Brainstem BOLD response to visual and acoustic stimuli in people with post-stroke spasticity

Spasticity, defined as velocity-dependent resistance to passive stretch, is common after stroke and imposes significant therapeutic challenges. It is believed that disinhibition of brainstem nuclei is responsible for spasticity, but there is debate on which individual nuclei within the brainstem, i.e. the lateral vestibular nuclei or pontine reticular formation within the whole reticular formation, are primarily involved. As such, we aimed to localize the activity of these individual brainstem nuclei via 3T functional magnetic resonance imaging (fMRI) in 10 people with post-stroke spasticity and compared the data with 11 age-matched healthy individuals. We used both acoustic and visual stimuli aimed at activating the pontine reticular formation and lateral vestibular nuclei. Visual stimuli were presented in the form of a moving checkerboard evoking illusionary self-motion to activate the vestibular network. Acoustic stimuli used loud (Sound pressure level [SPL] $= 100$ dB) acoustic bursts, expected to evoke a startle reflex and therefore activate both pontine reticular formation and lateral vestibular nuclei. We expected to find greater asymmetry in activation of brainstem nuclei in post-stroke compared to healthy individuals. We did not observe any difference in lateral symmetry between the two groups. However, we found that chronic stroke individuals exhibited three significant ($p\gt 0.05$) effects: 1) there were different delays in response to visual stimuli compared to acoustic stimuli; 2) the level of activation of the vestibular nuclei in post-stroke individuals was correlated to age, time since stroke, and brainstem volume); 3) brainstem volume of chronic stroke participants was smaller than in healthy individuals. These findings suggest that further efforts would be useful to better characterize functional activation of brainstem nuclei, especially in pathologies such as stroke.