Stroke

Strokes are a highly prevalent condition that are the leading cause of chronic disability, the second leading cause of dementia 1, and the fifth leading cause of death in the US 2. Roughly 795,000 have a stroke each year in the U.S. 3. A stroke results in brain tissue death, leading to cognitive impairments, motor issues (lack of sensation or control in certain areas), headaches, and vision problems 4.

Recent research found significant benefits of HBOT during the chronic phase of stroke recovery. After receiving 40 HBOT treatments, patients who had suffered from a stroke 6 months to 3 years prior experienced significant improvements in neurologic functions, ADLs (activities of daily living), brain metabolism, and quality of life. Brain scans showed that the inactive areas of the brain that were damaged due to stroke were significantly healed and reactivated in more than half of the patients 5.

HBOT Research Shows Improvements To:

  • Brain damaged area
  • Cognitive function
  • Motor function
  • Quality of life 
  • Independence & activities of daily living

Stroke

Strokes are a highly prevalent condition that are the leading cause of chronic disability, the second leading cause of dementia 1, and the fifth leading cause of death in the US 2. Roughly 795,000 have a stroke each year in the U.S. 3. A stroke results in brain tissue death, leading to cognitive impairments, motor issues (lack of sensation or control in certain areas), headaches, and vision problems 4.

Recent research found significant benefits of HBOT during the chronic phase of stroke recovery. After receiving 40 HBOT treatments, patients who had suffered from a stroke 6 months to 3 years prior experienced significant improvements in neurologic functions, ADLs (activities of daily living), brain metabolism, and quality of life. Brain scans showed that the inactive areas of the brain that were damaged due to stroke were significantly healed and reactivated in more than half of the patients 5.

  • Improvements in damaged brain area
  • Improved cognitive function
  • Improved motor function
  • Improved quality of life
  • Improved activities of daily living

Benefits of HBOT for Stroke:

Maximizes Oxygen Transport

Allows for 100% saturation of hemoglobin molecules. Additional O2 molecules then dissolve directly into the plasma (the fluid component of blood) for transport.

Preserves, Repairs, & Enhances Cellular Functions

Boosts cellular metabolism, promotes rapid cell reproduction, and enhances collagen synthesis. Collagen is a protein in connective tissues like skin.

Improves Circulation

Bypasses blood vessels in damaged tissues by inducing the formation of new ones; improving the circulation, oxygenation, and perfusion of regular and deficient tissues.

A Dual Role for Hyperbaric Oxygen in Stroke Neuroprotection: Preconditioning of the Brain and Stem Cells.

Stroke continues to be an extremely prevalent disease and poses a great challenge in developing safe and effective therapeutic options. Hyperbaric oxygen therapy (HBOT) has demonstrated significant pre-clinical effectiveness for the treatment of acute ischemic stroke, and limited potential in treating chronic neurological deficits. Reported benefits include reductions in oxidative stress, inflammation, neural apoptosis, and improved physiological metrics such as edema and oxygen perfusion, all of which contribute to improved functional recovery.

Targeting vascular inflammation in ischemic stroke: Recent developments on novel immunomodulatory approaches.

Ischemic stroke is a devastating and debilitating medical condition with limited therapeutic options. However, accumulating evidence indicates a central role of inflammation in all aspects of stroke including its initiation, the progression of injury, and recovery or wound healing. A central target of inflammation is disruption of the blood brain barrier or neurovascular unit. Here we discuss recent developments in identifying potential molecular targets and immunomodulatory approaches to preserve or protect barrier function and limit infarct damage and functional impairment.

The Effect of Hyperbaric Oxygen Therapy on Functional Impairments Caused by Ischemic Stroke.

While research suggests a benefit of hyperbaric oxygen therapy (HBOT) for neurologic injury, controlled clinical trials have not been able to clearly define the benefits. To investigate the effects of HBOT on physical and cognitive impairments resulting from an ischemic stroke. Using a within-subject design a baseline for current functional abilities was established over a 3-month period for all subjects (n=7). Each subject then received two 4-week periods of HBOT for a total of 40 90-minute treatments over a 12-week period. Subjects completed a battery of assessments and had blood drawn six times over the 9-month total duration of the study.

Increased circulating endothelial progenitor cells and improved short-term outcomes in acute non-cardioembolic stroke after hyperbaric oxygen therapy.

