Damage to the spinal cord resulting in temporary or permanent loss of motor, sensory, or autonomic function below the level of injury.

Exam domain	One-glance essentials
Definition / diagnosis	Traumatic or non-traumatic damage producing motor, sensory and autonomic dysfunction below the lesion ^[1] Complete and incomplete syndromes have different prognoses ^[1]
Epidemiology / risks	High-energy trauma, older-person falls and spinal stenosis increase risk ^[1] Hypotension and delayed immobilisation worsen secondary injury ^[1]
Core mechanism	Primary compression/contusion is followed by oedema, ischaemia and inflammatory injury ^[1] Cervical lesions can impair ventilation and sympathetic tone ^[1]
Clinical picture	Weakness, sensory level, areflexia initially and bladder/bowel dysfunction ^[1] Neurogenic shock causes hypotension with inappropriate bradycardia ^[1]
Investigations	ABCDE with full spinal examination and ASIA grading ^[2] CT defines bone injury; MRI assesses cord, discs and ligaments ^[2]
Management	Immobilise, maintain oxygenation/perfusion and obtain urgent spinal surgical review ^[3] Decompress/stabilise selected injuries and start early multidisciplinary rehabilitation ^[3]
Complications	Respiratory failure, pressure injury, VTE and autonomic dysreflexia ^[4] Neurogenic bladder, infection, spasticity and chronic pain are common ^[4]
Prevention / follow-up	Road/falls prevention and safe transfer reduce injury ^[3] Pressure care, VTE prophylaxis, bowel/bladder programmes and vaccination prevent secondary harm ^[3]
Exam traps	*Spinal shock is transient areflexia; neurogenic shock is haemodynamic failure* ^[2] Steroids are not routine treatment for acute traumatic spinal cord injury ^[3]

References

^[1] Lecture slides: GC 110. Paraplegia Spinal cord compression Transverse myelitis Spinal dysraphism Neuroimaging III Spinal Cord.pdf

^[2] Lecture slides: GC 110. Paraplegia Spinal cord compression Transverse myelitis Spinal dysraphism Neuroimaging III Spinal Cord.pdf

^[3] Lecture slides: GC 110. Paraplegia Spinal cord compression Transverse myelitis Spinal dysraphism Neuroimaging III Spinal Cord.pdf

^[4] Lecture slides: GC 110. Paraplegia Spinal cord compression Transverse myelitis Spinal dysraphism Neuroimaging III Spinal Cord.pdf

Spinal Cord Injuries

A spinal cord injury (SCI) is damage to the spinal cord that results in temporary or permanent changes in its motor, sensory, and/or autonomic function below the level of the lesion. The term breaks down from Latin/Greek roots: "spinal" (from Latin spina = thorn/backbone), "cord" (the cylindrical neural structure within the vertebral canal), and "injury" (from Latin injuria = wrongful damage).

SCI can be:

Primary injury: the immediate mechanical disruption of neural tissue at the time of trauma (contusion, laceration, compression, distraction) — this is essentially irreversible at the moment it occurs.
Secondary injury: the cascade of ischaemia, oedema, inflammation, excitotoxicity, and apoptosis that follows the primary insult, causing delayed neurological deterioration ^[1]. This is the window where early intervention can make a difference.

"Acute paraplegia is an EMERGENCY" — the spinal cord is "very unforgiving," and sphincter dysfunction represents a point of no return ^[1].

Key Concept

The distinction between primary and secondary injury is critical: you cannot undo primary mechanical damage, but you CAN mitigate secondary injury through rapid immobilisation, haemodynamic optimisation, and timely surgical decompression.

2. Epidemiology

Global incidence: approximately 250,000–500,000 new SCI cases per year worldwide (WHO estimate). Traumatic SCI incidence is roughly 10–80 per million population per year depending on region.
Hong Kong: SCI incidence is approximately 20–30 per million per year. Queen Mary Hospital and Princess Margaret Hospital are the major SCI referral centres.
Prevalence: due to improved survival, the global prevalence of SCI is rising; estimated 2–3 million people living with SCI worldwide.

Bimodal distribution ^[2]:
- Young adults (15–35 years): predominantly high-energy trauma (road traffic accidents, falls from height, sports injuries, assaults) ^[2]
- Older adults (≥ 65 years): predominantly low-energy trauma in the setting of osteoporotic bone and pre-existing spinal stenosis (meaning a minor fall can cause cord injury in an already narrow canal) ^[2]
Male:Female ratio ≈ 3–4:1 (young males are overrepresented due to high-risk behaviours and occupational hazards)

Falls (most common overall, especially in children and the elderly) ^[3]
Road traffic accidents (RTA) (most common cause of death < 40) ^[4]^[3]
Assaults (knife/bullet injuries — these produce specific injury patterns such as Brown-Séquard syndrome) ^[1]^[5]
Sports/recreation-related injuries (diving into shallow water, rugby, equestrian)
In Hong Kong, falls from height (especially construction-related) and RTAs are the leading causes.

50% cervical ^[6] — this is the most mobile segment of the spine and has the least bony protection relative to the range of movement
15% associated with non-adjacent level injuries ^[6] — meaning if you find one spinal fracture, you must image the entire spine because there may be another fracture elsewhere
25% associated with other organ injuries ^[6] — polytrauma is the norm, not the exception

Polytrauma involves injuries to the spine in up to 30% of cases. Multiple spinal fractures occur in 3 to 5% — examine and XR the whole spine. ^[2]

Exam Pearl

A common mistake is to stop looking after finding one spinal fracture. Up to 15% of spinal injuries are non-contiguous (at a different level), and polytrauma patients may have 2–3 fractures. Always image the whole spine.

Category	Risk Factors	Mechanism
Demographic	Young males (15–35), elderly (≥ 65)	High-energy behaviour; osteoporotic/stenotic spine
Pre-existing spinal disease	Pre-existing spinal stenosis, cervical spondylosis, OPLL, ankylosing spondylitis	Already narrowed canal → minor trauma causes disproportionate cord injury
Bone quality	Osteoporosis, metabolic bone disease, chronic steroid use	Vertebral body fractures occur with minimal force
Connective tissue disorders	Down syndrome (absent/lax transverse ligament), Marfan syndrome, Ehlers-Danlos	Ligamentous hyperlaxity → atlantoaxial instability
Inflammatory	Rheumatoid arthritis (atlantoaxial subluxation), ankylosing spondylitis (bamboo spine)	Weakened transverse ligament (RA); rigid ankylosed spine fractures like a long bone (AS)
Behavioural	Alcohol/drug intoxication, high-risk sports, occupational hazards (construction workers)	Impaired judgment, high-energy mechanisms
Iatrogenic	Spinal surgery, intubation in unstable C-spine	Direct mechanical injury during procedures

4. Anatomy and Function of the Spinal Cord

Understanding the anatomy is essential because the clinical features of SCI are a direct map of which tracts and segments are damaged.

