This Collateral sprouting by spared descending Motor axons in the spinal cord should be distinguished from Axon Regeneration by transected axons. Axon regeneration, also called regenerative synaptogenesis, is the actual regrowth of a damaged axon across the site of injury. It does not appear commonly in the spinal cord, though it is a common recovery mechanism in Peripheral nerves.

LMN weakness recovers primarily by motor axon sprouting in muscle. This growth of new neuromuscular synapses by spared motor axons compensates for LMNs degenerating due to the trauma. Perhaps as many as 75% of the muscle fibers can lose their innervation and still be reinnervated by the remaining 25% of motor axons.

Conduction block in LMNs may resolve as a basis for some recovery; however, our observations suggest this is an uncommon mechanism after a Cervical cord injury.

In both UMN and LMN weakness, muscle fiber strengthening must occur to complete the motor recovery. This muscle strengthening depends upon resistance exercises and develops gradually over several months.

Although some recovery occurs spontaneously, more is achieved - and it is achieved faster - through Rehabilitation, which may include the use of medications, adaptive equipment, strengthening exercises and Functional training. Optimal rehabilitation requires targeting specific recovery mechanisms with specific rehabilitation interventions. Rehabilitation interventions should therefore be individualized to specific patients, specific muscles and specific time periods to achieve the best possible outcome.

Here are four considerations based on our preliminary results that can guide rehabilitation interventions.

1. The non-invasive methods used in these studies can be applied to routine diagnosis and monitoring of arm weakness in tetraplegic subjects.
2. Recovery from UMN weakness by collateral sprouting in the spinal cord may be enhanced by active use of those pathways, while recovery from LMN weakness may be compromised by overuse.
3. The type of recovery may impose consequences on the functional capacity of the limb. For example, recovery via LMN axon sprouting may result in muscles that fatigue more readily and are susceptible to late deterioration, as seen in post-polio patients. Muscles recovering from UMN involvement may develop Spasticity, which can limit voluntary movement.
4. Some upper limb recovery mechanisms act over a period of many months, perhaps a year or more, meaning that some recovery develops after initial rehabilitation is completed. Follow-up of tetraplegic individuals should include reassessment of arms and hands to discover if late recovery warrants additional functional training or a change in adaptive equipment. The timing of procedures such as tendon transfers and implantable functional electrical stimulation must be carefully considered in light of this potential for late recovery.

REFERENCES

1. Wu L, Marino RJ, Herbison GJ et al.: Recovery of zero-grade muscles in the zone of partial Preservation in motor complete Quadriplegia. Arch Phys Med Rehabil 1992;73:40-43
2. Ditunno JF, Stover SL, Freed MM et al.: Motor recovery of the upper extremities in traumatic quadriplegia: a multicenter study. Arch Phys Med Rehabil 1992;73:431-436
3. Mange KC, Ditunno JF, Herbison GF et al.: Recovery of strength at the zone of injury in motor complete and motor incomplete cervical spinal cord injured patients. Arch Phys Med Rehabil 1990;71:562-565
4. Haughton JF, Powers RK, Robinson LR et al.: The ratio of electrically induced to voluntarily recruited electromyographic activity for evaluating upper Motoneuron weakness. Arch Phys Med Rehabil 1992;73:968
5. Little JW, Moore D, Brooke M et al.: Electromyographic evidence for motor axon sprouting in recovering upper extremities of acute quadriplegics. J Am Para Soc 1990;13:16
6. Yang JF, Stein RB, Jhamandas J et al.: Motor unit numbers and contractile properties after spinal cord injury. Ann Neurol 1990;28:496-502

Fall 1993