Dexterous finger movements in primate without monosynaptic corticomotoneuronal excitation.

Abstract

It is generally accepted that the precision grip and independent finger movements (IFMs) in monkey and man are controlled by the direct (monosynaptic) corticomotoneuronal (CM) pathway. This view is based on previous observations that pyramidotomy causes near permanent deficits of IFMs. However, in addition to the direct CM pathway, pyramidotomy interrupts several corticofugal connections to the brain stem and upper cervical segments. Indirect (oligosynaptic) CM pathways, which are phylogenetically older, have been considered to be of little or no importance in prehension. In three adult macaque monkeys, complete transection of the direct CM pathway was made in C4/C5, which is rostral to the forelimb segments (C6-Th1). Electrophysiological recordings revealed lack of the direct lateral corticospinal tract (LCST) volley, monosynaptic extracellular field potentials in the motor nuclei, and monosynaptic CM excitation. However, a disynaptic volley, disynaptic field potentials and disynaptic CM excitation mediated via C3-C4 propriospinal neurons remained after the lesion. Thus the lesion interrupted the monosynaptic CM pathway and oligosynaptic LCST pathways mediated by interneurons in the forelimb segments. Precision grip and IFMs were observed already after 1-28 days postoperatively. Weakness in force and deficits in preshaping remained for an observation period of 3 mo. Indirect CM pathways may be important for neuro-rehabilitation.