There is a prevalence of insomnia seen in psychiatric illness although insomnia itself can be a risk factor for psychiatric disorders. That’s according to research presented here on at the annual meeting of the American Psychiatric Association (APA).
“Clearly, of those with and without insomnia, the insomnia group has a higher incidence of depression and anxiety disorders,” said Meera Narasimhan MD, Professor of Psychiatry, Director, Biological Research, Dept. of Neuropsychiatry and Behavioral Sciences, University of South Carolina School of Medicine, Columbia, United States.
Narasimhan said 50% to 80% of patients with major depressive disorder (MDD) have insomnia. And a persistent case of insomnia augments a lifetime risk of MDD.
There is an invisible patient population where 70% of people with insomnia never discuss the problem with treating physicians. Only 8% of those with insomnia manage to see a psychiatrist and of that group, 52% have one-to-three comorbid illnesses. Sixty-nine percent have four or more comorbidities. “We need to do a better job accessing these individuals,” said Narasimhan.
Some of the comorbid conditions include:
• bipolar disorders with prevalence rates of circadian rhythm instability and insomnia as high as 77%
• post-traumatic stress disorder (PTSD) with prevalence rates as high as 70%
• schizophrenia, which is a condition frequently associated with sleep disturbance and insomnia.
Some more common causes of insomnia include primary sleep disorders, medical illness, mood disorders, dementia, psychosis, anxiety, medications, and psychosocial stress. The impact of insomnia include exacerbation of psychiatric symptoms and increased risk of relapse; reduction in mental performance and motor functioning; accidents; suicide; inability to accomplish daily tasks and interpersonal difficulties with families, friends, and at work.
Drugs can cause insomnia and the most likely culprits include illicit drugs, alcohol, caffeine, nicotine, stimulants, medications such as beta blockers and calcium channel blockers, and even some antidepressants.
“The common denominator in insomnia is hyperarousal and an activation of the HPA axis,” said Narasimhan, who also noted there is an activation of the autonomic nervous system with EEG changes and an increased metabolic rate. There is a shared neurobiology that explains the commonality of insomnia and depression. Candidate genes are currently being studied as well as serotonin gene polymorphisms.
Some of the risk factors for insomnia in depression, Narasimhan said, are age, female sex, single marital status, lower socioeconomic status, sleep abnormalities in endogenous MDD, early morning awakening, increased wakefulness, decreased arousal threshold, prolonged sleep latency, and shortened REM latency, and HPA activation in depression.
“It makes sense to use an antidepressant,” said Narasimhan “We know that they act beyond the surface and in looking at neurotrophic factors, which may in turn explain restoration of homeostasis, they may play role in plasticity.”
Narasimhan suggests that psychiatrists get a good initial assessment in patients with insomnia and psychiatric illness by checking the following:
• sleep history
• a sleep diary
• rule in/out primary psychiatric disorders
• rule out adverse effects of medications
• sleep hygiene measures
• daytime naps
• bedtime mood
• psychotrophic use
• treatments to decrease rates of relapse
“Insomnia and psychiatric disorders go hand in hand and they can overlap in neurobiology substrate and circuitry that require early recognition, accurate diagnosis, and we need to promote treatment,” Narasimhan concluded. “Good sleep hygiene is a vital component of treatment.”
[Presentation title: Making Every Sheep Count: Evidence-Based Approaches to Treating Insomnia. Abstract 581]
By Kristina R. Anderson