Hyperbaric Oxygen Induces Late
Neuroplasticity in Post Stroke Patients
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Recovery after stroke correlates with
non-active (stunned) brain regions, which
may persist for years. The current study
aimed to evaluate whether increasing the
level of dissolved oxygen by Hyperbaric
Oxygen Therapy (HBOT) could activate
neuroplasticity in patients with chronic neurologic deficiencies due to stroke.
Methods and Findings
A prospective, randomized, controlled trial including 74 patients (15 were excluded). All participants suffered a stroke 6–36 months prior to inclusion and had at least one motor dysfunction. After inclusion, patients were randomly assigned to “treated” or “cross” groups. Brain activity was assessed by SPECT imaging; neurologic functions were evaluated by NIHSS, ADL, and life quality. Patients in the treated group were evaluated twice: at baseline and after 40 HBOT sessions. Patients in the cross group were evaluated three times: at baseline, after a 2-month control period of no treatment, and after subsequent 2-months of 40 HBOT sessions. HBOT protocol: Two months of 40 sessions (5 days/week), 90 minutes each, 100% oxygen at 2 ATA. We found that the neurological functions and life quality of all patients in both groups were significantly improved following the HBOT sessions while no improvement was found during the control period of the patients in the cross group. Results of SPECT imaging were well correlated with clinical improvement. Elevated brain activity was detected mostly in regions of live cells (as confirmed by CT) with low activity (based on SPECT) – regions of noticeable discrepancy between anatomy and physiology.
The results indicate that HBOT can lead to significant neurological improvements in post stroke patients even at chronic late stages. The observed clinical improvements imply that neuroplasticity can still be activated long after damage onset in regions where there is a brain SPECT/CT (anatomy/physiology) mismatch.
Rationale of Hyperbaric Oxygenation in Cerebral Vascular Insult
Fischer BR, Palkovic S, Holling M, Wolfer J, Wassmann H
Curr Vasc Pharmacol. 2010 Jan: 8(1): 35-43
Cerebrovascular diseases and especially ischemic stroke are a leading cause of death. They occur mostly due to an insufficient oxygen (O2) supply to the central neural tissue as a result of thromboembolic events and/or obstructive vessel disease. The primary damage of the brain tissue cannot be restored. However, adequate therapy could minimize secondary impairment of brain tissue and restore neuronal function in the so-called “penumbra region”. Apart from reopening occluded vessels, additional O2 supply is essential for survival of malfunctioning neural tissue. Breathing of 100% O2 under hyperbaric conditions, hyperbaric oxygenation (HBO), is the only method to increase the O2 concentration in tissue with impaired blood supply. Experimental as well as clinical studies have reported a positive effect of HBO therapy. Survival rate has increased under HBO therapy and neurological outcome has improved. The optimal levels of pressure as well as duration and numbers of HBO sessions need to be specified to avoid undesirable effects. Unfortunately, many questions remain unanswered before routinely recommending HBO as additional therapy in clinical practice. In this review we consider the (patho-)physiological background of HBO-therapy, the latest results of experimental and clinical studies and stress the evidence in patients with cerebrovascular disease.
Oxygen Therapy in Stroke: Past, Present, and Future
Int J Stroke. 2006 Nov;1(4):191-200
Oxygen is frequently administered to patients with suspected stroke. However, the role of oxygen therapy in ischemic stroke remains controversial in light of the failure of three clinical trials of hyperbaric oxygen therapy to show efficacy, and the fear of exacerbating oxygen free radical injury. The previous trials had several shortcomings, perhaps because they were designed on basis of anecdotal case reports and little preclinical data. Most animal studies concerning oxygen therapy in stroke have been conducted over the last 6 years. Emerging data suggests that hyperbaric and even normobaric oxygen therapy can be effective if used appropriately, and raises the tantalizing possibility that hyperoxia can be used to extend the narrow therapeutic time window for stroke thrombolysis. This article reviews the history, rationale, mechanisms of action and adverse effects of hyperoxia, the key results of previous hyperoxia studies, and the potential role of oxygen therapy in contemporary stroke treatment.
Involvement of the Mitochondrial ATP-Sensitive Potassium Channel in the Neuroprotective Effect of Hyperbaric Oxygenation after Cerebral Ischemia
Lou M, Chen Y, Ding M, Eschenfelder CC, Deuschl G.
Brain Res Bull. 2006 Mar 31;69(2):109-16. Epub 2005 Dec 15.
In the present study, we investigated whether activation of mitochondrial ATP-sensitive potassium channel is involved in the neuroprotective effect offered by early hyperbaric oxygenation after cerebral ischemia. The selective mitochondrial ATP-sensitive potassium channel antagonist 5-hydroxydecanoate was infused intracerebroventricularly before hyperbaric oxygenation treatment initiated 3 h after middle cerebral artery occlusion for 90 min. Neurological status was evaluated and brains were removed for the measurement of infarct size and immunohistochemical evaluation of apoptosis 24 h after middle cerebral artery occlusion. Early hyperbaric oxygenation treatment improved neurologic deficits and reduced infarct volume, while these effects were reversed by the administration of 5-hydroxydecanoate. Furthermore, early hyperbaric oxygenation significantly decreased the number of apoptotic cells in the peri-infarct cortex 24 h after ischemic insult and this effect was also blocked by 5-hydroxydecanoate. The present findings suggest that early hyperbaric oxygenation therapy prevents apoptosis and promotes neurologic functional recovery after focal cerebral ischemia, and the opening of mitochondrial ATP-sensitive potassium channel plays a role in this antiapoptotic effect of early hyperbaric oxygenation.
Min Lou, Yizhang Chen, Meiping Ding, Christoph C. Eschenfelder, Günther Deuschl, Involvement of the mitochondrial ATP-sensitive potassium channel in the neuroprotective effect of hyperbaric oxygenation after cerebral ischemia, Brain Research Bulletin, Volume 69, Issue 2, 31 March 2006, Pages 109-116, ISSN 0361-9230, 10.1016/j.brainresbull.2005.11.009.
Keywords: Hyperbaric oxygenation; Ischemia; Middle cerebral artery occlusion; Mitochondria; Potassium channels; Rats