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Query: UMLS:C0001175 (AIDS)
 120,706 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

HIV-associated neurological manifestations: dementia, myelopathy, and neuropathy, have become one of the commonest causes of neurological disorders in young people. Cognitive impairment develops in about 30 p. 100 of patients with AIDS and frank dementia in 15 to 20 p. 100 with an annual incidence after AIDS of approximatively 7 p. 100. Typically, the onset of dementia is relatively abrupt over a few weeks or months. The clinical manifestations of the encephalopathy now termed "HIV-dementia", suggest predominant subcortical or frontal involvement. Typical presentation includes apathy and inertia, memory loss and cognitive slowing, minor depressive symptoms and withdrawal from usual activities. Neurological examination may show hypertonia of lower limbs, tremor, clonus, frontal release signs and hyperactive reflexes. Terminally, the patient is bedbound, incontinent, abulic or mute with decorticate posturing leading to death over 3 to 6 months. However, a stabilisation and even a regression of the cognitive disorders have been observed following antiretroviral treatment. Radiological features of HIV dementia include both central and cortical atrophy and white matter rarefaction. However they are neither invariable nor specific. Together with CSF examination, they are more important to exclude opportunistic infections. Indeed, although a completely normal CSF profile may reasonably exclude the diagnosis; at present, no single test or combination of tests can reliably diagnose HIV dementia. Although the clinical characteristics of HIV-dementia are now clearly established, its pathogenesis is unclear and its pathological counterpart remains a matter of debate. A number of "HIV-induced" lesions may be found in the brain of AIDS patients and their causative role in HIV-dementia has been considered. They include HIV encephalitis due to productive CNS infection by the virus, diffuse white matter pallor "HIV-leukoencephalopathy" reflecting an abnormality of the blood brain barrier, involvement of the grey matter, "diffuse poliodystrophy", with neuronal loss that results, at least partly, from a process of programmed cell death and axonal damage. These changes are variably associated in patients with HIV dementia, however none of them can be closely related to the cognitive disorders. This suggests that the neuronal dysfunction underlying HIV-dementia results from different mechanisms that are variably associated and may interact mutually. These include production of viral proteins, microglial activation with consequent production of neurotoxic factors such as proinflammatory cytokines, free radicals, derivates of arachidonic acid, or quinoleic acid, and blood borne neurotoxic factors in particular cytokines.
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PMID:[Dementia and human inmmunodeficiency virus infection]. 983 49

We report on a rare case of foot and ankle clonus as the initial presentation of progressive multifocal leukoencephalopathy in a young patient with no known history of HIV or AIDS and no significant past medical or social history. The patient came to the emergency department with a chief complaint of muscle spasms in his lower extremities and unsteadiness in gait. The patient was diagnosed as having bilateral ankle clonus. Work-up revealed an absolute lymphocyte CD4+ count of 18, an HIV viral load of 1,690,000, and a positive John Cunningham virus polymerase chain reaction in the cerebral spinal fluid, indicating that the patient had progressive multifocal leukoencephalopathy and AIDS. The diagnosis of progressive multifocal leukoencephalopathy should be in the foot and ankle surgeon's differential diagnosis when a patient presents with neurological symptoms in the lower extremities.
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PMID:Bilateral ankle clonus as initial manifestation of progressive multifocal leukoencephalopathy: a case report. 2527 49