Spinal cord injury is usually associated with major force, such as occurs with significant trauma. The most common causes of traumatic paraplegia are motor vehicle accidents and sports-related injuries, although gunshot injuries are increasingly more common. Trauma can result in contusion, acute edema, compression secondary to epidural hematoma, or actual transection.

Initial examination shows weak, flaccid muscles, absent reflexes, and sensory loss below the level of the lesion (spinal shock). Bowel and bladder dysfunction is typical. Autonomic disturbance (e.g., sweating, piloerection) is usually found below the level of the lesion. Over a period of weeks to months, flaccidity evolves into spasticity, hyperreflexia, and extensor plantar responses.

The neck must be stabilized in a cervical collar until the stability of the cervical spine is established. Magnetic resonance imaging (MRI) should be done to differentiate contusion or transection from epidural hematoma. Plain radiographs or computed tomography (CT) of the spine may also be helpful to evaluate for vertebral fractures and dislocations.

Spinal cord infarction is usually the result of occlusion of the anterior spinal artery, which supplies blood to the ventral two-thirds of the cord. The most common causes in children are dissection secondary to trauma, infection, emboli in patients with cardiac disease, or thrombosis in patients with hypercoagulable states.

Patients with spinal cord infarction present with flaccid motor paralysis, are-flexia, and dissociated sensory loss (loss of pain and temperature sensation with sparing of vibration and position sense) below the level of arterial occlusion.
Bowel and bladder dysfunction are usual. Back pain is sometimes present. Over weeks to months, flaccidity evolves into spasticity, with hyperreflexia, clonus, and extensor plantar responses.

An MRI of the spine should be performed to look for evidence of cord infarction. A spinal arteriogram should also be considered. Evaluations for cardiac disease and hypercoagulable states should be performed if there is no obvious cause for the occlusion.

Transverse myelitis is an acute inflammatory, demyelinating disorder of the cord. It can occur as a complication of systemic viral infections (infectious mononucleosis [Epstein–Barr virus], varicella, mumps, rabies, rubella, rubeola, influenza, HIV) or bacterial infections (cat-scratch disease, Mycoplasma pneumoniae), autoimmune disorders (lupus), immunizations (rare), and multiple sclerosis.

The mean age of onset is 9 years. The patient presents with thoracic back pain, lower extremity numbness, leg weakness (symmetric or asymmetric), and progressive urinary retention or incontinence. Initial findings include weak, flaccid muscles (symmetric or asymmetric); absent reflexes; and sensory loss below the level of the lesion. Optic disc swelling and decreased vision or vision loss are often present in patients with Devic disease (i.e., transverse myelitis accompanied by optic neuritis), although the ocular symptoms may occur after the onset of spinal symptoms. Spasticity, hyperreflexia, clonus, and extensor plantar responses are seen later in the course of the disease.

A lumbar puncture (LP) should be performed to check for cerebrospinal fluid (CSF) opening pressure (normal to slightly elevated), protein level (usually increased) and electrophoresis (looking for oligoclonal bands), and cell count (usually a mixed pleocytosis of <200 cells/mm³). Spinal MRI often shows swelling and abnormal signal at the level of the lesion. Head MRI should also be performed to look for other areas of demyelination suggestive of MS. Viral serologies (including HIV) may be helpful in identifying a triggering viral infection. Antinuclear antibody panel and complement levels should be considered as a screen for an autoimmune disorder.

Viral myelitis is the acute segmental infection of anterior horn cells. Viruses most commonly responsible include poliovirus, group B coxsackievirus, and echoviruses.

The patient usually has a history of malaise, myalgias, low-grade fever, and upper respiratory tract symptoms progressing to severe headache and nuchal rigidity. Areflexia and flaccidity and weakness of the muscles (usually asymmetric) are often heralded by pain in the spine and affected limbs. Bulbar weakness may also be present. There are usually no sensory symptoms.