There is a model of a human being (or any animal) in which the brain is the control center, directing the movements of the body. Your brain signals your heart to beat and stomach to digest. It tells your muscles when and how to contract in order to move your skeleton. When movement problems arise, when a person is incapable of initiating or controlling physical motion, most treatments focus on restoring brain function. For example, most medications for Parkinson’s disease target cerebral neurotransmitters. Such an approach seems to make perfect sense. Fix the control center, and it can get back to its supervisory role. But new developments in neuroplasticity and treating movement impairments show that such a top-down, brain-focused approach might not be the most effective path to recovery. And as a result, we may need to rethink our brain-first model.
A Brain Locked in a Body
A recent Chicago Tribune article profiles Jose Rodriguez Jr., who has a rare condition known as locked-in syndrome. In 2013, Rodriguez suffered a stroke at the age of thirty-one. He underwent surgery to remove the blood clot that caused his stroke, a procedure which left him in a coma for twelve days. When he awoke, he was unable to move any part of his body except for his eyes. Rodriguez couldn’t walk, talk, swallow or breathe on his own. His brain could not even regulate his body temperature. He underwent more surgery for a tracheotomy to attach a ventilator through his throat to keep him breathing. Hospital staff packed him in ice and directed fans at him to keep him from overheating. But he could still feel his body—he flinched every day when a nurse pinched his finger to test his reactions.
Locked-in syndrome can develop from a stroke, tumor, injury, amyotrophic lateral sclerosis or any disorder that disables the brain stem and prevents it from relaying signals for functions like movement, breathing and heart rate. About half of locked-in sufferers can eventually breathe on their own. Most don’t regain speech or voluntary movement.
Treatment of locked-in syndrome typically involves getting the patient as functional as possible within the range of available movements. Practitioners, family and friends are encouraged to establish eye-coded communication with the patient (e.g. look up for “yes” and down for “no,” or using eye movement to indicate a spoken or written letter). Devices like infrared eye tracking may allow patients to speak through a computer with an artificial voice and type messages. Once communication has been established, treatment moves to the rehabilitation of the small voluntary movements that remain or recover naturally. Movement therapy focuses on developing any existing or burgeoning movements as opposed to redeveloping movements that have been completely lost because recovery of near-normal motor control, including speaking, swallowing and walking, is extremely unusual.
Movement Through Constraint
In contrast to traditional therapies, Rodriguez went through a variation of constraint-induced therapy, which attempts to introduce new movements and promote new connections and functions between nerve cells, a process called neuroplasticity. Constraint-induced therapy involves restricting less-affected movements, such as with a sling or mitt on a patient’s arm or hand, while focusing on restoring impaired movements. The therapy helps patients develop fine motor skills by performing tasks like moving checkers. According to constraint-induced therapy creator Dr. Edward Taub, the key is to slowly increase the difficulty of the task to continually challenge the patient to improve. These repetitive motions and more challenging therapeutic approach encourage the brain to rewire itself by growing new connections.
Following his tracheotomy, therapists had Rodriguez perform some physical movement every day. By the time he left the hospital, he was able to open his mouth. He then regained the ability to breathe on his own and was referred to the Rehabilitation Institute of Chicago (now the Shirley Ryan AbilityLab). Next, he continued to work on moving his head from side to side in order to control a motorized wheelchair. He practiced chewing gum with a string attached to it so he could pull the gum out without swallowing. He later graduated to eating pureed food.
Therapists also used a robotic exoskeleton to help him walk. The skeleton did all the work to start, then less and less as Rodriguez regained his own movement capabilities. Neuroplasticity experts believe this process is crucial to relearning movement. Once again, slowly increasing the difficulty of the task encourages the brain to rewire neurons in order to advance to the next stage. Just moving the body passively does not have the same effect. It’s the same principle as any sort of physical training. If you keep the same exercise routine week after week, you’ll stop making gains in strength and endurance. You need to increase the difficulty of your workouts over time to force your body to continually adapt. Constraint-induced therapy also shows that movement adaptation is a result of the synchronized development of body and mind.
