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Updated: Sep 21, 2025

A Contusive Model of Unilateral Cervical Spinal Cord Injury Using the Infinite Horizon Impactor
Published on: July 24, 2012
Spinal Cord Injury and Loss of Cortical Inhibition
Bruno Benedetti1,2,3, Annika Weidenhammer1,2, Maximilian Reisinger1,2
1Institute of Experimental Neuroregeneration, Paracelsus Medical University, 5020 Salzburg, Austria.
Abstract:
After spinal cord injury (SCI), the destruction of spinal parenchyma causes permanent deficits in motor functions, which correlates with the severity and location of the lesion. Despite being disconnected from their targets, most cortical motor neurons survive the acute phase of SCI, and these neurons can therefore be a resource for functional recovery, provided that they are properly reconnected and retuned to a physiological state. However, inappropriate re-integration of cortical neurons or aberrant activity of corticospinal networks may worsen the long-term outcomes of SCI. In this review, we revisit recent studies addressing the relation between cortical disinhibition and functional recovery after SCI. Evidence suggests that cortical disinhibition can be either beneficial or detrimental in a context-dependent manner. A careful examination of clinical data helps to resolve apparent paradoxes and explain the heterogeneity of treatment outcomes. Additionally, evidence gained from SCI animal models indicates probable mechanisms mediating cortical disinhibition. Understanding the mechanisms and dynamics of cortical disinhibition is a prerequisite to improve current interventions through targeted pharmacological and/or rehabilitative interventions following SCI.

