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.