Acute ischemic stroke is a leading cause of mortality and long-term disability, and profiles of endothelial progenitor cells (EPCs) reflect the degree of endothelial impairment. This study tested the hypothesis that hyperbaric oxygen therapy (HBOT) both improves the clinical short-term outcomes and increases the number of circulating EPCs and antioxidant capacity. The numbers of circulating EPCs [CD133/CD34 (%), KDR/CD34 (%)], biomarkers for oxidative stress (thiols and thiobarbituric acid-reactive substances), and clinical scores (National Institutes of Health Stroke Scale [NIHSS], Barthel index [BI],

Cerebral arterial gas embolism from attempted mechanical thrombectomy: recovery following hyperbaric oxygen therapy.

Cerebral arterial gas embolism is a recognised complication of endovascular intervention with an estimated incidence of 0.08%. Its diagnosis is predominantly clinical, supported by neuroimaging. The treatment relies on alleviating mechanical obstruction and reversing the proinflammatory processes that contribute to tissue ischaemia. Hyperbaric oxygen therapy is an effective treatment and has multiple mechanisms to reverse the pathological processes involved in cerebral arterial gas embolism. Symptomatic cerebral arterial gas embolism is a rare complication of endovascular intervention for acute ischaemic stroke.

Hyperbaric Oxygen Therapy in the Treatment of Acute Severe Traumatic Brain Injury: a Systematic Review.

There has been no major advancement in a quarter of a century for the treatment of acute severe traumatic brain injury (TBI). This review summarizes 40 years of clinical and pre-clinical research on the treatment of acute TBI with hyperbaric oxygen therapy (HBO2) in the context of an impending National Institute of Neurologic Disorders and Stroke (NINDS)-funded, multicenter, randomized, adaptive Phase II clinical trial – the Hyperbaric Oxygen Brain Injury Treatment (HOBIT) trial. Thirty studies (8 clinical and 22 pre-clinical) that administered HBO2 within 30 days of a TBI were identified from PubMed searches. The pre-clinical studies consistently reported positive treatment effects across a variety of outcome measures with almost no safety concerns, thus providing strong proof-of-concept evidence for treating severe TBI in the acute setting.

Hyperbaric oxygen in patients with ischemic stroke following cardiac surgery: a retrospective observational trial.

Hyperbaric oxygenation (HBO₂) involves breathing 100% oxygen under elevated ambient pressure in a hyperbaric chamber, thereby dissolving oxygen in the plasma. This results in an increase of arterial partial pressure of oxygen (pO₂). Though well established in experimental studies, HBO₂ treatment for ischemic stroke is still under discussion. From 2002-2014 HBO₂ (2.2 bar, 90 minutes one/day; average number per patient: 4.7) was applied in 49 consecutive patients (32 males, 17 females, mean age: 68.8 years, range 31.2 – 83.9) with acute neurological deficit following cardiac surgery (CABG 15; combined surgery 14; valve surgery 11; aneurysm repair 8;

Current treatment of central retinal artery occlusion: a national survey.

Central retinal artery occlusion (CRAO) is an ophthalmological emergency, the retinal analog of a stroke. To date there is no consensus or national guidelines on how this disorder should be managed. As academic neurologists and ophthalmologists treat CRAO frequently, we set out to understand how these clinicians approach patients with CRAO with a national survey. We identified university-associated teaching hospitals offering vascular neurology, neuro-ophthalmology and/or retina fellowships in the US and asked the directors of the programs to respond to questions in an open response format to profile the acute management of CRAO at their institution.

Sirt1 mediates improvement in cognitive defects induced by focal cerebral ischemia following hyperbaric oxygen preconditioning in rats.

Hyperbaric oxygen preconditioning (HBO-PC) has been proposed as a safe and practical approach for neuroprotection in ischemic stroke. However, it is not known whether HPO-PC can improve cognitive deficits induced by cerebral ischemia, and the mechanistic basis for any beneficial effects remains unclear. We addressed this in the present study using rats subjected to middle cerebral artery occlusion (MCAO) as an ischemic stroke model following HBO-PC. Cognitive function and expression of phosphorylated neurofilament heavy polypeptide (pNF-H) and doublecortin (DCX) in the hippocampus were evaluated 14 days after reperfusion

Hyperbaric oxygen-associated seizure leading to stroke.

Oxygen toxicity seizures are a well-known complication of hyperbaric oxygen treatment (HBOT). Until now, there have not been any reported cases of an acute ischaemic event (stroke) as the result of a HBOT-associated oxygen toxicity seizure. We report an event in which a seizure and stroke occurred together and consider that the stroke may have been caused by seizure-induced demand ischaemia. This challenges the generally held view that oxygen toxicity seizures in the clinical hyperbaric setting are benign. A discussion of the literature on the subject of seizure-induced brain injury is included. Risk factors for cerebrovascular disease should be taken into consideration in determining treatment pressures for HBOT, as reducing pressure reduces seizure risk.

Additional Research

A Dual Role for Hyperbaric Oxygen in Stroke Neuroprotection: Preconditioning of the Brain and Stem Cells.

