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Biomedical subjects

H V Vinters

Publications and source records attributed to H V Vinters.

At least 127 records · Page 7Linked to original sources
PubMed1993

AIDS dementia complex complicated by cytomegalovirus encephalopathy.

We have studied longitudinally ten patients with AIDS encephalopathy with respect to pathogenetic roles of human immunodeficiency virus (HIV) and cytomegalovirus (CMV). Three patients manifested typical AIDS dementia complex (ADC) (initially without retinitis and with slowly progressive cognitive, motor and behavioral abnormalities which were zidovudine-responsive, and relatively preserved CD4+ T cells), and seven patients presented with AIDS dementia complex complicated by CMV encephalopathy (ACE) (with CMV retinitis, peripheral neuropathy, altered sensorium, and rapidly declining clinical and immunological status). Whereas only HIV antibody was elevated in the spinal fluid of patients with ADC, both virus infections were active in the central nervous system of patients with ACE as shown by HIV p24 antigenemia and antigenrrhachia, elevated HIV and CMV antibody in the spinal fluid, disseminated CMV infection with retinitis, and basilar ventriculoencephalitis with multinucleated cytomegalic cells containing CMV and HIV proteins and CMV DNA. The recognition of ADC and ACE is important, since some patients with ACE may respond to ganciclovir or foscarnet.

AIDS Dementia Complex↗
PubMed1993

Progressive multifocal leukoencephalopathy in AIDS: a clinicopathologic study and review of the literature.

We reviewed the clinical, radiographic, and pathologic features of 15 patients with the acquired immune deficiency syndrome (AIDS) and progressive multifocal leukoencephalopathy (PML). Brain tissue from 10 autopsy and 6 biopsy specimens was studied using: in situ hybridization (ISH) for JC virus (JCV), immunohistochemistry for human immunodeficiency virus (HIV) p24 antigen, and electron microscopy. Thirteen patients presented with focal neurologic deficits, while 2 presented with a rapid decline in mental status. PML was commonly the initial opportunistic infection of AIDS and produced hemiparesis, dementia, dysarthria, cerebellar abnormalities, and seizures. Magnetic resonance imaging was more sensitive than computed tomography in detecting lesions, and often showed multifocal areas of PML. CD4+ T-cell counts were uniformly low (mean 84/mm3), except in 1 patient who improved on 3'-azido-3'-deoxythymidine (AZT). PML involved the cerebral hemispheres, brain stem, cerebellum, and cervical spinal cord. The distribution of brain involvement was consistent with hematogenous dissemination of the virus. In 2 brain specimens, multiple HIV-type giant cells were present within the regions involved by PML. When co-infection by HIV and papovavirus was present, PML dominated the pathological picture. ISH for JCV showed virus in the nuclei of oligodendrocytes and astrocytes. Occasionally there was staining for JCV in the cytoplasm of glial cells and in the neuropil, the latter possibly a correlate of papovavirus spread between myelin sheaths, as seen by electron microscopy. ISH demonstrated more extensive foci of PML than did routine light microscopy.

Acquired Immunodeficiency Syndrome↗
PubMed1993

Herpesviruses in chronic encephalitis associated with intractable childhood epilepsy.

Herpesviruses (especially cytomegalovirus [CMV] and Epstein-Barr virus [EBV]) have been implicated in the pathogenesis of chronic (Rasmussen) encephalitis associated with epilepsy. To assess the presence of herpesvirus genes in brain tissue from epileptic children with chronic (usually Rasmussen type) encephalitis, DNA was extracted from surgically resected brain tissue and studied by the polymerase chain reaction using primers specific for CMV, varicella zoster virus, herpes simplex virus, EBV, and human herpesvirus 6 genes. By this technique evidence for the presence of low levels of CMV and EBV genes was detected in most brain specimens from encephalitis patients and in several brain specimens from patients without encephalitis (eg, cortical dysplasia, gliosis, or encephalomalacia) who also had intractable epilepsy. Occasionally, both EBV and CMV genes were found in the same brain. Signal strength for both CMV and EBV was much lower in epileptic brains than in the brains of acquired immunodeficiency syndrome patients with CMV encephalitis or brain lymphoma. We found evidence for infection of the brain by human herpesvirus 6 in only one patient with encephalitis. Polymerase chain reaction technology applied to resected brain tissue from epileptic patients may provide evidence for or against viral-mediated pathogenesis of Rasmussen encephalitis or other types of encephalitis. The small amounts of EBV and CMV genes found suggest that herpesvirus infection of the brain does not directly cause Rasmussen encephalitis.

