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.

Monday, June 30, 2025

Research progress in the use of botulinum toxin type a for post-stroke spasticity rehabilitation: a narrative review

Let's examine how useless this is! NOTHING ON CURING SPASTICITY! Survivors want it cured, not reduced! Why the fuck can't you solve that problem? Are you too lazy to even try to solve the problem? Too hard for you?

 Research progress in the use of botulinum toxin type a for post-stroke spasticity rehabilitation: a narrative review


Qianwen Xu, Ya Wang Article: 2521427 Received 26 Oct 2024 Accepted 27 May 2025 Published online: 23 Jun 2025 Cite this article https://doi.org/10.1080/07853890.2025.2521427Additional information

Abstract

Stroke is a leading cause of long-term disability and death worldwide. Spasticity after stroke seriously affects patients’ quality of life. If this state persists for a long time, it will lead to severe joint atrophy, reduced motor coordination, and even permanent disability. Therefore, clinical research has focused on the treatment of spasticity and the recovery of motor function after stroke.

Aim

The aim of this paper is to explore the use of botulinum toxin type A in the rehabilitation of spasticity after stroke and to provide a theoretical basis for optimizing rehabilitation strategies, highlighting its potential value in reducing spasticity and improving motor function.

Method

This article reviews the latest research progress on the application of BTX-A in spasticity after stroke, discusses the potential and challenges of BTX-A in reducing spasticity and improving motor function in patients with stroke.

Result

Botulinum toxin type A (BTX-A) is a local muscle paralytic agent that has received extensive attention in recent years for its application in reducing muscle spasticity and promoting post-stroke rehabilitation.This article confirms that botulinum toxin type A has a significant clinical effect in treating muscle spasticity after stroke and also helps improve motor function restoration in patients. Studies have shown that botulinum toxin type A injections are effective in reducing spasticity and, when combined with rehabilitation training, can facilitate the recovery of motor function in post-stroke patients. Therefore, botulinum toxin type A has a broad application prospect in the rehabilitation of post-stroke spasticity.

KEY MESSAGES

The application of botulinum toxin type A (BTX-A) in post-stroke rehabilitation primarily focuses on reducing muscle spasticity and improving motor function.Spasticity is a common clinical manifestation of damage to the upper motor neurons. It is caused by the increased excitability of gamma motor neurons and manifests as excessive involuntary muscle contraction. Its causes include cerebral palsy, stroke, traumatic brain injury, multiple sclerosis, brain or spinal cord tumours, and spinal cord injuries

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