According to estimates from January 2008, up to 300,000 servicemen and women from the current Iraq and Afghanistan wars have PTSD (Post Traumatic Stress Disorder) or serious depression, 320,000 have had a TBI (Traumatic Brain Injury), and 82,000 have all three diagnosis. Treatment for PTSD and depression is available, however there is no established treatment for the combination diagnosis of PTSD and TBI residual symptoms.
HBOT is the treatment of basic disease processes using higher-than-atmospheric-pressure oxygen in an enclosed chamber. HBOT has generally been used for emergency situations and chronic wounds, but not for blast-induced TBI/PCS or PTSD. This particular case report is the first application of the authors’ low-pressure HBOT (M-HBOT) protocol for chronic brain injury to blast-induced TBI/ PCS and PTSD. An early version of this protocol was recently published in an animal model of persistent TBI that mimicked human symptoms.
The brain receives 15% of the cardiac output, consumes 20% of the total body oxygen, and utilizes 25% of the total body glucose. Still, this energy supply is only sufficient to keep about five to ten percent of the neurons active at any given time. Thus, at standard healthy condition and at any given time, the brain is utilizing almost all oxygen/energy delivered to it.
The regeneration process after brain injury requires much additional energy. This is where hyperbaric oxygen treatment can help – the increased oxygen level in the blood and body tissues during treatment can supply the energy needed for brain repair. Indeed, several previous studies have demonstrated that elevated levels of dissolved oxygen by HBOT can have several reparative effects on damaged brain tissues. Other studies revealed the beneficial effects of HBOT on the injured brain and cognitive functions of animal models.
The elevated oxygen levels can have a significant effect on the brain metabolism, largely regulated by the glial cells. Improved energy management leads to multifaceted repair, including activation of angiogenesis and triggering of neuroplasticity (reactivation of quiescent neurones; creation of new synapses and new axonal connections), and might even induce differentiation of neuronal stem cells. The idea that HBOT can promote brain repair is reasonable and has gained experimental support, yet is still largely dismissed by the medical community as is discussed next.
Hyperbaric Oxygen Therapy Can Improve Post Concussion Syndrome Years after Mild Traumatic Brain Injury – Randomized Prospective Trial
HBOT enhances oxygen distribution throughout the body by increasing the amount dissolved in plasma, hence raising blood oxygen saturation. The use of HBOT for TBI is based on the observation that hypoxia following the injury plays a significant role in subsequent brain injury. In the absence of adequate oxygenation, neurons return to anaerobic metabolism, resulting in an acidotic condition. Neurons are unable to sustain metabolic homeostasis in the presence of persistent hypoxia. These alterations eventually become irreversible, and cell death occurs as a result.
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 level of consciousness (a few minutes) from an Intermittent explosive disorder 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 (level of consciousness) within 15 months. After medical evaluation diagnoses were TBI/PCS, PTSD, depression, hearing loss, and tinnitus.
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 Fogarty2, Paul K Staab1 and Keith Van Meter1
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.
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 session of HBOT. After 12 sessions of HBOT, sleep disruption, depression, social withdrawal, and fatigue improved. At 25th HBOT session absence of PTSD symptoms.
Re-evaluation after 37 HBOT sessions, left eye blurred vision and depression primary problems improved.
SPECT (single-photon emission computerized tomography): heterogeneous with bilateral frontal and temporal defects-all improved post HBOT. (See Additional file 1, Figures 1 and 2. (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 project 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 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.
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.
Conclusion
Thirty nine low pressure HBOT treatments 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.
Recent clinical investigation have also examined the effects of HBOT on PTSD symptoms in patients with a history of TBI. These studies did not find a statistically significant difference between the treatment group (2.4 ATA, 100% O2 ) and the sham group (1.3 ATA, 21% FiO2 ) since both groups demonstrated improvement in PTSD symptoms.
Some have concluded that HBOT does not work in the treatment of TBI with associated PTSD symptoms due to the lack of statistically significant differences between the treatment and sham groups.
According to Harch (2013), the problem is in the concept of “sham-controlled,” which implies a placebo design. The 1.3 ATA sham treatment is essentially an HBOT treatment. The increased pressure raises plasma oxygen levels over what would be found at sea level. To establish a control group, increased pressure and hyperoxia would have to be removed. Thus, in these investigations, both dosages (hyperbaric oxygen and hyperbaric air) revealed net benefits in post-concussion syndrome and PTSD.
HBOT has been shown to be safe at dosages of 1.5 ATA, and even higher, for wound treatment (2.4 ATA), therefore this is not an issue. According to Dr. Harch, “hyperbaric oxygen therapy in mTBI PCS/PTSD has satisfied one of medicine’s basic rules, “First, Do No Harm.”
Dr. Harch also suggests that after all of the money spent on research to find effective treatments for TBI and PTSD, the Coverage with Evidence pathway might allow the Departments of Defense (DoD) and Veterans Affairs (VA) to begin treating active military and veteran casualties with hyperbaric therapy so that they can have a better quality of life (QoL).
References
Primary Source:
Case Report – 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
Authors: Paul G Harch*1, Edward F Fogarty2, Paul K Staab1 and Keith Van Meter
And
Blast-Traumatic Brain Injury (TBI) with Post-traumatic Stress Disorder (PTSD): A Treatable Condition?
Authors: Judy R. Wilson, PhD
1. Invisible Wounds of War: Psychological and Cognitive Injuries, Their Conse- quences, and Services to Assist Recovery Edited by: Tanielian TJaycox LH. 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.
3. Harch PG, Neubauer RA: The Textbook of Hyperbaric Medicine 3rd edi- tion. Edited by: Jain KK. 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: The Textbook of Hyperbaric Medicine 2nd edition. Edited by: Jain KK. 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 Hyper- baric Medicine 4th edition. Edited by: Jain KK. 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 metabolism 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
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