33 vertebrae: 7 cervical, 12 thoracic, 5 lumbar, 5 sacral (fused), 4 coccygeal (fused)
The spinal cord ends at approximately L1-L2 (conus medullaris) in adults. Below this, the cauda equina (Latin: "horse's tail") — a bundle of nerve roots, not spinal cord — occupies the vertebral canal.
Critical clinical implication: injuries above L1 cause spinal cord syndromes (UMN); injuries below L2 cause cauda equina syndrome (pure LMN) ^[7]^[8].

This is used for assessing stability of the lower cervical spine and thoracolumbar spine ^[3]:

Column	Components
Anterior column	Anterior 2/3 of vertebral body, disc, and anterior longitudinal ligament (ALL)
Middle column	Posterior 1/3 of vertebral body, disc, and posterior longitudinal ligament (PLL)
Posterior column	Remaining posterior arch (pedicles, laminae, facet joints, spinous processes, interspinous and supraspinous ligaments)

Unstable fracture if 2/3 segments are disrupted ^[3]. This is the key principle — if two or more columns are broken, the spine cannot hold itself together and the cord is at risk of further damage from instability.

The cross-section of the spinal cord contains:

Structure	Location	Function	What happens if damaged?
Corticospinal tract (lateral)	Lateral white matter	Voluntary motor (UMN) — fibres have already crossed in the medullary pyramids	Ipsilateral UMN weakness below the lesion (spasticity, hyperreflexia, upgoing plantars)
Dorsal columns (gracilis & cuneatus)	Posterior white matter	Proprioception, vibration, fine touch — fibres ascend ipsilaterally, cross in medulla	Ipsilateral loss of proprioception and vibration below lesion
Spinothalamic tract	Anterolateral white matter	Pain and temperature — fibres cross within 1–2 segments of entering the cord	Contralateral loss of pain and temperature (the crossing happens at the level of entry, which matters for central cord syndrome)
Anterior horn cells	Central grey matter (ventral)	LMN cell bodies	LMN signs at the level of lesion (flaccid weakness, fasciculations, areflexia)
Intermediolateral cell column	Lateral grey matter (T1–L2)	Sympathetic preganglionic neurons	Autonomic dysfunction (neurogenic shock, autonomic dysreflexia)
Sacral parasympathetic nuclei	S2–S4	Bladder, bowel, sexual function	Bladder/bowel/sexual dysfunction

Anterior spinal artery (ASA): supplies the anterior 2/3 of the cord (corticospinal tracts, spinothalamic tracts, anterior horns). This is a single vessel — a "watershed" area vulnerable to ischaemia.
Paired posterior spinal arteries (PSA): supply the posterior 1/3 (dorsal columns).
Segmental radicular arteries: feed into the ASA and PSA. The most important is the artery of Adamkiewicz (usually arises T9–T12 on the left) — occlusion causes devastating anterior cord syndrome.
Venous drainage: internal vertebral venous plexus (Batson's plexus) — valveless, which is why metastases from prostate, breast, lung, kidney, and thyroid spread to the spine so readily.

Why does anterior cord syndrome spare proprioception?

Because proprioception travels in the dorsal columns, which are supplied by the posterior spinal arteries. Anterior spinal artery occlusion therefore spares them while destroying motor function and pain/temperature sensation.

Dermatome	Landmark
C4	Clavicle / shoulder cape
C6	Thumb
C7	Middle finger
C8	Little finger
T4	Nipple line
T10	Umbilicus
L1	Inguinal ligament
L4	Medial leg / knee
L5	Dorsum of foot / great toe
S1	Lateral foot / sole
S2-S4	Perianal ("saddle") area

Root	Key Muscle	Action
C5	Biceps/deltoid	Elbow flexion
C6	Wrist extensors	Wrist extension
C7	Triceps	Elbow extension
C8	Finger flexors (FDP to middle finger)	Finger flexion
T1	Hand intrinsics (abductor digiti minimi)	Finger abduction
L2	Iliopsoas	Hip flexion
L3	Quadriceps	Knee extension
L4	Tibialis anterior	Ankle dorsiflexion
L5	Extensor hallucis longus	Great toe extension
S1	Gastrocnemius/soleus	Ankle plantarflexion

The diaphragm is innervated by the phrenic nerve (C3-C5). This is clinically critical:

Respiratory arrest if injury above C3 (loss of control of diaphragm → cannot breathe at all) ^[8]
Diaphragmatic breathing if C5 or below (loss of control of intercostal muscles, but diaphragm preserved) ^[8]
Paradoxical ventilation ^[6]: when intercostal muscles are paralysed, diaphragmatic contraction during inspiration draws the rib cage inward instead of expanding it — the chest and abdomen move out of phase.

C3, 4, 5 keeps the diaphragm alive

This classic mnemonic reminds you that C3-5 injuries are life-threatening because they compromise diaphragmatic function. Any cervical SCI patient needs immediate airway assessment.

5. Etiology (Focus on Hong Kong)

Trauma is the commonest cause of acute paraplegia ^[1]^[7].

Mechanism	Examples	Hong Kong Context
Falls	Falls from height (construction), falls at home (elderly)	Leading cause in HK — construction industry falls, elderly falls at home
RTA	Motor vehicle collisions, motorcycle accidents, pedestrian struck	Second most common; high-speed collisions on highways
Assault	Stab wounds (knife), gunshot wounds	Gang fights with chopped/stabbed wounds can cause nerve and vascular injury ^[5]
Sports	Diving into shallow water, rugby, equestrian	Diving injuries particularly cause cervical SCI
Iatrogenic	Surgical positioning, epidural haematoma post-spinal anaesthesia	Rare but important

