Traumatic Brain Injury
Click on the publications below to view and close the abstracts
<strong>Hyperbaric oxygen therapy improves neurogenesis and brain blood supply in piriform cortex in rats with vascular dementia</strong><br /> Zhang T, Yang QW, Wang SN, Wang JZ, Wang Q, Wang Y, Luo YJ<br /> Brain Inj. 2010 Aug 17.
BACKGROUND: Neural stem cell treatment and neurogenesis stimulation have gained attention as potential treatments for vascular dementia (VD). Currently, research mainly focuses on neurogenesis occurring in the sub-ventricular zone and dentate gyrus, while the research of the piriform cortex (Pir) is limited. Few results showed that weak neurogenesis exists in the Pir of adult rats. Since neurogenesis occurs in the Pir and is closely related to cognitive function, this study addressed the question of whether neurogenesis occurs in the Pir of an animal with the VD. PRIMARY OBJECTIVE AND HYPOTHESIS: This study investigated the effects of hyperbaric oxygen therapy on brain blood supply and neurogenesis in the piriform cortex (Pir) of rats with VD.
MAIN OUTCOMES AND RESULTS: Compared to non-VD control rats (NC), rats with VD showed reduced rCBF, increased rCBV and slower MTT in the Pir. However, following hyperbaric oxygen (HBO) treatment in VD rats, rCBF increased, rCBV decreased and MTT increased. To determine whether the restoration in brain blood supply was associated with increased neurogenesis, immunohistochemical detection of nestin and doublecortin (DCX) was used. In the Pir of both normal and VD rats, nestin positive cells were localized to layer II (superficial cellular layer) and layer III (deep cellular layer). Nestin expression was increased in Pir cells in VD rats and was even more intensely expressed after the HBO treatment. DCX positive cells were mostly located in layer II from amygdaline fissure to rhinal fissure.
CONCLUSION: These results suggest that HBO therapy can improve the blood supply and promote the neurogenesis in the Pir of adult rats with the VD.
<strong>Hyperbaric oxygen preconditioning reduces ischemia-reperfusion injury by stimulating autophagy in neurocyte</strong><br /> Wang YC, Zhang S, Du TY, Wang B, Sun XQ<br /> Brain Res. 2010 Apr 6; 1323C:149-151. Epub 2010 Feb 1.
Cerebral ischemia-reperfusion injury (IRI) is a complex process resulting in cellular damage and death. Many studies have reported that an ischemic preconditioning could induce protection against ischemic insult. However, the safety concerns and practical feasibility have limited the application of ischemia preconditioning in practice.
Subsequently, a number of substances including endotoxin and cytokines etc. have proven effective in inducing ischemic tolerance in the neurocyte. Unfortunately, the application of these substances to the clinical practice of neurosurgery still remains questionable for their toxicity or side effects.
Therefore, a novel therapy to protect against cerebral IRI requires further study. Several recent studies confirmed that repeated hyperbaric oxygen preconditioning (HBO-PC) prior to cerebral ischemia or spinal cord ischemia can provide neuroprotection. HBO as a therapeutic measure has been widely accepted for its convenience and safety. However, information about the mechanism of how this neuroprotection works is still very limited.
We hypothesize that autophagy induction is involved in HBO-PC induced neuroprotection on IRI in neurocyte. The hypothesis reveals that autophagy may be a new therapeutic target for cerebral IRI.
Copyright 2010 Elsevier B.V. All rights reserved.
<strong>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</strong><br /> Harch PG, Fogarty EF, Staab PK and Van Meter K<br /> Cases Journal 2009, 2:6538
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.
<strong>Case report: Treatment of mild traumatic brain injury with hyperbaric oxygen</strong><br /> Wright JK1, Zant E, Groom K, Schlegel RE, Gilliland K.<br /> Undersea Hyperb Med. 2009 Nov-Dec;36(6):391-9.
Two United States Air Force Airmen were injured in a roadside improvised explosive device (IED) blast in Iraq in January 2008. Both airmen suffered concussive injuries and developed irritability, sleep disturbances, headaches, memory difficulties and cognitive difficulties as symptoms of mild traumatic brain injury (mTBI).
Six months after injury, repeat Automated Neuropsychological Assessment Metrics (ANAM) testing showed deterioration, when compared to pre-injury baseline ANAM assessment, in all measured areas (simple reaction time, procedural reaction time, code substitution learning, code substitution delayed, mathematical processing, and matching to sample).
The airmen were treated with hyperbaric oxygen in treatments of 100% oxygen for one hour at 1.5 atmospheres absolute, resulting in rapid improvement of headaches and sleep disturbances, improvement in all symptoms and resolution of most symptoms.
