Subacute normobaric oxygen and hyperbaric oxygen therapy in drowning, reversal of brain volume loss: A case report

Abstract

A 2-year-old girl experienced cardiac arrest after cold water drowning. Magnetic resonance imaging (MRI) showed deep gray matter injury on day 4 and cerebral atrophy with gray and white matter loss on day 32. Patient had no speech, gait, or responsiveness to commands on day 48 at hospital discharge. She received normobaric 100% oxygen treatment (2 L/minute for 45 minutes by nasal cannula, twice/day) since day 56 and then hyperbaric oxygen treatment (HBOT) at 1.3 atmosphere absolute (131.7 kPa) air/45 minutes, 5 days/week for 40 sessions since day 79; visually apparent and/or physical examination-documented neurological improvement occurred upon initiating each therapy. After HBOT, the patient had normal speech and cognition, assisted gait, residual fine motor and temperament deficits. MRI at 5 months after injury and 27 days after HBOT showed near-normalization of ventricles and reversal of atrophy. Subacute normobaric oxygen and HBOT were able to restore drowning-induced cortical gray matter and white matter loss, as documented by sequential MRI, and simultaneous neurological function, as documented by video and physical examinations.

Full text

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IntroductIon
Pediatric drowning1–3 is treated with normobaric 100%
oxygen to maintain adequate systemic oxygenation.1 Serious
cases cause angiosomic-based4 deep gray matter and cortical5
injury with resultant atrophy/ventricular dilatation.5,6 To our
knowledge and investigation reversal of gray matter (cortical
volume loss) and white matter atrophy (ventricular dilatation)
are unreported with any therapy. We report subacute treatment
of a severe pediatric drowning case with repetitive short-
duration normobaric oxygen and then hyperbaric oxygen that
resulted in visually apparent and/or physical examination-
documented neurological improvement with each therapy and
near-complete reversal of cortical and white matter atrophy
on magnetic resonance imaging (MRI).
case rePort
A 2-year-old girl was resuscitated at Washington Regional
CASE REPORT
Medical Center, Fayetteville, AR, USA, from a Glasgow
Coma Scale (GCS) of 3, xed dilated pupils, and body tem-
perature of 85.1°F (28.9°C) after a 15-minute submersion in
41°F (5°C) water. After 100 minutes of cardio-pulmonary
resuscitation, the arterial pH was 6.53. Following hypo-
thermia, vasopressors, ventilator support (10 days), and
critical care at Arkansas Children’s Hospital, Little Rock,
AR, USA, the patient was discharged home 35 days post
drowning unresponsive to all stimuli, immobile with legs
drawn to chest, and with constant squirming and head
shaking. MRIs at 3 (Figure 1) and 31 (Figure 2) days post
drowning showed thalamic injury then generalized atrophy
with evolving gray and white matter injury.
Author Paul G. Harch was consulted and commenced
2 L/minute nasal cannula 100% oxygen for 45 minutes
twice/day bridging normobaric oxygen therapy at 55 days
post-drowning. Within hours the patient was more alert,
awake, and stopped squirming (see the movie at https://
Subacute normobaric oxygen and hyperbaric oxygen therapy in
drowning, reversal of brain volume loss: a case report
Paul G. Harch1, *, Edward F. Fogarty2
1 Department of Medicine, Section of Emergency Medicine, University Medical Center, Louisiana State University School of
Medicine, New Orleans, LA, USA
2 Department of Radiology, University of North Dakota School of Medicine, Bismarck, ND, USA
*Correspondence to: Paul G. Harch, M.D., paulharchmd@gmail.com or pharch@lsuhsc.edu.
orcid: 0000-0001-7329-0078 (Paul G. Harch)
A 2-year-old girl experienced cardiac arrest after cold water drowning. Magnetic resonance imaging (MRI) showed deep gray mat-
ter injury on day 4 and cerebral atrophy with gray and white matter loss on day 32. Patient had no speech, gait, or responsiveness to
commands on day 48 at hospital discharge. She received normobaric 100% oxygen treatment (2 L/minute for 45 minutes by nasal
cannula, twice/day) since day 56 and then hyperbaric oxygen treatment (HBOT) at 1.3 atmosphere absolute (131.7 kPa) air/45 minutes,
5 days/week for 40 sessions since day 79; visually apparent and/or physical examination-documented neurological improvement oc-
curred upon initiating each therapy. After HBOT, the patient had normal speech and cognition, assisted gait, residual ne motor and
temperament decits. MRI at 5 months after injury and 27 days after HBOT showed near-normalization of ventricles and reversal of
atrophy. Subacute normobaric oxygen and HBOT were able to restore drowning-induced cortical gray matter and white matter loss, as
documented by sequential MRI, and simultaneous neurological function, as documented by video and physical examinations.
