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.

Showing posts with label supraspinal. Show all posts
Showing posts with label supraspinal. Show all posts

Thursday, June 18, 2015

New insights into the pathophysiology of post-stroke spasticity

Using a bunch of big words to disguise the fact they know nothing about spasticity; why it occurs; how to fix it.
http://www.ncbi.nlm.nih.gov/pubmed/25914638

Abstract

Spasticity is one of many consequences after stroke. It is characterized by a velocity-dependent increase in resistance during passive stretch, resulting from hyperexcitability of the stretch reflex. The underlying mechanism of the hyperexcitable stretch reflex, however, remains poorly understood. Accumulated experimental evidence has supported supraspinal origins of spasticity, likely from an imbalance between descending inhibitory and facilitatory regulation of spinal stretch reflexes secondary to cortical disinhibition after stroke. The excitability of reticulospinal (RST) and vestibulospinal tracts (VSTs) has been assessed in stroke survivors with spasticity using non-invasive indirect measures. There are strong experimental findings that support the RST hyperexcitability as a prominent underlying mechanism of post-stroke spasticity. This mechanism can at least partly account for clinical features associated with spasticity and provide insightful guidance for clinical assessment and management of spasticity. However, the possible role of VST hyperexcitability cannot be ruled out from indirect measures. In vivo measure of individual brainstem nuclei in stroke survivors with spasticity using advanced fMRI techniques in the future is probably able to provide direct evidence of pathogenesis of post-stroke spasticity.

Friday, February 13, 2015

Preservation of common rhythmic locomotor control despite weakened supraspinal regulation after stroke

No clue what this means so ask your doctor how this knowledge will help you recover.
http://journal.frontiersin.org/Journal/10.3389/fnint.2014.00095/full?
Taryn Klarner1,2,3, Trevor S. Barss1,2,3, Yao Sun1,2,3, Chelsea Kaupp1,2,3 and E. Paul Zehr1,2,3,4*
  • 1Exercise Science, Physical and Health Education, University of Victoria, Victoria, BC, Canada
  • 2Centre for Biomedical Research, University of Victoria, Victoria, BC, Canada
  • 3International Collaboration on Repair Discoveries, Vancouver, BC, Canada
  • 4Division of Medical Sciences, University of Victoria, Victoria, BC, Canada
The basic pattern of arm and leg movement during rhythmic locomotor tasks is supported by common central neural control from spinal and supraspinal centers in neurologically intact participants. The purpose of this study was to test the hypothesis that following a cerebrovascular accident, shared systems from interlimb cutaneous networks facilitating arm and leg coordination persist across locomotor tasks. Twelve stroke participants (>6 months post CVA) performed arm and leg (A&L) cycling using a stationary ergometer and walking on a motorized treadmill. In both tasks cutaneous reflexes were evoked via surface stimulation of the nerves innervating the dorsum of the hand (superficial radial; SR) and foot (superficial peroneal; SP) of the less affected limbs. Electromyographic (EMG) activity from the tibialis anterior, soleus, flexor carpi radialis, and posterior deltoid were recorded bilaterally with surface electrodes. Full-wave rectified and filtered EMG data were separated into eight equal parts or phases and aligned to begin with maximum knee extension for both walking and A&L cycling. At each phase of movement, background EMG data were quantified as the peak normalized response for each participant and cutaneous reflexes were quantified as the average cumulative reflex over 150 ms following stimulation. In general, background EMG was similar between walking and A&L cycling, seen especially in the distal leg muscles. Cutaneous reflexes were evident and modified in the less and more affected limbs during walking and A&L cycling and similar modulation patterns were observed suggesting activity in related control networks between tasks. After a stroke common neural patterning from conserved subcortical regulation is seen supporting the notion of a common core in locomotor tasks involving arm and leg movement. This has translational implications for rehabilitation where A&L cycling could be usefully applied to improve walking function.