Repeat ANAM testing after completion of the hyperbaric treatments – nine months after initial injury – showed improvement in all areas, with most measures improving to pre-injury baseline levels. The airmen received no other treatment besides medical monitoring. Repeat neuropsychologic testing confirmed the improvement.
We conclude that the improvement in symptoms and ANAM performance is most likely attributable to HBO treatment.
<strong>A Hyperbaric oxygen in traumatic brain injury</strong><br /> Rockswold SB, Rockswold GL, Defillo<br /> Neurol Res. 2007 Mar; 29(2):162-72
OBJECTIVES: This critical literature review examines historical and current investigations on the efficacy and mechanisms of hyperbaric oxygen (HBO) treatment in traumatic brain injury (TBI). Potential safety risks and oxygen toxicity, as well as HBO’s future potential, are also discussed.
METHODS: Directed literature review.
RESULTS: Historically, cerebral vasoconstriction and increased oxygen availability were seen as the primary mechanisms of HBO in TBI. HBO now appears to be improving cerebral aerobic metabolism at a cellular level, namely, by enhancing damaged mitochondrial recovery. HBO given at the ideal treatment paradigm, 1.5 ATA for 60 minutes, does not appear to produce oxygen toxicity and is relatively safe.
DISCUSSION: The use of HBO in TBI remains controversial. Growing evidence, however, shows that HBO may be a potential treatment for patients with severe brain injury. Further investigations, including a multicenter prospective randomized clinical trial, will be required to definitively define the role of HBO in severe TBI.
<strong>Hyperbaric oxygen and cerebral physiology</strong><br /> Calvert JW, Cahill J, Zhang JH<br /> Neurol Res. 2007 Mar; 29(2):132-41
Hyperbaric oxygen (HBO) therapy is defined by the Undersea and Hyperbaric Medical Society (UHMS) as a treatment in which a patient intermittingly breathes 100% oxygen under a pressure that is greater than the pressure at sea level [a pressure greater than 1 atmosphere absolute (ATA)].
HBO has been shown to be a potent means to increase the oxygen content of blood and has been advocated for the treatment of various ailments, including air embolism, carbon monoxide poisoning, wound healing and ischemic stroke.
However, definitive established mechanisms of action are still lacking. This has led to uncertainty among clinicians, who have understandingly become hesitant in regard to using HBO therapy, even in situations where it could prove beneficial. Therefore, this review will summarize the literature regarding the effects of HBO on brain oxygenation, cerebral blood flow and intracranial pressure in both the healthy and injured brains, as well as discuss how changes in these three factors can impart protection.
<strong>Hyperbaric oxygen therapy improves spatial learning and memory in a rat model of chronic traumatic brain injury</strong><br /> Harch PG, Kridt C, Van Meter KW and Sutherland RJ<br /> Brain Research 1174 (2007) 120-129
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.
<strong>Improving neuropsychological function after chronic brain injury with hyperbaric oxygen</strong><br /> Golden Z, Golden C, Neubauer RA<br /> Disability and Rehabilitation, November 2006; 28(22): 1379 – 1386 Toggle title
PURPOSE: One suggested treatment for chronic brain injury (CBI) is the use of hyperbaric oxygen therapy (HBOT). The present study was an evaluation of neuropsychological improvement after HBOT in CBI patients.
METHOD: Study 1 compared test – retest results of 21 CBI children treated with HBOT against test – retest results of 42 untreated brain injured and normal children. Study 2 compared 21 CBI adults treated with HBOT against 42 untreated normal and brain injured adults. In each study, subjects received pre and post assessments to evaluate neuropsychological function.
RESULTS: The HBOT-treated children showed significant improvement when compared with the two control groups on measures of daily living, socialization, communication, and motor skills. The treated adults made significant gains in all neuropsychological areas tested as compared to controls.
CONCLUSION: The studies were strongly supportive of HBOT as a treatment for lessening the neurological impact of CBI. These studies indicate that HBOT can be an effective aid in ameliorating the neuropsychological and physiological effects of CBI. The absence of a clear sham HBOT treatment group is an issue as it could be that there was a placebo effect, but it should be noted that the controls were receiving more traditional interventions during the study.
