Corticospinal projection patterns following unilateral section of the cervical spinal cord in the newborn and juvenile macaque monkey.

Immediately following a unilateral section of the midcervical spinal cord that interrupts the dorsolateral, lateral, and ventral columns, the macaque monkey has a severe flaccid paralysis on the side of the lesion. Recovery of hand function is rapid, and, although it is incomplete, within a few months, the monkey uses the initially disabled hand and fingers with considerable skill. We examined the accompanying changes in the pattern of projection of corticospinal neurons to the cervical spinal cord that occurred following such a lesion. Spinal section was done both in newborn and juvenile macaques, and the postlesion period was followed for up to 150 weeks. Corticospinal neuron populations were visualized by using both anterogradely and retrogradely transported labels, and their origins, spinal pathways, and terminations were examined at intervals during the period of recovery of hand function. Immediately following unilateral section of the spinal cord at C3, sampled counts of soma profiles of retrogradely labeled neurons indicated that there was a profound reduction in the corticospinal projection to the hemicord caudal to the lesion. The few labeled corticospinal axons spared by the lesion bypassed the spinal lesion by descending in the contralateral cord and then crossing the midline caudal to the lesion. A few corticospinal axons may also have bypassed the lesion in the ipsilateral ventromedial column when this was not fully interrupted by the lesion. In every monkey, we observed a similar, profound reduction in the corticospinal (and rubrospinal) projections to the hemicord caudal to the lesion: This pattern did not alter significantly over an extended recovery period. An unchanging corticospinal projection to the cervical spinal cord contralateral to the lesion was also visualized in each monkey and resembled that seen in the normal macaque. Although the resolution of the labeling and counting procedures used precluded the identification of small increases in the numbers of corticospinal neurons projecting to the hemicord caudal to the lesion, we concluded that there was no substantial reconstruction of this projection over a recovery period of more than 2 years.