Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acquired immunodeficiency syndrome (AIDS) has become an epidemic in the United States. AIDS dementia complex (ADC) is a neurological dysfunction which has been indicated in 25-90% of AIDS patients, 30-40% of HIV-infected patients, and may be the only presenting manifestation of AIDS. Researchers have investigated many aspects of ADC including clinical features, etiology, epidemiology and prevalence, diagnosis (psychological parameters and laboratory investigations such as CSF, EEG, CT, MRI, PET, and ERP), assessment, neurological features (including neuropsychiatric and neuropsychological measures, and neuropathology), prognosis, and treatment. The research is controversial, complex, and contradictory. A discussion of the many areas of ADC and many hypotheses will be included.
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PMID:Acquired immunodeficiency syndrome dementia complex. 935 7

We correlated MRI features with histopathological findings in an HIV-positive patient with vacuolar myelopathy. On MRI symmetrical nonenhancing high-signal areas in the posterior columns on T2-weighted images result from extensive vacuolation visible on histological sections.
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PMID:Spinal MRI in vacuolar myelopathy, and correlation with histopathological findings. 945 12

A twenty-six year old, previously healthy nurse presented with new onset of seizures and was given a clinical diagnosis of herpes simplex encephalitis. After treatment with acyclovir there was incomplete resolution of the lesions by MRI scans and within a few months the patient's neurologic symptoms worsened, prompting a stereotactic biopsy. A diagnosis of progressive multifocal leukoencephalopathy (PML) was made using electron microscopy, and in situ hybridization studies. Subsequent to this biopsy, she was shown to be infected with human immunodeficiency virus (HIV) and had a CD4 T-cell count of 63. She had no known risk factors for HIV infections and had been tested as recently as eighteen months previously during her pregnancy. Neither the husband nor the child were positive for HIV. PML as a presenting sign of HIV infection is rare.
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PMID:Case of the month: September 1997--a 26 year old woman with new onset seizures. 945 83

In patients with acquired immuno-deficiency syndrome, the differential diagnosis between primary brain lymphoma and toxoplasma encephalitis is not radiologically always straightforward, especially in the presence of a solitary cerebral lesion. In this context, involvement of the corpus callosum is almost exclusively associated with primary brain lymphoma. We describe here an HIV-infected patient who presented with a single and large cerebral lesion affecting the corpus callosum, suggestive of primary brain lymphoma on MRI-scan but who nonetheless responded clinically and radiologically to an anti-toxoplasma drug trial confirming the diagnosis of toxoplasma encephalitis.
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PMID:Toxoplasma encephalitis in a HIV patient: unusual involvement of the corpus callosum. 949 8

In this short review, the Author evaluates the most important diagnostic problems about tuberculous meningoencephalitis. Any inadequate therapy can alternate the clinical picture and the results of the cerebrospinal fluid examination, and the clinical evaluation may become very difficult. The neuroradiological findings (CT and MRI), even when correlated to the typical neuropathological features of the disease, could be very sensitive but not specific. An accurate evaluation of the clinical context and, above all, of the clinical history, is the best way to avoid a tardive diagnosis and inappropriate therapies, and to choose which diagnostic procedures must be performed. In the latest years, the immunodeficiency status related to HIV infection, and the mobility of many persons from geographic areas endemic for TBC stressed the importance of this diagnosis. The extreme variability of the clinical picture is discussed, and the author describes the common manifestations as well as the rare syndromes associated with this disorder. The review indicates also the diseases with which the neurologist must challenge for a differential diagnosis. Some practical suggestions indicate how to minimize a diagnostic and therapeutic delay, for a disorder that in many cases is still lethal or leading to serious neurological complications or sequelae.
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PMID:[Clinical evaluation in the early diagnosis of tuberculous meningoencephalitis]. 952 6

In herpes simplex encephalitis (HSE), simultaneous electro-encephalogram (EEG) and evoked potential studies have not been reported, although EEG changes have been described. In this communication, EEG, somatosensory and motor evoked potentials have been reported in 9 patients with HSE. The patients' age ranged between 2 and 70 years and 3 were females. Seven patients had seizures, CT scan was abnormal in 6 and MRI in remaining 3 patients. Seven patients received acyclovir therapy; one patient died and 6 had poor outcome. The initial EEG was carried out within 5 days of ictus and was abnormal in all the patients. The EEG abnormalities included frontotemporal delta slowing in 5, periodic lateralised epileptiform discharge in 3, runs of spike and periodic activity in one patient each. At 3 months, EEG was normal in 6 patients but it did not correlate with clinical recovery. Central motor conduction time (CMCT) to upper limb and median somatosensory evoked potential (SEP) were normal in all. CMCT to lower limbs and tibial SEPs were unrecordable in one patient who had wide spread herpes simplex virus (HSV-1) infection associated with AIDS, and died on 18th day of illness. From this study, we conclude that EEG although is frequently abnormal and may provide useful diagnostic information in a setting of encephalitis but evoked potential changes are infrequent; and if present an association of HIV infection should be considered.
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PMID:Neurophysiological studies in herpes simplex encephalitis. 963 44

