On date unavailable, commented:

None

On 2016 Jan 10, Paul Harch commented:

The response by Dr. Cifu is non-responsive to the scientific points raised in my Comment. In keeping with the purpose of PubMed Commons, an open, non-personal scientific exchange, the request is repeated to respond to the scientific points raised, specifically: 1. Cifu, et al,¹ and all of the DoD HBOT TBI studies,² are dose-finding non-controlled studies, according to a physiologic scientific definition of HBOT. None of them are sham controlled. 2. Cifu, et al,¹ showed no effect of 3 combination doses of hyperbaric therapy on mTBI PPCS and PTSD except in the 2.0 ATA 100% oxygen group which demonstrated a statistically significant improvement in PTSD symptoms. 3. Cifu, et al,¹ attributes the positive outcomes of civilian and other DoD-sponsored HBOT TBI studies to non-treatment effects such as placebo, relocation to a subtropical environment, Hawthorne Effect, etc., yet 5 of 6 outcomes for Cifu, et al,¹ are not positive. 4. This author is requesting that Dr. Cifu and co-investigators reconcile their neutral results with the positive and negative results of other studies on the same subject population. The maximal salutary environment of Pensacola, FL should have generated the most positive results of all studies, if in fact the outcomes are due to the non-treatment effects enumerated by Cifu, et al,¹ yet it did not. The major differences in all of these studies were the doses of hyperbaric therapy employed. The doses in Cifu, et al¹ were ineffective. 5. The claim that the results of HBOT in acute severe TBI are “inconclusive” is contrary to the results of multiple randomized trials.

The points raised in the previous Comment and this Rebuttal are not “…any of a shifting number or false arguments…” They are the same points raised in the peer-reviewed published Letter to the Editor (LTE),³ of the Wolf/Cifu, et al,⁴ paper which informed the data of Wolf/Cifu, ,⁴ et al, and invalidated their conclusions. To this date, the authors have not responded to this Letter to the Editor. I would ask Dr. Cifu again to review the referenced sampling in that LTE³ and the plethora of scientific literature accumulated over the past 70 years showing that small increases in ambient pressure are bioactive across the entire phylogenetic spectrum, including humans.⁵ This is old science just recently brought to the fore³ in the clinical hyperbaric medicine community and is best described as an inconvenient truth, rather than “ridiculous and embarrassing.” Instead of addressing this science Dr. Cifu has lodged the convenient claim of financial incentive to dismiss my Comment: “…the clinicians and lobbyists who make their livings using HBOT for a wide range of neurologic disorders…” This evasive charge was previously lodged by VA researchers in a critique⁶ of this author’s report⁷ and addressed by this author.⁸ The charge is inconsistent with nearly three decades of basic science and clinical research and more consistent with the conflict of interest of VA researchers.⁸ A final point: in no publication has the claim regarding effectiveness of HBOT in mTBI PPCS been predicated on an exclusive or even dominant anti-inflammatory effect of HBOT. Rather, the argument is based on the known micro-wounding of brain white matter in mTBI,⁹ and the known gene-modulatory,¹⁰ trophic wound-healing effects of HBOT in chronic wounding.¹¹ The preponderance of literature in HBOT-treated chronic wound conditions,¹¹ is contrary to Dr. Cifu’s statement of HBOT as a “useless technology.”<br> The implications of getting this science correct and clarifying the confusion in the medical and lay community caused by the confounding DoD studies’ conclusions are enormous. Millions of civilians and brain-injured military service personnel with PPCS or residual neurocognitive sequelae of moderate and severe TBI can be helped by this biological repair therapy. The only “false hope” by patients would be in Cifu, et al,¹ where the patients, by and large, did not improve. In nearly all other studies where proper doses of hyperbaric therapy were employed the “false hope” resulted in positive outcomes.