Autoradiography↗
PubMed1993

Multifocal necrotizing leukoencephalopathy with pontine predilection in immunosuppressed patients: a clinicopathologic review of 16 cases.

Multifocal necrotizing leukoencephalopathy (MNL) is characterized by multiple, usually microscopic, foci of necrosis confined primarily to the white matter of the basis pontis, but sometimes found elsewhere in the central nervous system. All 16 patients in whom we identified MNL had underlying immunosuppression, either naturally occurring or iatrogenic, including the acquired immunodeficiency syndrome (seven patients), acute leukemias (four patients), and lymphoma (one patient). One patient each had severe combined immunodeficiency, orthotopic liver transplantation, Shwachman-Diamond syndrome, and idiopathic thrombocytopenic purpura treated with high-dose steroids. Histologically, lesions of MNL show demyelination, spongiosis, axonal swelling, minimal histiocytic infiltrates, and frequent axonal calcification. Multifocal necrotizing leukoencephalopathy lesions were found in the pons of all patients, most commonly in the crossing pontocerebellar fibers, but often in the descending white matter tracts and rarely in the tegmentum. Three cases also showed nonpontine foci of MNL involving the white matter of the medulla, cerebellum, and cerebral hemispheres. Multifocal necrotizing leukoencephalopathy is a distinct entity usually localized to the basis pontis and is most consistently associated with immunosuppression, but as yet lacks other clearly defined clinical correlates.

Adult↗
PubMed1993

Communication deficits in children undergoing temporal lobectomy.

OBJECTIVE: To examine formal thought disorder and discourse (cohesive) devices that make speech coherent prospectively in seven children, aged 5.7 to 16.7 years, before and after temporal lobectomy for intractable cut points determined from sensitivity and specificity analyses of formal thought disorder and discourse measures in 22 children with complex partial seizure disorder and 45 normal children. RESULTS: Before surgery, the mean illogical thinking and discourse scores of the surgical candidates were in the pathological range. After a mean postoperative follow-up period of 15.1 months, their illogical thinking (but not their discourse scores) decreased significantly to the normal range. CONCLUSIONS: These preliminary findings are discussed in terms of the possible role of postsurgical changes in seizure control, behavior, antiepileptic drugs, cognition, and prefrontal function.

Adolescent↗
PubMed1993

Neurological reactions in HIV-infected patients treated with trichosanthin.

Trichosanthin is a ribosome-inactivating protein that is being studied as a possible treatment for patients infected with human immunodeficiency virus (HIV). We report the clinical and pathological features in two patients who experienced neurological reactions to trichosanthin. Both patients were neurologically asymptomatic prior to treatment but developed coma and multifocal neurological deficits after treatment. Neuropathological examination revealed regions of severe, multifocal necrosis with histiocytic infiltrates. These reactions to trichosanthin may be mediated by soluble factors released by HIV-infected macrophages.

Acquired Immunodeficiency Syndrome↗
PubMed1992

Differential expression of arachidonate 5-lipoxygenase transcripts in human brain tumors: evidence for the expression of a multitranscript family.

In addition to the important role of leukotrienes as mediators in allergy and inflammation, these compounds are also linked to pathophysiological events in the brain including cerebral ischemia, brain edema, and increased permeability of the blood-brain barrier in brain tumors. Although brain tumors have been shown to secrete leukotrienes, no studies to date have provided evidence for the tumor expression of genes encoding enzymes involved in leukotriene production. Therefore, the present study determined the abundance of the mRNA for arachidonate 5-lipoxygenase (5-LO; arachidonate:oxygen 5-oxidoreductase, EC 1.13.11.34), which is the rate-limiting enzyme in leukotriene synthesis, in a series of human brain tumors. Macrophage/monocyte infiltration of the tumor was estimated by measuring the abundance of the transcript for the 91-kDa glycoprotein phagocyte-specific oxidase (gp91-phox), which is the phagocyte-specific cytochrome b heavy chain. The present study shows that (i) the 5-LO transcript is expressed in normal bovine brain and in human brain tumors; (ii) the 5-LO gene in human brain tumors and in the dimethyl sulfoxide-induced promyelocytic human leukemic HL-60 cells is expressed as a multitranscript family (2.7, 3.1, 4.8, 6.4, 8.6 kilobases); and (iii) the abundance of 5-LO transcripts, the expression of the larger transcripts, and the 5-LO/gp91-phox ratio correlate with the tumor malignancy. Overall, the present study supports the hypothesis that the 5-LO gene product may play a role in human tumor-induced brain edemas and provides evidence for tumor-associated expression of high molecular weight 5-LO transcripts in human brain tumors.

