Parkinson’s Disease

By Peter Galvin, MD

For two centuries, Parkinson’s disease has been diagnosed clinically based on the characteristic motor syndrome of bradykinesia (lack of movement) along with a resting tremor, rigidity, and postural reflex impairment (e.g., dizziness upon rapidly standing from a sitting of lying position [orthostatic hypotension]), all the result of dopamine-based dysfunction in the brain. Primarily a disease of older individuals, its incidence is rising because of our aging population. There is a male:female ratio of 2:1, with white individuals more commonly affected than Asian or Black people. However, the incidence of Lewy bodies, a hallmark of Parkinson’s, found in the brain at autopsy is the same across all races. In the U.S., the economic burden of the disease is predicted to rise from $52 billion in 2017 to $79 billion in 2037.

While Parkinson’s is generally considered to be a movement disease, it actually affects multiple organ systems. Nonmotor symptoms include sleep disorders, cognitive impairment, altered mood and affect, autonomic dysfunction (constipation, urinary dysfunction, and orthostatic hypotension), and sensory impairments (hyposmia [decreased sense of smell]) and pain. Sleep disorders, specifically REM sleep behavior disorder, which is characterized by flailing and kicking during REM sleep (normally, atonia [paralysis] is present during REM sleep), and hyposmia often predate outright Parkinsonian symptoms by many years, which suggests they may be prodromal (predictor) symptoms of Parkinson’s.

Parkinson’s is thought to have multiple causes. About 20% of cases are genetic. Dose-dependent residential or occupational exposure to pesticides and chlorinated solvents (trichloroethylene and perchloroethylene) have been associated with an increased risk of Parkinson’s in many studies, as has a history of mild-to-moderate head trauma. Also implicated are exposure to metals, diabetes mellitus type 2, and certain infections and inflammatory disorders. A decreased risk of Parkinson’s is associated with cigarette smoking (don’t), caffeine consumption, and increased physical activity.

As Parkinsonian symptoms worsen over time, there is an increased risk of functional impairment and loss of independence, often from the combined effects of cognitive and motor decline, falls, and fractures. There is no current pharmacological therapy for slowing the progression of the disease, despite over four decades of research to find and identify such agents. Current advice includes eating a healthy diet, regular exercise, and quality sleep. The main treatment for motor symptoms (rigidity, tremor, and bradykinesia) are oral formulations of levodopa. If patients do not respond to levodopa, the diagnosis should be reconsidered. The treatment of nonmotor symptoms, especially dementia, is more problematic. Currently, rivastigmine is the only clinically useful drug for dementia, according to the International Parkinson and Movement Disorder Society. Recently, deep brain stimulation (DBS), which involves the placement of electrodes deep within the brain that are connected to a neurostimulator which is usually placed under the skin below the clavicle, or collar bone, has shown promise to aid those who no longer respond to oral medications.

While research into gene therapies and the use of stem cells has been ongoing, so far none of these therapies have received regulatory approval. But with time and improving technologies, the hope is that one day soon we will be able to identify those at risk of Parkinson’s before they actually have symptoms and slow or stop disease progression.

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