Recognizing and Treating Nonmotor Aspects of Parkinson’s Disease
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This article is the second in a series of three from the author on Parkinson’s disease.
In his “Essay on the Shaking Palsy,”1 James Parkinson described a condition with both motor and nonmotor aspects. Until recently, however, most attention was given to the motor aspects of the disease such as tremor and gait disturbance. This was reinforced in the 1960s with the advent of levodopa therapy.2 The innovation of augmenting brain dopamine levels with oral levodopa was an elegant demonstration that pharmacologic replacement of a depleted neurotransmitter could actually improve function. And motor function was indeed improved: tremor, rigidity, and bradykinesia all responded to this remarkable new therapy.
As treatment of motor symptoms continues to improve, with such added innovations as dopamine agonists and deep brain stimulation, it has become more obvious that myriad nonmotor symptoms such as depression, sleep disorders, and cognitive decline contribute not only to impaired function but to poor quality of life.3-5 Simultaneously, those studying the pathophysiology of the disease have expanded their focus from the events within the substantia nigra to other brain regions, the peripheral and autonomic nervous systems and areas such as the myenteric plexus and olfactory apparatus, where the disease may actually have its origin.6-8
This article will give a brief overview of some of the nonmotor features of Parkinson’s disease (PD), with some suggestions for management. The next article in the series will address another important category of nonmotor symptoms: neuropsychiatric manifestations such as dementia, depression, and hallucinations.
Sleep Disturbance
Persons with Parkinson’s disease experience a wide variety of problems with their sleep. Sleep architecture, already altered by aging, may be further disturbed as PD evolves to include brain regions such as the pedunculopontine nucleus, which is involved in the regulation of rapid eye movement (REM) sleep.9
Because of the brainstem involvement, one very common problem in PD is REM sleep behavior disorder (RSBD), in which patients act out their dreams instead of being paralyzed during them, as is normal. This is estimated to occur in up to 47% of persons with PD9 and is one of several nonmotor symptoms that may precede the motor aspects of the disorder.10,11 As with most sleep disturbances, this can be demonstrated during polysomnography. RSBD may be aggravated or precipitated by a variety of medications, including tricyclic antidepressants, selective serotonin reuptake inhibitors, and monoamine oxidase inhibitors.10 In the absence of complicating factors such as snoring or dementia, RSBD is often treated successfully with a small dose of clonazepam. If there is a suggestion of obstructive sleep apnea (OSA), also common in PD,12 this should be diagnosed and treated before sedating medications are prescribed.
One of the most commonly encountered sleep issues in PD is “wearing-off” of medication effect during the night, or even prior to sleep onset. This makes it difficult or even impossible to change position or adjust the bedclothes. Some patients describe waking up each morning in the exact same position in which they retired for the night, leading to complications produced by immobility, such as compression neuropathies or skin breakdown.
Sometimes, when the medication wears off, the patient is awakened by a sensation of uncomfortable warmth and experiences pronounced diaphoresis. When the medication effect wears off before bedtime, the patient may have difficulty getting comfortable enough to go to sleep and may even experience restless legs syndrome (RLS). Most of these problems can be addressed by adjusting the dopaminergic medication to cover these periods.
Depression is another common factor in parkinsonian sleep disturbance, often causing early morning awakening.
References
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