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 19, 2023

Association of Dual-Task Gait Cost and White Matter Hyperintensity Burden Poststroke: Results From the ONDRI

 This is still useless since you're predicting stuff rather than delivering EXACT REHAB PROTOCOLS!

Association of Dual-Task Gait Cost and White Matter Hyperintensity Burden Poststroke: Results From the ONDRI

Abstract

Background

Acute change in gait speed while performing a mental task [dual-task gait cost (DTC)], and hyperintensity magnetic resonance imaging signals in white matter are both important disability predictors in older individuals with history of stroke (poststroke). It is still unclear, however, whether DTC is associated with overall hyperintensity volume from specific major brain regions in poststroke.

Methods

This is a cohort study with a total of 123 older (69 ± 7 years of age) participants with history of stroke were included from the Ontario Neurodegenerative Disease Research Initiative. Participants were clinically assessed and had gait performance assessed under single- and dual-task conditions. Structural neuroimaging data were analyzed to measure both, white matter hyperintensity (WMH) and normal appearing volumes. Percentage of WMH volume in frontal, parietal, occipital, and temporal lobes as well as subcortical hyperintensities in basal ganglia + thalamus were the main outcomes. Multivariate models investigated associations between DTC and hyperintensity volumes, adjusted for age, sex, years of education, global cognition, vascular risk factors, APOE4 genotype, residual sensorimotor symptoms from previous stroke and brain volume.

Results

There was a significant positive global linear association between DTC and hyperintensity burden (adjusted Wilks’ λ = .87, P = .01). Amongst all WMH volumes, hyperintensity burden from basal ganglia + thalamus provided the most significant contribution to the global association (adjusted β = .008, η2 = .03; P = .04), independently of brain atrophy.

Conclusions

In poststroke, increased DTC may be an indicator of larger white matter damages, specifically in subcortical regions, which can potentially affect the overall cognitive processing and decrease gait automaticity by increasing the cortical control over patients’ locomotion.

Introduction

Mobility and cognitive impairments co-exist and have intertwined relationships in patients who experience vascular white matter lesions caused by a stroke.1 Current theoretical framework suggests that mobility and cognition share common brain networks that may be damaged by cerebrovascular disease.2 Dual-task gait cost (DTC), or the acute change in gait performance when simultaneously performing a mental task,3,4 was found to be higher in individuals with cognitive and motor syndromes. Furthermore, DTC is a predictor of motor5,6 and cognitive7,8 disabilities in individuals with history of stroke (poststroke) and accelerated brain degeneration.10-12 However, there is insufficient evidence of an independent association between DTC and hyperintensity signals (white matter lesions),13 particularly regarding its location, in Poststroke.
Increased DTC has been related to reduced cognitive5,6,14 and neural efficiency15 in frontal lobe regions in poststroke. A recent study, in healthy older adults, suggested that global microstructural white matter defects mediates the relationship between neural efficiency in prefrontal cortex and dual-task gait performance.16 White matter lesions are expected to reduce processing speed17 which consequently may affect the ability to walk and talk due to increased processing demands for task switching, as suggested by previous studies in Poststroke.6,14 White matter hyperintensity (WMH) is a typical macrostructural brain tissue alteration, detected with magnetic resonance imaging, in poststroke,11,12,18-22 and a strong predictor of fast progression to dementias,18-21 particularly when concentrated in the frontal lobe.11,12,22 Previous studies in older adults also have found global association between slow gait performance under dual-task conditions and larger WMH volumes and mostly focused on cortical regions.23,24 Notably, the investigation on the association between WMH burden in the parietal, occipital, temporal lobes and gait performance have been neglected, although pathology in these cortical regions can be directly or indirectly linked with mobility impairments.25 Moreover, despite subcortical regions, including basal ganglia and thalamus be known for its strong involvement with subconscious/well-learnt/automatic sensorimotor processing,26-28 studies also have shown that these subcortical regions are important to support cognitive processes occurring in frontal lobe regions during complex goal-directed actions.26,27,29 Hence, an independent association between subcortical WMH burden and increased DTC would suggest increased cognitive load for gait control driven by subcortical dysfunction (ie, decreased motor automaticity). However, it is unknown whether and how WMH burden in these regions would be associated with gait and DTC.
We hypothesize that increased DTC (ie, percentage of gait slowing from single- to dual-task testing conditions), will be cross-sectionally associated with larger WMH volumes in cortical and subcortical regions while controlling associations for potential confounders including atrophy.30 It is expected that increased DTC will be globally associated with larger WMH burden with greater contributions from aforementioned brain regions closely involved with complex thinking and sensorimotor processing for gait control. Importantly, because brain atrophy is quite prevalent in poststroke31 and strongly linked with worse gait performance in individuals with cerebrovascular disease,30 we also tested whether the normal appearing volumes would mediate the expected association between DTC and WMH. To test these hypotheses, we examined the cerebrovascular disease (CVD) cohort from the Ontario Neurodegenerative Disease Research Initiative (ONDRI),32 which is exclusively composed by patients with clinically confirmed history of stroke.
 
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