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Letter to the Editor

The Association Between PTSD and ADHD: Does the Association Reveal a PTSD-Somatoform Subtype?

Keith Fluegge, BA

Published: September 28, 2016

See reply by Spencer and Biederman and article by Spencer et al

This work may not be copied, distributed, displayed, published, reproduced, transmitted, modified, posted, sold, licensed, or used for commercial purposes. By downloading this file, you are agreeing to the publisher’s Terms & Conditions.

The Association Between PTSD and ADHD: Does the Association Reveal a PTSD-Somatoform Subtype?

To the Editor: Spencer et al1 recently published the findings of their meta-analysis in which they report a robust bidirectional association between attention-deficit/hyperactivity disorder (ADHD) and posttraumatic stress disorder (PTSD). One of the most peculiar results found by Spencer et al was that "the increased risk for PTSD in individuals with ADHD cannot be explained solely by an increased rate of trauma exposure in this population,"1(p80) suggesting other environmental and biological factors may be involved.

Schottenfeld and Cullen2 discussed a PTSD subtype that may clinically present as a somatoform disorder and is quite likely attributable to hypersensitivity to certain occupational-induced exposures including air pollution ("All of the patients with atypical posttraumatic stress disorder attempted to avoid exposure to such odors, often by limiting work, hobbies, or other activities. One patient habitually wore a gas mask whenever she left her house"2[p200]). Giacobo et al3 showed that subjects with ADHD exhibit functional somatic symptoms, suggesting that atypical PTSD may share some physiological similarities with diagnosed ADHD.

Geracioti et al4 demonstrated higher norepinephrine concentrations in the cerebrospinal fluid of male combat veterans versus healthy male controls, suggesting that a heightened central noradrenergic baseline may characterize typical PTSD pathology. Certain environmental exposures, though, may elicit similar neurologic effects as those found in typical PTSD and thus contribute to not only an atypical presentation of PTSD (ie, without trauma) but ADHD as well.

I have previously suggested that daily exposure to certain environmental air pollutants, principally nitrous oxide (N2O), may contribute to the development of neuropathology, including ADHD.5 Zhang et al6 reported that the analgesic action of N2O is thought to involve the release of norepinephrine in the spinal cord and that certain pharmaceutical agents, like naltrexone, can abrogate this action. This pharmacologic property may explain why naltrexone has been repeatedly found to be an effective treatment in the management of PTSD and associated comorbidities.7,8

This discussion posits a neurobiological explanation for the association between PTSD and ADHD, as shown by Spencer et al1 in their meta-analysis. More work is needed to better characterize the nature of this association and the underlying physiological mechanisms and determine whether certain subtypes of the disorders (ie, atypical vs typical PTSD, hyperactive versus inattentive ADHD) are more closely associated than others. Understanding these neurobiological interactions may be helpful for clinicians and scientists in their efforts to better monitor and treat patients with various presentations of the 2 disorders (typical PTSD, atypical PTSD with comorbid ADHD, etc).

References

1. Spencer AE, Faraone SV, Bogucki OE, et al. Examining the association between posttraumatic stress disorder and attention-deficit/hyperactivity disorder: a systematic review and meta-analysis. J Clin Psychiatry. 2016;77(1):72-83. PubMed doi:10.4088/JCP.14r09479

2. Schottenfeld RS, Cullen MR. Occupation-induced posttraumatic stress disorders. Am J Psychiatry. 1985;142(2):198-202. PubMed doi:10.1176/ajp.142.2.198

3. Giacobo RS, Jané MC, Bonillo A, et al. ADHD and functional somatic symptoms: structural equations of a conceptual model. Child Adol Ment H-UK. 2014;19(2):83-89. doi:10.1111/camh.12026

4. Geracioti TD Jr, Baker DG, Ekhator NN, et al. CSF norepinephrine concentrations in posttraumatic stress disorder. Am J Psychiatry. 2001;158(8):1227-1230. PubMed doi:10.1176/appi.ajp.158.8.1227

5. Fluegge K. A reply to Wang T, Shan L, Du L, Feng J, Xu Z, Staal WG, Jia F. Serum concentration of 25-hydroxyvitamin D in autism spectrum disorder: a systematic review and meta-analysis. Eur Child Adolesc Psychiatry. 2016;25(4):453-454. 10.1007/s00787-015-0786-1 PubMed

6. Zhang C, Davies MF, Guo TZ, et al. The analgesic action of nitrous oxide is dependent on the release of norepinephrine in the dorsal horn of the spinal cord. Anesthesiology. 1999;91(5):1401-1407. PubMed doi:10.1097/00000542-199911000-00033

7. Foa EB, Yusko DA, McLean CP, et al. Concurrent naltrexone and prolonged exposure therapy for patients with comorbid alcohol dependence and PTSD: a randomized clinical trial. JAMA. 2013;310(5):488-495. PubMed doi:10.1001/jama.2013.8268

8. Qazi H, Wijegunaratne H, Savajiyani R, et al. Naltrexone and prazosin combination for posttraumatic stress disorder and alcohol use disorder. Prim Care Companion CNS Disord. 2014;16(4):10.4088/PCC.14l01638. 10.4088/PCC.14l01638 PubMed

Keith Fluegge, BAa

[email protected]

aInstitute of Health and Environmental Research, Cleveland, Ohio

Potential conflicts of interest: None.

Funding/support: None.

J Clin Psychiatry 2016;77(9):e1149

dx.doi.org/10.4088/JCP.16lr10630

© Copyright 2016 Physicians Postgraduate Press, Inc.

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