Spinal Cord Injury (SCI)

Populations and Risk Factors

• Males affected approximately 4:1 over females; peak incidence between ages 16 and 30
• Motor vehicle accidents are the leading cause (~38%), followed by falls (~30%), violence (~14%), and sports/recreation (~8%)
• Second peak in older adults (>65) from falls, often with pre-existing cervical stenosis or spondylosis that predisposes to central cord syndrome from hyperextension injuries
• Sports-related SCI most commonly from diving into shallow water (cervical), football, rugby, hockey, and equestrian sports
• Pre-existing spinal canal narrowing (congenital stenosis, osteophytes, OPLL) increases the severity of injury from the same mechanical force
• Alcohol and substance use are contributing factors in approximately 25% of traumatic SCIs

Causes and Pathophysiology

Primary Injury

• Mechanical disruption: The spinal cord is damaged by compression, contusion, laceration, or distraction forces at the moment of trauma. The most common mechanism is a flexion-compression injury (e.g., diving) or hyperextension injury (e.g., rear-end collision in an elderly patient with stenosis). The vertebral column fails — fracture, dislocation, or burst fracture — and the cord is compressed or sheared within the spinal canal.
• Level determines presentation: Injuries at C1–C8 produce tetraplegia (all four limbs affected); injuries at T1 and below produce paraplegia (lower limbs affected, upper limbs spared). Higher cervical injuries (C1–C4) compromise diaphragmatic innervation (phrenic nerve: C3–C5), requiring ventilator support. C5 injuries spare the deltoid and biceps; C6 spares wrist extensors (enabling tenodesis grasp); C7 spares triceps and wrist flexors; C8 spares intrinsic hand muscles partially.

Secondary Injury Cascade

• Inflammation and edema: Within minutes to hours, the primary mechanical damage triggers an inflammatory cascade — hemorrhage, edema, release of excitotoxic glutamate, free radical production, and ischemia from vascular disruption. This secondary injury expands the zone of necrosis beyond the original mechanical lesion, often destroying 1–2 additional spinal cord segments.
• Ischemic penumbra: Surrounding the central hemorrhagic necrosis is a zone of tissue that is viable but vulnerable. Edema, vasospasm, and thrombosis in spinal cord microvasculature can convert this penumbra into permanent necrosis over the first 24–72 hours — the clinical rationale for emergency decompression surgery and methylprednisolone protocols.
• Wallerian degeneration: Axons severed by the primary or secondary injury degenerate distally over weeks, completing the circuit disruption and making the loss permanent once regeneration fails.

ASIA Impairment Scale

• The American Spinal Injury Association (ASIA) Impairment Scale classifies completeness of injury from A to E:
• A — Complete: No motor or sensory function preserved in the sacral segments S4–S5 (no perianal sensation, no voluntary anal contraction)
• B — Sensory incomplete: Sensory function preserved but no motor function below the neurological level, including the sacral segments S4–S5
• C — Motor incomplete: Motor function preserved below the neurological level; more than half of key muscles below the level have a muscle grade less than 3
• D — Motor incomplete: Motor function preserved below the neurological level; at least half of key muscles below the level have a muscle grade of 3 or more
• E — Normal: Sensory and motor function normal (patient may still have neurological deficits from previous SCI)
• Neurological level is determined by dermatomal sensory testing (light touch and pinprick) and myotomal motor testing (10 key muscle groups bilaterally). The neurological level is the most caudal segment with intact sensation and at least Grade 3 motor function.

Spinal Shock and Spasticity Development

• Spinal shock occurs immediately after injury: temporary areflexia, flaccid paralysis, and loss of all autonomic function below the lesion. This is not structural destruction of LMN — it is a temporary cessation of all spinal cord activity below the lesion due to loss of descending facilitatory input.
• Resolution timeline: Spinal shock resolves over days to weeks (rarely up to months). The first sign of resolution is the return of the bulbocavernosus reflex (S2–S4). As isolated spinal cord segments below the lesion recover intrinsic reflex activity without descending inhibition, the presentation evolves:
• Flaccidity gives way to spasticity — UMN pattern (velocity-dependent increased resistance to passive movement)
• Hyperreflexia emerges — exaggerated deep tendon reflexes
• Clonus develops — repetitive involuntary muscle contractions, especially at the ankle
• Positive Babinski sign — great toe extension with fanning of other toes
• At the lesion level: The anterior horn cells at the level of injury are destroyed (LMN damage). These segments remain permanently flaccid and areflexic — a narrow band of LMN presentation between normal function above and UMN spasticity below.

