Showing posts with label brain. Show all posts
Showing posts with label brain. Show all posts

Friday, September 20, 2013

Autism marked by Brain Inflammation. HBO reduces inflammation!



Autism Marked by Widespread Brain Inflammation

HBOT reduces the inflammation and restores circulation!


NEW YORK (Reuters Health) Nov 18 - Brains obtained at autopsy from autism patients show widespread neuroglial activation and inflammation, according to a report in the November 15th online edition of Annals of Neurology.

Despite suggestions that immune dysfunction plays a role in the pathogenesis of autism, the authors explain, neuropathological studies have given little attention to immune and neuroglial activity in autism.
Dr. Carlos A. Pardo from Johns Hopkins University School of Medicine, Baltimore, and colleagues studied brain tissues obtained at autopsy from 11 autistic patients and cerebrospinal fluid from 6 living autistic patients.  Neuropathological examination of autistic brains revealed extensive neuroglial responses, along with patchy loss of neurons in the Purkinje cell layer and granular cell layer of the cerebellum.  "The marked neuroglial activity in the cerebellum is consistent with previous observations that the cerebellum is one focus of pathological abnormalities in morphological and neuroimaging studies of patients with autism," Dr. Pardo commented.  There was, however, no evidence of adaptive immune reactions in autistic brains, the authors report.

Brain tissues from autistic patients showed increased levels of proinflammatory cytokines, the results indicate, particularly in the region of the anterior cingulate gyrus. Cytokines originated principally from reactive astrocytes.

Cerebrospinal fluid from living autistic patients showed significant increases in MCP-1, IL-6, IFN-gamma, IL-8, MIP-1beta, and other proinflammatory cytokines and modulatory cytokines.
"These cytokines play important roles in immune mediated processes, and their presence in the CSF in autistic patients may reflect an ongoing stage of inflammatory reactions likely associated with neuroglial activation and/or neuronal injury," Dr. Pardo explained.  "At present, there is no indication for using anti-inflammatory medications in patients with autism," Dr. Pardo cautioned. "There are ongoing experimental studies to examine the effect of drugs that limit the activation of microglia and astrocytes, but their use in humans must await further evidence of their efficacy and safety."

Hyperbaric Oxygen Therapy is known for its ability to dramatically reduce inflammation!


Ann Neurol 2004.
Printed with Permission
Rapid Recovery Hyperbarics 909-889-7626
www.hbot4u.com

Wednesday, June 27, 2012

HBOT after Blast Brain Injury, Study


Hyperbaric Oxygen Treatment after the Blast Injury of Rabbitbrain the Expression of AQP4 and PWI in the Study Phase

Title
Hyperbaric Oxygen Treatment after the Blast Injury of Rabbit brain the Expression of AQP4 and PWI in the Study Phase
Abstract
Objective:To establish explosive brain injury model in rabbits;To investigate the expression of aquaporin 4(AQP4) in model of explosive brain of rabbits injury,and perfusion changes in the expression, to explore the formation of brain edema after blast injury mechanism, and early hyperbaric oxygen treatment of traumatic brain edema formation and development of the role of early treatment for clinical hyperbaric oxygen provide the basis for traumatic brain edema.Method:30 New Zealand white rabbits, weighing 2.0 ~ 2.5kg, in accordance with the vertical distance between the detonators and the skull group, were randomly divided into groups 5.0cm, 6.5cm group, 8.0cm group, n = 10. 600mg TNT equivalent of paper detonators were used to explode respectively 5.0cm, 6.5cm, and 8.0cm vertical distance from the top of the rabbit head, observing animal survival after injury, and using magnetic resonance imaging methods to understand the pathology and brain damage in each group.150 New Zealand rabbits were randomly divided into non-treatment group, treatment group and control group, and 10 rabbits were in the latter. Explosive brain injury model was made by paper detonator. Injuryed rabbits were randomly divided into 1h6h12h24h72h7d14d ,14 groups according to a further killed time points after injury, and each group has 10 rabbits. Using dry weight to measure the content water in brain tissue, and using RT-PCR method and image analysis to detect the group at different time points aquaporin 4 (AQP4)mRNA expression, and Western blotting to measure the expression of AQP-4 in brain tissue. Using magnetic resonance perfusion imaging ( PWI) injury time points detected in brain tissue blood perfusion. Finally, it was used for statistical analysis.Results:5 rabbits died immediately after injury and 4 rabbits died within 3 days in group 5.0cm,and only one survived more than 7 days;The rabbit has appeared most extensive brain contusion, cortical surface vessel rupture occurs, and significant fragmentation in brain tissue, large subdural hematoma, and significant brain stem contusion. All rabbits in group 6.5cm survived more than 7 days,except that 1 rabbit died on the 4th day after injury because of inability eating. 4 rabbits occurred epilepsy and got paralysis of limbs; Pathology observed in the survival of the rabbits had cerebral cortex partial rupture of blood vessels, brain edema and obvious laceration and contusion lesions clear boundary with the surrounding brain tissue. All rabbits in group 8.0cm survived, but showed no significant changes in the brain.Blast injury after contusion brain 1h aquaporin 4 (AQP4) mRNA expression increased, and in turn increased, 72h peak (P <0.05), 7d pm down. Brain tissue aquaporin 4 (AQP4) began to express 1h after injury increases, and 72h reached its peak (P <0.05), it turned to down after 7d, but it still maintained on a high level. Brain tissue water content and water aquaporin 4 (AQP4) expression were the same. The correlation analysis, aquaporin 4 (AQP4) expression and brain tissue water content was positively correlated (r=0.8767,P<0.001). The hyperbaric oxygen treatment, aquaporin 4 (AQP4) expression at different time points are different degrees of decline, aquaporin 4 (AQP4) expression of injury group compared with control group at after 6h points were lower (P <0.05 ). Blast injury after contusion brain 1h AQP4 mRNA expression increased, and in turn increased, 72h peak (P <0.05), 7d pm down, but still maintain a high level. After intervention by hyperbaric oxygen, in 6h, AQP4 mRNA expression was significantly lower than the injury to 14d is still significantly lower (P <0.05). Post-traumatic cerebral contusion early peripheral blood perfusion decreased significantly to 6 hours after injury, blood perfusion decreased to the lowest (P <0.05), then gradually increased, and maintain a perfusion (close to the control group) for 2 weeks. The hyperbaric oxygen treatment group than in the early trauma group (1-6 hours after injury) perfusion decreased more significantly. 12 hours after infusion began to rise, and non-treatment group was essentially flat.Conclusion:Detonators and the vertical distance of the skull 6.5cm, can produce good stability, repeatability strong blast injury model of rabbit brain.The expression of post-traumatic brain aquaporin 4 (AQP4) in traumatic brain is closely related to the formation and development of injury and brain edema. Aquaporin 4 (AQP4) expression may be associated with brain ischemia and hypoxia in the Hyperbaric oxygen intervention aquaporin 4 (AQP4) expression was significantly reduced. Instead, the blood perfusion than the control group and non-treatment group decreased significantly, suggesting that brain tissue oxygen levels of early trauma and aquaporin 4 (AQP4) expression is closely related to early hyperbaric oxygen therapy on the relief plays an important role in traumatic brain edema. Early hyperbaric oxygen therapy can improve cerebral blood oxygen contusion, increased blood oxygen content, ease the secondary cerebral hypoxia caused by cerebral edema.