Key words: normobaric oxygen; hyperbaric oxygen; drowning; magnetic resonance imaging; brain volume; gray matter; white matter
doi: 10.4103/2045-9912.208521
How to cite this article: Harch PG, Fogarty EF. Subacute normobaric oxygen and hyperbaric oxygen therapy in drowning, reversal of
brain volume loss: a case report. Med Gas Res. 2017;7(2):144-149.
Abstract
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www.youtube.com/watch?v=Pdy9w_3x2Lw&feature=yo
utu.be. Entire movie is pre-, and post-drowning up to pre-
and post-normobaric oxygen therapy, shown at 7 minutes
40 seconds mark and then 9 minutes mark). Neurological
improvement rate increased over the ensuing 23 days with
laughing, increased movement of arms, hands, grasp with
the left hand, partial oral feeding, eye tracking, and short
sentence speech (pre-drowning speech level, but with di-
minished vocabulary). Physical (PT), occupational (OT),
and speech therapy (ST) were added on the 10th day for 2
weeks.
Seventy-eight days post-drowning, hyperbaric oxygen
treatment (HBOT) commenced with compressed air at 1.3
atmosphere absolute (1 ATA = 131.7 kPa) for 45 minutes
total treatment time, once daily. Within hours the patient
experienced decreased tone, increased gross motor ac-
tivity, vocabulary, and alertness. After 10 sessions of
HBOT, the patient’s mother reported that the patient
was “near normal, except for gross motor function;”
PT was then reinstituted. After 39 sessions of HBOT,
the patient exhibited: assisted gait, speech level greater
than pre-drowning, near normal motor function, normal
cognition, improvement on nearly all neurological exam
abnormalities, discontinuance of all medications (buspar,
propranolol, baclofen), and residual emotional, gait, and
temperament decits (Additional Video 1). Gait improve-
ment was documented immediately upon return home at
https://www.youtube.com/watch?v=m2SBmdY4RXg&f
eature=youtu.be. MRI at 27 days after 40-session HBOT
and 162 days post-drowning demonstrated mild residual
injury and near-complete reversal of cortical and white
matter atrophy (Figures 3–6), while further improved
gait was documented at: https://www.youtube.com/watc
h?v=UjtucZa7zmw&feature=youtu.be.
dIscussIon
Due to concern for oxygen toxicity,7,8 continuous nor-
mobaric oxygen in acute cerebral injury is only used for
normalization of systemic oxygenation.1 Short duration
normobaric oxygen has been applied to acute focal stroke9
and traumatic brain injury,10 yet is unexplored in subacute
hypoxic/ischemic encephalopathy (HIE). Short duration
hyperoxia at or slightly above the equivalent level of
normobaric oxygen in our case, in the form of hyperbaric
oxygen or air, has been achieved in chronic toxic brain
injury,11 traumatic brain injury,12,13 autism,14 and cerebral
palsy15,16 where it is used for deoxyribonucleic acid (DNA)
signal transduction17,18 in combination with increased baro-
metric pressure.19,20 Intermittent hyperoxia and increased
atmospheric pressure up- or down-regulate 8,101 genes in
human endothelial cells.21 Sequential application of normo-
baric oxygen and hyperbaric oxygen in our patient caused
visually apparent and/or physical examination-documented
neurological improvements consistent with gene signaling
effects of oxygen and then pressure20 as well as the clinical
effects demonstrated in chronic neurological disorders.11-16
Eight weeks post-drowning, our patient exhibited severe
predictable1,2 neurological decits and MRI ndings4-6,22 that
were reversed by short-duration normobaric oxygen and hy-
perbaric oxygen therapy. The decision to apply normobaric
100% oxygen was dictated by author PGH’s inability to obtain
HBOT in the patient’s location and PGH’s experience using
normobaric 100% oxygen in unpublished cases of chronic
multi-infarct dementia, traumatic brain injury and extremity
ulcers. Cortical cystic lesion and cortical atrophy regression
has been reported in a 2-year-old post-neonatal HIE, but
white matter loss was unchanged.23 Spontaneous regression
Figure 1: Magnetic resonance imaging at 3 days after injury of the
2-year-old girl who experienced cardiac arrest after cold water drowning.
