This page contains a Flash digital edition of a book.
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


Accordingly,


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


US NEUROLOGY


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


Management


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.


Others


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


Page 1  |  Page 2  |  Page 3  |  Page 4  |  Page 5  |  Page 6  |  Page 7  |  Page 8  |  Page 9  |  Page 10  |  Page 11  |  Page 12  |  Page 13  |  Page 14  |  Page 15  |  Page 16  |  Page 17  |  Page 18  |  Page 19  |  Page 20  |  Page 21  |  Page 22  |  Page 23  |  Page 24  |  Page 25  |  Page 26  |  Page 27  |  Page 28  |  Page 29  |  Page 30  |  Page 31  |  Page 32  |  Page 33  |  Page 34  |  Page 35  |  Page 36  |  Page 37  |  Page 38  |  Page 39  |  Page 40  |  Page 41  |  Page 42  |  Page 43  |  Page 44  |  Page 45  |  Page 46  |  Page 47  |  Page 48  |  Page 49  |  Page 50  |  Page 51  |  Page 52  |  Page 53  |  Page 54  |  Page 55  |  Page 56  |  Page 57  |  Page 58  |  Page 59  |  Page 60  |  Page 61  |  Page 62  |  Page 63  |  Page 64  |  Page 65  |  Page 66  |  Page 67  |  Page 68  |  Page 69  |  Page 70  |  Page 71  |  Page 72  |  Page 73  |  Page 74  |  Page 75  |  Page 76  |  Page 77  |  Page 78  |  Page 79  |  Page 80  |  Page 81  |  Page 82  |  Page 83  |  Page 84  |  Page 85  |  Page 86  |  Page 87  |  Page 88  |  Page 89  |  Page 90  |  Page 91  |  Page 92  |  Page 93  |  Page 94  |  Page 95  |  Page 96  |  Page 97  |  Page 98  |  Page 99  |  Page 100  |  Page 101  |  Page 102  |  Page 103  |  Page 104  |  Page 105  |  Page 106  |  Page 107  |  Page 108