Ascending vestibular drive is asymmetrically distributed to the inferior oblique motoneuron pools in a subset of hemispheric stroke survivors
Spasticity is a frequent and often disabling sequel to hemispheric stroke (Watkins et al., 2002; Urban et al., 2010; Wissel et al., 2013). It is characterized by a velocity-dependent increase in the resistance of a limb to passive stretch, coupled with exaggerated tendon jerks resulting from hyperexcitability of the segmental reflex arc (Dietz and Sinkjaer, 2007; Lance, 1980). The etiology of spasticity is complex, and while emerging evidence implicates changes in motoneuron excitability (i.e., decreased reflex threshold; spontaneous motoneuron firing at sub-threshold levels) as central to the genesis of post-stroke spasticity (Chung et al., 2008; Mottram et al., 2009; Hu et al., 2015), the physiological drivers underlying hyperexcitability are incompletely understood (Katz and Rymer, 1989; Burke et al., 2013).
Source: Clinical Neurophysiology - Category: Neuroscience Authors: Derek M. Miller, James F. Baker, W. Zev Rymer Source Type: research