PubMed Health⌕ Search

Biomedical subjects

W E Ballinger

Publications and source records attributed to W E Ballinger.

At least 19 recordsLinked to original sources
PubMed1992

Absence of cortical white matter changes in three patients undergoing long-term vigabatrin therapy.

Chronic administration of the experimental antiepileptic drug vigabatrin (gamma-vinyl GABA) to animals has been shown to cause dose-dependent neuropathological changes characterized by a microvacuolation in specific white matter tracts. This finding has led to some concern as to whether similar pathologic changes might occur in patients taking this medication. Here we report on analysis of tissue specimens taken during neurosurgery from three patients undergoing chronic vigabatrin therapy (4 g/day). The first patient, a 34-year-old woman, had taken vigabatrin for 2 years prior to surgery, the second, a 50-year-old man, had taken the drug for 1 year, and a 34-year-old man had taken the drug for 5.3 years. For comparison, similar specimens were taken from three other patients not taking vigabatrin who were undergoing surgery for intractable epilepsy. Specimens from each subject were prepared in an identical manner and examined with light and electron microscopy. All specimens were examined in a blinded fashion. There was some minor nonspecific myelinic splitting seen in both controls and vigabatrin-treated patients but there was no evidence for any drug-induced lesions similar to that seen in experimental animals.

Adult↗
PubMed1992

Insulin-like growth factor I receptor binding in brains of Alzheimer's and alcoholic patients.

Patients with chronic alcoholism and/or Alzheimer's disease show degenerative changes in the cerebral cortex and hippocampus. To investigate possible changes in insulin-like growth factor I receptor binding sites in brain tissue of patients with these pathological conditions, the number of 125I-insulin-like growth factor I binding sites was determined in tissues obtained from control patients and those with Alzheimer's and/or with a history of alcoholism. The four experimental groups examined consisted of patients from similar age groups. Postmortem histology and a clinical history were used for the diagnosis of Alzheimer's disease and alcoholism, respectively. Careful clinical records were kept concerning other variables such as immediate cause of death and medications administered before death. Specific binding of 125I-insulin-like growth factor I to homogenates prepared from cerebral cortex of Alzheimer's, alcoholic, alcoholic Alzheimer's, and age-matched control patients was similar, although Alzheimer's patients tended to have slightly higher binding values. No significant differences in insulin-like growth factor I binding in cerebral cortex were found with regard to age of patients, the interval between death and autopsy, and CNS-active medications. No statistical differences in 125I-insulin-like growth factor I binding were noted in hippocampal tissue from the four patient groups. Thus, human insulin-like growth factor I binding sites in cerebral cortex and hippocampus appear unaffected by several variables.

Alcoholism↗
PubMed1992

Aluminium intoxication in undialysed adults with chronic renal failure.

The dialysis encephalopathy syndrome (DES) consists of altered mental status, communication difficulty, seizures and myoclonus. It has been attributed to elevated serum aluminium (A1) levels. Two undialysed patients with chronic renal failure who presented with the characteristic syndrome are reported. The first, a 48 year old female, had used A1 containing phosphate binders for two years. Her serum A1 level was 25.34 mumol/L. Despite treatment with desferoximine and dialysis, she died. Necropsy revealed elevated A1 levels in the cerebral cortex (19 mcg/gm) and spongioform change in the outer three cortical layers. The second patient, a 46 year old woman, had a serum A1 of 8.70 mumol/L. She had never taken A1 containing phosphate binders but had taken several grams/day of citrate for at least six months. Treatment with haemodialysis and discontinuation of the citrate produced a resolution of symptoms and return of the A1 level to normal. During two years of haemodialysis there has been no recurrence.

Aluminum↗
PubMed1991

Binding of [125I]-insulin-like growth factor-1 (IGF-1) in brains of Alzheimer's and alcoholic patients.

