Psychosomatics 39:168-171, April 1998
© 1998 The Academy of Psychosomatic Medine
Posttraumatic Stress Disorder and Obstructive Sleep Apnea Syndrome
James M. Youakim, M.D.,
Karl Doghramji, M.D., and
Sharon L. Schutte, M.D.
Received May 30, 1996; revised August 28, 1996; accepted September 20, 1996. From the Sleep Disorders Center, Department of Psychiatry and Human Behavior, Jefferson Medical College, Philadelphia, Pennsylvania. Address reprint requests to Dr. Youakim, 1025 Walnut St., Suite 316, Philadelphia, PA 19107.
Key Words: Case Report • Posttraumatic Stress Disorder • PTSD • Sleep Apnea • Obstructive Sleep Apnea Syndrome • OSAS
Sleep complaints are an essential component of the constellation of symptoms that make up posttraumatic stress disorder (PTSD). Recurrent distressing dreams and difficulty falling asleep or staying asleep are salient features of the disorder.1 Attempts to explain the physiology of PTSD must account for these sleep symptoms. Ross et al.2–4 have suggested that rapid eye movement (REM) sleep mechanisms in particular are dysfunctional in patients with PTSD. Others have reported nightmares episodes during both REM and Stage II sleep.1
Obstructive sleep apnea syndrome (OSAS) is a common disorder in which disturbed breathing during sleep, usually attributable to obstruction of the airway, leads to oxyhemoglobin desaturations with concomitant hypercapnia. The resulting interruptions disrupt normal sleep architecture and lead to excessive daytime somnolence. Obstructive apneas are often more common in REM sleep than in non-REM stages of sleep, because the decreased tone of muscle of the airway during REM is more likely to lead to partial or complete upper airway obstruction. Thus, OSAS generally disrupts the continuity of REM periods and decreases the proportion of REM sleep per night. OSAS also decreases the amount of delta (Stages 3 and 4) sleep. The severity of OSAS is determined by nocturnal polysomnography. The number of abnormal respiratory events per hour of sleep, as determined by polysomnography, is called the apnea-hypopnea index.6
We report the case of a man with PTSD and severe obstructive OSAS whose PTSD symptoms abated when his OSAS was successfully treated. This case supports the notion that treatment of PTSD will be more successful if treatment of sleep complaints is emphasized and if sleep apnea and other sleep disorders are treated aggressively. The possibility of a connection between sleep-disordered breathing and PTSD, as seen in this case and also described elsewhere,7 has implications for understanding the physiology and treatment of PTSD.
Case Report
Mr. A. was a 42-year-old Vietnam veteran who came to the Sleep Disorders Center with a chief complaint of frequently interrupted sleep at night. He also reported a 10-year history of sleep-related symptoms witnessed by his wife. These included snoring that had become progressively louder over the previous 3 years. His wife also reported frequent breathing pauses, lasting at least 10 seconds, when Mr. A. was asleep. Occasionally, he awakened gasping and snorting. He noted that alcohol aggravated these symptoms. In addition, he complained of early morning headaches. He felt fatigued and unrefreshed in the morning despite an adequate amount of sleep.
Mr. A. had gained about 80 lbs. in the previous 10 years. His weight gain seemed to correlate with increased snoring volume.
Daytime symptoms included excessive sleepiness, which had become progressively worse over the past 10 years. He fell asleep readily during inactive situations, such as while reading or watching television. He denied sleep attacks or episodes of cataplexy, hypnagogic hallucinations, or sleep paralysis.
Past psychiatric history was significant for PTSD. The patient had returned from Vietnam in November 1969. PTSD symptoms began in 1970, after the patient was discharged from the hospital for a gunshot wound to the right leg. Nightmares occurred nightly, usually in the early part of the night. These nightmares, permeated by the smells of kerosene and gunpowder, consisted almost exclusively in which friends around him were killed, but he survived. Mr. A. dreaded bedtime, and anticipation of the nightmares made it difficult for him to fall asleep. During the day, the patient had an exaggerated startle response, flashbacks, and intense psychological distress with any exposure to events or substances that evoked memories of Vietnam (such as the smell of diesel fuel and the sound of firecrackers). Mr. A. reported that these symptoms had become more intense over the past 10 years and had necessitated 4 hospitalizations. Pharmacological treatment modalities had included courses of doxepin and other hypnotic agents, which Mr. A. discontinued because of limited success and a feeling of increased grogginess. At the time of presentation to the Sleep Disorders Center, the patient was no longer taking any psychotropic medications. However, he had outpatient appointments as needed with a psychiatrist at a Veterans Affairs clinic.
Past medical history was significant for diabetes mellitus and hypertension. Mr. A. used insulin on a daily basis.
Mr. A. had abused amphetamines during the war. He began heavy alcohol abuse shortly after returning to the United States. He successfully completed a drug detoxification program in 1988 and denied using these or any illicit substances at the time of evaluation. He also denied any consumption of caffeine.
Physical examination was remarkable for a thick, muscular neck; a thick, elongated uvula; and redundant tissue in the oral pharynx. The patient was 71 inches tall and weighed 318 lbs.
Nocturnal polysomnography and daytime multiple sleep latency testing were performed. The first night of testing revealed a large number of apneic events during sleep, the majority of which were of the obstructive type, associated with significant decrements in oxygen desaturation and significant sleep fragmentation, confirming the diagnosis of OSAS (Table 1). The multiple sleep latency test showed a pathologically severe level of daytime somnolence. The patient was treated with continuous positive airway pressure (CPAP) the following night, with tremendous improvement in all sleep parameters. He was titrated to a CPAP pressure of 14 cm H2O.
