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Spinal Cord Injury & Cord Syndromes

Orthopaedics · Spine · lean revision notes

Spinal Cord Injury & Cord Syndromes

Spinal cord injury (SCI) is a high-yield orthopaedic-cum-neurosurgical emergency where rapid recognition of the level, completeness, and syndrome changes both immediate management and long-term prognosis. This topic spans trauma resuscitation, neuroanatomy of cord tracts, the ASIA grading system, and the named cervical fractures—each a favourite NEET PG single-best-answer trap.


1. Basic definitions & classification

Spinal cord injury is damage to the cord resulting in temporary or permanent loss of motor, sensory, or autonomic function below the level of the lesion.

Injury is classified along several axes:

  • Mechanism: primary (mechanical disruption at impact) vs secondary (ischaemia, oedema, excitotoxicity, free-radical injury developing over hours—the target of neuroprotection).
  • Completeness: complete (no motor/sensory function in lowest sacral segments S4–S5) vs incomplete (some preservation, including sacral sparing).
  • Level: the lowest segment with normal motor (≥grade 3 with the segment above grade 5) AND sensory function bilaterally — the neurological level of injury (NLI).
  • Stability: stable vs unstable (Denis three-column concept).

High-yield: Sacral sparing (perianal sensation, voluntary anal contraction, great-toe flexor activity) is the single most important sign that an injury is incomplete, and it carries a far better prognosis. Always do a per-rectal exam.

Denis three-column concept (stability)

Column Structures Note
Anterior Anterior longitudinal ligament, anterior ⅔ vertebral body & annulus
Middle Posterior ⅓ body, posterior annulus, posterior longitudinal ligament The key column
Posterior Pedicles, facets, laminae, spinous process, posterior ligamentous complex

High-yield: Disruption of ≥2 of 3 columns = unstable. The middle column is the critical determinant of stability.


2. Spinal shock vs neurogenic shock

These two are the classic two-by-two confusion and are almost guaranteed in any SCI question set.

Feature Spinal shock Neurogenic shock
Nature Physiological loss of all cord function below lesion Haemodynamic / circulatory shock
Findings Flaccid paralysis, areflexia, loss of sensation, absent reflexes Hypotension + bradycardia + warm dry skin
Cause Transient cord "stunning" Loss of sympathetic outflow (T1–L2), unopposed vagal tone
Typical level Any cord injury Usually injuries above T6
Recovery marker Return of bulbocavernosus reflex Resolves with fluids ± vasopressors/atropine
Treatment Supportive; time IV fluids → vasopressors (noradrenaline), atropine for bradycardia

High-yield: Bradycardia with hypotension in a trauma patient = neurogenic shock (NOT haemorrhagic, which gives tachycardia). But always rule out concurrent blood loss first.

High-yield: End of spinal shock = return of the bulbocavernosus reflex (squeeze glans/tug Foley → reflex anal sphincter contraction). Only after this returns can you reliably call an injury complete vs incomplete. It typically returns within 24–48 hours.

Reflex sequence after SCI: Flaccid areflexia (spinal shock) return of bulbocavernosus/anal reflexes gradual emergence of spasticity, hyperreflexia, clonus, and upgoing plantars (UMN pattern) over weeks.


3. ASIA Impairment Scale (AIS)

The American Spinal Injury Association (ASIA) standard is the universal language of SCI severity.

Grade Definition
A Complete — no motor or sensory function in S4–S5
B Sensory incomplete — sensation (incl. S4–S5) preserved, no motor below level; no motor >3 levels below
C Motor incomplete — motor preserved below level, >½ of key muscles below have grade <3
D Motor incomplete — motor preserved, ≥½ of key muscles below have grade ≥3
E Normal motor and sensory
  • Sensory tested at 28 dermatomes each side (light touch + pinprick), scored 0–2.
  • Motor tested in 10 key muscles each side (5 upper-limb, 5 lower-limb), scored 0–5.

High-yield: AIS grade C vs D hinges on whether at least half the key muscles below the NLI are grade 3 or better. Grade D ≈ ambulatory potential.

