Insomnia Insomnia

82 Attarian
was confirmed by research done in the 1980s. It was also documented that this is a
distinct form of insomnia by showing that childhood-onset insomnia was different
from adult-onset insomnia on polysomnographic grounds (5) and that it could be
distinguished from other types of insomnia in a cluster analysis (6).
EPIDEMIOLOGY
Idiopathic insomnia is rarely seen in its pure form. Chronic and serious insomnia
over a lifetime almost always leads to other factors such as maladaptive behaviors;
poor sleep hygiene, and emotional disturbances that further complicate the
picture (7). A predisposition toward poor sleep exists in many insomniacs. However,
in its pure form, idiopathic insomnia represents less than 5% of all insomniacs
(8). Evidence shows that idiopathic insomnia often, but not always, has familial
patterns of inheritance (1).
ETIOLOGY
Idiopathic insomnia may be due to some dysfunction in the brain’s sleep–wake
center. It may represent either hyperactivity in the wake center or hypoactivity in
the sleep center (5,9). Another, and more commonly accepted theory, is that patients
with idiopathic insomnia are just simply organically hyperaroused (10).
PATHOGENESIS AND PATHOPHYSIOLOGY
Sleep–wake centers include the sleep-promoting center present in the anterior
hypothalamus, the raphe nuclei, and medial forebrain area, and the wake-promoting
center in the ascending reticular-activating system including the posterior
hypothalamus (7,9). Whether a person is awake or asleep depends on the neurophysiological
balance between the reticular-activating system and the sleep-inducing
maintenance systems (11). Idiopathic insomnia presumably is due to a shift of
this balance toward arousal. Either hyperactivity in the arousal system or
hypoactivity in the sleep system may cause idiopathic insomnia (9). Patients suffering
from idiopathic insomnia may have a neurochemical, neuroanatomical, or neurophysiological
dysfunction or lesions interfering with normal sleep (11). Idiopathic
insomniacs are often hyperaroused during wakefulness on questionnaires, auditoryevoked
potentials, and electroencephalogram (EEG) (12). Physiological
hyperarousal in many systems (cardiac, core temperature, corticosteroids, etc.) is
not confined to patients with idiopathic insomnia but is frequently found in all primary
insomniacs (10). Despite animal data showing the creation of insomniac animals
with medial forebrain and the medial preoptic area (13), no direct human
evidence for structural neuropathology exists (14). Difficult birth and prematurity
are likely risk factors for the development of idiopathic insomnia (1).
CLINICAL MANIFESTATIONS
Idiopathic insomnia is a chronic and serious inability to initiate and maintain
sleep that can often be observed as early as the first few weeks of life. Parents often