Friday, March 16, 2012

HBOT & Blast-induced Traumatic Brain Injury and PTSD, military


Journal List > Cases J > v.2; 2009 Formats: Abstract | Full Text | PDF (360K)
Cases J. 2009; 2: 6538. Published online 2009 June 9. doi: 10.1186/1757-1626-0002-0000006538 PMCID: PMC2740054 Copyright ©2009 licensee BioMed Central Ltd.


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 Paul G Harch,1 Edward F Fogarty,2 Paul K Staab,1 and Keith Van Meter1 1Section of Emergency Medicine, Department of Medicine, Louisiana State University Health Sciences Center, 2021 Perdido St, Room W535, New Orleans, Louisiana, 70112, USA 2Department of Radiology, University of North Dakota School of Medicine and Health Sciences, Post Office Box 1975, 515 ½ East Broadway Avenue, Suite 106, Bismarck, North Dakota, 58502, USA Corresponding author. Paul G Harch: paulharchmd@aol.com; Edward F Fogarty: efogarty@medicine.nodak.edu; Paul K Staab:pstaab@wjmc.org; Keith Van Meter: kvanmeter@aol.com Received March 12, 2009; Accepted April 4, 2009. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. This article has been cited by other articles in PMC. Other Sections▼

Abstract A 25-year-old male military veteran presented with diagnoses of post concussion syndrome and post traumatic stress disorder three years after loss of consciousness from an explosion in combat. The patient underwent single photon emission computed tomography brain blood flow imaging before and after a block of thirty-nine 1.5 atmospheres absolute hyperbaric oxygen treatments. The patient experienced a permanent marked improvement in his post-concussive symptoms, physical exam findings, and brain blood flow. In addition, he experienced a complete resolution of post-traumatic stress disorder symptoms. After treatment he became and has remained employed for eight consecutive months. This case suggests a novel treatment for the combined diagnoses of blast-induced post-concussion syndrome and post-traumatic stress disorder.

Other Sections▼ Introduction By January, 2008 it was estimated that as many as 300,000 servicemen and women from the current Iraq and Afghanistan Wars have PTSD or major depression, 320,000 have experienced a TBI, and 82,000 have all three diagnoses [1]. Treatment is available for PTSD and depression, but there is no proven therapy for the dual diagnoses of PTSD and the residual effects of TBI, the PCS [2]. HBOT is the use of greater than atmospheric pressure oxygen in an enclosed chamber to treat basic disease processes [3]. HBOT has been traditionally applied to certain emergent conditions and chronic wound conditions, but not to blast-induced TBI/PCS or PTSD. This case report is the first application of the authors' low pressure HBOT protocol for chronic brain injury to blast-induced TBI/PCS and PTSD. An early version of this protocol was recently reported in an animal model of chronic TBI that duplicated the human experience [4].

Other Sections▼ Case presentation A 25-year-old retired Caucasian male U.S. Marine presented with headaches, tinnitus, and sleep disturbance. Three years before evaluation the patient sustained LOC (a few minutes) from an IED explosion with anterograde memory loss and confusion (one hour), and persistent right ear tinnitus, headaches, imbalance, and sleep disturbance. He developed PTSD symptoms within 3 months and experienced six more explosions with near LOC within 15 months. After medical evaluation diagnoses were TBI/PCS, PTSD, depression, hearing loss, and tinnitus. Prioritized Symptom List: 1) Constant headaches with intermittent confusion, irritability, tunnel vision, and dizziness, 2) Bilateral tinnitus, 3) Sleep disruption, 4) Left eye blurred vision, 5) Irritability, 6) Depression, social withdrawal; Additional Symptoms: 7) Fatigue, 8) Decreased hearing, 9) Imbalance, 10) Cognitive problems-memory, attention, decreased speed of thinking, 11) Back pain, 12) Bilateral knee pain, 13) PTSD symptoms: intrusive thoughts, combat thoughts, nightmares, tachycardia.
Med-Surg, Medications: None. FH, ROS, and PHIS: non-contributory or negative.PSH: Engaged, no children, lives with parents, 3 years college education, no tobacco or drugs, one to two beers/week. Neuro PEx Abnormalities: Slight deviation of right eye laterally, bilateral: decreased hearing to softly rubbing fingers at one foot, noxious response to 512 Hz tuning fork, decreased finger tapping speed, unstable: rotation exam, tandem gait, and Romberg. Treatment and testing: MRI brain-normal. SPECT brain imaging pre-HBOT and 72 h after the 39th HBOT.

The patient underwent 39 HBOT's in 26 calendar days at 1.5 ATA/60 minutes total dive time, twice/day, five days/week in a monoplace chamber with 100% oxygen. Outcome: Headache permanently gone after the 1st HBOT. After 12 HBOT's symptoms 3, 6, and 7 improved. At 25th HBOT absence of PTSD symptoms. Re-evaluation after 37 HBOT's: 1) 4/6 primary problems improved (#'s 1, 3, 5, 6), 2/6 no change, 2) 4/7 additional symptoms improved (7, 9, 10, 13), 3/7 no change, 3) 6/6 abnormal exam findings retested improved, 1 finding not retested (right eye deviation). SPECT: heterogeneous with bilateral frontal and temporal defects-all improved post HBOT. (See Additional file 1, Figures Figures11 and and2.2. (Figure (Figure1):1): Pre-HBOT SPECT brain scan three dimensional surface reconstruction and processed transverse images. Pre-HBOT scan was rendered in three dimensional surface reconstruction format by PJT based on the method developed and taught by Picker International using Picker software. In this method brain blood flow is computer indexed to frontal lobe blood flow. A frontal lobe surface defect was identified on a selected transverse slice. Processed/filtered transverse slices were then featured with a 100% window such that all pixels render a white image. Counts were slowly subtracted by decreasing the window threshold until the defect was visible as a full thickness black defect in the contour of the cortex. As the defect emerged and was registered in proper anatomic proportion to the rest of frontal cortical blood flow the numerical window level was taken as the determination threshold. Three separate determinations were made for each scan and the final threshold taken as an average of the three determinations. The technologist was blind to the final image reconstruction due to software restrictions that only allow threshold determination. The surface reconstruction image at this threshold is featured in the image above. Color is aesthetic. Note bilateral orbital frontal and temporal lobe defects, areas typically injured in traumatic brain injury, consistent with processed transverse images in the right hand columns. Processed images also show an abnormal diffuse heterogeneous pattern of
blood flow. Description of processing is in (SD1). (Figure (Figure2):2):