Category	Examples	Notes
Degenerative	Spondylotic myelopathy (MC non-traumatic), OPLL	Very common in elderly HK population; chronic canal narrowing
Neoplastic	Primary or secondary tumours	Metastases from paired organs: thyroid, breast, lung, kidney, prostate (spread via Batson's plexus) ^[7]
Infective	TB spine (Pott's disease), epidural abscess, spondylodiscitis, viral myelitis	TB spine is particularly relevant in HK due to higher prevalence of TB compared to Western countries
Inflammatory	Transverse myelitis, MS, NMO, radiation myelopathy, paraneoplastic myelopathy	MS less common in HK Chinese population vs Caucasians; NMO (Devic's) relatively more common in Asians
Vascular	Spinal infarct (anterior spinal artery syndrome), vascular malformations (AVM, dural AVF)	Spinal infarct may follow aortic surgery or hypoperfusion states
Congenital/Developmental	Spinal dysraphism, syringomyelia, hereditary spastic paraplegia, Friedreich's ataxia	Spina bifida incidence reduced by folate supplementation
Degenerative (neurological)	MND, spinocerebellar ataxia	Progressive, no acute presentation
Metabolic	Subacute combined degeneration (B12 deficiency)	Combined posterior and lateral column disease
Disc herniation	Prolapsed intervertebral disc (PID)	L4/5 and L5/S1 most common levels; can cause cauda equina if massive central herniation

Common causes of paraplegia: Spinal trauma, Spinal tumours, Degenerative conditions, Infection, Spinal dysraphism ^[1]

6. Pathophysiology

These are the immediate mechanical forces applied to the cord at the moment of injury:

Compression: most common — fractured vertebral body or disc material pushes into the cord. Think of a burst fracture where bone fragments retropulse into the canal.
Contusion: cord is bruised by transient compression/impact. The cord bounces back to normal position but the internal damage is done — central haemorrhagic necrosis of grey matter with relative white matter sparing (explains central cord syndrome).
Laceration/transection: complete or partial cutting of the cord (e.g., knife or bullet wound — produces Brown-Séquard).
Distraction: the cord is stretched longitudinally beyond tolerance (e.g., seatbelt injuries, hangings).
Vascular disruption: tearing of vessels supplying the cord → ischaemia.

After the primary insult, a devastating cascade unfolds over hours to weeks:

Key points:

Ischaemia is the main driver of secondary injury — the cord's blood supply is disrupted and autoregulation fails
Excitotoxicity: damaged neurons release excessive glutamate → overactivation of NMDA receptors → massive calcium influx → cell death
Inflammation: neutrophils infiltrate within hours, followed by macrophages — this initially worsens damage but is also necessary for debris clearance
Oedema: vasogenic and cytotoxic oedema expand the zone of injury cranially and caudally
Glial scar: astrocytes form a barrier (the "glial scar") that prevents axonal regeneration — this is why spinal cord injuries are so permanent

Secondary neurological injury occurs from instability due to bony and ligamentous injuries, and haematoma → this leads to delayed neurological deterioration ^[1]

Why is early immobilisation so important?

Because secondary injury is worsened by ongoing mechanical instability. If a spine is unstable (2/3 columns disrupted), any movement allows further compression, distraction, and vascular disruption of the already-injured cord. This is why we immobilise first and investigate later.

Spinal shock has TWO meanings ^[1]:

Meaning	Mechanism	Clinical Features	Duration
1. Neurological spinal shock	Flaccid paralysis and areflexia for 1–2 weeks after injury — peripheral neurons become temporarily unresponsive to brain stimuli due to sudden loss of tonic descending excitatory input	Flaccid paralysis (NOT spastic), absent deep tendon reflexes, absent bulbocavernosus reflex	1–2 weeks (then hyperreflexia of UMN lesion occurs later) ^[1]
2. Neurogenic (haemodynamic) shock	Interruption of sympathetics → loss of vasomotor tone below the lesion (T1–L2 sympathetic outflow disrupted)	Vasodilatation → hypotension, bradycardia (because unopposed vagal tone), warm flushed skin (unlike hypovolaemic shock where skin is cold and clammy)	Days to weeks

Treatment of neurogenic shock: IV fluids and vasopressors/inotropes ^[1]

Feature	Spinal Shock	Neurogenic Shock
BP/Pulse	Hypotension, Bradycardia	Hypotension, Bradycardia
Bulbocavernosus reflex	Absent	Present
Motor	Flaccid paralysis	Normal (motor deficit is from the cord injury itself, not the shock)

The bulbocavernosus reflex (squeeze glans penis or tug on Foley catheter → anal sphincter contraction) is the first reflex to return after spinal shock resolves. Its return signals the end of spinal shock — at that point, whatever deficits remain are likely permanent.

Don't confuse these two!

Students commonly conflate neurological spinal shock (a period of areflexia) with neurogenic shock (a cardiovascular state of hypotension + bradycardia from sympathetic disruption). They are different phenomena that can coexist. Also, don't confuse neurogenic shock with hypovolaemic shock — in neurogenic shock, the patient is warm and bradycardic; in hypovolaemic shock, the patient is cold and tachycardic.

This is a chronic complication but worth understanding the pathophysiology now ^[8]:

Lesion at or above T6 disrupts descending sympathetic regulation
A noxious stimulus below the lesion (full bladder, constipation, skin pressure) generates a massive afferent signal
This triggers a reflex sympathetic discharge below the lesion → vasoconstriction → severe hypertension (the brain cannot send inhibitory signals down through the damaged cord)
The brain detects the hypertension via baroreceptors → sends vagal reflex → bradycardia + vasodilation above the lesion only (because the sympathetic inhibition cannot pass through the cord lesion)
Result: paroxysmal HTN, throbbing headache, excessive sweating and flushing above the lesion, bradycardia, anxiety ^[8]

7. Classification

The American Spinal Injury Association (ASIA) Impairment Scale classifies the severity of SCI:

Sensory: test pinprick and touch in each dermatome Motor: test the 10 key motor functions ^[1]^[6]

Grade	Type	Description
A	Complete	No motor, No sensory, No sacral sparing below the neurological level
B	Incomplete	No motor, sensory only preserved below the level (including sacral segments S4-S5)
C	Incomplete	Motor function preserved below level, but > 50% of key muscles below the level have a muscle grade < 3 (cannot raise arms or legs off bed)
D	Incomplete	Motor function preserved below level, and ≥ 50% of key muscles below the level have a muscle grade ≥ 3 (can raise arms or legs off bed)
E	Normal	Motor and sensory function are normal

Sacral Sparing — The Key Distinction

The difference between ASIA A (complete) and ASIA B (incomplete) is sacral sparing — if the patient has any sensation at S4-S5 (perianal area) or voluntary anal contraction, the injury is INCOMPLETE. This matters enormously for prognosis because incomplete injuries have far better recovery potential.

