Chapter
Parkinsonism
Claudia Trenkwalder and Isabelle Arnulf
Abstract
Altered sleep and vigilance are among the most frequent
nonmotor symptoms in parkinsonism. As many as 60%
patients with Parkinson’s disease (PD) suffer from insomnia,
15% to 59% from rapid eye movement (REM) sleep behavior
disorder (RBD), and 30% from excessive daytime sleepiness.
These frequencies are even higher in atypical parkinsonism.
Insomnia in parkinsonism is mainly a distressing difficulty in
maintaining sleep, promoted by motor disability, painful dys-
tonia, restless legs syndrome, dysuria, anxiety, and depressed
mood. Improving the motor control continuously during the
night with levodopa, transdermal or long-acting dopamine
agonists, or bilateral subthalamus stimulation can improve
sleep continuity, as does the specific treatment of dysuria,
anxiety, and depression.
RBD is violent, enacted dreaming that exposes the patients
or their bed partners to nighttime injuries. It is probably
caused by lesions in the REM sleep atonia system. Recent lon-
gitudinal studies indicate that RBD, when it affects middle-
aged patients, might precede parkinsonism (or dementia of
Lewy body type) for several years. In this case, it is often
associated with early markers of neurodegenerative diseases,
including olfactory, cognitive, and autonomic disturbances,
decreased dopaminergic transmission in functional imaging,
Parkinsonism is a common and disabling condition that
affects 1% to 2% of adults older than 65 years. During the
last several decades, there have been major advances in
optimizing the treatment of motor symptoms, at least in
idiopathic Parkinson’s disease (PD), whereas falls and
dementia (which determine the prognosis of the disease)
still remain difficult to treat. The interest for sleep disor-
ders in this already complex picture has increased within
the movement-disorders community. For decades, abnor-
mal sleep in parkinsonian patients was mostly considered
a collateral damage until key observations were made since
the 1990s.
DEFINITION
Parkinsonism
Parkinsonism (or parkinsonian syndrome, or Parkinson
syndrome) is defined by the association of slow movements
(bradykinesia) with either muscle rigidity (hypertonia), 4
to 6 Hz resting tremor, or postural instability.1 The main
cause of parkinsonism is idiopathic Parkinson’s disease
(PD), a neurodegenerative disorder with a progressive (but
not exclusive) loss of dopaminergic neurons. PD is char-
acterized by asymmetrical parkinsonism, progressive
worsening, and important initial benefit from levodopa.
When PD is fully developed, the clinical picture is
unmistakable.2
PD is primarily a disease of the elderly. Its prevalence
increases with age from about 0.9 % among persons 65 to
980
87
and slowed electroencephalographic (EEG) rhythms. Move-
ments that seem almost impossible can be restored for short
moments during RBD in some PD patients. That is different
from the sleep benefit, a motor improvement after a night’s
sleep and before drug intake reported by 33% to 55% of
patients. PD patients with RBD are less likely to be tremor-
predominant and are more exposed to hallucinations and
cognitive impairment than patients without RBD. When violent,
RBD can be treated with clonazepam and melatonin.
Daytime sleepiness and a narcolepsy-like phenotype (irrup-
tions of REM sleep episodes during daytime) is also part of PD.
In addition, the use of dopamine agonists exposes patients to
more frequent sleep attacks, especially when driving, suggest-
ing an interaction of drug and disease. Patients with multiple
system atrophy are disposed to develop a progressive, life-
threatening laryngeal obstruction (stridor) during sleep that
should be rapidly treated with positive airway pressure.
The disruption of the normal sleep and wakefulness in
patients with parkinsonism may be caused by neurodegenera-
tive damage in the brain area responsible for sleep and
arousal regulation; by behavioral, respiratory, and motor
system phenomena accompanying the disease; and by delete-
rious effects of medications. All of these effects on sleep have
implications for treatment planning.
69 years old to 5% among persons 80 to 84 years old, with
a slight male preponderance.3 Only a small percentage of
patients, mostly with the genetic forms, develop parkin-
sonism before the age of 45 years.
Major therapeutic advances have been accomplished in
PD during the last decades, including fine dopamine sub-
stitution and functional neurosurgery. After several years
of honeymoon on dopaminergic treatment, most patients
develop motor complications, including dyskinesia (abnor-
mal involuntary movements) at the peak of effect of
levodopa and painful dystonia (often confused with cramps)
at the beginning or the end of effect of levodopa, or early
in the morning. Patients use dopaminergic substitutive
treatment on daily schedules that becomes stricter and
more frequent as the disease progresses. Currently, it is
common to treat patients with a 10-year duration with 20
tablets per day, including small doses of levodopa every 3
hours, dopamine agonists every 5 hours, and various pills
to prevent the side effects (nausea, orthostatic hypoten-
sion, hallucinations) of these treatments.
The improvements brought by dopamine substitution
can also unmask the nondopaminergic and nonmotor
symptoms (mood, cognitive, psychiatric, sleep, and vegeta-
tive disturbances) that are not alleviated or are poorly
alleviated by these treatments. The most important of
these dopamine-unresponsive symptoms are falls (with the
risk of fractures) and dementia (which is the major motive
for placement in an institution).
Sleep disturbances are common—and newly recog-
nized—nonmotor symptoms. They include insomnia,