Stroke continues to be an extremely prevalent disease and poses a great challenge in developing safe and effective therapeutic options. Hyperbaric oxygen therapy (HBOT) has demonstrated significant pre-clinical effectiveness for the treatment of acute ischemic stroke, and limited potential in treating chronic neurological deficits. Reported benefits include reductions in oxidative stress, inflammation, neural apoptosis, and improved physiological metrics such as edema and oxygen perfusion, all of which contribute to improved functional recovery.

Targeting vascular inflammation in ischemic stroke: Recent developments on novel immunomodulatory approaches.

Ischemic stroke is a devastating and debilitating medical condition with limited therapeutic options. However, accumulating evidence indicates a central role of inflammation in all aspects of stroke including its initiation, the progression of injury, and recovery or wound healing. A central target of inflammation is disruption of the blood brain barrier or neurovascular unit. Here we discuss recent developments in identifying potential molecular targets and immunomodulatory approaches to preserve or protect barrier function and limit infarct damage and functional impairment.

The Effect of Hyperbaric Oxygen Therapy on Functional Impairments Caused by Ischemic Stroke.

While research suggests a benefit of hyperbaric oxygen therapy (HBOT) for neurologic injury, controlled clinical trials have not been able to clearly define the benefits. To investigate the effects of HBOT on physical and cognitive impairments resulting from an ischemic stroke. Using a within-subject design a baseline for current functional abilities was established over a 3-month period for all subjects (n=7). Each subject then received two 4-week periods of HBOT for a total of 40 90-minute treatments over a 12-week period. Subjects completed a battery of assessments and had blood drawn six times over the 9-month total duration of the study.

Increased circulating endothelial progenitor cells and improved short-term outcomes in acute non-cardioembolic stroke after hyperbaric oxygen therapy.

Acute ischemic stroke is a leading cause of mortality and long-term disability, and profiles of endothelial progenitor cells (EPCs) reflect the degree of endothelial impairment. This study tested the hypothesis that hyperbaric oxygen therapy (HBOT) both improves the clinical short-term outcomes and increases the number of circulating EPCs and antioxidant capacity. The numbers of circulating EPCs [CD133/CD34 (%), KDR/CD34 (%)], biomarkers for oxidative stress (thiols and thiobarbituric acid-reactive substances), and clinical scores (National Institutes of Health Stroke Scale [NIHSS], Barthel index [BI],

Cerebral arterial gas embolism from attempted mechanical thrombectomy: recovery following hyperbaric oxygen therapy.

Cerebral arterial gas embolism is a recognised complication of endovascular intervention with an estimated incidence of 0.08%. Its diagnosis is predominantly clinical, supported by neuroimaging. The treatment relies on alleviating mechanical obstruction and reversing the proinflammatory processes that contribute to tissue ischaemia. Hyperbaric oxygen therapy is an effective treatment and has multiple mechanisms to reverse the pathological processes involved in cerebral arterial gas embolism. Symptomatic cerebral arterial gas embolism is a rare complication of endovascular intervention for acute ischaemic stroke.

Hyperbaric Oxygen Therapy in the Treatment of Acute Severe Traumatic Brain Injury: a Systematic Review.

There has been no major advancement in a quarter of a century for the treatment of acute severe traumatic brain injury (TBI). This review summarizes 40 years of clinical and pre-clinical research on the treatment of acute TBI with hyperbaric oxygen therapy (HBO2) in the context of an impending National Institute of Neurologic Disorders and Stroke (NINDS)-funded, multicenter, randomized, adaptive Phase II clinical trial – the Hyperbaric Oxygen Brain Injury Treatment (HOBIT) trial. Thirty studies (8 clinical and 22 pre-clinical) that administered HBO2 within 30 days of a TBI were identified from PubMed searches. The pre-clinical studies consistently reported positive treatment effects across a variety of outcome measures with almost no safety concerns, thus providing strong proof-of-concept evidence for treating severe TBI in the acute setting.

Hyperbaric oxygen in patients with ischemic stroke following cardiac surgery: a retrospective observational trial.

Hyperbaric oxygenation (HBO₂) involves breathing 100% oxygen under elevated ambient pressure in a hyperbaric chamber, thereby dissolving oxygen in the plasma. This results in an increase of arterial partial pressure of oxygen (pO₂). Though well established in experimental studies, HBO₂ treatment for ischemic stroke is still under discussion. From 2002-2014 HBO₂ (2.2 bar, 90 minutes one/day; average number per patient: 4.7) was applied in 49 consecutive patients (32 males, 17 females, mean age: 68.8 years, range 31.2 – 83.9) with acute neurological deficit following cardiac surgery (CABG 15; combined surgery 14; valve surgery 11; aneurysm repair 8;

Current treatment of central retinal artery occlusion: a national survey.