Note: (A) Axial diffusion weighted image at three days post drowning, showing
increased signal from acute ischemic injury to both thalami; (B) Coronal T2
weighted mid thalamic image 3 days post-drowning, showing subtle diffuse
thalamic signal changes, normal ventricles, and normal cortical sulcal cerebro-
spinal uid spaces.
Figure 2: Magnetic resonance imaging at 31 days after injury of
the 2-year-old girl who experienced cardiac arrest after cold water
drowning.
Note: (A) Axial uid attenuated inversion recovery (FLAIR) image at the level of
the basal ganglia at 31 days post-drowning, showing subtle persistent diffuse
signal irregularities in the gray and white matter (yellow arrows), diffuse gray
matter atrophy (enlarged sulcal spaces), and white matter atrophy (enlarged
lateral and third ventricles); (B) Coronal T2 image at the level of the thalami 31
days post-drowning, showing gray matter atrophy with increased cerebro-spinal
uid spaces at temporal and parietal lobes (green arrows) and cerebellar lobes
(red arrows), and white matter atrophy with thinned corpus callosum (yellow
arrow) and enlarged ventricles.
A AB B
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Figure 3: T2 coronal MRI images and axial uid attenuated inversion recovery (FLAIR) image of the 2-year-old girl who experienced cold water drowning.
Note: (A) T2 coronal images at the level of the thalami from left to right at 3, 31, and 162 days post-drowning, showing reversal of white matter and cortical
atrophy. Corpus callosum white matter and temporal lobe gray matter calculations embedded: 3.17, 2.00, 3.57 mm, and 8.10, 6.31, and 7.75 mm, at 3, 31, and
162 days respectively. (B) Axial FLAIR image at the level of the basal ganglia 162 days post-drowning, showing scattered residual signal change in the white
matter (yellow arrows) despite apparent global return to normal tissue volumes. MRI: Magnetic resonance imaging.
Figure 4: Three-dimensional DWI volumes obtained from the level of the pons to the centrum semi-ovale as viewed from a caudal-oblique projection
in the 2-year-old girl who experienced cold water drowning.
Note: Axial images at 3, 31, and 162 days (left to right) post-drowning with iso-contour three-dimensional brain volume calculations of 697, 611, and 696 cm3,
respectively. There is smaller volume and worsening of surface texture in the middle image and reversal of both in the third image. DWI: Diffusion weighted imaging.
Figure 5: Partial T2 coronal MRI images at the level of the thalami at 3, 31, and 162 days post-drowning of the 2-year-old girl who experienced cold
water drowning.
Note: (A) Partial T2 coronal image at the level of the thalami at 3 days post-drowning with right temporal lobe gray matter (2.70
–
3.87 mm) and corpus callosum
white matter (3.71
–
4.11 mm) thickness measurements. (B) Partial T2 coronal image at the level of the thalami 31 days post-drowning with right temporal lobe
gray matter (2.39
–
2.65 mm) and corpus callosum white matter (1.88
–
3.91 mm) thickness measurements. (C) Partial T2 coronal image at the level of the thalami
162 days post-drowning with right temporal lobe gray matter (2.56
–
4.01 mm) and corpus callosum white matter (3.67
–
4.37 mm) thickness measurements. MRI:
Magnetic resonance imaging.
A B
CB
A
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it is impossible to conclude from this single case if the
sequential application of normobaric oxygen then HBOT
would be more effective than HBOT alone.
conclusIon
Short duration normobaric oxygen and hyperbaric oxygen
therapy in the subacute phase of drowning recovery resulted
in video-documented near-complete resolution of severe
neurological decits and near-complete reversal of gray and
white matter atrophy on MRI. Hyperoxic and hyperbaric
gene signaling-induced growth of both gray and white mat-
ter is the most likely explanation.