Arachidonate 5-Lipoxygenase↗
PubMed1992

Reversible in vitro growth of Alzheimer disease beta-amyloid plaques by deposition of labeled amyloid peptide.

The salient pathological feature of Alzheimer disease (AD) is the presence of a high density of amyloid plaques in the brain tissue of victims. The plaques are predominantly composed of human beta-amyloid peptide (beta A4), a 40-mer whose neurotoxicity is related to its aggregation. Radioiodinated human beta A4 is rapidly deposited in vitro from a dilute (less than 10 pM) solution onto neuritic and diffuse plaques and cerebrovascular amyloid in AD brain tissue, whereas no deposition is detectable in tissue without performed plaques. This growth of plaques by deposition of radiolabeled beta A4 to plaques is reversible, with a dissociation half-time of approximately 1 h. The fraction of grey matter occupied by plaques that bind radiolabeled beta A4 in vitro is dramatically larger in AD cortex (23 +/- 11%) than in age-matched normal controls (less than 2%). In contrast to the human peptide, rat/mouse beta A4 (differing at three positions from human beta A4) does not affect the deposition of radiolabeled human beta A4. beta A4 has no detectable interaction with tachykinin receptors in rat or human brain. The use of radioiodinated beta A4 provides an in vitro system for the quantitative evaluation of agents or conditions that may inhibit or enhance the growth or dissolution of AD plaques. This reagent also provides an extremely sensitive method for visualizing various types of amyloid deposits and a means for characterizing and locating sites of amyloid peptide binding to cells and tissues.

Aged↗
PubMed1992

Cerebral hemorrhage with biopsy-proved amyloid angiopathy.

Clinical, radiological, and immunohistochemical findings in brain biopsy specimens from six patients with cerebral amyloid angiopathy-associated intracerebral hemorrhage were reviewed. Acute clinical presentations included headache, nausea and vomiting, loss of consciousness, and focal neurological deficits such as hemiplegia and blindness. Transient ischemic attacks experienced by one patient and referable to one hemisphere did not indicate impending hemorrhage in that region. Computed tomographic scans revealed acute, irregular, superficial, lobar hemorrhage with occasional ring enhancement. Immunohistochemical studies were performed on biopsy specimens using primary antibodies against portions of the Alzheimer A4 (beta-) peptide or gamma-trace peptide (the vascular amyloid protein in patients with hereditary cerebral hemorrhage with amyloidosis-Icelandic type). In all patients, anti-A4 and anti-gamma-trace labeled cerebral microvessels. Immunoreactive senile plaques were few compared with the numbers of stained microvessels. Reactive astrocytes in some patients were labeled by both antiserum samples, suggesting uptake or production of these proteins by the astrocytes. This study demonstrates the heterogeneous clinical and radiological features of cerebral amyloid angiopathy-related brain hemorrhage and the value of anti-A4 and anti-gamma-trace immunohistochemical study of biopsy material from patients with suspected cerebral amyloid angiopathy-related intraparenchymal bleeding.

Aged↗
PubMed1992

Neuropathologic findings in surgically treated hemimegalencephaly: immunohistochemical, morphometric, and ultrastructural study.

Tissues from three cases of hemimegalencephaly (HME) causing intractable seizures treated by cortical resection were studied using immunohistochemical, ultrastructural, and morphometric techniques. Severe cortical dysplasia was seen in all cases and included lesions best characterized as hemilissencephaly and polymicrogyria. Blurring of the cortex-white matter junction, the presence of large neuronal heterotopias, and neuronal cytomegaly were frequent observations. Immunohistochemical analysis demonstrated cellular colocalization of astrocytic markers glial fibrillary acidic protein and vimentin in one case of hemilissencephaly. Morphometric data showed significant increases over controls in neuronal profile area in all cases of HME. Neuronal cell density was increased significantly above controls in one of the cases. The study shows that HME results from severe cortical dysplasia which may be caused by multiple insults, manifest in one of several ways, and reflects abnormal or altered signals that regulate cortical morphogenesis.

