PubMed Health⌕ Search

Biomedical subjects

C G Harper

Publications and source records attributed to C G Harper.

At least 19 recordsLinked to original sources
PubMed1992

Brain stem serotonin-synthesizing neurons in Alzheimer's disease: a clinicopathological correlation.

The location and number of brain stem serotonin-synthesizing neurons were analyzed in 11 patients with Alzheimer's disease (AD) and 5 age-matched controls using immunohistochemical techniques. In addition, the number of neuritic plaques and neurofibrillary tangles in the cortex and brain stem raphe was evaluated, as was the number of Nissl-stained raphe neurons. AD patients could be classified into two groups based on their raphe pathology; patients with such pathology (AD+) and those without (AD-). The number of large raphe neurons correlated significantly with the number of serotonin-synthesizing neurons in control material, indicating that all large neurons were serotonergic. This relationship was not apparent in AD+ patients, in whom the number of serotonin-synthesizing neurons correlated with the number of neurofibrillary tangles in the raphe of these patients. This indicates that in AD+ patients the serotonin-synthesizing neurons were selectively affected. There was no correlation between raphe and cortical pathology or raphe pathology and patient sex, age, mini-mental score or depression score, even when such scores were weighted for the interval between testing and death. There was a trend for the raphe pathology to correlate with the age of onset and duration of dementia and the Blessed dementia score in AD+ patients. Most AD+ patients with severe raphe lesions had clinical dementia only, while AD- patients had additional clinical features. The raphe lesions were more dramatic in AD+ patients with a rapid progression of symptoms.

Aged↗
PubMed1992

Amino acid neurotransmitter receptor changes in cerebral cortex in alcoholism: effect of cirrhosis of the liver.

Gamma-aminobutyric acidA/benzodiazepine receptor binding sites and the N-methyl-D-aspartate subclass of glutamate receptor sites were assessed in synaptic plasma membrane homogenates of cerebral cortex tissue obtained at autopsy from cirrhotic and noncirrhotic alcoholic patients and matched control subjects. The alcoholic patients consumed an average of greater than 80 g of ethanol/day, the control subjects less than 20 g/day. Postmortem delays up to approximately 100 h caused no significant loss of any of the binding sites; the patient and subject groups were closely matched for age. The affinities (KD) of the receptor sites did not differ between the patient and subject groups, nor between cortical regions. Using three different radioligands ([3H]muscimol, [3H]flunitrazepam, and [3H]diazepam), the gamma-aminobutyric acidA/benzodiazepine receptor complex was found to have greater density (Bmax) in superior frontal gyrus in alcoholic patients (which selectively shows morphological change in alcoholic patients), but was unchanged in motor cortex. Alcoholic patients with cirrhosis had much less pronounced changes. The density of the N-methyl-D-aspartate subclass of glutamate receptors, assessed with [3H]MK-801, did not vary across patient and subject groups.

Adult↗
PubMed1991

Central tumour necrosis: a cause for the acute presentation of benign meningiomas.

Occasionally, large benign intracranial tumours which have existed for many years present as a relatively acute problem. The mechanisms underlying the sudden change are sometimes unclear but infarction of the benign tumour, subsequent cerebral oedema and an increase in intracranial pressure have been reported. The authors describe such a case of focal infarction in a meningioma with a precise chronology of the clinical, radiological and pathologic findings.

