Muscle Spasms in C5-C6 Spinal Cord Compression
Muscle spasms from spinal cord compression at C5-C6 result from two primary mechanisms: loss of spinal inhibitory control and increased motoneuron excitability, not from increased excitatory input. 1
Primary Pathophysiological Mechanisms
Loss of Inhibitory Control
Impaired synaptic inhibition is the dominant mechanism causing spasms after spinal cord injury. 1 Research demonstrates that inhibitory inputs to motoneurons become significantly impaired following chronic spinal cord injury, leading to uninhibited reflex activity below the level of compression. 1, 2
When synaptic inhibition is blocked pharmacologically in experimental models, even normal spinal cords become spastic, but injured cords generate substantially longer spasms, confirming that loss of inhibitory interneuron function is central to spasm generation. 1
The velocity-dependent tone and spasms characteristic of spinal cord injury manifest through uninhibited reflex activity of muscles below the injury level. 2
Increased Motoneuron Excitability
Motoneurons below the level of compression develop increased persistent inward currents, making them hyperexcitable. 1 This heightened excitability means that even normal sensory inputs can trigger prolonged muscle contractions and spasms.
Hyperexcitability of anterior horn cells develops following disturbance of spinal inhibitory interneurons, creating an abnormal network within the spinal cord that perpetuates spasm activity. 3
Excitatory Input Remains Unchanged
- Contrary to common assumptions, excitatory postsynaptic currents (EPSCs) in motoneurons show no difference in amplitude or conductance between injured and normal spinal cords. 1 This finding is critical because it explains why current pharmacological approaches targeting excitatory inputs often fail and may worsen motor function.
Secondary Contributing Factors
Reperfusion Injury
- In surgical decompression cases, transient spinal cord disturbance can occur from reperfusion after chronic compression is relieved. 4 This reperfusion phenomenon may trigger additional spinal cord dysfunction manifesting as muscle weakness or spasms in the immediate postoperative period.
Nerve Root Trauma
Abnormal afferent neuronal input from traumatized nerve roots at the compression site can trigger formation of secondary abnormal networks in the spine, perpetuating spasm activity. 3
Stenosis of the C4-C5 intervertebral foramen (adjacent to C5-C6 compression) represents a risk factor for developing postoperative complications including altered muscle tone. 5
Clinical Implications
The current standard approach of suppressing excitatory inputs with medications is misdirected because excitatory mechanisms remain unaltered after spinal cord injury. 1 This explains why many antispasmodic medications provide limited benefit and may cause additional motor weakness.
More effective therapeutic targets include:
- Restoring synaptic inhibition (e.g., baclofen, which enhances GABA-mediated inhibition) 1, 3
- Modulating motoneuron excitability directly 1
- Addressing abnormal afferent input through nerve blocks when conservative measures fail 3
Common Pitfalls
Avoid relying solely on medications that suppress excitatory transmission, as this approach targets an unchanged mechanism and risks further compromising motor recovery. 1
Recognize that spasms may develop or worsen immediately after surgical decompression due to reperfusion injury, not necessarily indicating inadequate decompression. 4
Multiple cervical segments are often involved beyond the primary compression level, so spasms may affect muscle groups beyond those directly innervated by C5-C6. 4