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Summary Table

Category	Details
Risk Factors	Young males (motor vehicle collisions, sports injuries, diving), elderly (falls, cervical spondylosis narrowing the canal), penetrating trauma, osteoporosis, ankylosing spondylitis, rheumatoid arthritis with atlantoaxial instability
Etiology	Mechanical disruption of the spinal cord via fracture, dislocation, or ligamentous injury causing compression, contusion, or transection; secondary injury from edema, ischemia, and inflammatory cascades
Patient Presentation	Loss of motor and/or sensory function below the level of injury; urinary retention; hypotension with bradycardia (neurogenic shock); respiratory failure if cervical level
Classic Physical Exam	Flaccid paralysis and areflexia acutely (spinal shock); sensory level on exam; priapism; loss of rectal tone and bulbocavernosus reflex; paradoxical (diaphragmatic) breathing in high cervical injuries
Key Diagnostic Results	CT of the spine is the best initial imaging; MRI for cord compression, ligamentous injury, and edema; plain films have limited sensitivity; ASIA Impairment Scale for classification
Management	Immobilization, airway protection, hemodynamic support with MAP goal of 85 to 90 mmHg for 5 to 7 days, urgent surgical decompression if structural compression is present, DVT prophylaxis, bladder catheterization
Keywords	"Sensory level," "flaccid paralysis after trauma," "loss of rectal tone," "hypotension with bradycardia," "priapism," "diaphragmatic breathing," "bulbocavernosus reflex"

1. Pathophysiology

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.

2. Classification and Clinical Manifestation

ASIA Impairment Scale

Grade	Description
A (Complete)	No motor or sensory function preserved in the sacral segments S4-S5
B (Sensory Incomplete)	Sensory but no motor function preserved below the level, including S4-S5
C (Motor Incomplete)	Motor function preserved below the level; more than half of key muscles have a grade less than 3
D (Motor Incomplete)	Motor function preserved below the level; at least half of key muscles have a grade of 3 or more
E (Normal)	Motor and sensory function are normal

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.

Syndrome	Mechanism	Motor Deficit	Sensory Deficit	Key Distinguishing Feature
Central Cord Syndrome	Hyperextension in elderly with cervical spondylosis	Upper extremities worse than lower ("cape-like" distribution)	Variable; pain and temperature may be affected in upper limbs	Arms weaker than legs; elderly patient who falls; best prognosis among incomplete syndromes
Brown-Sequard Syndrome	Hemisection of cord (penetrating trauma, e.g., stab wound)	Ipsilateral motor loss (corticospinal tract)	Ipsilateral loss of proprioception/vibration (dorsal columns); contralateral loss of pain/temperature (spinothalamic tract)	Dissociated sensory loss with ipsilateral motor paralysis; best overall prognosis for functional recovery
Anterior Cord Syndrome	Flexion injury or anterior spinal artery occlusion	Bilateral motor paralysis below the level	Bilateral loss of pain and temperature (spinothalamic tracts)	Preserved proprioception and vibration (dorsal columns intact); worst prognosis among incomplete syndromes
Posterior Cord Syndrome	Rare; hyperextension	Motor function preserved	Loss of proprioception and vibration bilaterally	Pain and temperature preserved; motor function intact; very rare and low yield
Cauda Equina Syndrome	Injury below L1-L2 (not true cord injury; affects nerve roots)	Lower motor neuron pattern: flaccid paralysis, areflexia	Saddle anesthesia (perineal area)	Bowel/bladder dysfunction (urinary retention, fecal incontinence); asymmetric leg findings; this is a surgical emergency
Conus Medullaris Syndrome	Injury at L1-L2 (the terminal cord)	Mixed upper and lower motor neuron signs	Perianal sensory loss, symmetric	Early and prominent bowel/bladder dysfunction; symmetric findings; compared with cauda equina, onset is more sudden and symmetric

Neurogenic Shock vs. Spinal Shock

Feature	Neurogenic Shock	Spinal Shock
Nature	Cardiovascular (distributive shock)	Neurological phenomenon
Mechanism	Loss of sympathetic tone	Transient suppression of spinal reflexes
Findings	Hypotension + bradycardia + warm, dry skin	Flaccid paralysis, areflexia, absent rectal tone
Level	Injuries at T6 or above	Any level
Resolution marker	Hemodynamic stabilization with fluids and vasopressors	Return of bulbocavernosus reflex

