pii: jc-17- 00218http://dx.doi.org/10.5664/jcsm.6642
LE TTER S TO T H E EDITOR
Should Hyperarousal and Sleep Fragmentation Be Additional Treatment Targets When Treating OSA in PTSD With CPAP?
Response to Goldstein et al. Advancing treatment of comorbid PTSD and OSA. J Clin Sleep Med. 2017;13(6):843–844 and Lettieri et al. Challenges in the management of sleep apnea and PTSD: is the low arousal threshold an unrealized target? J Clin Sleep Med. 2017;13(6):845–846. Madhulika A. Gupta, MD, FAASM, RST Department of Psychiatry, Schulich School of Medicine and Dentistry, University of Western Ontario, London, Ontario, Canada
Lettieri and colleagues1 and Goldstein and colleagues2 have raised very important points that are central to managing obstructive sleep apnea (OSA) in posttraumatic stress disorder (PTSD). Lettieri and colleagues1 report that the profile of their OSA patients with PTSD is similar to that of OSA patients with the low arousal threshold (LAT) phenotype, who sometimes benefit from use of sedatives that increase the arousal threshold.3 In my experience, the LAT type OSA presentation encountered in the PTSD patient is highly state dependent and variable (ie, OSA associated with LAT occurs only when the patient is experiencing sympathetic activation, hyperarousal, and sleep fragmentation, with resultant upper airway instability). In such situations use of a sedative-hypnotic agent may be beneficial. Alternately, a mood-stabilizing agent such as valproate can prevent the occurrence of extreme sympathetic activation, and/or mitigate the central effects of sympathetic activation in the PTSD patient and decrease sleep fragmentation. Goldstein and colleagues2 very rightly stress the need to approach OSA and PTSD as independent disorders. PTSD is a multidimensional disorder,4 and aspects of PTSD that contribute to OSA are mainly related to hyperarousal, which constitute only a minority of symptoms and do not necessarily directly address acute sleep-related complaints (Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition).4 Changes in global PTSD severity scores may therefore not necessarily reflect statistically significant changes in hyperarousal or sleep symptoms. Among the 20 core PTSD symptoms (Criteria B to E) in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition,4 Criterion E addresses hyperarousal and consists of the following 6 items (2 of the 6 are required for PTSD diagnosis): (1) irritable behavior and angry outbursts, (2) reckless or self-destructive behavior, (3) hypervigilance, (4) exaggerated startle response, (5) problem with concentration, and (6) sleep disturbance (eg, difficulty falling or staying asleep or restless sleep). The selective serotonin reuptake inhibitor/serotonin-norepinephrine reuptake inhibitor antidepressants are the recommended PTSD pharmacotherapies2; they have a pharmacologically activating effect and can further exacerbate the insomnia and OSA in PTSD patients. A systematic review of
the literature concluded that there is limited evidence that valproate reduces hyperarousal symptoms in PTSD.5 Management of OSA in PTSD should also concurrently target underlying hyperarousal and sleep fragmentation. C I TAT I O N Gupta MA. Should hyperarousal and sleep fragmentation be additional treatment targets when treating OSA in PTSD with CPAP? J Clin Sleep Med. 2017;13(6):847. R E FE R E N CES 1. Lettieri CJ, Collen JF, Williams SG. Challenges in the management of sleep apnea and PTSD: is the low arousal threshold an unrealized target? J Clin Sleep Med. 2017;13(6):845–846. 2. Goldstein LA, Colvonen PJ, Sarmiento KF. Advancing treatment of comorbid PTSD and OSA. J Clin Sleep Med. 2017;13(6):843–844. 3. Edwards BA, Eckert DJ, McSharry DG, et al. Clinical predictors of the respiratory arousal threshold in patients with obstructive sleep apnea. Am J Resp Crit Care Med. 2014;190(11):1293–1300. 4. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5th ed. Arlington, VA: American Psychiatric Association; 2013. 5. Adamou M, Puchalska S, Plummer W, Hale AS. Valproate in the treatment of PTSD: systematic review and meta-analysis. Curr Med Res Opin. 2007;23(6):1285–1291.
SUBMISSION & CORRESPONDENCE INFORMATION Submitted for publication April 25, 2017 Submitted in final revised form April 26, 2017 Accepted for publication April 27, 2017 Address correspondence to: Dr. Madhulika A. Gupta, 585 Springbank Drive, Suite 101, London, Ontario, N6J 1H3, Canada; Tel: (519) 641-1001; Fax: (519) 641-1033; Email: [email protected]
D I SCLO S U R E S TAT E M E N T Dr. Gupta has indicated no financial conflicts of interest.
