) infection, predominantly sensory neuropathy, affects 10-30% of patients with acquired immunodeficiency syndrome (AIDS). From 40 individuals with peripheral neuropathy and HIV infection, we have identified 26 patients with this syndrome. All had constitutional symptoms when neuropathic symptoms developed; 20 had AIDS and six had AIDS-related complex. The most common complaint was pain on the soles. Paresthesias were frequent and usually involved the entire foot. Signs of peripheral neuropathy were present in all; the most frequent finding was absent or reduced ankle reflexes. Electrophysiologic studies revealed abnormal sensory and motor conduction, studies suggesting a dying-back axonopathy. Over time, the neuropathy progressed in all except one patient with ARC, who had spontaneous subjective improvement. Tricyclic antidepressants provided partial symptomatic relief. In three patients, the neuropathy did not change during azidothymidine treatment. Predominantly sensory neuropathy in HIV infection appears to be a distal axonal degeneration primarily involving sensory neurons. The mechanism is unknown, but the neuropathy is associated with the late manifestations of HIV infection.
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PMID:Predominantly sensory neuropathy in patients with AIDS and AIDS-related complex. 283 69

The histopathological and immunopathological features of peripheral neuropathy were investigated in 21 patients with the acquired immunopathological syndrome (AIDS) or AIDS-related complex (ARC). Clinical syndromes observed in the 11 (52%) symptomatic patients included distal symmetrical polyneuropathy (DSPN) and chronic inflammatory demyelinative polyneuropathy (CIDP). Specimens from 19 of 20 patients (95%), both symptomatic and asymptomatic, had histopathological evidence of moderate or severe demyelination (79%), axonal degeneration (36%), and mononuclear cell inflammation (37%). Nerves from patients with CIDP and DSPN showed similar degrees of demyelination and axonal degeneration, but inflammation was more intense in CIDP. Immunohistochemical staining identified the majority of inflammatory cells as T lymphocytes or macrophages, with a predominance of CD8+ cytotoxic/suppressor cells. Diffuse immunostaining for human leukocyte antigen (HLA)-DR was present on endothelial cells, mononuclear inflammatory cells, and Schwann cells, and variable patchy immunostaining for HLA-DR was present on nerve fibers. Control nerve specimens showed staining for HLA-DR limited to endothelial, and a few mononuclear cells. The patterns of immunostaining were similar for AIDS and ARC patients. Human immunodeficiency virus (HIV) was cultured from peripheral nerve in 3 patients, but HIV antigen was not detected by immunohistochemical staining of 8 specimens. The findings implicate HIV infection in nerve, with T cell- and macrophage-mediated tissue destruction as the pathogenetic mechanism of the AIDS/ARC neuropathy.
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PMID:Peripheral neuropathy in the acquired immunodeficiency syndrome. 283 6

Neuromuscular disorders reported in association with human immunodeficiency virus (HIV) infection include several forms of peripheral neuropathy and polymyositis. We report 11 patients with HIV-associated myopathy. Five patients with acquired immunodeficiency syndrome (AIDS), 2 with AIDS-related complex, and 4 otherwise asymptomatic HIV-infected patients developed progressive proximal muscle weakness. Serum creatine phosphokinase levels were elevated and electromyography revealed abnormal spontaneous activity and myopathy in most patients. All 8 muscle biopsy specimens showed fiber necrosis. Four had inflammatory infiltrates, and nemaline rod bodies were prominent in 3. Immunosuppressant therapy in 5 patients resulted in improvement. Attempts at viral localization in 4 muscle biopsy specimens were unsuccessful. These findings suggest a distinct association between HIV infection and myopathy with features atypical for polymyositis.
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PMID:Human immunodeficiency virus-associated myopathy: analysis of 11 patients. 284 80

The purpose of this study was to assess systematically morphology of peripheral nerves from patients with human immunodeficiency virus infection (acquired immunodeficiency syndrome [AIDS] and AIDS-related complex) examined at autopsy. Sural nerve specimens were taken from 25 patients (mean age 44 years) and evaluated by routine procedures used in our laboratory. In 13 cases no detectable abnormality was seen. Twelve patients (48%) showed loss of myelinated fibers with disproportionately greater loss of large myelinated fibers. Three of these patients showed severe myelinated fiber loss; 2 had no documented symptoms and no other known predisposing factors for a peripheral neuropathy. Changes suggestive of wallerian degeneration were occasionally seen, as were epineurial and endoneurial inflammatory infiltrates. Segmental demyelination was not identified in any nerve examined. Electron microscopy revealed thickened basement membranes around small blood vessels, Schwann cells, and fibroblasts. Peripheral nerve abnormalities in patients with AIDS or ARC are frequent and their pathogenesis remains unclear.
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PMID:Abnormalities of peripheral nerve in patients with human immunodeficiency virus infection. 284 21

