A recent paper in the journal Nature Medicine sheds some important new light on the underlying mechanisms of spasticity that often develops after a spinal cord injury. Involuntary contractions of muscles, or spasticity, can have potentially serious consequences, and although medications are available that reduce spasticity, they can also interfere with positive motor functions or rehabilitation.
Although spasticity represents an involuntary movement of muscle, the muscular activity originates with excited neurons telling the muscles to constantly move and contract (hyperexcitability). Previous dogma held this hyperexcitability to be related to uncontrolled intracellular levels of sodium and calcium in the nerve cells.
This new paper identifies changes in intracellular chloride levels as a potentially important regulator of spasticity. The authors, Boulenguez et al, also identify possible “upstream” mechanisms, including decreases in the neurotransmitter BDNF, as responsible for controlling the chloride levels, thus hinting at new targets available for therapeutic intervention.
An accompanying editorial by Drs. V. Reggie Edgerton (pictured) and Roland Roy states that, “Further study of these adaptive events is likely to lead to a better understanding of the phenomena that underlie spasticity and ultimately provide ways to alleviate its symptoms in a safe and effective way. Dr. Edgerton is a member of the Reeve Foundation’s International Consortium on Spinal Cord Injury and its science advisory council.
The research was partially supported by a grant from the Reeve Foundation to the lead author Laurent Vinay, as is ongoing follow-up work on this project.
Douglas S. Landsman, Ph.D.
Director, Individual Research Grants Program