Key motor levels (memorise the ladder):

Root Action
C5 Elbow flexion (biceps)
C6 Wrist extension
C7 Elbow extension (triceps)
C8 Finger flexion (FDP middle finger)
T1 Finger abduction (small finger)
L2 Hip flexion
L3 Knee extension
L4 Ankle dorsiflexion
L5 Great-toe extension (EHL)
S1 Ankle plantarflexion

Sensory landmarks: C4 clavicle, T4 nipple, T6 xiphisternum, T10 umbilicus, L1 inguinal, S1 lateral foot, S4–S5 perianal.


4. Incomplete cord syndromes

This is the most heavily tested section. Anchor each to its cross-sectional tract anatomy.

(a) Central cord syndrome — the commonest

  • Mechanism: hyperextension injury in an older patient with pre-existing cervical spondylosis (cord pinched between osteophytes anteriorly and buckled ligamentum flavum posteriorly). Often without fracture.
  • Pathology: central grey matter and the medially placed cervical fibres of the corticospinal tract bear the brunt.
  • Clinical: weakness greater in UPPER limbs than lower limbs, distal > proximal, with variable sensory loss and bladder dysfunction. "Man-in-a-barrel" pattern.
  • Prognosis: generally good; recovery order = legs → bladder → proximal arms → hands (hands recover last/least).

High-yield: Central cord syndrome = elderly + hyperextension (fall on face/forehead) + arms worse than legs. Most common incomplete syndrome.

(b) Anterior cord syndrome — the worst prognosis

  • Mechanism: flexion injury or anterior spinal artery infarction (e.g., aortic surgery, thrombosis).
  • Tracts lost: corticospinal (motor) + spinothalamic (pain/temperature). Dorsal columns spared.
  • Clinical: complete motor paralysis below level + loss of pain and temperature, with preserved proprioception, vibration, and light touch.
  • Prognosis: worst of the incomplete syndromes (~10–20% useful recovery).

High-yield: Anterior cord syndrome → motor + pain/temp lost, vibration/proprioception preserved (dorsal columns are posterior and spared). Poorest recovery.

(c) Brown-Séquard syndrome — cord hemisection

  • Mechanism: penetrating trauma (stab/gunshot), lateral mass fracture, or tumour — classically a hemisection.
  • Clinical triad below the lesion:
    • Ipsilateral loss of motor power (corticospinal, decussates in medulla).
    • Ipsilateral loss of vibration/proprioception/fine touch (dorsal columns, decussate in medulla).
    • Contralateral loss of pain & temperature, beginning 1–2 segments below the lesion (spinothalamic, decussates in cord).
  • Prognosis: best of all the syndromes for ambulation.

High-yield: Brown-Séquard = ipsilateral paralysis + ipsilateral dorsal-column loss + contralateral pain/temperature loss. Best functional outcome.

(d) Posterior cord syndrome (rare)

  • Loss of proprioception, vibration, fine touch below the lesion → sensory ataxia, positive Romberg; motor preserved. Seen in tabes dorsalis, B12 deficiency (subacute combined degeneration), posterior trauma.

(e) Conus medullaris vs cauda equina

Feature Conus medullaris Cauda equina
Level Cord tip ~L1–L2 vertebra Lumbosacral roots below L2
Lesion type UMN ± LMN (mixed) Pure LMN
Onset Sudden, bilateral, symmetric Gradual, often asymmetric
Pain Less, bilateral Severe radicular, often unilateral
Saddle anaesthesia Symmetric, prominent Asymmetric, may be incomplete
Bladder/bowel Early, marked retention/incontinence Late, but a red flag
Reflexes Ankle jerk may be preserved (knee jerk lost) Areflexic (knee + ankle lost)
Recovery Poorer Better (LMN roots)

High-yield: Cauda equina syndrome is a surgical emergency. Red flags: bilateral sciatica, saddle anaesthesia, urinary retention with overflow incontinence, reduced anal tone, loss of bulbocavernosus reflex. Urgent MRIdecompression ideally within 24–48 hours for the best bladder recovery.

Flow for suspected cauda equina: Bilateral leg symptoms + bladder/bowel change PR exam (tone, sensation) + post-void residual bladder scan urgent MRI whole spine emergency surgical decompression (discectomy/laminectomy).