Disorders of the peripheral nervous system occur at all stages of HIV infection. From 13 patients referred for a peripheral neuropathy, 9 were known to be HIV seropositive and 4 were found to be seropositive. All were Caucasian males aged 27 to 58. Ten were homosexual, 2 were drug-addicts. Patients fell into several groups: the first group was made of 5 patients, 4 asymptomatic and 1 AIDS-related-complex (ARC), with an inflammatory demyelinating polyneuropathy, acute in 1 case and subacute in 4; the CSF showed pleiocytosis in all cases. Motor conduction nerve velocities were markedly reduced and motor distal latencies prolonged. Three patients recovered spontaneously, 1 responded to corticosteroids, 1 to plasmapheresis. In the second group, 4 patients, 1 asymptomatic and 3 ARC, had a distal symmetrical polyneuropathy; CSF was normal in 2 cases. Electrophysiological studies and nerve biopsies indicated a mixed axonal-demyelinating polyneuropathy. Three patients recovered spontaneously, 1 is unchanged. Among both groups, an infiltration of mononuclear cells was found on nerve biopsies in 4 cases. The third group was made of 3 patients with AIDS who presented with a painful sensory polyneuropathy involving the distal lower limbs. Electrophysiological and pathological study of the nerve indicated axonal degeneration. No cell infiltration was found. The last patient with AIDS had a progressive meningoradiculopathy. These 4 patients died within 6 months after the onset of the neuropathy. These findings are close to those previously reported, and confirm the wide spectrum of disorders of the peripheral nervous system associated to HIV infection.
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PMID:[The peripheral nervous system and HIV infection. 13 cases]. 285 39

HIV-infected patients are at markedly increased risk for neurological dysfunction, which may occur at any level of the neuraxis (see Table 1). The most common syndromes--AIDS dementia complex, vacuolar myelopathy, and possibly distal symmetric peripheral neuropathy--appear to be related to HIV infection within the nervous system, rather than due to the immunoincompetence caused by HIV. However, the mechanism(s) by which HIV causes these syndromes, e.g., infecting neurons or oligodendroglia directly, interfering with neurotrophic factors, effecting toxic monokine production, etc., is unknown. Early, albeit incomplete, success with azidothymidine is encouraging. Less commonly, neurological syndromes may be secondary to the immunoincompetence produced by HIV. Many different etiologies--most of which are treatable--have been encountered, but a few of these (cerebral toxoplasmosis, cryptococcal meningitis, primary CNS lymphoma, and progressive multifocal leukoencephalopathy) are responsible for most of the opportunistic complications. Marked differences in symptoms and signs between AIDS patients and immunologically normal patients may complicate recognition of some of these diseases (e.g., herpes simplex encephalitis). Finally, some HIV-associated syndromes, e.g., inflammatory demyelinating polyradiculoneuropathy and retinal microvasculopathy, are of unknown etiology.
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PMID:The neurology of human immunodeficiency virus infection. 285 54

Plasma exchange was used in three cases of peripheral neuropathy of polyradiculoneuritis type in patients with AIDS. The neurologic lesion in the first case was due to a cytomegalovirus, and plasma exchange appeared to provide additional benefits (to antiviral treatment) during the first attack of polyradiculoneuritis. The peripheral neurologic disorders were probably related to the HIV itself in the other two cases, and plasma exchange was carried out only briefly because of the seriousness of the situation, which was unaffected. Although plasma exchange is possible, if particular technical precautions are taken, in patients with AIDS, the present series is too small for valid scientific evaluation.
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PMID:[Plasma exchange in polyradiculoneuritis in AIDS]. 326 34

We report on 79 patients of different stages of human immune deficiency virus (HIV) infection according to the Walter-Reed staging classification (WR). Comparing the HIV antibody content per weight IgG in serum and cerebrospinal fluid (CSF), 54 patients (68%) showed higher antibody activity in CSF than in serum, indicating intrathecal antibody production and thus a local challenge with the virus. The percentage of patients with these antibodies in CSF increased from stage WR 1 (33%) to WR 5 (90%). It decreased again in WR 6 (68%). Twenty-one patients with intrathecally produced antibodies but without evidence for opportunistic or preexistent neuropsychiatric diseases were further analyzed. Even in stages WR 1 and 2 these patients showed distinct clinical signs. These consisted mostly in apathic personality change (n = 13), peripheral neuropathy (n = 8) or mild hemisyndrome (n = 9). Progression to severe dementia solely caused by HIV encephalitis seems to be possible. More often acceleration of the mental disorder indicates a synergistic action of other pathogens. Our study gives further evidence for very frequent, early and clinically active involvement of the nervous system by the HIV infection.
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PMID:Early involvement of the nervous system by human immune deficiency virus (HIV). A study of 79 patients. 337 87

A patient with positive serological HIV-II reactions is presented, who lived for many years in North and West Africa and on the Arabian peninsula, and who developed asthenica, incontinence, gait disturbances, impaired mental function, personality changes and finally spastic paraplegia and peripheral neuropathy. He was shown to have a chronic inflammatory process of the central nervous system with cerebral atrophy.
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PMID:HIV-II infection with initial neurological manifestation. 338 48

Unilateral facial palsies were observed in three patients with positive serology for HIV. Two patients presented a second unilateral peripheral seventh nerve palsy after extraction of a tooth. Recovery was complete in each case. Peripheral neuropathies are present in 20% of cases with AIDS but cranial neuropathies are uncommon, affecting only 2 to 3% of patients. The seventh and the fifth are the most frequent cranial nerves involved. The reported isolation of HIV in the cerebrospinal fluid and from the nerve suggests a direct role of this agent. In this study an indirect mechanism such as a vascular spasm may also favour the occurrence of these facial palsies.
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PMID:[Isolated and recurrent peripheral facial paralysis in human infection with human immunodeficiency virus (HIV)]. 341 62


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