Acknowledgments
We thank Chris and Kristal Carlson for allowing us to report
the treatment of their daughter, Henry Arnold, a Certicate of
Artistry Media Arts senior student at Lusher Charter School,
New Orleans, LA, USA for his expeditious and skilled editing
of the nal video used in this report, and Juliette Lucarini,
R.N., research nurse for the Family Physicians Center and
Harch Hyperbarics, Inc., New Orleans, LA, USA, for her
counseling/interface with the family during the normobaric
oxygen administration and facilitation of their eight week
sojourn to New Orleans. We would also like to acknowledge
the use of Osirix Open-source workstation software without
which the image analysis would not have been possible.
Author contributions
PGH consulted on the patient during the patient’s hospital-
ization and after discharge from the hospital, evaluated the
patient, performed the hyperbaric treatment, videoed the
patient, drafted, and revised the manuscript. EFF reviewed,
analyzed, chose the representative slices, formatted, and
performed all of the calculations on the imaging, drafted,
and revised the manuscript.
Conflicts of interest
PGH is co-owner of Harch Hyperbarics, Inc., a corporation
that performs hyperbaric medicine consulting and expert
witness testimony/opinions. He is also on the board of di-
rectors of the International Hyperbaric Medical Association
(IHMA), a non-prot corporation. He derives no income
of both cortical and white matter atrophy is contrary to the
natural evolution of non-neonatal HIE.24 T2 signal changes
on days 4 and 32 indicated permanent brain tissue injury or
loss (increased uid spaces) and limited tissue salvage/future
neurological improvement. The diffuse regrowth of tissue
was validated by visual inspection and multiple calculations.
A minimum 12.3% volume loss (86 cm3, underestimated due
to inclusion of enlarged ventricles) was restored to the normal
volume of a 24–36-month-old child.
Functional imaging has been used since 1990 in chronic
neurological disorders,25-43 to document HBOT-induced neu-
rological improvements. These improvements have evaded
anatomical imaging due to the paucity of subacute pediatric
cases, treatment of severe cases with large tissue loss, and the
inability to capture metabolic25,29,30 and microscopic chang-
es,31,35,42,44 including microscopic neurogenesis.42,45 The star-
tling macroscopic regrowth of tissue in this case is explicable
by early intervention prior to long-term tissue degeneration
(e.g., Wallerian degeneration, apoptosis) in a growing child.
The synergy of increased oxygen and increased oxygen with
pressure in the hormone-rich childhood cerebral milieu is con-
sistent with the synergy of growth hormones and hyperbaric
oxygen17,18 caused by normobaric and hyperbaric oxygen-
induced gene signaling trophic,21,46 anti-inammatory,21,46 and
anti-apoptotic effects21,46 on brain tissue.47 Trophism is the
basis of oxygen and hyperbaric oxygen based wound-healing
in animals and humans,48 including central nervous system
injuries48 and is underscored in this patient by the concomitant
rapid neurological improvements.
Substantial animal and human literature has demonstrated
benecial effects of hyperacute HBOT for resuscitation
and post-resuscitation recovery from global ischemia/an-
oxia.49 Late application to drowning patients32,36 and other
global ischemia patients28,49,50 produces more modest effects.
When hyperacute HBOT is precluded by availability or
other non-medical factors bridging short-duration repetitive
normobaric oxygen therapy may be an option until HBOT
is available. Such low-risk medical treatment may have a
profound effect on recovery of function in similar patients
who are neurologically devastated by drowning; however
Figure 6: T2 coronal MRI images of
the thalami in the 2-year-old girl who
experienced cold water drowning.
Note: T2 coronal images at the level of the
thalami of MRI 3 (A), 31 (B), and 162 days
(C) post-drowning with manually drawn
surface area calculations of 77.8, 59.9,
and 72.0 cm2, respectively. MRI: Magnetic
resonance imaging.
A B C
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Harch and Fogarty. / Med Gas Res www.medgasres.com
from the IHMA. EFF is president of the International
Hyperbaric Medical Foundation (IHMF), a non-prot
corporation that promotes education, research, and teach-
ing in hyperbaric medicine. He derives no income from
the IHMF.
Declaration of patient consent
The authors certify that they have obtained all appropriate
patient consent forms. In the form the patient's parents have
given her consent for her images and other clinical infor-
mation to be reported in the journal. The patient’s parents
understand that their names will be published.
