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Repairing the Damaged Spinal Cord

Nov 7, 2008 | Staff | Scientific American News

For Chinese gymnast Sang Lan, the cause was a highly publicized headfirst fall during warm-ups for the 1998 Goodwill Games. For Richard Castaldo of Littleton, Colo., it was bullets; for onetime football player Dennis Byrd, a 1992 collision on the field; and for a child named Samantha Jennifer Reed, a fall during infancy. Whatever the cause, the outcome of severe damage to the spinal cord is too often the same: full or partial paralysis and loss of sensation below the level of the injury.

Ten years ago doctors had no way of limiting such disability, aside from stabilizing the cord to prevent added destruction, treating infections and prescribing rehabilitative therapy to maximize any remaining capabilities. Nor could they rely on the cord to heal itself. Unlike tissue in the peripheral nervous system, that in the central nervous system (the spinal cord and brain) does not repair itself effectively. Few scientists held out hope that the situation would ever change.

Then, in 1990, a human trial involving multiple research centers revealed that a steroid called methylprednisolone could preserve some motor and sensory function if it was administered at high doses within eight hours after injury. For the first time, a therapy had been proved to reduce dysfunction caused by spinal cord trauma. The improvements were modest, but the success galvanized a search for additional therapies. Since then, many investigators-including us- have sought new ideas for treatment in studies of why an initial injury triggers further damage to the spinal cord and why the disrupted tissue fails to reconstruct itself.

In this article we will explain how the rapidly burgeoning knowledge might be harnessed to help people with spinal cord injuries. We should note, however, that workers have also been devising strategies that compensate for cord damage instead of repairing it. In the past two years, for example, the U.S. Food and Drug Administration has approved two electronic systems that regulate muscles by sending electrical signals through implanted wires. One returns certain hand movements (such as grasping a cup or a pen) to patients who have shoulder mobility; another restores a measure of control over the bladder and bowel.

A different approach can also provide grasping ability to certain patients. Surgeons identify tendons that link paralyzed forearm muscles to the bones of the hand, disconnect them from those muscles and connect them to arm muscles regulated by parts of the spine above the injury (and thus still under voluntary control). Further, many clinicians suspect that initiating rehabilitative therapy early-exercising the limbs almost as soon as the spine is stabilized-may enhance motor and sensory function in limbs. Those perceptions have not been tested rigorously in people, but animal studies lend credence to them.

The Cord at Work
The organ receiving all this attention is no thicker than an inch but is the critical highway of communication between the brain and the rest of the body. The units of communication are the nerve cells (neurons), which consist of a bulbous cell body (home to the nucleus), trees of signal-detecting dendrites, and an axon that extends from the cell body and carries signals to other cells. Axons branch toward their ends and can maintain connections, or synapses, with many cells at once. Some traverse the entire length of the cord.

The soft, jellylike cord has two major systems of neurons. Of these, the descending, motor pathways control both smooth muscles of internal organs and striated muscles; they also help to modulate the actions of the autonomic nervous system, which regulates blood pressure, temperature and the body's circulatory response to stress. The descending pathways begin with neurons in the brain, which send electrical signals to specific levels, or segments, of the cord. Neurons in those segments then convey the impulses outward beyond the cord.