<strong>Late Treatment of Severe Brain Injury with Hyperbaric Oxygenation</strong><br /> Neubauer RA, Neubauer V, Gerstenbrand F<br /> Journal of American Physicians and Surgeons Volume 10 Number 2 Summer 2005
Controlled studies have demonstrated safety and efficacy of hyperbaric oxygenation therapy (HBOT) in the treatment of anoxic, traumatic, ischemic, or thrombotic brain injury. Over the past 15 years, our clinic has treated 350 seriously brain-injured patients, from six months to 14 years after the event, many of whom suffered from various degrees of the apallic syndrome ranging from 1 to 8. Despite the hopeless prognosis that most patients were given by their physicians, varying degrees of clinical improvement occurred, along with substantial reductions in the cost of ongoing care. Clinical improvements were correlated with increased perfusion and metabolism, with reactivation of idling neurons demonstrated by sequential single photon emission computerized tomographic (SPECT) scanning.
<strong>Improvement in motor and cognitive impairment after hyperbaric oxygen therapy in a selected group of patients with cerebrovascular disease: a prospective single-blind controlled trial</strong><br /> Vila JF, Balcarce PE, Abiusi GR, Dominguez RO, Pisarello JB<br /> Undersea Hyperb Med. 2005 Sep-Oct; 32(5):341-9
BACKGROUND: Clinical and experimental evidence suggests that a localized decrease in oxygen brain tissue availability contributes to the neurological deficit in patients with cerebrovascular disease (CVD) who also present with frontal leukoaraiosis (LA) (periventricular hypodensity on CT scan) and lacunar infarcts. In a prospective controlled trial blinded to patients but not to investigators, we tested the effect of HBO2 on this group of patients.
METHODS: Selected patients with symptomatic CVD, LA and lacunar infarcts received daily exposures of 45 minutes for 10 days to hyperbaric oxygen (n=18, HBO2 group) or hyperbaric air (n=8, control group). The control group subsequently received HBO2. Scores of conventional scales for motor and cognitive functions were obtained and videotaped before and after exposure. After the exposures, participants were followed on a monthly basis with systematic clinical neurological examination for up to 6 months. Results. There was a statistically significant improvement in all scales for the HBO2 group compared with the placebo group and in the placebo group after receiving HBO2 (p<0.05). Neurological improvement persisted in the majority of patients for up to 6 months. Repetition of the HBO2 protocol in 9 patients in whom symptoms recurred after 6 months resulted in improvement of symptoms.
CONCLUSIONS: These data provide evidence consistent with the notion that HBO2 improves neurological function in patients with CVD, lacunar infarcts and frontal LA. Because of the lack of investigator blinding and a relatively small sample size in this study, larger, randomized controlled studies are needed to further test this hypothesis and to further define the role of oxygen therapy for brain repair in chronic brain disease.
<strong>Hyperbaric oxygen in the treatment of patients with cerebral stroke, brain trauma, and neurologic disease</strong><br /> Al-Waili NS, Butler GJ, Beale J, Abdullah MS, Hamilton RW, Lee BY, Lucus P, Allen MW, Petrillo RL, Carrey Z, Finkelstein M<br /> Adv. Ther. 2005 Nov-Dec; 22(6):659-78.
Hyperbaric oxygen (HBO) therapy has been used to treat patients with numerous disorders, including stroke. This treatment has been shown to decrease cerebral edema, normalize water content in the brain, decrease the severity of brain infarction, and maintain blood-brain barrier integrity. In addition, HBO therapy attenuates motor deficits, decreases the risks of sequelae, and prevents recurrent cerebral circulatory disorders, thereby leading to improved outcomes and survival.
Hyperbaric oxygen also accelerates the regression of atherosclerotic lesions, promotes antioxidant defenses, and suppresses the proliferation of macrophages and foam cells in atherosclerotic lesions. Although no medical treatment is available for patients with cerebral palsy, in some studies, HBO therapy has improved the function of damaged cells, attenuated the effects of hypoxia on the neonatal brain, enhanced gross motor function and fine motor control, and alleviated spasticity.
In the treatment of patients with migraine, HBO therapy has been shown to reduce intracranial pressure significantly and abort acute attacks of migraine, reduce migraine headache pain, and prevent cluster headache. In studies that investigated the effects of HBO therapy on the damaged brain, the treatment was found to inhibit neuronal death, arrest the progression of radiation-induced neurologic necrosis, improve blood flow in regions affected by chronic neurologic disease as well as aerobic metabolism in brain injury, and accelerate the resolution of clinical symptoms.
Hyperbaric oxygen has also been reported to accelerate neurologic recovery after spinal cord injury by ameliorating mitochondrial dysfunction in the motor cortex and spinal cord, arresting the spread of hemorrhage, reversing hypoxia, and reducing edema. HBO has enhanced wound healing in patients with chronic osteomyelitis.
The results of HBO therapy in the treatment of patients with stroke, atherosclerosis, cerebral palsy, intracranial pressure, headache, and brain and spinal cord injury are promising and warrant further investigation.