Aberrant crossed corticospinal facilitation in muscles distant from a spinal cord injury.

Crossed facilitatory interactions in the corticospinal pathway are impaired in humans with chronic incomplete spinal cord injury (SCI). The extent to which crossed facilitation is affected in muscles above and below the injury remains unknown. To address this question we tested 51 patients with neurological injuries between C2-T12 and 17 age-matched healthy controls. Using transcranial magnetic stimulation we elicited motor evoked potentials (MEPs) in the resting first dorsal interosseous, biceps brachii, and tibialis anterior muscles when the contralateral side remained at rest or performed 70% of maximal voluntary contraction (MVC) into index finger abduction, elbow flexion, and ankle dorsiflexion, respectively. By testing MEPs in muscles with motoneurons located at different spinal cord segments we were able to relate the neurological level of injury to be above, at, or below the location of the motoneurons of the muscle tested. We demonstrate that in patients the size of MEPs was increased to a similar extent as in controls in muscles above the injury during 70% of MVC compared to rest. MEPs remained unchanged in muscles at and within 5 segments below the injury during 70% of MVC compared to rest. However, in muscles beyond 5 segments below the injury the size of MEPs increased similar to controls and was aberrantly high, 2-fold above controls, in muscles distant (>15 segments) from the injury. These aberrantly large MEPs were accompanied by larger F-wave amplitudes compared to controls. Thus, our findings support the view that corticospinal degeneration does not spread rostral to the lesion, and highlights the potential of caudal regions distant from an injury to facilitate residual corticospinal output after SCI

The translational dialogue in spinal cord injury research

Background: Although the emphasis in clinical spinal cord injury (SCI) research has been directed towards the evaluation of clinical assessments (standards in neurological examination) and the appreciation of outcome measures (that is, extent and pattern of clinical recovery from SCI), the underlying neurological mechanisms for recovery from SCI are not well documented in humans. However, to improve the translational research, a meaningful preclinical-clinical dialogue is required, with an appreciation for both fundamental neural mechanisms and what makes human SCI unique. This holds true both for potential interventions in rehabilitation and novel drug or cell-based treatment approaches in acute SCI.Objectives:The gap in translational research that needs to be approached from both ends not only includes the appreciation of principal neural mechanisms (repair, sprouting, plasticity) and their assumed impact onto outcomes (even though humans and non primate animals may rely on slightly different supraspinal control for some movements), but also includes an understanding of the spatial (location and size of lesion) and temporal (timelines of damage and recovery) factors in spinal cord damage that can vary considerably between the different species being studied.Conclusion:The preclinical-clinical dialogue should be encouraged as a venue to improve the appreciation of discoveries in basic research, and to power valid discoveries towards a meaningful translation into advanced treatments downstream. Similarly, the upstream identification of appropriate clinical targets that take into account clinical constraints depends on reliable and advanced clinical information being provided to preclinical investigators.Spinal Cord advance online publication, 8 November 2011; doi:10.1038/sc.2011.113