Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Sunday, June 30, 2024

Hyperbaric Oxygen Post Established Stroke

 I can't see any use for HBOT unless it's delivered in the first week and there are vastly easier options for delivering oxygen than that.

  • oxygen delivery (29 posts to January 2020) Many ideas in here, if your doctor isn't already using them to save neurons immediately post stroke; you don't have a functioning stroke doctor!

Hyperbaric Oxygen Post Established Stroke

David W. Harrison Penny M. BrasherJanice J. EngDevin HarrisAlison M. HoensAfshin KhazeiJennifer K. YaoRiyad B. Abu-Laban

Published: June 28, 2024

DOI: 10.7759/cureus.63395

Peer-Reviewed

Cite this article as: Harrison D W, Brasher P M, Eng J J, et al. (June 28, 2024) Hyperbaric Oxygen Post Established Stroke. Cureus 16(6): e63395. doi:10.7759/cureus.63395

Abstract

Background and purpose: Hyperbaric oxygen therapy (HBOT) has been reported to improve neurological function in the chronic phase of stroke in a single trial having significant limitations, including a lack of a sham control.

Methods: We conducted a single-center, parallel-group, randomized trial to determine the effectiveness of HBOT compared with a sham control in adults who were 6 to 36 months post-ischemic stroke. The treatment group received 40 sessions of HBOT at the Vancouver General Hospital Hyperbaric Unit. The control group received 40 sessions of sham treatment designed to replicate an HBOT experience.

Due to recruitment challenges and timeline/feasibility tracking by the research team, the control arm was altered after 20 months to a waitlist in the hope of increasing participation. In the second phase, participants were randomized to receive HBOT immediately or following an eight-week observation period.

The primary outcome was the post-treatment Stroke Impact Scale-16 (SIS-16). Secondary outcomes included the National Institute of Health Stroke Scale, Berg Balance Test, Digit Symbol Substitution Test, 5-Metre Walk Test, 6-Minute Walk Test, Grip Strength, Montreal Cognitive Assessment, Box/Block Test, and Center for Epidemiological Studies - Depression and Short Form-36. Based on detecting a clinically important between-group difference of 10 on the SIS-16 score, our target sample size was 68 participants per arm. 

Results: From January 5, 2016 to October 9, 2018, 34 participants were enrolled in the trial, 27 during the first phase and seven in the second phase. The study was stopped after 36 months, and prior to meeting the sample size target, due to low recruitment. At the end of treatment, the difference in the SIS-16 between groups was 5.5 (95% CI: 1.3 to 9.7, p = 0.01) in favor of the sham group.

Conclusions: Our results exclude a clinically important benefit of HBOT on the primary outcome of the SIS-16. These findings do not support the use of HBOT in chronic stroke survivors.

Introduction

Stroke is a major cause of mortality and long-term disability. The lifetime risk of stroke is approximately 25% [1]. Over half of stroke victims have some disability at one year [2]. Furthermore, stroke accounts for over 4% of all direct healthcare costs in high-income countries [3]. The estimated annual stroke-related cost of healthcare, lost wages, and decreased productivity in Canada is approximately $3.6 billion [4].

Most of the neurological improvement among stroke survivors occurs in the first 30 to 90 days [5]. Further modest functional improvements are possible after this period with interventions from an interdisciplinary rehabilitation team, but major disability often persists [2]. Hyperbaric oxygen therapy (HBOT) has been advocated and used by some healthcare providers as a therapy to improve disability post-stroke. HBOT involves the administration of inhaled 100% oxygen at increased ambient pressure inside a closed vessel, producing greatly elevated arterial and tissue oxygen tensions, and a wide variety of physiological effects at the cellular and sub-cellular levels [6,7].

HBOT has been studied as a treatment in the acute/subacute phase and chronic (3-6 months post-stroke) phase of stroke. A 2014 Cochrane systematic review of HBOT for acute ischemic stroke found that "there was no good evidence to show that HBOT improves clinical outcomes when applied during acute presentation of ischemic stroke", although the possibility of clinical benefit had not been excluded [8].

The use of HBOT in chronic stroke has been less studied. A PubMed search for randomized controlled trials of HBOT in chronic stroke (Hyperbaric Oxygenation/ AND (Stroke Rehabilitation/ OR Stroke/) AND randomized controlled trial.pt.) published between 1960 and 2024 identified one publication. There were significant limitations with the trial: it used a waitlist control, which can lead to overestimates of treatment effects [9,10], and the validity of the primary outcome, NIHSS, is uncertain in chronic stroke [11].

In an attempt to more definitively evaluate the use of HBOT as a treatment in the chronic phase of ischemic stroke, we designed a randomized clinical trial comparing the effect of sham HBOT and true HBOT on the neurological status of participants who were between six months and three years post-stroke. We hypothesized that a course of 40 treatments of HBOT would improve neurological function, as reflected in Stroke Impact Scale-16 (SIS-16) scores.

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