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, July 14, 2016

The Effects of Stroke Type, Locus, and Extent on Long-Term Outcome of Gait Rehabilitation The LEAPS Experience

What really needs to come out of this research is a gait protocol.
http://nnr.sagepub.com/content/30/7/615?etoc
  1. Stephen E. Nadeau, MD1,2⇑
  2. Bruce Dobkin, MD3
  3. Samuel S. Wu, PhD4
  4. Qinglin Pei, PhD4
  5. Pamela W. Duncan, PhD5
  6. for the LEAPS Investigative Team
  1. 1Malcom Randall VA Medical Center, Gainesville, FL, USA
  2. 2University of Florida College of Medicine, Gainesville, FL, USA
  3. 3Geffen/UCLA School of Medicine, Los Angeles, CA, USA
  4. 4University of Florida Colleges of Medicine and Public Health and Health Professions, Gainesville, FL, USA
  5. 5Wake Forest School of Medicine, Winston-Salem, NC, USA
  1. Stephen E. Nadeau, MD, Research Service (151), Malcom Randall VA Medical Center, 1601 SW Archer Road, Gainesville, FL 32608-1197, USA. Email: snadeau@ufl.edu

Abstract

Background. Paresis in stroke is largely a result of damage to descending corticospinal and corticobulbar pathways. Recovery of paresis predominantly reflects the impact on the neural consequences of this white matter lesion by reactive neuroplasticity (mechanisms involved in spontaneous recovery) and experience-dependent neuroplasticity, driven by therapy and daily experience. However, both theoretical considerations and empirical data suggest that type of stroke (large vessel distribution/lacunar infarction, hemorrhage), locus and extent of infarction (basal ganglia, right-hemisphere cerebral cortex), and the presence of leukoaraiosis or prior stroke might influence long-term recovery of walking ability. In this secondary analysis based on the 408 participants in the Locomotor Experience Applied Post-Stroke (LEAPS) study database, we seek to address these possibilities. Methods. Lesion type, locus, and extent were characterized by the 2 neurologists in the LEAPS trial on the basis of clinical computed tomography and magnetic resonance imaging scans. A series of regression models was used to test our hypotheses regarding the effects of lesion type, locus, extent, and laterality on 2- to 12-month change in gait speed, controlling for baseline gait speed, age, and Berg Balance Scale score. Results. Gait speed change at 1 year was significantly reduced in participants with basal ganglia involvement and prior stroke. There was a trend toward reduction of gait speed change in participants with lacunar infarctions. The presence of right-hemisphere cortical involvement had no significant impact on outcome. Conclusions. Type, locus, and extent of lesion, and the loss of substrate for neuroplastic effect as a result of prior stroke may affect long-term outcome of rehabilitation of hemiparetic gait.
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