Parkinson's Disease
PD is characterized by bradykinesia, resting tremor, cogwheel rigidity, postural reflex impairment, progressive course, and good response to dopaminergic therapy. Other distinct forms of parkinsonism include relatively rare genetic forms and the less common neurodegenerations with multiple system involvement or significant striatal lesions (for example, progressive supranuclear palsy or multiple system atrophy). Parkinsonism secondary to external causes, such as manganese poisoning or carbon monoxide poisoning, although now rare, is referred to as secondary parkinsonism. Because the burden of these diseases to the patient is similar to or greater than that for PD and there is no evidence for addressing these disorders separately, they will not be distinguished here.
Prevalence, Incidence Rate, and Mortality
Prevalence estimates vary widely across populations (Tanner and Goldman 1996; Zhang and Roman 1993). Recent reports, contrary to previous reports, suggest that the prevalence in developing and developed countries may be similar (Marras and Tanner 2002). Few incidence studies have been performed, and none in developing countries. Van Den Eeden and others (2003) report the incidence rate of PD in the United States as approximately 13 per 100,000 person-years. Men are affected more commonly than women (Tanner and Goldman 1996). Lower PD incidence in African Americans—and by extension Africans—has been suggested but is controversial (Van Den Eeden and others 2003). Most mortality estimates available for developed countries show about a twofold overall increased mortality, independent of age, in those with PD (Berger and others 2000).
Causes and Risk Factors
The cause of PD is unknown. A specific environmental risk factor has not been identified. Pure genetic forms account for 10 to 15 percent of cases or fewer. Increasing age and male gender are risk factors worldwide (Marras and Tanner 2002). Exposure to toxins, head trauma, frequent infections, diets high in animal fat, and midlife adiposity have been reported to increase PD risk, but none do so consistently (Tanner and Goldman 1996). The most consistent association is an inverse association with cigarette smoking and caffeine consumption, suggesting a protective effect (Ascherio and others 2001).
Burden of Disease
The BOD estimates for PD include Parkinson's disease and secondary parkinsonism. Mathers and others (2003) estimate the DALYs for PD as 2,325,000, with the burden being slightly higher in females (1,202,000) than males (1,124,000). Though male gender is a risk factor for PD, the higher burden in females may reflect their longer life span. As PD is a disease of older ages, the burden from PD is generally higher in high-income countries, where life expectancy is higher, diagnosis is better, and better treatment leads to increased longevity. However, the burden is high in East Asia and the Pacific and South Asia relative to that in other regions (table 32.1).
The economic burden of PD includes direct costs, such as for medication, physicians, hospitals, and chronic care facilities. Estimated indirect costs resulting from the loss of labor of both patients and caregivers typically exceed direct costs. The quality of life of both patients and caregivers is adversely affected.
Interventions
Treatment of PD is based on symptomatic relief, except for preventing secondary parkinsonism caused by neurotoxins.
Population-based Interventions
No determinants of PD amenable to population-based interventions have been identified.
Personal Interventions
Specific curative or neuroprotective treatments for PD have not been established. Interventions are primarily directed at palliation of symptoms and include pharmaceuticals, surgery, physical therapy, and—in some countries—traditional medicines.
Levo-dopa (l-dopa), l-dopa/decarboxylase inhibitor is the most widely used therapy for PD. It provides partial relief of all PD symptoms. Despite its benefits, chronic side effects after long-term use can cause significant morbidity.
Researchers in developing countries have studied the use of traditional medicines for PD. Clinical trials have shown that the seeds of Mucuna pruriens, which contain l-dopa, are a safe and effective treatment for PD (Parkinson's Disease Group 1995), and in animal studies, they are two to three times more effective than synthetic l-dopa dose per dose (Hussain and Manyam 1997). This substance is available in ayurvedic formulations in India at a much lower cost than that of synthetic antiparkinsonian drugs. Another traditional medicine is derived from Banisteriopsis caapi, which tribal societies of the Amazonian jungle use to make a potent hallucinogenic brew. It reportedly showed dramatic positive effects on rigidity and akinesia in 15 patients with postencephalitic parkinsonism (Lewin and Schuster 1929). A third traditional option is tai chi, a basic exercise in traditional Chinese medicine that may help with some of the motor deficits of PD.
Surgical treatment for PD by deep brain stimulation is generally recommended to address the loss of efficacy of dopaminergic drugs. For most patients, it is not effective independent of drugs. Although a few will have dramatic improvement and may be able to reduce or stop drugs, this effect is generally temporary. Criteria for selection of patients for deep brain stimulation include those with advanced disease who are responsive to l-dopa, not demented, and in good general health. Additional considerations are the high cost of the equipment, the need for trained personnel to program the device, and—in most cases—the need for several visits to a medical center to program the stimulator correctly, with periodic returns to adjust the settings.
