Quality of life in Parkinson's disease--Indian scenario.

The subjective sense of well being is central to the concept of quality of life (QoL) and a good QoL should be the ultimate goal to any therapeutic measure. In Parkinson's disease (PD), several rating scale are in vogue to measure the QoL, namely PDQ-39, PDQ-8, SF-36, Likert scale etc. Parkinson's Impact Scale (PIMS) has been used in this study to assess the QoL which includes 10 items. METHODOLOGY: Thirty two patients of Parkinson's disease satisfying the UK Parkinson's disease brain bank diagnostic criteria, ranging from HY stage I to IV have been recruited. UPDRS was also administered to them. Statistical analysis was performed using Spearman rank correlation and multivariate stepwise regression analysis using SPSS for windows. RESULT: Seventy two percents were male, all getting levodopa, 72% got anticholinergics. Monthly income varied from Rs.800 (US dollars 17.10) to Rs.15,000 (US dollars 320) pm. Eighty eight percent belonged to HY II-III. UPDRS score ranged from 3-85 (40.4 +/- 18.6). PIMS total score ranged from 1-22 (10.4 +/- 6.1). DISCUSSION AND CONSLUSION: The QoL deteriorates with H-Y staging, the UPDRS score, not with advancing age as seen in other studies. It is also significantly influenced by duration of the disease and financial security. Surprisingly, the family and community relations were not significantly affected with advancing disease, perhaps due the close family and social tie up among Indians. So, measurement of QoL should be made an essential part to the routine assessment of PD patients to get a complete scenario of the problem. PIMS can serve as a comprehensive tool for the same suitable for use in the OPD.

Terapia neuroprotectora de la Enfermedad de Parkinson / Neuroprotective therapy in Parkinson's Disease

With the current limitations on treating Parkinsonãs disease, neuroprotection should be looked at as a possible way of slowing the varying processes involved in the onset of the disease. A review was made of the work of NINDS experts, who evaluated 59 drugs resulting from their Medline and Pub Med search. Twelve drugs, those considered the most promising, were included in the final analysis. We look at such substances as caffeine, coenzyme q10, estrogens, minocycline, nicotine, rasagiline-selegiline, and ropinirole-pramipexole. These agents acted dissimilarly, but favorably, on some of the diseaseãs processes or on its underlying pathogenesis, although the mechanisms involved and the duration of the beneficial effects were not clear. The challenge is to overcome the difficulties that make the results of the few current studies uncertain, using new methods, such as transgenic models, to maintain hope for effective future treatments.

Escolha do tratamento da narcolepsia / The treatment of narcolepsy

O tratamento da narcolepsia visa seus dois sintomas principais, a sonolência excessiva diurna e a cataplexia. A primeira é usualmente controlada com anfetmina, metilfenidato e pemoline. Mais recentemente, inibidores da MAO, e principalmente os inibidores seletivos de MAO-A e B têm mostrado resultados promissores, com a selegilina. Modafinil, um estimulante alfa-1-adrenérgico tem também evidenciado bons resultados. A cataplexia, por sua vez, é geralmente tratada com antidepressivos tricíclicos. Dentre as novas drogas, sem efeito colateral antropínico, temos o hidrocloreto de viloxazina, um bloqueador de recaptaçäo da noradrenalina

Rationale for (-) deprenyl (Selegiline) therapy in Parkinson's disease and Alzeheimer's disease / Razöes da terapêutica com (-) deprenil (Selegilina) na doença de Parkinson e na doença de Alzeheimer

(-) Deprenil (Selegiline, Jumex, Eldepryl, Movergan), a close structural relative to phenylethylamine (PEA), is a drug with a unique pharmacological spectrum. It is a highly potent and selective, irreversible inhibitor of B-type monoamine oxidase (MAO), a predominantly glial enzyme in the brain. The activity of this enzyme significantly increases with age. (-) Deprenyl, the first slective inhibitor of MAO-B described in literature, has become the universally used research tool for selectively blocking B-type MAO. It is the only selectively inhibitor in clinical use. (-) Deprenyl interferes with the uptake of catecholamines and indirectly acting sympathomimetics beacuse it is handled by the catecholaminergic neuron in a way similar to the physiological substances transported through the axonal and organ and vesicular membrane. The unique behavior or (-)deprenyl is that, in striking contrast to PEA and its relatives, it does not displace the transmitter from storage, ie, it is not a releaser. The net result is that (-)de inhibits the releasing effect of tyramine, and, at present, is the only safe MAO inhibitor than can be administered without dietary precautions. Maintenance on (-)deprenyl selectively enhances superoxide dismutase (SOD) and catalase activity in the striatum. This effect is unrelated to its effect on MAO-B and the inhibitory effects of thhe drug on neurotransmitter uptake. Maintenance on (-)deprenyl facilitates the activity of the catecholaminergic system in the brain, and this effect, too, is unrelated to either its effects on MAO or on neurotransmitter uptake. (-)Deprenyl protects the nigrostriatal dopaminergic neurons against selective neurotoxins (6-hydroxy-dopamine, MPTP,DSP-4). Maintenance on (-)deprenyl prevents the characteristic age-related morphological changes in the neuromelanin granules of the neurocytes in the substantia nigra. All in all, (-)deprenyl increases the activity of the nigrostriatal dopaminergic system and slows its age-related decline. Maitenance of male rats on (-)deprenyl delays the loss of the capacity to ejaculate, slows the decline of learning and memory, and significanthy lengthens the lifespan as compared with saline-treated rats. Parkinson's disease patients on levodopa plus (-)deprenyl (1o mg daily) live significanthy longer than those on levodopa alone. (-)Deprenyl is the first drug that retards the progress of Parkinson's disease patients maintained on (-)deprenyl need levodopa significanthy later than their placebo-treated peers. Maintenance on (-)deprenyl improves significantly the performance of patients with Alzheimer's disease. It is concluded that Parkinson's disease patients need to be treated daily with 10 mg (-)deprenyl from diagnosis until death, irrespective of other medication. We propose that the healthy be maintained on 10-15 mg (-)deprenyl weekly starting at 45 in order to combat the age-related decline of the nigrostriatal dopaminergic neurons. Prophylactic (-)deprenyl medication seems to offer a reasonable prospect of improving the quality of life in the later decades, delaying the time of natural death and decreasing the susceptibility of age-related neurological diseases, like Parkinson's disease and Alzheimer's disease