Traumatic brain injury (TBI) is a common and potentially devastating clinical problem. Because prompt proper management of TBI sequelae can significantly alter the clinical course especially within 48 h of the injury, neuroimaging techniques have become an important part of the diagnostic work up of such patients. In the acute setting, these imaging studies can determine the presence and extent of injury and guide surgical planning and minimally invasive interventions. Neuroimaging also can be important in the chronic therapy of TBI, identifying chronic sequelae, determining prognosis, and guiding rehabilitation.

Neuroimaging in traumatic brain imaging

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/60min 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.

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A phase I study of low-pressure hyperbaric oxygen therapy for blast-induced post-concussion syndrome and post-traumatic stress disorder.

Background
Traumatic brain injury is a common health problem with significant effect on quality of life. Each year in the USA approximately 0.56% of the population suffer a head injury, with a case fatality rate of about 40% for severe injuries. These account for a high proportion of deaths in young adults. In the USA, 2% of the population live with long-term disabilities following head injuries. The major causes are motor vehicle crashes, falls, and violence (including attempted suicide). Hyperbaric oxygen therapy (HBOT) is the therapeutic administration of 100% oxygen at environmental pressures greater than 1 atmosphere absolute (ATA). This involves placing the patient in an airtight vessel, increasing the pressure within that vessel, and administering 100% oxygen for respiration. In this way, it is possible to deliver a greatly increased partial pressure of oxygen to the tissues. HBOT can improve oxygen supply to the injured brain, reduce the swelling associated with low oxygen levels and reduce the volume of brain that will ultimately perish. It is, therefore, possible that adding HBOT to the standard intensive care regimen may reduce patient death and disability. However, a concern for patients and families is that using HBOT may result in preventing a patient from dying only to leave them in a vegetative state, entirely dependent on medical care. There are also some potential adverse effects of the therapy, including damage to the ears, sinuses and lungs from the effects of the pressure and oxygen poisoning, so the benefits and risks of the therapy need to be carefully evaluated.

Objectives
To assess the effects of adjunctive HBOT for traumatic brain injury.

Search methods
We searched CENTRAL, MEDLINE, EMBASE, CINAHL and DORCTHIM electronic databases. We also searched the reference lists of eligible articles, handsearched relevant journals and contacted researchers. All searches were updated to March 2012.

Selection criteria
Randomised studies comparing the effect of therapeutic regimens which included HBOT with those that did not, for people with traumatic brain injury.

Data collection and analysis
Three authors independently evaluated trial quality and extracted data.

Main results
Seven studies are included in this review, involving 571 people (285 receiving HBOT and 286 in the control group). The results of two studies indicate use of HBOT results in a statistically significant decrease in the proportion of people with an unfavourable outcome one month after treatment using the Glasgow Outcome Scale (GOS) (relative risk (RR) for unfavourable outcome with HBOT 0.74, 95% CI 0.61 to 0.88, P = 0.001). This five-point scale rates the outcome from one (dead) to five (good recovery); an 'unfavourable' outcome was considered as a score of one, two or three. Pooled data from final follow-up showed a significant reduction in the risk of dying when HBOT was used (RR 0.69, 95% CI 0.54 to 0.88, P = 0.003) and suggests we would have to treat seven patients to avoid one extra death (number needed to treat (NNT) 7, 95% CI 4 to 22). Two trials suggested favourably lower intracranial pressure in people receiving HBOT and in whom myringotomies had been performed. The results from one study suggested a mean difference (MD) with myringotomy of -8.2 mmHg (95% CI -14.7 to -1.7 mmHg, P = 0.01). The Glasgow Coma Scale (GCS) has a total of 15 points, and two small trials reported a significant improvement in GCS for patients treated with HBOT (MD 2.68 points, 95%CI 1.84 to 3.52, P < 0.0001), although these two trials showed considerable heterogeneity (I2 = 83%). Two studies reported an incidence of 13% for significant pulmonary impairment in the HBOT group versus 0% in the non-HBOT group (P = 0.007).

In general, the studies were small and carried a significant risk of bias. None described adequate randomisation procedures or allocation concealment, and none of the patients or treating staff were blinded to treatment.

Authors' conclusions
In people with traumatic brain injury, while the addition of HBOT may reduce the risk of death and improve the final GCS, there is little evidence that the survivors have a good outcome. The improvement of 2.68 points in GCS is difficult to interpret. This scale runs from three (deeply comatose and unresponsive) to 15 (fully conscious), and the clinical importance of an improvement of approximately three points will vary dramatically with the starting value (for example an improvement from 12 to 15 would represent an important clinical benefit, but an improvement from three to six would leave the patient with severe and highly dependent impairment). The routine application of HBOT to these patients cannot be justified from this review. Given the modest number of patients, methodological shortcomings of included trials and poor reporting, the results should be interpreted cautiously. An appropriately powered trial of high methodological rigour is required to define which patients, if any, can be expected to benefit most from HBOT.

Hyperbaric oxygen therapy for the adjunctive treatment of traumatic brain injury

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.

Hyperbaric oxygen in the treatment of patients with cerebral stroke, brain trauma, and neurologic disease.

Persistent post-concussion syndrome caused by mild traumatic brain injury has become a major cause of morbidity and poor quality of life. Unlike the acute care of concussion, there is no consensus for treatment of chronic symptoms. Moreover, most of the pharmacologic and non-pharmacologic treatments have failed to demonstrate significant efficacy on both the clinical symptoms as well as the pathophysiologic cascade responsible for the permanent brain injury. This article reviews the pathophysiology of PCS, the diagnostic tools and criteria, the current available treatments including pharmacotherapy and different cognitive rehabilitation programs, and promising new treatment directions. A most promising new direction is the use of hyperbaric oxygen therapy, which targets the basic pathological processes responsible for post-concussion symptoms; it is discussed here in depth.

Treatment of persistent post-concussion syndrome due to mild traumatic brain injury: current status and future directions

Objective: To evaluate the effects of hyperbaric oxygen (HBO) therapy on patients with postbrain injury neural status. Methods: Two to 4 courses of HBO therapy and/or medications were used to treat 320 patients who were randomly divided into two groups. Assessment was made with 99m Tc-ethyl cysteinate dimer ( 99m Tc-ECD) single photon emission computed tomography (SPECT) before and after treatment. Results: There was a significant difference between the HBO therapy group and the non-HBO therapy group. HBO therapy was superior to medication treatment alone in the recovery of clinical symptoms, control of epilepsy, and resolution of hydrocephalus (P 0.01). Conclusions: HBO therapy has specific curative effects on patients with postbrain injury neural status, and 99m Tc-ECD SPECT could play an important role in diagnosing postbrain injury neural status and monitoring the therapeutic effects of HBO.

Jian-xiu Bao

Papers

Cerebral perfusion SPECT imaging for assessment of the effect of hyperbaric oxygen therapy on patients with postbrain injury neural status.