The phrase “spinal cord seizure” describes severe, involuntary muscle movements originating in the spinal cord. True epileptic seizures, however, are defined by abnormal electrical activity starting in the brain. These spinal events are more accurately characterized as severe muscle spasms or spasticity resulting from excessive nerve activity below the neck. They are a manifestation of spinal cord hyperexcitability, often following a neurological injury or disease.
The Mechanism of Spinal Hyperexcitability
The spinal cord maintains a balance between signals that excite muscles and signals that inhibit them. This equilibrium relies heavily on inhibitory neurotransmitters, primarily Gamma-aminobutyric acid (GABA) and Glycine. These chemicals dampen motor neuron activity, ensuring muscles only contract when intended.
When the spinal cord is damaged or inflamed, this system is disrupted, resulting in a loss of inhibitory control. Damaged areas below the injury site may reduce the effectiveness of GABAergic and glycinergic signals. This lack of inhibition allows excitatory signals to dominate the local spinal circuits.
This imbalance causes motor neurons to become hypersensitive and fire spontaneously or excessively. The resulting involuntary muscle contractions occur without input from the brain’s motor cortex, distinguishing them from voluntary movement.
Observable Signs and Physical Symptoms
The physical manifestations of spinal hyperexcitability are categorized into three types of involuntary muscle activity.
Tonic Spasms
A tonic spasm involves sustained, rigid muscle contractions lasting from seconds to minutes. These spasms result in stiffness, causing the limbs or trunk to lock into a fixed posture.
Clonic Spasms
A clonic spasm presents as rhythmic, alternating contractions and relaxations of muscle groups. This results in a repetitive jerking or shaking movement of the affected limbs. Both tonic and clonic spasms frequently involve the trunk and lower limbs, making sitting or walking difficult.
Myoclonus
Myoclonus is characterized by sudden, brief, shock-like jerks of a muscle or group of muscles. These movements are rapid, often occurring irregularly and feeling like an electric jolt. Spinal events are typically stimulus-sensitive, meaning they can be triggered by minor external factors like a light touch, a sudden noise, or an emotional surge.
Common Conditions Leading to Spinal Spasms
These spinal events are typically a secondary symptom arising from an underlying neurological disorder or injury.
Spinal Cord Injury (SCI)
SCI is a frequent cause, as trauma severs the descending inhibitory pathways from the brain. The spinal segments below the level of the injury become functionally isolated, leading to chronic hyperexcitability and spasticity.
Multiple Sclerosis (MS) and Transverse Myelitis
MS can cause these symptoms due to inflammatory damage to the myelin sheath insulating nerve fibers. Lesions in the spinal cord disrupt signal transmission, contributing to a state of disinhibition. Transverse Myelitis, which involves inflammation across the width of the spinal cord, is another cause, leading to demyelination and subsequent muscle stiffness and spasms.
Stiff-Person Syndrome (SPS)
Specific autoimmune disorders, such as SPS, offer a direct example of spinal hyperexcitability. In SPS, the body produces antibodies that target components of the GABAergic inhibitory system, notably the GAD enzyme. This autoimmune attack severely compromises inhibitory signals, leading to profound muscle rigidity and stimulus-induced spasms.
Identifying and Treating Spinal Events
Healthcare professionals rely on a clinical examination to distinguish these spinal events from other movement disorders. Diagnosis often requires neurophysiological testing to pinpoint the origin of the abnormal muscle activity.
Diagnosis
Electromyography (EMG) is used to record electrical activity in affected muscles, confirming that spontaneous firing originates from spinal motor neurons. An Electroencephalogram (EEG) may be performed concurrently to definitively rule out a cortical seizure by monitoring electrical patterns in the brain. If an autoimmune cause is suspected, specialized blood tests can detect antibodies, such as the anti-GAD65 antibodies associated with Stiff-Person Syndrome. Imaging scans like MRI are also used to visualize structural damage, lesions, or inflammation in the spinal cord.
Treatment
Management focuses on reducing the hyperexcitability of spinal cord circuits to improve function and comfort. Pharmacological interventions often include muscle relaxants, such as Baclofen, which acts as a GABA-mimetic to enhance inhibitory signaling. Benzodiazepines may also be prescribed, as they increase the effect of GABA to further dampen nerve activity. Certain antiepileptic medications can help stabilize nerve membranes and reduce the pathological firing of motor neurons. Physical therapy is an important component of the overall management strategy, focusing on stretching and strengthening exercises. This helps maintain joint mobility and prevent muscles from shortening due to chronic stiffness. Therapy also aids in identifying and avoiding specific sensory triggers.