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Summary Table

Category	Details
Risk Factors	Young males (most common demographic for traumatic SCI), high-speed motor vehicle accidents, falls from height, diving injuries, contact sports, penetrating trauma (gunshot/stab wounds), pre-existing spinal stenosis
Etiology	Acute spinal cord injury (SCI) causing sudden loss of all supraspinal descending input to the cord below the level of injury; the cord becomes transiently "electrically silent" due to motor neuron hyperpolarization
Patient Presentation	A trauma patient (often immobilized on a backboard) with complete flaccid paralysis, loss of all sensation, and absent reflexes below a defined neurological level. Often accompanied by urinary retention, fecal incontinence, and in males, priapism
Classic Physical Exam	Flaccid (not spastic) paralysis below the lesion; areflexia (absent deep tendon reflexes below the injury); absent anal sphincter tone on rectal exam; absent bulbocavernosus reflex; loss of all sensory modalities below the lesion; priapism in males
Key Diagnostic Results	Clinical diagnosis confirmed by areflexia + flaccid paralysis below the level of injury. MRI of the spine is the gold standard for cord injury characterization. CT identifies bony fractures/dislocations. Return of the bulbocavernosus reflex signals resolution of spinal shock
Management	ABCDE trauma protocol with strict spinal immobilization; hemodynamic support targeting MAP $\geq$ 85 mmHg for 3 to 7 days (ICU monitoring); IV fluids and vasopressors (norepinephrine preferred); Foley catheter for urinary retention; DVT prophylaxis; early surgical decompression (<24 hours) if structurally indicated; methylprednisolone is not routinely recommended
Keywords	"Flaccid paralysis after trauma," "areflexia below the level of injury," "absent bulbocavernosus reflex," "loss of anal tone," "warm and dry extremities with bradycardia," "priapism," "hypotension with bradycardia after spinal injury"

1. Pathophysiology

Spinal shock is a transient physiological phenomenon, not a permanent anatomical destruction. When the spinal cord sustains an acute injury, there is an abrupt loss of all tonic excitatory input from the brain (the reticulospinal, vestibulospinal, and corticospinal tracts) to the spinal neurons below the level of injury. Without this constant descending facilitation, the lower motor neurons and interneurons below the lesion become hyperpolarized and electrically unresponsive. The result is complete areflexia and flaccid paralysis, even in cases where the cord is not fully transected.

This explains why the paralysis in spinal shock is flaccid, not spastic. Spasticity and hyperreflexia are features of an upper motor neuron lesion that has had time to reorganize. In the acute phase, the cord below the injury simply cannot generate any reflex arc because its neurons have lost the background excitation they depend on. The deep tendon reflexes, cutaneous reflexes, and the bulbocavernosus reflex all vanish.

The autonomic nervous system is equally disrupted. The sympathetic chain originates from T1 through L2. In cervical or high thoracic injuries (above T6), the loss of sympathetic outflow causes unopposed vagal (parasympathetic) tone. This produces the classic hemodynamic picture: hypotension with paradoxical bradycardia, warm and vasodilated extremities, and impaired thermoregulation. This cardiovascular component is what some sources call neurogenic shock, which is the hemodynamic consequence that frequently coexists with the neurological phenomenon of spinal shock.

Loss of sacral parasympathetic and somatic efferents produces urinary retention (detrusor areflexia), loss of rectal tone, and priapism in males (due to unopposed parasympathetic vasodilation of penile vasculature when sympathetic tone is absent). Each of these findings connects directly back to the loss of integrated autonomic regulation.

The critical concept to understand is that spinal shock is time-limited. Over days to months, the spinal cord neurons below the injury gradually develop intrinsic excitability through denervation supersensitivity, receptor upregulation, and synaptogenesis. The reflex arc re-emerges, and flaccid paralysis transitions into spastic paralysis with hyperreflexia. The return of the bulbocavernosus reflex (an S2 through S4 polysynaptic reflex) has traditionally been used as the clinical marker signaling that spinal shock has ended. Once this reflex returns, any persistent motor or sensory deficit indicates a true, structural cord injury rather than physiological suppression.