Post-HBOT SPECT brain scan three dimensional surface reconstruction and processed transverse images. Three dimensional surface image was prepared in identical fashion to the image in Figure Figure1.1. Note relative improvement in brain blood flow to bilateral focal frontal and temporal defects, consistent with processed transverse images in the right hand columns. Transverse slices also show normalization of the blood flow to a more homogeneous pattern.
Figure 1 Pre-HBOT SPECT brain scan three dimensional surface reconstruction and processed transverse images. Note bilateral orbital frontal and temporal lobe defects and diffuse heterogeneous pattern of blood flow.
Figure 2 Post-HBOT SPECT brain scan three dimensional surface reconstruction and processed transverse images. Note relative improvement in brain blood flow to bilateral focal frontal and temporal defects and overall normalization of blood flow to a more homogeneous (more ...) Discussion The present case is the first application of the author's HBOT protocol to blast-induced TBI/PCS and PTSD. The patient's symptomatic, physical exam, and SPECT improvements are similar to ours [3,5,6,9] and others' [7,8] previous cases/case series of non-blast TBI suggesting common pathophysiology. The unexpected result was the complete resolution of PTSD. With the overlap of symptoms, pathophysiology, and anatomy in TBI/PCS and PTSD [10] HBOT is likely impacting common shared targets in this case. Conclusion Thirty-nine low pressure HBOT's caused a reduction in symptoms and signs of chronic mild-moderate blast-induced TBI/PCS and PTSD.
The resolution of symptoms and signs of TBI/PCS and PTSD were reflected in global and focal improvements in brain blood flow imaging, suggesting a novel treatment for these combined diagnoses. Patient's perspective Patient has declined to submit his perspective due to privacy concerns.
List of abbreviations ATA: Atmospheres absolute; ECD: Ethyl cysteinate dimer; FH: Family history; HBOT: Hyperbaric oxygen therapy; HPI: History of present illness; IED: Improvised explosive device; LOC: Loss of consciousness; MRI: Magnetic resonance imaging; PCS: Post-concussion syndrome; PEx: Physical exam; PHIS: Prior head injury history; PMH: Past medical history; PSH: Personal and Social history; PTSD: post-traumatic stress disorder; ROS: Review of systems; SPECT: Single photon emission computed tomography; TBI: Traumatic brain injury. Consent Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal. In addition, this case was approved by the LSU School of Medicine's Institutional Review Board as a case report. Competing interests The authors declare competing interests. The primary author has a small corporation, Harch Hyperbarics, Inc. that does hyperbaric consulting. Author KVM has a corporation that leases hyperbaric oxygen chambers and a corporation that contracts to provide hyperbaric oxygen and woundcare services. None of the authors have personal or financial relationships with people or organizations that would influence the interpretation of data in this report. Authors' contributions PGH evaluated the patient, ordered the treatment and imaging, and wrote the draft of the manuscript. EFF analyzed and presented the SPECT imaging and assisted in writing the manuscript. PKS assisted in the treatment of the patient and assisted in writing the manuscript. KVM assisted in development of the hyperbaric protocol and writing the manuscript. All authors read and approved the final manuscript. Other Sections▼ Supplementary Material
Additional file 1 Side by side Pre and Post HBOT processed transverse SPECT brain blood flow images. Pre-HBOT scan is on the left and post-HBOT on the right. Click on either image to initialize movie. Images were obtained on a Picker Prism 3000 triple-head gamma camera. Both scans were processed by technologist PJT: 25 mCi of ECD was prepared with the standard manufacturer's kit and injected in a peripheral vein in a low noise low light area while the patient was quiet and motionless. One hour after injection acquisition proceeded with a 360 degree rotation and 40 stops, 20 seconds/stop on a 128 x 128 matrix, using low energy high resolution fan beam collimators. Motion correction was used for minor movement. Raw data was processed by transverse reconstruction using 360 degree filtered back projection and a ramp filter, followed by a LoPass filter, order 2.2. Cutoff was taken at the intersection of the best fit LoPass filter and noise on the power spectrum graph. Per file attenuation correction and best fit ellipse were applied. Images were oblique reformatted with slice thickness at 4 mm (2 pixels), aligned, and off-center zoom applied (20 cm2 area). Images were presented in all 3 orthogonal planes. Transverse processed images were analyzed with Osirix Open-source software (version 3.3.2) and windowed at a level of 1000 with a window width of 2000. They were subsequently rendered in QuickTime movie format starting from vertex and proceeding through the base of the brain. Images are in standard SPECT format and orientation. Color map is red, yellow, green, blue, and violet from highest brain blood flow to lowest. Note the marked generalized increase in perfusion on the post-HBOT scan Click here for file(3.2M, mov) Acknowledgements The authors are indebted to nuclear technologist Philip J. Tranchina for expert processing and three dimensional thresholding of the SPECT brain imaging.

Other Sections▼ References 1. Tanielian TJaycox LH, editor. Invisible Wounds of War: Psychological and Cognitive Injuries, Their Consequences, and Services to Assist Recovery. Center for Military Health Policy Research, the Rand Corporation; 2008. 2. King NS. PTSD and traumatic brain injury: Folklore and fact? Brain Injury. 2008;22:1–5. doi: 10.1080/02699050701829696. [PubMed] [Cross Ref] 3. Harch PG, Neubauer RA. In: The Textbook of Hyperbaric Medicine. 3. Jain KK, editor. Hogrefe and Huber; 1999. pp. 318–349. 4. Harch PG, Kriedt C, Van Meter KW, Sutherland RJ. Hyperbaric oxygen therapy improves spatial learning and memory in a rat model of chronic traumatic brain injury. Brain Res.2007;1174:120–129. doi: 10.1016/j.brainres.2007.06.105. [PubMed] [Cross Ref] 5. Harch PG, Van Meter KW, Neubauer RA, Gottlieb SF. In: The Textbook of Hyperbaric Medicine. 2. Jain KK, editor. Hogrefe and Huber; 1996. pp. 480–491. 6. Harch PG, Neubauer RA. In: The Textbook of Hyperbaric Medicine. 4. Jain KK, editor. Hogrefe & Huber; 2004. Hyperbaric oxygen therapy in global cerebral ischemia/anoxia and coma; pp. 223–262. 7. Neubauer RA, Gottlieb SF, Pevsner NH. Hyperbaric oxygen treatment of closed head injury.South Med J. 1994;87:933–936. [PubMed] 8. Golden ZL, Neubauer RA, Golden CJ. Improvement in cerebral metabol-ism in chronic brain injury after hyperbaric oxygen therapy. Int J Neurosci. 2002;112:119–131. doi: 10.1080/00207450212027. [PubMed] [Cross Ref] 9. Harch PG, Gottlieb SF, Van Meter KW, Staab P. HMPAO SPECT brain imaging and low pressure HBOT in the diagnosis and treatment of chronic traumatic, ischemic, hypoxic and anoxic encephalopathies. Undersea & Hyperbaric Medicine. 1994;21:30. 10. Kennedy JE, Jaffee MS, Leskin GA. Posttraumatic stress disorder and posttraumatic stress disorder-like symptoms and mild traumatic brain injury. J Rehab Res Devel. 2007;44:895–920. doi: 10.1682/JRRD.2006.12.0166. [PubMed] [Cross Ref]

