The Upper Motor Neuron (UMN) system serves as the command center for initiating and controlling voluntary movement. These neurons originate in the motor areas of the cerebral cortex and various nuclei within the brainstem. Their function is to translate thought and planning into a coordinated motor signal that descends through the central nervous system. UMNs do not directly connect to muscle fibers; instead, they operate as the first leg of a two-neuron relay system that delivers the brain’s instructions to the muscles.
The Primary Target: Lower Motor Neurons
The most direct target of the Upper Motor Neuron is the Lower Motor Neuron (LMN), which acts as the “final common pathway” for all motor commands. LMN cell bodies are located in the brainstem’s cranial nerve nuclei and the spinal cord’s ventral horn. They are the only neurons that physically connect the central nervous system to skeletal muscle, triggering contraction.
The UMN’s primary role is to synapse onto these LMNs, either directly or indirectly, to activate or inhibit them. UMNs targeting the body and limbs terminate on LMNs in the spinal cord’s ventral horn. For movements of the face, head, and neck, UMNs synapse with LMNs in the cranial nerve motor nuclei within the brainstem. The excitatory neurotransmitter glutamate typically transmits the chemical signal between the UMN and LMN.
A single LMN and the muscle fibers it innervates constitute a motor unit. This two-neuron chain is fundamental to voluntary movement, with the UMN providing the command and the LMN executing the action.
Modulating the Signal: Spinal Interneurons
While UMNs directly target LMNs, the majority of the UMN signal is relayed through spinal interneurons. These interneurons are local circuit cells within the spinal cord’s gray matter, refining and distributing the motor command. They integrate descending UMN input with local sensory information before the signal reaches the LMNs.
Interneurons facilitate coordination by processing and modifying the command from the brain. They mediate reciprocal inhibition, where the command to contract one muscle group is accompanied by an inhibitory signal to the opposing group. This prevents co-contraction, allowing for smooth movement.
UMNs exert both excitatory and inhibitory control over the LMN pool via these interneurons. This modulation ensures the final output to the muscle is precisely calibrated. This allows for the fine-tuning of motor output and the regulation of basic reflexes.
The Major Descending Pathways
UMN signals travel from the cerebral cortex and brainstem to their targets through descending motor tracts. The two most prominent are the Corticospinal Tract and the Corticobulbar Tract, which form the pyramidal system responsible for voluntary movement. These tracts define the anatomical route UMNs take to reach LMNs and interneurons.
Corticospinal Tract
The Corticospinal Tract controls the body and limbs, particularly fine, skilled movements of the hands and fingers. Its UMN axons descend through the brainstem and cross over (decussate) in the lower medulla oblongata. About 90% of fibers form the Lateral Corticospinal Tract on the opposite side of the spinal cord. This crossing means the motor cortex controls movement on the opposite side of the body.
Corticobulbar Tract
The Corticobulbar Tract is the pathway for the muscles of the head and face. These UMNs descend to the brainstem where they synapse on the LMNs of the cranial nerves, controlling functions like chewing, swallowing, and facial expression. Unlike the Corticospinal Tract, the Corticobulbar Tract often provides bilateral input to the LMNs for many cranial nerves.
Consequences of Damage to the UMN Circuit
Damage to the UMN circuit, often caused by stroke or spinal cord injury, results in a distinct set of symptoms because LMNs are deprived of modulatory input. Loss of UMN inhibition leads to an overactive LMN reflex arc. Symptoms include spasticity (increased muscle tone) and hyperreflexia (exaggerated deep tendon reflexes). Although muscles are weak due to lost voluntary control, they exhibit only mild atrophy because the LMNs remain intact.
Lower Motor Neuron Damage
Damage to the LMN itself produces a different clinical picture. Since the LMN is the final pathway to the muscle, its destruction results in flaccid paralysis, where the muscle becomes limp and unresponsive. This damage also causes severe muscle wasting (atrophy) and the absence of reflexes (areflexia). Distinguishing between UMN and LMN symptom patterns allows clinicians to precisely localize the site of neurological injury.