Trauma Medulla Spinalis

01Pathophysiology

Spinal cord trauma involves two phases of injury that you must understand separately, because exam questions will test your ability to distinguish between them and to recognize which interventions target which phase.

Primary injury is the immediate mechanical damage at the moment of impact. This includes compression, contusion, laceration, or transection of the cord. The cord may be damaged by displaced bone fragments, herniated disc material, or ligamentous disruption leading to subluxation. The mechanism matters: hyperflexion injuries are most common (as in head-on collisions), hyperextension injuries are classic in elderly patients with pre-existing cervical spondylosis who fall forward, and axial loading (vertical compression) causes burst fractures, classically seen in diving accidents.

Secondary injury begins within minutes and evolves over hours to days. This cascade includes vasospasm, ischemia, release of excitotoxic glutamate, calcium influx, free radical generation, inflammatory cell infiltration, and progressive edema. The cord swells within the rigid spinal canal, which further compromises perfusion and extends the zone of injury. This is why maintaining adequate spinal cord perfusion pressure is a cornerstone of acute management: the secondary injury is the modifiable target.

The reason a patient presents with flaccid paralysis and areflexia acutely (rather than spasticity) is because of spinal shock, a transient suppression of all reflex activity below the level of injury. This is not the same as neurogenic shock, a concept that exam questions love to confuse. Spinal shock is a neurological phenomenon (loss of reflexes), while neurogenic shock is a cardiovascular phenomenon (loss of sympathetic tone causing vasodilation, hypotension, and bradycardia). Neurogenic shock occurs in injuries at T6 or above, because the sympathetic outflow from T1 to L2 is disrupted while vagal (parasympathetic) tone is unopposed.

The resolution of spinal shock is marked by the return of the bulbocavernosus reflex. Only after this reflex returns can you determine whether the injury is truly complete or incomplete. This is a heavily tested concept.

02Classification and Clinical Manifestation

ASIA Impairment Scale

Incomplete Cord Syndromes

This table is one of the highest-yield topics in this subject. You must be able to identify each syndrome from a clinical vignette.

Neurogenic Shock vs. Spinal Shock

03Diagnostic Workup

When a trauma patient arrives with suspected spinal injury, CT is the first-line imaging study. Plain radiographs are no longer recommended as the primary screen in most modern guidelines because of their poor sensitivity for detecting fractures, particularly at the craniocervical and cervicothoracic junctions. If the patient has a neurological deficit, is obtunded, or has a concerning mechanism, go straight to CT.

MRI is not the initial test but is essential when there is a neurological deficit. MRI answers the question: "Is there something compressing the cord that needs surgical decompression?" It identifies cord edema (which appears as T2 hyperintensity), cord hemorrhage (which carries a worse prognosis), epidural hematoma, and ligamentous disruption. MRI should be obtained urgently when the clinical picture suggests cord compression that may benefit from surgery.

For clearance of the cervical spine in alert, sober, neurologically intact patients, the NEXUS criteria and the Canadian C-Spine Rule are used to determine whether imaging is needed at all. The NEXUS criteria state that the cervical spine can be cleared clinically (no imaging needed) if all five conditions are met: no midline tenderness, no focal neurological deficit, normal alertness, no intoxication, and no painful distracting injury. Exam questions frequently present a patient who meets all NEXUS criteria, and the correct answer is clinical clearance without imaging.

04Management and Treatment

Acute stabilization follows standard trauma principles: airway, breathing, circulation. The critical trap is recognizing that neurogenic shock is a distributive shock, not hypovolemic shock. In a trauma patient who is hypotensive with bradycardia and warm extremities, the reflex is to give fluids. Fluids alone will not correct neurogenic shock because the problem is loss of vascular tone and cardiac sympathetic drive, not volume depletion. Vasopressors (norepinephrine is first-line) are required. However, you must always rule out hemorrhagic shock first in a trauma patient, because the two can coexist.

The MAP target of 85 to 90 mmHg for 5 to 7 days is based on the principle that the injured cord is vulnerable to ischemia from secondary injury, and augmenting perfusion pressure may limit the extent of damage. This is a guideline-supported recommendation (AO Spine, AANS).

Methylprednisolone deserves a special note because it is a classic exam topic. The NASCIS II and III trials originally suggested a benefit when high-dose methylprednisolone was started within 8 hours of injury (30 mg/kg bolus followed by 5.4 mg/kg/hr for 23 to 48 hours). However, subsequent analysis and guideline panels have concluded that the evidence is weak and the risks (infection, pneumonia, sepsis, GI hemorrhage, hyperglycemia) outweigh any potential benefit. Current guidelines from the AANS/CNS recommend against its routine use. If an exam question asks for the standard of care, the answer is not methylprednisolone. If the question asks about a historical protocol or what was previously recommended, then know the dosing regimen.

Autonomic dysreflexia is a late complication tested frequently. It occurs in patients with injuries at T6 or above, typically weeks to months after injury. A noxious stimulus below the level of injury (most commonly a distended bladder from a blocked catheter, but also fecal impaction, pressure ulcers, or tight clothing) triggers a sympathetic surge that cannot be modulated because descending inhibitory signals are blocked at the injury level. This produces severe, paroxysmal hypertension with reflex bradycardia, pounding headache, diaphoresis and flushing above the level, and pallor below the level. The first step in management is to sit the patient upright (to lower BP via orthostasis) and identify and remove the offending stimulus (straight catheterize the bladder, disimpact the rectum). If hypertension persists, use a fast-acting antihypertensive such as nifedipine or nitropaste.

05Differential Diagnosis and Distractors

06Traps and High-Yield Pearls

The most common way students lose points on spinal cord trauma questions is by confusing neurogenic shock with hypovolemic shock. The trauma setting creates a strong bias toward thinking "bleeding," but the vignette will describe hypotension with bradycardia and warm skin, which is the opposite hemodynamic profile of hemorrhage. The correct next step is vasopressors, not just fluids, though you must always exclude hemorrhage first. If the question stem gives you a normal FAST exam and no evidence of blood loss, neurogenic shock is the answer.

A second common trap involves the incomplete cord syndromes. Vignettes will describe a pattern of motor and sensory loss, and the student must match it to the correct syndrome. The discriminating detail is usually which modalities are preserved: if proprioception and vibration are intact but motor function and pain/temperature are lost, that is anterior cord syndrome. If the arms are weaker than the legs in an elderly patient after a fall, that is central cord syndrome. If there is ipsilateral motor loss with contralateral pain/temperature loss, that is Brown-Sequard.

A third trap is declaring a complete cord injury too early. During spinal shock, a patient may appear to have a complete injury (ASIA A), but once the bulbocavernosus reflex returns and spinal shock resolves, some function may be recovered, reclassifying the injury as incomplete. Exam questions test whether you know that completeness of injury can only be determined after spinal shock resolves.

Finally, students forget that methylprednisolone is no longer the standard of care. An older question bank may present it as the correct answer, but current guidelines do not recommend it. If the question uses language like "most appropriate next step" or "current guideline-recommended therapy," steroids are not the answer. The correct acute intervention is hemodynamic optimization and surgical decompression if indicated.

The core competency being tested across all spinal cord trauma questions is your ability to localize the lesion anatomically based on the deficit pattern, distinguish between shock types in a trauma setting, and sequence the workup and management correctly.