Patients with chronic alcoholism and/or Alzheimer's disease suffer from degenerative changes in the cerebral cortex and hippocampus. To investigate possible changes in IGF-1 receptor binding sites in brain tissue of patients with these pathological conditions, the binding of [125I]-IGF-1 was determined in tissues obtained from control, Alzheimer's and/or patients with a history of alcoholism. The four experimental groups examined consisted of patients from similar age groups. Specific binding of [125I]-IGF-1 to cerebral cortical membranes from Alzheimer's patients had significantly more binding sites than age-matched controls, alcoholic patients and alcoholic patients with Alzheimer's disease. Regression analyses indicated that there were no significant differences in [125I]-IGF-1 binding in cerebral cortex with regard to age of patients (1.1% of total variance with a range of 52 to 92 years). Likewise, the time interval between death and autopsy contributed only 1.4% to the total variance in IGF-1 binding. No statistical differences in [125I]-IGF-1 binding were noted in hippocampal tissue from the various patient groups. Thus, human IGF-1 binding sites in cerebral cortex and hippocampus appear to be relatively stable for a number of variables. The increase in cerebral cortical [125I]-IGF-1 binding sites could be due to upregulation of IGF-1 receptors resulting from a decrease in IGF-1 levels in Alzheimer's patients.

Alcoholism↗
PubMed1991

Long-term follow-up of radiotherapy for pituitary adenoma: the absence of late recurrence after greater than or equal to 4500 cGy.

Recent literature has suggested that late recurrence of pituitary adenoma after radiotherapy is common. We hypothesized that late failures might be a result of inadequate dose (less than 4500 cGy). To investigate, we analyzed 105 patients treated at our institution between 1965 and 1986 (analysis, 2/89). The minimum observation time was greater than or equal to 5 years in 58% and greater than or equal to 10 years in 30% of the patients. All patients received megavoltage radiotherapy (range, 4200-5500 cGy; mean, 4821 cGy) at a mean dose per fraction of 172 cGy; 100 patients received greater than or equal to 4500 cGy tumor dose. Twenty-nine patients received radiotherapy alone, and 76 had postoperative radiotherapy after frontal craniotomy (20 patients) or transsphenoidal hypophysectomy (56 patients). At presentation, 71% of patients had extrasellar disease, 57% had visual field deficits, and 50% had endocrinopathy. Of patients treated postoperatively, 74% had gross residual disease. Four local failures occurred at 13, 16, 57, and 64 months after postoperative radiotherapy, all within the irradiated volume (tumor doses of 4700, 4715, 5000, and 5100 cGy). All four patients had presented with moderate to extensive extrasellar disease with visual field defects. Two of the four remain free of second recurrence at 7 and 13 years after salvage transsphenoidal hypophysectomy. The local control rate with radiotherapy (product-limit method) at 10 years was 100% in the radiotherapy-alone group and 92% in the postoperative radiotherapy group (95% for all patients). To prevent bias, seven patients who received bromocriptine, none of whom demonstrated a recurrence, were censored from the local control analysis at the initiation of the drug. No patient in this study suffered recurrence greater than 64 months after radiotherapy, with 31 patients (none with bromocriptine) observed 10 to 21 years. We conclude that treatment of pituitary adenoma with greater than or equal to 4500 cGy in 25 fractions can result in a high (greater than or equal to 90%) probability of stable long-term control.

Adenoma↗
PubMed1991

Anatomic examination of a case of open trigeminal nucleotomy (nucleus caudalis dorsal root entry zone lesions) for facial pain.

Nucleus caudalis dorsal root entry zone lesions (open trigeminal nucleotomy) are a surgical procedure which can achieve pain control without major complications in the difficult clinical setting of deafferentation-type facial pain. Two patients are reported, who had relief of pain, but also experienced neurological complications. One patient succumbed to pulmonary complications, which provided the opportunity for anatomic analysis of the lesioned area, which is discussed in detail. Potential modifications of the surgical technique are suggested.

Afferent Pathways↗
PubMed1991

Loss of synaptic receptors can precede morphologic changes induced by alcoholism.

