The post-concussion syndrome (PCS) is a complex of symptoms consisting of headaches, dizziness, imbalance, vertigo, fatigue, changes in sleep pattern, neuropsychiatric symptoms, and cognitive impairments (in memory, attention, concentration and executive functions). PCS is most often described in the setting of mTBI, but may also occur after moderate and severe TBI. In Eight to Ninty percent of mTBI cases, the symptoms fade away in 7–10 days. Still, in 10–20 percent, PCS may persist for weeks or months due to structural and/or metabolic brain damage. Twenty-five to thirty-three percent of those retain a permanent brain injury and experience persistent PCS; the symptoms turn chronic and endure more than 6 months.
The existing pharmacologic and non-pharmacologic treatments have mostly failed to elicit efficacious results in both the clinical symptoms and the pathophysiologic cascade leading to permanent brain injury. In recent years, both basic (animal models) and clinical studies have shown that hyperbaric oxygen therapy (HBOT) can improve PCS by targeting the basic pathological processes responsible for post-concussion symptoms. HBOT can induce brain angiogenesis, demonstrated by perfusion MRI with significant increase in CBF and CBV following HBOT along with significant cognitive improvement in patients post TBI.
In a study by Sigal Tal, Amir Hadanny, Efrat Sasson, Gil Suzin and Shai Efrati, fifteen patients with chronic cognitive impairment due to TBI who were treated at the Sagol Center for Hyperbaric Medicine and Research between September 2013 and December 2015. The mean age was 35.8±3.5 years (21–70), and 53% (8/15)were males. All patients had documented traumatic brain injury6 months to 27 years (mean 6.7±2.1 years) prior to HBOT. Seven patients (46.7%) suffered from moderate to severe TBI, and8 (53.3%) suffered from PCS after mTBI.
Along with the structural changes, HBOT induces angiogenesis, as shown by the increase of CBF and CBV in this study as well as in previous study . The injured areas in the brains post TBI experience hypoxia and hypo perfusion, which serve as a rate-limiting factor for any regenerative process. HBOT-induced angiogenesis has been amply confirmed in pre-clinical models and can be deduced from brain SPECTs of patients post stroke and post TBI even years after the acute insult.
The generation of new micro vessels renders the local environment non-hypoxic, thus able to induce brain plasticity, enhance neurogenesis and synaptogenesis and foster functional recovery. Unsurprisingly, CBV and CBF increased in the long association fiber tracts discussed above, including corpus callosum, association fibers (SLF, IFOF) and cingulum. Angiogenesis and increased perfusion to the malfunctioning tissue, seen in DSC, serve as infrastructure for the regenerative process and the preservation of newly generated metabolic functioning of the axonal microstructure seen in DTI.
HBOT can induce cerebral angiogenesis and recovery of brain microstructure in patients with chronic cognitive impairments due to TBI months to years after the acute injury. The increased integrity of brain fibers correlates with the functional cognitive improvement. The mechanism by which HBOT can induce brain neuroplasticity can be demonstrated by highly sensitive perfusion MRI and DTI. Further studies, using DTI – MRI, are needed in order to gain better understanding of the neuroplasticity effect of HBOT in a larger cohort of patients with different types of brain injuries.
Sigal Tal, Amir Hadanny, Efrat Sasson, Gil Suzin and Shai Efrati (2017); Hyperbaric Oxygen Therapy Can Induce Angiogenesis and Regeneration of Nerve Fibers in Traumatic Brain Injury Patients.
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