Post-traumatic cauda equina concussion: Definition and description of the injury mechanism.

Despite being a prevalent clinical condition, cauda equina concussion has not been thoroughly elucidated in the literature. The aim of this study is to delineate the etiology and pathogenesis of cauda equina concussion and its associated clinical manifestations. Patients exhibiting clinical manifestations indicative of spinal cord injury and transient neurological deficits after spinal trauma were evaluated retrospectively. The pathogenesis was elucidated through correlating clinical presentations with radiological findings. Neurological deficits were categorized into two principal groups, symmetrical and asymmetrical. Non-penetrating fractures were classified to ascertain the relationship between the type of trauma and the ensuing neurological deficits. A cohort of 82 patients was diagnosed with cauda equina concussion. Among these, 58 had experienced vertical trauma resulting from falls, while 24 had encountered axial trauma in vehicular accidents. Stable spinal fractures were identified in 52 patients across multiple levels, whereas single-level fractures were observed in 30. Asymmetrical neurological deficits were detected in 51 (62.19%) patients, with a notably higher incidence among those subjected to vertical trauma (p < 0.014). The mean recovery time was 14.25 ± 15.16 h for sensory deficits and 11.25 ± 13.36 h for motor deficits in those patients. Notably, motor deficits resolved more expeditiously than sensory deficits in all cases presenting with both. Cauda equina concussion emerges as a frequently encountered clinical phenomenon attributable to the impact of high-energy vertical forces. Neurological deficits commonly manifest asymmetrically. The rapid resolution of neurological deficits presents challenges for the diagnostic process.