Complete injury — prognosis is generally poor. Incomplete injury — prognosis highly variable. ^[1]

Level	Term	Key Features
C1–C4	High cervical tetraplegia	Respiratory failure (C3-5 → phrenic nerve), ventilator-dependent
C5–C8	Low cervical tetraplegia	Upper and lower limb involvement, variable hand function
T1–T12	Paraplegia	Lower limbs affected, upper limbs spared; above T6 → risk of autonomic dysreflexia
L1–L2	Conus medullaris	Mixed UMN + LMN signs, early bladder/bowel involvement
Below L2	Cauda equina	Pure LMN, saddle anaesthesia, bladder/bowel dysfunction

7.3 By Spinal Cord Syndrome — Clinical Patterns

These are the classic incomplete cord syndromes ^[7]^[8]:

Features: Loss of all sensory modality below lesion; LMN loss at level, UMN loss below level; Spastic bladder (or DSD)
Causes: Trauma, transverse myelitis, acute compression; Benign tumours, spondylosis
Pathophysiology: complete disruption of all ascending and descending tracts

Features: Loss of pain and temperature below; UMN loss below with spastic bladder
Causes: SC infarct, prolapsed disc; Radiation myelopathy, HTLV-1
Pathophysiology: anterior spinal artery occlusion → infarction of the anterior 2/3 of the cord (corticospinal tracts + spinothalamic tracts + anterior horns). Dorsal columns are spared because they are supplied by posterior spinal arteries.

Features: Loss of proprioception and vibration below; Variable weakness and bladder dysfunction
Causes: Epidural metastasis; Spondylosis, MS, subacute combined degeneration, Friedreich's ataxia
Pathophysiology: damage to dorsal columns. Motor function relatively preserved because corticospinal tracts are lateral.

Features: Ipsilateral weakness + loss of proprioception; Contralateral loss of pain and temperature
Causes: Knife or bullet injury; Tumour, spondylosis, MS, radiation necrosis
Pathophysiology: hemisection of the cord. Motor tracts (corticospinal) and dorsal columns have already crossed above (or don't cross until the brainstem), so damage is ipsilateral. Spinothalamic tracts cross within 1–2 segments of entry, so the contralateral pain/temperature loss is from fibres that have already crossed from the opposite side.
Best prognosis of all incomplete syndromes (because at least half the cord is intact)

Features: Segmental suspended spinothalamic loss; Segmental ± UL > LL long-tract weakness; ± "cape-like" loss of pain and temperature
Causes: Spinal stroke, traumatic contusion, transverse myelitis; Syringomyelia, intramedullary tumour
Pathophysiology: the central cord is damaged first. The spinothalamic fibres cross centrally (in the anterior white commissure) → suspended (segmental) pain/temperature loss at the level of the lesion. The corticospinal tract is arranged somatotopically with cervical fibres medially and sacral fibres laterally (lamination) → central damage preferentially affects upper limb motor fibres → UL weakness > LL weakness. In syringomyelia, the expanding syrinx gradually destroys crossing spinothalamic fibres → "cape-like" dissociated sensory loss.
Most common incomplete SCI in the elderly — typically from hyperextension injury in a patient with pre-existing cervical spondylosis.

Features: Mixed LMN + UMN signs + saddle anaesthesia; Paralytic bladder and bowel incontinence
Causes: Prolapsed IVD, trauma; Tumours
Pathophysiology: the conus (L1-L2 level) contains the sacral parasympathetic outflow (S2-4) and the terminal portion of the cord where UMN and LMN overlap → mixed picture. Early bladder/bowel involvement because the sacral micturition centre is located here.

Features: Pure LMN signs + saddle anaesthesia; Paralytic bladder and bowel incontinence
Causes: Prolapsed IVD (L4/5, L5/S1); Tumours, spinal stenosis
Pathophysiology: below L2, there is no spinal cord — only nerve roots (cauda equina). Compression produces purely peripheral nerve damage (LMN). Compression of cauda equina (below L2) ^[7].
Key difference from conus: no UMN signs; pain is more prominent and radicular; bladder involvement may present later but is often irreversible once established.

Conus vs Cauda Equina

Feature	Conus Medullaris	Cauda Equina
Motor	Mixed UMN + LMN	Pure LMN
Pain	Less prominent, bilateral	Prominent, often unilateral/radicular
Bladder/bowel	Early, severe	Late, but irreversible
Sensory	Saddle, bilateral, symmetric	Saddle, may be asymmetric
Reflexes	Variable (UMN and LMN mixed)	Absent (LMN)

7.4 AO Classification of Cervical Spine Fractures [3]

Region	Injury Type
Type 1: Occipital condyle, cranio-cervical junction	Type A: Bony injury only
Type 2: C1 ring, C1/2 joint	Type B: Tension band injuries
Type 3: C2 and C2/3 joint	Type C: Translation injuries

Injury Type
Type A: Compression injuries
Type B: Distraction injuries
Type C: Translation injuries
Type F: Facet joint injuries

Stable injury: ligaments not damaged ^[6]
Unstable injury: ligaments disrupted ^[6]
Mechanism of injury helps determine degree of stability ^[6]

Clinical signs of instability:

"Step over spinous processes" for any tenderness, swelling or gap between spinous processes ^[6] — a gap indicates rupture of the interspinous ligament (i.e., unstable injury)

8. Clinical Features

8.1 Symptoms

Symptom	Pathophysiological Basis
Weakness/paralysis of limbs below the lesion	Disruption of descending corticospinal tracts → loss of voluntary motor commands to anterior horn cells below the level
Tetraplegia (all four limbs)	Cervical cord injury → both upper and lower limb corticospinal tracts interrupted
Paraplegia (lower limbs only)	Thoracic or lumbar cord injury → lower limb corticospinal tracts interrupted, upper limbs spared
Clumsiness/loss of fine motor control	Damage to corticospinal tract (which carries fine, fractionated finger movements) and/or dorsal columns (loss of proprioceptive feedback)
Upper limb > lower limb weakness (central cord)	Central cord syndrome — somatotopic arrangement of corticospinal tract with cervical fibres medially → damaged first by central lesion

Symptom	Pathophysiological Basis
Numbness/anaesthesia below a sensory level	Disruption of ascending sensory tracts (spinothalamic and/or dorsal columns)
Paraesthesia (tingling/pins and needles)	Partial damage to sensory tracts → aberrant signal transmission
Saddle anaesthesia	Damage to S2-S4 nerve roots or conus → loss of sensation in perineum, inner thighs, and perianal area
Band-like sensation at the level of injury	Segmental irritation of dorsal root at the level of the lesion
Dissociated sensory loss	Selective tract damage: anterior cord → lose pain/temperature but keep proprioception; dorsal cord → lose proprioception but keep pain/temperature
"Cape-like" loss of pain and temperature	Central cord / syringomyelia → crossing spinothalamic fibres at multiple segmental levels destroyed → bilateral suspended sensory loss in a cape distribution