2. Classification and Clinical Manifestation

Ditunno Four-Phase Model of Spinal Shock

Phase	Timeframe	Underlying Mechanism	Clinical Features
Phase 1	0 to 24 hours	Loss of descending facilitation; motor neuron hyperpolarization	Complete areflexia or hyporeflexia below the lesion; flaccid paralysis; loss of all sensation; absent anal tone; absent bulbocavernosus reflex. The delayed plantar reflex is typically the first pathological reflex to appear near the end of this phase
Phase 2	Day 1 to Day 3	Denervation supersensitivity; receptor upregulation on post-synaptic neurons	Initial return of some cutaneous reflexes (bulbocavernosus, cremasteric). Deep tendon reflexes remain absent. Sympathetic dysfunction may cause bradyarrhythmias, AV conduction blocks, and hypotension
Phase 3	Day 4 to ~1 month	Axon-supported synapse growth; new synaptic connections forming	Early hyperreflexia begins. Deep tendon reflexes return (ankle jerk before knee jerk). Babinski sign becomes positive. Detrusor hyperreflexia may begin
Phase 4	1 to 12 months	Soma-supported synapse growth; long-axon sprouting	Established spasticity and hyperreflexia. Autonomic dysreflexia may develop (in injuries above T6). Bladder transitions from areflexic to hyperreflexic pattern

Spinal Shock vs. Neurogenic Shock

Feature	Spinal Shock	Neurogenic Shock
Definition	Transient loss of all spinal cord function (motor, sensory, reflex, autonomic) below the injury	Cardiovascular collapse from loss of sympathetic tone
Primary Finding	Areflexia + flaccid paralysis	Hypotension + bradycardia
Mechanism	Loss of descending excitatory input to spinal neurons	Loss of sympathetic vasomotor tone, causing vasodilation and decreased venous return
Injury Level	Any level of spinal cord injury	Typically injuries above T6 (the higher the injury, the more pronounced the effect)
Duration	Days to months	Hours to days (usually resolves faster)
Hallmark	Absent bulbocavernosus reflex	Warm, vasodilated extremities with low BP and low HR

ASIA Impairment Scale (Used After Resolution of Spinal Shock)

Grade	Description
A (Complete)	No motor or sensory function preserved in sacral segments S4/S5
B (Sensory Incomplete)	Sensory but not motor function preserved below the neurological level, including sacral segments
C (Motor Incomplete)	Motor function preserved below the level; more than half of key muscles below the level have a grade less than 3
D (Motor Incomplete)	Motor function preserved below the level; at least half of key muscles below the level have a grade of 3 or more
E (Normal)	Motor and sensory function normal

A critical point: the ASIA classification cannot reliably determine completeness of injury while the patient is still in spinal shock. The bulbocavernosus reflex must return before you can classify an injury as "complete" (ASIA A). Until then, the apparent absence of all function below the lesion may simply reflect ongoing physiological suppression rather than true anatomical transection.

3. Diagnostic Workup

Test	Role	Key Findings
Clinical Examination	Best initial test	Flaccid paralysis + areflexia + absent anal tone + absent bulbocavernosus reflex below a defined neurological level, in the setting of acute trauma
Bulbocavernosus Reflex	Marker for resolution of spinal shock	Absent during spinal shock; its return signals the end of spinal shock. Tested by squeezing the glans penis/clitoris or tugging the Foley catheter while palpating anal sphincter contraction on digital rectal exam
CT of the Spine	Best initial imaging for bony injury	Identifies fractures, dislocations, bony fragment retropulsion. Fast and widely available in trauma settings
MRI of the Spine	Gold standard for cord pathology	Directly visualizes spinal cord edema, hemorrhage, compression, disc herniation, and ligamentous injury. Determines the extent and nature of cord damage
Plain Radiographs	Largely replaced by CT	May still be used for initial screening in low-resource settings; poor sensitivity for detecting subtle fractures and cord injury
ASIA/ISNCSCI Exam	Standardized neurological assessment	Performed serially; documents motor (key muscles) and sensory (dermatomes to light touch and pinprick) function. Determines neurological level and injury completeness once spinal shock resolves

The diagnosis of spinal shock is primarily clinical. When a trauma patient presents with flaccid paralysis, complete sensory loss, and areflexia below a defined level, alongside absent anal tone and an absent bulbocavernosus reflex, the clinical picture is essentially diagnostic. No laboratory test "confirms" spinal shock as a standalone entity; instead, the workup aims to identify the underlying spinal cord injury and guide surgical decision-making.

The best initial imaging study in the trauma setting is a CT scan of the spine, which rapidly identifies fractures, dislocations, and retropulsed bony fragments that may be compressing the cord. It is fast, highly sensitive for bony pathology, and available in virtually all trauma centers.

The most accurate test for evaluating the spinal cord itself is MRI. MRI directly visualizes cord edema, intramedullary hemorrhage (which carries a worse prognosis), disc herniation, epidural hematoma, and ligamentous injury. It is the study that informs whether surgical decompression is indicated and helps predict functional recovery. MRI findings of cord hemorrhage strongly correlate with a complete injury and poor neurological outcome.

The bulbocavernosus reflex deserves its own emphasis. This is a polysynaptic reflex mediated through sacral segments S2 to S4. It is tested by performing a digital rectal examination while simultaneously squeezing the glans penis or clitoris (or tugging on an indwelling Foley catheter). A positive reflex is a palpable contraction of the anal sphincter. During spinal shock, this reflex is absent. Its return (usually within 24 to 72 hours) marks the resolution of spinal shock, and it is at this point that a complete neurological assessment can reliably classify the injury as complete or incomplete using the ASIA scale.

