The lack of quality evidence limits the choices of treatments in this area. Most trials have low methodological quality. Few trials provide the results to allow reliable comparisons of different treatments; in such cases comparisons are possible only between treatments without regard to whether the groups were representative of patients in a practice. It is likely that some treatments will be shown to be more effective than others based on their frequency of use; for this reason there is no good evidence as to which treatment is most effective.
There is evidence that many parasomnias, often as a result of psychiatric or other chronic disease, persist irrespective of treatment. The evidence for the use of the anticonvulsant carbamazepine is less convincing and needs further study.
A wide range of potential etiologies can cause parasomnias, ranging from physiological causes (e.g., hyperthyroidism, hypoxic deprivation) to psychological and psychiatric conditions: e.g., anxiety, major depressive disorder, panic disorder, and social phobia. Given that no cure for parasomnias is known, the focus for treatment is on relieving symptoms, addressing triggers, and managing secondary comorbidities. Psychological counseling is also very helpful. Furthermore, most children with behavioral disorders respond well to psychotherapy and/or medication.
In patients who have suffered a traumatic brain injury (TBI), the most common presenting complaint is somnolence. One third of patients with TBI complain of excessive sleepiness and more than one-third reported trouble falling asleep. This suggests that sleep disorders are frequent in traumatic brain injury, and the differential evaluation may help determine a patient's postconcussion syndrome.
About 2 million people are currently or previously diagnosed as having idiopathic paroxysmal hyperkinesia. Paroxysmal hyperkinesia is often associated with other behavioral/organic disorders and is usually not associated with psychiatric disorders. If this is the case, patients will seek medical attention for idiopathic paroxysmal hyperkinesia.
The most common indications are sleep-related behaviours such as snoring, day-time sleepiness, sleep restriction, nocturnal awakenings, sleep terrors and nocturnal enuresis. The prevalence of snoring increases during adolescence, and sleep terrors peak at the age of 25-30 years.
The prevalence of sleep-related parasomnias in the family appears to be similar in healthy and non-healthy first-degree relatives of a patient with somnolence of excessive arousal (SUEA, EDS or hypersomnia), suggesting a genetic component in some families. SUEA is more common in families of sleep onset insomnia patients than in families of EDS patients, suggesting that an alteration of vigilance circadian phase is more likely to occur in the familial environment of EDS patients, than in the familial environment of SUEA patients. The presence of parasomnias has also been associated with a familial trait related to daytime somnolence, namely insomnia nocturnal awakenings or nighttime sleep complaints.
In view of the modest number of patients included in cbt-p, further studies involving larger numbers of patients must be encouraged. However, we have found some interesting aspects of the drug: firstly, it seems effective. Secondly, it may be used with some degree of security with an advantage over hypnotics, which in turn may not be at all effective.
Findings from a recent study found that CBT-p is efficacious in treating sleep and sleep-related symptoms in children for a variety of severities of CPS. Sleep specialists should therefore incorporate CBT-p therapy along with other behavioral, medical, or pharmacological treatment approaches. In children and adolescents, long-term effectiveness for treatment with CBT was determined with minimal residual symptoms at posttreatment. Thus, CBT may be an important treatment avenue for CPS, and future longitudinal studies would be useful to determine CBT's long-term effectiveness.
The main side effect of cbt-p is insomnia and sleepiness at bed time and early morning awakening, sleepiness and a lower quality of sleep in general in the daytime. Other common side effects include dizziness, headache, nausea, constipation, vomiting, rash, urinary urgency and increased appetite.
Parasymnia symptoms occur widely in older patients. One of the most useful tools for the identification of syndromal causes of parasomnias is the assessment of sleep arousal, which can help differentiating among a large number of clinical and pathologic potential causes. If symptoms persist over a period of months to years, it is unlikely to be related to an actual organic cause, and treatment should be directed toward symptomatic treatment with medications most likely to disrupt sleep and sleep apnea-like events, such as a beta1-adrenergic agonist.
The most recent, relevant research suggests that sleep disorders may contribute to the development of parasomnias. Studies have failed to replicate the presence of sleep terrors, but more recent research suggests that other parasomnias, including night terror and sleep-related movement disorders, may be related. It remains unclear whether the relationship between sleep disorders and parasomnias is the result of sleep apnea or other undiagnosed sleep disorders. There is also still a lack of evidence pertaining to the link between sleep disorders and daytime sleep behaviours. Further research, using prospective and longitudinal studies, is needed to elucidate the causal pathway underlying these diverse associations.