Symptom	Pathophysiological Basis
Painless acute retention of urine (AROU)	Loss of descending control to sacral micturition centre (S2-4) → detrusor cannot contract; loss of sensation → patient doesn't feel the full bladder ^[1]^[6]
Overflow urinary incontinence	Bladder fills beyond capacity → passive overflow due to paralysed detrusor
Faecal incontinence / constipation	Loss of voluntary control of external anal sphincter and disruption of colonic motility
Sexual dysfunction / impotence	Disruption of parasympathetic (S2-4 erection) and sympathetic (T11-L2 ejaculation) pathways
Priapism	Loss of sympathetic tone → unopposed parasympathetic vasodilation of penile blood vessels → sustained erection ^[6] — this is an ominous sign of severe SCI
Respiratory difficulty	Cervical injuries → loss of intercostal muscle function (T1-T12) and/or diaphragm (C3-5)

Pain Type	Pathophysiological Basis
Back/neck pain at the level of injury	Bony, ligamentous, and soft tissue damage; nerve root compression
Radicular pain (shooting, dermatomal)	Compression or irritation of individual nerve roots at the fracture level
Neuropathic pain (burning, electric)	Damage to spinothalamic tract and/or posterior horn → aberrant pain signalling

8.2 Signs

During spinal shock phase (first 1–2 weeks):

Sign	Pathophysiological Basis
Flaccid paralysis below the lesion	Spinal shock → temporary complete loss of all reflex activity below the lesion due to sudden withdrawal of tonic descending facilitation ^[1]
Areflexia (absent deep tendon reflexes)	Same mechanism — the reflex arc's excitability depends on descending supraspinal facilitation, which is suddenly lost
Absent bulbocavernosus reflex	The sacral reflex arc is temporarily suppressed

After spinal shock resolves (weeks to months):

Sign	Pathophysiological Basis
Spastic paralysis below the lesion	Hyperreflexia of UMN lesion occurs later ^[1] — loss of descending inhibitory pathways → anterior horn cells become hyperexcitable
Hyperreflexia	Loss of inhibitory UMN influence on spinal reflex arcs → exaggerated stretch reflexes
Clonus	Sustained rhythmic involuntary contraction due to hyperexcitable stretch reflex loop
Upgoing plantars (Babinski sign)	Loss of corticospinal tract input → primitive flexion withdrawal reflex (normally suppressed) re-emerges
Increased muscle tone / spasticity	Loss of descending inhibition → increased gamma motor neuron activity → increased muscle spindle sensitivity
LMN signs at the level of the lesion	Destruction of anterior horn cells at the injury level → flaccid weakness, muscle wasting, fasciculations at that specific segment

Sign	Pathophysiological Basis
Sensory level (sharp dermatomal boundary)	All ascending sensory fibres interrupted at a specific cord level → sensory loss below, normal above. The highest intact dermatome defines the "sensory level."
Segmental sensory loss at the level	Damage to entering dorsal root fibres at the injury level
Dissociated sensory loss	Selective tract involvement — depends on which syndrome
Lhermitte's sign (electric shock sensation down spine with neck flexion)	Demyelinated dorsal columns in the cervical cord are mechanically sensitive → flexion stretches them → paroxysmal discharge

Sign	Pathophysiological Basis
Neurogenic shock: hypotension, bradycardia, warm flushed skin	Interruption of sympathetics → loss of vascular tone (vasodilatation) and loss of cardiac sympathetic drive (T1-T4) → unopposed vagal bradycardia ^[1]^[8]
Paradoxical ventilation	When intercostal muscles are paralysed, diaphragmatic muscle contraction during inspiration draws the rib cage inward ^[6]
Diaphragmatic breathing	Loss of intercostal muscle innervation → sole reliance on diaphragm for ventilation
Lax anal tone	Loss of S2-4 innervation to external anal sphincter → flaccid ^[1]^[6]
Priapism	Loss of sympathetic tone → unopposed parasympathetic → sustained erection ^[6]
Distended bladder (palpable/percussable)	AROU from neurogenic bladder
Ileus / absent bowel sounds	Neurogenic ileus — loss of autonomic input to bowel → atonic gut
Poikilothermia (body temperature varies with environment)	Impaired thermoregulation ^[8] — loss of sympathetic control of cutaneous vasomotor responses and sweating below the lesion
Pressure sores	Loss of sensation → patient cannot feel prolonged pressure → tissue ischaemia → ulceration ^[8]

Initial Assessment Checklist for SCI

On initial assessment, look for ^[6]:

"Step over spinous processes" for tenderness, swelling, or gap
Neurogenic shock signs: paradoxical ventilation, bradycardia, hypotension
Neurological deficits: flaccid limbs, sensory level
Anogenital signs: painless AROU, lax anal tone, priapism

A 28-year-old man sustained a fall from height. On admission, he was fully conscious. He was unable to move his lower limbs. His upper limbs were normal. ^[1]

What other symptoms and signs should you look for? UMN/LMN signs; sensory level & segmental loss; saddle anaesthesia; AROU; lax anal tone; spinal shock ^[1]

What was the likely level of spinal cord injury? Likely below T1; see sensory level ^[1]

What was the extent of injury? Determined by ASIA classification — need to assess motor and sensory function systematically.

9. Special Considerations

Detrusor sphincter dyssynergia (DSD) ^[8]^[9]:

Cause: spinal cord injury, pontine stroke
Mechanism: interruption of descending control by pontine micturition centre → failure of detrusor-sphincter coordination → synchronous contraction of both detrusor and sphincters
Consequence: ↑↑urinary tract pressure → upper tract damage

This is different from the initial areflexic bladder during spinal shock (where the detrusor is flaccid). After spinal shock resolves:

Suprasacral lesion → spastic (reflex) bladder with DSD
Sacral lesion / cauda equina → flaccid (paralytic) bladder → overflow incontinence

Patients with long-term indwelling catheters have a 16–20x risk of developing SCC (squamous cell carcinoma) in the bladder (NOT UCC, because of chronic irritation by catheter in bladder) ^[10].

