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

We investigated the binding of the gp120 glycoprotein of the human immunodeficiency virus (HIV-1) to neural glycolipids and glycoproteins by ELISA. The gp120 protein bound to sulfatide (GalS), a sulfated glycolipid autoantigen implicated in sensory neuritis, and to the myelin associated glycoprotein (MAG), an autoantigen in demyelinating neuropathy. Binding of gp120 to MAG was inhibited by the HNK-1 antibody, which recognizes a sulfated glucuronic acid epitope, suggesting that the interaction involves carbohydrate determinants. Sulfatide and MAG are potential receptors for gp120 in peripheral nerve and may have a role in the neuropathy associated with HIV-1 infection.
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PMID:The gp120 glycoprotein of HIV-1 binds to sulfatide and to the myelin associated glycoprotein. 128 33

A retrospective study of the neurological problems arising in HIV-I seropositive patients in a single defined geographical area was undertaken. Ninety patients were referred for a neurological opinion from a total known HIV-I seropositive population of 436. Minor problems were frequently encountered early in the course of disease (20 at CDC stage II, 12 at CDC stage III), including seizures related to drug abuse in six. The most frequent neurological problem in those patients in CDC group IV (58 patients) were the AIDS dementia complex (14 patients), an axonal sensorimotor neuropathy (12), toxoplasmosis (nine) and cryptococcal meningitis (three). All patients with a structural lesion had appropriate focal signs on examination. The value and role of CT cranial scanning in the diagnosis of toxoplasmosis is discussed and the importance of recognizing potentially treatable causes of both intellectual impairment and cytomegalovirus-related neuropathies is stressed. This is the first report of an unselected series of patients at all stages of HIV-I related neurological disease from a single UK centre.
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PMID:The neurological features of HIV-positive patients in Glasgow--a retrospective study of 90 cases. 132 56

In the 1990s, HIV has replaced syphilis as the "great masquerader." Virtually every level of the neuraxis may be affected in a patient with HIV infection. The superimposition of multiple levels of neuropathology further complicate the bedside neurologic diagnosis of an AIDS patient. This article has reviewed the variety of forms of peripheral neuropathy that may be associated with HIV infection and its treatment. Distal symmetrical polyneuropathy may be produced in patients with HIV infection by neurotoxic drugs (e.g., vincristine, INH, ddC, or ddI) or by vitamin B12 deficiency or may develop in the later stages of HIV infection without identifiable cause. GBS and CIDP occur with increased frequency in early HIV infection owing to presumed autoimmunity, and these IDPs respond to plasmapheresis or prednisone, similar to HIV-seronegative patients. A limited distribution of mononeuropathy simplex or multiplex occurs in patients with CD4 counts greater than 200; the neuropathy will usually spontaneously improve in these patients. Widespread mononeuropathy multiplex may occur in patients with AIDS and CD4 counts less than 50 and is then usually caused by CMV infections; those neuropathies are usually progressive unless antiviral treatment is given. Progressive polyradiculopathy usually occurs in patients with AIDS and low CD4 counts. If the cerebrospinal fluid has a polymorphonuclear pleocytosis, CMV infection is almost always present, and progression is expected unless ganciclovir therapy is promptly started. Finally, mild autonomic neuropathy is commonly present in HIV-infected patients. Protocols for the evaluation and therapy of cranial and peripheral neuropathies are presented (Figs. 6 and 7). It is unfortunate but likely that increasing numbers of "neuro-AIDS" patients will be encountered, not only in urban medical centers but also in general community practice. The pace at which research in the field of HIV research has proceeded is unprecedented. It is, therefore, important that neurologists stay at the forefront of investigation and clinical care of these complex disorders.
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PMID:Peripheral neuropathies associated with human immunodeficiency virus infection. 132 49

A subacute advanced severe sensorimotor polyneuropathy developed over 6 months in a 47-year-old patient in stage 5 of an HIV infection (Walter Reed Hospital classification). Clinical examination, cranial computed tomography and spinal nuclear magnetic imaging failed to demonstrate any central nervous system complication. Cerebrospinal fluid showed a lymphocytic pleocytosis of 57/3 cells and total protein raised to 132 mg/dl as sign of an abnormal blood-brain barrier. Circulating immune complex in blood was raised to 30%. Assuming an immune-complex mediated neuropathy treatment with oral steroids was started, initially 150 mg daily. The signs of polyneuropathy regressed almost completely, even after prednisolone was discontinued. The proportion of circulating immune complexes in blood fell within 7 weeks to 10% during this treatment. It is suggested that in HIV-infected patients severe polyneuropathies may develop as part of a humoral immune reaction in which immunosuppressive treatment can be effective. Even in advanced HIV infection high-dosage and prolonged steroid treatment can be undertaken, under strictest indications, and may have impressive results.
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PMID:[Subacute progressive polyneuropathy syndrome in HIV infection. The efficacy of immunosuppressive treatment?]. 138 20