References:

1. Cifu DX, et al. J Head Trauma Rehabil. 2013 Sep 18. [Epub ahead of print]. DOI: 10.1097/HTR.0b013e3182a6aaf0.<br>
2. Weaver LK, et al. Undersea Hyper Med. 2012;39(4):807–814.
3. Harch PG. J Neurotrauma. 2013 Oct 11. [Epub ahead of print]. doi:10.1089/neu.2012.2799.
4. Wolf G,et al. J Neurotrauma. 2012;29:1–7.
5. Macdonald AG, Fraser PJ. Comparative Biochemistry and Physiology Part A. 1999;122:13-36.
6. Wortzel HS, et al. J Neurotrauma. 2012;29(14):2421-4.
7. Harch PG, et al. J Neurotrauma. 2012;29:168–185.
8. Harch PG, et al. J Neurotrauma. 2012;29:2425-2430.
9. Ryu J, et al. (2014). Acta Neuropathologica Communications. 2014;2:153.
10. Godman CA, et al. Cell Stress Chaperones. 2010;15:431–442.
11. Gesell LB, ed. Hyperbaric Oxygen Therapy Indications. The Hyperbaric Oxygen Therapy Committee Committee Report. 12th ed. Durham, NC: Undersea and Hyperbaric Medical Society;2008.

On 2016 Jan 03, David X Cifu commented:

Mild Traumatic Brain Injury ("Concussion") of any etiology is a complex injury that typically (>95%) has an excellent and rapid recovery. Individuals who have persistent symptoms for more than 3 months after a concussion will commonly have a number of number of factors (related and not related to the initial mTBI) contributing to the chronicity of their symptoms, which makes further improvement challenging. Multimodal interventions, delivered by knowledgeable and experienced individuals who work in an interdisciplinary fashion, emphasize progressive increases in physical and cognitive activity, stress the importance of a return to normal and full pre-injury activity, de-emphasize the need for diagnostics, encourage self-management to enhance resiliency, avoid unproven and fringe treatments, and utilize psychological techniques (e.g. CBT) to ameliorate behavioral and cognitive dysfunction, are the only proven effective strategies. While current research has identified a potential role for chronic inflammation contributing to neurodegeneration in the miniscule subset of individuals who develop early onset dementia (chronic traumatic encephalopathy), persistent inflammation has not been identified in the vast majority of individuals and has not been associated with the persistence of symptoms. There is no reason to believe that an intervention like HBOT that purports to decrease inflammation would have any meaningful effect on the persistence of symptoms after concussion. Three well-controlled, independent studies (funded by the Department of Defense and published in a range of peer reviewed journals) involving more than 200 active duty servicemen subjects have demonstrated no durable or clinically meaningful effects of HBOT on the persistent (>3 months) symptoms of individuals who have sustained one or more concussions. Despite these scientifically rigorous studies, the clinicians and lobbyists who make their livings using HBOT for a wide range of neurologic disorders (without scientific support) have continued to advocate the use of HBOT for concussion. They purport that either the elevated pressures or the slightly higher than room oxygen content (1.2 vs 1.0) of the sham procedures used as part of the scientific control are confounding the research trials. These claims are ridiculous and embarrassing. These distractors would rather attack highly controlled and peer supported research publications by any of a shifting number or false arguments than admit they are advocating a useless technology. HBOT does not work on any level for the persistent symptoms seen after concussion. As a clinician and an academician, I would never recommend its usage and would advise any patient or clinician to avoid this inappropriate intervention. We have evidence-based and clinically sound treatments for post-concussive symptoms (as noted above). Let's employ these proven tools, help our patients, and cease with purveying false hopes.

