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Biomedical subjects

A H Rajput

Publications and source records attributed to A H Rajput.

13 recordsLinked to original sources

Oxygen free radical producing activity of polymorphonuclear leukocytes in patients with Parkinson's disease.

Oxygen free radicals (OFRs) have been suggested in the pathogenesis of Parkinson's disease (PD). These free radicals exert their cytotoxic effect by peroxidation of lipid membrane resulting in the formation of malondialdehyde (MDA). Polymorphonuclear (PMN) leukocyte is one of the major sources of OFR. However, the oxygen free radical producing activity of PMN leukocytes in patients with PD is not known. We therefore studied the oxygen free radical producing activity of polymorphonuclear leukocytes and MDA levels in the serum of healthy subjects and in patients with Parkinson's disease. The oxygen free radical producing activity of PMN leukocytes in blood and the MDA content in serum were significantly higher in patients with Parkinson's disease than in healthy subjects. These results indicate a possible role of oxygen free radicals in the pathogenesis of Parkinson's disease.

Aged

Serum antioxidant enzyme activity in Parkinson's disease.

The activities of superoxide dismutase (SOD; EC 1.15.1.1) and glutathione peroxidase (GSHPx; EC 1.11.1.9), the enzymes that metabolize the superoxide anion and hydrogen peroxide, respectively, were measured in serum from healthy subjects and patients with Parkinson's disease (PD). The activities of SOD and GSHPx in patients with PD were higher than those in normal healthy individuals. These results suggest that the increased activities of these enzymes could be due to oxidative stress in the initial stages of this disease.

Aged

Frequency and cause of Parkinson's disease.

Parkinson syndrome (PS) is a common disorder in the North American population. The annual incidence rate is 20.5/100,000 population and the mean survival after onset is approximately 12.3 years. The estimated prevalence rate is about 300/100,000 population. The incidence and prevalence rates rise with advancing age. Both the widespread use of levodopa and the improved health care in general have increased the longevity in PS. The survival in PS from the time of the first clinic visit is still significantly shorter when compared with the regional age and sex matched population. The cause of IPD may be related to some environmental factor(s)--most likely a toxin. Genetic factors are not the cause but in some families, may predispose to IPD.

Humans

National conference on Parkinson's disease.

A National Conference on Parkinson's disease was held on September 7th-8th, 1990 in Victoria, British Columbia. The scientific program included 11 formal presentations, 10 small group workshops and video presentations of interesting examples of movement disorders. The subjects discussed ranged from epidemiology and etiology to current and possible future modes of management of Parkinson's disease.

Humans

Accuracy of clinical diagnosis in parkinsonism--a prospective study.

Clinical diagnosis of Parkinson's syndrome (PS) is reasonably easy in most cases but the distinction between different variants of PS may be difficult in early cases. The correct diagnosis is not only important for counselling and management of patients but also in conducting pharmacological and epidemiological studies. There is very little critical literature on the pathological verification of the clinical diagnosis in PS. We report our 22 years experience to address that issue. Between 1968 and 1990, 65 PS patients came to autopsy. Complete data are available in 59 (M-50, F-19) cases. The initial diagnosis made by a qualified neurologist was idiopathic Parkinson's disease (IPD) in 43 cases. Of those 28 (65%) had Lewy body pathology. After a mean duration of 12 years the final diagnosis was IPD in 41 cases which was confirmed in 31 (76%). The IPD could not be clinically distinguished from cases with severe substantia nigra neuronal loss without inclusions or from those with neurofibrillary tangle inclusions and neuronal loss at the anatomical sites typically involved in IPD. All progressive supra-nuclear palsy, olivopontocerebellar atrophy, Jakob-Creutzfeldt's disease and the majority of the multiple system atrophy cases were diagnosed correctly during life. The correct clinical diagnosis in most non-IPD variants of PS was possible within 5 years of onset (range: 2 months to 18 years). We recommend that studies aimed at including only the IPD cases restrict the enrollment to those cases that have had PS motor manifestations for five years or longer duration.

Brain

Occurrence of resting tremor in Parkinson's disease.

Several previous studies have noted that resting tremor (RT) is absent in 10% to 30% of idiopathic Parkinson's disease (IPD) patients. We report our 22-year observations in 47 pathologically verified parkinsonian patients. In all the IPD cases with median follow-up of 3.7 years, RT was noted on at least one evaluation. Among other parkinsonian syndrome variants characterized by widespread subcortical pathology with median follow-up of 2.86 years, RT was seen in 31% of the cases. Our data indicate that the sites typically involved in IPD are sufficient to produce RT.

Female

Clinicopathologic observations in essential tremor: report of six cases.

Essential tremor (ET) is the most common pathologic tremor, but only eight cases have been studied pathologically. We report detailed clinical and neuropathologic studies of six additional patients. We did not find any neuropathologic lesions that might be specific for ET. Moreover, there were no abnormalities of the substantia nigra consistent with Parkinson's disease. The neuropathologic substrate of ET remains unknown.

Aged

Dysautonomia in Parkinsonism: a clinicopathological study.

Necropsy studies were done on six patients with idiopathic paralysis agitans, one with multiple system atrophy including features of Parkinsonism, and one control. Autonomic functions had been evaluated during life to a varying degree. Intra-arterial blood pressure studies were carried out on two patients with paralysis agitans (cases 4 and 6) and the one with multiple system atrophy (case 7). Lewy bodies with or without cell loss were seen in the sympathetic ganglia of five cases of paralysis agitans. Three of these had orthostatic hypotension and the severity of the lesion approximately correlated with the degree of hypotension. It is concluded that the lesions of the sympathetic ganglia may play a major role in the production of orthostatic hypotension in idiopathic paralysis agitans.

Aged

Postural hypotension in idiopathic Parkinson's disease. Etiopathology.

Postural changes in blood pressure were recorded in all 391 patients suffering from Parkinson's syndrome over a period of six years. Intraarterial blood pressure studies were carried out in those with significant postural hypotension. Histological examination of the entire central nervous system and the sympathetic ganglia was performed in six patients suffering from idiopathic Parksinson's disease. Five of the six patients had Lewy bodies in the sympathetic ganglia. Loss of nerve cells was noted in the sympathetic ganglia in those patients that demonstrated postural hypotension. The severity of the lesions in the ganglia correlated with the severity of postural hypotension in idiopathic Parkinson's disease, One case of Shy-Drager syndrome was similarly studied to demonstrate the differences in spinal cord and sympathetic ganglia lesions in the two conditions.

Aged

Relative efficacy of alcohol and propranolol in action tremor.

Thirty-nine patients with a variety of diseases, including essential tremor, Parkinson's Disease, olivopontocerebellar degeneration, ataxia telangiectasia, and cervical cord injury with action tremor, were evaluated for the effect of one ounce of absolute alcohol ingestion. Tremor significantly subsided in 61.9% of E.T.; 46.6% of P.D.; one patient with A.T.; and one patient with C6 lesion. The tremor became worse in one patient with O.P.C.D. Twenty of these patients were treated with propranolol, an average dose of 92 mgm. per day, and re-evaluated three to six months later. All those who improved on alcohol improved on propranolol and the one whose tremor accentuated with alcohol had a similar response to propranolol. It is concluded that the tremorilytic effect of alcohol is neither specific for, nor limited to, essential tremor and is of no value in differentiating various neurological disorders which manifest as action tremor. It is recommended that one ounce of absolute alcohol by mouth be used as an office procedure to predict the response of patients' tremor to propranolol.

Adult