With the help of his therapist and exoskeleton, Rodriguez learned to stand, then take a few steps, then walk seventy feet. He also learned to operate a power wheelchair using one hand and to communicate by typing letters using his eye movement and an eye-tracking device. After that, he developed the ability to type with one finger. He was released from the hospital and continues his rehabilitation from home. He writes a series of sci-fi/fantasy books on his laptop, does his daily exercises and takes occasional trips around his neighborhood and to stores and movies. Over five years since his stroke, he can now speak a word or two at a time.
Rodriguez’s experience with locked-in syndrome and constraint-induced therapy demonstrates the interconnection between brain and body. The brain is not the command center directing the movement of the body; it needs movement in order to function properly. And it needs new and constantly evolving movements in order to repair itself or grow. It appears the brain and body function as a cohesive system, both growing and changing to meet challenges in the external environment.
Movement As Medicine
It turns out that more difficult challenges may lead to even better outcomes. Researchers at Northwestern Medicine and the University of Colorado School of Medicine recently discovered that not only is high-intensity exercise safe for patients with Parkinson’s disease, it actually prevents disease symptoms from getting worse.
According to the Parkinson’s foundation, 60,000 Americans are diagnosed with the disease each year. About one million Americans currently suffer from the disease, more than the number patients with muscular dystrophy, Lou Gehrig’s disease or multiple sclerosis. The disease results from the impairment or death of brain cells that affect movement. As a result, Parkinson’s causes difficulties with balance, posture, walking and speech.
Previous studies have examined the effect of low-intensity endurance exercise on Parkinson’s symptoms. But this recent study is the first to investigate high-intensity training. Many doctors believed that strenuous exercise could prove hazardous to Parkinson’s patients. To test this hypothesis, the Northwestern and Colorado researchers assigned 127 subjects to one of three groups. The first group followed a high-intensity treadmill workout regimen for six months, the second followed a moderate treadmill regimen for six months and the third group did not exercise during that time period. None of the subjects took any medication for their condition during the experimental period. Parkinson’s symptoms of the disease did not change significantly for subjects in the high-intensity group but worsened by 7.5% percent for those in the moderate group and by 15% for those in the control group.
Daniel Corcos, a professor of physical therapy and human movement sciences at Northwestern’s Feinberg School of Medicine and one of the lead authors of the paper, said the study provides additional evidence that “exercise is medicine.” He added, “The real question is: Is there any disease or any disorder for which exercise is not good?”
Geoffrey Rogers was one of the subjects in the study’s high-intensity group. He was diagnosed with Parkinson’s five years ago at the age of sixty-four and noted that exercise improved his symptoms. “I can’t speak as a researcher or as an authority on this,” he said, “But the cumulative effect was that the tremor was less intense going forward. When I finished with a workout, the tremor would be under control, I wouldn’t be going crazy with it. And that would last twenty minutes, an hour.”
For now, these findings are preliminary. Researchers need to perform another clinical trial to conclusively demonstrate the benefits of high-intensity workouts on Parkinson’s disease. But Corcos hypothesized that improved blood flow to the brain because of exercise might explain the results. And he emphasized that consistency is critical to achieving lasting benefits. “It has to be a sustained lifetime commitment,” he said.
A New Brain-Body Model
At the very least, the benefits of high-intensity exercise for Parkinson’s disease patients support the brain-body synchronization demonstrated by locked-in syndrome and constraint-induced therapy. Treating brain disorders seems to require more than brain-centric therapy. These disorders manifest themselves through impaired motor function, and restoring movement is key to recovering brain function. The success of constraint-induced therapy and high-intensity exercise in treating locked-in syndrome and Parkinson’s disease suggest that the control center model of the brain is wrong, that the brain is not the underlying cause of these disorders. Rather, the brain and body function, learn and adapt together. So treatment should address both physical actions and cognitive processes. And the treatment stimulus must be demanding enough to require adaptations from the brain and body that will allow them to regrow, heal and improve together.