HBOT for post concussion and PTSD

J Neurotrauma. 2012 Jan 1;29(1):168-85. Epub 2011 Nov 22. A phase I study of low-pressure hyperbaric oxygen therapy for blast-induced post-concussion syndrome and post-traumatic stress disorder. Harch PG, Andrews SR, Fogarty EF, Amen D, Pezzullo JC, Lucarini J, Aubrey C, Taylor DV, Staab PK, Van Meter KW. Source Department of Medicine, Section of Emergency and Hyperbaric Medicine, School of Medicine, Louisiana State University Health Sciences Center, New Orleans, Louisiana 70112, USA. paulharchmd@gmail.com

Abstract
This is a preliminary report on the safety and efficacy of 1.5 ATA hyperbaric oxygen therapy (HBOT) in military subjects with chronic blast-induced mild to moderate traumatic brain injury (TBI)/post-concussion syndrome (PCS) and post-traumatic stress disorder (PTSD).

Sixteen military subjects received 40 1.5 ATA/60 min HBOT sessions in 30 days. Symptoms, physical and neurological exams, SPECT brain imaging, and neuropsychological and psychological testing were completed before and within 1 week after treatment. Subjects experienced reversible middle ear barotrauma (5), transient deterioration in symptoms (4), and reversible bronchospasm (1); one subject withdrew.

Post-treatment testing demonstrated significant improvement in: symptoms, neurological exam, full-scale IQ (+14.8 points; p<0.001), WMS IV Delayed Memory (p=0.026), WMS-IV Working Memory (p=0.003), Stroop Test (p<0.001), TOVA Impulsivity (p=0.041), TOVA Variability (p=0.045), Grooved Pegboard (p=0.028), PCS symptoms (Rivermead PCSQ: p=0.0002), PTSD symptoms (PCL-M: p<0.001), depression (PHQ-9: p<0.001), anxiety (GAD-7: p=0.007), quality of life (MPQoL: p=0.003), and self-report of percent of normal (p<0.001), SPECT coefficient of variation in all white matter and some gray matter ROIs after the first HBOT, and in half of white matter ROIs after 40 HBOT sessions, and SPECT statistical parametric mapping analysis (diffuse improvements in regional cerebral blood flow after 1 and 40 HBOT sessions).

Forty 1.5 ATA HBOT sessions in 1 month was safe in a military cohort with chronic blast-induced PCS and PTSD. Significant improvements occurred in symptoms, abnormal physical exam findings, cognitive testing, and quality-of-life measurements, with concomitant significant improvements in SPECT.
PMID: 22026588 [PubMed - in process]

Hyperbaric oxygen therapy improves spatial learning and memory

Brain Res. 2007 Oct 12;1174:120-9. Epub 2007 Aug 16. Hyperbaric oxygen therapy improves spatial learning and memory in a rat model of chronic traumatic brain injury. Harch PG, Kriedt C, Van Meter KW, Sutherland RJ. Source Department of Medicine, LSU Health Sciences Center in New Orleans, Harvey, Louisiana 70058, USA. paulharchmd@aol.com
ABSTRACT:
In the present experiment we use a rat model of traumatic brain injury to evaluate the ability of low-pressure hyperbaric oxygen therapy (HBOT) to improve behavioral and neurobiological outcomes. The study employed an adaptation of the focal cortical contusion model. 64 Male Long-Evans rats received unilateral cortical contusion and were tested in the Morris Water Task (MWT) 31-33 days post injury. Rats were divided into three groups: an untreated control group (N=22), an HBOT treatment group (N=19) and a sham-treated normobaric air group (N=23).

The HBOT group received 80 bid, 7 days/week 1.5 ATA/90-min HBOTs and the sham-treated normobaric air group the identical schedule of air treatments using a sham hyperbaric pressurization. All rats were subsequently retested in the MWT. After testing all rats were euthanized. Blood vessel density was measured bilaterally in hippocampus using a diaminobenzadine stain and was correlated with MWT performance. HBOT caused an increase in vascular density in the injured hippocampus (p<0.001) and an associated improvement in spatial learning (p<0.001) compared to the control groups. The increased vascular density and improved MWT in the HBOT group were highly correlated (p<0.001).

In conclusion, a 40-day series of 80 low-pressure HBOTs caused an increase in contused hippocampus vascular density and an associated improvement in cognitive function. These findings reaffirm the clinical experience of HBOT-treated patients with chronic traumatic brain injury.
PMID: 17869230

