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Biomedical subjects

F Gray

Publications and source records attributed to F Gray.

At least 145 records · Page 8Linked to original sources
PubMed1992

[AIDS-related progressive multifocal leukoencephalopathy limited to U fibers, responsible for subacute encephalopathy with normal CT scan findings].

A 41-year-old male homosexual with AIDS was hospitalized for temperature elevation to 40 degrees C with confusion. Neurologic evaluation found psychomotor slowing and temporospatial disorientation with no focal signs. The CD4 count was 100/mm3. CSF analysis and the CT scan were normal. Despite antiviral treatment the patient died fifteen days after admission. Gross appearance of the brain was normal. Histologic examination disclosed multiple, small foci of demyelination characteristic of progressive multifocal leukoencephalopathy. These foci were disseminated among the U fibers. In situ hybridization and immunocytochemical studies demonstrated papovavirus particles in oligodendrocytes and a few astrocytes. This case shows that papovavirus infection in AIDS patients may be responsible for a diffuse febrile encephalopathy with normal CT scan findings and a rapidly progressive course.

AIDS-Related Opportunistic Infections↗
PubMed1992

Low levels of human immunodeficiency virus replication in the brain tissue of children with severe acquired immunodeficiency syndrome encephalopathy.

The authors examined the autopsy brain samples of nine children infected with human immunodeficiency virus (HIV) at birth by histology, immunologic staining, and in situ hybridization. Surprisingly, although seven of these children presented with typical AIDS encephalopathy, the authors could detect a multifocal HIV infection in the brains of only three of these patients. The authors could not detect any significant HIV replication in the brain of four other children despite severe neurologic disease. However, HIV DNA was detected by polymerase chain reaction (PCR) in the central nervous system (CNS) of all patients. In addition, the authors found associated lesions in the brains of three of these four patients. This study shows that severe AIDS encephalopathy exists in children and therefore might exist in adults with few signs or without any signs of HIV replication or inflammation in the CNS. Understanding the pathogenesis of this neurologic disease and the kinetics of HIV replication in brain tissue of children with AIDS encephalopathy is essential to determine the best therapeutic strategy.

Acquired Immunodeficiency Syndrome↗
PubMed1991

Prominent cortical atrophy with neuronal loss as correlate of human immunodeficiency virus encephalopathy.

A 25-year-old homosexual AIDS patient presented with progressive cognitive, motor and behavioral disturbances consistent with HIV encephalopathy. CT scans demonstrated progressive diffuse brain atrophy. Neuropathology showed predominant cortical changes including severe neuronal loss corroborated by morphometry. Only minimal changes were found in the white matter and basal ganglia. Immunocytochemistry for HIV stained occasional microglial cells more markedly in the cerebral cortex. This suggests that HIV infection of the brain may cause predominant cortical nerve cell loss, and that HIV encephalopathy is not necessarily due to white matter lesions.

AIDS Dementia Complex↗
PubMed1991

Ischaemic myelopathy secondary to disseminated intravascular coagulation in AIDS.

A 39-year-old patient with AIDS presented with a rapidly progressive myelopathy with a partial Brown-Séquard syndrome. He died, 9 weeks after onset of the first neurological signs, from diffuse encephalopathy. Neuropathological examination revealed multiple, usually small, frequently haemorrhagic, infarcts or various ages and numerous fibrin thrombi in medium and small penetrating vessels and capillaries of the brain and spinal cord, characteristic of disseminated intravascular coagulation. There were no inflammatory changes. Immunohistochemical studies for human immunodeficiency virus, cytomegalovirus, varicella zoster virus, herpes simplex virus type 1 and type 2 were negative. Ischaemic spinal cord lesions due to disseminated intravascular coagulation may represent an unusual cause of focal, non-inflammatory, non-tumoral, myelopathic syndrome in AIDS.

Acquired Immunodeficiency Syndrome↗
PubMed1991

Cerebral lymphoma and HIV encephalitis in a case of paediatric AIDS, with pre-existing multicystic encephalomalacia.

A case of intracerebral malignant B cell lymphoma associated with encephalitis typical of Human Immunodeficiency Virus (HIV) infection is described in a 4 year old child, with post-transfusion Acquired Immune Deficiency Syndrome (AIDS) and severe pre-existing cystic encephalomalacia. This report further documents B cell lymphoma as the commonest cause of an intracerebral mass, and an important cause of death in paediatric AIDS. That more than one pathological process may be responsible for neurological symptoms in paediatric AIDS is also emphasised.

AIDS Dementia Complex↗
PubMed1991

Multifocal multinucleated giant cell myelitis in an AIDS patient.

