Enhanced Reticulospinal Output in Subacute Spinal Cord Injury Patients with Spasticity

In the chronic phase of spinal cord injury (SCI), damage to the reticulospinal and corticospinal tracts has been associated with the development of spasticity. Because spasticity can emerge within just a few weeks postinjury, this suggests that reorganization of these motor pathways may begin during the subacute phase. To test this hypothesis, we assessed the StartReact response-an involuntary release of a planned movement via a startling stimulus that engages the reticulospinal tract-by measuring reaction times from electromyographic activity, motor evoked potentials (MEPs) by stimulating the leg motor cortex using transcranial magnetic stimulation, and maximal voluntary contractions (MVCs) in the quadriceps femoris muscle. Participants included males and females with subacute (1 month post-injury) incomplete SCI with and without spasticity and age-matched controls. Spasticity was evaluated using clinical and kinematic data. We found that patients with spasticity exhibited shorter reaction times to startle stimuli compared with both patients without spasticity and control subjects. In contrast, MEP amplitudes and MVCs were similarly reduced in both SCI groups compared with control subjects. Follow-up assessments conducted in a subset of participants with spasticity at 1 year post-injury revealed persistent exaggerated StartReact responses alongside reduced MEP amplitudes compared with controls. These findings indicate that, in subacute SCI, spasticity is associated with enhanced reticulospinal influences, whereas corticospinal output is reduced regardless of spasticity. The upregulation of reticulospinal pathways, 1 month post-injury, may play a critical role in the development of spasticity.