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Biomedical subjects

S K Shankar

Publications and source records attributed to S K Shankar.

At least 127 records · Page 7Linked to original sources
PubMed1989

Neuronal degeneration and neurofilament accumulation in the trigeminal ganglia in Creutzfeldt-Jakob disease.

We report the pathological and immunohistochemical changes in the first-order neurons in the trigeminal ganglia in Creutzfeldt-Jakob disease (CJD). Degenerative changes consisted of cytoplasmic vacuolation and fenestration, abundant satellite cells, neurofilament accumulation in neurons, and axonal dystrophy with spheroid formation and torpedolike structures arising from the neuronal cytoplasm. Dystrophic axons, axonal spheroids, and some ganglion cells were labeled with monoclonal antibodies to a phosphorylated epitope of neurofilaments (200 kDa). Polyclonal antibodies to purified scrapie-associated fibril/prion protein (molecular weight 27-30 kDa) extracted from scrapie-infected hamster brains, as well as polyclonal and monoclonal antibodies to a synthetic 15-amino acid polypeptide of the 27- to 30-kDa protein, demonstrated variable immunoreactivity with degenerating neurons in the CJD cases, but not in the controls. Furthermore, some of the satellite cells and dystrophic axons were stained by the antibodies to the synthetic peptide. These data indicate that the first-order neurons of the trigeminal ganglia may form a route by which the CJD agent may travel from the brain to the periphery or vice versa. As in other chronic neurodegenerative diseases, disturbances of neuroaxonal transport seem to occur in CJD.

Adult↗
PubMed1989

Immunocytochemical characterization of neurofibrillary tangles in amyotrophic lateral sclerosis and parkinsonism-dementia of Guam.

Cryostat-cut sections of formalin-fixed and unfixed hippocampus from 23 Guamanian Chamorros with clinically and neuropathologically verified amyotrophic lateral sclerosis (ALS) (8 cases) and parkinsonism-dementia (PD) (15 cases) and from 12 neurologically normal Guamanians (5 with and 7 without neurofibrillary degeneration) were evaluated by the immunoperoxidase technique, using monoclonal antibodies against phosphorylated neurofilament, human fetal microtubule-associated protein tau, and paired helical filaments. On immunostaining, all three antibodies showed intracellular tangles in the hippocampal neurons of patients with ALS, patients with PD, and in neurologically normal Guamanians with neurofibrillary pathology, but the correlation of immunostaining between these antibodies was not absolute. Extracellular or ghost tangles were immunostained only with the antibody against paired helical filaments. Our immunocytochemical data indicate that the antigenic composition of neurofibrillary tangles in Guamanian ALS and PD is similar to that of Alzheimer's disease, suggesting a common pathogenetic pathway for neurofibrillary tangle formation in these neurodegenerative disorders.

Adult↗
PubMed1989

Low-calcium, high-aluminum diet-induced motor neuron pathology in cynomolgus monkeys.

Long-term epidemiological studies indicate that environmental factors play a causative role in high-incidence amyotrophic lateral sclerosis (ALS) and parkinsonism-dementia (PD) in the western Pacific. An increased risk for disease is acquired in youth and remains for life. The low concentrations of calcium and magnesium and high levels of aluminum in the soil and drinking water, along with the relative isolation of these populations, constitute an unusual environmental feature common to all three high-incidence foci. Studies of mineral deposition in brain tissue of Guamanian ALS and PD patients, as well as of neurologically normal Guamanians with neurofibrillary degeneration, demonstrate accumulations of calcium, aluminum and silicon in neurofibrillary tangle-bearing neurons. In an attempt to duplicate the low calcium and high aluminum and manganese in soil and drinking water in these foci, we maintained juvenile cynomolgus monkeys for 41 to 46 months on a low-calcium diet with or without supplemental aluminum and manganese. Experimental animals exhibited mild calcium and aluminum deposition and degenerative changes, compatible with those of early ALS and PD, in motor neurons of the spinal cord, brain stem, substantia nigra and cerebrum. Neuropathological findings included chromatolysis, aberrant perikaryal accumulation of phosphorylated neurofilament, neurofibrillary tangles, axonal spheroids, and basophilic and hyaline-like inclusions consisting of abnormal cytoskeletal elements by electron microscopy. The magnitude and extent of these lesions far exceeded those found in normal aged monkeys.

Aluminum↗
PubMed1989

Role of squash-smear technique for rapid diagnosis of neurosurgical biopsies--a cytomorphological evaluation.

The biopsy material obtained from lesions of CNS are subjected to squash smear technique for rapid diagnosis as it is easier to make and the cytological features of cells are well preserved. During the year 1982-1983 one hundred and seventy eight squash smears were made to offer rapid diagnosis to the operating surgeon. The diagnosis was verified on paraffin sections. Correct diagnosis was made in 87% of cases. Various lesions have distinct cytomorphological features on smears. These distinct characters and efficacy of the method are discussed.

Biopsy↗
PubMed1987

Localization of amyloid beta protein messenger RNA in brains from patients with Alzheimer's disease.

