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Older men. Although older adults are more likely to experience falls, their injuries typically result in fractures or degenerative conditions rather than acute traumatic SCIs. Their lower participation in high-risk behaviors reduces their overall risk compared to young men. Therefore, they are not the primary target for SCI prevention education.

Teenage girls. Teenage girls have a significantly lower incidence of SCIs compared to males of the same age group. While they may experience injuries from sports or accidents, the overall frequency is much less. Thus, prevention programs targeting them would have a limited impact on reducing the total burden of SCIs.

Elementary school–age children. Children in this age group are vulnerable to injuries such as bicycle or playground accidents, but these rarely result in SCIs compared to adolescent trauma. Their risk is considerably lower than that of young adult men. For this reason, they are not the priority group for SCI prevention efforts.

Paraplegia with a flaccid paralysis. Paraplegia indicates lower limb involvement only, which would occur in thoracic or lumbar injuries, not a cervical injury at C7. While flaccidity is seen in spinal shock, the distribution here is incomplete for the described injury. Therefore, this option does not accurately reflect the clinical picture.

Total hemiplegia with sensory and motor loss. Hemiplegia affects only one side of the body and is more typical of conditions like stroke rather than SCI. A C7 lesion produces bilateral deficits, not unilateral weakness. This makes hemiplegia inconsistent with spinal shock presentation.

Spastic tetraplegia with loss of pressure sensation. Spasticity occurs after spinal shock resolves as reflex activity returns, not during the acute phase. Early spinal shock is marked by flaccidity, not spasticity. Thus, this option describes a later stage, not the initial findings of spinal shock.

Anterior cord syndrome. This syndrome results from damage to the anterior spinal artery or anterior cord structures, leading to loss of motor function, pain, and temperature sensation below the level of injury. However, it typically spares posterior column functions such as position sense and vibration. It does not present with the disproportionate upper extremity weakness seen in central cord syndrome.

Posterior cord syndrome. This is a rare condition that causes loss of proprioception, vibration, and fine touch while preserving motor function and pain/temperature sensation. Patients may have difficulty with balance and coordination, but motor weakness is not a primary feature. Thus, it does not match the clinical description of greater upper extremity weakness.

Cauda equina and conus medullaris syndromes. These syndromes involve damage to the lumbosacral nerve roots or the distal spinal cord, causing flaccid paralysis, sensory loss in a saddle distribution, and bowel/bladder dysfunction. Because they affect the lower body, they cannot explain weakness that is more severe in the upper extremities.

Damage to the most distal cord and nerve roots, resulting in flaccid paralysis of the lower limbs and areflexic bowel and bladder. This describes cauda equina syndrome, which involves injury to the lumbosacral nerve roots, not hemisection of the spinal cord. Unlike Brown-Séquard syndrome, it produces flaccid paralysis, saddle anesthesia, and severe bladder/bowel dysfunction.

Rare cord damage resulting in loss of proprioception below the lesion level with retention of motor control and temperature and pain sensation. This describes posterior cord syndrome, which affects the dorsal columns. While proprioception is impaired, motor strength and pain/temperature sensation are preserved, making it inconsistent with Brown-Séquard syndrome.

Often caused by flexion injury with acute compression of cord resulting in complete motor paralysis and loss of pain and temperature sensation below the level of injury. This describes anterior cord syndrome, caused by flexion or vascular compromise of the anterior spinal artery. It produces complete motor loss and loss of pain/temperature sensation but spares proprioception, differing from the pattern seen in Brown-Séquard syndrome.

Edematous compression of the cord above the level of the injury. While edema can worsen neurological deficits, it usually occurs at the site of injury rather than strictly above it. It contributes to secondary injury but does not fully explain the conversion to complete damage.

Continued trauma to the cord resulting from damage to stabilizing ligaments. Ligament damage may cause instability and additional trauma, but this is more related to mechanical factors. The critical progression to complete injury stems from pathophysiologic secondary changes, not repeated trauma alone.

Mechanical transection of the cord by sharp vertebral bone fragments after the initial injury. This represents a primary injury mechanism leading to immediate complete cord damage. It does not describe the process by which an initially incomplete injury worsens to complete.