Nervous system: Organization of motor neurons

The organization of upper motor neurons (UMNs), lower motor neurons (LMNs), and sensory neurons creates a feedback system that modulates the strength of muscle contraction, maintains passive muscle tone, and mitigates stretch and spinal reflexes. UMNs are motor neurons that have cell bodies in the precentral gyrus of the brain and project their axons from the brain to synapses on lower motor neurons (LMNs) in the ventral horn of the spinal cord. LMNs are motor neurons that project from their respective spinal segments onto muscles at neuromuscular junctions to promote muscle contraction. LMNs in the ventral horn also receive input from spinal interneurons, as well as sensory input from type Ia sensory axons. This organization is summarized in Figure 1.

Figure 1 Hierarchical organization of somatic motor systems

During a reflex contraction, such as a knee-jerk or patellar reflex, specialized cells called muscle spindles sense increased tension in a muscle or tendon; when stretched, they trigger type Ia sensory axons to fire action potentials, which then excite alpha motor neurons in the ventral horn, causing the muscle to contract. This contraction is modulated by UMNs, which can send inhibitory signals to suppress or dampen the activity of spinal reflex arcs, or excitatory signals that can enhance the responsiveness of reflex movements when appropriate, allowing for coordinated motor responses.

Conversely, when a muscle becomes increasingly relaxed, slackened muscle spindles cease firing. A special type of LMN, called a gamma motor neuron, responds to this decreased firing and causes the muscle spindle to contract. This is known as a gamma loop and maintains passive muscle tone.

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease caused by progressive degeneration of both UMNs and LMNs. It can be distinguished from other neurological disorders that only involve UMNs or LMNs by its unique set of symptoms. Specifically, symptoms of muscle atrophy, weakness, either increased or decreased muscle tone, and concurrent symptoms of spasticity and exaggerated deep tendon reflexes, are hallmarks of the disease.