Thursday, February 2, 2012

Football head injuries: Testimony

1
Written Testimony
Ann C. McKee, M.D.
Associate Professor of Neurology and Pathology
Boston University School of Medicine
Director of the VISN-1 Neuropathology Laboratory for the New England Veterans
Administration Medical Centers
Director of the Brain Banks for the Boston University Alzheimer’s Disease Center,
Framingham Heart Study, and Centenarian Study
Co-Director, Center for the Study of Traumatic Encephalopathy
Hearing before the House Judiciary Committee
Legal Issues Relating to Football Head Injuries
October 28, 2009
2
3
Mr. Chairman and Members of the Committee:
Thank you for the invitation to testify today on legal issues relating to football head
injuries. My name is Dr. Ann McKee. I am an associate professor of Neurology and
Pathology at Boston University School of Medicine, and I am the Director of the
Neuropathology Laboratory for the New England Veterans Administration Medical
Centers at the Bedford VA Medical Center, the Director of the Brain Banks for the
Boston University Alzheimer’s Disease Center, the Framingham Heart Study, and the
Centenarian Study, and I am a co-director for the Center for the Study of Traumatic
Encephalopathy at Boston University.
I received my medical degree in 1979, and I am board certified in both Neurology and
Neuropathology. I have extensive experience in neuropathology of neurological disease
and have written extensively on the neuropathology of many neurodegenerative
diseases, including Alzheimer’s disease, Parkinson’s disease, and Frontotemporal
Dementia, as well as normal aging. For the past 23 years, I have been studying the
brains of individuals after death and correlating the pathological findings to the patient’s
clinical symptoms during life. I have examined thousands of brains, brains from people in
all walks of life including brains from individuals who have lived to be well over the age of
100. In addition, for most of my professional career, I have been focused on tau protein,
a protein that becomes toxic when abnormally phosphorylated and builds up in the
brains of patients with some neurodegenerative diseases, including Alzheimer’s disease,
but is found only in very limited quantities in the brains of normally functioning people.
In January of 2003, as part of my work with the Boston University Alzheimer’s Disease
Center and the Bedford VA, I examined the brain of a man who died at the age of 72
after 15 years of severe dementia requiring institutionalization. The man had been a
4
world champion boxer and had been clinically diagnosed with Alzheimer’s disease
beginning at the age of 58. However, when I looked at his brain on post-mortem
examination, I found that there was absolutely no evidence of Alzheimer’s disease;
there was no evidence of beta amyloid, a protein that accumulates in the brain in people
with Alzheimer’s disease and is thought by many to be the cause of Alzheimer’s disease.
Instead, the brain of this world champion boxer showed a massive build-up of the toxic
form of tau protein as neurofibrillary tangles (NFTs) and glial tangles throughout his
brain. The neurofibrillary and glial tangles were also distributed in a unique pattern, a
pattern not found in any neurodegenerative condition except Chronic Traumatic
Encephalopathy, or CTE. In CTE, tau protein builds up in individual nerve cells and
prevents them from making normal connections with other nerve cells, eventually killing
the cells. In this man’s brain, there were massive numbers of NFTs and glial tangles, so
many in fact that you could see the abnormalities on the glass slides without the use of a
microscope, as you can see in the right panels of Figure 1. There is tremendous
accumulation of tau protein that appears as a brown pigment. All the brown pigment you
see is abnormal, please compare what you see on the right to the brain of a normal 65
year old man on the left, all the slides are prepared and stained in exactly the same way,
and there is absolutely no brown pigment visible in the normal individual. When you look
at the brain microscopically as in the lower panels, you can see that many individual
nerve cells of the boxer contain NFTs – they are found in nearly every nerve cell and
there are almost no normal appearing cells. This individual, a former professional boxer,
was clinically diagnosed with Alzheimer’s disease during life, but the disease that
actually caused his tragic 15 year decline in intellect and eventually killed him, was CTE,
a disorder that would have been entirely prevented if he hadn’t suffered repeated head
injury in his younger years as a boxer.
5
My second case of CTE came in 2004, again when I was examining the brain of a man
who had been clinically diagnosed with Alzheimer’s disease when he was alive. When I
looked at the slides, I immediately realized that the changes found in this individual were
nearly identical to those that I had found in the world champion boxer, but in this case,
the medical records did not indicate that he had ever had any head injury. So I called the
patient’s daughter, and sure enough, it turned out that the man had been a professional
boxer during his twenties. Again, his post-mortem examination indicated that his
functional deterioration, dementia and placement in a nursing home were not due to
Alzheimer’s disease, but instead due to CTE, a disorder that could have been entirely
prevented. Over the ensuing years, I examined several other cases of CTE in
professional boxers, all with a similar appearance and pattern of abnormalities.
I met Chris Nowinski in the summer of 2007 and through Chris’s efforts in early 2008, I
had my first opportunity to examine the brain of a retired professional football player. It
was the brain of John Grimsley, a former linebacker for the Houston Oilers who had died
of an accidental gunshot wound while cleaning his gun at the age of 45. According to his
wife, he was concussed 3 times during his college football years, and at least 8 times
during his NFL career, however, only one "cerebral concussion" was medically
confirmed. He was never formally diagnosed with post-concussion syndrome and never
sought medical attention for residual cognitive and behavioral difficulties. There was no
history of ever losing consciousness for more than a few seconds and he never required
being carried off the field or hospitalization. He never took any performance-enhancing
drugs or used illicit drugs. He was a nonsmoker and there was no known family history
of dementia.
6
According to his wife and close friends, he began showing changes in his behavior and
cognitive decline at age 40. He developed difficulties in short-term memory, attention,
concentration, organization, planning, problem-solving, judgment, and the ability to
juggle more than one task at a time. For example, he would ask the same questions
repeatedly over the course of the day and he would ask to rent a movie that he had
already seen. He had difficulty assembling his tax records, shopping alone, and
understanding television. His symptoms gradually progressed and became quite severe
by the end of his life. He also developed a “shorter and shorter fuse” and would become
angry and verbally aggressive over seemingly trivial issues.
When I first looked at his brain (it had been previously dissected by the coroner), I didn’t
see any gross changes. Yet when the microscopic slides were prepared, they showed
the exact same pattern of changes that I had found in the brains of the boxers with CTE.
There were large numbers of tau containing neurofibrillary tangles throughout all parts of
the brain and there was absolutely no evidence of beta amyloid protein or Alzheimer’s
disease. The brain of this 45 year old husband and father, at the prime of his life,
showed profound neurofibrillary degeneration, changes of CTE that were identical in
nature to the changes I found in the brains of the boxers, but were now in a football
linebacker some 30 years younger. In John Grimsley’s brain, there were striking
changes in regions of the brain controlling personality and behavior, such as the frontal
lobes, profound changes in the areas controlling impulsivity and rage behavior such as
the amygdala, and severe changes in anatomic structures that are responsible for
memory, such as the hippocampus, mammillary bodies and thalamus. In Figure 1, the
brain of John Grimsley is seen in the middle; in the top middle panel, you can see severe
tau deposition in the frontal lobe and microscopically; in the bottom middle panel, you
can see numerous nerve cells containing tau and NFTs.
7
Figure 1
In a normal 45 year old, absolutely none of these changes would be found. Indeed these
