Cervical myelopathy is a neurological condition resulting from compression of the spinal cord within the neck, or cervical spine. This pressure is often caused by age-related changes like bone spurs or disc herniation that narrow the spinal canal. Although the injury site is in the neck, the most debilitating symptoms frequently appear in the legs and lower body. Understanding how the spinal cord functions as a comprehensive information pathway explains this connection.
The Spinal Cord Pathway
The spinal cord communicates between the brain and the body, carrying motor commands down and sensory information back up. Signals controlling leg movement start in the brain and descend through the spine via specific nerve bundles known as the corticospinal tracts. These tracts carry the brain’s instructions for voluntary movement.
These tracts pass directly through the narrow cervical spine before reaching the lower segments that innervate the legs. Since the cervical spine is the uppermost gateway for all descending motor signals, pressure at this level threatens the function of nerves controlling the body below. The nerve fibers responsible for leg movement are positioned centrally within the spinal cord’s white matter when passing through the neck. This central location makes these fibers highly susceptible to damage when the spinal canal is squeezed.
How Compression Interrupts Signals
Spinal canal narrowing causes damage through two primary mechanisms: mechanical force and reduced blood flow. Static pressure from degenerative changes like thickened ligaments or bone spurs, combined with the dynamic stress of neck movement, exerts direct strain on the nerve fibers. This mechanical stress can physically damage the protective insulating layer around the nerve axons, a process called demyelination. Demyelination slows or halts the transmission of signals.
Ischemia is the second mechanism, where sustained pressure restricts the small blood vessels supplying the cord tissue. This loss of adequate blood flow starves the nerve cells of oxygen and nutrients, leading to cellular dysfunction and eventual death. Oligodendrocytes, the cells responsible for maintaining the myelin sheath, are vulnerable to this oxygen deprivation. This interruption prevents the brain’s motor commands from traveling clearly, resulting in unreliable and uncoordinated communication with the leg muscles.
Specific Lower Body Symptoms
The disruption of the descending motor tracts results in Upper Motor Neuron (UMN) symptoms, which are most noticeable in the lower body. The earliest symptom is a change in walking, referred to as a myelopathic gait. Individuals often describe their legs as feeling heavy or dragging, leading to an unsteady, clumsy, or broad-based walking pattern.
Signal interruption also causes muscle stiffness (spasticity) and increased reflexes (hyperreflexia) in the legs, which are hallmarks of UMN damage. The sensory tracts responsible for proprioception—the body’s sense of where its limbs are in space—are also affected by the compression. This sensory loss contributes to poor balance and coordination, making it difficult to walk heel-to-toe or navigate uneven surfaces.