There has been some discussion among researchers and health providers about the timing and intensity of rehabilitation. In North America, the overall view is that the earlier rehabilitation starts after stroke (and other brain injury) the better (although probably not always practiced!). However I did meet a young physician from China at a neuroscience conference and he reported to me that people who have a stroke in his facility remain on bedrest for at least a week. His rationale was that some animal research suggested that early rehabilitation worsened the extent of the brain damage and impeded recovery. Hmmmmm…
My view is that my colleague is both right and wrong in his approach.
In 1996, researchers in the Schallert lab at University of Texas at Austin reported that rats that were placed in body casts for 15 days to force the use of the impaired forelimb directly following brain lesion surgery, did poorly. The animals also had worsening of the extent of the brain lesions compared to rats with the affected limb casted or no cast at all.
My first thought about this study is that there are issues with both timing and intensity of ‘rehabilitation’. First of all, a rat undergoes a fairly significant procedure and wakes up to find that one forelimb is casted to its body (24 hrs per day for 15 days) and the other forelimb is non functional. The rat would be stressed and unable to eat, groom or defend itself properly so worsening of the brain lesion and poor recovery is no surprise. Although it is important to determine the threshold of timing and intensity of rehabilitation, the intensity of this method of ‘forced-use’ is unrealistic and the timing (while the animal is still anesthetised for the brain surgery) is extreme. I find it hard to believe that it mimics the human experience of brain injury in any way. Researchers in the same lab in a paper published in 1998 (by Humm and group) replicated the experiment except they had two additional groups; group 1. Casted for the first seven days (Day 0-7) and group 2.,Casted for the second seven days (Day 7-15). They found both groups did poorly but the later casting group had less brain tissue loss. This suggests to me that delaying the casting and ‘rehabilitation’ did not seem to change the outcome very much-the intensity is probably still too extreme- a very important finding. In this study, the brain injury was induced by electrical injury to the brain’s cortex. I am not sure if the brain damage, induced by electrical injury, is similar enough to brain injury mechanisms in humans. How brain cells die using this method may be quite different than stroke or trauma.
Another study by Risedal in 1999 revisited the issue of timing and intensity. They used a rat model of brain blood vessel blockage to induce a small stroke. They instituted 1 hr/day of training beginning 24 hrs or 7 days following the stroke. Both groups improved compared to the ‘no rehab’ group but the early group had larger lesions. The delayed group had the best outcome. So it seems that beginning rehabilitation within the first 24 hours after stroke would be ill-advised (even just an hour a day)….but should we wait as long as 7 days?
The timing and intensity of rehabilitation after a brain injury is a very important research question that can really only be answered using animal models. Doing this type of work in humans is obviously unethical. Biernaskie and Corbett address it again in a paper published in 2004. Rats underwent 5 weeks of rehabilitation (enriched cages and up to 6 hrs of reach training 5 days per week) beginning 5, 14 and 30 days after stroke. The stroke was fairly substantial and larger than the previous studies mentioned above. In terms of the extent of the brain damage, there were no differences among the groups; that is, starting rehab earlier did not worsen the injury as suggested by previous studies. Furthermore the Day 5 group recovered better than the 14 and 30 day start groups with more dendritic branching occurring in the opposite brain hemisphere. Interestingly, beginning rehab at 30 days after stroke did not benefit the animals at all.
I know I am presenting a lot of research stuff here but it is important to appreciate that the answer about timing and intensity is not clear cut. The take home message to me is that beginning intensive rehabilitation before 5 days after injury would not be advised. Perhaps the threshold can be 2 , 3 or 4 days but we don’t know. Who knows if timelines established in rat brain injury parallel those in the human world? In the case of my Chinese colleague, perhaps 7 days of bedrest is the other extreme and also probably not beneficial. I would suggest that there is other literature that supports that people on bedrest for that length of time would have muscle atrophy and be at risk for blood clots. It is rare that someone who has had had a stroke in the past week would be well enough to participate in intensive tasks anyway. Early rehabilitation often focuses on sitting up, moving about in bed and balance. It does not seem to make sense to me to delay this type of intervention.
What I surmise from research findings so far is that, in terms of intensity, any type of constraint of the unaffected limb to force use of weaker limb is not advised within the first two weeks after brain injury. Training targeted to increase motor recovery of the arm and hand for up to 6 hrs per day is probably fine after 5 days but I have not heard of such intense practice at any time in rehabilitation other than Constraint-induced Movement Therapy (which I plan to discuss in later posts).
If I were to advise a biomedical stroke researcher on further work in this area, my thoughts are,
1. Choose an animal model closely aligned to brain injury in humans.
2. Try different intensities of training (1,2,3,4, 5 hrs per day) beginning 2,3,or 4 days after injury.
3. Try restraint of the unaffected arm 20 or 30 days after brain injury to determine the time threshold for hyper-intense interventions (this could be important as we advance in our rehabilitation methods), and,
4. Find out why and how brain lesions are worsened by some interventions. ..perhaps vulnerable neurons are stressed or
killed off by some chemical response.
That’s my two cents worth.