The pyramidal fibers originating in the motor cortex and extending down the spinal cord where they synapse on alpha motoneurons. They connect to the extrafusal muscles of the hand and fingers with just one synapse, and thus are referred to as being ‘monosynaptic’. In the newborn macaque monkey, fibers of this tract have reached all levels of the spinal cord white matter (a process already underway by mid-gestation), but their penetration into gray matter by means of axonal growth cones is by no means complete. Their maturation is complete by two years of age, at least according to myelination and sprouting of terminal axonal collaterals that make multiple synaptic contacts on both motoneurons and interneurons. In the subsequent five months, projections to the intermediate zone show marked increases, and approximately at the same time dexterous finger movements become evident. Thus, this corticospinal system is thought to be a prerequisite for the ability to move the fingers independently of each other as required, for example, with a pincer grasp. As for the human, based on transcranial magnetic stimulation, controversy exists as to when in postnatal development these tracts become functional, with some arguing that there is evidence already in the newborn period (but certainly not functional in sense of, for example, a one year-old infant). The index of dexterity, a measure of independent finger movement, is 2 in the cat (indicating of very restricted capacity for such movements), 5 for the squirrel monkey (but it has no pincer grasp or the ability for within-hand manipulations), 6 for the macaque and 7 in humans. Finally, an intriguing point about the tracts is that they are almost entirely inhibitory. How can this be if they are the most important central pathway influencing voluntary movement? – a question once asked by the eminent neurophysiologist John C. Eccles (1903-1997). The answer is that the tracts reciprocally inhibit muscles in a selective manner that are antagonistic to those being voluntary contracted (i.e., the agonist muscles). When they fail to do so, the result is co-contractions or loss of reciprocal relaxation of antagonist muscles (and thus of voluntary motor control), and ultimately spasticity.
See Agonist muscle, Alpha (α) motoneuron, Antagonist muscle, Corticospinal tracts (CST), Extrafusal muscle fibers, Extrapyramidal system, Gray matter, Interneurons, Motor cortex, Motoneurons, Motor cortex, Myelination, Palmar grasp, Pincer grasp (or grip), Primary motor cortex, Spasticity, Spinal cord, Synapse, Transcranial magnetic stimulation (TMS), White matter