Autonomic Dysreflexia

• Mechanism: In injuries at T6 and above, the major splanchnic sympathetic outflow (T5–L2) is isolated from descending brainstem inhibition. A noxious stimulus below the lesion level (full bladder, fecal impaction, pressure sore, tight clothing, catheter kink, rapid temperature change) triggers a massive unmodulated sympathetic discharge → widespread vasoconstriction below the lesion → dangerous blood pressure elevation.
• Baroreceptor response: Carotid and aortic baroreceptors detect the hypertension and signal the brainstem → parasympathetic response via the vagus nerve → bradycardia and vasodilation above the lesion. However, the descending inhibitory signals cannot pass the cord lesion, so vasoconstriction below persists → BP remains dangerously elevated.
• Clinical presentation: Pounding headache, flushing and sweating above the lesion, goosebumps and pallor below the lesion, nasal congestion, blurred vision, anxiety, bradycardia. Untreated, BP can reach 300/200 mmHg → stroke, seizure, cardiac arrest, death.
• MT relevance: Any physical stimulus the therapist applies to insensate areas can trigger an episode. The therapist must know the protocol: stop all treatment immediately, sit the client upright (gravity-assisted BP reduction), identify and remove the trigger, call emergency services if BP does not reduce within minutes.

Neurogenic Bowel and Bladder

• Injuries above the sacral cord (S2–S4) produce a UMN bladder — the bladder contracts reflexively but without voluntary control, causing reflex incontinence. The external sphincter is spastic, leading to incomplete emptying and high post-void residuals.
• Injuries at or below S2–S4 produce a LMN bladder — the detrusor is flaccid, the bladder overfills without reflexive contraction, and overflow incontinence occurs.
• Most SCI clients use intermittent catheterization or an indwelling catheter. The therapist must be aware of catheter placement, avoid disturbing the catheter or tubing, and recognize that a kinked or blocked catheter is the most common trigger for autonomic dysreflexia.

Poikilothermy

• Below the lesion level, the hypothalamic thermoregulatory pathway is interrupted. The body cannot vasoconstrict or vasodilate, sweat, or shiver below the injury level in response to environmental temperature changes. The client's body temperature passively follows ambient temperature (poikilothermy).
• Clinical significance: The treatment room must be maintained at a comfortable, neutral temperature. Insensate areas cannot provide feedback about excessive heat or cold, and thermoregulatory failure means the body cannot compensate.

Incomplete Spinal Cord Syndromes

Heterotopic Ossification (HO)

• Ectopic bone formation in periarticular soft tissues below the injury level, typically around the hips, knees, and elbows. Occurs in approximately 20–30% of SCI patients, usually within the first 2–6 months after injury.
• Mechanism: Not fully understood; likely related to aberrant mesenchymal stem cell differentiation in response to immobilization, vascular disruption, and neurogenic inflammation in denervated tissues.
• Palpation significance: Presents as a warm, firm, non-mobile periarticular mass with progressive ROM restriction. Must be differentiated from DVT (which also presents with warmth and swelling). HO is confirmed by radiograph. Do not mobilize aggressively through an HO-restricted range — risk of fracture.

Deep Vein Thrombosis (DVT)

• SCI clients are at extremely high risk for DVT due to loss of the skeletal muscle pump in paralyzed limbs, immobility, and altered blood flow. DVT risk is highest in the first 3 months post-injury.
• Clinical significance for MT: Unilateral limb swelling, warmth, and erythema in a paralyzed limb must be assumed to be DVT until proven otherwise. Do not massage the affected limb — risk of pulmonary embolism.

Tenodesis Grasp

• In C6 complete injuries, the wrist extensors (extradorsalcarpi radialis longus and brevis) are preserved but finger flexors are paralyzed. When the client actively extends the wrist, the passive tension in the paralyzed finger flexor tendons produces a functional finger flexion — a tenodesis grasp.
• MT relevance: Do not stretch or mobilize the finger flexors in a C6 client — the functional shortening of these tendons is what enables their only grasp function. Lengthening them destroys the tenodesis mechanism.

