Researchers are investigating overlapping neural pathways for anxiety, arousal, and circadian disturbance as a potential pathophysiological link between insomnia and depression (Benca, 2005b).
Depressed patients exhibit hypermetabolism in the brain's emotional pathways, including the amygdala, anterior cingulate cortex, and related structures, during both waking and NREM sleep.
A 1985 study by Reynolds et al. published in Biological Psychiatry examined EEG sleep patterns in elderly subjects categorized as depressed, demented, or healthy.
A 2003 systematic review and meta-analysis published in the American Journal of Psychiatry identified risk factors for depression among elderly community subjects.
Nofzinger et al. (2004a) found increased activation of the anterior paralimbic and executive cortex when transitioning from waking to REM sleep in patients with depression.
Untreated residual insomnia is a risk factor for the recurrence of depression.
The Institute of Medicine (US) Committee on Sleep Medicine and Research associates chronic sleep loss and sleep disorders with an increased risk of hypertension, diabetes, obesity, depression, heart attack, and stroke.
Depressed patients exhibit less pronounced decreases in brain metabolism during sleep compared to healthy individuals.
Limbic and paralimbic structures that regulate basic emotions and instinctual behaviors—specifically the amygdala, hippocampus, ventromedial prefrontal cortex, and anterior cingulate cortex—are abnormally active during sleep in individuals with primary insomnia and secondary insomnias related to depression, as reported by Nofzinger et al. (2004a, 2005).
Nofzinger et al. (2005) hypothesize that the amygdala and other limbic structures of the brain are common pathways linking insomnia and depression.
Insomnia is associated with depression, acting as both a risk factor and a manifestation of the condition.
Secondary cases of narcolepsy or hypersomnia can occur in the context of psychiatric disorders (e.g., depression), central nervous system tumors (notably in the hypothalamus), neurodegenerative disorders (e.g., Parkinson’s disease), inflammatory disorders (e.g., multiple sclerosis or paraneoplastic syndromes), traumatic disorders (e.g., head trauma), vascular disorders (e.g., median thalamic stroke), and genetic disorders (e.g., myotonic dystrophy or Prader-Willi syndrome).
In patients with depression, sleep abnormalities may persist even after the depression episode has remitted.
Insomnia is a common complication of stroke that may result from medication, inactivity, stress, depression, and brain damage.
Perlis et al. (2005) hypothesize that chronic insomnia increases activity of the hypothalamic-pituitary-adrenal axis, which contributes to the development of depression.
Livingston G, Blizard B, and Mann A investigated whether sleep disturbance predicts depression in elderly people in a study conducted in inner London, published in the British Journal of General Practice in 1993.
In the study of 1,007 young adults by Breslau et al. (1996), the adjusted odds of developing depression after a history of insomnia were 3.95 (95% CI, 2.2–7.0).
Riemann and Voderholzer (2003) suggest that treating insomnia may prevent some cases of depression, though data supporting this are limited.
Riemann and Voderholzer (2003) identified primary insomnia as a potential risk factor for the development of depression.
Nofzinger et al. (2005) hypothesize that increased metabolism in emotional pathways in depressed patients may increase emotional arousal, which adversely affects sleep.
A study tracking more than 1,000 male physicians for 40 years found a longitudinal association between insomnia and depression.
The cumulative effects of sleep loss and sleep disorders are associated with an increased risk of hypertension, diabetes, obesity, depression, heart attack, and stroke.
Insomnia is associated with depression, acting as both a risk factor for and a manifestation of the condition (Ford and Kamerow, 1989; Livingston et al., 1993; Breslau et al., 1996; Weissman et al., 1997; Chang et al., 1997; Ohayon and Roth, 2003; Cole and Dendukuri, 2003).
Chronic sleep loss and sleep disorders are associated with an increased risk of hypertension, diabetes, obesity, depression, heart attack, and stroke.
In a study sample, 16 percent of individuals with a history of insomnia at baseline developed depression, compared to 4.6 percent of individuals without a history of insomnia.
Cancer patients often suffer from pain or depression, which contributes to difficulty sleeping.
Other polysomnographic abnormalities associated with depression include a shortened initial REM period, increased REM density, and slow-wave deficits, according to Benca (2005a).
Increased metabolism in emotional pathways associated with depression may increase emotional arousal and adversely affect sleep.
Insomnia in young men is associated with subsequent depression, according to the Johns Hopkins precursors study published in the American Journal of Epidemiology in 1997.
Rao et al. (1996) studied the relationship between longitudinal clinical course and changes in sleep and cortisol levels in adolescents with depression.
The shorter REM latency observed in depressed individuals persists even after treatment for depression, according to Benca (2005a).
Many cancer patients experience difficulty sleeping due to pain or depression, which requires treatment similar to other patients with these conditions.