On 2016 Jan 02, Paul Harch commented:

Cifu, et al¹ characterize the Department of Defense HBOT TBI studies^1-3 as sham-placebo controlled clinical investigations. A sham group “omits a key therapeutic element of the treatment or procedure under investigation”⁴ and a placebo must be inert.⁵ The key therapeutic elements in hyperbaric therapy are pressure and hyperoxia, neither of which are inert.⁶ Therefore, Cifu et al¹ is neither sham, placebo, nor controlled; all groups contain either increased pressure, hyperoxia, or both.^6,7<br> Cifu, et al¹ define HBOT as involving “…breathing high levels of oxygen…at… at least 1.4 times greater than …(1 atmosphere absolute…ATA)…. ¹ This non-physiologic definition sets an arbitrary threshold for HBOT that excludes the contribution of lesser elevated pressures and degrees of hyperoxia (e.g. 1.39999 ATA hyperbaric oxygen is not HBOT?). Hyperbaric oxygen therapy is a combination intervention of increased pressure and hyperoxia,^6,7 that up- and down-regulates both independent and overlapping pressure and oxygen-sensitive genes^6,8-10 to produce well-known clinical effects.¹¹ Cifu et al¹ purported to test the doses of HBOT in previous publications.^12-14. It did not. Cifu et al¹ studied 3 composite doses of hyperbaric therapy by using different doses of oxygen, a single dose of pressure (2.0 ATA), and changing doses of oxygen and pressure during compression and decompression that have not been previously tested in mTBI/PPCS and PTSD. Cifu, et al¹ stands in contrast to Wolf, et al^2, which initially showed statistically significant beneficial effects of two different composite doses of hyperbaric therapy in mTBI/PPCS and PTSD (1.3 ATA air and 2.4 ATA 100% oxygen), and other studies using 1.5 ATA 100% oxygen.^12,15-17 (Wolf, et al’s² findings have been qualified in a subset analysis that demonstrated a trend toward harm with 2.4 ATA oxygen in PPCS).¹⁸ According to Cifu, et al^1, the results of Wolf, et al² and “…prior case reports^14,19-22 are explained by factors other than the effect of HBO2 on PPCS,” i.e., placebo, relocation, reduced duty schedules, Hawthorne Effect, leisure time and activities in a noncombat, semitropical beach environment, and other non-biologic effects of the hyperbaric chamber experience. This explanation has merit if Cifu, et al’s¹ data were uniformly positive. However, it is not, despite the maximal salutary environment of Pensacola, FL. The most logical explanation for Cifu, et al’s¹ data is the independent and differing bioactivity of different combination doses of pressure and hyperoxia on gene expression. ^9,10 Cifu, et al¹ have demonstrated the ineffectiveness of 2 new composite doses of hyperbaric therapy on PTSD and 3 new doses on PPCS, and the effectiveness of one dose on PTSD. The PPCS findings are consistent with the literature on HBOT in chronic traumatic brain injury cited by Cifu and others^{1-3,6,7,12-16,23} that reveal no evidence for the effectiveness of 2.0 ATA of pressure or oxygen on chronic TBI, and negative/toxic effects ≥ 2.0 ATA in acute severe TBI.^24,25 Cifu, et al¹ finish with a claim that the results of HBOT in acute severe TBI are “inconclusive.” There are five randomized clinical trials on HBOT in acute severe TBI,^26-30 a comparative dosing study,²⁵ and two Cochrane reviews^21,31 demonstrating a significant reduction in mortality^26,28-31 (~60%) and improvement in outcome.