Make them walk funny and look lousy in shorts forever!

Warning: ENDING THE USE OF AN AFO CAN LEAD TO FALLS AND INJURIES.

Never discontinue the use of an orthotic without first consulting the appropriate health care provider. Then call your doctor. Then have your doc talk to any other providers as needed. Then discuss it some more. Thank you.

It seems like a no-brainer. “Ted”, has hemiparesis and the classic signs of drop foot: Emerging spasticity in the super-strong muscles that push the foot down at the ankle. He also has a weakness of the muscles that lift the foot. On top of that, he has balance problems and weakness the muscles that stabilize the ankle. The safety imperative is intense. Everybody hates falls.

AFOs solve all of these problems and allow for an almost immediate functional gait. This allows stroke survivors to get on their feet, out the door and on with their life. AFOs work really well. They do the job. They allow survivors to be functional.

But “functional” sometimes collides with “recovery”.

What would recovery be in Ted’s case? Let’s define “recovery” as “progress towards being the same as prior to the stroke.” Will the AFO help or hurt recovery?

Consider what is happening in Ted’s brain. The area of stroke is infracted. This area is now devoid of living neurons and will soon be completely filled with cerebral spinal fluid. There is an area surrounding the infarct called the penumbra. This area is kept alive through anastomosis. Like cars going around a traffic jam by taking the back roads, blood cells are delivered through smaller, secondary vessels. This allows the neurons in the penumbra to stay alive--barely. 
But neurons in the penumbra have problems besides just a reduction in blood flow. The intense biological processes initiated by the stroke soaks the penumbric neurons in a metabolic soup. This further “stuns” the neurons.

That’s what’s happening in Ted’s brain. But what is happening in Ted’s life?

The PT's initial assessment of Ted’s gait is that there is a clear need for an AFO. Once the order is written, the AFO will take 2-3 weeks to fabricate. In the meantime therapists have begun gait training using an ace bandage tied to his lower leg. This forces the foot up and stabilizes the ankle. Ted is given a cane. Ted does well with this system and is able to walk 20 yards. He still fatigues easily, so a recumbent stepper is used to build cardiovascular strength.

Okay, now back to Ted’s brain. The neurons stunned by the stroke are starting to come back “on line”. The blockage has cleared in the primary artery. The metabolic soup that provided such a harsh environment for the neurons has dissipated. The neurons are ready to go back and do what they’ve always done; help Ted walk. But these neurons are never called upon.

They never will be.

Once the AFO arrives, Ted takes to it well. The gait training and cardio work he's done pays off. The AFO works so much better than the ace bandage that Ted immediately walks longer than he ever has. Ted is functional.

Meanwhile, the area of the cortex jam-packed full of neurons that control the ankle is shrinking. Rapidly. In a process known as learned nonuse the area will shrink to half its size in just a few weeks. Languishing for long enough will force the remaining neurons to migrate to some other task. Other neurons will go through "synaptic pruning" and they'll communicate less and less with the neurons around them. The muscles of that push the foot down may atrophy and will certainly shorten. The muscles that pull the foot up at the ankle are not called upon. The AFO does that work. The muscles that pull the foot up are small to begin with (relative to the muscles that push the foot down). And they begin to atrophy. Ted will have the AFO as a lifelong companion. The orthotic will substantially change his style of walking and may have future orthopedic implications.

What's the alternative? Managed care leaves few options and little time. Stroke survivors want to go home and their caregivers want them home. This is why AFOs seem like a blessing. 

      But a new perspective is emerging. There are researchers that advocate early electrical stimulation (e-stim) as a possible hedge against learned nonuse. E-stim has the potential to jump start movement, promote muscle building, calm spasticity and may even have an impact cortically. Repetitive practice with and without the help of robotics, gaming applications and task specific training may begin to bring the stunned cells of the penumbra back on line. A menagerie of emerging treatment options from mirror therapy to bilateral training to lower extremity constraint induced therapy also seem to have potential. But there are more flies in the ointment than ointment at this point. Research is far from definitive answers. One thing we do know is that the brain is a market economy. The “goods” (neurons) go to the “customers” (whatever movement is asked for). If nothing is asked of them neurons will find something else to do. As recovery is unmasked after stroke, every effort should be made to guide neurons “back home”. This will require more time to allow the arc of natural recovery to emerge. It will also require more focus on what is not easily seen: neuroplastic change in the brain. “Seeing” neuroplastic change requires sensitive, stroke-specific outcome measures.

    In other words, this shift in treatment philosophy, from “focus on functional” to “realizing recovery” is as much a work in progress for therapists as it is researchers.