Stimulating the Facial Nerve to Treat Ischemic Stroke: A Systematic Review

 Is this the best way to increase cerebral blood flow or is more oxygen delivery better?

If your doctor is doing nothing about oxygen delivery to the brain s/he is letting more neurons die than should. ARE YOU OK WITH THAT? Mine let 5.4 billion neurons die that first week.

No protocol, you need to fire the complete stroke department, starting with the board of directors.  I would suggest one of these:

Possible solutions: Obviously not vetted coming from me. Don't do them.

You can look at the years these were reported on and tell how long your hospital has been incompetent.

• Normobaric oxygen (10 posts to January 2020)

• oxygen delivery (4 posts to January 2020)

• brain blood flow (3 posts to April 2019) 

 

How to Improve Your Brain Function with An Oxygen Concentrator April 2018 

Or is it more important to increase the loading ability of red blood cells to carry more oxygen? 

Like this?

University of Glasgow Study Demonstrates the Ability of Oxycyte® to Supply Oxygen to Critical Penumbral Tissue in Acute Ischemic Stroke  August 2012

Or like this?

chronic cannabis users have higher cerebral blood flow and extract more oxygen from brain blood flow than nonusers. August 2017   

Vinpocetine increases cerebral blood flow and oxygenation in stroke patients: a near infrared spectroscopy and transcranial Doppler study May 2015 

Or this? having red blood cells release more oxygen.

Methylene blue shows promise for improving short-term memory

HOW FUCKING LONG WILL YOU LET YOUR INCOMPETENT STROKE HOSPITAL STILL TREAT PATIENTS LIKE NOTHING NEW HAS OCCURRED IN THE PAST 50 YEARS?

 

Or maybe this newest one I found about on Shark Tank, what is the downside? You can't listen to anything I have to say, I'm not medically trained, is your doctor?

Boost Oxygen on Shark Tank highlights

The latest here:

Stimulating the Facial Nerve to Treat Ischemic Stroke: A Systematic Review

Turner S. Baker^1,2*†, Justin Robeny^1,2†, Danna Cruz^2,3, Alexis Bruhat^1,2, Alfred-Marc Iloreta⁴, Anthony Costa^1,2 and Thomas James Oxley^1,2

• ¹Department of Neurosurgery, Icahn School of Medicine at Mount Sinai, New York, NY, United States
• ²Sinai BioDesign, Icahn School of Medicine at Mount Sinai, New York, NY, United States
• ³The Grove School of Engineering, The City College of New York, New York, NY, United States
• ⁴Department of Otolaryngology, Icahn School of Medicine at Mount Sinai, New York, NY, United States

Acute ischemic stroke (AIS) is a common devastating disease that has increased yearly in absolute number of cases since 1990. While mechanical thrombectomy and tissue plasminogen activator (tPA) have proven to be effective treatments, their window-of-efficacy time is very short, leaving many patients with no viable treatment option. Over recent years there has been a growing interest in stimulating the facial nerves or ganglions to treat AIS. Pre-clinical studies have consistently demonstrated an increase in collateral blood flow (CBF) following ganglion stimulation, with positive indications in infarct size and neurological scores. Extensive human trials have focused on trans-oral electrical stimulation of the sphenopalatine ganglion, but have suffered from operational limitations and non-significant clinical findings. Regardless, the potential of ganglion stimulation to treat AIS or elongate the window-of-efficacy for current stroke treatments remains extremely promising. This review aims to summarize results from recent trial publications, highlight current innovations, and discuss future directions for the field. Importantly, this review comes after the release of four important clinical trials that were published in mid 2019.

Introduction

Acute Ischemic Stroke

Stroke is the leading cause of disability and the fifth leading cause of death in the United States (US). Approximately 795,000 people experience a new or recurrent stroke each year (1). Acute ischemic stroke (AIS) occurs when an obstruction within a blood vessel decreases cerebral blood flow, depriving nerve cells of oxygen and leading to severe metabolic failure and neural death (2–4). Immediately following stroke, a section of the brain referred to as the ischemic core is subject to extreme hypoxia, leading to irreversible brain damage (5). The area surrounding the ischemic core, the ischemic penumbra, is severely hypoperfused and non-functioning, yet can regain functionality if blood flow is restored to the area (5, 6). This recovery is highly time-dependent, as the penumbra rapidly evolves into the ischemic core (6, 7). The recovery of the penumbra has been demonstrated to have a significant effect on clinical outcomes; Meretoja et al. showed that for every 20-min reduction in time to reperfusion increases the average disability-free life span by 3 months (8).

More at link.