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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 post-injury, 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) over the leg motor cortex using transcranial magnetic stimulation, and maximal voluntary contractions (MVCs) in the quadriceps femoris muscle in males and females with subacute (approximately one-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 cues compared to patients without spasticity and control subjects. In contrast, MEP size and MVCs were reduced similarly in both groups of patients compared to control subjects. Notably, we were able to complete follow-up measurements in some participants with spasticity one-year post-injury and found persistent exaggerated StartReact responses and reduced MEP amplitudes in spastic patients compared with controls. These findings indicate that, in subacute SCI, spasticity is associated with heightened reticulospinal influences, whereas corticospinal responses are reduced regardless of spasticity. The upregulation of reticulospinal pathways, approximately one-month post injury, appears critical for the development of spasticity.<b>Significance Statement</b> Although spasticity is a common complication after spinal cord injury (SCI), its underlying mechanisms have remained poorly understood. Our findings show that, in the subacute phase (approximately one-month post-injury) after SCI, spasticity is characterized by increased reticulospinal influence that persists chronically. Notably, this upregulation of reticulospinal pathways was specific to individuals who developed spasticity, whereas corticospinal responses are reduced regardless of spasticity. These results suggest that early enhancement of reticulospinal drive following injury plays a critical role in the pathogenesis of spasticity.