Signs and Symptoms

By Level

By Completeness

General Signs and Symptoms

• Spasticity (UMN, below lesion): velocity-dependent increased resistance to passive movement; flexor spasms (LE) or extensor spasms; can be painful, disruptive to sleep, and functionally limiting — but also functionally useful (supports standing transfers in some paraplegics)
• Flaccidity (LMN, at lesion level): absent reflexes, absent tone, progressive muscle atrophy in the affected myotome
• Neuropathic pain: burning, stabbing, or electric pain at or below the lesion level; often most severe at the transition zone between innervated and denervated segments; present in approximately 60–70% of SCI patients; responds poorly to standard analgesics
• Decubitus ulcers (pressure injuries): loss of sensation eliminates the discomfort signal that prompts repositioning; loss of vasomotor control impairs local tissue perfusion; sacrum, ischial tuberosities, greater trochanters, and heels are highest risk; can progress to deep tissue destruction and osteomyelitis
• Respiratory compromise: cervical injuries impair diaphragm (C3–C5), intercostals (T1–T11), and abdominals (T7–T12); reduced cough effectiveness → secretion retention → pneumonia (leading cause of death in chronic SCI)
• Orthostatic hypotension: loss of sympathetic vasoconstriction below the lesion → blood pools in lower extremities when upright → lightheadedness, syncope; managed with abdominal binders, compression stockings, and gradual position changes
• Poikilothermy: inability to regulate body temperature below lesion level
• Heterotopic ossification: ectopic bone formation around joints below the lesion, particularly hips and knees
• Sexual dysfunction: erectile dysfunction in males (reflex erections may be preserved in UMN injuries but psychogenic erections lost); reduced sensation and lubrication in females

Assessment Profile

Subjective Presentation

• Chief complaint: highly variable depending on level, completeness, and chronicity — chronic SCI clients typically present for management of spasticity, pain, contracture prevention, or compensatory overuse in innervated regions (shoulder pain from wheelchair propulsion, cervical pain from adaptive postures); newly referred clients may describe muscle tightness, spasms, or stiffness in affected limbs
• Pain quality: neuropathic pain at the transition zone (burning, electric, shooting); musculoskeletal pain in overloaded innervated regions (aching, constant shoulder/neck pain from wheelchair use); spasticity-related deep cramping; the client may report pain in areas where they have no sensation (central/deafferentation pain)
• Onset: traumatic — usually a clearly recalled event (MVA, fall, diving accident, assault); the client will know their neurological level and ASIA classification; ask about the date of injury, current medications (baclofen for spasticity, gabapentin for neuropathic pain), and any recent medical changes
• Aggravating factors: prolonged sitting without pressure relief (pressure injury risk); cold environments (poikilothermy — unable to warm below lesion); full bladder, constipation, tight clothing (autonomic dysreflexia triggers in T6-and-above injuries); rapid position changes (orthostatic hypotension)
• Easing factors: regular pressure relief and repositioning; baclofen or other antispasmodics for spasticity; slow sustained stretching for tone reduction; warmth to the environment (not direct heat to insensate skin)
• Red flags: Autonomic dysreflexia (T6 and above): sudden pounding headache, flushing/sweating above the lesion, pallor/goosebumps below the lesion, hypertension → STOP treatment, sit client upright, identify trigger, call emergency services if unresolved within minutes. New onset of increased spasticity, fever, or worsening pain → screen for UTI, pressure injury, or DVT. Unilateral leg swelling → DVT — do not massage; refer immediately.

Observation

• Local inspection: Wheelchair type indicates functional level (power chair with head controls → high cervical; manual wheelchair → thoracic or low cervical); muscle atrophy below the lesion level with bulk preserved above; trophic skin changes in insensate areas (thin, shiny, hairless skin); existing pressure injuries or healed scars over sacrum, ischial tuberosities, greater trochanters, or heels; indwelling catheter or leg bag may be visible; abdominal binder or compression stockings for orthostatic hypotension management
• Posture: Seated posture in wheelchair — kyphotic thoracic posture with forward head position from prolonged sitting; scoliotic curvature possible from asymmetric trunk muscle innervation in incomplete injuries; shoulder elevation and protraction from compensatory upper trapezius and pectoral overuse during transfers and wheelchair propulsion; wrist positioning in C6 injuries — wrist held in slight extension to maintain tenodesis grasp
• Gait: Absent in complete injuries above L1; in incomplete injuries or lower-level injuries, gait may be present with orthotics and assistive devices — steppage gait (foot drop from weak dorsiflexors), circumduction gait (spastic LE), wide-based ataxic gait (proprioceptive loss); many SCI clients are full-time wheelchair users and gait assessment is not applicable