^25-27,29,30 There is nothing inconclusive about this data, however it’s inclusion in a report on mTBI PPCS is inappropriate. In summary, Cifu, et al¹ is mis-described as a sham placebo controlled study based on a non-physiologic definition of hyperbaric therapy that omits the bioactivity of increased pressure. On this foundation Cifu, et al¹ combine their data with Wolf, et al² and offer sweeping erroneous conclusions about the effectiveness of hyperbaric therapy in PPCS of mTBI and acute severe TBI. Cifu, et al¹ is a 3 dose study of different combinations of pressure and oxygen that demonstrates the ineffectiveness of two doses of hyperbaric therapy in patients with PPCS and PTSD and the effectiveness of a third dose in PTSD and possibly PPCS. Their data complement the effectiveness of multiple other doses of hyperbaric therapy in mTBI PPCS^{2,12,15-17,23} and PTSD^2,12,15,17 which they refer to incorrectly as showing “no symptom relief with HBO2,” and an animal model of HBOT in chronic mTBI.³² The Cifu,¹ Wolf,² and civilian studies^12,15,16 must be appreciated In terms of the effects of different doses of hyperbaric therapy (increased pressure and hyperoxia) on PPCS and PTSD whose doses have different physiologic and gene profiles. Some of these doses are effective while others are not. Conflict of Interest: The author is the co-owner of Harch Hyperbarics, Inc., a C-corporation that provides expert witness testimony and hyperbaric consulting. References: 1. Cifu DX, et al. J Head Trauma Rehabil. 2013 Sep 18. [Epub ahead of print]. DOI: 10.1097/HTR.0b013e3182a6aaf0.<br> 2. Wolf G, et al.. J Neurotrauma. 2012;29:1–7. 3. Weaver LK, et al. Undersea Hyper Med. 2012;39(4):807–814 4. Sham. Available at: http://www.merriam-webster.com/medical/sham. 5. Placebo. Available at: http://medical-dictionary.thefreedictionary.com/placebo+effect. 6. Harch PG. J Neurotrauma. 2013 Oct 11. [Epub ahead of print]. doi:10.1089/neu.2012.2799. 7. Harch P. Undersea Hyper Med. 2013;40(5):469-70. 8. Godman CA, et al. Cell Stress Chaperones. 2010;15:431–442. 9. Chen Y, et al. Neurochem. Res. 2009; 34:1047–1056. 10. Oh S, et al. Cell Stress and Chaperones. 2008;13:447-458. 11. Gesell LB, ed. Hyperbaric Oxygen Therapy Indications. The Hyperbaric Oxygen Therapy Committee Committee Report. 12th ed. Durham, NC: Undersea and Hyperbaric Medical Society;2008. 12. Harch PG, et al. J Neurotrauma. 2012;29:168–185. 13. Rockswold SB, et al. J Neurosurg. 2010;112:1080–1094. 14. Harch PG. In: Joiner JT, ed. Proceedings of the 2nd International Symposium on Hyperbaric Oxygenation for Cerebral Palsy and the Brain-Injured Child. Flagstaff, AZ: Best Publishing Co;2012:31–56. 15. Harch, PG, et al. Cases Journal. 2009;2:6538. http://casesjournal.com/casesjournal/article/view/6538. 16. Wright JK, et al. Undersea Hyper Med. 2009;36:391–399. 17. Data on Cifu, et al1, Wolf, et al3, and HOPPS Army study presented at the 46th Annual UHMS Scientific Meeting in Orlando, FL 6/15/2013 in a special symposium. 18. Scorza KA, et al. Abstract C27, Friday, 6/14/2013, 8:12 a.m. Undersea and Hyperbaric Medical Society Annual Meeting, Orlando, FL. 19. Rockswold SB, et al. Neurol Res. 2007;29(2):162–172. 20. Bennett MH. Extrem Physiol Med. 2012;1(1):14.<br> 21. Bennett MH, et al. Cochrane Database Syst Rev. 2004;(4):CD004609. 22. McDonaugh M, et al. Arch Phys Med Rehabil. 2004;85(7):1198-1204. 23. Harch PG, et al. Hyperbaric oxygen therapy in global cerebral ischemia/anoxia and coma. In: Jain KK, ed. Textbook of Hyperbaric Medicine, 5th revised edition Chapter 19. Seattle, WA: Hogrefe and Huber Publishers;2009:235–274. 24. Holbach KH, et al. J Neurol. 1977;217:17-30. 25. Holbach, KH. In: Schurmann K, ed. Advances in Neurosurgery, Vol. 1. Berlin: Springer;1973:158-163. 26. Holbach KH, et al. Acta Neurochir (Wien). 1974;30:247–256, (Ger) 27. Artru F., et al. Eur Neurol. 1976;14:310-318. 28. Rockswold GL, et al. J Neurosurg. 1992;76:929–934. 29. Ren H, et al. Chinese Journal of Traumatology (English Edition). 2001;4(4):239-241. 30. Rockswold SB, et al. J Neurosurg. 2013;118(6):1317-28. 31. Bennett MH, et al. Cochrane Database Syst Rev. 2012;12:CD004609. doi: 10.1002/14651858.CD004609.pub3. Review. 32. Harch, PG, et al. Brain Res. 2007. 1174, 120–129.

