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

Motor Cortex Activation During Treatment May Predict Therapeutic Gains in Paretic Hand Function After Stroke

 WHAT EXACT PROTOCOL WILL GUANANTEE THESE THERAPEUTIC GAINS?  If you can't provide that your research is mostly useless! The whole fucking point of stroke research is to get survivors recovered. This DOESN'T DO THAT! Look at all these supposedly smart Ph.D's that don't understand that.

Send me hate mail on this: oc1dean@gmail.com. I'll print your complete statement with your name and my response in my blog. Or are you afraid to engage with my stroke-addled mind? What is your reason for doing stroke research? Getting published is not the correct answer.

Motor Cortex Activation During Treatment May Predict Therapeutic Gains in Paretic Hand Function After Stroke

Yun Dong, MD, PhD; Bruce H. Dobkin, MD; Steven Y. Cen, PhD; Allan D. Wu, MD; Carolee J. Winstein, PhD 
Background and Purpose

Functional brain imaging after stroke offers insight into motor network adaptations. This exploratory study examined whether motor cortical activation captured during arm-focused therapy can predict paretic hand functional gains. 

Methods

Eight hemiparetic patients had serial functional MRI (fMRI) while performing a pinch task before, midway, and after 2 weeks of constraint-induced therapy. The Wolf Motor Function Test (WMFT) was performed before and after intervention. 

Results

There was a linear reduction in ipsilateral (contralesional) primary motor (M1) activation (voxel counts) across time. The midpoint M1 Laterality Index anticipated post-therapeutic change in time to perform the WMFT. The change in ipsilateral M1 voxel count (pre- to mid-) correlated with the change in mean WMFT time (pre- to post-). 

Conclusions

The relationship between brain activation during treatment and functional gains suggests a use for serial fMRI in predicting the success and optimal duration for a focused therapeutic intervention. (Stroke. 2006;37:1552- 1555.) Key Words: magnetic resonance imaging rehabilitation Functional MRI (fMRI) has revealed reorganization in the primary and secondary motor cortices during poststroke recovery and after therapeutic interventions. 

1 Few studies have explored the evolution of brain activation in relation to behavioral gains in a “one-to-one” correspondence during a specific rehabilitation intervention. 2 This exploratory study examined whether the brain activation midway through a 2-week arm-focused intervention might capture adaptations induced by the initial week of training and, in turn, could be used to anticipate post-therapeutic behavioral changes in paretic hand function. If so, this brain– behavior correspondence may offer guidance to determine an optimal duration for task-specific therapy. 2 Subjects and Methods Eight patients with hemiparetic stroke (Fugl-Meyer [FM] motor score 33 to 62) participated. Inclusion criteria were 3 months after stroke, ability to perform the fMRI task, and a minimum of 10° of voluntary wrist and finger extension.(Well, that excludes a huge portion of survivors that have spasticity, so massive cherry picking) Lesions varied in location, but all spared the hand motor representation (M1). No alternative therapy group was studied. Seven healthy volunteers were scanned twice to test the reproducibility of fMRI activation. Physical Therapy and Functional Measure All patients received constraint-induced therapy for 2 weeks as defined for the EXCITE trial. 3 The Wolf Motor Function Test (WMFT) 4 was performed before and after intervention. The behavioral outcome measure consisted of 6 dexterity items from the full 15-item WMFT (Lift Can; Lift Pencil; Lift Paper Clip; Stack Checkers; Flip Cards; Turn Key in Lock) that most directly captured fine motor control(If you can do most of these, you're a high-functioning survivor, thus more cherry picking). The change in mean WMFT (mWMFT) time for the 6-item subset was correlated with that for the 15-item test (r=0.98), indicating reliability and validity for the subset. The pre-mWFT–post-mWFMT (absolute time) difference was used as a proxy for functional change in motor skill. fMRI Acquisition fMRI acquisition parameters were described previously. 5 fMRI sessions were performed before intervention, midintervention, and after intervention, each with 4 30-s bouts of repetitive pinch alternating with 5 30-s rest periods. The pinch apparatus included a vertical plastic tube connected to a pressure transducer. The task required tube compression with the index and middle fingers against the thumb, creating enough pressure to match 50% of maximum, viewed through goggles as a target line, and paced by auditory cues at 75% maximum rate. These parameters were maintained constant across the 3 sessions. Practice before each fMRI session minimized unwanted movements and deviations from consistent task performance. Data Analysis fMRI data were analyzed as described previously. 5,6 Volumes related to head motion (2 mm), and associated movements (visually identified from videotape) were excluded. Z statistic images were thresholded at Z3.1, and significant clusters were defined at P0.01 (corrected for multiple comparisons). Regions of interest (ROIs) were set in bilateral M1 and dorsal premotor (PMd) areas. Percentage signal change (% SC) and voxel counts (VCs) within each ROI were measured and a Laterality Index [LI=(contra- lateral-ipsilateral)/(contralateral+ipsilateral)] (contralateral and ip- silateral activation to the hand movement. LI ranges from -1 [all ipsilateral activation] to 1 [all contralateral activation]) was calculated using VC for each ROI. Linear Mixed Model was used for intersession comparisons of fMRI variables (% SC, VC), pinch pressure, and rate, separately. Individual linear regression analyses were performed between LI, VC (M1 and PMd; independent variable) pre-, mid-, and post- and the post-pre–mWMFT time difference (dependent variable). Pearson correlation coefficient anal- ysis was used to assess the relationship between changes in fMRI measures and changes in mWMFT time. Preintervention fMRI from patients 5 and 6 was technically unusable. Results Prefunctional to postfunctional gains (mWMFT) varied across patients, but the group 6-item time decreased for the paretic hand after therapy (P=0.03; Table). No differences were detected in pinch pressure or rate across sessions (P0.1). Intersession comparisons of M1 activation in healthy volunteers showed no differences (Table). Group analysis for the paretic hand showed a continuous reduction of VC in ipsilateral M1 (P=0.02; P=0.006 linear trend) across time (Table). No differences in M1 activation across time were found for the less-affected hand (P0.1; data not shown). We observed 4 patterns of LI evolution for M1, including a progressive increase (patients 3, 4, and 7; Figure 1A), a midpoint-only increase (patient 8), a midpoint decrease (patient 1; Figure 1B), and nearly no change (patient 2). Among the 3 showing “progressive increase,” patients 3 and 4 (FM score 53 and 54, respectively) had either an increase in contralateral or a decease in ipsilateral M1 activation across time, whereas patient 7 (FM score 45) demonstrated a continuous reduction in bilateral M1 activation but more so ipsilaterally. The “midpoint decrease” in patient 1 (FM score 62), who was well recovered and showed the least functional improvement, was attributed to a pre- to mid- reduction in contralateral M1 activation. The “midpoint-only increase” in patient 8 (FM score 34), who showed the most functional improvement, resulted from a pre- to mid- decrease in ipsilateral M1 activation. There was no correlation between post-pre change in mWMFT time and change in activation (VC or % SC) in M1 or PMd (ipsilateral or contralateral), except for that between post-pre change in mWMFT time and pre- to- mid- change in ipsilateral M1 activation (VC; r=0.82; P=0.05). The mid-point and postintervention LI for M1 and midpoint ipsilateral M1 VC, but not that for PMd, did predict the post-pre mWMFT time change (6-item; Figure 2).

More at link with figures.

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