Supraspinal control of automatic postural responses in people with multiple sclerosis

- Supraspinal causes of delayed automatic postural responses in people with MS are unknown.
- We correlated supraspinal structural connectivity to postural response latency.
- Pedunculopontine nucleus structural connectivity was worse in people with MS.
- Pedunculopontine nucleus connectivity was correlated to tibialis onset latency.
- Altered supraspinal connectivity may contribute to delayed postural responses in MS.

The neural underpinnings of delayed automatic postural responses in people with multiple sclerosis (PwMS) are unclear. We assessed whether white matter pathways of two supraspinal regions (the cortical proprioceptive Broadman's Area-3; and the balance/locomotor-related pedunculopontine nucleus) were related to delayed postural muscle response latencies in response to external perturbations. 19 PwMS (48.8 ± 11.4 years; EDSS = 3.5 (range: 2-4)) and 12 healthy adults (51.7 ± 12.2 years) underwent 20 discrete, backward translations of a support surface. Onset latency of agonist (medial-gastrocnemius) and antagonist (tibialis anterior) muscles were assessed. Diffusion tensor imaging assessed white-matter integrity (i.e. radial diffusivity) of cortical proprioceptive and balance/locomotor-related tracts. Latency of the tibialis anterior, but not medial gastrocnemius was larger in PwMS than control subjects (p = 0.012 and 0.071, respectively). Radial diffusivity of balance/locomotor tracts was higher (worse) in PwMS than control subjects (p = 0.004), and was significantly correlated with tibialis (p = 0.002), but not gastrocnemius (p = 0.06) onset latency. Diffusivity of cortical proprioceptive tracts was not correlated with muscle onset. Lesions in supraspinal structures including the pedunculopontine nucleus balance/locomotor network may contribute to delayed onset of postural muscle activity in PwMS, contributing to balance deficits in PwMS.