In a mouse model of stroke, Johns Hopkins researchers have found that intrinsic nervous system repair mechanisms could allow mice to recover more quickly. Specifically, mice partially lost the use of their front paws following an initial stroke, but were able to successfully grab food pellets after a second stroke.
The research appeared in the online journal Neurorehabilitation and Neural Repair.1
The scientists first trained animals to perform a grasping task then gave them a stroke using photocoagulation. After 7 days, the animals were retrained in the reaching task, for a total of nineteen days. The animals did not fully recover, and were given a second stroke. The researchers then retrained the animals in the reaching task after only one day post-recovery, for a total of nine days. The animals fully recovered to normal performance following the second stroke.
The findings build upon the idea that neurons may have more plasticity, i.e., capacity for repair in adulthood, than previously believed.
The authors noted in their report that the findings in no way suggest that inducing a stroke is a viable treatment option. However, the findings do open up the intriguing possibility that the nervous system has intrinsic repair mechanisms that could be exploited. If the mechanisms mediating repair after a second stroke could be uncovered, this might open up new avenues for stroke treatments and for the prevention of neural damage following stroke.
“If we can better understand how to reopen or extend the optimal recovery period after a stroke, then we might indeed change how we treat patients for the better,” remarked Steven Zeiler, MD, PhD, in a press release. Zeiler is an assistant professor of neurology at the Johns Hopkins University School of Medicine. “Our study adds new strong and convincing evidence that there is a sensitive period following stroke where it’s easiest to relearn motor movements — a topic that is still debated among stroke researchers” he added.
The research is a follow-up to a prior Johns Hopkins study, which identified the first seven days as the optimal recovery time following induced stroke in mice.2 However, in this study the scientists were able to extend the stroke recovery window by giving animals the antidepressant fluoxetine right after the stroke. Because fluoxetine works as a serotonin reuptake inhibitor, the effects observed could be due to actions on the serotonergic system.
The antidepressant increased the animals’ ability to learn the same pellet-grabbing task. However, the study did not show that it could be possible to reopen the learning period. These new results suggest that learning can indeed occur again.
In their study report, the investigators concluded “New ischemia can reopen a sensitive period of heightened responsiveness to training and mediate full recovery from a previous stroke.”
The research could have implications for recovery of function in individuals who have suffered more than one stroke. However, at present the results have only been observed in an animal model. Further investigations of recovery of function following stroke and the mechanisms underlying it need to be conducted in humans.
1. Zeiler SR, et al. Paradoxical motor recovery from a first stroke after induction of a second stroke: reopening a postischemic sensitive period. Neurorehabil Neural Repair. 2015 Dec 31.
2. Johns Hopkins Medicine. Research in mice shows potential value of common antidepressant in stroke victims too sick for immediate rehab. 31 Aug 2015.