Adult↗
PubMed1991

Increased central immunoreactive beta-endorphin content in patients with Wernicke-Korsakoff syndrome and in alcoholics.

beta-endorphin, adrenocorticotrophin, and alpha-melanocyte stimulating hormone were measured by radioimmunoassay in three areas of human brain at necropsy in seven subjects with Wernicke-Korsakoff syndrome and in 52 controls. Thiamin concentration in six brain areas was also measured. Mamillary body beta-endorphin concentrations were significantly increased in those with the syndrome compared with controls, and those controls with high alcohol intake showed increased mamillary body beta-endorphin compared with controls with low alcohol intake. Brain thiamin concentration was similar in both groups, with the exception of the brainstem, where it was reduced in subjects with Wernicke-Korsakoff syndrome. Thalamic beta-endorphin in controls was inversely correlated with thiamin in frontal white matter, frontal cortex, parietal white matter and parietal cortex, while beta-endorphin in the hypothalamus of patients was inversely correlated with thiamin in frontal cortex, parietal white matter, thalamus and brainstem. These results suggest that there is a disturbance of the endorphinergic system in Wernicke-Korsakoff syndrome which may be related to alcohol intake.

Adrenocorticotropic Hormone↗
PubMed1990

Neurocysticercosis--two Australian cases.

Two cases of neurocysticercosis, one with multiple small lesions and the other with a single cerebral cyst, are reported. Both patients presented with focal seizures and headaches years after likely exposure to Taenia solium eggs. These cases represent susceptible populations in Australia--migrants from and travellers in endemic areas.

Adult↗
PubMed1990

Neuropathology of alcoholism.

There are wide ranging effects of alcohol on the nervous system. Some interfere with physiological and neurochemical functions but ultimately structural damage occurs. During life one of the most impressive changes is brain shrinkage which can be visualized using neuroradiological imaging techniques. This article reviews the pathological explanations for brain shrinkage and addresses the question of the pathogenesis of the reversible component of this damage in relation to prolonged abstinence from alcohol. This shrinkage seems to relate to a loss of white matter. However, the cortex is also abnormal in that there is a loss of neurones from the frontal region. In this and other regions of the cortex examined there is shrinkage of the neuronal soma. This is reflected in a retraction of the neuronal dendritic arbor which plays a crucial role in cell-to-cell communication. In addition, the cerebellum appears to be vulnerable in alcoholic patients although it may well be that associated nutritional deficiencies play an important role. The Wernicke-Korsakoff syndrome is another important deficiency disorder which is seen most frequently in alcoholic patients. Two important population groups which are considered in this review are females and moderate ('social') drinkers. Females are thought to be more susceptible to the damaging effects of alcohol than males and this is examined in the light of the scant data available. Similarly, there are few neuropathological data on people who drink 30-80 grams of alcohol per day. In order to assess so-called 'safe levels of drinking' this is an important group to study.

Alcohol Amnestic Disorder↗
PubMed1990

Brain and liver dolichol in chronic alcoholism: a necropsy study.

Cerebral gray and white matter and liver dolichol levels were measured in postmortem samples from chronic alcoholics and nonalcoholic controls following recent suggestions that dolichol levels may be used as a marker for alcoholism. No significant differences in brain dolichol were found between the control and alcoholic groups. A significant reduction in the liver dolichol was observed in the alcoholic group. This was most marked in those alcoholics with liver disease.

Adult↗
PubMed1990

The effects of alcohol on the female brain: a neuropathological study.

This quantitative neuropathological study compared the brains of seventeen alcoholic females with twenty non-alcoholic female controls. There was a significant (P less than 0.001) increase in the pericerebral space value (control 9.5; alcoholic 16.3) indicating shrinkage of the brain. Cerebral grey and white matter volumes were determined morphometrically. There was a significant decrease in the cerebral white matter volume (P less than .02) in the alcoholics. The cerebral grey matter volume was unchanged. These changes parallel those described previously in male alcoholics. Further studies will be necessary to establish the relative severity of the brain damage in males and females.

Alcohol Drinking↗
PubMed1989

Cortical dihydropyridine binding sites are unaltered in human alcoholic brain.

The density and affinity of sites labeled by the 1,4-dihydropyridines, [3H]nitrendipine and (+) [3H]PN 200-110, were not significantly different in superior frontal and parietal cortical membranes from alcoholic patients and nonalcoholic control patients. This is in contrast to the increased number of dihydropyridine receptors and increased functional activity of calcium channels reported in brain from rats treated chronically with ethanol and in neural cell lines grown in the presence of ethanol. These results indicate that 1,4-dihydropyridine-sensitive calcium channels (L type) in the brain, despite possible acute changes, are unaltered following long-term ethanol exposure in humans.

