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.

Friday, September 10, 2021

Brain Function and Upper Limb Outcome in Stroke A Cross-Sectional fMRI Study

I got nothing out of this.

Brain Function and Upper Limb Outcome in Stroke A Cross-Sectional fMRI Study


  • Floor E. Buma, 
  • Mathijs Raemaekers, 
  • Gert Kwakkel, 
  • Nick F. Ramsey
PLOS
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Abstract

Objective

The nature of changes in brain activation related to good recovery of arm function after stroke is still unclear. While the notion that this is a reflection of neuronal plasticity has gained much support, confounding by compensatory strategies cannot be ruled out. We address this issue by comparing brain activity in recovered patients 6 months after stroke with healthy controls.

Methods

We included 20 patients with upper limb paresis due to ischemic stroke and 15 controls. We measured brain activation during a finger flexion-extension task with functional MRI, and the relationship between brain activation and hand function. Patients exhibited various levels of recovery, but all were able to perform the task.

Results

Comparison between patients and controls with voxel-wise whole-brain analysis failed to reveal significant differences in brain activation. Equally, a region of interest analysis constrained to the motor network to optimize statistical power, failed to yield any differences. Finally, no significant relationship between brain activation and hand function was found in patients. Patients and controls performed scanner task equally well.

Conclusion

Brain activation and behavioral performance during finger flexion-extensions in (moderately) well recovered patients seems normal. The absence of significant differences in brain activity even in patients with a residual impairment may suggest that infarcts do not necessarily induce reorganization of motor function. While brain activity could be abnormal with higher task demands, this may also introduce performance confounds. It is thus still uncertain to what extent capacity for true neuronal repair after stroke exists.

Introduction

Stroke is a leading cause of disability in western society [1]. The European Registers of Stroke study (EROS) show that of 2000 patients with first-ever strokes, 40% had a poor outcome in terms of a Barthel Index (BI) below 12 points at 3 months post stroke [2]. In the United States, 50% of stroke survivors suffer from hemiparesis [3,4]. Physical therapy aimed at restoring activities of daily living (ADL) remains the gold standard of treatment but outcomes are variable [5]. Recently, two independent studies have shown that an early return of some shoulder abduction and finger extension within 72 hours post stroke is highly predictive for outcome of upper limb function [68]. The patients’ ability to extend the paretic fingers voluntary is seen as an early sign of some intactness of corticospinal tract system (CST) after stroke [7,9]. In addition, in rehabilitation medicine voluntary control of finger extension is judged as a key function for achieving of some dexterity with the paretic limb [6,8,10].

An approach to improve our understanding of the mechanisms underlying functional recovery is to investigate the neural correlates of movement of the affected hand. Many cross-sectional as well as longitudinal studies have previously demonstrated a relationship between various patterns of fMRI brain activation and post-stroke outcome in patients with infarcts that spare M1. Correlations have been found between outcome after stroke, and increased (but also decreased) activation in secondary motor areas (such as PM and SMA), ipsilesional M1 overactivation, contralesional M1 activity as well as more bilateral activation patterns within the motor network, including the cerebellum [1113]. While there is variation in results of these studies, a recent meta-analysis has shown a consistent pattern of higher contralesional M1 activity and generally more widespread activity in secondary motor areas in stroke patients [14].

The relationship between these changes in brain activation and recovery of motor function is however not necessarily straightforward. Task parameters defining quality of motor performance as well as the occurrence of mirror movements are often not monitored in fMRI and may confound the interpretation of fMRI [12]. In addition, a number of recent longitudinal studies suggest that improvement of upper limb function after stroke is mainly driven by learning compensation strategies rather than by actual neuronal repair [15,16]. In animal studies compensatory strategies as correlates of recovery have also been shown after photothrombotic stroke [17,18]. Patients might learn to deal with impairments by using the affected limb to perform a task in a different way than before the stroke using alternative neuronal pathways, for example by reducing the number of degrees of freedom during movement [16,1921]. While such strategies may underlie clinical improvement, they do not constitute true neuronal plasticity or repair.

In the present fMRI study brain activity during motor function while performing an isolated, voluntary finger extension motor paradigm, is compared between patients with damage to the corticospinal tract and healthy controls. The patients are measured >6 months after stroke, when most of the recovery would be expected to have taken place. In addition, the quality of task performance was closely monitored with kinematic measurements to detect potential performance confounds, so that observed differences in brain activation between patients and control subjects can potentially be directly linked to neuronal plasticity [12]. We hypothesize that extent of functional recovery after stroke is associated with reorganization of brain function during a motor task, as proposed in literature [9,22]. We expect task-related brain activation to differ between subjects that have shown some motor recovery of the upper paretic limb, and healthy, age-matched controls. Specifically, we expect to find in stroke patients 1) elevated activation of secondary motor areas, 2) a more bilateral activation pattern across the motor network, as well as 3) a correlation between brain activity and functional outcome. However, we observed that under these well controlled conditions, there were differences in brain activation between patients and control subjects.

 

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