Brain↗
PubMed1992

Neuropathologic findings in cortical resections (including hemispherectomies) performed for the treatment of intractable childhood epilepsy.

Despite the use of hemispherectomy in the treatment of medically refractory seizures since the early 1950's, few studies published have documented neuropathologic findings in the resected specimens. This report describes the neuropathologic findings in 38 children who underwent either hemispherectomy or multilobar cortical resection as treatment for medically intractable epilepsy between 1986 and 1990. Examination of the resected specimens revealed a variety of abnormalities which fell into four broad categories. Malformations or hamartomatous lesions were the dominant finding in 15 patients, whereas encephalomalacic lesions were the most prominent abnormality in 16; chronic pathogen-free encephalitits (Rasmussen's encephalitis) was present in 3 and an additional 3 children had Sturge-Weber-Dimitri syndrome. There were no gross or microscopic abnormalities in 1 patient. This report provides the first comprehensive description of the pathologic findings in a series of children with refractory epilepsy of varying types treated by hemispherectomy-multilobar resection.

Brain Ischemia↗
PubMed1992

Correlation of neuromuscular pathology in acquired immune deficiency syndrome patients with cytomegalovirus infection and zidovudine treatment.

Peripheral nerve and skeletal muscle specimens from 115 autopsied adult AIDS patients were examined for types and incidence of histological abnormalities. Focal perivascular chronic inflammatory infiltrates featuring plasma cells were found in 85% of nerve and muscle specimens. These foci were specifically associated with cytomegalovirus (CMV)-infected capillary or venous endothelial cells in neuromuscular specimens of 31/115 patients, with increasing incidence in patients surviving longer with the diagnosis of AIDS. Neuromuscular CMV was identified histologically in 19% of AIDS patients with an AIDS-defining illness for 3 months or less, with the incidence increasing to 46% of patients who had the diagnosis for 2 years or longer. Vascular damage from CMV endothelial infection may result in regional ischemic and/or inflammatory damage to nerves, producing myelinated fiber loss and axonal degeneration, leading to denervation atrophy of myofibers found in skeletal muscle specimens in a majority of the patients. Myelinated fiber loss within the sural nerve was determined by morphometric quantitation for a subset of 50 patients, and correlated with the presence of histologically identifiable neuromuscular CMV, clinical history of zidovudine administration, and chemotherapy for alleviation of Kaposi's sarcoma. CMV infection and zidovudine treatment were both positively correlated with myelinated fiber loss, while Kaposi's sarcoma chemotherapy did not independently increase the incidence of myelinated fiber loss.

Acquired Immunodeficiency Syndrome↗
PubMed1992

Morphological substrates of infantile spasms: studies based on surgically resected cerebral tissue.

Extensive surgical resections of neocortical cerebral tissue (including hemispherectomies) from 13 infants and children with infantile spasms showed that 12 of 13 specimens contained either malformative and dysplastic lesions of the cortex and white matter (sometimes with associated hamartomatous proliferation of globular cells), or destructive lesions possibly acquired as a result of anoxic-ischemic injury, or a combination of the two. In brain tissue from 4 patients, coarse neuronal cytoplasmic fibrils resembling neurofibrillary tangles were seen in areas of dysplastic brain on silver-stained (Bielschowsky technique) sections. Immunohistochemical (immunoperoxidase) study of cortical lesions containing globular cells employing primary antibodies to glial fibrillary acidic protein and synaptophysin as markers of astrocytic and neuronal differentiation, respectively, revealed that many cells showed astrocytic and/or neuronal features, suggesting the local proliferation of primitive or multipotential neuroectodermal cells as one substrate for this seizure disorder. Morphological abnormalities of a severe degree and wide extent in the resected tissue (e.g., in one patient with hemimegalencephaly) often showed features to suggest that they may represent variants of tuberous sclerosis. These most likely result from abnormal movement and/or local proliferation of neuroectodermal precursors that have migrated from the germinal matrix to the cortical mantle. Cellular, molecular and neurophysiological study of these abnormalities is likely to yield information about basic molecular mechanisms of brain malformation and injury important in the pathogenesis of infantile spasms and other forms of focal or generalized epilepsy.