On 2016 Jan 02, Paul Harch commented:

Cifu, et al¹ characterize the Department of Defense HBOT TBI studies^1-3 as sham-placebo controlled clinical investigations. A sham group “omits a key therapeutic element of the treatment or procedure under investigation”⁴ and a placebo must be inert.⁵ The key therapeutic elements in hyperbaric therapy are pressure and hyperoxia, neither of which are inert.⁶ Therefore, Cifu et al¹ is neither sham, placebo, nor controlled; all groups contain either increased pressure, hyperoxia, or both.^6,7<br> Cifu, et al¹ define HBOT as involving “…breathing high levels of oxygen…at… at least 1.4 times greater than …(1 atmosphere absolute…ATA)…. ¹ This non-physiologic definition sets an arbitrary threshold for HBOT that excludes the contribution of lesser elevated pressures and degrees of hyperoxia (e.g. 1.39999 ATA hyperbaric oxygen is not HBOT?). Hyperbaric oxygen therapy is a combination intervention of increased pressure and hyperoxia,^6,7 that up- and down-regulates both independent and overlapping pressure and oxygen-sensitive genes^6,8-10 to produce well-known clinical effects.¹¹ Cifu et al¹ purported to test the doses of HBOT in previous publications.^12-14. It did not. Cifu et al¹ studied 3 composite doses of hyperbaric therapy by using different doses of oxygen, a single dose of pressure (2.0 ATA), and changing doses of oxygen and pressure during compression and decompression that have not been previously tested in mTBI/PPCS and PTSD. Cifu, et al¹ stands in contrast to Wolf, et al^2, which initially showed statistically significant beneficial effects of two different composite doses of hyperbaric therapy in mTBI/PPCS and PTSD (1.3 ATA air and 2.4 ATA 100% oxygen), and other studies using 1.5 ATA 100% oxygen.^12,15-17 (Wolf, et al’s² findings have been qualified in a subset analysis that demonstrated a trend toward harm with 2.4 ATA oxygen in PPCS).¹⁸ According to Cifu, et al^1, the results of Wolf, et al² and “…prior case reports^14,19-22 are explained by factors other than the effect of HBO2 on PPCS,” i.e., placebo, relocation, reduced duty schedules, Hawthorne Effect, leisure time and activities in a noncombat, semitropical beach environment, and other non-biologic effects of the hyperbaric chamber experience. This explanation has merit if Cifu, et al’s¹ data were uniformly positive. However, it is not, despite the maximal salutary environment of Pensacola, FL. The most logical explanation for Cifu, et al’s¹ data is the independent and differing bioactivity of different combination doses of pressure and hyperoxia on gene expression. ^9,10 Cifu, et al¹ have demonstrated the ineffectiveness of 2 new composite doses of hyperbaric therapy on PTSD and 3 new doses on PPCS, and the effectiveness of one dose on PTSD. The PPCS findings are consistent with the literature on HBOT in chronic traumatic brain injury cited by Cifu and others^{1-3,6,7,12-16,23} that reveal no evidence for the effectiveness of 2.0 ATA of pressure or oxygen on chronic TBI, and negative/toxic effects ≥ 2.0 ATA in acute severe TBI.^24,25 Cifu, et al¹ finish with a claim that the results of HBOT in acute severe TBI are “inconclusive.” There are five randomized clinical trials on HBOT in acute severe TBI,^26-30 a comparative dosing study,²⁵ and two Cochrane reviews^21,31 demonstrating a significant reduction in mortality^26,28-31 (~60%) and improvement in outcome.