A 19-year-old male intravenous drug abuser, was admitted to hospital with a one-week history of lower limb weakness and urinary retention. He was known to have been HIV-seropositive for 3 years and had been treated for cerebral toxoplasmosis. Neurological examination confirmed flaccid paraparesis with weak ankle jerks and bilateral extensor plantar responses. There was no obvious sensory deficit. Neurological examination was otherwise normal. CSF contained 63 mg/dl protein and 10 leucocytes/mm3. Myelography was normal. He died 1 month later from septic peritonitis. Neuropathological examination showed chronic lesions of toxoplasmosis in brain. Small necrotic foci with myelin loss, proliferation of microglia, macrophages and multinucleated giant cells (MGC) were disseminated in the whole spinal cord, mostly in the white matter, but the brain was spared. Immunohistochemistry demonstrated p24 and p17 HIV antigens in macrophages, MGC and microglial cells. These lesions resemble those of so called 'multifocal giant cell encephalitis'. The present case demonstrates that HIV-related multifocal inflammatory changes may be restricted to the spinal cord and may be a cause of myelopathy in AIDS patients.

Acquired Immunodeficiency Syndrome↗
PubMed1991

Fulminating multiple sclerosis-like leukoencephalopathy revealing human immunodeficiency virus infection.

A 66-year-old French homosexual man and a 42-year-old Brazilian man with no known risk factors for HIV infection developed headaches, asthenia, and neurologic episodes of abrupt onset. CT showed multiple hypodense, nonenhancing lesions. Serology for HIV was positive. They died respectively 2 months and 1 month after onset of the illnesses. Autopsy in both cases showed multiple, well-demarcated, demyelinating foci in the white matter of the cerebral hemispheres, brainstem, and cerebellum with histologic features characteristic of recent plaques of multiple sclerosis. There were no multinucleated giant cells or microglial nodules. Immunostaining for HIV was negative. Although a random coincidence of MS and HIV infection cannot be ruled out, the close temporal relationship between the 2 disorders suggests a possible etiologic association.

Adult↗
PubMed1991

[Neuropathologic study of 135 adult cases of acquired immunodeficiency syndrome (AIDS)].

The central nervous system was examined in 135 adult AIDS patients who died between August 1982 and December 1990. Twenty two brains showed non-diagnostic changes including microglial nodules, discrete myelin pallor with reactive astrocytosis, mineralization of blood vessels and granular ependymitis. In 105 brains with specific changes, toxoplasmosis was the most frequent finding (55 cases) manifested by multifocal necrotic lesions or diffuse pseudo-encephalitic process. Other opportunists included cytomegalovirus (21 case), progressive multifocal leukoencephalopathy (1 cases), cryptococcosis (6 cases), mycobacterium avium intracellulaire (2 cases), varicella-zoster virus (2 cases), aspergillosis (1 case) and multiple bacterial microabscesses (1 case). Multinucleated giant cells were found in 52 cases. In 40 cases, they were widely disseminated throughout the brain and in 39 cases, they were associated with diffuse or multifocal white matter changes. Fifteen cases had a cerebral lymphoma, 9 hepatic encephalopathy, 1 centropontine myelinolysis and 1 focal pontine leukoencephalopathy. Three cases had a cerebral haemorrhage due to disseminated intravascular coagulation, antithrombin therapy and amyloid angiopathy. Spinal changes in 13 cases included vacuolar myelopathy (7 cases), HIV myelitis (1 case) and ganglio-radiculitis (1 cases), cytomegalovirus myelo-radiculitis (1 case) secondary spread from a lymphoma (1 case) and spinal infarcts due to disseminated intravascular coagulation (1 case). These lesions were frequently atypical and various combinations of all these pathologies were encountered in the same brain, sometimes in the same area and occasionally in the same cell. Chronological variations in the incidence of some complications could be related to changes in treatment.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Immunohistochemical study of cerebral amyloid angiopathy. III. Widespread Alzheimer A4 peptide in cerebral microvessel walls colocalizes with gamma trace in patients with leukoencephalopathy.