Recent evidence suggests that the delayed plantar reflex may actually return before the bulbocavernosus reflex in some patients. However, for examination purposes, the bulbocavernosus reflex remains the most traditionally tested and most commonly referenced marker.

4. Management and Treatment

Phase	Intervention	Details
Prehospital	Spinal immobilization	Cervical collar + backboard; maintain in-line stabilization during transport
Primary Survey	ABCDE protocol	Airway (intubation if high cervical injury compromises respiratory drive), Breathing (watch for diaphragmatic breathing in C3 to C5 injuries), Circulation (fluid resuscitation + vasopressors), Disability, Exposure
Hemodynamic Support	MAP target $\geq$ 85 mmHg	IV crystalloid first; if inadequate, add vasopressors. Norepinephrine is preferred (alpha + beta agonism). Maintain for 3 to 7 days in an ICU setting
Bradycardia Management	Atropine or pacing if symptomatic	Due to unopposed vagal tone; watch for AV conduction abnormalities
Surgical Decompression	Early surgery within 24 hours	Recommended when there is structural compression (fracture, disc herniation, epidural hematoma) amenable to decompression
Methylprednisolone	Not routinely recommended	AO Spine 2017 guidelines: a 24-hour infusion may be offered if started within 8 hours of injury, but this remains controversial and is not standard of care
DVT Prophylaxis	Chemical prophylaxis within 72 hours	Low-molecular-weight heparin (enoxaparin 40 mg SC daily or equivalent); mechanical compression devices as adjunct
Bladder Management	Indwelling Foley catheter acutely	Transition to intermittent catheterization as clinical status stabilizes
GI Prophylaxis	Stress ulcer prevention, bowel program	H2 blockers or proton pump inhibitors; monitor for paralytic ileus (common in acute phase)
Skin and Positioning	Pressure injury prevention	Turn patient every 2 hours; specialized mattress; meticulous skin care
Respiratory Support	Varies by injury level	C3 to C5 injuries may require mechanical ventilation (phrenic nerve involvement). Early tracheostomy is recommended for high cervical injuries

Acute stabilization begins with the trauma ABCDE protocol. The most immediate life-threatening concern in high spinal cord injuries is respiratory failure. The phrenic nerve arises from C3, C4, and C5. Injuries at or above this level can abolish diaphragmatic function entirely, requiring emergent intubation and mechanical ventilation. Injuries just below this level still compromise intercostal and abdominal muscle function, resulting in a restrictive pattern with poor cough and eventual atelectasis.

Hemodynamic management is the cornerstone of acute care. The AO Spine/Praxis 2024 guidelines suggest augmenting MAP to at least 75 to 80 mmHg as the lower limit, but not actively augmenting beyond 90 to 95 mmHg as the upper limit, to optimize spinal cord perfusion. However, traditional neurosurgical guidelines recommend a MAP goal of 85 to 90 mmHg for 7 days. For exam purposes, the tested answer is typically MAP $\geq$ 85 mmHg for 5 to 7 days. Initial resuscitation begins with isotonic crystalloid (normal saline or lactated Ringer's). If fluid resuscitation alone does not achieve the MAP target, norepinephrine is the preferred vasopressor because it provides both alpha-adrenergic (vasoconstriction) and beta-adrenergic (chronotropic) activity, addressing both the hypotension and the bradycardia seen in neurogenic shock.

Methylprednisolone is a frequently tested topic. The NASCIS II and III trials suggested a potential benefit of high-dose methylprednisolone (30 mg/kg IV bolus followed by 5.4 mg/kg/hour infusion for 23 hours) if initiated within 8 hours of injury. However, current guidelines from AANS/CNS state that methylprednisolone is not recommended for routine use in acute SCI, and it is not FDA-approved for this indication. The risks (infection, GI bleeding, hyperglycemia, avascular necrosis) generally outweigh the marginal benefits. The exam-tested answer: methylprednisolone is not standard of care, but a 24-hour infusion may be considered if the patient presents within 8 hours. A 48-hour infusion is never recommended.

Early surgical decompression (within 24 hours of injury) is recommended when there is identifiable structural compression of the spinal cord. This has been shown to correlate with improved neurological outcomes compared to delayed surgery.

Supportive care includes Foley catheterization for urinary retention (the bladder is areflexic during spinal shock, and overdistension can cause permanent detrusor damage), DVT prophylaxis with low-molecular-weight heparin (SCI patients carry an exceptionally high risk of venous thromboembolism), stress ulcer prophylaxis, bowel management to prevent ileus, and rigorous pressure ulcer prevention with scheduled repositioning.

