Neuronal migration is an essential process in the development of the nervous system. Neurons are born in one location and migrate sizable distances to their final location. In many other developmental processes, cells migrate as collectives, where the migration of one cell influences the migration of another cell; this process has yet to be shown in the developing central nervous system. Using the conserved tangential migration of facial branchiomotor neurons (FBMNs), I aim to determine the nature of the collective migration in the developing nervous system. Here, two models of FBMN collective migration are tested: the “Pioneer” model, where following FBMNs migrate intimately on the axon of the first neuron to migrate and the “Contact inhibition of locomotion (CIL)” model, where transient cell-cell contacts are the driving influence of the proper caudal migration of FBMNs. Using fixed tissue imaging, it was found that early born FBMNs do not contact the axon. In contrast, they are more likely to make soma-soma contact and display morphology typical of CIL. FBMNs that do contact the axon do not display an elongated morphology that is predicted of a cell using the leader axon as a substrate for migration. Further, wild-type FBMNs are able to rescue PCP-deficient FBMNs. Therefore, blastula-stage transplantation of PCP-deficient neurons into wild-type hosts allows us to live image the method of collective migration. CIL events were observed between PCP-deficient neurons and wild-type neurons, indicating that PCP is not required for CIL. In addition, PCP-deficient neurons making sustained contact with wildtype axons were not rescued, arguing against the Pioneer model. Taken together, these observations are more consistent with the “CIL” model of FBMN collective migration in which transient soma-soma interactions are required for the coordinated movement of neurons as they migrate in the developing nervous system.