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  • Any combination of resting tremor, bradykinesia, rigidity, and postural instability (late feature). Bradykinesia is a required feature for diagnosis.

  • Asymmetric onset is the norm.

  • Responds well to levodopa in most cases.

  • Diagnostic accuracy improves with observation over time.

General Principles

Parkinson disease (PD) is the second most common chronic progressive neurodegenerative disorder, after Alzheimer disease. It affects an estimated 1% of people older than age 65 years and up to 3% older than age 85 years, or approximately 1.5 million people in the United States and >5 million people worldwide. With the aging of the world’s population, and with age being the strongest risk factor for PD, incidence is expected to rise dramatically in coming decades. By 2050, some researchers project >2.5 million cases in the United States.

PD is generally considered a disease of the older adult, but it can affect younger age groups. The mean age of onset is about age 60 to 65 years. Several key points should be emphasized about the care of older PD patients. The differential diagnosis of parkinsonian symptoms in patients older than the age of 75 years is mostly limited to either idiopathic PD or secondary parkinsonism, as onset of atypical etiologies is rare in this age group. Older PD patients often present with an akinetic-rigid syndrome, more nonmotor symptoms, and less tremor. Levodopa is the drug of choice in patients older than age 70 years because dopamine agonists (eg, pramipexole and ropinirole), amantadine, and anticholinergics are poorly tolerated in this age group.


The clinical presentation of PD was first described by James Parkinson in his 1817 “Essay on Shaking Palsy.” It was not until the 20th century that the pathologic hallmarks of PD, α-synuclein–positive Lewy bodies and dopaminergic cell loss of the substantia nigra, were described. It is estimated that by the time the first symptoms emerge, 60% of substantia nigra neurons have already died. Neurochemically, this results in dopamine depletion in the nigrostriatal pathway. Physiologically, this leads to inhibition of the thalamus and reduced excitation of the motor cortex, manifesting as the cardinal motor features of PD (bradykinesia and rigidity).

A fundamental shift in our understanding of PD pathology has occurred in recent years. It has long been known that the pathology spreads beyond the substantia nigra as PD progresses, which explains much of the disabling nonmotor features of advanced PD, such as dementia, depression, and autonomic failure. However, we now know that even before any motor symptoms occur, pathology has spread through specific areas of the olfactory system, lower brainstem, and peripheral nervous system. This “premotor” prodrome of PD can manifest as hyposmia, sleep disorders, mood disorders, and constipation. In summary, from the earliest to the most advanced stages, PD pathology occurs in a much wider distribution of the central and peripheral nervous ...

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