3. Diagnostic Workup

Test	Role	Key Findings
CT of the spine (non-contrast)	Best initial imaging test for bony injury	Fractures, dislocations, bone fragments in the canal, burst fractures
MRI of the spine	Most accurate test for cord and soft tissue evaluation	Cord edema, hemorrhage, contusion, disc herniation, ligamentous injury, epidural hematoma
Plain radiographs (X-ray)	Limited role; may be used where CT is unavailable	Alignment abnormalities, obvious fractures; misses up to 50% of injuries
CT angiography (vertebral arteries)	If cervical fracture involves the transverse foramen	Vertebral artery dissection or occlusion
ASIA motor and sensory exam	Clinical classification	Determines level and completeness of injury after spinal shock resolves

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.

4. Management and Treatment

Phase	Intervention	Details
Prehospital	Spinal immobilization	Rigid cervical collar, spine board, log-roll precautions
Airway	Early intubation if needed	Injuries at C3-C5 ("C3, 4, 5 keeps the diaphragm alive") compromise respiratory function; use in-line stabilization during intubation
Hemodynamic support	IV fluids + vasopressors	Target MAP 85 to 90 mmHg for 5 to 7 days to optimize spinal cord perfusion; use norepinephrine or phenylephrine for neurogenic shock; avoid pure fluid resuscitation alone (will not correct the bradycardia or loss of vascular tone)
Atropine	For symptomatic bradycardia	Neurogenic shock causes unopposed vagal tone
Surgical decompression	Urgent if structural compression exists	Within 24 hours of injury if there is ongoing cord compression on MRI; earlier intervention is associated with better neurological outcomes
Methylprednisolone	Controversial; NOT standard of care	No longer recommended by most guidelines (AANS/CNS); associated with increased infection risk, GI bleeding, and hyperglycemia without proven benefit
DVT prophylaxis	Mechanical + pharmacological	Pneumatic compression devices immediately; low-molecular-weight heparin started within 72 hours once hemostasis is secure
Bladder management	Intermittent catheterization	Urinary retention is nearly universal in acute cord injury; avoid indwelling catheters long-term due to infection risk
Pressure ulcer prevention	Repositioning every 2 hours	Insensate skin below the level of injury is extremely vulnerable
Autonomic dysreflexia management	Identify and remove the trigger	Occurs in injuries at T6 or above during the chronic phase; presents with severe hypertension, headache, flushing above the level, and bradycardia; most common trigger is bladder distension

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.

5. Differential Diagnosis and Distractors

Differential	Why It Is Similar	Key Discriminator
Hemorrhagic (hypovolemic) shock	Trauma patient with hypotension	Hypovolemic shock presents with tachycardia and cool, clammy skin; neurogenic shock presents with bradycardia and warm, dry skin
Guillain-Barre Syndrome	Ascending paralysis, areflexia, possible respiratory failure	GBS has no trauma history, is preceded by infection (Campylobacter, viral URI), shows ascending weakness starting in the legs, and CSF shows albuminocytologic dissociation
Transverse Myelitis	Acute bilateral weakness and sensory level	No trauma; often post-infectious or autoimmune; MRI shows cord inflammation without fracture or mechanical compression
Epidural Abscess	Back pain, neurological deficits, sensory level	Fever, elevated WBC and ESR/CRP, history of IV drug use or recent spinal procedure; no acute trauma
Aortic Dissection	Acute back pain with neurological deficits	Tearing chest/back pain radiating between the scapulae; blood pressure differential between arms; widened mediastinum on chest X-ray
Cauda equina from disc herniation	Saddle anesthesia, urinary retention, bilateral leg symptoms	No trauma history; progressive low back pain radiating to legs; large midline disc herniation on MRI at L4-L5 or L5-S1
Spinal epidural hematoma (spontaneous)	Acute cord compression, sensory level	Often in patients on anticoagulants; no trauma; sudden onset back pain progressing to weakness

6. Traps 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.

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