Sleep disturbances in Alzheimer’s disease are associated with behavioral symptoms including aggressiveness and depression, though the pathophysiology of this association is unknown.
One hypothesis for the link between insomnia and depression is that chronic insomnia increases activity of the hypothalamic-pituitary-adrenal axis, which contributes to depression (Perlis et al., 2005).
Cole and Dendukuri conducted a systematic review and meta-analysis on risk factors for depression among elderly community subjects, published in the American Journal of Psychiatry in 2003.
Raison CL and Miller AH discussed the neuroimmunology of stress and depression in Seminars in Clinical Neuropsychiatry in 2001.
Polysomnography detects abnormalities in depressed individuals including shortened initial REM periods, increased REM density, and slow-wave deficits, according to Benca (2005a).
Depressed individuals exhibit specific polysomnographic abnormalities, including shorter rapid eye movement (REM) latency, which is the time elapsed from the onset of sleep to the onset of REM sleep.
When transitioning from waking to non-REM (NREM) sleep, depressed subjects show smaller decreases in relative metabolism in regions of the frontal, parietal, and temporal cortex compared to healthy individuals, according to Nofzinger et al. (2005) using positron emission tomography.
It is essential to exclude secondary causes, such as head trauma or hypersomnia resulting from depression, when diagnosing idiopathic hypersomnia, as noted by Roth (1976) and Billiard and Dauvilliers (2001).
Sleep-onset abnormalities during adolescence are associated with an increased risk of depression in later life, according to Rao et al. (1996).
Periodic limb movement disorder is associated with above-average rates of depression, memory impairment, attention deficits, oppositional behaviors, and fatigue, according to the American Academy of Sleep Medicine (2005).
Treating insomnia may prevent some cases of depression, though limited data are available to support this possibility (Riemann and Voderholzer, 2003).
The adjusted odds of developing depression for individuals with a history of insomnia were 3.95 (95% CI, 2.2–7.0).
Nofzinger et al. (2005) documented alterations in regional cerebral glucose metabolism across waking and non-rapid eye movement sleep in patients with depression.
Associations between sleep disturbance and behavioral symptoms in Alzheimer’s disease patients include aggressiveness (Moran et al., 2005) and depression (Tractenberg et al., 2005).
Researchers hypothesize that insomnia and depression may be linked by common pathophysiology involving overlapping neural pathways for anxiety, arousal, and/or circadian disturbance, as suggested by Benca (2005b).
The adjusted odds of developing a psychiatric disorder following a history of insomnia were highest for depression, with an odds ratio of 3.95 (95% CI, 2.2–7.0).
A 2003 study by Riemann and Voderholzer published in the Journal of Affective Disorders examined whether primary insomnia acts as a risk factor for the development of depression.
Raison and Miller (2001) explored the neuroimmunology of stress and depression.
The 2005 NIH State of the Science Conference on the Manifestations and Management of Chronic Insomnia concluded that while available behavioral and pharmacological therapies may provide benefit, more research and randomized clinical trials are required to verify their efficacy, particularly for long-term illness management and the prevention of complications such as depression.
A 1997 study by Reynolds et al. published in the American Journal of Psychiatry investigated which elderly patients with remitted depression remain well when treated with continued interpersonal psychotherapy after discontinuing antidepressant medication.
Associations between sleep disturbance and behavioral symptoms in Alzheimer’s disease patients include aggressiveness (Moran et al., 2005) and depression (Tractenberg et al., 2005).
Depressed individuals exhibit shorter rapid eye movement (REM) latency, defined as a shorter period between sleep onset and REM sleep onset, which persists even after depression treatment.
A longitudinal study of 1,007 young adults at a health maintenance organization found that a history of insomnia at baseline predicted the new onset of depression and other psychiatric disorders, including anxiety, alcohol abuse, drug abuse, and nicotine dependence, over a 3.5-year period.
Fava M identified daytime sleepiness and insomnia as correlates of depression.
Cytokines used as biotherapy adjuncts, specifically interferon, interleukin-2, and tumor necrosis factor, are associated with side effects including daytime sleepiness, disturbed sleep, and depression.
A 1997 study published in the American Journal of Epidemiology titled 'Insomnia in young men and subsequent depression' found a link between insomnia in young men and the subsequent development of depression.
Individuals with insomnias associated with depression exhibit abnormal activity in neocortical structures responsible for controlling executive function and modulating behavior related to basic arousal and emotions, according to Nofzinger et al. (2004a, 2005).
Insomnia worsens clinical outcomes in patients with depression, schizophrenia, and alcohol dependence.
One hypothesis for the link between insomnia and depression is that common neural pathways involve the amygdala and other limbic structures of the brain (Nofzinger et al., 2005).
Most potential mechanisms explaining sleep changes in psychiatric disorders focus specifically on the relationship between insomnia and depression.
Sleep abnormalities in patients with depression may persist even after the depressive episode has remitted (Fava, 2004).