changes would not be found in a normal 65 year old, 85 year old or 110 year old.
8
The next football player’s brain that I examined was that of Tom McHale, a 45 year old
retired offensive lineman for the Tampa Bay Buccaneers. He was a husband and father
of 3 young boys. After a 3 year decline in his ability to make sound business decisions,
increasing apathy, depression, and memory loss, he died as a result of substance
abuse. His wife did not know of any reported formal concussions during his year as a
lineman. His brain too showed profound tau immunoreactive neurofibrillary
degeneration in areas controlling memory, impulsivity, organization and problem solving
(as you can see in Figure 2) and again with no evidence of any other disorder other than
CTE.
Figure 2
The third brain of a professional football player I examined was that of Wally Hilgenberg,
a 66 year old former linebacker who died from complications related to Amyotrophic
Lateral sclerosis or Lou Gehrigs disease. He played 16 seasons with the Minnesota
Vikings and had at least 10 concussions, including losing consciousness on 1 or 2
occasions. He began showing slow and steady cognitive decline at the age of 56. His
cognitive difficulties were manifest mainly by “not understanding things at a deeper level”
and he had difficulties with executive functioning, including worsening organization and
9
planning skills. His cognitive decline progressed with worsening memory and language
functions. In his last year, he stopped being able to read and was completely unable to
learn how to operate an assistive communication device, even using the simplest level of
commands. Inspection of his brain showed damage to the frontal cortex in a pattern that
suggested it had been used as a battering ram, and the interior spinal fluid spaces were
enlarged suggesting that the volume of the brain had declined. Microscopically the brain
was densely riddled by tau containing NFTs and glial tangles throughout the cerebral
cortex, basal ganglia, thalamus, and brainstem in the unique pattern that defines CTE,
and again, in the complete absence of Alzheimer’s disease and beta amyloid.
Furthermore, the damage found in his brain was far greater in density and the damage
was much more widespread than anything that I have ever found in Alzheimer’s disease
or any of the other common neurodegenerative disorders.
Figure 3
10
The fourth, fifth and sixth brains from former NFL football players that I examined,
including one individual who took his own life, all showed the same distinctive,
characteristic changes of CTE. The seventh brain of a former NFL player I analyzed was
that of Louis Creekmur, a former offensive lineman for the Detroit Lions and an eighttime
Pro Bowler. Louis Creekmur played ten seasons for the Lions, and was famous for
suffering at least thirteen broken noses and 16 concussions. Beginning at the age of 58,
he began to show increasing cognitive and behavioral difficulties including memory loss,
problems with attention and organization, and outbursts of anger and aggression. He
died from complications of dementia at the age of 82. The brain of Mr. Creekmur showed
extensive damage including marked shrinkage of medial temporal lobe structures that
control memory, shrinkage of the frontal and temporal lobes, and marked dilation of the
spinal fluid cavities that line the brain’s interior. There was widespread and severe tau
deposition as NFTs throughout the frontal and temporal lobes, amygdala, hippocampus,
thalamus and brainstem in the unique pattern that is only found in CTE. In Mr.
Creekmur’s case, the abnormalities were profound, they were severe, and they
paralleled the changes found in the world champion professional boxer. Mr. Creekmur
was also a member the NFL’s Plan 88. Yet again, there was absolutely no evidence of
Alzheimer’s disease or any other neurodegenerative disorder, and the findings indicated
that if Mr. Creekmur had not sustained repetitive head trauma during the play of football,
he would be alive and well and enjoying his family and grandchildren today.
11
Figure 4
I have also examined the brain of a former college football player, Mike Borich, a former
wide receiver for Snow College and Western Illinois University who died at the age of 42
after a several-year period of increasing irritability, aggressive and violent outbursts, and
drug and alcohol abuse. His brain, too, showed CTE affecting widespread parts of his
cerebral cortex and deep brain nuclei. Brains from 3 other college football players
showed similar changes.
Lastly, I have had the opportunity to examine the brain of a high school football player
who died at the age of 18. He had played football and other sports for 4 years and
suffered several concussions. The brain of an 18 year old should be pristine, there
should be no abnormalities anywhere, no abnormalities whatsoever. But in the brain of
this young man, a brain that should be entirely normal, there were spots of undeniable
pathology. They were 4 areas of damage in the frontal lobe that you could see even
looking at the slides with your naked eye (Figure 5). In those areas, there were hundreds
of degenerating nerve cells containing tau neurofibrillary tangles and disordered nerve
12
cell processes. Even in this 18 year old high school student, with only a few years
experience playing football, there were signs of the earliest stages of CTE. Had he lived
longer, this 18 year old would have almost certainly developed the same full blown CTE
that we found in the other college and professional football players.
Figure 5
I have now examined the brains of 7 former NFL players, and 4 college layers, and all 11
have shown profound and widespread changes of CTE. I have also found CTE in a
college level player and the earliest signs of CTE in a high school football player. I
realize that this is just a handful of cases, so – so what? -what can you say from just 11
cases? Well, I can say that for the past 23 years, I have looked at thousands of brains,
from individuals from all walks of life, of all ages, and during the past 20 years, I have
primarily focused on abnormalities of tau protein. But I have only seen this unique
13
pattern of changes, in this severity, in individuals with a history of repetitive head trauma,
including boxers and football players. These changes are dramatically not normal -there
is no way these pathological changes represent a variation in normal that we find under
a bell shaped curve. We have found these changes in every professional football
players’ brain that has come into my laboratory at the BU Center for the Study of
Traumatic Encephalopathy and I have never seen this in 20 plus years of examining
brains. I have had colleagues of mine from other institutions – leading neuropathologists
from Harvard and Mt. Sinai—independently examine these brains, and they have come
up with the same diagnosis as I had, CTE. I know that the argument is often made that
there are hundreds of thousands of former football players, including former professional
football players, with no signs of any cognitive decline or memory loss or personality
change, but what I don’t understand is why are we expecting that this exposure to
repetitive head trauma will have 100% penetrance into the population and cause disease
in every football player? Do we expect 100% of cigarette smokers will develop lung
cancer? Do we expect 100% of children who play with matches or even chain saws will
get hurt? No. Even if the percentage of affected players is 20%, or 10%, there are still
thousands of kids and adults out there, right now, playing football at all levels -who will
eventually come down with this devastating and debilitating disorder. And as a doctor
and as a mother, I think this calls for immediate action. We need to take radical steps to
change the way football is played and we need to make those changes today.
14
B.U. Center for the Study of Traumatic Encephalopathy Grant Support
Title: Development of Pathology Diagnostic Criteria for Chronic Traumatic
Encephalopathy
Co-Principal Investigators: Ann McKee and Robert Stern
Type of Grant: Supplement to P30 Center Grant (N. Kowell, P.I); P30-AG13846
Funding Agency: National Institute on Aging
Years Funded: 2009-2010
Total Direct Costs: $83,287
Title: Neuropathologic Examination of Traumatic Encephalopathy in Athletes with
Histories of Repetitive Concussion
Co-Principal Investigators: Ann McKee and Robert Stern
Type of Grant: Supplement to P30 Center Grant (N. Kowell, P.I); P30-AG13846
Funding Agency: National Institute on Aging
Years Funded: 2008-2009
Total Direct Costs: $100,000

