1. What are the diagnostic criteria for idiopathic Parkinson disease?

2. What is the differential diagnosis of a patient with parkinsonian symptoms?

3. What is the pathophysiology of Parkinson disease?

4. What treatments are available? How do they relate to the underlying pathophysiology?

5. What side effects and long-term effects may occur in a patient with Parkinson disease who is on medication?

6. What complications may occur when a patient with Parkinson disease is admitted to the hospital?

Parkinson disease (PD) develops in 12 to 20/100,000 people yearly, with a prevalence as high as 1% in those older than 65 years. With appropriate treatment, there appears to be no significant effect on life expectancy. However, quality of life is markedly reduced due to a variety of factors, some of which have only recently been recognized, such as autonomic system dysfunction.

Estimates of the economic burden of PD in various countries range from $4,000 to$20,000 per patient yearly, including roughly 33% to 40% in indirect costs, such as lost productivity. On average, PD-affected patients can no longer work full time by 3.4 years after diagnosis, and most file for disability by 5 years. In addition, PD is a risk factor for nursing home placement.

PD is associated with the loss of dopaminergic neurons located in the midbrain, in the substantia nigra pars compacta (SNc). Patients who are still early in their clinical course have lost ˜80% of the SNc neurons, implying that the degenerative process begins long before motor symptoms appear, and that the basal ganglia are able to compensate until there is a critical loss of dopaminergic neurons. How the loss of dopamine disrupts normal functioning of the basal ganglia is not fully understood, but it appears to result in pathologic synchronization of neuronal firing throughout the region that interferes with both voluntary and involuntary movements. PD has many nonmotor symptoms as well, suggestive of a more widespread neurodegenerative process involving neurotransmitters other than dopamine. There is increasing evidence for more extensive involvement of the brainstem and cortex, perhaps explaining the effects of PD on cognition, behavior, and sleep.

In most cases, the cause of PD is unknown. Mutations in single genes such as parkin, DJ-1, and LRRK2 are responsible for only a minority of cases of PD but are more prominent in patients who develop symptoms before the age of 50. The relationship of these mutations to neuronal death is not known, but it may involve several mechanisms, including protein misfolding, defective protein degradation by proteosomes, and increased oxidative stress. Recently, an association of PD with relatively common mutations in the gene for the lysosomal enzyme glucocerebrosidase has been described.

The pathological hallmark of PD is the presence of Lewy bodies in the neurons of the SNc. Lewy bodies may be more widely distributed and are found in the cortex in the related disorder known as dementia with Lewy bodies. Lewy bodies are composed of intracellular ...

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