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Journal of Clinical Sleep Medicine, Vol. 13, No. 6, 2017
LE TTER S TO T H E EDITOR
Should Hyperarousal and Sleep Fragmentation Be Additional Treatment Targets When Treating OSA in PTSD With CPAP?
Response to Goldstein et al. Advancing treatment of comorbid PTSD and OSA. J Clin Sleep Med. 2017;13(6):843–844 and Lettieri et al. Challenges in the management of sleep apnea and PTSD: is the low arousal threshold an unrealized target? J Clin Sleep Med. 2017;13(6):845–846. Madhulika A. Gupta, MD, FAASM, RST Department of Psychiatry, Schulich School of Medicine and Dentistry, University of Western Ontario, London, Ontario, Canada
Lettieri and colleagues1 and Goldstein and colleagues2 have raised very important points that are central to managing obstructive sleep apnea (OSA) in posttraumatic stress disorder (PTSD). Lettieri and colleagues1 report that the profile of their OSA patients with PTSD is similar to that of OSA patients with the low arousal threshold (LAT) phenotype, who sometimes benefit from use of sedatives that increase the arousal threshold.3 In my experience, the LAT type OSA presentation encountered in the PTSD patient is highly state dependent and variable (ie, OSA associated with LAT occurs only when the patient is experiencing sympathetic activation, hyperarousal, and sleep fragmentation, with resultant upper airway instability). In such situations use of a sedative-hypnotic agent may be beneficial. Alternately, a mood-stabilizing agent such as valproate can prevent the occurrence of extreme sympathetic activation, and/or mitigate the central effects of sympathetic activation in the PTSD patient and decrease sleep fragmentation. Goldstein and colleagues2 very rightly stress the need to approach OSA and PTSD as independent disorders. PTSD is a multidimensional disorder,4 and aspects of PTSD that contribute to OSA are mainly related to hyperarousal, which constitute only a minority of symptoms and do not necessarily directly address acute sleep-related complaints (Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition).4 Changes in global PTSD severity scores may therefore not necessarily reflect statistically significant changes in hyperarousal or sleep symptoms. Among the 20 core PTSD symptoms (Criteria B to E) in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition,4 Criterion E addresses hyperarousal and consists of the following 6 items (2 of the 6 are required for PTSD diagnosis): (1) irritable behavior and angry outbursts, (2) reckless or self-destructive behavior, (3) hypervigilance, (4) exaggerated startle response, (5) problem with concentration, and (6) sleep disturbance (eg, difficulty falling or staying asleep or restless sleep). The selective serotonin reuptake inhibitor/serotonin-norepinephrine reuptake inhibitor antidepressants are the recommended PTSD pharmacotherapies2; they have a pharmacologically activating effect and can further exacerbate the insomnia and OSA in PTSD patients. A systematic review of
the literature concluded that there is limited evidence that valproate reduces hyperarousal symptoms in PTSD.5 Management of OSA in PTSD should also concurrently target underlying hyperarousal and sleep fragmentation. C I TAT I O N Gupta MA. Should hyperarousal and sleep fragmentation be additional treatment targets when treating OSA in PTSD with CPAP? J Clin Sleep Med. 2017;13(6):847. R E FE R E N CES 1. Lettieri CJ, Collen JF, Williams SG. Challenges in the management of sleep apnea and PTSD: is the low arousal threshold an unrealized target? J Clin Sleep Med. 2017;13(6):845–846. 2. Goldstein LA, Colvonen PJ, Sarmiento KF. Advancing treatment of comorbid PTSD and OSA. J Clin Sleep Med. 2017;13(6):843–844. 3. Edwards BA, Eckert DJ, McSharry DG, et al. Clinical predictors of the respiratory arousal threshold in patients with obstructive sleep apnea. Am J Resp Crit Care Med. 2014;190(11):1293–1300. 4. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5th ed. Arlington, VA: American Psychiatric Association; 2013. 5. Adamou M, Puchalska S, Plummer W, Hale AS. Valproate in the treatment of PTSD: systematic review and meta-analysis. Curr Med Res Opin. 2007;23(6):1285–1291.
SUBMISSION & CORRESPONDENCE INFORMATION Submitted for publication April 25, 2017 Submitted in final revised form April 26, 2017 Accepted for publication April 27, 2017 Address correspondence to: Dr. Madhulika A. Gupta, 585 Springbank Drive, Suite 101, London, Ontario, N6J 1H3, Canada; Tel: (519) 641-1001; Fax: (519) 641-1033; Email: [email protected]
D I SCLO S U R E S TAT E M E N T Dr. Gupta has indicated no financial conflicts of interest.
847
Journal of Clinical Sleep Medicine, Vol. 13, No. 6, 2017
