Abstract
Background.
Proprioception of fingers is essential for motor control. Reduced
proprioception is common after stroke and is associated with longer
hospitalization and reduced quality of life. Neural correlates of
proprioception deficits after stroke remain incompletely understood,
partly because of weaknesses of clinical proprioception assessments.
Objective.
To examine the neural basis of finger proprioception deficits after
stroke. We hypothesized that a model incorporating both neural injury
and neural function of the somatosensory system is necessary for
delineating proprioception deficits poststroke.
Methods. Finger
proprioception was measured using a robot in 27 individuals with chronic
unilateral stroke; measures of neural injury (damage to gray and white
matter, including corticospinal and thalamocortical sensory tracts),
neural function (activation of and connectivity of cortical sensorimotor
areas), and clinical status (demographics and behavioral measures) were
also assessed. Results. Impairment in finger proprioception was
present contralesionally in 67% and bilaterally in 56%. Robotic measures
of proprioception deficits were more sensitive than standard scales and
were specific to proprioception. Multivariable modeling found that
contralesional proprioception deficits were best explained (r2 = 0.63; P
= .0006) by a combination of neural function (connectivity between
ipsilesional secondary somatosensory cortex and ipsilesional primary
motor cortex) and neural injury (total sensory system injury).
Conclusions.
Impairment of finger proprioception occurs frequently after stroke and
is best measured using a quantitative device such as a robot. A model
containing a measure of neural function plus a measure of neural injury
best explained proprioception performance. These measurements might be
useful in the development of novel neurorehabilitation therapies.
No comments:
Post a Comment