Thursday, March 29, 2012
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Friday, March 16, 2012
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: firstname.lastname@example.org; Edward F Fogarty: email@example.com; Paul K Staab:firstname.lastname@example.org; Keith Van Meter: email@example.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 . 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 . HBOT is the use of greater than atmospheric pressure oxygen in an enclosed chamber to treat basic disease processes . 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 .
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  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]
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]
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.
Sunday, March 4, 2012
A of A Science Summary: Autism behaviors may be eased by gluten-free, casein-free diet: Penn State College of Medicine
Autism behaviors may be eased by gluten-free, casein-free diet: Penn State College of Medicine Posted on February 29, 2012 by Stone Hearth News A gluten-free, casein-free diet may lead to improvements in behavior and physiological symptoms in some children diagnosed with an autism spectrum disorder (ASD), according to researchers at Penn State. The research is the first to use survey data from parents to document the effectiveness of a gluten-free, casein-free diet on children with ASD. Research has shown that children with ASD commonly have GI [gastrointestinal] symptoms, said Christine Pennesi, medical student at Penn State College of Medicine. Notably, a greater proportion of our study population reported GI and allergy symptoms than what is seen in the general pediatric population. Some experts have suggested that gluten- and casein-derived peptides cause an immune response in children with ASD, and others have proposed that the peptides could trigger GI symptoms and behavioral problems. The team which included Laura Cousino Klein, associate professor of biobehavioral health and human development and family studies asked 387 parents or primary caregivers of children with ASD to complete a 90-item online survey about their childrens GI symptoms, food allergy diagnoses, and suspected food sensitivities, as well as their children’s degree of adherence to a gluten-free, casein-free diet. The teams results appeared online this month in the journal Nutritional Neuroscience. Pennesi and Klein and their team found that a gluten-free, casein-free diet was more effective in improving ASD behaviors, physiological symptoms and social behaviors for those children with GI symptoms and with allergy symptoms compared to those without these symptoms. Specifically, parents noted improved GI symptoms in their children as well as increases in their children’s social behaviors, such as language production, eye contact, engagement, attention span, requesting behavior and social responsiveness, when they strictly followed a gluten-free, casein-free diet. According to Klein, autism may be more than a neurological disease — it may involve the GI tract and the immune system. There are strong connections between the immune system and the brain, which are mediated through multiple physiological symptoms,” Klein said. “A majority of the pain receptors in the body are located in the gut, so by adhering to a gluten-free, casein-free diet, you’re reducing inflammation and discomfort that may alter brain processing, making the body more receptive to ASD therapies. The team found that parents who eliminated all gluten and casein from their children’s diets reported that a greater number of their childrens ASD behaviors, physiological symptoms and social behaviors improved after starting the diet compared to children whose parents did not eliminate all gluten and casein. The team also found that parents who implemented the diet for six months or less reported that the diet was less effective in reducing their childs ASD behaviors.
According to the researchers, some of the parents who filled out the surveys had eliminated only gluten or only casein from their children’s diets, but survey results suggested that parents who completely eliminated both gluten and casein from their childs diet reported the most benefit. While more rigorous research is needed, our findings suggest that a gluten-free, casein-free diet might be beneficial for some children on the autism spectrum, Pennesi said. It is also possible that there are other proteins, such as soy, that are problematic for these children. The reason Klein and Pennesi examined gluten and casein is because they are two of the most common diet offenders. “Gluten and casein seem to be the most immunoreactive, Klein said. A childs skin and blood tests for gluten and casein allergies can be negative, but the child still can have a localized immune response in the gut that can lead to behavioral and psychological symptoms. When you add that in with autism you can get an exacerbation of effects. Kleins advice to parents of children with ASD? If parents are going to try a gluten-free, casein-free diet with their children, they really need to stick to it in order to receive the possible benefits, she said. It might give parents an opportunity to talk with their physicians about starting a gluten-free, casein-free diet with their children with ASD.
The Cascade EffectThe Cascade Effect
Torn or damaged tissues release fluids into interstitial spaces, the space between cells, causing edema (swelling). As swelling increases, this causes more pressure on surrounding cells, tissues and blood vessels. As these areas are squeezed from the increase of fluid and from the natural body response to increase inflammation (as a component of “first response” to an injury), more tissues die, more fluids are released and edema increases. As edema increases, there is more potential for this cascade effect to continue, causing more damage. This is especially significant in cerebral edema as injury to the brain is compounded by swelling around the site of the initial injury, and extensive swelling within 48 hours may result in additional long-term disabilities from the destruction of brain tissue. Hyperbaric oxygen reduces edema. Reducing swelling in the brain lowers intracranial pressure and this reduction in edema decreases the cascade effect on compromised tissues, and the oxygen promotes the repair and healing of these areas. Trapped fluid as the result of a disruption in the lymph or circulatory system can be reduced well after the initial trauma took place, which will promote healing to the area.
Certain sports injuries and trauma to the body also are affected by the inflammation response by the body to the injury, as well as from the swelling caused by the damage to the tissues in the affected site. HBOT is proving a useful adjunct in treating trauma to the body. All of this normally happens when the treatment series is over. Normally about 40 hours or more is depending upon the type of injury.