Spinal cord injury: sensory level, motor deficits, anal tone should be assessed as part of head injury evaluation ^[3]. In polytrauma, always assume a spinal injury until proven otherwise.

Long-term issues include: dysreflexia, neurogenic bladder, spasticity, contracture, and skin problems ^[1]

High Yield Summary

SCI = primary (irreversible) + secondary (preventable) injury. Early immobilisation and haemodynamic support reduce secondary damage.
Epidemiology: bimodal (young males — high energy trauma; elderly — low energy + stenosis). 50% cervical. 15% non-contiguous. Always image the whole spine.
Three-column theory: unstable if ≥ 2/3 columns disrupted.
Spinal shock ≠ Neurogenic shock: Spinal shock = flaccid paralysis + areflexia (1–2 weeks). Neurogenic shock = hypotension + bradycardia from sympathetic disruption. Key differentiator: bulbocavernosus reflex absent in spinal shock, present in neurogenic shock.
ASIA classification: A = complete (no sacral sparing); B = sensory only; C = motor < grade 3 in > 50%; D = motor ≥ grade 3 in ≥ 50%; E = normal. Sacral sparing differentiates A from B.
Cord syndromes: Complete, Anterior (lose pain/temp + motor, keep proprioception), Dorsal (lose proprioception, keep motor), Brown-Séquard (ipsilateral motor + proprioception, contralateral pain/temp — best prognosis), Central (UL > LL weakness, cape-like sensory loss — most common in elderly with spondylosis), Conus (mixed UMN/LMN + early bladder), Cauda equina (pure LMN + saddle anaesthesia).
C3, 4, 5 keeps the diaphragm alive — injuries above C3 → respiratory arrest.
Autonomic dysreflexia: lesion at or above T6, noxious stimulus below → reflex sympathetic surge → severe HTN + bradycardia.
Initial assessment: step over spinous processes, neurogenic shock signs, neurological deficits (flaccid limbs + sensory level), anogenital signs (AROU, lax anal tone, priapism).
Prognosis: Complete injury — recovery rare. Incomplete injury — most recovery within 6 months. Loss of sphincter function is a poor prognostic factor. Methylprednisolone is NOT recommended (higher morbidity).
Long-term problems: autonomic dysreflexia, neurogenic bladder (DSD), spasticity, contractures, pressure sores, impaired thermoregulation.

Active Recall - Spinal Cord Injuries

^[1] Lecture slides: GC 110. Paraplegia Spinal cord compression Transverse myelitis Spinal dysraphism Neuroimaging III Spinal Cord.pdf ^[2] Lecture slides: GC 227. Cervical Spine Pathology.pdf (slides on epidemiology and polytrauma) ^[3] Senior notes: maxim.md (Section 2.7 Spine trauma) ^[4] Senior notes: Ryan Ho Radiology.pdf (p1 — Trauma deaths) ^[5] Lecture slides: GC 182. Chopped and stabbed wound in gang fight Nerves and vascular injury; Classification of injuries.pdf ^[6] Senior notes: Ryan Ho Neurology.pdf (Section 9.6 Spinal Trauma, p176-177) ^[7] Senior notes: maxim.md (Section 2.3 Approach to spine diseases — Cauda equina syndrome) ^[8] Senior notes: Ryan Ho Fundamentals.pdf (Section 3.4.9 Paraplegia, p334-335) ^[9] Senior notes: Ryan Ho Urogenital.pdf (p164 — Detrusor sphincter dyssynergia) ^[10] Senior notes: felixlai.md (Section on bladder cancer risk factors — SCC in SCI patients)

Differential Diagnosis of Spinal Cord Injury

When a patient presents with acute neurological deficit suggestive of spinal cord dysfunction — weakness, sensory level, sphincter disturbance — the differential diagnosis is not simply "trauma vs. not trauma." The real clinical challenge is threefold:

Is this truly a spinal cord lesion? (vs. brain, peripheral nerve, NMJ, or functional)
If spinal cord, what is the aetiology? (trauma, tumour, infection, vascular, inflammatory, degenerative, congenital)
Is there a surgically treatable compressive lesion? (because this is a time-critical emergency)

The approach hinges on the tempo of onset (acute vs. subacute vs. chronic), the pattern of deficit (which cord syndrome), and the clinical context (trauma, cancer history, immunosuppression, etc.).

"The spinal cord is very unforgiving. Acute paraplegia is an EMERGENCY. Sphincter dysfunction — a point of no return." ^[1]

Before committing to a spinal cord differential, you must confirm the lesion is actually in the cord and not elsewhere. The clinical features of a spinal cord lesion are distinctive ^[11]:

Spinal Cord	Brain (Hemispheric / Brainstem)	Peripheral Nerve / Cauda Equina
UMN signs below level, LMN at level	Contralateral UMN + higher cortical deficits (aphasia, neglect) or cranial nerve palsies (brainstem)	Pure LMN signs (flaccid, areflexic, wasting)
Sensory level on trunk	Hemisensory loss (face + arm + leg on same side)	Dermatomal / peripheral nerve distribution
Sphincter disturbance (early in conus, late in cord)	Sphincters usually spared (cortical lesions rarely cause incontinence acutely unless bilateral)	Sphincter dysfunction in cauda equina (late, irreversible)
Bilateral leg involvement common	Usually unilateral (hemiplegia)	May be unilateral or bilateral, asymmetric
No cranial nerve involvement	Cranial nerve involvement (brainstem) or cortical signs	No cranial nerve involvement

Key mimics of spinal cord disease ^[12]^[13]:

Stroke or TIA: occurs more rapidly, typically "negative" symptoms (weakness/numbness rather than tingling), unilateral, associated cortical signs ^[13]
Migraine aura: spreading tingling or paraesthesia followed by numbness, evolves over 20–30 minutes over one half of body ^[13]
Guillain-Barré syndrome (GBS): ascending weakness with areflexia, but sensory level is absent; CSF shows albuminocytological dissociation
Bilateral cerebral lesions (e.g., parasagittal meningioma, bilateral ACA territory infarct): can cause bilateral leg weakness mimicking paraplegia, but typically with cortical features
Psychogenic / functional: bizarre distribution not conforming to known anatomical patterns ^[13]

How to Tell Cord from Cauda Equina

Both cause weakness + sensory loss + sphincter problems. The key difference: cord = UMN signs (spastic, hyperreflexic, upgoing plantars) with a sensory level. Cauda equina = LMN signs (flaccid, areflexic) with saddle anaesthesia and radicular pain. In practice, the conus medullaris at L1-2 can give a mixed picture.

