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Biomedical subjects

J M Murthy

Publications and source records attributed to J M Murthy.

At least 55 records · Page 3Linked to original sources
PubMed1986

Parasitic intracranial space-occupying lesions in children in India.

A study was carried out on parasitic intracranial space-occupying lesions in children in south India. Such lesions constitute a fraction of 1% of intracranial space-occupying lesions in India. This paper discusses three cases of cerebral and two cases of intradiploic cranial hydatid cysts, as well as six cases of cysticercosis, of which three were solitary cysts and the remainder were pseudotumors with visual deterioration.

Adolescent↗
PubMed1981

Vascular changes in leprosy and its role in the pathogenesis of leprous neuritis.

The arteriographic pattern of left hand vessels was studied in 20 patients in leprosy by percutaneous brachial arteriography. Arteriographic abnormalities noted consisted of occlusion, narrowing, tortuosity, dilatation, irregularity and incomplete filling of the lumen by contrast medium. Such abnormal findings were seen in all the arteriograms studied and more than one vessel involvement was noted in over 50 percent cases. This study clearly demonstrated that arterial involvement in leprosy was frequent. No correlation was found between motor weakness and vascular abnormalities. There was no difference in arterial lesions between the patients with and without trophic changes. There was also no correlation between the severity of vascular changes and decline in motor nerve conduction. Degree of histopathological abnormalities in the sural nerve biopsy from these patients showed no features of micro angiopathic neuropathy. It is concluded that the observed vascular abnormalities do not contribute significantly in the genesis of neurological deficit in leprosy.

Adult↗
PubMed1980

Role of porta systemic shunt and hepatocellular damage in the genesis of hepatic neuropathy.

A study was undertaken to evaluate the relative role of porta-systemic shunts and hepatocellular damage in the genesis of neuropathy in chronic liver disease. Two of the 14 patients with non-alcoholic cirrhosis showed clinical evidence of neuropathy, whereas none of the patients with idiopathic portal fibrosis had evidence of neuropathy clinically. Decreased motor conduction velocities were present in some cases of idiopathic portal fibrosis as well as non-alcoholic cirrhosis. Subclinical evidence of histopathological neuropathy in the form of segmental demyelination and remyelination as well as myelin fiber loss was seen in 10 out of 11 sural nerves studied in idiopathic portal fibrosis group and in all the 10 patients in the non-alcoholic cirrhosis group. No correlation was found between histological features and various parameters studied. It is postulated that the development of clinical or subclinical neuropathy in chronic liver disease depends on two factors, being collateral shunting and hepatocellular damage or both and probably related to abnormalities of nitrogen metabolism.

Adult↗
PubMed1980

Paralytic rabies: a clinico-pathological study.

Clinical and pathological features of 11 cases of paralytic rabies have been described, with a detailed study of the peripheral nerves. The mean incubation period was forty-nine days (range 7-90 days). The mean interval between the onset of symptoms and death was 8.4 days (range 7-11 days). A history of animal bite was available in 9 cases. Pain and paraesthesiae at the site of the bite, followed by paralysis, were the main presenting symptoms. Motor weakness and involvement of the respiratory muscles was present in all cases. Histopathological features in the spinal cord and brain were (i) an inflammatory cellular reaction, (ii) vascular changes and (iii) inclusion bodies. Pathological changes were more severe in the spinal cord and brain-stem than in the cerebral cortex. Peripheral nerves showed segmental demyelination and remyelination. Wallerian degeneration, myelinated fibre loss and axonal loss. The changes were of variable degree. In 9 nerves segmental demyelination was the primary lesion. Wallerian degeneration and segmental demyelination were seen in 6 peripheral nerves. All the spinal nerves showed evidence of Wallerian degeneration as well as segmental demyelination. It is suggested that some protein component of rabies virus may produce primary demyelination in peripheral nerves by a cross-antigenic action on myelin protein, but that the pathological features in the spinal cord and brain are due to virus infection per se.

Adolescent↗