^25-27,29,30 There is nothing inconclusive about this data, however it’s inclusion in a report on mTBI PPCS is inappropriate. In summary, Cifu, et al¹ is mis-described as a sham placebo controlled study based on a non-physiologic definition of hyperbaric therapy that omits the bioactivity of increased pressure. On this foundation Cifu, et al¹ combine their data with Wolf, et al² and offer sweeping erroneous conclusions about the effectiveness of hyperbaric therapy in PPCS of mTBI and acute severe TBI. Cifu, et al¹ is a 3 dose study of different combinations of pressure and oxygen that demonstrates the ineffectiveness of two doses of hyperbaric therapy in patients with PPCS and PTSD and the effectiveness of a third dose in PTSD and possibly PPCS. Their data complement the effectiveness of multiple other doses of hyperbaric therapy in mTBI PPCS^{2,12,15-17,23} and PTSD^2,12,15,17 which they refer to incorrectly as showing “no symptom relief with HBO2,” and an animal model of HBOT in chronic mTBI.³² The Cifu,¹ Wolf,² and civilian studies^12,15,16 must be appreciated In terms of the effects of different doses of hyperbaric therapy (increased pressure and hyperoxia) on PPCS and PTSD whose doses have different physiologic and gene profiles. Some of these doses are effective while others are not. Conflict of Interest: The author is the co-owner of Harch Hyperbarics, Inc., a C-corporation that provides expert witness testimony and hyperbaric consulting. References: 1. Cifu DX, et al. J Head Trauma Rehabil. 2013 Sep 18. [Epub ahead of print]. DOI: 10.1097/HTR.0b013e3182a6aaf0.<br> 2. Wolf G, et al.. J Neurotrauma. 2012;29:1–7. 3. Weaver LK, et al. Undersea Hyper Med. 2012;39(4):807–814 4. Sham. Available at: http://www.merriam-webster.com/medical/sham. 5. Placebo. Available at: http://medical-dictionary.thefreedictionary.com/placebo+effect. 6. Harch PG. J Neurotrauma. 2013 Oct 11. [Epub ahead of print]. doi:10.1089/neu.2012.2799. 7. Harch P. Undersea Hyper Med. 2013;40(5):469-70. 8. Godman CA, et al. Cell Stress Chaperones. 2010;15:431–442. 9. Chen Y, et al. Neurochem. Res. 2009; 34:1047–1056. 10. Oh S, et al. Cell Stress and Chaperones. 2008;13:447-458. 11. Gesell LB, ed. Hyperbaric Oxygen Therapy Indications. The Hyperbaric Oxygen Therapy Committee Committee Report. 12th ed. Durham, NC: Undersea and Hyperbaric Medical Society;2008. 12. Harch PG, et al. J Neurotrauma. 2012;29:168–185. 13. Rockswold SB, et al. J Neurosurg. 2010;112:1080–1094. 14. Harch PG. In: Joiner JT, ed. Proceedings of the 2nd International Symposium on Hyperbaric Oxygenation for Cerebral Palsy and the Brain-Injured Child. Flagstaff, AZ: Best Publishing Co;2012:31–56. 15. Harch, PG, et al. Cases Journal. 2009;2:6538. http://casesjournal.com/casesjournal/article/view/6538. 16. Wright JK, et al. Undersea Hyper Med. 2009;36:391–399. 17. Data on Cifu, et al1, Wolf, et al3, and HOPPS Army study presented at the 46th Annual UHMS Scientific Meeting in Orlando, FL 6/15/2013 in a special symposium. 18. Scorza KA, et al. Abstract C27, Friday, 6/14/2013, 8:12 a.m. Undersea and Hyperbaric Medical Society Annual Meeting, Orlando, FL. 19. Rockswold SB, et al. Neurol Res. 2007;29(2):162–172. 20. Bennett MH. Extrem Physiol Med. 2012;1(1):14.<br> 21. Bennett MH, et al. Cochrane Database Syst Rev. 2004;(4):CD004609. 22. McDonaugh M, et al. Arch Phys Med Rehabil. 2004;85(7):1198-1204. 23. Harch PG, et al. Hyperbaric oxygen therapy in global cerebral ischemia/anoxia and coma. In: Jain KK, ed. Textbook of Hyperbaric Medicine, 5th revised edition Chapter 19. Seattle, WA: Hogrefe and Huber Publishers;2009:235–274. 24. Holbach KH, et al. J Neurol. 1977;217:17-30. 25. Holbach, KH. In: Schurmann K, ed. Advances in Neurosurgery, Vol. 1. Berlin: Springer;1973:158-163. 26. Holbach KH, et al. Acta Neurochir (Wien). 1974;30:247–256, (Ger) 27. Artru F., et al. Eur Neurol. 1976;14:310-318. 28. Rockswold GL, et al. J Neurosurg. 1992;76:929–934. 29. Ren H, et al. Chinese Journal of Traumatology (English Edition). 2001;4(4):239-241. 30. Rockswold SB, et al. J Neurosurg. 2013;118(6):1317-28. 31. Bennett MH, et al. Cochrane Database Syst Rev. 2012;12:CD004609. doi: 10.1002/14651858.CD004609.pub3. Review. 32. Harch, PG, et al. Brain Res. 2007. 1174, 120–129.