Palpation

• Tone: Two distinct zones: (1) at the lesion level — LMN flaccidity, absent tone, soft atrophied muscle in the affected myotome; (2) below the lesion — UMN spastic hypertonia (velocity-dependent increased resistance to passive movement); hip adductors, knee flexors, and plantarflexors are typically most spastic; above the lesion — muscles are neurologically intact but frequently hypertonic from compensatory overuse (upper trapezius, levator scapulae, cervical extensors, rotator cuff, pectorals in wheelchair users). In incomplete injuries, tone distribution is mixed and asymmetric.
• Tenderness: Compensatory overuse pain in innervated regions — bilateral shoulder girdle tenderness from wheelchair propulsion (supraspinatus, infraspinatus, posterior deltoid, biceps tendon, upper trapezius); cervical paraspinal tenderness from forward head posture; trigger points in upper trapezius and levator scapulae are common. In insensate areas below the lesion, tenderness cannot be assessed — the client has no pain feedback. The therapist must rely on visual and palpatory tissue assessment rather than client report for pressure guidance.
• Temperature: Below the lesion, skin temperature passively follows ambient conditions (poikilothermy) — extremities may feel cool in a normal room temperature environment; this is baseline, not pathology. Localized warmth in an insensate area is significant: warm, firm periarticular mass → heterotopic ossification; unilateral limb warmth with swelling → DVT — do not massage; refer. Above the lesion, temperature is normal.
• Tissue quality: Below the lesion — muscle atrophy (soft, reduced bulk, loss of contractile tissue); skin over pressure points may be thin, fragile, or scarred from previous pressure injuries; fascial mobility markedly reduced in chronically immobile segments; edema common in dependent paralyzed limbs (loss of muscle pump). Above the lesion — compensatory hypertrophy in wheelchair-propulsion muscles; ropy, fibrotic trigger points in chronically overloaded upper trapezius and shoulder girdle; may palpate joint crepitus in overused glenohumeral joints.

Motion Assessment

• AROM: Absent below the lesion in complete injuries; in incomplete injuries, reduced and weak in partially innervated segments — test each myotomal level to establish the neurological level; above the lesion, AROM is full but may be limited by pain from compensatory overuse (shoulder flexion and abduction limited by impingement from wheelchair propulsion overload); cervical AROM may be restricted by chronic forward head posture and upper trapezius hypertonicity
• PROM / end-feel: Below the lesion, PROM assesses for contracture development — the critical clinical question is whether range loss is from spasticity (elastic-muscular end-feel that yields to slow sustained pressure) or from established contracture (firm/hard end-feel that does not yield). Slow PROM through a spastic range will achieve more motion than rapid movement (velocity-dependent nature of spasticity); if clonus is triggered by rapid dorsiflexion at the ankle, slow the velocity. At joints with heterotopic ossification, end-feel is bony/hard with progressive range loss — do not force.
• Resisted testing: Meaningful only in the transition zone and above; test key muscles to confirm neurological level: C5 — biceps/deltoid; C6 — wrist extensors; C7 — triceps/wrist flexors; C8 — finger flexors; T1 — finger abductors; L2 — hip flexors; L3 — knee extensors; L4 — ankle dorsiflexors; L5 — great toe extensors; S1 — ankle plantarflexors. Below the neurological level, resisted testing is not applicable in complete injuries.

Special Test Cluster

UMN vs. LMN in SCI — the two-zone model:

| Feature | At lesion level (LMN) | Below lesion level (UMN) | |––––-|–––––––––––|––––––––––––-| | Tone | Flaccid | Spastic (velocity-dependent) | | Reflexes | Absent or diminished | Hyperreflexic, clonus | | Babinski | Negative | Positive | | Atrophy | Severe — denervation atrophy | Moderate — disuse atrophy | | Clinical significance | Identifies exact level of cord damage | Confirms intact but isolated reflex arcs below |

Differential Diagnoses