Chapter 17

A systematic search of the medical literature was performed in January, 2008. The search, limited to human subjects and English language journals, included the National Guideline Clearinghouse, the Cochrane database, PubMed, UpToDate®, and PIER.

One of the most common neurological disorders of the aging population, Parkinson disease (PD) is the best understood with respect to the specific neurochemical and pathological changes in the brain. The characteristic motor impairments are mostly the consequence of the selective loss of several hundred thousand neurons in the substantia nigra,1 but the cause of this loss is unknown. PD has a number of treatment options ranging from medications to surgical treatments.2

The clinical presentation can be distinctive but is not always diagnostic, even when the full Parkinsonian syndrome is present. Parkinsonian syndrome consists of PD or others disorders with similar motor impairments. It is characterized by one or more of the following: tremors of a limb or face at rest, cogwheel-type rigidity, slowed movements with diminished dexterity, facial masking, forward flexed posture, and imbalance.3

Idiopathic PD is the most common etiology when signs and symptoms develop slowly.4 Often, PD starts on one side just with a resting tremor. Other presentations quite distinctive for PD include handwriting that trails off (micrographia), decreased arm swing, and a shuffling gait. It is not necessary for all symptoms to be present to make a diagnosis of PD. Conversely, a diagnosis of PD cannot be made on the basis of symptoms alone. Additional information from medical history and medication response may be necessary. PD should not cause increased muscle stretch reflexes (hyperreflexia), Babinski signs, eye movement disturbance, impairment of cerebellar system function, or cognitive decline as early features. Neuroimaging studies such as head CT or MRI scans are normal in idiopathic PD, and can be used to assess for other syndromes with Parkinsonian symptoms, including strokes, normal pressure (communicating) hydrocephalus, or a structural lesion such as a subdural hematoma.

PD can present a diagnostic challenge because the deficits evolve gradually and can caricature other illnesses often associated with advanced age.5 The forward flexed posture can resemble changes in the spine in osteoporosis. Decreased arm swing can mimic frozen shoulder. The decreased clarity of voice and diminished facial animation can resemble depression. Tremors in the hand and elsewhere can resemble side effects of medications or essential tremor. PD subjects often complain of generalized weakness and easy fatigue although formal testing generally reveals slowed movements with decreased dexterity rather than loss of muscle power.

There is no pathognomonic testing for PD outside of research settings, in which radiotracer neuroimaging can explore the dopaminergic lesion in vivo.6 However, responsiveness to medications like levodopa can help greatly in making the diagnosis. Such medication trials are especially important for differentiating PD from Parkinson-plus disorders (Table 17-1). In the initial stages, these disorders, including progressive supranuclear palsy, ...

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