Low pressure hyperbaric oxygen therapy and SPECT brain imaging

Case report
Open Access
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
Paul G Harch1*, Edward F Fogarty2, Paul K Staab1 and Keith Van Meter1
Addresses: 1Section of Emergency Medicine, Department of Medicine, Louisiana State University Health Sciences Center, 2021 Perdido St, Room
W535, New Orleans, Louisiana, 70112, USA and 2Department of Radiology, University of North Dakota School of Medicine and Health Sciences,
Post Office Box 1975, 515 ½ East Broadway Avenue, Suite 106, Bismarck, North Dakota, 58502, USA
Email: PGH* - paulharchmd@aol.com; EFF - efogarty@medicine.nodak.edu; PKS - pstaab@wjmc.org; KVM - kvanmeter@aol.com
* Corresponding author
Published: 5 June 2009 Received: 12 March 2009
Accepted: 4 April 2009
Cases Journal 2009, 2:6538 doi: 10.4076/1757-1626-2-6538
This article is available from: http://casesjournal.com/casesjournal/article/view/6538
© 2009 Harch et al; licensee Cases Network Ltd.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0),
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
A 25-year-old male military veteran presented with diagnoses of post concussion syndrome and post
traumatic stress disorder three years after loss of consciousness from an explosion in combat. The
patient underwent single photon emission computed tomography brain blood flow imaging before
and after a block of thirty-nine 1.5 atmospheres absolute hyperbaric oxygen treatments. The patient
experienced a permanent marked improvement in his post-concussive symptoms, physical exam
findings, and brain blood flow. In addition, he experienced a complete resolution of post-traumatic
stress disorder symptoms. After treatment he became and has remained employed for eight
consecutive months. This case suggests a novel treatment for the combined diagnoses of blastinduced
post-concussion syndrome and post-traumatic stress disorder.
Introduction
By January, 2008 it was estimated that as many as 300,000
servicemen and women from the current Iraq and Afghanistan
Wars have PTSD or major depression, 320,000 have
experienced a TBI, and 82,000 have all three diagnoses [1].
Treatment is available for PTSD and depression, but there is
no proven therapy for the dual diagnoses of PTSD and the
residual effects of TBI, the PCS [2].
HBOT is the use of greater than atmospheric pressure
oxygen in an enclosed chamber to treat basic disease
processes [3]. HBOT has been traditionally applied to
certain emergent conditions and chronic wound conditions,
but not to blast-induced TBI/PCS or PTSD. This case
report is the first application of the authors’ low pressure
HBOT protocol for chronic brain injury to blast-induced
TBI/PCS and PTSD. An early version of this protocol was
recently reported in an animal model of chronic TBI that
duplicated the human experience [4].
Case presentation
A 25-year-old retired Caucasian male U.S. Marine presented
with headaches, tinnitus, and sleep disturbance.
Three years before evaluation the patient sustained LOC
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(a few minutes) from an IED explosion with anterograde
memory loss and confusion (one hour), and persistent
right ear tinnitus, headaches, imbalance, and sleep
disturbance. He developed PTSD symptoms within
3 months and experienced six more explosions with near
LOC within 15 months. After medical evaluation diagnoses
were TBI/PCS, PTSD, depression, hearing loss, and
tinnitus.
Prioritized Symptom List: 1) Constant headaches with
intermittent confusion, irritability, tunnel vision, and
dizziness, 2) Bilateral tinnitus, 3) Sleep disruption, 4) Left
eye blurred vision, 5) Irritability, 6) Depression, social
withdrawal; Additional Symptoms: 7) Fatigue, 8)
Decreased hearing, 9) Imbalance, 10) Cognitive problemsmemory,
attention, decreased speed of thinking, 11) Back
pain, 12) Bilateral knee pain, 13) PTSDsymptoms: intrusive
thoughts, combat thoughts, nightmares, tachycardia.
Med-Surg, Medications: None. FH, ROS, and PHIS: noncontributory
or negative. PSH: Engaged, no children, lives
with parents, 3 years college education, no tobacco or
drugs, one to two beers/week. Neuro PEx Abnormalities:
Slight deviation of right eye laterally, bilateral: decreased
hearing to softly rubbing fingers at one foot, noxious
response to 512 Hz tuning fork, decreased finger tapping
speed, unstable: rotation exam, tandem gait, and Romberg.
Treatment and testing: MRI brain-normal. SPECT
brain imaging pre-HBOT and 72 h after the 39th HBOT.
The patient underwent 39 HBOT’s in 26 calendar days at
1.5 ATA/60 minutes total dive time, twice/day, five days/
week in a monoplace chamber with 100% oxygen.
Outcome: Headache permanently gone after the 1st
HBOT. After 12 HBOT’s symptoms 3, 6, and 7 improved.
At 25th HBOT absence of PTSD symptoms. Re-evaluation
after 37 HBOT’s: 1) 4/6 primary problems improved
(#’s 1, 3, 5, 6), 2/6 no change, 2) 4/7 additional symptoms
improved (7, 9, 10, 13), 3/7 no change, 3) 6/6 abnormal
exam findings retested improved, 1 finding not retested
(right eye deviation). SPECT: heterogeneous with bilateral
frontal and temporal defects-all improved post HBOT. See:
Movie 1, Figures 1 and 2. (Movie 1): Side by side Pre and
Post HBOT processed transverse SPECT brain blood flow
images-movie. File Format: Quicktime Video. Description
of Data: Pre-HBOT scan is on the left and post-HBOT on
the right. Click on either image to initialize movie. Images
were obtained on a Picker Prism 3000 triple-head gamma
camera. Both scans were processed by technologist PJT:
25 mCi of ECD was prepared with the standard manufacturer’s
kit and injected in a peripheral vein in a low
noise low light area while the patient was quiet and
motionless. One hour after injection acquisition proceeded
with a 360 degree rotation and 40 stops,
20 seconds/stop on a 128 x 128 matrix, using low energy
high resolution fan beam collimators. Motion correction
was used for minor movement. Raw data was processed by
transverse reconstruction using 360 degree filtered back
projection and a ramp filter, followed by a LoPass filter,
order 2.2. Cutoff was taken at the intersection of the
best fit LoPass filter and noise on the power spectrum
graph. Per file attenuation correction and best fit ellipse
were applied. Images were oblique reformatted with slice
thickness at 4 mm (2 pixels), aligned, and off-center zoom
Figure 2. Post-HBOT SPECT brain scan three dimensional
surface reconstruction and processed transverse images.
Note relative improvement in brain blood flow to bilateral
focal frontal and temporal defects and overall normalization of
blood flow to a more homogeneous pattern.
Figure 1. Pre-HBOT SPECT brain scan three dimensional
surface reconstruction and processed transverse images.
Note bilateral orbital frontal and temporal lobe defects and
diffuse heterogeneous pattern of blood flow.
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applied (20 cm2 area). Images were presented in all
3 orthogonal planes. Transverse processed images were
analyzed with Osirix Open-source software (version 3.3.2)
and windowed at a level of 1000 with a window width of
2000. They were subsequently rendered in QuickTime
movie format starting from vertex and proceeding through
the base of the brain. Images are in standard SPECT format
and orientation. Color map is red, yellow, green, blue, and
violet from highest brain blood flow to lowest. Note the