5. Differential Diagnosis and Distractors

Differential	Why It Is Similar	Key Discriminator
Neurogenic shock	Also occurs after spinal cord injury; also presents with hypotension. Students often confuse the two as the same entity	Neurogenic shock is a hemodynamic phenomenon (hypotension + bradycardia from sympathetic loss). Spinal shock is a neurological phenomenon (areflexia + flaccid paralysis). They frequently coexist but are conceptually distinct. A question asking "what is spinal shock" wants you to answer areflexia, not hypotension
Hypovolemic/hemorrhagic shock	Trauma patient with hypotension; easy to assume blood loss after a major accident	Hemorrhagic shock produces tachycardia (sympathetic compensation) and cool, clammy skin. Neurogenic/spinal shock produces bradycardia and warm, dry, vasodilated skin. This is the single most important discriminator
Guillain-Barre Syndrome (GBS)	Ascending flaccid paralysis with areflexia; can look identical on exam	GBS is a post-infectious, ascending process (usually after a GI or respiratory illness). It develops over days to weeks, not acutely after trauma. There is no sensory level. CSF shows albuminocytologic dissociation (elevated protein with normal cell count)
Transverse myelitis	Bilateral weakness and sensory loss at a spinal cord level; areflexia may be present acutely	Transverse myelitis is inflammatory and subacute (develops over hours to days, not instantaneously after trauma). MRI shows cord inflammation/enhancement. Often follows viral infections or is associated with autoimmune conditions (e.g., MS, neuromyelitis optica)
Cauda equina syndrome	Lower extremity weakness, urinary retention, saddle anesthesia, decreased rectal tone	Cauda equina involves peripheral nerves (lower motor neuron), not the spinal cord itself. Findings are purely lower motor neuron: flaccid paralysis that does not transition to spasticity over time. Asymmetric involvement is common. Injury is at or below L1 to L2
Anterior spinal artery syndrome	Sudden-onset bilateral motor paralysis and loss of pain/temperature below a level, with preserved proprioception and vibration	This is a vascular event, not trauma (though trauma can cause it). The hallmark is dissociated sensory loss: pain and temperature are lost (anterolateral columns), but proprioception and vibration are preserved (dorsal columns). In pure spinal shock, all modalities are lost

6. Traps and High-Yield Pearls

The most common way students get questions about spinal shock wrong is by confusing it with neurogenic shock. These two entities frequently coexist in the same patient, but the question is asking which concept you understand. If the vignette emphasizes areflexia, flaccid paralysis, and absent reflexes below a level, the answer is spinal shock. If it emphasizes hypotension with bradycardia and warm extremities, the answer is neurogenic shock. Read the question stem carefully for what it is actually asking.

A second frequent trap is premature classification of injury completeness. Students see a trauma patient with zero motor and sensory function below a level and immediately label it "complete cord transection" (ASIA A). This is wrong if the bulbocavernosus reflex has not yet returned. While the patient is still in spinal shock, you cannot determine whether the injury is complete or incomplete because the areflexia and paralysis may simply reflect physiological suppression. The correct answer is: "reassess after spinal shock resolves (after the bulbocavernosus reflex returns) before determining completeness."

Third, do not confuse the flaccid paralysis of spinal shock with a lower motor neuron lesion. Early spinal shock mimics a lower motor neuron pattern (flaccid, areflexic), but the underlying lesion is an upper motor neuron injury. The key proof: once spinal shock resolves, the patient transitions to spasticity, hyperreflexia, and positive Babinski signs, all upper motor neuron findings. If a vignette describes a trauma patient who initially had flaccid paralysis and weeks later develops spasticity, this is the expected evolution of spinal shock resolving, not a new pathology.

Fourth, know the hemodynamic distinction cold: hemorrhagic shock = tachycardia + cold/clammy skin; neurogenic shock = bradycardia + warm/dry skin. A trauma patient with hypotension and bradycardia who has a spinal cord injury should not receive aggressive blood transfusion as the first-line treatment; the answer is IV fluids and vasopressors (norepinephrine). Conversely, do not assume a spine-injured patient cannot also be bleeding. If there is tachycardia, look for a concurrent hemorrhagic source.

Finally, remember the methylprednisolone pearl: it is not recommended as routine standard of care for acute SCI. If the question asks for the "next best step" in managing a spinal shock patient, the answer is hemodynamic support and surgical evaluation, not steroids. Methylprednisolone is only a consideration (not a recommendation) if the patient presents within 8 hours, and even then, it is a weak suggestion with significant side-effect risk.

The core competency being tested with spinal shock questions is your ability to recognize the acute clinical picture (flaccid paralysis + areflexia + absent bulbocavernosus reflex after trauma), distinguish it from neurogenic shock, understand that it is a temporary phenomenon, and know that definitive neurological classification must wait until the bulbocavernosus reflex returns.

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