Neuropsychological deficits including dementia in some alcoholics may potentially result from progressive, submicroscopic loss of synaptic receptors in the absence of morphological lesions. The densities of two types of synaptic receptors were determined in autopsy brain homogenates from several brain regions of not grossly demented alcoholics and non-alcoholic controls. In alcoholics, muscarinic cholinergic receptors were decreased by 40% in frontal cortex, temporal cortex and putamen and by 30% in hippocampus. Benzodiazepine receptors were decreased by 30% in hippocampus and by 25% in frontal cortex but not in temporal cortex or putamen. These changes occurred in histologically normal brains in the absence of Wernicke's encephalopathy, coma, liver cirrhosis and cholinergic or benzodiazepine medications. A computer data base matched for differences in death-autopsy time intervals, age and hypoxia. We conclude that chronic exposure to alcohol results in a loss of synaptic receptors with their synapses. To what extent such receptor losses could result in impairment of cognitive function is currently unknown but will depend on other factors such as the availability of spare receptors and what subtypes of receptors are involved. A rationale may emerge for using in alcoholics the cholinergic treatments currently being developed for the cognitive deficits of Alzheimer's disease.

Alcoholism↗
PubMed1989

Loss of muscarinic cholinergic receptors from the temporal cortex of alcohol abusers.

It is currently controversial whether all the brain damage in alcohol abusers in the result of thiamine deficiency (Wernicke-Korsakoff's disease) or whether, in addition, alcohol abuse may affect the brain by other mechanisms as well. The purpose of this study was to determine if alcohol abuse affects muscarinic cholinergic and benzodiazepine receptors in histologically normal brains obtained at autopsy in a general hospital population. Patients were excluded from this study if they had clinical brain diseases (including Wernicke's disease), died in coma, or had liver disease, significant brain atrophy, or dementia severe enough to require institutionalization. We found that muscarinic cholinergic synaptic receptor density determined with [3H] quinuclidinly benzilate was decreased by 40% in homogenates of the tempeoral cortex of 26 alcohol abusers compared with 26 matched nonalcoholic controls. The affinities of the muscarinic receptors were not significantly different between the two groups. In contrast, receptor densities and affinities of benzodiazepine receptors determined with [3H]flunitrazepam were not significantly different in the two groups. Age and death-autopsy time interval had no significant effects on either wet tissue protein concentrations, yields of protein after centrifugation, or receptor binding. The contributions of age and time interval were each less than 2% of the total variance of protein concentrations and receptor binding. When patients were excluded or included who had received cholinergic, anticholinergic, or benzodiazepine medications before death, no significant effects on the final results were observed. Pneumonia, known to be associated with acute hypoxia, and chronic obstructive pulmonary disease, known to be associated with chronic hypoxia, where approximately equally distributed between the two groups and had no significant effects on the results reported here. The loss of muscarinic and the sparing of benzodiazepine receptors occurs in the temporal cortex of histologically normal brains in the absence of significant atrophy and of gross dementia. This means that these changes are early in the development of an alcohol encephalopathy. We have previously reported a decrease in both muscarinic and benzodiazepine receptor binding in the frontal cortex and a decreasing muscarinic but not benzodiazepine receptors in the temporal cortex of alcohol abusers. Taken together, these findings suggest that alcohol neurotoxicity does not simply result in a random loss of neurons and or their associated synapses with their receptors. Instead, different types of receptors, depending upon their location in different brain regions, are specifically affected or spared. This suggests the involvement of region- and receptor-specific mechanisms in chronic alcohol toxicity.(ABSTRACT TRUNCATED AT 400 WORDS)

Aged↗
PubMed1989

The incidence of unexpected pathological findings in an image-guided biopsy series: a review of 100 consecutive cases.

Despite the widespread availability of image-guided stereotactic biopsy, the need for such procedures in patients with "clear-cut" clinical and radiographic diagnoses is still frequently discussed. In an attempt to ascertain the incidence of unexpected pathological findings, 100 consecutive stereotactic biopsies have been reviewed. Twelve patients were found to have diagnoses of pathological conditions that preoperatively were considered unlikely, or not considered at all. The details of these "diagnostically discordant" cases are discussed.

Adult↗
PubMed1989

Neuroreceptor changes in the putamen of alcohol abusers.

