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Biomedical subjects

H V Vinters

Publications and source records attributed to H V Vinters.

234 records · Page 13Linked to original sources
PubMedDate not supplied

Necrotizing vasculitis of the nervous system in a patient with AIDS-related complex.

A patient with AIDS-related complex (ARC) presented with a fulminant neurologic syndrome suggestive of ascending myelopathy, and died approximately 48 h after admission to hospital. At necropsy, there was evidence of a severe necrotizing vasculitis affecting the nervous system most severely, with multifocal haemorrhagic necroses of the spinal cord and cauda equina. Although a rare intranuclear inclusion suggestive of herpesvirus infection was seen in the predominantly lympho-histiocytic infiltrate in and around blood vessel walls, the precise aetiology of the angiitis was not apparent. It may represent a response to AIDS virus infection of one or more components of the blood vessel wall.

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

Surgery for intractable infantile spasms: neuroimaging perspectives.

Twenty-three infants and children underwent cortical resection (n = 15) or hemispherectomy (n = 8) for intractable infantile spasms. Infantile spasms were present at the time of surgery in 17 of the 23 patients; in six, spasms had evolved to other seizure types during surgical evaluation. Children with a remote history of infantile spasms were excluded from this study. Focal or hemispheric lesions were identified by magnetic resonance imaging in seven children; an additional two showed focal atrophy without a discrete lesion. Positron emission tomography (PET) showed lateralized or localized abnormalities of cerebral glucose utilization in all patients; in 14, PET was the only neuroimaging modality to identify the epileptogenic cortex. When this occurred, neuropathological examination of resected brain tissue typically showed malformative and dysplastic cortical lesions. Focal interictal and/or ictal electrographic abnormalities were present in all patients, and corresponded well with localization from neuroimaging. None of the patients were subjected to chronic invasive electrographic monitoring with intracranial electrodes. At follow-up (range 4-67 months; mean 28.3 months), 15 children were seizure-free, three had 90% seizure control, one had 75% seizure control, and four failed to benefit from surgery with respect to seizure frequency.

Brain↗
PubMedDate not supplied

Neuropathologic study of resected cerebral tissue from patients with infantile spasms.

Studies to date on the neuropathologic substrates of infantile spasms have largely utilized autopsy material of children who die after a long and complicated seizure history. This makes the interpretation of primary versus secondary changes in the cerebral tissue difficult if not impossible. We have recently had the opportunity to review the neuropathologic changes in cortical tissue resected from infants and children with a history of infantile spasms. The major identifiable abnormalities were destructive lesions, sometimes classifiable as cystic-gliotic encephalomalacia, and dysplastic changes of varying degree. The cortical dysplasias had some similarity to cerebral changes described in tuberous sclerosis, including the presence of bizarre gemistocytic "balloon" cells, and secondary cytoskeletal changes within neuronal cell bodies. Such material provides an opportunity to apply immunohistochemical and molecular techniques to epileptic tissue in an attempt to understand the morphologic substrates of infantile spasms and other types of generalized epilepsy.

Brain↗
PubMedDate not supplied

Lymphomatosis cerebri presenting as a rapidly progressive dementia: clinical, neuroimaging and pathologic findings.

Primary central nervous system lymphoma (PCNSL) usually presents with clinical and neuroimaging findings consistent with single or multiple intracranial mass lesions. On cranial magnetic resonance imaging (MRI), such lesions are nearly always contrast enhancing, reflecting disruption of the blood-brain barrier at the site of tumor nodules. We describe 2 cases from the UCLA Medical Center who developed a rapidly progressive dementia due to extensive gray and white matter cerebral lesions involving much of the brain. In the patient who came to autopsy, widely infiltrating, focally necrotic B-cell plasmacytoid lymphoma was noted throughout the cerebral neuraxis. MRI findings in case 2 were consistent with diffuse lymphomatous brain infiltration without mass lesions, which was biopsy proven. We conclude that PCNSL may occur in a diffusely infiltrating form which may occur without MRI evidence of mass lesions or blood-brain barrier compromise. We refer to this entity as 'lymphomatosis cerebri' and add it to the differential diagnosis of a rapidly progressive dementia.

Adult↗
PubMedDate not supplied

Pediatric cortical dysplasia: correlations between neuroimaging, electrophysiology and location of cytomegalic neurons and balloon cells and glutamate/GABA synaptic circuits.

