Polysomnographic Features of Sleep in Psychiatric Disorders

Polysomnographic Features of Sleep in Psychiatric Disorders

More studies of sleep and sleep-related phenomenology have been conducted in depression than in any other disorder. De-spite the common clinical impression that early morning wake-fulness is a predominant symptom in depression, most of the objective measures in recent years have implicated abnormali-ties occurring at sleep onset and during the first non-REM and REM periods: prolonged sleep latency; reduced stages 3 and 4 sleep; increased duration and REM density of the first REM period; and associated neuroendocrine abnormalities, including growth hormone, thyroid-stimulating hormone and melatonin. Furthermore, some studies have suggested that short REM la-tency or reduced delta sleep ratio (amount of delta waves in first non-REM periods compared with second non-REM periods) may predict relapse in depressed patients. Some of these sleep-related abnormalities appear to persist during periods of clinical remis-sion, such as short REM latency, loss of stages 3 and 4 sleep, and blunted nocturnal growth hormone release. Genetic factors may influence some of these measures, including short REM latency. Preliminary data suggest that short REM latency may be a ge-netic marker for depression in first-degree relatives of patients with mood disorders.

Even though the polygraphic sleep findings in depression do not appear to be diagnostically specific, they remain among the best documented biological abnormalities of any psychiatric disorder at this time. One challenge is to understand their patho-physiological mechanism. Because of the shallow, fragmented sleep and response to sleep deprivation, the sleep of patients with depression has been described as “overaroused”. For instance, the antidepressant response of sleep deprivation may “dampen down” an overly aroused limbic system in a subgroup of patients. Several studies have shown that responders to sleep deprivation differ from nonresponders at baseline assessment before sleep deprivation by having a higher level of metabolic activity in the cingulate gyrus and that this overactivity approaches normality with clinical improvement.

The sleep disturbances of schizophrenic patients are of-ten similar to those of depressed patients, including short REM latency and reduced delta sleep, total sleep time and sleep ef-ficiency. Interestingly, while making nightly “sleep checks” on hospitalized patients, nurses are more accurate in judging sleep time in schizophrenic patients than in depressive patients, who often appear to be asleep when they are actually awake.

Although less well studied, the sleep of patients with anxi-ety disorders, such as generalized anxiety disorder, panic dis-order, obsessive–compulsive disorder, acute stress disorder and PTSD, is often disturbed. Panic attacks, for example, may occur occasionally during sleep itself, usually at the transition between stage 2 and delta sleep. Patients with panic disorders during sleep are also likely to experience panic attacks during wakefulness either with relaxation or after sleep deprivation.

Patients with obsessive–compulsive disorder frequently endure difficulties in the initiation and maintenance of sleep. They often have elaborate compulsive rituals before going to bed, for example, concerns about “germs” may necessitate long showers and fresh, clean “sterilized” pajamas and sheets each night. Polysomnographic features are sometimes similar to those described in major depressive disorder, even though the patients do not have symptoms that meet full diagnostic criteria for major depressive disorder.

Classic symptoms of post traumatic stress disorder in-clude nightmares, night terrors and violent thrashing about dur-ing sleep. These patients are easily aroused. Combat survivors with PTSD sometimes seek a physically “secure” sleeping en-vironment in which to sleep and wake up frequently during the night to “check the perimeter”. These sleep problems in Vietnam veterans who suffer from PTSD are often complicated by chronic conditioning, alcohol and substance abuse, depression, anxiety, and significant interpersonal and social problems. Total sleep time is usually reduced with variable and inconsistent distur-bances of REM sleep. Successful treatment of the disorder and the sleep complaints has been traditionally difficult. The night-mares of PTSD appear to occur in both non-REM and REM sleep. While SSRIs are often recommended in the treatment of PTSD, some of the activating antidepressants appear to worsen subjec- tive complaints of sleep. Nefazodone, a sedative antidepressant, slowly improved subjective sleep quality, mood, and the number of reported nightmares. Phenelzine and other MAOIs have also been reported to improve sleep and nightmares, but the possi-bility of serious drug interactions, alcoholism and poor compli-ance limit their usefulness. More recently, Raskin and colleagues have reported a significant reduction in nightmares and overall improvement in combat veterans with PTSD who were treated with prazosin, an alpha-1-adrenergic receptor antagonist (Taylor and Raskin, 2002).

Changes in sleep patterns may occur in patients with eat-ing disorders. Night bingeing and increased sleep after eating are commonly reported in bulimic patients, who are also reported to eat and shop for food while sleepwalking. The patient frequently does not remember these nocturnal episodes; they often become known from family or friends who have observed the behavior or from physical evidence of shopping or eating behaviors. Patients with anorexia are often hyperactive, needing little sleep. Given the degree of physical and psychic stress associated with eating disorders, it is surprising how limited are the objective sleep dis-turbances associated with these disorders.