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Non-motor Symptoms in Parkinson’s Disease

Inadequate glottis control can lead to recurrent microaspiration, which can further impair lung parenchymal function. Cough strength is generally low, impairing the ability to remove aspirated secretions and food particles. In addition to microaspiration, aspiration pneumonia is the leading cause of death in PD. Expiratory muscle strength training can increase cough strength independent of other respiratory parameters,119,120 although whether this affects the incidence or severity of aspiration has not yet been tested. Independent of pulmonary function, patients with PD may have reduced coordination between breathing and locomotion.121

It is

therefore plausible that breathing during activities of daily living is less efficient, thus contributing to a feeling of breathlessness. Despite these potential barriers owing to abnormal respiration, patients with mild to moderate PD are reliably able to exercise to maximum intensity and achieve peak oxygen consumption and workloads that are similar to age-matched controls.118,122

However, unlike healthy controls who

terminate maximum exercise owing to muscle fatigue, PD patients are more likely to terminate exercise owing to breathlessness.118


mild to moderate PD patients likely can participate in aerobic exercise programs and might be offered the same cardiovascular, metabolic, and psychological benefits as individuals without PD.

Sleep Sleep Fragmentation

Most patients with PD will have disturbed nocturnal sleep at some point during the course of their disease, and for about one-third of them it is considered a moderate to severe problem.123

Sleep disturbances worsen as

Sleep fragmentation—that is, a lack of sleep continuity owing to frequent awakenings—is the most common complaint for these patients in this regard. Fragmented sleep may be caused by a concomitant sleep disorder, such as obstructive sleep apnea (OSA) (see below) or nocturia, but a return of PD motor symptoms or medication effects is often at fault.125

PD progresses, and become more common in patients with higher Hoehn and Yahr stages.124

Recurrence of tremor or the inability to turn over in bed most often occurs in light non-REM sleep (N1, N2), thereby leading to difficulty initiating sleep or re-initiating sleep after an awakening. Treatment with levodopa, as well as implantation of a deep brain stimulator, has been shown to improve these troubling symptoms.126,127

On the other hand,

dopamine agonists can actually potentiate nocturnal motor activity and lead to resultant sleep fragmentation in some patients.128,129

In those who

are disturbed by increased dyskinesias, nightmares, and hallucinations, a reduction in evening medication doses may be helpful.

Restless Leg Syndrome and Periodic Limb Movements of Sleep

Restless leg syndrome (RLS) and the related periodic limb movements of sleep (PLMS) can cause sleep-onset insomnia or sleep fragmentation, and have been found by some authors to be increased in PD patients.130,131 While it is tempting to think that RLS would naturally be increased in PD because both conditions are attributable to a dopaminergic deficiency state and respond to levodopa or dopamine agonists, it is likely that dopaminergic pathways other than the nigrostratal system (which is central to PD) are involved in RLS.132

Moreover, the association

between RLS/PLMS and PD may not necessarily implicate a common pathophysiology, but rather reflect distinct processes that are more common in older individuals (e.g. iron deficiency, use of antidepressants). Regardless, the common responsiveness to dopaminergic therapy allows


for treatment of both conditions in comorbid individuals with the same or similar treatment regimens.

Obstructive Sleep Apnea

OSA has been claimed to be more frequent in PD than in the general population in some studies133

but not in others.134 Again, as the number

of obstructive apneas and hypopneas per hour of sleep increase with age,135

EDS in these patients is correlated with PD severity, cognitive decline, and longer use of levodopa and dopamine agonists.137–139 Although agonists have been considered to be a major cause of EDS and ‘sleep attacks,’ it appears that the total load of both types of medications leads to excessive sleepiness in susceptible patients.140 While the previously described sleep fragmentation would be expected to cause daytime sleepiness, some investigators have failed to find that it is a major cause of EDS in PD compared with age-matched controls.136 Of interest, a narcolepsy-like state, complete with sleep-onset REM periods and short mean sleep latency on the multiple sleep latency test, has been found to cause EDS in some PD patients. Unlike typical narcolepsy, cataplexy is not seen in these PD patients.141

the purported association between PD and OSA may only reflect conditions that are more common with advancing age. Nevertheless, like most patients with OSA, many of those with PD have excessive daytime sleepiness (EDS), which may raise clinical concern for OSA in these individuals. In point of fact, more than 15 % of PD patients, compared with 4 % of age-matched controls with diabetes, have EDS.123,136


of EDS includes excluding other causes, such as depression, decreasing or changing levodopa/dopamine agonists, and using stimulants such as modafinil.142

It is important to recall that depression is much more common in PD than in the general elderly population52

well as insomnia) is a common clinical feature in affected individuals. Regardless of the cause, sleepy drivers with PD have an increased crash risk and should be restricted from driving until effectively treated.143

Rapid Eye Movement Sleep Behavior Disorder REM sleep behavior disorder (RBD) is characterized by increased EMG activity and dream enactment behavior during REM, when atonia usually renders individuals motionless. RBD is not only common in PD, perhaps affecting as much as 50 % of this population, but may be a harbinger for the later development of PD or other synucleinopathies in otherwise asymptomatic individuals.144

RBD has been shown to antedate the onset

of PD by as much as 50 years in some patients and its presence increases the likelihood of the later development of dementia.145

Similar to a

As in

patients with idiopathic RBD, affected PD patients can often be treated successfully with clonazepam, and there are reports that donepezil, melatonin, and pramipexole may also be helpful.146–148 RLS/PLMS, RBD may be caused or aggravated by antidepressants,149

fact that should be borne in mind by clinicians. As with any patient suffering from RBD, making the sleeping environment safe and protecting bed partners from inadvertent injury are of paramount importance.


Weight loss is frequently observed in PD, and is associated with severity of parkinsonism, hallucinations, cognitive decline, and eating and swallowing difficulty.150–155

Successful DBS treatment is associated with weight gain.156,157 Loss of smell is frequent in PD, as in other neurodegenerative disorders (e.g. Alzheimer’s disease), and may antedate the diagnosis by many years.158

117 and EDS (as

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