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Biomedical subjects

M Honavar

Publications and source records attributed to M Honavar.

At least 37 records · Page 2Linked to original sources
PubMed1994

Neocortical cholinergic activities differentiate Lewy body dementia from classical Alzheimer's disease.

Activity of the enzyme which synthesizes acetylcholine, choline acetyltransferase, was estimated in the neocortex of three series of control and demented cases. Clinically demented cases were divided into those with the classical neuropathological features of Alzheimer's disease (numerous neocortical plaques and tangles) and those with Lewy bodies in the brain stem and cortex (together with plaques and variable neurofibrillary pathology). In the Lewy body cases neocortical choline acetyltransferase was consistently lower than in the classical Alzheimer-type cases. Two of the Lewy body cases with extremely low cholinergic activity were responders in therapeutic trials of the cholinesterase inhibitor, tacrine, and the combined data suggest that cholinergic therapy may be particularly relevant to patients with Lewy body type dementia.

Alzheimer Disease↗
PubMed1994

Infantile axonal neuropathy in two siblings.

Two siblings presented with a recurrent axonal neuropathy associated with intercurrent infection. One child had mild global developmental delay. The CSF was normal and haematological and biochemical tests failed to reveal a metabolic disorder. Nerve conduction studies in both children showed a mixed sensory and motor axonal neuropathy. Sural nerve biopsies showed severe ongoing axonal degeneration. At post mortem examination peripheral nerves showed widespread axonal loss with a marked reduction of anterior horn and posterior root ganglion cells. Mild diffuse endoneurial cell inflammation was present in the peripheral nerves and some posterior roots. We believe that these siblings died from a genetically determined axonal neuropathy with central nervous system involvement.

Axons↗
PubMed1993

Preliminary observations on the neuromuscular abnormalities in patients with organ failure and sepsis.

OBJECTIVE: To estimate the incidence and nature of neuromuscular abnormalities in a representative group of ITU patients. DESIGN: Prospective sequential study. SETTING: Teaching hospital ITU. PATIENTS: 23 patients who eventually stayed > 7 days on ITU who had no contraindication to muscle biopsy and whose relatives gave informed consent. MEASUREMENTS AND RESULTS: Muscle histopathology, neurophysiological studies, record of all drugs administered, APACHE II score, organ system failure score, presence or absence of sepsis, clinical evaluation of neuromuscular problems, time to hospital discharge. Heterogeneous neuromuscular abnormalities were present in 22 out of 23 patients studied and included axonal neuropathy, denervation, generalised fibre atrophy, non-specific myopathy and necrotising myopathy. CONCLUSION: Neuromuscular abnormalities are almost invariable in longstay intensive care patients and the resulting weakness may seriously delay hospital discharge. Various abnormalities were seen but no obvious aetiological factors were identified. The origin of the abnormalities is probably multifactorial.

Adolescent↗
PubMed1993

The St. George's dementia bed investigation study: cardiovascular, neurological and neuropsychological correlates.

The results of the cardiovascular, neurological and neuropsychological examination of a series of patients admitted to the St. George's dementia investigation bed and who later came to postmortem are compared in relation to their pathological diagnosis. Individual clinical signs were not found to differentiate between cases of dementia with vascular versus those with Alzheimer's disease pathology, although multivariate analysis suggested that there was a pattern of signs associated with cerebrovascular disease. A vascularity index was constructed from these signs; it achieved a useful level of discrimination between vascular and nonvascular causes of dementia.

Aged↗
PubMed1993

Control of temporal lobe epilepsy following en bloc resection of low-grade tumors.

Thirty-one patients with a mean age of 18.9 years (range 3 to 53 years) who underwent temporal lobe surgery for tumor-related epilepsy over a 14-year period are presented. All had suffered chronic drug-resistant temporal lobe seizures (mean age at onset 6.9 years, range 0 to 30 years; mean duration of condition 11.9 years, range 3 to 39 years). Preoperative interictal scalp electroencephalography tracings indicated unilateral localized epileptic foci in 90% of patients, and computerized tomography scans showed abnormalities within the temporal lobe in 87%. All patients underwent en bloc temporal lobectomy. No patient received adjuvant radiotherapy or chemotherapy. Review of the histological material showed dysembryoplastic neuroepithelial tumor in 27 (87%) of the specimens and microscopic evidence of incomplete removal of tumor in 22 (71%). At long-term follow-up evaluation (mean duration 5.8 years, range 1 to 14 years), 81% of patients were completely free of seizures (Engel grade I) and 10% were almost seizure free (Engel grade II) with no deaths reported in either early or late follow-up review. Only one patient in the series failed to benefit from the surgery. Four patients suffered permanent neurological deficit causing a mild disability. Psychological assessment showed no significant fall in verbal or performance intelligent quotient for the group, but a mild memory impairment was evident in 32%. Behavioral and social aspects improved in nearly all (94%) cases. Relief of seizures could not be predicted by intraoperative electrocorticography, and outcome was independent of the completeness of tumor resection. Postoperative electroencephalographic findings identified epileptiform potentials in 65% of patients, which were associated with a worse seizure-control outcome grade.

Adolescent↗
PubMed1992

Neuropathology of biotinidase deficiency.

