Clinical ReviewInsomnia in central neurologic diseases – Occurrence and management
Introduction
There is increasing awareness that sleep disorders are frequently associated with neurological diseases. Most studies in the field cover the whole array of sleep disorders or focus on excessive daytime sleepiness, periodic limb movement disorder (PLMD), and rapid eye movement (REM) sleep behavior disorder (RBD). Despite its high prevalence ranging from 30 to 100%1 in neurodegenerative disease, the topic of studying insomnia in neurological diseases has been largely neglected. It is assumed that the impact of insomnia on the course and long-term outcome of neurological diseases is underestimated. This may be due to the lack of a specific pathophysiological model of insomnia associated with neurological diseases, which would allow identifying insomnia as a co-morbid sleep disorder or secondary to depression, pain or other features associated with the underlying neurological disease. The World Health Organization developed an interview to assess the general impact of co-morbid diseases in health burden.2 Among the most important factors were neurological disease, insomnia and major depression. To underline the importance of insomnia this article will describe the present state of the art of diagnostic instruments, prevalence and management of insomnia in central neurological diseases.
Section snippets
Definition of insomnia
Insomnia can be classified according to the diagnostic and statistical manual of mental disorders (DSM) IV,3 international classification of sleep disorders (ICSD) 24 or international classification of diseases (ICD) 10. The criteria for primary (DSM-IV)3 and non-organic insomnia (ICD-10) strongly overlap: difficulty initiating or/and maintaining sleep, non-restorative sleep for at least one month coupled with impaired daytime functioning. DSM-IV3 differentiates primary insomnia from secondary
Pathophysiology of insomnia
The pathophysiology of insomnia per se is not yet fully understood. State of the art models of primary insomnia are mainly based on the hyperarousal concept9 which assumes psychological and physiological hyperarousal at the core of chronic insomnia. Psychobiological studies demonstrated that patients with chronic primary insomnia display increased levels of subjective and autonomous, neuroendocrine, neurophysiologic and brain metabolic activity compared to good sleepers. A widely accepted model
Search strategy
Several electronic literature databases were searched including MEDLINE, PUBMED, EMBASE, WEB OF SCIENCE, and Cochrane. The search was performed for the years 1986–2010 restricted to literature on adult subjects. The search terms were “insomnia in neurologic disease” and “insomnia in central neurologic diseases”. Language was restricted to English.
Selection criteria: The literature had to contain at least a definition of insomnia that is compatible with the standard classification systems. All
Diagnostic instruments for insomnia in neurological disorders
The evaluation of insomnia in patients with neurological disorders requires a detailed medical and sleep history plus a physical and psychiatric examination. Specific sleep diaries to assess sleep habits (bedtimes, etc), sleep parameters (sleep onset latency, wake time after sleep onset, etc), drug and alcohol intake, etc., for periods of 7–14 days should be filled out by patients regularly on a daily basis.24 The Pittsburgh Sleep Quality Index,25 Sleep Disorders Questionnaire,26 and Insomnia
Frequency of insomnia in neurological disorders
Studies reporting the frequency of insomnia in central neurological diseases are summarized in Table 1.
Management of insomnia in neurological diseases
The first step in managing insomnia in neurological diseases is to establish a correct diagnosis. If the sleep disorder is co-morbid with a medical or psychiatric condition such as pain, depression, anxiety, or RLS, the underlying disease has to be treated. However, if the treatment of the co-morbid disorder alone does not relieve insomnia a management of insomnia symptoms per se has to be performed to prevent the consequences.
Sleep disorders may be the result of adverse effects of medications
Conclusion
The frequency of insomnia in central neurological diseases is high. Only a few studies on the topic are of sufficient quality. Insomnia definitions used in hitherto published studies are often not in line with the international classifications. There are many confounders like co-morbid depression, pain and/or other sleep disorders that make it difficult to evaluate the impact of one symptom on the burden of disease. In addition the assessment of insomnia by clinical interview and or by
Conflicts of interest
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Yves Dauvilliers has consulted and/or gave talks for UCB Pharma, Cephalon, Sanofi-Aventis, Bioprojet, and Boehringer Ingelheim.
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Geert Mayer is participating in advisory boards of UCB and Sanofi-Aventis. He received speaker’s honoraria from Cephalon, Sanofi-Aventis and UCB and was the recipient of research support from Cephalon and UCB.
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Poul Jennum is participating in an advisory board of UCB
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Dieter Riemann has received speaker’s honoraria from Sanofi-Aventis, Lundbeck, Servier, GSK, Cephalon and
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