Brain tissue from 11 patients with cerebral amyloid angiopathy, changes of Alzheimer's disease, and variable degrees of subcortical leukoencephalopathy was examined by immunohistochemical methods, using primary antibodies to peptide segments representing portions of the Alzheimer A4 (beta-) peptide or gamma-trace peptide (seen most commonly in Icelandic patients with cerebral hemorrhage (hereditary cerebral hemorrhage with amyloidosis [HCHWA-I]). Variable A4 immunostaining was seen within cortical (and rarely white matter) parenchyma in the form of senile plaques (with or without central cores), and within capillary and arteriolar walls. Within individual patients, A4 deposits were often primarily parenchymal or vascular, and when they were vascular they tended to be more prominent in arteriolar than in capillary wall segments. Perivascular A4 deposits were often detected around strongly immunoreactive microvessels. Gamma-trace immunoreactivity was noted in many A4-positive microvessel walls, but staining was always less intense than with the anti-A4 antibody. We conclude that patients with severe cerebral amyloid angiopathy may show wide variation in the severity and topography of A4 deposits within brain parenchyma. A4 may colocalize with gamma-trace peptide, suggesting that A4 and gamma-trace forms of cerebral amyloid angiopathy may not be as biochemically distinctive as has been suggested. Other proteases or protease inhibitors may contribute to the pathogenesis of cerebral amyloid angiopathy or cerebral amyloid angiopathy-related stroke syndromes.

Amyloid↗
PubMed1990

Spinal cord lesions in the acquired immune deficiency syndrome (AIDS).

Spinal cord involvement in AIDS is not uncommon. Different types of lesions corresponding to varying pathogenetic mechanisms have been reported. Vacuolar myelopathy is the most frequently found. The symptoms and pathological changes resemble those of subacute combined degeneration; however, cobalamine or folate levels have always been found normal. Its frequent association with the multi-nucleated giant cells characteristic of HIV encephalitis makes it likely that the virus plays a role in its pathogenesis. Cytomegalovirus may be responsible for acute myeloradiculitis involving the spinal roots of the cauda equina and inferior part of the spinal cord. In cases of Herpes simplex virus myelitis has been reported; they are usually associated with cytomegalovirus infection and are due to herpes simplex virus type II. Secondary spread from systemic lymphomas may involve the subarachnoid space of the cord and the spinal roots. Compression of the spinal cord by epidural lymphomatous masses has also been described. Spinal infarcts may be secondary to acute or chronic vasculitis or to less specific vascular processes such as disseminated intravascular coagulation.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Cytomegalovirus (CMV) encephalomyeloradiculitis and human immunodeficiency virus (HIV) encephalitis: presence of HIV and CMV co-infected multinucleated giant cells.

A 25-year-old homosexual male with AIDS presented with a cauda equina syndrome clinically suggestive of cytomegalovirus (CMV) myeloradiculitis. He was treated with ganciclovir with transient improvement of neurological signs and died 4 months after onset of neurological signs. Neuropathological examination revealed human immunodeficiency virus (HIV) encephalitis, CMV subependymal encephalitis and CMV myeloradiculitis. The latter was characterised by myelin loss, Schwann cell proliferation and presence of CMV early antigens in the nuclei of S-100 protein-positive cells in the spinal roots. In the subependymal regions, morphologically characteristic multinucleated giant cells, positive for CD68, contained early CMV antigens (E13) in their nuclei and HIV antigens (gp41 and p24) in their cytoplasm. The observation that HIV and CMV can co-infect the same cell in vivo raises the possibility of a direct synergistic interaction of both viruses at cell level. This suggests that CMV may play a role as a co-factor in the pathogenesis of HIV encephalopathy.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Cerebral amyloid angiopathy and granulomatous angiitis: immunohistochemical study using antibodies to the Alzheimer A4 peptide.

Neuropathologic study of an 82-year-old male who died from massive cerebral hemorrhage showed extensive amyloid angiopathy, with morphologic and immunohistochemical characteristics similar to those observed in Alzheimer's disease, associated with granulomatous angiitis, including the presence of numerous giant cells. Some of the giant cells contained, in their cytoplasm, congophilic material immunoreactive for the Alzheimer A4 peptide, supporting the hypothesis that the granulomatous angiitis may, in part, represent a foreign body reaction to A4 amyloid deposition.

Aged↗
PubMed1990

Cytomegalovirus encephalopathy in an infant with congenital acquired immuno-deficiency syndrome.

A female infant born pre-term to a HIV seropositive mother presented at birth with seropositivity for HIV and CMV viruria. At five months of age she developed an AIDS-related complex. Six months later she died from rapidly progressive diffuse encephalopathy. Post mortem examination revealed generalized CMV infection. Neuropathological examination showed a nodular encephalitis with occasional cytomegalic cells containing characteristic CMV inclusion bodies. There was no evidence of HIV encephalitis; immunostaining for HIV antigen (gp 41) was negative. Opportunistic infections in infants with congenital AIDS are the exception. To our knowledge, only one case of CMV encephalitis in an infant with congenital AIDS has been reported previously. In that case, as in the present one, a reactivation of a congenital CMV infection is likely.

AIDS-Related Complex↗