Spasms, or spasticity, are a common, involuntary consequence of a spinal cord injury (SCI), characterized by sudden, uncontrolled muscle contractions and increased muscle tone below the level of the injury. While these muscle movements are frequent for many individuals with SCI, the exact neurological mechanics that drive them are complex. This article explains the underlying physiological changes that transform normal muscle reflexes into uncontrollable spasms.
How Spinal Cord Damage Changes Nerve Signaling
The fundamental cause of spasms begins with physical damage to the spinal cord, which severs the two-way communication between the brain and the body below the injury site. The central nervous system normally relies on the brain to send continuous “descending inhibitory signals” down the spinal cord to regulate muscle activity and tone. These regulatory signals travel via tracts like the corticospinal pathway.
A spinal cord injury creates a structural block that prevents these inhibitory messages from reaching the motor neurons that command muscles to contract. This damage is classified as an upper motor neuron lesion. Without the constant, modulating influence of the brain, the spinal circuits below the lesion become functionally isolated. This loss of supraspinal modulation over muscle reflexes sets the stage for hyperactivity.
The Phenomenon of Hyperexcitability
When the descending inhibitory signals are lost, the local reflex circuits within the spinal cord below the injury become hypersensitive, a state known as hyperexcitability. The basic reflex arc is no longer dampened by the brain’s regulatory control. This loss of inhibition means that a minor sensory stimulus can trigger a massive, uncontrolled motor response.
At the cellular level, this hyperexcitability is driven by significant changes within the alpha motor neurons themselves. These motor neurons develop an enhanced intrinsic excitability, largely due to the emergence of persistent inward currents (PICs). These currents, often mediated by voltage-gated L-type calcium channels, allow the motor neurons to generate prolonged, self-sustained firing after only a brief input. The presence of PICs means that a motor neuron can remain active and command a muscle contraction for an extended period, which is the physical manifestation of a sustained spasm.
The inhibitory pathways within the spinal cord itself also become impaired. Synaptic inhibition, which normally functions to suppress reflex activity, is significantly reduced. For example, the function of interneurons that typically inhibit the motor neurons, such as the Renshaw cells, is diminished. This maladaptive neuronal plasticity contributes to hyperactive reflexes, as the motor neurons are no longer held in check by local inhibitory circuits.
This neurological reorganization leads to a lower threshold for activation of the reflex arc. The spinal cord circuits below the injury become hyper-reflexive, meaning they are easily triggered and produce an exaggerated response. The combination of lost descending control and increased intrinsic excitability creates a hair-trigger system that translates small sensory inputs into large, involuntary muscle spasms.
External and Internal Spasm Triggers
While hyperexcitability provides the mechanism for spasms, a specific stimulus is usually required to initiate the event. These triggers send a sensory signal into the hyperactive spinal reflex arc, causing the explosive motor response. Triggers are broadly categorized as external, involving contact or environmental factors, or internal, relating to bodily changes or discomfort.
External triggers typically involve direct stimulation of the skin or muscle. These include sudden movements, passive stretching of the limb, or changes in temperature, such as exposure to a cold environment. Even light touch, tight clothing, or minor irritations like an ingrown toenail can generate enough sensory input to set off the uncontrolled muscle contraction.
Internal triggers signal a physiological problem or distress within the body below the level of injury. Common examples include a full bladder or bowel, which causes visceral stretching that generates a strong sensory signal. Other internal triggers are a urinary tract infection, a skin breakdown or pressure sore, or undiagnosed pain like a fracture. These internal signals flood the hyper-reflexive spinal cord circuits, leading to a massive, uncontrolled motor output that manifests as a spasm.