Biomedical subjects
V P Sweeney
Publications and source records attributed to V P Sweeney.
Prevalence of multiple sclerosis in British Columbia.
A province wide prevalence study on multiple sclerosis (MS) was conducted in British Columbia (B.C.). The prevalence date was July 1, 1982. The major portion of this study was a review of all the files of neurologists practicing in B.C. as this was judged to be the most accurate source for identifying MS patients. 239,412 neurologists' files were hand searched by one researcher using modified Schumacher criteria for classification. Other sources used during the study for identifying MS patients were the MS Clinic, general practitioners, ophthalmologists, urologists, specialized facilities such as long term care facilities and rehabilitation centres, and patient self-referrals. A total of 4,620 non-duplicated cases were identified and classified. 4,112 of these (89%) were classified according to information contained in neurologists' records. The prevalence estimate for definite/probable MS in B.C. was 93.3/100,000 population. This increased to 130.5/100,000 population if possible MS and optic neuritis were also included. These rates are among the highest reported in Canada or elsewhere. The cooperation of B.C. neurologists made this study unique in its scope and accuracy of diagnosis.
Brain gamma-aminobutyric acid and benzodiazepine receptor binding in dialysis encephalopathy.
We measured gamma-aminobutyric acid (GABA) and benzodiazepine binding in autopsied frontal cortex of 8 patients dying with dialysis encephalopathy (DE). No alteration in [3H] GABA binding was observed. However, a mild reduction (-23%, P less than 0.05) of [3H] flunitrazepam-binding density was found in DE cortex. The magnitude of this reduction was similar to that observed in frontal cortex of amygdala-kindled rats [10]. We suggest that a reduction in benzodiazepine receptor number, in combination with markedly reduced GABA concentration in DE cerebral cortex may contribute to some of the clinical features (especially seizures) characteristically observed in this syndrome.
Neurochemical abnormalities in brains of renal failure patients treated by repeated hemodialysis.
We examined autopsied brain from 10 patients with end-stage renal failure who had undergone repeated hemodialysis. Eight had classic symptoms, and two had suggestive symptoms of dialysis encephalopathy. Findings were compared with those in autopsied brain from control adults who had never been hemodialyzed. Mean gamma-aminobutyric acid (GABA) contents were significantly reduced in frontal and occipital cortex, cerebellar cortex, dentate nucleus, caudate nucleus, and medial-dorsal thalamus of the hemodialyzed patients, the reduction being greater than 40% in cerebral cortex and thalamus. Choline acetyltransferase activity was reduced by 25-35% in three cortical regions in the hemodialyzed patients. These two abnormalities were observed in the brain of each hemodialyzed patient, regardless of whether or not the patient died with unequivocal dialysis encephalopathy. Pyridoxal phosphate contents were substantially reduced in brains of the hemodialyzed patients, but metabolites of noradrenaline, 3,4-dihydroxyphenylethylamine (dopamine), and 5-hydroxytryptamine (serotonin) were present in normal amounts. Aluminum levels were abnormally high in frontal cortical gray matter in the hemodialyzed patients. Although this study does not clarify the role played by aluminum toxicity in the pathogenesis of dialysis encephalopathy, the abnormalities we found suggest the need for further neurochemical investigations in this disorder.
Brain gamma-aminobutyric acid deficiency in dialysis encephalopathy.
We measured levels of gamma-aminobutyric acid (GABA) in the CSF and in the autopsied brain of patients with dialysis encephalopathy. GABA concentrations were low in the CSF of three of five living patients. Mean GABA content was reduced by 30 to 50% in five brain regions (frontal, occipital, and cerebellar cortex, caudate nucleus, and medial dorsal thalamus) in five fatal cases. GABA content was normal in brain regions where GABA is characteristically reduced in Huntington's disease. Choline acetyltransferase activity was diminished (by 25 to 35%) in cerebral cortex of the dialysis encephalopathy patients.
Neoplastic angioendotheliosis. The case of the missed primary?
Two patients are described, of whom one suffered from progressive dementia, the other with a picture suggestive of Guillain-Barré syndrome. Both were found at necropsy to have small vessels throughout the body clogged with malignant cells with resultant cerebral infarcts. The source in one case was a 1-cm tumor in the thyroid, in the other a microscopic focus in the pancreas. It is suggested that most cases described as neoplastic angioendotheliosis involving the brain represent vascular dissemination of an unrecognized primary carcinoma rather than a miraculously widespread malignant endothelial transformation.
Use of discriminant analysis. II. Identification of persons with glaucomatous visual field defects.
Thirty-three ocular, systemic, and laboratory variables were used in a discriminant analysis to separate 219 patients suffering from chronic open-angle glaucoma from 100 people who did not have the disease. The analysis used seven of the variables to separate 93% of the patients correctly. Without intraocular pressure, a 90% separation was obtained.
Migrainous hemiplegia during breast-feeding.
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Factors involved in the production of low tension glaucoma.
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Shock-induced optic neuropathy: a cause of nonprogressive glaucoma.
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Studies of factors involved in the production of low tension glaucoma.
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Ischaemic optic neuropathy in chronic simple glaucoma.
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Optic neuritis and compressive neuropathy associated with cat scratch disease.
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Acute intermittent porphyria. Increased ALA-synthetase activity during an acute attack.
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Haemorrhage on the disc--a sign of acute ischaemic optic neuropathy in chronic simple glaucoma.
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Cerebro-vascular studies in chronic simple glaucoma.
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An acute syndrome of ocular oscillations and truncal myoclonus.
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