Step 2: Differential Diagnosis by Tempo of Onset

This is the most clinically useful way to organise the differential, because the speed of onset narrows the aetiology dramatically ^[6]^[8]:

Aetiology	Key Features	Why It Presents Acutely
Spinal trauma	History of trauma, bony tenderness, neurogenic shock	Direct mechanical destruction of cord tissue at the moment of impact
Spinal infarct (anterior spinal artery syndrome)	Sudden onset, anterior cord syndrome (motor + pain/temp loss, proprioception spared), risk factors: DM, AF, aortic surgery, hypotension ^[8]^[11]	Vascular occlusion → immediate ischaemic necrosis of the anterior 2/3 of cord (analogous to a stroke but in the cord)
Spinal epidural/subdural haematoma	Anticoagulant use, post-procedure, sudden back pain → progressive deficit	Rapid blood accumulation compresses the cord
Acute disc herniation (massive central)	Preceded by back pain, heavy lifting; cauda equina or conus syndrome	Large disc fragment suddenly compresses neural elements
Vascular malformation (AVM) with haemorrhage	Sudden deficit ± subarachnoid haemorrhage (SAH)	Rupture of abnormal vessels → haemorrhage into or around the cord

Aetiology	Key Features	Why It Presents Subacutely
Transverse myelitis	Acute/subacute progressive paraparesis, sensory level, autonomic dysfunction; may be idiopathic or a/w MS, NMO, SLE ^[14]	Inflammatory demyelination and oedema evolve over days
Epidural abscess	Fever, severe back pain, progressive neurological deficit; risk factors: IVDU, immunosuppression, diabetes	Infection forms and enlarges over days, causing progressive compression and direct cord inflammation
Spondylodiscitis / TB spine (Pott's disease)	Subacute back pain, constitutional symptoms, kyphosis; cord compression present at diagnosis in 40–70% ^[15]	Vertebral body destruction + abscess formation → gradual cord compression; TB classically disc-sparing early
Viral myelitis	Post-viral prodrome, rapidly ascending weakness	Direct viral invasion or post-infectious immune-mediated damage
Acute cord compression from metastasis	Known cancer, progressive back pain worse at night/lying down, rapid neurological deterioration	Tumour grows or pathological fracture collapses → acute-on-chronic compression
Guillain-Barré syndrome (mimic)	Ascending weakness, areflexia, no sensory level	Autoimmune peripheral nerve demyelination — NOT cord, but must be excluded

Aetiology	Key Features	Why It Presents Chronically
Spondylotic (cervical) myelopathy	Most common cause of cervical cord lesion in pt > 50 years ^[8]; insidious gait unsteadiness, clumsy hands, myelopathic hand signs	Slow osteophyte growth / ligamentum flavum hypertrophy → gradual canal narrowing; cord adapts until a critical threshold
Primary or secondary tumours	Progressive deficit, worse at night (intradural tumours), weight loss; metastases from thyroid, breast, lung, kidney, prostate	Tumour growth is slow (primary) or stepwise (metastatic with pathological fracture)
Syringomyelia	Cape-like dissociated sensory loss, central cord syndrome, may be a/w Chiari I malformation	Slowly expanding fluid-filled cavity (syrinx) within the cord
Multiple sclerosis	Relapsing-remitting course, optic neuritis, Lhermitte's sign, periventricular lesions on brain MRI; d/dx includes neurofibroma, syringomyelia, early MND ^[8]	Inflammatory demyelinating plaques accumulate over time
Subacute combined degeneration	B12 deficiency → posterior + lateral column disease (loss of proprioception + vibration + UMN signs); megaloblastic anaemia, glossitis	Demyelination from impaired myelin synthesis due to lack of B12 as a cofactor in methionine synthase
Motor neurone disease (MND)	Pure motor (no sensory loss), combined UMN + LMN signs, fasciculations, bulbar symptoms	Progressive degeneration of motor neurons
Hereditary spastic paraplegia	Family history, slowly progressive spastic paraparesis, usually minimal sensory involvement	Genetic → axonal degeneration in corticospinal tracts
Friedreich's ataxia	Onset < 25 years, ataxia, absent reflexes (despite UMN signs), cardiomyopathy, scoliosis	Trinucleotide repeat → mitochondrial iron accumulation → dorsal columns + corticospinal tracts + cerebellum degeneration
Spinal dysraphism / tethered cord	History from birth, lumbosacral skin abnormalities, progressive LL weakness + bladder dysfunction with growth	Congenital failure of neural tube closure; tethering stretches the cord as the child grows
Radiation myelopathy	History of radiation therapy, delayed onset (months to years), progressive myelopathy	Radiation-induced vasculopathy and demyelination
HTLV-1 associated myelopathy	Tropical spastic paraparesis, slowly progressive, anterior cord pattern	Retroviral-induced chronic inflammation
Spinal stenosis	Neurogenic claudication (leg pain with walking, relieved by sitting/flexion), chronic	Degenerative narrowing of the spinal canal → positional compression

Differential diagnosis of back pain: Degeneration (spondylosis), Prolapsed intervertebral disc, Spinal stenosis, Cauda equina syndrome, Muscle/ligamentous injury (muscle strain), Fractures/injuries, Infection (TB spine, epidural abscess), Tumour (primary, metastases e.g. lung, breast, prostate), Inflammation (AS, PSA, RA), Extra-spinal causes/Referred pain (pancreatitis, AAA, uro/gynae causes, zoster) ^[3]

The clinical pattern tells you the location of the lesion within the cord, which in turn narrows the aetiological differential ^[6]^[8]:

Syndrome	Differential Diagnosis	Reasoning
Complete cord	Trauma, transverse myelitis, acute compression, benign tumours, spondylosis	Total cross-sectional cord destruction → only severe/complete insults produce this
Anterior cord	SC infarct, prolapsed disc, radiation myelopathy, HTLV-1	Anterior spinal artery territory → vascular or ventral compressive causes
Dorsal cord	Epidural metastasis, spondylosis, MS, subacute combined degeneration, Friedreich's ataxia	Posterior column selective damage → metabolic, compressive from behind, or inflammatory
Brown-Séquard	Knife or bullet injury, tumour, spondylosis, MS, radiation necrosis	Hemisection → penetrating trauma is classic; lateral tumours/plaques can also do this
Central cord	Spinal stroke, traumatic contusion, transverse myelitis, syringomyelia, intramedullary tumour	Central damage → hyperextension in spondylotic canal (elderly); expanding syrinx (young)
Pure motor	Poliomyelitis, motor neurone disease, hereditary spastic paraplegias	Only motor tracts/neurons affected, no sensory involvement
Conus medullaris	Prolapsed IVD, trauma, tumours	Lesion at L1-2; sacral autonomic nuclei involved early → early bladder/bowel
Cauda equina	Prolapsed IVD (L4/5, L5/S1), tumours, spinal stenosis, arachnoiditis	Below L2 → pure peripheral nerve roots

