The AIDS dementia complex and HIV-1 brain infection: a pathogenetic model of virus-immune interaction.
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Biomedical subjects
Publications and source records attributed to B J Brew.
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Assessment of antibodies against human T-lymphotropic virus type I (HTLV-I) by enzyme-linked immunoassay, immunofluorescence, and Western blot was undertaken in patients with pathologically or clinically diagnosed acquired immunodeficiency syndrome-related vacuolar myelopathy to determine whether this retrovirus could be etiologically implicated in this disorder. No serological evidence for HTLV-I was found in the patients with vacuolar myelopathy, though 1 patient with an atypical myelopathy did have antibodies against HTLV-I.
Neurological manifestations of unknown cause occurring in patients who become or are HIV antibody positive with presumed normal immune function have been described recently. This report adds a further six cases, all of whom had normal CD4+ cell counts either throughout the period of observation or after the episode of seroconversion. Three had an acute presentation, two in the context of documented seroconversion consisting of one of the following: an encephalitis, an ataxia, and confusion with neuralgic amyotrophy. Three had a subacute disorder occurring at a later phase of HIV infection but before opportunistic infections or neoplasms, and marked by a static mild cognitive deficit. This report extends the range of abnormalities that may be seen at seroconversion and documents the presence of a non-progressive cognitive deficit occurring in the latent phase of HIV infection.
We prospectively evaluated CSF concentrations of beta 2 microglobulin (beta 2M) in 65 human immunodeficiency virus type 1 seropositive patients. The highest concentrations occurred in those with lymphoma, neurologic opportunistic infections, and acquired immune deficiency syndrome dementia complex (ADC). There was a high correlation between the CSF beta 2M concentration and ADC severity, suggesting that CSF beta 2M may be useful as a marker for the development, progression, and perhaps response to treatment of ADC. Elevated CSF beta 2M was not due to CSF pleocytosis and was usually independent of blood-brain barrier dysfunction.
Although merging clinically within the spectrum of the AIDS dementia complex, vacuolar myelopathy is a pathologically distinct entity detected in up to 30% of autopsied patients succumbing to the late complications of human immunodeficiency virus type 1 (HIV-1) infection. Using immunohistochemistry and in situ hybridization to detect an HIV-1 core protein and viral mRNA, respectively, in tissue sections, and culture isolation to assess infectious virus in tissue homogenates, we found that vacuolar myelopathy was independent of productive HIV-1 infection of the spinal cord and brain. These results indicate that AIDS-associated vacuolar myelopathy is either not related directly to spinal cord HIV-1 infection or involves nonproductive infection and pathobiological processes distinct from those responsible for the multinucleated-cell inflammatory infiltrates that serve as histopathologic markers of productive CNS HIV-1 infection.
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Tumours outside the central nervous system rarely prove to be intracranial glioma metastases. The mechanism of glioma metastasis has been thought to be related to dissemination of tumour cells either at the time of surgery or later through the surgical defect. However, 8 cases have been recorded to date in which metastases have occurred in the absence of surgery. This report details the clinical findings in 2 such patients. One presented with a pharyngeal mass that was found to be a metastasis from an anatomically remote parietal lobe astrocytoma. The other patient presented with a C8 nerve root tumour which was external to the dura. Biopsy revealed an astrocytoma that had metastasized from the roof of the lateral ventricle. Possible mechanisms of pathogenesis are discussed, including that of neural spread.
Neoplastic angioendotheliosis is a rare disease in which malignant cells are found within numerous blood vessels throughout the body in the absence of any detectable extravascular primary malignancy. The disorder has a propensity for clinical neurological involvement despite pathological evidence of systemic spread. To date 23 patients with neurological involvement have been described. This report adds a further 3 cases. There was no definite evidence to support the theory that the malignancy arises in endothelial cells; no primary extravascular tumour was found. At present a definite conclusion about the cause of the disease cannot be made.
The causes of visual loss in benign intracranial hypertension are related to long standing papilloedema, ischaemic optic neuropathy or haemorrhage into a subretinal neovascular membrane. Decompression procedures generally preserve or improve visual acuity but surgical treatment with subtemporal decompression may lead to visual impairment. Such a deficit has been recorded in the past as occurring with ventriculography. Postulated mechanisms have included brain herniation, spasm of vessels supplying the visual cortices or retinal vascular disturbance. To our knowledge treatment with lumboperitoneal shunting has not previously been reported as leading to further significant visual loss in this condition. This report describes such an occurrence in a patient. Retinal vascular disturbance is postulated on the basis of several normal CT scans, normal CSF pressure measured after surgery and visual evoked responses suggesting retinal or optic nerve damage.
Records of the emergency medical admissions to a large teaching hospital over a one year period were examined for evidence of Wernicke's encephalopathy or Korsakoff's syndrome. It was found that only 0.4% of the population studied had the classical triad of Wernicke's encephalopathy, namely confusion, ophthalmoplegia, and ataxia. If two of these three criteria are allowed in the absence of other causes then 2.2% of the population had this limited Wernicke's encephalopathy or Korsakoff's syndrome. It is concluded that the diagnosis of Wernicke's encephalopathy should not rely on the presence of all three criteria; any two of the three in the absence of other causes will suffice for the diagnosis.
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