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Biomedical subjects

R Raman

Publications and source records attributed to R Raman.

172 records · Page 10Linked to original sources
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Cognitive and motor function in patients with Parkinson's disease with and without depression.

The objective of this study was to define risk factors for depression in patients with idiopathic Parkinson's disease (PD) and to evaluate the correlation of depression with cognitive function and the primary domains of parkinsonian motor dysfunction tremor, bradykinesia, rigidity, gait and balance impairment. The risk factors for depression in patients with PD remain controversial. Several investigators have demonstrated a significant association between cognitive dysfunction and depression, but motoric and disease variables can confound this evaluation and have shown an inconsistent relation to depression. A consecutive series of 88 patients with PD were examined using the motor subscale of the Unified Parkinson's Disease Rating Scale (UPDRSm), Hoehn-Yahr stage (HY), and Hamilton Rating Scale for Depression (HRSD). Major depression was diagnosed according to the criteria in the Diagnostic and Statistic Manual of Mental Disorders, 4th edition. Gender, age, handedness, PD duration, side of PD onset, motor fluctuations, UPDRSm total score, daily Levodopa dose, and Mini-Mental State Examination score (MMSE) were analyzed using multivariate and univariate logistic regression, Fisher's Exact test, and Pearson correlations. Major depression was diagnosed in 12 patients (7.3%). Low MMSE score, axial bradykinesia, gait and balance impairment were strongly significant predictors of depression. In conclusion, depression and physical function are important factors impairing the quality of life for patients with PD, and regular depression screening and treatment should focus on patients with PD who have cognitive impairment, high axial bradykinesia, gait and balance impairment.

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Estrogen supplementation in the posthypoxic myoclonus rat model.

The objective of the study was to investigate the effects of estrogen on severity and duration of myoclonus in the rat cardiac arrest model of posthypoxic myoclonus. Female sex hormones affect a variety of movement disorders and alter dopaminergic and serotonergic pharmacology. Although women represented three-fourths of patients from the original report of Lance and Adams and 80% of the largest published series, the impact of estrogens on myoclonus has never been studied. Twelve previously ovariectomized female rats underwent 8 minutes of mechanically induced cardiac arrest and were resuscitated according to a standardized protocol. On the same day, they were randomly assigned to subcutaneous treatment with a 21-day, 0.5-mg, 17 beta-estradiol or matching placebo pellet. Animals were tested daily with 7 sets of 45 auditory stimuli for 10 days, and myoclonus scores were obtained using a 5-point interval scale. Comparisons were based on two-sample Wilcoxon rank-sum tests. Estrogen treatment significantly enhanced myoclonus intensity and duration: mean peak myoclonus score, 210.2 +/- 18.0 versus 180 +/- 28.5 (p = 0.031); mean number of days above baseline, 9.2 +/- 0.4 versus 5.7 +/- 2.3 (p = 0.004); mean score on day 10, 90.7 +/- 38.7 versus 27.0 +/- 20.6 (p = 0.016). All estrogen-treated animals were above baseline on day 10 compared with none in the placebo group. Estrogen enhances and prolongs posthypoxic myoclonus, suggesting that female gender and estrogen status may play a pivotal role as a risk factor for human posthypoxic myoclonus.

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Attrition and non-compliance in secondary stroke prevention trials.

BACKGROUND: Attrition and non-compliance of subjects in secondary stroke prevention trials due to study drug-induced adverse events and loss to follow-up could lead to bias and loss of information, thus affecting the analysis of study results. METHODS: We reviewed results from ten antiplatelet stroke prevention clinical trials: CAN TIA, DUTCH TIA, SWED ASA, SALT, UK TIA, CATS, TASS, ESPS, ESPS-2, and CAPRIE to tabulate the frequencies for total subject discontinuation, voluntary withdrawal, and loss to follow-up. RESULTS: Forty thousand seven hundred and thirty (40,730) subjects participated in the aforementioned secondary stroke prevention trials. The range of outcomes was 11.8-52.0% for subjects discontinued for any reason (n = 9 trials); 3.0-20.9% for study drug-induced adverse events (n = 9 trials), and 4.2-7.8% for voluntary withdrawal (n = 10 trials). CONCLUSION: There is a substantial discrepancy (up to 20%) between the frequencies of total subject discontinuation for any reason and the sum of study drug-induced adverse events, voluntary withdrawal and loss to follow-up. Underestimation of these important outcomes may limit the ability of clinicians to translate results from clinical trials into medical practice.

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Poor visual discrimination and visual hallucinations in Parkinson's disease.

This study examined the relationship between deficits in color and contrast discrimination and visual hallucinations (VH) in patients with Parkinson's disease (PD) and normal visual acuity. Thirty-five nondemented and nonpsychotic PD patients with normal visual acuity and without major ophthalmologic disease were interviewed twice and divided into two groups: hallucinators (n = 14) and non-hallucinating controls (n = 21). The groups were compared for color vision (assessed by Lanthony D-15 [LD] and Farnsworth-Munsell 100 hue [FM] tests), and for contrast sensitivity (tested by Vis tech tables [VT] and monocular and binocular Pelli-Robson test [PR]). There was no difference in age, duration or stage of PD, or dosage or duration of levodopa therapy between the two groups. Parkinson's disease patients showed impairment on all visual tests, with the hallucinators performing worse than the controls on all tests. This difference was significant for the LD (p < 0.007), the VT at 1.5 and 3 cycles per degree (p < 0.037 and 0.043, respectively) and the monocular PR tests (p < 0.049). The results led the authors to conclude that in patients with normal visual acuity, those with VH show added visual deficits of color and contrast discrimination. These ophthalmopathies may therefore be facilitating factors for visual hallucinations in PD and justify more focused research on the pathophysiology of visual hallucinations in Parkinson's disease.

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