Parkinson’s disease is the most common cause of Parkinsonism and is the second most common neurodegenerative disease, after Alzheimer’s disease. Although descriptions of the condition appeared before the nineteenth century, it was James Parkinson’s eloquent account in 1817 that fully documented the clinical features of the illness now bearing his name.
The identification of dopamine deficiency in the brains of people with Parkinson’s disease and the subsequent introduction of replacement therapy with levodopa represent a considerable success story in the treatment of neurodegenerative illness in general. There remain, however, a number of significant management problems in Parkinson’s disease, particularly in the advanced stages of the condition.
Parkinson’s disease affects 1% of the population over 65 years of age, rising to 2% over the age of 80. One in 20 patients is, however, diagnosed before their 40th year. It is estimated that 110,000 people have Parkinson’s disease in the UK. The condition is found worldwide, with variability in prevalence estimates most likely reflecting study methodology, rather than real differences.
Most epidemiological studies have indicated a small male-to-female predominance. Drug-induced Parkinsonism is also called as symptomatic Parkinsonism. It affects minor group of individuals who are exposed to dopamine receptor blocking agents including neuroleptics and some labyrinthine sedatives.
Both genetic and environmental factors have been implicated as a cause of Parkinson’s disease. While opinions were initially polarized, it now seems probable that in the majority of cases there is an admixture of influences, with environmental factors precipitating the onset of Parkinson’s disease in a genetically susceptible individual. Environmental factors became preeminent in the 1980s when drug addicts attempting to manufacture pethidine accidentally produced a toxin called MPTP (1-methyl-4-phenyl- 1,2,3,6-tetrahydropyridine). Ingestion or inhalation of MPTP rapidly produced a severe Parkinsonian state, indistinguishable from advanced Parkinson’s disease.
A number of factors which includes age, severity and type of disease (tremor-dominant versus bradykinesia-dominant) and co-morbidity, are taken into account for the treatment of Parkinson’s dsease. The efficacy and tolerability of levodopa in Parkinson’s disease were first described when the drug was started in low doses and gradually increased thereafter.
Examples of non-neuroleptic drugs associated with drug-induced Parkinsonism Sodium valproate Tetrabenazine Calcium channel blockers (e.g. cinnarizine) Amiodarone Lithiuma Phenelzineb Amphotericin Bc 5-Fluorouracilb Vincristine–adriamycinb Pethidineb a Lithium causes postural tremor.
This syndrome comprises premature wearing off of the antiparkinsonian effects of levodopa, and response fluctuations. The wearing-off effect is the time before a patient is due their next dose of medication, during which they become increasingly bradykinetic. Response fluctuations can include dramatic swings between gross involuntary movements (dyskinesias) and a frozen, immobile state.
The rapid and sudden switching between the dyskinetic state and profound akinesia is also termed the ‘on–off’ phenomenon. If this occurs rapidly and repeatedly, the term ‘yo-yo-ing’ is sometimes used. These problems emerge at a rate of approximately 10% per year so that by 10 years into their illness all Parkinson’s disease patients can expect to experience such unpredictable responses.
Notably, however, levodopa-induced dyskinesias and fluctuations develop earlier in younger Parkinson’s disease patients than in older patients. On–off episodes may be extremely disabling and remain a major therapeutic challenge in the management of Parkinson’s disease.
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