Open access statement
This is an open access article distributed under the terms
of the Creative Commons Attribution-NonCommercial-
ShareAlike 3.0 License, which allows others to remix,
tweak, and build upon the work non-commercially, as long
as the author is credited and the new creations are licensed
under the identical terms.
Contributor agreement
A statement of “Publishing Agreement” has been signed
by an authorized author on behalf of all authors prior to
publication.
Plagiarism check
This paper has been checked twice with duplication-
checking software iThenticate.
Peer review
A double-blind and stringent peer review process has been
performed to ensure the integrity, quality and signicance
of this paper.
Open peer reviewers
Reviewer 1, Lei Huang, Loma Linda University, USA;
Reviewer 2, Wen-wu Liu, Second Military Medical Uni-
versity, China.
Additional file
Additional Video 1: Author PGH video exams at hyper-
baric clinic pre- and post-hyperbaric oxygen therapy--Eden
Carlson.
references
1. Szpilman D, Bierens JJ, Handley AJ, Orlowski JP. Drowning.
N Engl J Med. 2012;366:2102-2110.
2. Wagner C. Pediatric submersion injuries. Air Med J. 2009;
28:116-119.
3. Felton H, Myers J, Liu G, Davis DW. Unintentional, non-fatal
drowning of children: US trends and racial/ethnic disparities.
BMJ Open. 2015;5:e008444.
4. Ishaque M, Manning JH, Woolsey MD, Franklin CG, Tullis
EW, Fox PT. Lenticulostriate arterial distribution pathology
may underlie pediatric anoxic brain injury in drowning. Neuro-
image Clin. 2016;11:167-172.
5. Huang BY, Castillo M. Hypoxic-ischemic brain injury: imaging
ndings from birth to adulthood. Radiographics. 2008;28:417-
439; quiz 617.
6. Dubowitz DJ, Bluml S, Arcinue E, Dietrich RB. MR of hy-
poxic encephalopathy in children after near drowning: corre-
lation with quantitative proton MR spectroscopy and clinical
outcome. AJNR Am J Neuroradiol. 1998;19:1617-1627.
7. Semple-Hess J, Campwala R. Pediatric submersion injuries:
emergency care and resuscitation. Pediatr Emerg Med Pract.
2014;11:1-21; quiz 21-22.
8. Gore A, Muralidhar M, Espey MG, Degenhardt K, Mantell
LL. Hyperoxia sensing: from molecular mechanisms to signi-
cance in disease. J Immunotoxicol. 2010;7:239-254.
9. Singhal AB, Benner T, Roccatagliata L, et al. A pilot study of
normobaric oxygen therapy in acute ischemic stroke. Stroke.
2005;36:797-802.
10. Rockswold SB, Rockswold GL, Zaun DA, et al. A prospective,
randomized clinical trial to compare the effect of hyperbaric
to normobaric hyperoxia on cerebral metabolism, intracranial
pressure, and oxygen toxicity in severe traumatic brain injury. J
Neurosurg. 2010;112:1080-1094.
11. Heuser G, Heuser SA, Rodelander D, Aguilera O, Uszler M.
Treatment of Neurologically Impaired Adults and Children
with “Mild” Hyperbaric Oxygen (1.3ATA and 24% Oxygen).
The Proceedings of the 2nd International Symposium on Hy-
perbaric Oxygenation for Cerebral Palsy and the Brain-Injured
Child; 2002; Flagstaff.
12. Wolf G, Cifu D, Baugh L, Carne W, Profenna L. The effect
of hyperbaric oxygen on symptoms after mild traumatic brain
injury. J Neurotrauma. 2012;29:2606-2612.
13. Miller RS, Weaver LK, Bahraini N, et al. Effects of hyperbaric
oxygen on symptoms and quality of life among service mem-
bers with persistent postconcussion symptoms: a randomized
clinical trial. JAMA Intern Med. 2015;175:43-52.
14. Rossignol DA, Rossignol LW, Smith S, et al. Hyperbaric treat-
ment for children with autism: a multicenter, randomized, dou-
ble-blind, controlled trial. BMC Pediatr. 2009;9:21.
15. Collet JP, Vanasse M, Marois P, et al. Hyperbaric oxygen for
children with cerebral palsy: a randomised multicentre trial.
HBO-CP Research Group. Lancet. 2001;357:582-586.