The purpose of this study was to determine if alcohol abuse affects muscarinic cholinergic and benzodiazepine receptors in histologically normal brains obtained at autopsy in a general hospital population. Patients were excluded from this study if they had clinical brain (including Wernicke's) disease, died in coma, had liver disease, significant brain atrophy, or dementia severe enough to require institutionalization. We found that muscarinic cholinergic synaptic receptor density determined with [3H]quinuclidinyl benzilate was decreased by 40% in homogenates of the putamen of 27 alcohol abusers compared with 37 matched nonalcoholic controls. In contrast, receptor densities and affinities of benzodiazepine receptors determined with [3H]flunitrazepam were not significantly different in the two groups. Age and death-autopsy time interval had no significant effects on either wet tissue protein concentrations, yields of protein after centrifugation, or receptor binding. The contributions of age and time interval were each less than 3% of the total variance of protein concentrations and receptor binding. When patients who had received cholinergic, anticholinergic, or benzodiazepine medications before death were excluded or included we observed no significant effects on the final results. Pneumonia, known to be associated with acute hypoxia, and chronic obstructive pulmonary disease, known to be associated with chronic hypoxia, were approximately equally distributed between the two groups and had no significant effects on the results reported here. It is significant that the loss of muscarinic and the sparing of benzodiazepine receptors in the putamen occurs in histologically normal brains in the absence of significant atrophy and gross dementia. It implies that these changes are early in the development of alcoholic encephalopathy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Effects of aging and alcohol on the biochemical composition of histologically normal human brain.

Human brains were removed at autopsy and examined grossly and histologically for any abnormality or evidence of disease. Sixty-two brains appearing normal by these criteria were examined further. First, a detailed record of alcohol consumption was obtained. Second, frozen punches of gray and white matter were used to determine the compositional change associated with age and drinking patterns. Increased age was associated with an increase in the water content, particularly in the white matter, a decline in RNA content in gray matter, a decline in total protein in white matter, and a decline in both myelin and the myelin-like subfraction. The loss of myelin membrane in white matter corresponded to a similar increase in water content, although there was an additional loss of some nonmyelin protein. There was no significant shift in the density between the myelin and the myelin-like membranes, and the protein composition of myelin was not significantly altered by age. A history of heavy alcohol consumption was associated with a relative increase in total protein in white matter even though heavy drinking accelerated the age-related loss of myelin. Presumably, alcohol produced a lag in the rate at which nonmyelin proteins are lost or accelerated the accumulation of abnormal protein. Alcohol consumption did not influence the myelin composition or the ratio of myelin and myelin-like membranes. The interval between patient death and autopsy was shown to have little or no effect on the samples used in this study. These data show that normal aging, uncomplicated by other disease processes, can have a significant effect on the composition of brain tissue, particularly the white matter, and that heavy alcohol consumption accelerates degenerative change, even in tissue appearing normal by histology.

Aged↗
PubMed1988

The meningioma controversy: postoperative radiation therapy.

Total surgical excision is the main goal of therapy for intracranial meningiomas. The controversy today involves the efficacy of postoperative radiation therapy. To evaluate this question, 132 patients with benign intracranial meningiomas, treated between October 1964 and April 1985, were evaluated. All patients had a minimum 2-year follow-up. The actuarial local control rates at 10 years for the three treatment groups were as follows: subtotal excision alone, 18%; subtotal excision plus postoperative radiation therapy, 82%; and total excision alone, 77%. The actuarial determinate survival rates at 10 years were 49%, 81%, and 93%, respectively. Postoperative radiation therapy was also effective for patients treated at the time of the first recurrence, with an actuarial local control rate at 10 years after salvage treatment of 30% for patients treated with surgery alone and 89% for patients receiving postoperative radiation therapy at the time of salvage. This analysis suggests that radiation therapy has a significant role in the treatment of subtotally excised and recurrent intracranial meningiomas.

Brain Neoplasms↗
PubMed1988

Loss of cholinergic muscarinic receptors in the frontal cortex of alcohol abusers.

