Blood pressure drug may prevent spasms caused by spinal cord injury
One of the serious and enduring side effects of a spinal cord injury can be the gradual development of regular muscle spasms, something that afflicts around 70 percent of sufferers, according to researchers at the University of Copenhagen. These scientists may have uncovered an effective new treatment for this side effect in the form of an existing blood pressure medication, which proved capable of halting its progression in mice.
Known as spasticity, this common side effect of spinal cord injuries is caused by a breakdown in communications from the brain that normally regulate one’s reflexes. The involuntary, sustained muscle spasms that result can occur in any part of the body impacted by the spinal cord injury, and can appear as soon as a few hours after the injury, or only begin to take hold some months later.
The University of Copenhagen researchers were experimenting with a drug called nimodipine, which has been approved for use since the 1980s to treat a number of conditions, including high blood pressure. In these experiments, mice with spinal cord injuries were given the nimodipine treatment for six weeks, and observed for a period of nine weeks.
The mice went on to develop only mild signs of spasticity, or none at all. What really surprised the researchers, however, was that the effects of the treatment seem to endure, keeping the spasticity at bay even after the treatment had stopped.
"We show that nimodipine by and large can prevent the development of spasticity after a spinal cord injury if administered soon after the injury and for an extended period of time,” says co-author Ole Kiehn, Professor at the Department of Neuroscience at the University of Copenhagen. “One of the most surprising and interesting elements in the study is that the effect continues, even after treatment has stopped.”
The researchers were also able to demonstrate why this might be the case. Nimodipine works by blocking calcium channels in nerve cells in the spinal cord, and by genetically removing one of those channels in the mice, known as the CaV1.3 channel, the researchers produced the same results in preventing spasticity.
The team believes this approach could even be applied to other conditions that can lead to spasticity, such as multiple sclerosis or stroke. The researchers are now focusing their attention on how these results might translate from mice to humans.
“We are quite optimistic that nimodipine will have the same effect in humans,” says Ole Kiehn. “But we cannot be certain. Nimodipine is an approved drug that easily enters the brain, and we will now begin trials together with other researchers where we test nimodipine on healthy test subjects to study the effect on various reflexes and motor skills. Subsequently, it may potentially be possible to test the drug on people with spasticity.”
The research was published in the journal Science Translational Medicine.
Source: University of Copenhagen