Insomnia Insomnia

Medical and Neurological Causes 117
residual cognitive dulling, lingering hypnotic effects, or uncomfortable side effects.
There may be a role for medications that have antidepressant or anxiolytic characteristics,
especially in the early stages following cancer diagnosis. Chronic treatment
may be better achieved by nonpharmacologic interventions (54,55) such as
cognitive therapy, relaxation therapy, biofeedback, and behavioral approaches to
improve sleep quality.
Degenerative conditions of the CNS alter the chemical and structural substrates
that regulate sleep; most of these produce fragmented sleep, with or without daytime
hypersomnia. Disrupted sleep patterns are common in Alzheimer’s Dementia
(56), and the difficulties produced by perceptual impairment may aggravate nocturnal
behaviors and confusion (57,58), characterized as a “sundown” syndrome. Cholinergic
agonists or cholinesterase inhibitors utilized to treat Alzheimer’s Dementia
may aggravate difficulties with sleep initiation, by augmenting cholinergic tone in
the basal forebrain and cerebral cortex, favoring the maintenance of wakefulness.
Parkinson’s disease (PD) may disrupt sleep by way of tremor, dystonia, or periodic
nocturnal movements, whereas the dopamine agonist medications used for treatment
of PD may also cause insomnia, dystonia, or dyskinesia. Thus, inadequate
symptomatic treatment at night or the side effects of treatment may cause sleep
disruption by similar mechanisms. The dopamine agonists tend to enhance dreaming,
and many patients report increased nightmares in association with bedtime
doses of levodopa and pergolide. These medications may also cause increased motor
activity during dreams. Lewy body dementia has a high incidence of REM behavior
disorder and sleep fragmentation (58a). The EEG in progressive supranuclear palsy
has been observed to include more elemental changes in sleep architecture, with
decreased total sleep time, decreased sleep spindles, and diminished REM sleep
(59,60). Multiple systems atrophy also produces considerable sleep disruption, with
increased arousal and diminished slow wave sleep (61). Huntington’s chorea has
been associated with decreased sleep efficiency, and sleep may become dramatically
fragmented as behavioral symptoms increase. Fatal Familial Insomnia is a
rare prion-associated spongeform encephalopathy with rapid progression through
fulminant insomnia to dementia and death over the course of months (62). Insomnia
is also commonly seen in association with Creutzfeldt-Jakob disease (63,64),
especially when the thalamic degeneration is disproportionately observed.
Neuropathy and radiculopathy are associated with chronic pain, fasciculations,
and muscle spasms that cause impaired sleep initiation/maintenance, and periodic
limb movements of sleep are augmented in peripheral nerve disorders, further
exacerbating difficulties with sleep maintenance. Muscular dystrophy and inflammatory
myopathies can cause insomnia by similar mechanisms, in addition to their
effects on ventilatory and pharyngeal musculature that lead to hypoventilation and
frequent aspiration. Most of the medications used to treat the symptoms of neuropathy
are sedating for the majority of people who take them, but the
anticonvulsants carbamazepine and lamotrigine have been reported to cause
insomnia. Myelopathy can also cause pain, muscle spasms, spasticity, constipation,