Insomnia Insomnia

Primary Sleep Disorders 143
architecture, with fragmented nocturnal sleep being a basic manifestation of this
dysregulation. Sleep paralysis and hypnogogic hallucinations can be unpleasant
enough to result in anxiety about sleeping. The stimulants and antidepressants used
to treat excessive daytime sleepiness and cataplexy can further contribute to difficulty
sleeping. The anxiety resulting from a nightmare may result in awakenings
and difficulty returning to sleep. With sleep starts, an awakening coincides with the
abnormal motor activity; when repetitive, this can result in difficulty falling asleep
or returning to sleep after awakening in the night.
In the primary sleep disorders, many patients do not develop a complaint of
insomnia despite demonstrable sleep fragmentation, suggesting individual differences
in susceptibility. Psychophysiological insomnia has been shown to have a
familial tendency (18), and genetic predisposition likely plays a role in the development
of an insomnia complaint in the primary sleep disorders. Additionally, poor
sleep hygiene often develops, leading to further difficulty sleeping. For instance, in
RLS, patients often report that they get their best sleep late in the morning, leading
to a tendency to sleep in late when possible, leading to further difficulties initiating
sleep. In any of the disorders, the perception of difficulty sleeping can lead to anxiety
directed toward sleep and therefore a secondary component of psychophysiological
insomnia.
PATHOGENESIS AND PATHOPHYSIOLOGY
In OSA, repetitive complete or partial occlusions of the upper airway result in
repetitive arousals during sleep. Pharyngeal patency is maintained by a balance of
outward forces created by actively contracting pharyngeal muscles such as the
genioglossus that are phasically active during inspiration, and negative intraluminal
forces created during inspiration (19). In OSA, this patency is compromised
through a narrowing of the upper airway through either anatomical means such as
hypertrophied tonsils, or dynamic means such as reduction of the phasic inspiratory
contractions. This leads to an increased effort of breathing and hypoxemia, resulting
in arousals or awakenings, associated with a surge in sympathetic nervous system
activity. Because most arousals and awakenings in OSA are brief, patients are
usually unaware of the frequency of awakenings. Some awakenings may be long
enough for the patient to recall, leading to an insomnia complaint. Apneas are sometimes
associated with a sensation of choking, not breathing, dyspnea, or tachycardia.
This can lead to a fear of sleep that can sometimes reach phobic levels. The
total number of apneic and hypopneic episodes per hour of sleep is called either the
apnea-hypopnea index (AHI) or the respiratory disturbance index (RDI), although
many laboratories include events such as respiration effort-related arousals or snore
arousals in the RDI. An AHI score of 5 or higher is enough to establish the diagnosis
of OSA syndrome.
The pathophysiology of RLS remains unclear. Most cases are idiopathic, but a
significant percentage are hereditary, with an autosomal-dominant pattern of inher-