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.

Wednesday, October 16, 2019

Cathodal transcranial direct current stimulation suppresses ipsilateral projections to presumed propriospinal neurons of the proximal upper limb

Whatever the fuck this says, I have no clue. Bet your doctor doesn't either.  And throwing in Motor Evoked Potentials to make this sound important is not helping any survivor get recovered.

So completely and totally fucking useless. 

Maybe that line will get a stroke medical professional to tell me exactly how I'm wrong and an idiot. 

 

Cathodal transcranial direct current stimulation suppresses ipsilateral projections to presumed propriospinal neurons of the proximal upper limb

Lynley V. Bradnam,
1,3
Cathy M. Stinear,
2,3
and Winston D. Byblow
1,3
1
 Movement Neuroscience Laboratory,
 2
 Department of Medicine, and
 3
Centre for Brain Research, The University of Auckland, Auckland, New Zealand
Submitted 14 December 2010; accepted in final form 7 March 2011
Bradnam LV, Stinear CM, Byblow WD.
 Cathodal transcranial direct current stimulation suppresses ipsilateral projections to presumed propriospinal neurons of the proximal upper limb.
 J Neuro- physiol
 105: 2582–2589, 2011. First published March 9, 2011;doi:10.1152/jn.01084.2010.—This study investigated whether cathodal transcranial direct current stimulation (c-tDCS) of left primary motor cortex (M1) modulates excitability of ipsilateral propriospinal premotoneurons (PNs) in healthy humans. Transcranial magnetic stimulation (TMS) of the right motor cortex was used to obtain motor evoked potentials (MEPs) from the left biceps brachii (BB) while participants maintained contraction of the left BB. To examine presumed PN excitability, left BB MEPs were compared with those conditioned by median nerve stimulation (MNS) at the left elbow.Interstimulus intervals between TMS and MNS were set to produce summation at the C3–C4 level of the spinal cord. MNS facilitated BBMEPs elicited at TMS intensities near active motor threshold but inhibited BB MEPs at slightly higher intensities, indicative of putative PN modulation. c-tDCS suppressed the facilitatory and inhibitory effects of MNS. Sham tDCS did not alter either component. There was no effect of c-tDCS and sham tDCS on nonconditioned left BBMEPs or on the ipsilateral silent period of left BB. Right first dorsal interosseous MEPs were suppressed by c-tDCS. These results indicatethat M1 c-tDCS can be used to modulate excitability of ipsilateral projections to presumed PNs controlling the proximal arm muscle BB.This technique may hold promise for promoting motor recovery of proximal upper limb function after stroke.human; motor evoked potential; biceps brachii
PROPRIOSPINAL NEURONS
 (PNs) located in the 3rd and 4th segments in the spinal cord (C3–C4) mediate descending com-mands for target reaching in the cat and nonhuman primate (Alstermark et al. 2007). Also known as cervical “premotoneurons,” presumed PNs integrate sensory feedback with descending cortical output to update rapidly the motor command during a reaching task (Pierrot-Deseilligny and Burke 2005). Inhuman and nonhuman primates, PNs are held under tonic suppression (Alstermark et al. 2007; Isa et al. 2006; Pierrot-Deseilligny 1996; Pierrot-Deseilligny and Burke 2005) that is released during activities requiring cocontraction of proximal and distal upper limb muscles (Iglesias et al. 2007; Nicolas etal. 2001; Roberts et al. 2008). As such, PNs facilitate the formation of muscle synergies (Pierrot-Deseilligny and Burke2005). Interestingly, descending inputs to presumed PNs orig-inate in both the contralateral hemisphere (Boudrias et al.2010; Mazevet et al. 1996; Nicolas et al. 2001) and ipsilateral hemisphere via the reticulospinal tract (Illert et al. 1978, 1981).Therefore, input from both hemispheres ultimately determines task-specific selective muscle activation and formation of nor-mal muscle synergies in the production of goal-directed upper limb movements such as reaching.The propriospinal system can be studied indirectly in hu-mans using single-pulse transcranial magnetic stimulation(TMS) combined with peripheral nerve stimulation. Usinginterstimulus intervals (ISIs) that permit summation at pre-sumed C3–C4 PNs (e.g., Nicolas et al. 2001), combining a weak cortical stimulus with submotor threshold peripheral stimulation facilitates contralateral motor evoked potentials(MEPs). Conversely, a stronger cortical stimulus and the same peripheral stimulus suppresses MEPs, presumably due to the cortical stimulus recruiting higher threshold descending path-ways reaching inhibitory interneurons within the spinal cord(Fig. 1; Iglesias et al. 2007; Nicolas et al. 2001; Roberts et al.2008; Stinear and Byblow 2004b). The present study examinedmodulation of inputs from the ipsilateral hemisphere to pre-sumed PNs during an upper limb task.Transcranial direct current stimulation (tDCS) is a noninvasive brain stimulation technique that can be used to transientlyalter membrane potential of neuronal populations within pri-mary motor cortex (M1), resulting in aftereffects that last several minutes. tDCS increases excitability when the anode is placed over M1, whereas with the cathode placed over M1,excitability is reduced (Lang et al. 2004; Nitsche and Paulus2000, 2001; Nitsche et al. 2003a,b, 2005). Interestingly, there have been reports of enhanced ipsilateral arm function after cathodal tDCs (c-tDCS) in healthy humans (Vines et al. 2006)and enhanced paretic arm function in stroke patients after tDCS(Boggio et al. 2007; Fregni et al. 2005). c-tDCS has been shown to decrease excitability of uncrossed projections to ipsilateral proximal upper limb

-motoneurons (MNs) (Brad-nam et al. 2010b), which may explain observed effects on the ipsilateral arm. Improvements in function may also be due to reduced transcallosal inhibition from stimulated to nonstimulated hemisphere following c-tDCS (Schlaug et al. 2008; Wil-liams et al. 2010).The aim of the current study was to examine whetherc-tDCS can indirectly downregulate presumed PNs and inhibitory interneurons intercalated in uncrossed pathways to the ipsilateral arm in healthy adults. Our hypothesis was thatc-tDCS of left M1 would suppress ipsilateral descending inputsto PNs and inhibitory interneurons. The aftereffects of tDCS were examined on presumed PNs converging onto
 
MNs of the ipsilateral (left) biceps brachii (BB) by applying single-pulse TMS to right M1 in conjunction with median nerve stimulation (MNS) at the left elbow. c-tDCS of left M1 was
Address for reprint requests and other correspondence: W. D. Byblow,Movement Neuroscience Laboratory, Centre for Brain Research, The Univ. of Auckland, Auckland 1142, New Zealand (e-mail: w.byblow@auckland.ac.nz).

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