The distribution of cells containing messenger RNA that encodes amyloid beta protein was determined in hippocampi and in various cortical regions from cynomolgus monkeys, normal humans, and patients with Alzheimer's disease by in situ hybridization. Both 35S-labeled RNA antisense and sense probes to amyloid beta protein messenger RNA were used to ensure specific hybridization. Messenger RNA for amyloid beta protein was expressed in a subset of neurons in the prefrontal cortex from monkeys, normal humans, and patients with Alzheimer's disease. This messenger RNA was also present in the neurons of all the hippocampal fields from monkeys, normal humans and, although to a lesser extent in cornu ammonis 1, patients with Alzheimer's disease. The distribution of amyloid beta protein messenger RNA was similar to that of the neurofibrillary tangles of Alzheimer's disease in some regions, but the messenger RNA was also expressed in other neurons that are not usually involved in the pathology of Alzheimer's disease.

Alzheimer Disease↗
PubMed1987

Sturge-Weber-Dimitri disease without facial nevus.

A patient with Sturge-Weber-Dimitri disease presented with intractable seizures and progressive intellectual deterioration. There was no facial nevus or focal neurologic abnormality. CT disclosed bilateral calcification in a parieto-occipital gyral pattern. Histopathology of the brain revealed extensive calcification of vessel wall in parieto-occipital cortices.

Angiomatosis↗
PubMed1986

Malignant fibrous histiocytoma arising from the meninges of the posterior fossa.

A case of malignant fibrous histiocytoma presenting as a cerebellar mass in a young man is described. The tumor was found to be arising from the dura mater and infiltrating the cerebellum. The ultrastructural and immunocytochemical studies confirmed the mesenchymal origin of the neoplasm. Focal reactive astrocytomalike areas were observed in the midst of this tumor.

Adult↗
PubMed1984

Monomelic amyotrophy.

From 1977 through 1981, we examined 23 patients with single-limb atrophy. Thirteen had upper-limb and ten had lower-limb involvement. The characteristic clinical features were insidious onset in the second and third decades, male preponderance, sporadic occurrence, wasting and weakness confined to one limb, and absence of involvement of the cranial nerves, cerebrum, brain stem, and sensory system. The electromyographic features, along with histologic features of neurogenic atrophy, were suggestive of an anterior horn cell lesion. The slow progression of illness for two to four years followed by a stationary phase was observed. There was no clinical evidence of involvement of the other three limbs even in patients with long-standing illness of ten to 15 years' duration.

Adolescent↗
PubMed1984

Neurological complications due to beta-propiolactone (BPL)-inactivated antirabies vaccination. Clinical, electrophysiological and therapeutic aspects.

Seventy six patients with neuroparalytic accidents due to antirabies vaccination (ARV) with BPL vaccine were studied. The mean age of incidence was 26.9 +/- 15.7 years. The suspected source of infection was by the bite of a dog in 72 (97.3%) out of 74. The mean duration of interval between the first dose of ARV and onset of neurological deficits was 12.2 +/- 8.4 days. The number of doses was 7 or less in 49 (65.3%) cases and more than 7 in 26 (34.7%) cases. With regard to neurological deficits, 6 (7.9%) had encephalopathy, 23 (30.3%) had encephalomyeloradiculopathy, 7 (9.2%) had myelopathy, 21 (27.6%) had myeloradiculopathy, 18 (23.7%) had polyradiculopathy and one had bilateral 7th cranial nerve palsies. Lumbar CSF analysis was done in 67 patients and was abnormal in 47 (70.1%) patients in the form of pleocytosis or raised protein or both. EEG, done in 30 patients, was abnormal in 13 (43.3%) and the abnormalities were not related to clinical features in 6. Electroneuromyography (ENMG) was done in 25 and was abnormal in 21 cases. Visual evoked potentials (VEP) was done in 11 cases and was abnormal in two. Sixty eight patients received steroids and 17 patients received cyclophosphamide in addition to steroids, 14 during the first admission and 3 during follow up when the recovery with steroids was not satisfactory. The therapeutic results were better in those who received cyclophosphamide and was statistically significant. Fourteen (18.4%) patients died and 6 were autopsied. The pathological features were essentially myeloradiculopathies, with variable degree of encephalic involvement. Two showed distinct necrotising myelopathy of immune type.

Adult↗
PubMed1983

Cerebral cladosporiosis--a neuropathological and microbiological study.

Cerebral cladosporiosis is a rare mycotic infection of the brain. So far only 21 culture-proven cases of cerebral cladosporiosis have been listed in literature (FETTER et al. 1967, FETTER and KLINTWORTH, 1978). In view of the rarity of this mycotic infection and its clinical importance we report two cases of culture-proven cerebral cladosporiosis. They presented as meningoencephalitis with extensive areas of haemorrhagic infarctions of frontoparietal lobes. Both patients were middle-aged farmers from Karnataka State, South India. The clinical, neuropathological and mycological features are presented.

Adult↗