http://nnr.sagepub.com/content/early/2015/10/22/1545968315613851.abstract?&location1=all&location2=all&row_operator2=and&term1a=neuroplasticity&term1b=neurogenesis&term_operator1=or&term_operator2=and&ct
- Stephen E. Nadeau, MD1,2⇑
- Bruce Dobkin, MD3
- Samuel S. Wu, PhD4
- Qinglin Pei, PhD4
- Pamela W. Duncan, PhD5
- for the LEAPS Investigative Team
- 1Malcom Randall VA Medical Center, Gainesville, FL, USA
- 2University of Florida College of Medicine, Gainesville, FL, USA
- 3Geffen/UCLA School of Medicine, Los Angeles, CA, USA
- 4University of Florida Colleges of Medicine and Public Health and Health Professions, Gainesville, FL, USA
- 5Wake Forest School of Medicine, Winston-Salem, NC, USA
- 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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