Relationships between REM sleep findings and PTSD symptoms during the early aftermath of trauma.

Laboratory sleep findings in posttraumatic stress disorder (PTSD) have been characterized as incongruent with subjective complaints. Most findings relate to rapid eye movement (REM) sleep. Chronicity confounds relationships between objective sleep and PTSD. The authors report relationships between PTSD symptoms and objective sleep measures from the early aftermath of trauma. Thirty-five patients received polsomnography and PTSD assessment within a month of traumatic injury. Posttraumatic stress disorder status was established at 2 months. The REM segment duration correlated negatively with initial PTSD and insomnia severity, which also correlated with total sleep time. Relative beta frequency during REM sleep from a subset of cases correlated negatively with PTSD and nightmare severity. These findings suggest a link between subjective symptoms and REM sleep phenomena acutely following trauma.

Insomnia.

Effective management of insomnia begins with recognition and adequate assessment. Family doctors and other health care providers such as practice nurses and psychologists should routinely enquire about sleep habits as a component of overall health assessment. Identification and treatment of primary psychiatric disorders, medical conditions, circadian disorders, or specific physiological sleep disorders--eg, sleep apnoea and periodic limb movement disorder--are essential steps in management of insomnia. Conditioned aspects of insomnia can be primary (psychophysiological insomnia) or may complicate sleep disturbance owing to other causes. Approved hypnotic drugs have clearly been shown to improve subjective and objective sleep measures in various short-term situations. Despite widespread use of standard hypnotics and sedating antidepressants for chronic insomnia, their role for this indication still remains to be further defined by research evidence. Non-pharmacological treatments, particularly stimulus control and sleep restriction, are effective for conditioned aspects of insomnia and are associated with durable long-term improvement in sleep.

Headache complaints in relation to nocturnal oxygen saturation among patients with sleep apnea syndrome.

BACKGROUND: Morning headaches are often ascribed to patients with sleep apnea syndrome (SAS) but the etiology of headaches in SAS is unclear. Given the relationship between oxygen and other headache syndromes, nocturnal hypoxia might be one factor contributing to headaches in SAS. METHODS: All subjects 18-80 years of age who were determined to have SAS and who underwent a continuous positive airway pressure trial in our sleep laboratory between March 1, 1997 and March 18, 1998 were considered for inclusion. Subjects were grouped according to whether they endorsed that waking with headaches is a problem for them. Polysomnography and standardized questionnaires were used to test the main hypothesis that patients with SAS and headaches would spend more time at lower oxyhemoglobin levels than those SAS patients without headache. RESULTS: Headache and non-headache patients did not differ in the percentage of time spent with an oxygen saturation less than 90%, either in total sleep time or in rapid eye movement sleep (REM). The headache patients were more likely to be female and spend a lower percentage of time in REM sleep. The REM sleep difference was not accounted for by the use of REM suppressing medications or by depression (as measured by the Zung scale). CONCLUSIONS: These data do not support the hypothesis that the duration of nocturnal hypoxemia relates to headache complaints in patients with SAS. The lower REM sleep percentage and higher variability in REM apnea index among the headache patients warrants further investigation.