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.

Thursday, December 5, 2024

Sub-acute stroke demonstrates altered beta oscillation and connectivity pattern in working memory

 

Big fucking whoopee.

 

 But you tell us NOTHING ABOUT A SOLUTION Useless!

Sub-acute stroke demonstrates altered beta oscillation and connectivity pattern in working memory

Abstract

Introduction

Working memory (WM) is suggested to play a pivotal role in relearning and neural restoration during stroke rehabilitation. Using EEG, this study investigated the oscillatory mechanisms of WM in subacute stroke.

Methods

This study included 48 first subacute stroke patients (26 good-recovery, 22 poor-recovery, based on prognosis after a 4-week period) and 24 matched health controls. We examined the oscillatory characteristics and functional connectivity of the 0-back WM paradigm and assessed their associations with prognosis.

Results

Patients of poor recovery are characterised by a loss of significant beta rebound, beta-band connectivity, as well as impaired working memory speed and performances. Meanwhile, patients with good recovery have preserved these capacities to some extent. Our data further identified beta rebound to be closely associated with working memory speed and performances.

Conclusions

We provided novel findings that beta rebound and network connectivity as mechanistic evidence of impaired working memory in subacute stroke. These oscillatory features could potentially serve as a biomarker for brain stimulation technologies in stroke recovery.

Introduction

Stroke is the third most common cause of morbidity and the second most common cause of dementia [1]. The most common symptoms of stroke include physical deficits (such as paralysis, and sensory loss) and dysfunction in learning, memory, and executive functions. When it comes to cognitive function, working memory (WM) has a fundamental role in performing complex behaviours and is associated with poor functional outcomes after a stroke [2, 3].

An abrupt, cliff-like decline in brain function represents a key difference between acute stroke and neurodegenerative cerebral disorders. More importantly, this pattern of cognitive decline exhibits reversibility within a defined temporal framework [4], which is critical for both neural restoration and clinical rehabilitation. In clinical practices, there is also evidence supporting the ability to regain partial functions or develop compensatory skills through the process of learning [5]. Notably, working memory underpins the learning processes [2], making it critical for neural restoration and clinical rehabilitation. It is therefore important to investigate the behavioural and neural dynamics of WM, offering insights for the development of more effective rehabilitation strategies.(WHOM SPECIFICALLY DID YOU CONTACT TO GET THAT RESEARCH DONE? NO ONE? So, you're a complete failure at doing your job?)

Working memory is defined as a multi-component system involved in goal-directed behaviours that involve retaining and manipulating information [6]. N-back task is a well-validated and widely used means of manipulating working memory capacity and its response requirements [7]. Among them, 0-back requires less workload, which is highly suitable for post-stroke individuals with significant cognitive impairment. It includes components such as sustained attention to a stimulus and continuous memory of the instructions. It is noted that clinical assessment of vascular cognitive impairment (VCI) predominantly relies on cognitive scales, with a paucity of concurrent evidence from cognitive tasks such as WM.

Using an electroencephalogram (EEG), previous studies have established the oscillatory mechanisms of WM. Most of the studies have identified increased power in the fast oscillatory ranges such as beta (13–30 Hz) and gamma (30–100 Hz) [8, 9]. In terms of the functioning, gamma oscillation is suggested to store memories, while beta oscillation is closely associated with attention and response selection [9,10,11]. However, the effects of stroke on neural oscillations underlying WM are largely unclear. A recent scoping review indicated a correlation between decreased fast waves (such as beta) and poor cognition following a stroke [12].

This study was designed to investigate the oscillatory characteristics of working memory in subacute stroke patients. Patients in the subacute stroke underwent a visual-spatial WM 0-back with EEG recordings. They were further classified as good-recovery (n = 26) and poor-recovery (n = 22) according to the modified Rankin Score (mRS). We hypothesized that stroke patients would demonstrate lower power in beta and gamma range compared to healthy controls. Moreover, patients with a poor recovery would have a more prominent decrease in beta and gamma oscillation.

More at link.

No comments:

Post a Comment