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AAPI’S NUTRITION GUIDE TO OPTIMAL HEALTH: USING PRINCIPLES OF FUNCTIONAL MEDICINE AND NUTRITIONAL GENOMICS improvements.(37) They concluded that HBOT was a new therapy for the treatment of ASD in Thai children. Because of its potential regenerative capacity, stem cell therapy has been proposed as a potential treatment for autism spectrum disorder.(38) HBOT has been shown to mobilize stem cells from the bone marrow and therefore may act to stimulate the body’s own native healing processes.(39,40) The mechanism of action of stem cell treatments in autism may be the regeneration of damaged nerve tissue and reduction of inflammation or immune modulation. Although many more studies are needed to evaluate the viability of this treatment option, it is interesting to consider the use of HBOT to stimulate the body’s native regenerative process. Autism is considered a multisystem disorder. Hyperbaric oxygen therapy may be beneficial to the treatment of autism because of its general effects on the body, with minor side effects (ear pain, sinus pain, claustrophobia). ASD is a complex neurodevelopmental disorder demonstrating brain inflammation, cerebral hypoperfusion in the temporal lobes, gut inflammation and dysbiosis. The central mechanism of this disorder may be inflammation and this could explain seemingly divergent symptoms present in this population. HBOT has been demonstrated to have anti-inflammatory effects, to improve cerebral perfusion, upregulate anti-oxidant enzyme systems, and reduce intestinal dysbiosis in scientific studies. It seems well founded that HBOT should continue to be explored in the treatment of ASD since its mechanism of action on the human body may directly counter many of the pathophysiological mechanisms of disease in this population. Traumatic Brain Injury Clinical Vignette CR is a 17 year old male who presented for further physical rehabilitation for gait ataxia due to 146 hemiparesis. Two years ago CR was hospitalized for 6 weeks after he sustained severe traumatic brain injury as an unrestrained motor vehicle passenger. CT scanning revealed multiple areas of brain trauma and hemorrhage involving the right temporal area, left internal capsule, right frontal lobe, and bilateral parietal lobes. CR received 14 months of residential and outpatient rehabilitation. A repeat CT scan at 19 months showed only a small lacunar infarct. Review of the Literature and Discussion Traumatic brain injury is a common cause for disability in young people. TBI is thought to affect approximately 530 per 100,000 people in the United States with the male to female incidence nearly double. TBI encompasses disorders of varying degrees of severity and disability. Pathologic consequences result from both primary injury (hypoxia, hemorrhage, diffuse axonal injury, etc.) and the subsequent inflammatory and reparative process that follows, often called secondary injury. (1) The majority of scientific and clinical efforts are being focused on mitigating the pathophysiologic consequences of the secondary injury since this appears to be modifiable. Cerebral ischemia, energy failure, inflammation, oxidative stress and neuronal death is the final outcome of the secondary injury.(2) Understanding the mechanism of the secondary injury will aid in establishing effective treatment strategies of which HBO therapy may be able to address.HBOT has been used for the treatment of brain injury for over forty years, with a large body of work from the Russian literature which we do not have access to.(3) An early prospective controlled trial of sixty patients evaluated HBOT for the treatment of head injury coma, finding that HBOT can counteract ischemia and edema.(4) In a group of severely brain injured pediatric patients, Brown et al. found that HBOT temporarily reduced intracranial pressure, however did not not demonstrate a clinical improvement in this group.(5) 2012
AAPI’S NUTRITION GUIDE TO OPTIMAL HEALTH: USING PRINCIPLES OF FUNCTIONAL MEDICINE AND NUTRITIONAL GENOMICS The use of HBO in the acute closed head injury was studied in 1992 by Rockswold et al. when they randomly selected for HBO treatment from 168 patients who had a Glascow Coma Score of 9 or less for at least 6 hours. HBOT did not increase the number of patients in the favorable outcome category. (6) It is now believed that there is a therapeutic window of between three and 6 hours for the treatment of TBI with HBOT(7), although delayed multiple HBO treatment may be beneficial.(8) HBO can protect the nervous system by improving brain metabolism, decreasing intracranial pressures, blunting the inflammatory response, improving the integrity of the blood brain barrier and reducing edema, and mitigating apoptosis.(9) HBOT was found to improve cerebral blood flow, as determined by SPECT scan, in a study of 50 patients with chronic brain injury (10) An improvement in aerobic brain metabolism was seen in 37 severely brain injured patients after they underwent up to seven one-hour treatments with HBOT. These authors demonstrated a reduction in cerebrospinal fluid lactate, a reduction in intracranial pressure, and an increased cerebral metabolic rate.(11) None of these studies looked at clinical outcomes. Longhi et al. reported later that there was no evidence of a clinical benefit of hyperoxia for head injury, demonstrating that the ratio between lactate and pyruvate, which they deemed a better indicator of brain metabolism, was unchanged after hyperoxia (not HBOT).(12) In a review of the literature, McDonagh et al. reported in 2004 that the clinical significance of HBOT on functional status was ‚unclear,‛ but that the evidence did support a small decrease in overall mortality.(13) Shi et al., however, concluded that HBO therapy had ‚specific curative effects‛ after studying the use of HBO therapy in320 patients post-brain injury. They measured the recovery of clinical symptoms, control of epilepsy, and resolution of hydrocephalus. SPECT imaging was performed before and after treatment to assess the therapeutic effects of HBOT. These 147 authors concluded HBO therapy was superior to medications alone and that SPECT imaging could be used to demonstrate those individuals with neurological dysfunction that may be amenable to HBO treatment.(14) HBOT has been used as an adjunct to radiationinduced necrosis of the brain which demonstrates its potential neuroprotective role.(15) The use of HBOT for bony injuries and soft tissue radiation injury was recommeded by Feldmeirer after a review of 74 studies in the literature. He further noted that there was increasing evidence in support of HBOT for radiation-induced brain necrosis.(16) Treatment frequency of HBOT has been found to be a factor in improving neuropsychiatric effects of chronic brain injury and this may occur via enhanced mitochondrial recovery. This benefit is proposed when HBO treatment is used at lower pressures and greater frequency. Many reports describe the use of ‚mild‛ hyperbaric oxygen therapy at pressures of 1.5 atmospheres or less and ongoing treatments.(17) This was illustrated by a pilot case study of a 54-year-old male who had sustained a TBI one year previous, causing permanent neurological symptoms. Electrophysiological, behavioral, and metabolic measures were obtained to evaluate the impact of HBOT on his neurocognitive function. After the first series of 20 treatments, the authors noted improvements in motor and sensory measures. These were paralleled by electrophysiological measures. The improvements were not sustained at one year. He then received a second series of 60 HBO treatments one year later.(18) Notable aspects of this case study are the documented measurable clinical improvements coincident with enhanced electrophysiological testing (P300 brainwave amplitude); however, there was no concomitant improvement in SPECT imaging seen. This may indicate that SPECT imaging is not the appropriate surrogate test to validate functional 2012
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