5. Named cervical spine fractures

A reliably tested cluster — link mechanism, stability, and management.

Fracture Site / mechanism Stability Key facts / management
Jefferson C1 burst (ring) from axial loading (diving) — ≥2 breaks in the ring Stable if transverse ligament intact; unstable if disrupted Rule of Spence: combined lateral mass overhang >6.9 mm on open-mouth view = transverse ligament rupture → unstable. Usually no cord injury (canal widens). Halo/collar; surgery if unstable
Hangman C2 bilateral pars (traumatic spondylolisthesis of axis) — hyperextension + distraction (road accidents now > hanging) Variable Often neurologically intact (canal widest here). Levine classification; mostly halo/collar, surgery for unstable types
Odontoid (dens) fracture C2 dens — flexion/extension Type II unstable Anderson-D'Alonzo: Type I (tip, stable), Type II (base — commonest, high non-union), Type III (into body, best healing). Type II → halo or surgical fixation
Clay-shoveler C7/T1 spinous process avulsion Stable Benign; conservative
Teardrop Flexion (anteroinferior body fragment) Highly unstable Severe cord injury, often anterior cord syndrome; surgical

High-yield: Odontoid Type II is the most common odontoid fracture and has the highest non-union rate (poor blood supply at the base). Type III heals best.

High-yield: Jefferson and Hangman fractures often spare the cord because each widens the canal at that level. Teardrop and bilateral facet dislocation are the dangerous ones.

Mnemonic — "JeffersON ONE ring" : Jefferson = C1; "Hang the TWO" → Hangman/odontoid = C2.


6. Initial assessment & investigation

Pre-hospital → ED flow (ATLS):

  1. A — Airway with cervical-spine control: rigid collar + manual in-line stabilisation; intubate without neck extension if needed.
  2. B — Breathing: high lesions (above C3–C5, the phrenic nerve, "C3-4-5 keeps the diaphragm alive") → diaphragmatic failure → ventilate.
  3. C — Circulation: treat haemorrhage first; suspect neurogenic shock if hypotensive + bradycardic.
  4. D — Disability: GCS, pupils, full ASIA exam including PR.
  5. E — Exposure / log-roll for spinal palpation.

Imaging:

  • CT is the investigation of choice for bony injury and clearing the cervical spine in trauma.
  • MRI is the investigation of choice for the cord, ligaments, disc, and haematoma — and is mandatory in cauda equina and in neurological deficit without obvious bony injury (SCIWORA — Spinal Cord Injury WithOut Radiographic Abnormality, classically in children).

High-yield: NEXUS criteria allow clinical clearance of the cervical spine without imaging if ALL are present: no midline tenderness, no focal deficit, normal alertness, no intoxication, no distracting injury. The Canadian C-spine rule is the alternative.


7. Management & drug of choice

Acute medical:

  • Maintain MAP 85–90 mmHg for the first ~7 days to optimise cord perfusion (vasopressors as needed).
  • High-dose methylprednisolone (NASCIS protocol) is now controversial and not routinely recommended — significant infection/GI risk often outweighs marginal benefit. Know it as a historical/contested answer.

Definitive:

  • Reduction of dislocations (e.g., Gardner-Wells tongs traction for cervical facet dislocation).
  • Surgical decompression + stabilisation: evidence (e.g., STASCIS) favours early decompression (<24 h) in incomplete cervical SCI to improve neurological recovery.
  • Stable injuries: orthosis (collar/halo/TLSO brace).

Long-term bladder management — a recurrent NEET PG theme:

Phase Bladder type Management
Spinal shock Areflexic / atonic (flaccid) Indwelling/intermittent catheterisation to prevent overdistension
After recovery (lesion above conus, UMN) Spastic / reflex (automatic) neurogenic bladder Clean intermittent catheterisation (CIC) ± anticholinergics; trigger voiding
Lesion at/below conus (LMN) Flaccid / autonomous bladder CIC ± Credé/Valsalva

High-yield: Clean intermittent self-catheterisation (CISC) is the GOLD STANDARD for long-term neurogenic bladder — lowest rates of infection, stones, and upper-tract damage compared with indwelling catheters. Goal: keep detrusor pressures low to protect the kidneys (the leading cause of late mortality historically).