A patient with biotinidase deficiency and a progressive neurological disorder died just before the biochemical diagnosis was established. Post-mortem examination of the brain and spinal cord revealed necrotising lesions similar to those in Leigh's disease and Wernicke's encephalopathy. Unlike these two conditions, the regions affected included the hippocampus and parahippocampal cortex. In addition there was severe focal oedema in deep cerebral grey matter, the brain stem, and the spinal cord. These lesions appear to result from a number of severe metabolic disturbances, perhaps linked to an underlying disordered pyruvate metabolism. The nature of the pathology explains why a neurological deficit may persist despite treatment.

Amidohydrolases↗
PubMed1992

Rasmussen's encephalitis in surgery for epilepsy.

Nineteen patients with Rasmussen's encephalitis were studied, using light-microscopy, immunohistochemistry and in some cases electron-microscopy. Although there was inflammation, no causative agent was identified. 10 patients underwent hemispherectomy and with one exception did well, while local resection for seven produced little or no improvement. For two patients biopsy with subpial transection was beneficial, although a third had a poor response, necessitating subsequent hemispherectomy. Surgical treatment of these patients is justified by a beneficial outcome. Neuropathological study of the resected material is essential for diagnosis and management of this condition.

Cerebral Cortex↗
PubMed1992

The St. George's dementia bed investigation study: a comparison of clinical and pathological diagnosis.

Sixty-four elderly patients who had been admitted to the St. George's Hospital Alzheimer's disease evaluation project during 1981-1989 were followed up to postmortem examination. Comparison between clinical diagnoses and neuropathological diagnoses indicated positive predictive values for the antemortem diagnoses of 50-67%. Existing clinical criteria may not be accurate enough to permit firm antemortem diagnosis of older people for either research or clinical purposes.

Aged↗
PubMed1991

A clinicopathological study of the Guillain-Barré syndrome. Nine cases and literature review.

The postmortem findings are reported from 9 cases of the Guillain-Barré syndrome with survival between 10 days and 1 yr. In 8 cases there was multifocal loss of myelin throughout the peripheral nervous system with relative preservation of axons. In 1 case there was predominant loss of axons. Inflammatory mononuclear cell infiltration was present in the peripheral nervous system of all cases except 1 case surviving a year. The extent and severity of cell infiltration was variable, usually being less prominent than in previous reports, and sometimes sparing nerves in which myelin destruction was severe. Vesicular dissolution of myelin noted by electron microscopy was considered to be a postmortem artefact. In cases examined within 30 days after the onset, immunohistochemical studies with monoclonal antibodies identified more leucocytes (PD7/2B11+) and T cells (UCHL1+) in the endoneurium than in cases examined later or control cases. These findings and recent single case reports indicate that the pathology of the Guillian-Barré syndrome is variable. This variability may reflect differences in pathogenesis, with greater cell-mediated immunity in some cases and greater antibody targeted macrophage-mediated demyelination in others.

Adolescent↗
PubMed1991

Malignant glioma in laboratory workers.

In 1989 an increased risk of cancer, with a higher than expected incidence of brain tumours, was reported in laboratory workers at the Pasteur Institute, Paris. Three cases of primary brain tumours occurring in three laboratory workers from one laboratory in a district general hospital also came to light. Although this may have been due to coincidence or geographic clustering, the need for stringent safety standards in all laboratories is reiterated, and it is proposed that a national register should be established to record the causes of death in laboratory workers.

Adult↗
PubMed1989

Pure akinesia due to lewy body Parkinson's disease: a case with pathology.

The case of a patient with levodopa-responsive pure akinesia and freezing of gait for 17 years, whose brain showed the classical changes of Lewy body Parkinson's disease at postmortem is presented. A short trial of DL-threo-DOPS was ineffective. Intellectual function was preserved despite the presence of Lewy bodies and mild cell loss in subcortical cholinergic nuclei. Pure akinesia is likely to be a heterogeneous condition, with most cases having little or no response to levodopa therapy. However, this case demonstrates that this clinical picture may be caused by Lewy body Parkinson's disease.

Antiparkinson Agents↗
PubMed1988

Diagnosing dementia: do we get it right?

To find out whether the diagnosis of dementia agreed with findings at necropsy a detailed assessment of 27 elderly patients (mean age 82 (range 70-94] presenting with dementia was conducted at a combined department of geriatric medicine and psychiatry for the elderly. On the basis of the results the cause of the dementia was diagnosed clinically. Neuropathological examinations were performed after death. The clinical diagnosis made during life was not supported by the findings at necropsy in 11 cases. Alzheimer's disease was overdiagnosed in life (13 cases, of which only six were confirmed at necropsy). Although the clinical investigation was limited by availability of resources, neither cranial computed tomography nor the Hachinski score helped to distinguish between multi-infarct dementia and Alzheimer's disease in this age group. This study confirms the value of neuropathological studies in the precise diagnosis of dementia.

Aged↗
PubMed1987

Ultrastructural changes in the frontal cortex and hippocampus in the ageing marmoset.

The ultrastructure of the cells and capillaries of the frontal cortex and hippocampus was studied in marmosets to assess age-related changes. The appearances in the brains of four marmosets, more than 12 years of age, were compared with those of two young marmosets aged 26 and 21 months. There was widespread accumulation of lipofuscin in neurons, glial cells, perivascular macrophages and pericytes, but not in endothelial cells. Many of the nerve cell nuclei showed marked membrane infolding, alteration of nuclear morphology and occasional inclusions. A few degenerated and dystrophic axons containing abnormal organelles were seen. The capillaries displayed irregularly thickened and split basal laminae. No neurofibrillary tangles, neuritic plaques, amyloid deposits or granulovacuoles were present. These changes are compared to those occurring in other animal species and in man during ageing.

Aging↗