Traumatic brain injury (TBI) is a disorder of major public health significance. Each year in the United States alone there are 100 new cases/100,000 population and 52,000 deaths (NIH Consensus, 1999). Most patients survive and add to an increasing prevalence of chronic TBI, estimated at 2.5 – 6.5 million individuals in 1998 (NIH Consensus, 1999).
HBOT is the use of greater than atmospheric pressure oxygen as a pharmacologic treatment of basic disease processes/states and their diseases (Harch and Neubauer, 1999). HBOT has a variety of physiological effects depending on the chronicity of the underlying pathology. When delivered repetitively in chronic shallow perfusion gradient wounds (Marx and Johnson, 1988) HBOT repairs wounds through stimulated fibroblast replication (Hehenberger et al., 1997), collagen synthesis (Ishii et al., 1999), and ultimately angiogenesis (Marx et al., 1990). The mechanisms are postulated to be a combination of upregulation of key growth hormone receptors (Bonomo et al., 1998) and hormones (Sheikh et al.,2000), improved wound responsiveness to growth hormones (Wu et al., 1995), and DNA signaling (Siddiqui et al., 1997; Ishii et al., 1999).
In the early 1990s, Paul G. Harch, Christopher Kriedt, Keith W. Van Meter and Robert James Sutherland found that a lower pressure/dose of HBOT than traditionally employed for diving cases could be used to successfully treat delayed, recalcitrant, and chronic cases of decompression illness (Harch, 1996). The durable clinical improvements (cognitive, social, work/school, emotional, and neurological) were mirrored by improvements in SPECT brain imaging (Harch, 1996). They and others subsequently applied this low-pressure HBOT protocol to additional chronic cerebral disorder cases, including chronic traumatic brain injury, with similar clinical and SPECT improvements (Neubauer et al., 1992, 1994, 2004; Harch et al., 1996a, 2004;
Neubauer and James, 1998; Harch and Neubauer, 1999, 2004; Golden et al., 2002).
In an experiment of 2007, the authors used 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 the hippocampus using a diaminobenzidine 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.
Paul G. Harch, Christopher Kriedt, Keith W. Van Meter and Robert James Sutherland (2007). Hyperbaric oxygen therapy improves spatial learning and memory in a rat model of chronic traumatic brain injury. Brain Research.
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