marked generalized increase in perfusion on the post-
HBOT scan. (Figure 1): Pre-HBOT SPECT brain scan three
dimensional surface reconstruction and processed transverse
images. Pre-HBOT scan was rendered in three
dimensional surface reconstruction format by PJT based
on the method developed and taught by Picker International
using Picker software. In this method brain blood
flow is computer indexed to frontal lobe blood flow. A
frontal lobe surface defect was identified on a selected
transverse slice. Processed/filtered transverse slices were
then featured with a 100% window such that all pixels
render a white image. Counts were slowly subtracted by
decreasing the window threshold until the defect was
visible as a full thickness black defect in the contour of the
cortex. As the defect emerged and was registered in proper
anatomic proportion to the rest of frontal cortical blood
flow the numerical window level was taken as the
determination threshold. Three separate determinations
were made for each scan and the final threshold taken as
an average of the three determinations. The technologist
was blind to the final image reconstruction due to software
restrictions that only allow threshold determination. The
surface reconstruction image at this threshold is featured
in the image above. Color is aesthetic. Note bilateral
orbital frontal and temporal lobe defects, areas typically
injured in traumatic brain injury, consistent with processed
transverse images in the right hand columns.
Processed images also show an abnormal diffuse heterogeneous
pattern of blood flow. Description of processing
is in (Movie 1). (Figure 2): Post-HBOT SPECT brain scan
three dimensional surface reconstruction and processed
transverse images. Three dimensional surface image was
prepared in identical fashion to the image in Figure 1.
Note relative improvement in brain blood flow to bilateral
focal frontal and temporal defects, consistent with
processed transverse images in the right hand columns.
Transverse slices also show normalization of the blood
flow to a more homogeneous pattern.
Discussion
The present case is the first application of the author’s
HBOT protocol to blast-induced TBI/PCS and PTSD. The
patient’s symptomatic, physical exam, and SPECT
improvements are similar to ours [3,5,6,9] and others’
[7,8] previous cases/case series of non-blast TBI suggesting
common pathophysiology. The unexpected result was the
complete resolution of PTSD. With the overlap of
symptoms, pathophysiology, and anatomy in TBI/PCS
and PTSD [10] HBOT is likely impacting common shared
targets in this case.
Conclusion
Thirty-nine low pressure HBOT’s caused a reduction in
symptoms and signs of chronic mild-moderate blastinduced
TBI/PCS and PTSD. The resolution of symptoms
and signs of TBI/PCS and PTSD were reflected in global
and focal improvements in brain blood flow imaging,
suggesting a novel treatment for these combined
diagnoses.
Patient’s perspective
Patient has declined to submit his perspective due to
privacy concerns.
List of abbreviations
ATA, Atmospheres absolute; ECD, Ethyl cysteinate dimer;
FH, Family history; HBOT, Hyperbaric oxygen therapy;
HPI, History of present illness; IED, Improvised explosive
device; LOC, Loss of consciousness; MRI, Magnetic resonance
imaging; PCS, Post-concussion syndrome; PEx,
Physical exam; PHIS, Prior head injury history; PMH, Past
medical history; PSH, Personal and Social history; PTSD,
post-traumatic stress disorder; ROS, Review of systems;
SPECT, Single photon emission computed tomography;
TBI, Traumatic brain injury.
Consent
Written informed consent was obtained from the patient
for publication of this case report and accompanying
images. A copy of the written consent is available for
review by the Editor-in-Chief of this journal. In addition,
this case was approved by the LSU School of Medicine’s
Institutional Review Board as a case report.
Competing interests
The authors declare competing interests. The primary
author has a small corporation, Harch Hyperbarics, Inc.
that does hyperbaric consulting. Author KVM has a
corporation that leases hyperbaric oxygen chambers and
a corporation that contracts to provide hyperbaric oxygen
and woundcare services. None of the authors have
personal or financial relationships with people or organizations
that would influence the interpretation of data in
this report.
Authors’ contributions
PGH evaluated the patient, ordered the treatment and
imaging, and wrote the draft of the manuscript. EFF
analyzed and presented the SPECT imaging and assisted in
writing the manuscript. PKS assisted in the treatment of
the patient and assisted in writing the manuscript. KVM
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assisted in development of the hyperbaric protocol and
writing the manuscript. All authors read and approved the
final manuscript.
Acknowledgements
The authors are indebted to nuclear technologist Philip J.
Tranchina for expert processing and three dimensional
thresholding of the SPECT brain imaging.
References
1. Tanielian T, Jaycox LH, Eds: Invisible Wounds of War: Psychological
and Cognitive Injuries, Their Consequences, and
Services to Assist Recovery. Center for Military Health Policy
Research, the Rand Corporation, Arlington, VA, 2008.
2. King NS: PTSD and traumatic brain injury: Folklore and fact?
Brain Injury 2008, 22:1-5.
3. Harch PG, Neubauer RA: Hyperbaric oxygen therapy in global
cerebral ischemia, anoxia, and coma. In The Textbook of
Hyperbaric Medicine, Chapter 18, 3rd Edition. Edited by Jain KK. Seattle,
Washington, Hogrefe and Huber; 1999:318-349.
4. Harch PG, Kriedt C, Van Meter KW, Sutherland RJ: Hyperbaric
oxygen therapy improves spatial learning and memory in a
rat model of chronic traumatic brain injury. Brain Res 2007,
1174:120-129.
5. Harch PG, Van Meter KW, Neubauer RA, Gottlieb SF: Use of
HMPAO SPECT for assessment of response to HBO in
ischemic/hypoxic encephalopathies. In The Textbook of Hyperbaric
Medicine. Chapter 35, Appendix 2. 2nd Edition. Edited by Jain KK.
Seattle, Washington, Hogrefe and Huber; 1996:480-491.
6. Harch PG, Neubauer RA: Hyperbaric oxygen therapy in global
cerebral ischemia/anoxia and coma. In The Textbook of Hyperbaric
Medicine. Chapter 18, 4th Revised Edition. Edited by Jain KK. Seattle,
Washington, Hogrefe & Huber; 2004:223-262.
7. Neubauer RA, Gottlieb SF, Pevsner NH: Hyperbaric oxygen
treatment of closed head injury. South Med J 1994, 87:933-936.
8. Golden ZL, Neubauer RA, Golden CJ et al.: Improvement in
cerebral metabol-ism in chronic brain injury after hyperbaric
oxygen therapy. Int J Neurosci 2002, 112:119-131.
9. Harch PG, Gottlieb SF, Van Meter KW, Staab P: HMPAO SPECT
brain imaging and low pressure HBOT in the diagnosis and
treatment of chronic traumatic, ischemic, hypoxic and
anoxic encephalopathies. Undersea & Hyperbaric Medicine 1994,
21:30.
10. Kennedy JE, Jaffee MS, Leskin GA et al.: Posttraumatic stress
disorder and posttraumatic stress disorder-like symptoms
and mild traumatic brain injury. J Rehab Res Devel 2007,
44:895-920.
Movie 1. Side by side Pre and Post HBOT processed
transverse SPECT brain blood flow images-movie. Click on
this link to activate the video: http://casesjournal.com/
casesjournal/article/downloadFile/6538/303311
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Cases Journal 2009, 2:6538 http://casesjournal.com/casesjournal/article/view/6538
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