8. Complications

  • Autonomic dysreflexia (lesions above T6): a noxious stimulus below the lesion (commonly bladder distension/blocked catheter, faecal impaction) → massive sympathetic surge → severe hypertension, pounding headache, sweating/flushing above the lesion, pallor/piloerection below, with reflex bradycardia. Life-threatening (stroke, seizure).
    • Management flow: Sit the patient up → loosen constrictions → find & remove the trigger (unblock/empty bladder, disimpact rectum) → antihypertensive (GTN, nifedipine) if BP persists.
  • DVT/PE — high risk; prophylaxis essential.
  • Pressure ulcers — over sacrum/heels; meticulous turning.
  • Respiratory failure / pneumonia — leading acute cause of death in high lesions.
  • Heterotopic ossification, spasticity, contractures.
  • Orthostatic hypotension, temperature dysregulation (poikilothermia).
  • Neuropathic pain, depression.

High-yield: Autonomic dysreflexia = injury above T6 + sudden severe hypertension + headache + bradycardia. First step is sit the patient upright and hunt for a blocked catheter — do NOT just give antihypertensives blindly.


9. Key differentials

  • Transverse myelitis / demyelination (MS, NMO): subacute, no trauma, MRI cord signal change.
  • Spinal epidural abscess/haematoma: fever/anticoagulants, MRI compression.
  • Cord tumour / metastatic cord compression: progressive, MRI with contrast; oncological emergency.
  • Guillain-Barré syndrome: ascending flaccid areflexic paralysis but symmetric, no sensory level, no bladder early — distinguishes from cord lesion.
  • Anterior spinal artery infarct: mimics anterior cord syndrome without trauma.
  • B12 deficiency / SCD: dorsal column + corticospinal (mimics posterior/combined patterns).

Recently asked / exam angle

  • Image/clinical-vignette of an elderly man falling forward, arms weaker than legs → identify central cord syndrome and its mechanism (hyperextension, spondylosis).
  • Stab wound to back, ipsilateral weakness + contralateral pain lossBrown-Séquard, asked to identify the spared modality side.
  • Trauma patient with hypotension + bradycardia → distinguish neurogenic from hypovolaemic shock; first-line = fluids then vasopressors/atropine.
  • "End of spinal shock is marked by return of which reflex?"bulbocavernosus reflex.
  • Rule of Spence / 6.9 mm overhangJefferson fracture, transverse ligament integrity.
  • Most common odontoid fracture / highest non-unionType II.
  • Gold-standard long-term bladder care in SCIclean intermittent catheterisation.
  • Quadriplegic with sudden severe headache + hypertensionautonomic dysreflexia, first step sit upright + check catheter.
  • Investigation of choice for cord/ligament vs boneMRI vs CT respectively; SCIWORA in children needs MRI.

Rapid revision

  1. Sacral sparing = incomplete injury = better prognosis; always do PR exam.
  2. Bulbocavernosus reflex return marks the end of spinal shock (24–48 h).
  3. Neurogenic shock = hypotension + bradycardia + warm skin (injuries above T6); haemorrhagic shock gives tachycardia.
  4. ASIA A = complete (no S4–S5 function); C vs D decided by ≥half key muscles ≥grade 3.
  5. Central cord = elderly + hyperextension + arms worse than legs; commonest, good prognosis.
  6. Anterior cord = motor + pain/temp lost, dorsal columns spared; worst prognosis.
  7. Brown-Séquard = ipsilateral motor/dorsal column + contralateral pain/temp; best prognosis.
  8. Cauda equina = LMN, areflexic, saddle anaesthesia, retention → emergency MRI + decompression.
  9. Jefferson (C1) burst — Rule of Spence overhang >6.9 mm = unstable; Hangman (C2) pars; both often spare cord.
  10. Odontoid Type II = commonest + highest non-union; Type III heals best.
  11. CT for bone, MRI for cord/ligament; remember SCIWORA in children.
  12. CIC is gold-standard long-term bladder care; autonomic dysreflexia (above T6) → sit up + clear catheter first.