Alcohol abuse causes impairment of cognitive function ranging from mild forms to end-stage dementia. Alcohol-related dementia accounts for nearly 20% of all admissions to state mental hospitals and may result from head trauma, thiamine deficiency, Alzheimer's, and other brain diseases that can be diagnosed conclusively only at autopsy. However, we postulate that after all these conditions have been excluded, an "alcohol encephalopathy" remains. This is characterized by impaired synaptic function, which underlies the continuum of impaired intellectual function. We found in 79 histologically normal brains of a nondemented general hospital population a 40% decrease in the density of cholinergic muscarinic receptors in the frontal cortex of alcoholics when compared with matched controls of the same age. Only alcohol abuse and not aging, postmortem changes, medications, clinical (including liver) diseases, or differences in causes of death could account for this loss.

Age Factors↗
PubMed1988

Intramedullary spinal tuberculoma.

A case report of intramedullary spinal tuberculomas presenting as cervical myelopathy is described. The rarity of these lesions in North America make this case unique. The use of modern neurodiagnostic and microsurgical techniques as well as the use of postoperative antituberculous drugs resulted in a good outcome. The first known description of magnetic resonance imaging of intramedullary spinal tuberculomas is presented. The gross and microscopic appearances of the lesion are given.

Aged↗
PubMed1987

Brain heterotopia and anencephaly.

This report describes the finding of nodular collections of heterotopic brain tissue in the lungs of a stillborn anencephalic infant. Immunoperoxidase staining was performed on the nodules and on the neural tissue found at the infant's cranial defect, for neuron-specific enolase, glial-fibrillary acidic protein, carcinoembryonic antigen, and epithelial membrane antigen. The nodules were shown to consist of neurons and neuroglia. Epithelium-lined channels within the nodules were shown to have the same staining characteristics as bronchi and bronchioles in the lung, and to be different from ependyma. To our knowledge, ours is the first report of immunoperoxidase techniques being used to objectively characterize the makeup of the lesions in a case of brain heterotopia.

Anencephaly↗
PubMed1987

Multiple sclerosis mimicking primary brain tumor.

Surgical biopsy specimens of multiple sclerosis plaques have been only infrequently reported, and the scanty descriptions of these specimens have generally emphasized the inflammatory nature of the lesion. We present surgical specimens from four patients with multiple sclerosis on whom biopsies were performed because of clinical features mimicking brain tumor. Both general pathologists and neuropathologists involved with these cases experienced difficulty in arriving at the correct diagnosis. In all four cases, the lesions were remarkably uniform in microscopic appearance, consisting of monotonous sheets of gemistocytic astroglia interspersed by numerous foamy macrophages. In sections stained with hematoxylin-eosin, the most helpful diagnostic features were the even distribution of the foamy macrophages and the absence of associated necrosis. In each case, the diagnosis was confirmed with special stains that disclosed total destruction of myelin sheaths with relative preservation of axons. Significant inflammatory infiltration was present in only one of five biopsy specimens.

Adult↗
PubMed1986

Regeneration in peripheral nerve grafts to the cat spinal cord.

Peripheral nervous system grafts have long been known to promote CNS axonal elongation in the rodent. To investigate whether these principles also apply to a higher order animal, more suitable for physiologic studies, we performed autogenous sciatic nerve grafts to the adult cat spinal cord. This report is a brief, initial study of these grafts. In an effort to study both descending and ascending fibers as separately as possible, laminectomies were performed at both thoracic (T2-T9) and lumbar (L2-L4) levels. Aspiration lesions were made in the left side of the cord and the sciatic grafts were introduced. Three cats were studied with standard histological techniques, confirming previous reports of glial scar formation, collagen deposition, and cyst formation at the graft-CNS junction. In 7 other animals, at 146-179 days after the initial operation, the axonal origins were traced retrogradely using horseradish peroxidase and the tetramethyl benzidine technique. Reinnervation of the graft was found by intrinsic spinal cord neurons and dorsal root ganglia neurons. The number of reinnervating neurons was found to be greater than previously reported in the rodent. There was, however, no evidence of regeneration from brainstem nuclei when the grafts were placed at spinal levels where this has been seen in the rat. This may support an absolute maximum for regenerative distances vs a relative one. Although the amount of data was limited, it did support previous reports that peripheral axotomy enhances the regenerative response seen in primary sensory neurons.

Animals↗