Cerebral Cortex↗
PubMed1992

Neuropathologic findings after liver transplantation.

Neuropathologic findings are described in 37 patients autopsied after one or more orthotopic liver transplants. Gross or microscopic lesions were observed in almost all patients, including anoxic-ischemic change, hemorrhages and/or infarcts, and opportunistic infections by fungi (most commonly Aspergillus) and rarely viruses (cytomegalovirus). Central pontine and extra-pontine myelinolysis was commonly observed, and appeared to result from severe multifactorial metabolic abnormalities in the perioperative period. Low-grade (microglial nodule) encephalitis without an obvious pathogen was often encountered. Common clinical neurologic abnormalities included encephalopathy, seizures (myoclonic, focal or generalized), obtundation and coma. These were found more commonly than focal findings, but clinical features in a given patient were not uniformly predictive of underlying neuropathologic change.

Brain Diseases↗
PubMed1992

Late onset primary systemic carnitine deficiency exacerbated by carnitine-free parenteral nutrition.

We describe a 21-year-old male with previously normal plasma total and free carnitine levels who developed a deficiency manifest by decreased plasma and muscle total and free carnitine, decreased urine carnitine, severe hepatic steatosis, mediastinal lipomatosis, progressively impaired triglyceride clearance, myopathy and intermittent hypoglycemia. This case demonstrates that systemic carnitine deficiency may occur in some patients receiving long term carnitine-free TPN. Carnitine may be an essential element of the diet in this patient population.

Journal Article↗
PubMed1992

An assessment of the proliferative potential of 'balloon cells' in focal cortical resections performed for childhood epilepsy.

Cerebral cortical dysplasia is an uncommon pathological substrate of severe intractable childhood epilepsy, sometimes treated by hemispherectomy. Neuropathological findings include abnormal gyrus formation, loss of cortical lamination, unusual giant neurons and 'balloon cells' of indeterminate histogenesis similar in appearance to neoplastic gemistocytic astrocytes. In order to investigate the proliferative potential of 'balloon cells', we used Crocker's silver impregnation technique to demonstrate nucleolar organizer regions (AgNORs) involved in cellular proliferation, together with immunohistochemical evaluation of proliferating cell nuclear antigen (PCNA) expression. Balloon cells (5.56 +/- 0.24) had significantly (P < 0.001) greater AgNOR numbers than reactive astrocytes (3.89 +/- 0.15), neurons (2.30 +/- 0.13) or giant neurons (4.26 +/- 0.20). However, when corrected for nuclear size, results showed that 'balloon cells' (0.093 +/- 0.006) had significantly (P < 0.001) fewer AgNORs/square micrometre of nuclear area than reactive astrocytes (0.225 +/- 0.016) and had significantly (P < 0.001) more AgNORs/square micrometre of nuclear area than normal (0.048 +/- 0.003) or giant neurons (0.054 +/- 0.003). On the assumption that astrocytes are typical interphase cells and that normal neurons are post-mitotic, the results suggest that 'balloon cells' are unlikely to be undergoing proliferative activity and, when adjusted for nuclear size, the number of AgNORs/unit of nuclear area is more reflective of cellular ploidy than of proliferative activity in non-neoplastic neural tissues. The virtual absence of PCNA expression by 'balloon cell' nuclei supports such an interpretation of the AgNOR results.

Cell Count↗
PubMed1992

Temporal and extended temporal resections for the treatment of intractable seizures in early childhood.

In our series of 33 children who underwent temporal and extended temporal lobe resections because of seizures, the average age at surgery was 7 years, 11 months. Sixteen cases (48%) were diagnosed as having tumors: low-grade astrocytoma (6), hamartoma (5), and ganglioglioma/neuroma (5). Other pathologic diagnoses included one or more cytoarchitectural abnormalities and/or reactive changes. Due to a more aggressive and early radiologic and electrophysiologic investigation of children with seizures, a resectable focus, e.g. neoplasm or structural abnormality, was found in a much younger age group of patients than previously reported. In children who had intractable seizures but normal radiologic studies, positron emission tomography was of great value in localizing the seizure focus. In a group of children with infantile spasms, seizures were controlled following the identification and resection of a focal lesion. Prompt detection and precise localization of lesions in the temporal lobe in the pediatric population may lead to surgical management and seizure control.

Adolescent↗