16. Mukherjee A, Raison M, Sahni T, et al. Intensive rehabilita-
tion combined with HBO2 therapy in children with cerebral
palsy: a controlled longitudinal study. Undersea Hyperb Med.
2014;41:77-85.
17. Siddiqui A, Davidson JD, Mustoe TA. Ischemic tissue oxygen
capacitance after hyperbaric oxygen therapy: a new physiolog-
ic concept. Plast Reconstr Surg. 1997;99:148-155.
18. Zhao LL, Davidson JD, Wee SC, Roth SI, Mustoe TA. Effect
of hyperbaric oxygen and growth factors on rabbit ear ischemic
ulcers. Arch Surg. 1994;129:1043-1049.
19. Macdonald AG, Fraser PJ. The transduction of very small hy-
drostatic pressures. Comp Biochem Physiol A Mol Integr Physi-
ol. 1999;122:13-36.
20. Chen Y, Nadi NS, Chavko M, Auker CR, McCarron RM.
Microarray analysis of gene expression in rat cortical neu-
rons exposed to hyperbaric air and oxygen. Neurochem Res.
2009;34:1047-1056.
21. Godman CA, Chheda KP, Hightower LE, Perdrizet G, Shin
DG, Giardina C. Hyperbaric oxygen induces a cytoprotective
and angiogenic response in human microvascular endothelial
cells. Cell Stress Chaperones. 2010;15:431-442.
[Downloaded free from http://www.medgasres.com on Friday, July 7, 2017, IP: 154.16.64.198]

Medical Gas Research ¦ June ¦ Volume 7 ¦ Issue 2 149
Harch and Fogarty. / Med Gas Res www.medgasres.com
22. Grant PE, Yu D. Acute injury to the immature brain with hy-
poxia with or without hypoperfusion. Radiol Clin North Am.
2006;44:63-77, viii.
23. Bekiesinska-Figatowska M, Borszewska-Kornacka MK, Antc-
zak-Marach D, Szczepanik E. Regression of cystic lesions on
brain MRI in a child with hypoxic-ischemic encephalopathy
treated with selective head cooling. Ginekol Pol. 2013;84:151-
156.
24. Gutierrez LG, Rovira A, Portela LA, Leite Cda C, Lucato LT.
CT and MR in non-neonatal hypoxic-ischemic encephalopa-
thy: radiological ndings with pathophysiological correlations.
Neuroradiology. 2010;52:949-976.
25. Neubauer RA, Gottlieb SF, Kagan RL. Enhancing "idling" neu-
rons. Lancet. 1990;335:542.
26. Neubauer RA, Gottlieb SF, Miale A, Jr. Identication of hypo-
metabolic areas in the brain using brain imaging and hyperbaric
oxygen. Clin Nucl Med. 1992;17:477-481.
27. Neubauer RA, James P. Cerebral oxygenation and the recover-
able brain. Neurol Res. 1998;20 Suppl 1:S33-36.
28. Golden ZL, Neubauer R, Golden CJ, Greene L, Marsh J, Mleko
A. Improvement in cerebral metabolism in chronic brain injury
after hyperbaric oxygen therapy. Int J Neurosci. 2002;112:119-
131.
29. Van Meter KW, Weiss L, Harch PG, et al. Should the pressure
be off or on in the use of oxygen in the treatment of carbon
monoxide-poisoned patients? Ann Emerg Med. 1994;24:283-
288.
30. Harch PG, Van Meter KW, Neubauer RA, Gottlieb SF. Use of
HMPAO SPECT for assessment of response to HBO in isch-
emic/ hypoxic encephalopathies. In: Jain KK, ed. Textbook of
Hyperbaric Medicine. Seattle: Hogrefe & Huber Publishers;
1996:480-491.
31. Harch PG. Late treatment of decompression illness and use of
SPECT brain imaging. Treatment of Decompression Illness,
45th Workshop of the Undersea and Hyperbaric Medical So-
ciety; Undersea and Hyperbaric Medical Society, Kensington,
MD, USA. 1996; pp203-242.
32. Harch PG, Neubauer RA. Hyperbaric oxygen therapy in global
cerebral ischemia/anoxia and coma, Chapter 18. In: Jain KK,
ed. Textbook of Hyperbaric Medicine. Seattle: Hogrefe & Hu-
ber Publishers; 1999:318-349.