A pilot study of low contrast visual acuity testing using Regan Charts has been undertaken in 34 patients seropositive for Human Immuno-Deficiency Virus and 20 normal control subjects. Low contrast visual acuities of the HIV (+) patients both with and without HIV retinopathy were found to be significantly lower than the age-matched controls (p < 0.01). This finding is probably attributable to pathology related to HIV in the visual pathways/Central Nervous System. Lowest contrast Chart (Chart C) was found to be a useful diagnostic tool for HIV retinopathy and presumed neuropathy.
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PMID:Low contrast visual acuity changes in human immuno-deficiency virus (HIV) infection. 142 97

We describe a patient with human immunodeficiency virus (HIV) infection who developed mononeuritis multiplex associated with polyclonal (type III) cryoglobulinemia. The patient's symptoms stabilized following treatment with plasmapheresis and removal of the cryoglobulin. Our case represents the first report of polyclonal cryoglobulinemia in HIV disease and suggests that cryoglobulinemia may play an etiologic role in some patients with HIV-associated neuropathy.
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PMID:Mononeuritis multiplex associated with cryoglobulinemia in HIV infection. 143 18

Motor and sensory conduction of the right peroneal and sural nerves was studied in 28 children (17 HIV seropositive) with inherited hemostasis disorders, without any symptoms of neuropathy. The amplitude ratio of the evoked muscle potential (EMP) at distal stimulation to that at proximal stimulation at the right peroneal nerve was also studied. Thirty healthy aged-matched children were used as controls. There was no statistically significant difference in the distal latency, amplitude and conduction velocity of motor and sensory nerves between patients and controls. On the contrary, a great diminution of amplitude of the EMP during proximal stimulation of nerve was observed in patients, statistically very significant, as compared to controls. This difference was independent of patients' age, severity of hemostasis defect or HIV status. In 9 patients the amplitude was within normal limits. Intraneural oozing due to trivial trauma is postulated as a possible mechanism of peroneal nerve lesion.
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PMID:Subclinical neuropathy in children with inherited haemostasis disorders. 144 83

A prospective study of possible aetiological factors for neuropathy associated with HIV infection was performed in 80 patients and 28 homosexual controls. At entry to the study twelve patients (15 per cent) had evidence of a generalized neuropathy not due to any other cause and a further three patients developed symptomatic neuropathy during a mean (SD) follow-up of 20 (7.5) months. All but two of these neuropathies were of the distal symmetrical sensory type. Electrophysiology was consistent with an axonal pathology and nerve biopsy confirmed this as the major pathological change. Warming threshold was the diagnostic test most frequently abnormal, sometimes in the absence of other electrophysiological abnormalities. No association was seen with opportunistic infection (cytomegalovirus, herpes simplex, Pneumocystis pneumonia, toxoplasmosis, Cryptococcus infection or tuberculosis). HIV proviral DNA could not be detected in paraffin sections of peripheral nerve in six patients with neuropathy. The presence of the neuropathy did not show significant correlation with depression of the number of CD4+ T cells in the blood, impaired T cell function tests, or IgG, IgM, or IgA levels. Immune complexes containing C1q, but not those containing IgG, IgM, IgA or C3c, were significantly more common among neuropathic patients (p = 0.01).
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PMID:A study of neuropathy in HIV infection. 144 48

Nucleoside-induced neuropathy characteristically appears as a painful, symmetric, distal polyneuropathy. To evaluate the neurotoxic potential of zidovudine (ZDV, or azidothymidine), in persons with little confounding human immunodeficiency virus (HIV) neuropathy, we evaluated peripheral nerve function in persons completing placebo-controlled studies of ZDV in early HIV disease. Participants had been receiving placebo or ZDV at doses of 800-1,200 mg daily for a median 52 weeks at the time of evaluation. Neuropathic symptoms and abnormalities of motor and sensory function were present in fewer than 10% of both treatment groups. Depressed reflexes were found in 19% of the ZDV group and 18% of the placebo group. Quantitative sensory testing for vibration was abnormal in fewer than 10% of participants and the absolute scores favored the ZDV group. We thus found a low prevalence of peripheral nerve abnormalities and no evidence of ZDV neurotoxicity in this population.
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PMID:Peripheral nerve function in persons with asymptomatic or minimally symptomatic HIV disease: absence of zidovudine neurotoxicity. 165 10

Clinical and electrophysiologic features in 22 patients with HIV infection are reported. Four cases had chronic demyelinating polyneuropathy, two mononeuropathy multiplex, and nine symmetrical sensory-motor polyneuropathy. Seven cases had normal clinical and electromyographic examination. Electrophysiological study had a higher diagnostic yield (68%) than clinical examination (50%) for peripheral neuropathy diagnosis. Thus, peripheral nerve abnormalities are frequent in patients with different stages of HIV infection, although their pathogenesis remains unclear. Symmetrical sensory-motor polyneuropathy is the main type of neuropathy seen in ouvert AIDS, whereas chronic demyelinating polyneuropathy was mainly diagnosed in patients with asymptomatic HIV infection as first manifestation of the disease. Axonal or demyelinating nerve damage was established according to electrophysiological criteria. Frequently a mixture of both lesions was found. Electrophysiologic study is also a good index of neuropathy evolution in HIV infection and to follow-up of nerve abnormalities after treatment.
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PMID:Electrophysiologic study in peripheral neuropathy associated with HIV infection. 166 Aug 6


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