On 2016 Jan 03, David X Cifu commented:

Mild Traumatic Brain Injury ("Concussion") of any etiology is a complex injury that typically (>95%) has an excellent and rapid recovery. Individuals who have persistent symptoms for more than 3 months after a concussion will commonly have a number of number of factors (related and not related to the initial mTBI) contributing to the chronicity of their symptoms, which makes further improvement challenging. Multimodal interventions, delivered by knowledgeable and experienced individuals who work in an interdisciplinary fashion, emphasize progressive increases in physical and cognitive activity, stress the importance of a return to normal and full pre-injury activity, de-emphasize the need for diagnostics, encourage self-management to enhance resiliency, avoid unproven and fringe treatments, and utilize psychological techniques (e.g. CBT) to ameliorate behavioral and cognitive dysfunction, are the only proven effective strategies. While current research has identified a potential role for chronic inflammation contributing to neurodegeneration in the miniscule subset of individuals who develop early onset dementia (chronic traumatic encephalopathy), persistent inflammation has not been identified in the vast majority of individuals and has not been associated with the persistence of symptoms. There is no reason to believe that an intervention like HBOT that purports to decrease inflammation would have any meaningful effect on the persistence of symptoms after concussion. Three well-controlled, independent studies (funded by the Department of Defense and published in a range of peer reviewed journals) involving more than 200 active duty servicemen subjects have demonstrated no durable or clinically meaningful effects of HBOT on the persistent (>3 months) symptoms of individuals who have sustained one or more concussions. Despite these scientifically rigorous studies, the clinicians and lobbyists who make their livings using HBOT for a wide range of neurologic disorders (without scientific support) have continued to advocate the use of HBOT for concussion. They purport that either the elevated pressures or the slightly higher than room oxygen content (1.2 vs 1.0) of the sham procedures used as part of the scientific control are confounding the research trials. These claims are ridiculous and embarrassing. These distractors would rather attack highly controlled and peer supported research publications by any of a shifting number or false arguments than admit they are advocating a useless technology. HBOT does not work on any level for the persistent symptoms seen after concussion. As a clinician and an academician, I would never recommend its usage and would advise any patient or clinician to avoid this inappropriate intervention. We have evidence-based and clinically sound treatments for post-concussive symptoms (as noted above). Let's employ these proven tools, help our patients, and cease with purveying false hopes.