Mr. A. was seen for follow-up 4 months later. Polysomnographic study showed continued effective control of the patient's obstructive sleep apnea, normalization of his sleep architecture, and a decreased level of daytime somnolence with CPAP treatment (Table 1).
In addition, the patient reported dramatic improvement in his PTSD symptoms, with a decrease in nightmare frequency and intensity and a decreased startle response. The almost-nightly nightmares now occurred monthly, generally when the patient was under unusual stress. The nightmares also shifted in occurrence from the beginning to the end of the night and were usually not as terrifying as they had been before CPAP treatment. On occasion when he awakened, he recalled the same dream content as before, but the dreams were longer and began with events and scenes that were less anxiety-provoking. The effect of the CPAP was limited to its time of use. If his CPAP mask became dislodged, the nightmares returned in their original form.
Mr. A. also noticed a difference in daytime PTSD symptoms that he attributed to the change in his sleep. He could now smell diesel fuel, but he was able to "shake off" flashbacks because he had had "a full night's sleep." (Unfortunately, structured psychiatric assessments of Mr. A. were not done before or after CPAP treatment.) He felt less sleepy during the day. He also began to have pleasant dreams, which had previously been extremely uncommon.
Discussion
It is difficult to draw firm conclusions from a single case. However, the dramatic improvement in Mr. A.'s PTSD symptoms following CPAP treatment invites speculation on possible explanations of these changes based on the changes demonstrated in his sleep following treatment.
Effect on Sleep Architecture and Daytime Sleepiness.
The most dramatic change was the great decrease in the numbers of apneas and hypopneas and the number of associated arousals that caused marked disruption of normal sleep architecture and led to an associated excessive daytime somnolence. The number of arousals, sleep disruption, and daytime somnolence improved with CPAP treatment. It is possible that sleep deprivation and increased daytime somnolence increase susceptibility to posttraumatic flashbacks and other anxiety symptoms. There is evidence that sleep deprivation triggers panic attacks in sleep.8
Effect on REM Sleep.
CPAP treatment led to fewer disruptions of REM sleep and an increased percentage of REM sleep, that is, a reversal of the REM deprivation caused by sleep apnea. The frequent disruptions of REM sleep caused by these arousals might have led to increased recall of dreams occurring in REM sleep. It is also possible that chronic REM deprivation has anxiogenic effects. (Deprivation of delta sleep is another product of chronic sleep apnea, but in Mr. A.'s case, delta sleep did not return even with CPAP treatment and reduction in his PTSD symptoms.)
Effect on Oxygen Saturation.
Sleep apnea caused hypoxemia and presumably concomitant hypercapnia. Hypercapnia has been thought to have anxiogenic properties.9,10 It has also been suggested that the hypercapnia is a mechanism by which sleep deprivation induces panic attacks.11 Treatment of these desaturations with CPAP (from SaO2 as low as 49% on the first night of polysomnography to a lowest SaO2 of 92% with CPAP) may explain the decrease in anxiety symptoms.
The patient's nightmares seemed consistent with descriptions of PTSD dreams as both REM and NREM phenomena: they occurred earlier in the sleep cycle, were accompanied by body movement, and had elaborate content.5 Nightmares were reduced when CPAP restored normal sleep architecture, even though REM sleep was also restored. Therefore, this case does not support the notion that reduction of REM sleep would be therapeutic in PTSD patients.2
Polysomnographic studies of patients with PTSD have shown inconsistent results, but it has been argued that the posttraumatic anxiety dream is a phenomenon of REM sleep.2 Mellman et al.12 found in their sample that symptomatic arousals from sleep in patients with PTSD were disproportionally preceded by REM. Posttraumatic dreams seem to fit the description of dreams recalled from REM sleep more closely than those recalled from non-REM sleep, since they are in general more vivid, longer, more elaborate, and better organized and more easily recalled.13 If posttraumatic dreams are REM-related, as Ross et al.2 have proposed, PTSD patients might benefit from a reduction in REM sleep.
However, there has also been evidence that PTSD dreams occur in both REM and non-REM sleep.5 Traumatic dreams also are more likely to occur in the early part of the night, the time when non-REM sleep predominates over REM sleep and when parasomnias of non-REM sleep are more likely to occur. In addition, posttraumatic dreams are often accompanied by body movements, which are seen commonly in non-REM sleep. Normal REM sleep is characterized by muscle atonia.
Mr. A.'s nightmares seemed consistent with descriptions of PTSD dreams of both REM and non-REM phenomena; they occurred earlier in the sleep cycle, were accompanied by body movements, and had elaborate content. Nightmares were reduced when CPAP restored sleep architecture, even though REM sleep was also restored. Therefore, this case does not support the notion that the reduction of REM sleep would be therapeutic in PTSD patients. Rather, it seems likely that restoration of the quality of sleep architecture, including normal REM cycles, leads to decreased symptoms of PTSD.
We may conclude from this case that reduction of the number of arousals during sleep and of excessive daytime somnolence, whether they are secondary to sleep apnea or to another condition, should be emphasized in the treatment of PTSD. Each of the possible explanations of the association noted between PTSD and disrupted sleep caused by disordered breathing deserves further study.
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