Insomnia and Anxiety (Series in Anxiety and Related Disorders) by Jack D. Edinger Colleen E. Carney
Authors: Jack D. Edinger Colleen E. Carney
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course of this
disorder, the affected individual recognizes the obsessions and associated compul-
sions are irrational, but these symptoms persist over time despite this insight.
Compared to other anxiety disorders, obsessive–compulsive disorder is rela-
tively rare, albeit often very persistent and debilitating. Most epidemiological sur-
veys show a stable prevalence of obsessive–compulsive disorder with approximately
2% of the general population of Western societies meeting criteria for this condition.
Those with obsessive–compulsive disorder are not particularly prone to present in
Obsessive–Compulsive Disorder
41
primary care settings (Fireman, Koran, Leventhal, & Jacobson, 2001), but as many
as 9.2 % of those who seek psychiatric treatment suffer from this condition
(Hantouche, Bouhassira, Lancrenon, Ravily, & Bourgeois, 1995). These findings
are, perhaps, not surprising inasmuch as many as two thirds of those with obses-
sive–compulsive disorder present with comorbid mental disorders, particularly
mood or other anxiety disorders (Torres et al., 2006; Tukel, Meteris, Koyuncu,
Tecer, & Yazici, 2006). Obsessive–compulsive disorder tends to be chronic in as
many as 60% of affected individuals (Angst et al., 2004), and almost one half of
those who eventually achieve full symptomatic remission later suffer relapse (Eisen
et al., 1999). Whereas some persons with obsessive–compulsive disorder may suf-
fer surprisingly little social and vocational impairment, this condition often results
in considerable impairment of social and occupational functioning. In more pro-
tracted cases, this disorder may contribute to reduced quality of life, impairment of
family and social relationships, reduced productivity and heightened absenteeism
from work, chronic disability, and a markedly increased risk for suicide (American
Psychiatric Association, 1997; Kamath, Reddy, & Kandavel, 2007; Stengler-
Wenzke, Krolla, Matschingera, & Angermeyera, 2006; Torres et al., 2006).
Insomnia and other forms of sleep disturbance are not considered core symptoms
or primary associated features of obsessive–compulsive disorder (Stein & Mellman,
2005). However, one recent study (Voderholzer et al., 2007) indicated that those with
obsessive–compulsive disorder show relative disturbances of sleep continuity (i.e.,
more fragmented sleep) compared with well-matched noncomplaining normal
sleepers. Another recent study (Kluge, Schüssler, Künzel et al., 2007) showed that
obsessive–compulsive disorder sufferers displayed higher plasma concentration
levels of ACTH and cortisol during their sleep than did normal controls. Alterations
in REM and slow wave sleep architecture have also been noted in some (Insel et al.,
1982; Kluge, Schüssler, Dresler, Yassouridis, & Steiger, 2007) but not all obsessive–
compulsive sufferers (Hohagen et al., 1994; Robinson, Walsleben, Pollack, &
Lerner, 1998; Voderholzer et al., 2007). Considered collectively, these findings sug-
gest obsessive–compulsive disorder patients may have a relative propensity for dis-
rupted nocturnal sleep perhaps mediated by over-activity of the HPA axis. Of course,
insomnia may develop independently because of other factors and exist as a comor-
bid condition, as is the case with other anxiety disorders.
As noted by Smith and colleagues (Smith et al., 2005), compulsive behaviors
may sometimes play a role in insomnia complaints. For example, compulsive
checking that doors are locked or repetitive praying before retiring for the night
may interfere with the act of falling asleep and markedly delay sleep onset. Also,
given the recent findings implicating possible over-activity of the HPA axis in
obsessive–compulsive patients, excessive arousal during the nighttime may compli-
cate the sleep of some such patients. Furthermore, it is noteworthy that unhelpful
beliefs are thought to perpetuate the symptoms of at least some
disorder, the affected individual recognizes the obsessions and associated compul-
sions are irrational, but these symptoms persist over time despite this insight.
Compared to other anxiety disorders, obsessive–compulsive disorder is rela-
tively rare, albeit often very persistent and debilitating. Most epidemiological sur-
veys show a stable prevalence of obsessive–compulsive disorder with approximately
2% of the general population of Western societies meeting criteria for this condition.
Those with obsessive–compulsive disorder are not particularly prone to present in
Obsessive–Compulsive Disorder
41
primary care settings (Fireman, Koran, Leventhal, & Jacobson, 2001), but as many
as 9.2 % of those who seek psychiatric treatment suffer from this condition
(Hantouche, Bouhassira, Lancrenon, Ravily, & Bourgeois, 1995). These findings
are, perhaps, not surprising inasmuch as many as two thirds of those with obses-
sive–compulsive disorder present with comorbid mental disorders, particularly
mood or other anxiety disorders (Torres et al., 2006; Tukel, Meteris, Koyuncu,
Tecer, & Yazici, 2006). Obsessive–compulsive disorder tends to be chronic in as
many as 60% of affected individuals (Angst et al., 2004), and almost one half of
those who eventually achieve full symptomatic remission later suffer relapse (Eisen
et al., 1999). Whereas some persons with obsessive–compulsive disorder may suf-
fer surprisingly little social and vocational impairment, this condition often results
in considerable impairment of social and occupational functioning. In more pro-
tracted cases, this disorder may contribute to reduced quality of life, impairment of
family and social relationships, reduced productivity and heightened absenteeism
from work, chronic disability, and a markedly increased risk for suicide (American
Psychiatric Association, 1997; Kamath, Reddy, & Kandavel, 2007; Stengler-
Wenzke, Krolla, Matschingera, & Angermeyera, 2006; Torres et al., 2006).
Insomnia and other forms of sleep disturbance are not considered core symptoms
or primary associated features of obsessive–compulsive disorder (Stein & Mellman,
2005). However, one recent study (Voderholzer et al., 2007) indicated that those with
obsessive–compulsive disorder show relative disturbances of sleep continuity (i.e.,
more fragmented sleep) compared with well-matched noncomplaining normal
sleepers. Another recent study (Kluge, Schüssler, Künzel et al., 2007) showed that
obsessive–compulsive disorder sufferers displayed higher plasma concentration
levels of ACTH and cortisol during their sleep than did normal controls. Alterations
in REM and slow wave sleep architecture have also been noted in some (Insel et al.,
1982; Kluge, Schüssler, Dresler, Yassouridis, & Steiger, 2007) but not all obsessive–
compulsive sufferers (Hohagen et al., 1994; Robinson, Walsleben, Pollack, &
Lerner, 1998; Voderholzer et al., 2007). Considered collectively, these findings sug-
gest obsessive–compulsive disorder patients may have a relative propensity for dis-
rupted nocturnal sleep perhaps mediated by over-activity of the HPA axis. Of course,
insomnia may develop independently because of other factors and exist as a comor-
bid condition, as is the case with other anxiety disorders.
As noted by Smith and colleagues (Smith et al., 2005), compulsive behaviors
may sometimes play a role in insomnia complaints. For example, compulsive
checking that doors are locked or repetitive praying before retiring for the night
may interfere with the act of falling asleep and markedly delay sleep onset. Also,
given the recent findings implicating possible over-activity of the HPA axis in
obsessive–compulsive patients, excessive arousal during the nighttime may compli-
cate the sleep of some such patients. Furthermore, it is noteworthy that unhelpful
beliefs are thought to perpetuate the symptoms of at least some
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