A case is reported of idiopathic CD4+T lymphocytopenia with progressive multifocal leukoencephalopathy and cervical lymph node tuberculosis. A 57 year old Japanese man presented with cervical lymphadenopathy and progressive neurological deficits, and six months later he developed akinetic mutism. He had a persistent severely depressed number of circulating CD4+T lymphocytes in the absence of human immunodeficiency virus infection. T1 weighted MRI showed a diffuse decreased signal intensity limited to the white matter without mass effect. A brain biopsy specimen had a morphology similar to that of progressive multifocal leukoencephalopathy. Polyomavirus antigen was detected in the brain lesion, and viral DNA was identified in nucleated blood cells and urine. Unusually this serious medical condition has lasted for more than three years without remission. To our knowledge this is the first patient with CD4+T lymphocytopenia with progressive multifocal leukoencephalopathy, suggesting that similar opportunistic infections should be considered even in previously normal people.
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PMID:An unusual course of progressive multifocal leukoencephalopathy in a patient with idiopathic CD4+ T lymphocytopenia. 964 12

More than 50% of patients with acquired immunodeficiency syndrome (AIDS) present a lesion affecting parotid gland, lymph nodes, paranasal sinuses, pharyngo-larynx or temporal bone. In about 20% out of cases affected patients present different head and neck lesions at the time of evaluation. Most often, clinical examination and endoscopy are sufficient to perform diagnosis and to manage the disease. Imaging studies (CT or MRI) are indicated when the nature of the disease is unknown or when a map of the process is mandatory for therapeutic approach. Some imaging features are strongly suggestive of HIV infection: parotid cysts associated with hyperplasia of the nasopharynx and cervical lymph nodes enlargement; labyrinthitis and multinevritis; and head and neck squamous cell carcinomas in non alcoolo-tobacco addicted patients. Such diseases suggest the need for knowledge of the patient's seropositivity status.
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PMID:[Imaging of ORL diseases in acquired immunodeficiency syndrome]. 968 16

The non-convulsive status epilepticus (NCSE) is a complication of petit mal epilepsy or epilepsy with temporal lobe seizures. Very rarely it is the primary manifestation of a symptomatic epilepsy. This report is on a 30-year old female inpatient with NCSE as the primary manifestation of symptomatic epilepsy, occurring four years after HIV infection (stage B3 according to the CDC classification) through heterosexual contact. After an initial tonic-clonic seizure, the patient suffered from NCSE for four weeks with diminished consciousness and major cognitive deficits. During this whole time period the EEG showed bilateral synchrone 1-2 Hz spike-wave complexes. After several failed treatment attempts, the NCSE was successfully and permanently treated with a combination of valproic acid and ethosuximide. The cerebrospinal fluid, cranial CT and cranial MRI were completely uneventful with regard to a CNS infection by the HI-virus or other infectious agents. 20 days after the initial symptoms, MRI showed bilateral cortical-subcortical and bilateral hippocampal lesions which stood out as focal edema zones, gradually disappeared completely and occurred in combination with the development of a discrete brain and right sided hippocampal atrophy. The EEG continued to show signs of right-temporal epileptic discharges with tendencies to generalise after 3 months but normalised after 6 months. Epileptic seizures are rarely an initial clinical sign of an infection with the HI-Virus even if no signs of encephalitis is detectable in the cerebrospinal fluid or in the cerebral MRI.
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PMID:[Prolonged non-convulsive status epilepticus as an early clinical manifestation of epilepsy in connection with HIV infection--case report with EEG and MRI follow-up]. 969 7

A 38-year-old homosexual male with AIDS suffered four neurological episodes including headaches, confusion, visual impairment, memory disturbances, and dysarthria which resolved spontaneously in a few days. He was admitted to hospital during a fifth episode. Neurological examination revealed a cerebellar syndrome. General examination was normal. CD4 count was 90. CSF contained two WBCs/mm(3) and 12.30 mg/dL protein. MRI revealed diffuse ill defined increased signal on T2-weighted images in the white matter. His condition worsened rapidly with vomiting and he died 1 month after admission. Neuropathological examination revealed diffuse brain oedema with ventricular compression, central diencephalic herniation and bilateral tonsilar herniation in the absence of a focal lesion. Microscopical examination revealed predominant involvement of the white matter with diffuse myelin pallor and massive perivascular dilatation containing an exudate expressing serum proteins and occasional macrophages. The same exudate was also diffuse in the leptomeninges. Parenchymal damage predominated around the perivascular spaces and included loosening of tissue, axonal damage with spheroids and reactive astrocytosis. There was no evidence of productive HIV encephalitis, no multinucleated giant cells; p24 immunostaining and RT-PCR for HIV genome were negative. There was neither significant inflammation nor microglial activation. In this illustrative case, the relapsing course of the neurological signs, the diffuse topography of the blood-brain barrier breakdown and the absence of local cause make it likely that the diffuse leak and axonal damage could be related to circulating factors.
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PMID:Acute, relapsing brain oedema with diffuse blood-brain barrier alteration and axonal damage in the acquired immunodeficiency syndrome. 971 86


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