Paradoxical Motor Recovery From a First Stroke After Induction of a Second Stroke Reopening a Postischemic Sensitive Period

I would never voluntarily do a second stroke and I doubt this would ever get enough test subjects to prove if this works in humans. I would really question the conclusion that came out of this. Have you proven that the same exact area was infarcted?
Earlier reported here: But it seems to be the same research, just now in print.

'Window of recovery' can reopen after stroke

http://nnr.sagepub.com/content/30/8/794?etoc

1. Steven R. Zeiler, MD, PhD1⇑
2. Robert Hubbard1
3. Ellen M. Gibson1
4. Tony Zheng1
5. Kwan Ng, MD, PhD2
6. Richard O’Brien, MD, PhD3
7. John W. Krakauer, MD1

1. ¹Johns Hopkins University, Baltimore, MD, USA
2. ²UCLA, Los Angeles CA, USA
3. ³Duke University, Durham, NC, USA

1. Steven R. Zeiler, MD, PhD, The Johns Hopkins Hospital, Department of Neurology, Phipps 443, 600 N. Wolfe Street, Baltimore, MD 21287, USA Email: sz@jhmi.edu

Abstract

Background and objective. Prior studies have suggested that after stroke there is a time-limited period of increased responsiveness to training as a result of heightened plasticity—a sensitive period thought to be induced by ischemia itself. Using a mouse model, we have previously shown that most training-associated recovery after a caudal forelimb area (CFA) stroke occurs in the first week and is attributable to reorganization in a medial premotor area (AGm). The existence of a stroke-induced sensitive period leads to the counterintuitive prediction that a second stroke should reopen this window and promote full recovery from the first stroke. To test this prediction, we induced a second stroke in the AGm of mice with incomplete recovery after a first stroke in CFA.  

Methods. Mice were trained to perform a skilled prehension (reach-to-grasp) task to an asymptotic level of performance, after which they underwent photocoagulation-induced stroke in CFA. After a 7-day poststroke delay, the mice were then retrained to asymptote. We then induced a second stroke in the AGm, and after only a 1-day delay, retrained the mice.  

Results. Recovery of prehension was incomplete when training was started after a 7-day poststroke delay and continued for 19 days. However, a second focal stroke in the AGm led to a dramatic response to 9 days of training, with full recovery to normal levels of performance.  

Conclusions. New ischemia can reopen a sensitive period of heightened responsiveness to training and mediate full recovery from a previous stroke.