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.

Sunday, April 19, 2020

Position-Cortical Coherence as a Marker of Afferent Pathway Integrity Early Poststroke: A Prospective Cohort Study

Ooooo, big words and abbreviations, must be important. Hope your doctor understands them since I could never translate this into any kind of stroke rehab. And at the end they suggest further research because this research obviously failed at whatever it was trying to accomplish. 

Position-Cortical Coherence as a Marker of  Early Poststroke: A Prospective Cohort Study 

First Published March 4, 2020 Research Article Find in PubMed


Background.
Addressing the role of somatosensory impairment, that is, afferent pathway integrity, in poststroke motor recovery may require neurophysiological assessment.  
Objective.
We investigated the longitudinal construct validity of position-cortical coherence (PCC), that is, the agreement between mechanically evoked wrist perturbations and electroencephalography (EEG), as a measure of afferent pathway integrity.  
Methods.
PCC was measured serially in 48 patients after a first-ever ischemic stroke in addition to Fugl-Meyer motor assessment of the upper extremity (FM-UE) and Nottingham Sensory Assessment hand-finger subscores (EmNSA-HF, within 3 and at 5, 12, and 26 weeks poststroke. Changes in PCC over time, represented by percentage presence of PCC (%PCC), mean amplitude of PCC over the affected (Amp-A) and nonaffected hemisphere (Amp-N) and a lateralization index (L-index), were analyzed, as well as their association with FM-UE and EmNSA-HF. Patients were retrospectively categorized based on FM-UE score at baseline and 26 weeks poststroke into high- and low-baseline recoverers and non-recoverers.  
Results.
%PCC increased from baseline to 12 weeks poststroke (β = 1.6%, CI = 0.32% to 2.86%, P = .01), which was no longer significant after adjusting for EmNSA-HF and FM-UE. A significant positive association was found between %PCC, Amp-A, and EmNSA-HF. Low-baseline recoverers (n = 8) showed longitudinally significantly higher %PCC than high-baseline recoverers (n = 23). Conclusions.
We demonstrated the longitudinal construct validity of %PCC and Amp-A as a measure of afferent pathway integrity. A high %PCC in low-baseline recoverers suggests that this measure also contains information on cortical excitability. Use of PCC as an EEG-based measure to address the role of somatosensory integrity to motor recovery poststroke requires further attention.

Progress of time as a reflection of underlying spontaneous neurobiological recovery appears to account for 80% to 90% of the observed improvement in motor function and upper limb capacity in patients after stroke.1-3 This accounts for approximately 70% of patients in which some patients are expected to recover, that is, patients with a relatively high baseline motor function, while other patients are not, that is, patients with a low baseline motor function. It is unknown why 20% to 30% of patients, the so-called non-recoverers, with a low motor function at 26 weeks poststroke, fail to show spontaneous recovery.4
Patients with somatosensory impairments have a lower probability of regaining upper limb capacity than patients in whom this function is not affected.3 Somatosensory impairments may influence motor recovery due to a tight interaction of the afferent and efferent pathways with a supposed cortical loop.5,6 Disturbance of afferent pathway integrity is therefore important to study to understand motor recovery.7 The Erasmus modification of the Nottingham Sensory Assessment of the upper extremity (EmNSA-UE) is a common and reliable clinical measure of somatosensory impairment in patients with stroke.8 However, it is not a direct measure of afferent pathway integrity, and is not very responsive to change.8-10
Finger stimulation evoked somatosensory potentials could theoretically be an approach to study somatosensory processing, however, may not be recommend due to the lack in reliability.11 Cortical rebound responses in the beta band of the affected hemisphere measured with magnetoencephalography during manual passive finger movements, were found to correlate with the initial severity and recovery of motor activity as measured with the box and block test at 1 and 12 months poststroke.12 Joint position perturbations act as an external excitation signal for the proprioceptive system, primarily the Golgi tendon organs and muscle spindles, providing an interesting approach to study sensorimotor processing in severely affected patients.12 Coherence between mechanical perturbations and subsequent cortical responses as measured with EEG, that is, position-cortical coherence (PCC), represent the unidirectional information transfer across the afferent pathways.13,14 A cross-sectional study in stroke patients found significant differences in the presence of PCC between groups with poor and good motor function as measured by FM-UE using this system identification approach.14 A similar protocol was used by Vlaar et al,15 who reported a reduced amplitude in ipsilesional cortical responses, quantified by a signal-to-noise ratio, in patients with severe somatosensory impairment (reduced EnMSA-UE score for more than 2 subtests) in patients in the chronic phase after stroke.
To address the potential added value of neurophysiological measures, prospective studies are required with fixed moments of measurements poststroke to establish their construct validity.16 These neurophysiological biomarkers could help to improve the prediction of outcome, and enhance accurate selection of patients for clinical trials.17,18
We aimed to evaluate the longitudinal construct validity of PCC as a measure of afferent pathway integrity and its relation to poststroke recovery, in a prospective cohort study with repetitive measurements at fixed time points within 3 weeks and at 5, 12, and 26 weeks in patients after a first-ever ischemic stroke. We addressed the following research questions and corresponding hypotheses:
  1. How does PCC change over the first 26 weeks poststroke? We expected measures of PCC to show a significant change over time as a reflection of spontaneous neurobiological recovery. Because of these spontaneous neurobiological processes, we also expected this association over time to be influenced by the recovery of motor function, reflected by FM-UE and somatosensory function, reflected by EmNSA hand and finger subset (EmNSA-HF).
  2. Does PCC relate to clinical somatosensory scores, and how does this compare with motor recovery? We expected measures of PCC to represent somatosensory integrity, that is, to show a significant association with EmNSA-HF and not with FM-UE score. We hypothesized that these associations would be independent of time.
  3. How does PCC relate to motor recovery poststroke? We expected a higher PCC in recoverers compared with non-recoverers.
 More at link.

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