Seizures in cortical dysplasia (CD) could be from cytomegalic neurons and balloon cells acting as epileptic 'pacemakers', or abnormal neurotransmission. This study examined these hypotheses using in vitro electrophysiological techniques to determine intrinsic membrane properties and spontaneous glutamatergic and GABAergic synaptic activity for normal-pyramidal neurons, cytomegalic neurons and balloon cells from 67 neocortical sites originating from 43 CD patients (ages 0.2-14 years). Magnetic resonance imaging (MRI), (18)fluoro-2-deoxyglucose positron emission tomography (FDG-PET) and electrocorticography graded cortical sample sites from least to worst CD abnormality. Results found that cytomegalic neurons and balloon cells were observed more frequently in areas of severe CD compared with mild or normal CD regions as assessed by FDG-PET/MRI. Cytomegalic neurons (but not balloon cells) correlated with the worst electrocorticography scores. Electrophysiological recordings demonstrated that cytomegalic and normal-pyramidal neurons displayed similar firing properties without intrinsic bursting. By contrast, balloon cells were electrically silent. Normal-pyramidal and cytomegalic neurons displayed decreased spontaneous glutamatergic synaptic activity in areas of severe FDG-PET/MRI abnormalities compared with normal regions, while GABAergic activity was unaltered. In CD, these findings indicate that cytomegalic neurons (but not balloon cells) might contribute to epileptogenesis, but are not likely to be 'pacemaker' cells capable of spontaneous paroxysmal depolarizations. Furthermore, there was more GABA relative to glutamate synaptic neurotransmission in areas of severe CD. Thus, in CD tissue alternate mechanisms of epileptogenesis should be considered, and we suggest that GABAergic synaptic circuits interacting with cytomegalic and normal-pyramidal neurons with immature receptor properties might contribute to seizure generation.

Action Potentials↗
PubMedDate not supplied

Adenovirus encephalitis and widespread ependymitis in a child with AIDS.

A 4-year-old child with AIDS developed encephalitis 2 months prior to death. Adenovirus was cultured from the cerebrospinal fluid. At autopsy, sections of the brain revealed complete sloughing of the intracranial ependyma, with marked gliosis and edema of the periventricular white matter. Cells with large, dark, smudgy intranuclear inclusions, consistent with adenovirus inclusions, were also seen in subependymal locations. In situ hybridization studies confirmed the presence of adenovirus DNA in these cells. This represents a case of morphologically proven adenovirus encephalitis in a pediatric AIDS patient.

AIDS Dementia Complex↗
PubMedDate not supplied

Cerebral amyloid angiopathy: incidence and complications in the aging brain. I. Cerebral hemorrhage.

The clinical and pathologic findings in eleven patients with fatal cerebral hemorrhages related to cerebral amyloid angiopathy (CAA) are described. The hemorrhages were bihemispheric, though not necessarily of simultaneous onset in four patients, and favoured the fronto-parietal cortex and white matter in ten patients. Dissection into the subarachnoid space was common. Cerebrovascular lesions or cardiomegaly related to hypertension coexisted with those of CAA in three cases. Seven patients were not demented prior to the ictus. Ten of eleven brains contained abundant senile plaques and/or neurofibrillary tangles, whether or not the patient had been clinically demented. In the elderly, CAA is an important etiologic consideration for cerebral hemorrhage, especially if the hemorrhage occurs in a peripheral location in the brain and is superimposed on a history of dementia.

Aged↗
PubMedDate not supplied

Cerebral amyloid angiopathy: incidence and complications in the aging brain. II. The distribution of amyloid vascular changes.

Ten histologic sections were sampled from similar cortical regions in each of 84 autopsy brains removed from patients aged 60 to 97 years. The sections were stained by the Congo-red method and examined under polarized light for the presence of cortical (parenchymal) cerebral amyloid angiopathy (CAA). Some degree of CAA was found in 36% of all brains examined, with a higher proportion of patients affected in each successive decade of life. Angiopathy was seen most frequently and was of greater severity in the parietal and occipital gray matter. Overall, it was often a patchy and asymmetric lesion. There was sparing of subcortical white matter and the hippocampi. CAA was most severe in cases of Alzheimer's disease, but occurred in the absence of this condition.

Aged↗
PubMedDate not supplied

Demonstration of adenosine receptors on mouse cerebral smooth muscle membranes.

Adenosine receptors have been identified on brain cortical membranes and microvascular preparations. However, they have not been demonstrated on specific microvascular elements in isolation. 2-3H-chloroadenosine was used as a ligand to investigate the presence of adenosine receptors on isolated mouse cerebral smooth muscle membranes. The binding studies reveal the presence of a high affinity binding site with a Kd value of 33.3 nM and a maximal binding capacity (Bmax) of 283 fmol/mg protein. These findings demonstrate that there is an adenosine receptor on cerebral smooth muscle membranes.

2-Chloroadenosine↗
PubMedDate not supplied

A pathologic correlate of the 'steal' phenomenon in a patient with cerebral arteriovenous malformation.