Alcoholism↗
PubMed1989

Neuronal counts from four cortical regions of alcoholic brains.

Neuronal loss from the frontal superior cortex of the brains of alcoholics has recently been documented. In addition to this, a reduction in the mean neuronal area was also seen in the frontal and motor cortices. This suggested a regional specificity of neuronal damage in the brains of alcoholics. Further quantitation of other cortical regions of the same cases as used in the above study has been performed. The frontal cingulate and temporal cortices were examined and there was found to be no significant alteration in the number of neurons when compared to a control population. There was, however, a significant reduction in the mean size of the neuronal soma in the frontal cingulate cortex (P less than 0.05). These data support the hypothesis of regional variations in the severity of cerebral cortical damage in alcoholism with shrinkage of neurons in most regions examined but neuronal loss only in the superior frontal gyrus.

Adult↗
PubMed1988

Brain shrinkage in alcoholics is not caused by changes in hydration: a pathological study.

Measurement of the water content of the cerebral white matter in 26 control and 24 alcoholic cases supports in vivo MRI studies and previous necropsy studies which appeared to show an increase in the water content in the alcoholic group. This negates the hypothesis that reversible brain shrinkage in alcoholics is caused by changes in the state of hydration.

Aged↗
PubMed1988

Solitary cervical intra- and extramedullary schwannoma.

A case of solitary cervical intramedullary schwannoma with an extramedullary extension is reported. This case demonstrates the difficulty of radiologic diagnosis of these tumours and the necessity for pre-treatment biopsy.

Female↗
PubMed1988

Necropsy study of GABA/benzodiazepine receptor binding sites in brain tissue from chronic alcoholic patients.

Neurological and cognitive deficits occur in many chronic alcoholic patients. Quantitative studies reveal a significant reduction in the number of neurons in the superior frontal gyrus of chronic alcoholics, with no change in the motor cortex. Our studies are aimed at delineating which neurotransmitter systems are altered in alcoholics and to correlate these alterations with morphometry and, where possible, clinical signs. Much evidence suggests both short- and long-term effects of ethanol on GABA-mediated neurotransmission. GABA and benzodiazepines bind to distinct, but allosterically linked, sites on the GABA/benzodiazepine receptor complex. In the absence of any detected difference in the number of benzodiazepine receptors in both the frontal and motor cortex from alcoholic and control patients, a significant increase in the amount of GABA enhancement of [3H]diazepam binding was measured in frontal cortex membranes from patients with Wernicke's encephalopathy relative to non-alcoholic controls. This finding suggests an increased coupling of the GABA and benzodiazepine recognition sites in this area, which may be due to ethanol-induced conformational changes in the receptor complex.

Alcoholism↗
PubMed1987

A quantitative histological study of the cerebellar vermis in alcoholic patients.

A quantitative histological study was made of the cerebellar vermis in 10 male alcoholic and 8 age-matched control cases. The mean Purkinje cell loss was 21% in the alcoholic group. The small rostral and caudal lobes were most severely affected. The mean Purkinje cell density per unit length of foliae showed similar changes. Histological measurements of the area of the molecular, granular and medullary layers of the cerebellar vermis showed that the molecular layer varied in the degree of shrinkage between lobes (from 11 to 39%) while the granular layer showed a consistent shrinkage (9 to 10%). The molecular layer appears to be the most vulnerable region in chronic alcoholics. Brains taken from patients with Wernicke's encephalopathy had particularly low Purkinje cell counts and a large pericerebral space. Nutritional deficiency would seem to be an important factor in the causation of the observed neuropathology, with liver disease playing a lesser role. Evidence that repeated alcohol withdrawal can lead to further brain disturbances is reviewed.

Aged↗