Central retinal artery occlusion (CRAO) is an ophthalmological emergency, the retinal analog of a stroke. To date there is no consensus or national guidelines on how this disorder should be managed. As academic neurologists and ophthalmologists treat CRAO frequently, we set out to understand how these clinicians approach patients with CRAO with a national survey. We identified university-associated teaching hospitals offering vascular neurology, neuro-ophthalmology and/or retina fellowships in the US and asked the directors of the programs to respond to questions in an open response format to profile the acute management of CRAO at their institution.

Sirt1 mediates improvement in cognitive defects induced by focal cerebral ischemia following hyperbaric oxygen preconditioning in rats.

Hyperbaric oxygen preconditioning (HBO-PC) has been proposed as a safe and practical approach for neuroprotection in ischemic stroke. However, it is not known whether HPO-PC can improve cognitive deficits induced by cerebral ischemia, and the mechanistic basis for any beneficial effects remains unclear. We addressed this in the present study using rats subjected to middle cerebral artery occlusion (MCAO) as an ischemic stroke model following HBO-PC. Cognitive function and expression of phosphorylated neurofilament heavy polypeptide (pNF-H) and doublecortin (DCX) in the hippocampus were evaluated 14 days after reperfusion

Hyperbaric oxygen-associated seizure leading to stroke.

Oxygen toxicity seizures are a well-known complication of hyperbaric oxygen treatment (HBOT). Until now, there have not been any reported cases of an acute ischaemic event (stroke) as the result of a HBOT-associated oxygen toxicity seizure. We report an event in which a seizure and stroke occurred together and consider that the stroke may have been caused by seizure-induced demand ischaemia. This challenges the generally held view that oxygen toxicity seizures in the clinical hyperbaric setting are benign. A discussion of the literature on the subject of seizure-induced brain injury is included. Risk factors for cerebrovascular disease should be taken into consideration in determining treatment pressures for HBOT, as reducing pressure reduces seizure risk.

References
  1. Roger, Véronique L., Alan S. Go, Donald M. Lloyd-Jones, Robert J. Adams, Jarett D. Berry, Todd M. Brown, Mercedes R. Carnethon, et al. “Heart Disease and Stroke Statistics—2011 Update.” Circulation 123, no. 4 (February 1, 2011): e18–209. https://doi.org/10.1161/CIR.0b013e3182009701.
  2. George, Mary G. “CDC Grand Rounds: Public Health Strategies to Prevent and Treat Strokes.” MMWR. Morbidity and Mortality Weekly Report 66 (2017). https://doi.org/10.15585/mmwr.mm6618a5.
  3. “Stroke: Hope Through Research | National Institute of Neurological Disorders and Stroke.” Accessed June 13, 2019. https://www.ninds.nih.gov/Disorders/Patient-Caregiver-Education/Hope-Through-Research/Stroke-Hope-Through-Research#1105_1.
  4. “Stroke: Causes, Symptoms, Diagnosis, and Treatment.” Medical News Today. Accessed June 26, 2019. https://www.medicalnewstoday.com/articles/7624.php.
  5. Badr, A. E., W. Yin, G. Mychaskiw, and J. H. Zhang. “Dual Effect of HBO on Cerebral Infarction in MCAO Rats.” American Journal of Physiology. Regulatory, Integrative and Comparative Physiology 280, no. 3 (March 2001): R766-770. https://doi.org/10.1152/ajpregu.2001.280.3.R766.
  6. Yin, Dali, and John H. Zhang. “Delayed and Multiple Hyperbaric Oxygen Treatments Expand Therapeutic Window in Rat Focal Cerebral Ischemic Model.” Neurocritical Care 2, no. 2 (2005): 206–11. https://doi.org/10.1385/NCC:2:2:206.
  7. Efrati, Shai, Gregori Fishlev, Yair Bechor, Olga Volkov, Jacob Bergan, Kostantin Kliakhandler, Izhak Kamiager, et al. “Hyperbaric Oxygen Induces Late Neuroplasticity in Post Stroke Patients – Randomized, Prospective Trial.” PLOS ONE 8, no. 1 (January 15, 2013): e53716. https://doi.org/10.1371/journal.pone.0053716.
  8. Zhang, John H., Takkin Lo, George Mychaskiw, and Austin Colohan. “Mechanisms of Hyperbaric Oxygen and Neuroprotection in Stroke.” Pathophysiology 12, no. 1 (July 1, 2005): 63–77. https://doi.org/10.1016/j.pathophys.2005.01.003.

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