The nervous system directs voluntary movement through precise pathways of neurons that function as communication highways from the brain to the muscles. The primary route for conscious motor control is the corticospinal tract. This system is responsible for the fine, skilled movements required for tasks ranging from writing to playing a musical instrument.
The corticospinal tract is composed of millions of nerve fibers connecting the cerebral cortex to the spinal cord. Understanding its specific route is fundamental to comprehending how the brain orchestrates movement and what occurs when this system is disrupted.
Origin and Pathway of Upper Motor Neurons
Upper motor neurons (UMNs) are the first neurons in the command chain for voluntary movement, originating in the brain’s cerebral cortex. About 30% of these neurons arise from the primary motor cortex, another 30% from the premotor and supplementary motor areas, and the remaining 40% from regions like the somatosensory cortex. The largest of these UMNs are the giant pyramidal cells, known as Betz cells, located in the fifth layer of the primary motor cortex.
Once activated, their long projections, called axons, begin their descent toward the spinal cord. These axons first fan out into a structure known as the corona radiata before converging into a dense bundle called the internal capsule, a passageway deep within the brain.
From the internal capsule, the UMN axons continue into the brainstem. The tract passes through the midbrain as large bundles called the cerebral peduncles and continues downward through the pons. Throughout this course, the UMNs carry the blueprint for a specific movement toward the next neuron in the sequence.
The Medullary Pyramids as a Critical Junction
All upper motor neurons of the corticospinal tracts converge and pass through the medullary pyramids. These are two pyramid-shaped structures on the front side of the medulla oblongata, the lowest part of the brainstem, formed by the dense collection of descending corticospinal axons. This location serves as a bottleneck for motor command signals.
Within the lowest part of the medulla, a defining event occurs: the pyramidal decussation. Here, between 85% and 90% of the corticospinal fibers cross to the opposite side of the brainstem. This crossing is the anatomical reason the left hemisphere of the brain controls the right side of the body, and the right hemisphere controls the left.
The fibers that cross over form the lateral corticospinal tract, which travels down the spinal cord to control limb movements. The smaller portion of fibers, around 10-15%, that do not cross at the pyramids form the anterior corticospinal tract. These fibers are associated with control of the trunk and proximal muscles, and most will cross over at the spinal cord level before connecting with target neurons.
Synapsing with Lower Motor Neurons
After passing the medullary pyramids, upper motor neurons descend through the spinal cord’s white matter within their respective tracts. The axons travel with the lateral corticospinal tract being significantly larger than the anterior one. The final destination for these UMNs is the gray matter of the spinal cord, specifically a region known as the anterior horn.
In the anterior horn, the upper motor neuron forms a synapse, or connection, with a lower motor neuron (LMN). The LMN is the “final common pathway,” meaning it is the neuron that makes direct contact with the skeletal muscle fibers. The UMN delivers the motor command by releasing a neurotransmitter, glutamate, which excites the LMN.
Once activated, the lower motor neuron sends its own axon out of the spinal cord through a spinal nerve. This axon travels directly to a specific muscle. When the signal arrives at the neuromuscular junction, it triggers the muscle fibers to contract, producing the intended movement.
Clinical Signs of Upper Motor Neuron Lesions
Damage to upper motor neurons, from conditions like stroke, multiple sclerosis, or spinal cord injury, leads to a characteristic collection of symptoms. Because UMNs have an inhibitory influence on the reflex arcs of the spinal cord, their damage results in the loss of this regulation.
One of the primary signs is spastic paralysis or paresis, where muscles are weak yet exhibit increased muscle tone, making them stiff and resistant to passive movement. This is often accompanied by hyperreflexia, a condition where deep tendon reflexes, like the knee-jerk reflex, become exaggerated. Clonus may also appear, which involves a series of involuntary, rhythmic muscle contractions in response to stretching the muscle.
A classic diagnostic indicator of an upper motor neuron lesion is the Babinski sign. In a typical response, stroking the sole of the foot causes the toes to curl downward. When UMNs are damaged, this stimulus causes the big toe to extend upward while the other toes fan out. These signs stand in contrast to LMN lesions, which cause flaccid paralysis, muscle wasting (atrophy), and absent reflexes.