The corticospinal tract (CST) plays a major role for the control of dexterous finger movement. Previous studies showed that dysfunction of finger dexterity in macaque monkeys caused by a lesion of lateral CST at the C4/C5 segment of the spinal cord recovered within 1-3 months after the lesion. It is important to reveal the compensatory mechanism in the corticospinal projection during the recovery from spinal cord injury (SCI). To clarify the neuroanatomical basis of functional compensation, we investigated the axonal distribution of CST in cervical spinal cord of CST lesioned monkeys. We performed a unilateral lesion of the CST at the mid-cervical spinal segment in 7 rhesus monkeys. An anterograde neural tracer, biotinylated dextran amine (BDA), was injected into the ipsilesional or contralesional hand and arm area of the primary motor cortex (M1) after the spinal cord injury. Possibility of axonal sprouting was examined by counting of labeled axons in the lesioned monkeys and comparison with those of 4 intact monkeys. In the ipsilesional dorsolateral funiculus (DLF), the number of labeled axons was increased at the segments rostral to the lesion as compare to those of intact monkeys. Caudal to the lesion, axonal projections and button-like swellings from ipsilesional M1 were found at ipsilesional lamina IX. Labeled axons and button-like swellings from contralesional primary motor cortex were also found at lamina IX, though increase of uncrossed axons from contralesional M1 which descend in the contralesional DLF was not observed. These results suggest that collaterals of corticospinal axons were increased rostral to the lesion and projections to lamina IX were newly formed caudal to the lesion after they cross the midline. Such reorganization of corticospinal projections might contribute to the functional recovery of the finger dexterity after SCI.