Recovery of some upper limb function is common following a Cervical spinal cord injury. Patients with initial C4-level Tetraplegia often regain C5 muscle function, enabling them to eat and use a joystick hand control independently, while those with C5-level tetraplegia often regain C6 strength, making possible some independent grasp and pinch by using wrist extensor muscles and a splint.
Two factors that help predict this type of upper limb recovery have been identified. One is initial strength. Those muscles with some movement (muscle grade 1 to 2+) shortly after injury have an 82% likelihood of achieving anti-gravity strength by 6 months and a 90% chance after 12 months. However, muscles at the zone of injury with no movement by 72 hours have only a 36% chance of achieving anti-gravity strength by 6 months, and 45% and 64% likelihoods at 12 and 24 months, respectively.
A second predictor is voluntary movement in the lower limbs, which indicates a less severe cord injury, and therefore a greater probability of Functional recovery in the hands and arms as well as legs. Those with some initial voluntary movement (Frankel C or D) in the legs have been shown to have a greater chance for Motor recovery in the upper limbs than those with no leg movement (Frankel A or B).
Our recent work at the Seattle V.A. Medical Center and the University of Washington Department of Rehabilitation Medicine, funded by the Department of Veterans Affairs and by the Paralyzed Veterans of America, has examined this arm weakness and subsequent recovery in 41 tetraplegic individuals. By examining weak muscles during the period of Acute rehabilitation, using a variety of electrophysiologic tests, we have distinguished upper motor Neuron (UMN) and lower motor neuron (LMN) weakness and the different recovery mechanisms associated with these different types of weakness.
To assess LMNs, which connect the spinal cord to muscle, we measured the muscles’ response to electrical stimulation of the Peripheral nerve (M response amplitude). To assess UMNs, which connect the brain to the spinal cord, we measured the electrical activity generated during maximum voluntary effort and expressed it as a root mean square (RMS).
The ratio of M/RMS can be used to determine the degree of UMN weakness, with a higher ratio indicating greater UMN involvement. We also examined the motor-unit firing rate during maximum effort, as UMN weakness is associated with unusually slow firing rates at such times.
Weak arm muscles in acute tetraplegic patients demonstrate various combinations of UMN and LMN weakness. Approximately one-third of the muscles demonstrate UMN weakness, one-third demonstrate LMN weakness and one-third have mixed UMN and LMN weakness.
Our work and that of others has shown that UMN weakness recovers by a different neuromuscular mechanism than LMN weakness.
UMN weakness recovers because conduction is restored in dysfunctional but preserved axons that extend through the zone of cord injury; this may take place when pressure on the cord is relieved by surgery or when Glial Cells repair the insulating Myelin around axons. UMN weakness also recovers when spared axons that cross the zone of cord injury establish new synapses in the spinal cord. This growth of new connections in the spinal cord is called Collateral sprouting or reactive synaptogenesis, and it allows a reduced number of descending fibers from the brain to activate neurons in the spinal cord and thus produce functional movements in previously paralyzed muscles.
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
