Mona Ragothaman

Are current recommendations to diagnose orthostatic hypotension in Parkinson's disease satisfactory?

We interviewed 50 Parkinsons disease (PD) patients using a questionnaire to verify the reliability of orthostatic symptoms in warning the presence of orthostatic hypotension (OH). OH is defined as 20 mm Hg systolic or 10 mm Hg diastolic BP fall within 3 min of tilting or standing but if this fall occurs after 3 min we called it ‘late OH’ (L‐OH). We compared if OH in Parkinsons disease (PD) was more frequent after head‐up tilt or on standing and if the period of postural challenge matters in detecting OH. Twenty‐one (42%) patients had OH that occurred twice more often after tilting (n = 20) than on standing (n = 10). OH occurred within 3 min of tilting in 9 patients (18%) and appeared beyond the currently recommended 3 min in 11 patients (55%) (L‐OH). Ten of the 20 patients developing OH on tilting were symptomatic. The 10 patients who had OH on standing were asymptomatic. Reporting of symptoms was independent of age or severity of BP fall. Most (90%) patients reporting orthostatic symptoms on standing had OH on tilting for 3 min. Orthostatic symptoms in PD have a high specificity but low sensitivity in predicting OH. In Parkinsons disease OH occurs often after tilting than on standing and is delayed (after 3 min). As OH in PD is often asymptomatic and delayed it could contribute to falls and increase morbidity. We suggest routine evaluation of OH in PD by tilting them longer than the recommended 3 minutes to detect delayed OH.

Complex phenotypes in an Indian family with homozygous SCA2 mutations

We describe a consanguineous Indian family having spinocerebellar ataxia type 2 (SCA2) expansions with complex phenotypes (early‐onset, dopa‐responsive parkinsonism, ataxia and retinitis pigmentosa). The two probands having homozygous SCA2 mutations presenting with early‐onset dopa‐responsive parkinsonism without ataxia develop dyskinesias within a year of starting levodopa. Their siblings, heterozygous for SCA2 mutations, had retinitis pigmentosa with or without ataxia. Approximately 38% of family members with SCA2 mutations were asymptomatic.

Direct Costs of Managing Parkinson's Disease in India: Concerns in a Developing Country

Medicines and surgical interventions improve the quality of life of Parkinsons disease (PD) patients. These are still expensive options and are unaffordable to those living in developing countries. Managing PD in Indians who have a low annual gross national income (GNI; US

Lower risk of Parkinson's disease in an admixed population of European and Indian origins.

450–540) and for whom only a few (3%) have health insurance is a challenge. We interviewed 175 consecutive PD patients regarding health insurance and money spent for treatment. The annual income of nearly half the patients was less than rupees 50,000 (US

Validity of a modified Parkinson's disease screening questionnaire in India: effects of literacy of participants and medical training of screeners and implications for screening efforts in developing countries.

1,148.63). Patients in this study spend nearly 16% to 41.7% of the average Indian GNI to buy medicines. Costs of treating PD in India are lower than those in developed nations but are still out of reach for most Indian patients.

Homozygous SCA 2 mutations changes phenotype and hastens progression.

We studied whether the occurrence of Parkinsons disease (PD) in the Anglo‐Indians, an admixed population of European and Asian Indian origin, differs from Indians living in the same environment. Epidemiological studies show considerably higher prevalence of PD amongst white compared to non‐white populations. Normal Indians contain a ∼40% lower number of melanized nigral neurons compared to Caucasians from the UK. Anglo‐Indians are an admixed population of European and Indian origin. We used the UK Parkinsons Disease Society Brain Bank clinical diagnostic criteria (steps 1 and 2) to diagnose PD in 84 of 493 residents (Indians, 409; Anglo‐Indians, 84) living in elderly homes in Bangalore, India. Of these 84, 80 were Indians (19.5%) and 4 were Anglo‐Indians (4.8%). Occurrence of PD is nearly five times higher amongst Indians compared to the Anglo‐Indians (odds ratio, 3.9; 95% confidence interval, 1.3–12.9). We conclude that an admixture population of European and Indian origins, rather than averaging, might result in reduced occurrences of PD. Hence, studying an admixed population could provide crucial insights into understanding genetic mechanisms in the etiopathogenesis of PD.

Task-specific dystonia in tabla players

The prevalence of Parkinsons disease (PD) is low among Indians, except in the Parsis. Data for Indians come from studies using different screening tools and criteria to detect PD. An epidemiological study in India, which has nearly a billion people, more than 18 spoken languages, and varying levels of literacy, requires development and validation of a screening tool for PD. The objectives of this study are to (1) validate a modified version of a widely used screening questionnaire for PD to suit the needs of the Indian population; (2) compare the use of a nonmedical assistant (NMA) with the use of a medical person during screening; and (3) compare the effect of literacy of participants on the validity of the screening tool. The validity of the questionnaire was tested on 125 participants from a home for the elderly. NMAs of similar background and medical personnel administered the modified screening questionnaire. A movement disorder neurologist blind to the responses on the questionnaire, examined participants independently and diagnosed if participants had PD. The questionnaire was validated in the movement disorders clinic, on known PD patients and their family members without PD. In the movement disorders clinic, sensitivity and specificity of the questionnaire were 100% and 89%, respectively. Fifty‐seven participants were included for analysis. The questionnaire had a higher sensitivity when NMAs (75%) rather than the medical personnel (61%) administered it, and its specificity was higher with the medical personnel (61%) than with NMAs (55% and 25%). The questionnaire had a higher specificity in literates than illiterates, whereas sensitivity varied considerably. The modified questionnaire translated in a local Indian language had reasonable sensitivity and can be used to screen individuals for PD in epidemiological studies in India. This questionnaire can be administered by NMAs to screen PD and this strategy would reduce manpower costs. Literacy may influence epidemiological estimates when screening PD.

Elemental mercury poisoning probably causes cortical myoclonus

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Parkinsonism and personality changes following an acute hypoxic insult during mountaineering.

Task‐specific dystonia significantly impairs the performance of approximately 8% of musicians [Lederman RJ. Muscle Nerve 2003;27:549–561]. We describe hand dystonia in two professional musicians experienced while playing tabla, a percussion instrument.

The Indian turban trick : A novel sensory trick in blepharospasm

Mercury toxicity causes postural tremors, commonly referred to as “mercurial tremors,” and cerebellar dysfunction. A 23‐year woman, 2 years after injecting herself with elemental mercury developed disabling generalized myoclonus and ataxia. Electrophysiological studies confirmed the myoclonus was probably of cortical origin. Her deficits progressed over 2 years and improved after subcutaneous mercury deposits at the injection site were surgically cleared. Myoclonus of cortical origin has never been described in mercury poisoning. It is important to ask patients presenting with jerks about exposure to elemental mercury even if they have a progressive illness, as it is a potentially reversible condition as in our patient.