33. Harch PG, Neubauer RA, Uszler JM, James PB, Maxeld W.
Functional imaging. In: Jain KK, ed. Textbook of Hyperbaric
Medicine. Seattle: Hogrefe & Huber Publishers; 1999:616-625.
34. Van Meter K, Weiss L, Harch PG. Hyperbaric oxygen in emer-
gency medicine. In: Jain KK, ed. Textbook of Hyperbaric Medi-
cine. Seattle: Hogrefe & Huber Publishers; 1999:556-589.
35. Barratt DM, Harch PG, Van Meter K. Decompression illness in
divers: a review of the literature. Neurologist. 2002;8:186-202.
36. Harch PG. The Dosage of Hyperbaric Oxygen in Chronic Brain
Injury. The Proceedings of the 2nd International Symposium on
Hyperbaric Oxygenation for Cerebral palsy and the Brain-In-
jured Child. James T. Joiner (ed.). Best Publishing Co., Flag-
staff, AZ, USA. 2002; pp31-56.
37. Harch PG, Neubauer RA, Uszler JM, James PB. Appendix: di-
agnostic imaging and hbo therapy, Chapter 41. In: Jain KK, ed.
Textbook of Hyperbaric Medicine. Seattle: Hogrefe & Huber
Publishers; 2004:471-485.
38. Harch PG, Neubauer RA. Hyperbaric oxygen therapy in global
cerebral ischemia/anoxia and coma, Chapter 18. In: Jain KK,
ed. Textbook of Hyperbaric Medicine. Seattle: Hogrefe & Hu-
ber Publishers; 2004:223-261.
39. Neubauer V, Neubauer RA, Harch PG. HBO in the manage-
ment of cerebral palsy, Chapter 21. In: Jain KK, ed. Textbook
of Hyperbaric Medicine. Seattle: Hogrefe & Huber Publishers;
2004:287-296.
40. Harch PG, McCullough VE. The Oxygen Revolution. New
York: Hatherleigh Press; 2007.
41. Harch PG, Fogarty EF, Staab PK, Van Meter K. Low pressure
hyperbaric oxygen therapy and SPECT brain imaging in the
treatment of blast-induced chronic traumatic brain injury (post-
concussion syndrome) and post traumatic stress disorder: a
case report. Cases J. 2009;2:6538.
42. Harch PG, Andrews SR, Fogarty EF, et al. A phase I study
of low-pressure hyperbaric oxygen therapy for blast-induced
post-concussion syndrome and post-traumatic stress disorder. J
Neurotrauma. 2012;29:168-185.
43. Boussi-Gross R, Golan H, Fishlev G, et al. Hyperbaric oxy-
gen therapy can improve post concussion syndrome years after
mild traumatic brain injury-randomized prospective trial. PLoS
One. 2013;8:e79995.
44. Palmer AC, Calder IM, Yates PO. Cerebral vasculopathy in
divers. Neuropathol Appl Neurobiol. 1992;18:113-124.
45. Harch PG, Kriedt C, Van Meter KW, Sutherland RJ. Hyper-
baric oxygen therapy improves spatial learning and memory
in a rat model of chronic traumatic brain injury. Brain Res.
2007;1174:120-129.
46. Kendall AC, Whatmore JL, Harries LW, Winyard PG, Eggle-
ton P, Smerdon GR. Different oxygen treatment pressures alter
inammatory gene expression in human endothelial cells. Un-
dersea Hyperb Med. 2013;40:115-123.
47. Lin KC, Niu KC, Tsai KJ, et al. Attenuating inammation but
stimulating both angiogenesis and neurogenesis using hyper-
baric oxygen in rats with traumatic brain injury. J Trauma
Acute Care Surg. 2012;72:650-659.
48. Hyperbaric oxygen therapy indications. In: Weaver LK, ed. The
Hyperbaric Oxygen Therapy Committee Report. North Palm
Beach: Best Publishing Co.; 2014.
49. Harch PG. Hyperbaric oxygen therapy in global cerebral isch-
emia/anoxia and coma, Chapter 20. In: Jain KK, ed. Textbook
of Hyperbaric Medicine. Cham: Springer; 2017:269-319.
50. Churchill S, Weaver LK, Deru K, et al. A prospective trial of
hyperbaric oxygen for chronic sequelae after brain injury (HY-
BOBI). Undersea Hyperb Med. 2013;40:165-193.
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