A patient died after therapeutic bucrylate embolization and resection of a right occipital arteriovenous malformation, which received significant blood supply from the right posterior cerebral artery. At autopsy, there was marked diffuse neuron loss and gliosis in all cell layers of the right hippocampus--pathology which we hypothesize was secondary to a 'steal' of blood from this structure into the malformation. This report represents pathologic evidence for a phenomenon believed to be of major clinical importance in the symptomatology of many AVMs.

Brain↗
PubMedDate not supplied

Primary intraventricular hemorrhage in adults.

Five adults with primary intraventricular hemorrhage are described. The presenting features included headache, confusion and drowsiness. Focal neurological signs were minimal or absent. All five had a history of hypertension, three patients had bilateral internal carotid occlusion at its origin, one had unilateral occlusion of the left internal carotid artery with severe stenosis of the contralateral siphon. Unilateral occlusion of the middle cerebral artery were present in the fifth patient. Pathological examination of the brain from one patient showed the presence of severe hemorrhagic "lacunar" infarcts adjacent to the left lateral ventricle, one showing direct continuity of blood in the lacune with the massive intraventricular hematoma. We hypothesize that such a finding illustrates one possible mechanism for this unusual type of hemorrhage. Patients with longstanding hypertension and severe occlusive disease of the internal carotid arteries may be predisposed to this unusual complication.

Cerebral Angiography↗
PubMedDate not supplied

Alzheimer's disease or plaque disease? Two cases at the frontier of a definition.

Atypical dementias confront the adequacy of current diagnostic concepts. The two patients with atypical dementia syndromes described here shared common postmortem features of numerous neocortical neuritic (senile) plaques and microvascular amyloid, sparing of hippocampus and substantia nigra, and the virtual absence of neurofibrillary tangles. Microscopically, the two differed only by the presence of a few subcortical Lewy bodies in case 1. These similar morphologic features were associated with dramatically different clinical presentations. In the first patient, visual hallucinations, Capgras' syndrome, cognitive slowing, myoclonus, parkinsonism, and primitive reflexes evolved over 3 years. Memory and language were relatively spared. In the second, dysphagia, nonfluent aphasia, hypophonia, motor perseveration, and a severe disorder of attention developed during this 18-month illness. At autopsy, an unrecognized colon malignancy was found. Despite high neuritic plaque counts in cortex, neither the clinical nor the pathologic criteria for Alzheimer's disease adequately describe either case. The cases will be examined first as clinical, then as neuropathologic, entities. From this approach, we conclude that a specific clinical dementia syndrome may be expressed by several neuropathologic "diseases" and that a variety of clinical syndromes may represent a single neuropathologic diagnosis. This strategy identifies a conceptual dichotomy between Alzheimer's syndrome and postmortem Alzheimer's disease. Meticulous clinical and neuropathologic observation is essential in advancing an understanding of the relationship between the two.

Aged↗
PubMedDate not supplied

Microvasculature in brain biopsy specimens from patients with Alzheimer's disease: an immunohistochemical and ultrastructural study.

Brain biopsy specimens from five patients with Alzheimer's disease obtained in the course of a trial of intracerebroventricular bethanechol were studied by immunohistochemical (antibody to A4 peptide) and ultrastructural techniques, with particular emphasis on the microvessels. In some cases, numbers of A4-immunoreactive lesions (senile plaques) correlated well with numbers of plaques demonstrable by silver stains. Prominent A4-immunoreactive amyloid angiopathy was seen in one patient. The patient with severe cerebral amyloid angiopathy (CAA) showed extensive arteriolar deposition of amyloid filaments with apparent destruction of the media but remarkably intact endothelium. A cell of origin for amyloid filaments was not apparent, although close proximity to smooth muscle cell remnants in the arteriolar media suggested this as one possible cell of origin. Frequent vessels showed medial or adventitial collagen deposition, even when the amount of amyloid was minimal or negligible. Thus relatively severe CAA can exist in the absence of overt endothelial injury, although related studies on this tissue indicate definite abnormalities of the blood-brain barrier. Conversely, destruction of smooth muscle cells and collagen deposition in vessel walls may be the cellular correlates of arteriolar weakening that can lead to CAA-related brain hemorrhage.

Alzheimer Disease↗
PubMedDate not supplied

Development of the biologically active Guglielmi detachable coil for the treatment of cerebral aneurysms. Part II: an experimental study in a swine aneurysm model.

