This is fucking pathetic that we are still asking questions like these. It means that every stroke survivor is an unregistered clinical trial of one for walking rehabilitation. Because we have never had an objective stroke damage diagnosis.
https://ueaeprints.uea.ac.uk/55626/1/Does_Stroke_Location_Predict_Walk_Speed_Response_to_Gait_Rehabilitation.pdf
P. Simon Jones 1
, Valerie M. Pomeroy 2
, Jasmine Wang 3
, Gottfried Schlaug 3
, S. Tulasi Marrapu 1
, Sharon Geva 1
, Philip J. Rowe 4
, Elizabeth Chandler 2
, Andrew Kerr 4
, Jean+Claude Baron 1,5
, for the SWIFT+Cast
investigators.
Affiliations:
1.Stroke Research Group, Dept of Clinical Neuroscienc
es, University of
Cambridge, UK
2.Acquired Brain Injury Rehabilitation Alliance, Scho
ol of Health Sciences,
University of East Anglia, Norwich, UK
3.Department of Neurology, Beth Israel Deaconess Medi
cal Center, Harvard
Medical School Boston, USA.
4.Bioengineering Unit, University of Strathclyde, Gla
sgow, UK.
5.Inserm U894, Sorbonne Paris Cité, Centre Hospitalie
r Sainte+Anne, Paris,
France
Running head: Stroke location and walking rehabilit
ation
Correspondence:
Jean+Claude Baron
INSERM U894
2 ter rue d'Alésia
75014 Paris, France
tel: (33) (0)1 40788626
fax: (33) (0)1 45807293
email: jean+claude.baron@inserm.fr
Abstract
Objectives: Recovery of independent ambulation after stroke is a major goal.
However, which rehabilitation regimen best benefits each individual is unknown and
decisions are currently made on a subjective basis. Predictors of response to specific
therapies would guide the type of therapy most appropriate for each patient. Although
lesion topography is a strong predictor of upper limb response, walking involves more
distributed functions. Earlier studies that assessed the cortico+spinal tract (CST) were
negative, suggesting other structures may be important.
Experimental design: The relationship between lesion topography and response of
walking speed to standard rehabilitation was assessed in 50 adult+onset patients using
both volumetric measurement of CST lesion load and voxel+based lesion+symptom
mapping (VLSM) to assess non+CST structures. Two functional mobility scales, the
Functional Ambulation Category (FAC) and the Modified Rivermead Mobility Index
(MRMI) were also administered. Performance measures were obtained both at entry
into the study (3+42 days post+stroke) and at the end of a six+week therapy. Baseline
score, age, time since stroke onset and white matter hyperintensities score were
included as nuisance covariates in regression models.
Principal observations:
CST damage independently predicted response to therapy for FAC and MRMI, but not for Walk speed. However, using VLSM the latter was predicted by damage to the putamen, insula, external capsule and neighbouring white matter.
Conclusions:
Walk speed response to rehabilitation was affected by damage involving the putamen and neighbouring structures but not the CST, while the latter has modest but significant impact on everyday functions of general mobility and gait.
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