BACKGROUND AND PURPOSE: Ion implantation is a surface-modification technology that creates a borderless surface on protein-coated platinum; this change in physical and chemical properties on the surface of Guglielmi detachable coils (GDCs) appears to enhance cell proliferation and adhesion. Our purpose was to evaluate the effect of ion implantation on GDCs in an experimental aneurysm model. METHODS: GDCs were coated with either type I collagen, fibronectin, vitronectin, laminin, or fibrinogen. Using He+ or Ne+ 1 x 10(14-15) ions/cm2, ion implantation was performed on these protein-coated GDCs (GDC-Is). A total of 56 experimental aneurysms were constructed microsurgically in the common carotid arteries of 28 swine. These experimental aneurysms were embolized with standard GDCs (n = 23), collagen GDC-Is (n = 11), vitronectin GDC-Is (n = 6), laminin GDC-Is (n = 4), fibrinogen GDC-Is (n = 6), and fibronectin GDC-Is (n = 6). The animals were sacrificed at day 14 after coil embolization. The physical properties of the new coils (friction on delivery, deployment into aneurysms, trackability, etc) and the development of tissue scarring and neoendothelium across the aneurysm's orifice were evaluated macroscopically and microscopically. RESULTS: No evidence of increased coil friction/stiffness was observed during delivery of GDC-Is through microcatheters in this aneurysm model. A more intense scar formation and neoendothelium at the neck of aneurysms were observed macroscopically when treated with GDC-Is. Significant differences in the proportion of neck coverage between standard GDCs (48.3% +/- 20.5%) and all GDC-I groups were observed (collagen GDC-I-89.4% +/- 14.9%, P < .01; vitronectin GDC-I-71.5% +/- 7.0%, P < .05; laminin GDC-I-76.5% +/- 11.0%, P < .05; fibrinogen GDC-I-74.8% +/- 13.9%, P < .05; fibronectin GDC-I-87.5% +/- 15.0%, P < .01). Light microscopy showed a well-organized fibrous tissue bridging the aneurysm's neck when using GDC-Is, whereas only a fibrin-like thin layer covered the standard GDC surfaces. CONCLUSION: GDC-Is indicated a more intense inflammatory response in the aneurysm body and dome and faster re-endothelial coverage of the neck of the aneurysm. This accelerated histologic response may decrease the chances of coil compaction and aneurysm recanalization. This technology may improve anatomic and clinical outcomes in patients harboring intracranial aneurysms.

Animals↗
PubMedDate not supplied

Neuropathologic findings in the acquired immunodeficiency syndrome (AIDS).

The acquired immunodeficiency syndrome (AIDS) is characterized by a severe idiopathic deficiency in T-cell mediated immunity. Homosexuals, intravenous drug abusers and Haitians are predominantly affected, predisposing them to opportunistic infections and neoplasms. In this study, the central nervous system (CNS) was examined at autopsy in 29 AIDS patients. Significant CNS complications occurred in 55%, mainly related to opportunistic infections similar to those seen in patients with other causes of immunosuppression. Progressive multifocal leukoencephalopathy (three cases), cytomegalovirus (CMV) encephalitis (five cases), cryptococcal meningitis (four cases), Mycobacterium avium-intracellulare (three cases), and toxoplasmosis (one case) were found. Widespread microglial nodules were observed in 20 patients, 80% of whom had CMV inclusions elsewhere at autopsy. Primary cerebral lymphoma (one case) and lymphomatoid granulomatosis (one case) were present. Subarachnoid (five cases) and intraparenchymal (three cases) hemorrhage was seen although these were not usually clinically significant. A single case of embolic arterial obstruction with cortical infarction was due to non-bacterial thrombotic endocarditis.

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

Microscopic cortical dysplasia in infantile spasms: evolution of white matter abnormalities.

PURPOSE: To determine whether microscopic cortical lamination defects in patients with infantile spasms, not initially identifiable on MR, may be inferred from evolving changes in the adjacent white matter. METHODS: Three infants between 3 and 6 months of age presented with infantile spasms. Based on negative metabolic assessment and normal MR findings, they were classified as cryptogenic. Despite therapy the children deteriorated with seizure recurrence and the advent of lateralizing clinical and neurophysiologic findings. MR studies were repeated and positron emission tomography was done. RESULTS: The second MR studies demonstrated abnormalities of myelination, corresponding to localized clinical and neurophysiologic findings. Positron emission tomography findings did not show a strong correlation; one was normal, one showed no abnormality in the major area of MR abnormality, and one showed significantly less abnormality than on MR. Two patients have undergone surgery, both with good response. DISCUSSION: Subtle lamination defects may be identifiable on positron emission tomography but are usually not detectable on MR. White matter abnormality on MR images is usually attributable to primary disease. We suggest that in certain cases progressive white matter changes may be induced as a secondary phenomenon by overlying microscopic cortical lamination defects. Serial MR imaging may be beneficial in children with infantile spasms in whom signs of laterality evolve.

Cerebral Cortex↗