These are the conditions where delayed diagnosis leads to irreversible deficit:

Condition	Why It's Urgent	Key Clues
Epidural abscess	Cord compression + direct infection → irreversible paraplegia if not drained	Fever + back pain + progressive deficit; IVDU, DM, immunosuppression
Epidural haematoma	Expanding haematoma compresses cord	On anticoagulants, post-procedure, sudden back pain → rapid deficit
Cauda equina syndrome	"Point of no return" for sphincters; usually irreversible unless very early intervention ^[11]	Saddle anaesthesia, urinary retention, bilateral radicular pain
Metastatic cord compression	Tumour rapidly destroys cord; dexamethasone + urgent radiation/surgery needed	Known cancer + back pain worse lying down + progressive deficit
Unstable spinal fracture	Secondary neurological injury from instability ^[1] → further cord damage	Trauma + gap between spinous processes + neurological deficit

The 'Red Flags' for Serious Spinal Pathology

Always ask about:

Cauda equina syndrome: faecal incontinence, painless urinary retention ± incontinence, saddle anaesthesia ^[3]
Infection: fever, immunosuppression ^[3]
Fracture: chronic steroid use, osteoporosis / metabolic bone disease ^[3]
Malignancy: constitutional symptoms, history of cancer, age > 50 with new back pain
Neurological deficit: progressive weakness or sensory loss

Missing these means missing a surgical emergency.

Step 5: Diagnostic Differentiation by Context

The main differential is:

Traumatic SCI (obvious mechanism) — but you must also consider:
- Delay in diagnosis due to: unconscious patient, head injury, alcohol intoxication, multiple distracting injuries ^[2]
- Pre-existing pathology unmasked by minor trauma: cervical spondylotic myelopathy + hyperextension → central cord syndrome (elderly)
- Pathological fracture: metastasis or osteoporosis → low-energy mechanism causing fracture → cord compression
- Chronic condition with acute deterioration ^[1] — e.g., patient with ankylosing spondylitis whose rigid "bamboo spine" fractures like a long bone from a minor fall

The key differentiation is:

Compressive (tumour, abscess, disc, haematoma) — requires urgent surgical decompression → MRI is the modality of choice; plain XR cannot make or exclude diagnosis of cord compression ^[16]
Non-compressive (transverse myelitis, vascular, inflammatory, metabolic) — managed medically

D/dx of transverse myelitis includes: Non-inflammatory myelopathy by MRI spine (mechanical: disc herniation, vertebral body compression fractures...) ^[14]. The first step is always MRI to exclude compression.

Condition	Onset	Pain	Motor Pattern	Sensory Pattern	Sphincters	Special Features
Traumatic SCI	Acute	At injury site	Depends on level/completeness	Sensory level	Often early	History of trauma, neurogenic shock
Spinal infarct	Hyperacute (minutes)	Sudden back pain	Anterior cord (motor loss)	Pain/temp loss, proprioception spared	Spastic bladder	Risk factors: AF, DM, aortic surgery
Epidural abscess	Subacute (days)	Severe, localised	Progressive UMN	Sensory level	Late	Fever, ↑WBC/CRP, IVDU
TB spine	Subacute–chronic	Insidious back pain	UMN below	Sensory level	Late	Constitutional symptoms, kyphosis
Transverse myelitis	Subacute (hours–days)	Girdle-like	Bilateral, often complete	Sensory level	Early	Post-viral, a/w MS or NMO
Metastatic compression	Subacute–acute	Night pain, worse lying down	Progressive UMN	Dorsal cord pattern	Late	Known cancer, weight loss
Cervical spondylotic myelopathy	Chronic	Neck stiffness	UMN in legs, myelopathic hands	Often subtle	Very late	Age > 50, Lhermitte's sign
Syringomyelia	Chronic	Painless burns on hands	Central cord (UL > LL)	Cape-like dissociated	Late	Chiari I malformation
B12 deficiency	Chronic	None	UMN (lateral columns)	Posterior columns (proprioception, vibration)	Usually spared	Megaloblastic anaemia, glossitis
MS	Relapsing-remitting	Variable	Variable	Variable	Variable	Optic neuritis, Lhermitte's, brain lesions
Cauda equina	Variable	Radicular, bilateral	Pure LMN	Saddle	Late but irreversible	Usually L4/5 disc or tumour

In the polytrauma setting, hypotension must be differentiated ^[17]:

	Neurogenic Shock	Hypovolaemic Shock	Cardiogenic Shock
Mechanism	Interruption of neurogenic vasomotor control → inappropriate ↓HR, ↓SVR ^[17]	Blood loss → ↓preload	Pump failure → ↓CO
Heart Rate	Paradoxically slow HR (bradycardia)	Tachycardia	Variable
Skin	Warm, flushed, dry	Cold, clammy, pale	Cold, clammy
JVP/CVP	Low–normal	Low (↓CVP < 8)	High (↑CVP > 12)
Context	Compatible Hx of CNS injury ^[17]	Visible bleeding, pelvic fracture	MI, arrhythmia
Treatment	IV fluids + vasopressors	Volume resuscitation, stop bleeding	Inotropes, IABP

A Trap in Polytrauma

In a polytrauma patient with a spinal injury AND hypotension, always assume hypovolaemic shock first and look for bleeding (chest, abdomen, pelvis, long bones). Neurogenic shock is a diagnosis of exclusion. If you assume neurogenic shock and the patient is actually bleeding, they will die from uncontrolled haemorrhage.

When a patient presents with urinary symptoms and SCI is suspected, the differential for the bladder dysfunction itself includes ^[18]:

Neurogenic overactive bladder: Stroke, Spinal cord injury, Multiple sclerosis, Parkinson's disease
Non-neurogenic overactive bladder (idiopathic): post-operative pelvic surgery, secondary to bladder outlet obstruction
Detrusor underactivity: diabetic neuropathy, cauda equina

High Yield Summary — Differential Diagnosis of SCI

Confirm it's a cord lesion: UMN below + LMN at level + sensory level + sphincter disturbance = cord. Pure LMN = cauda equina or peripheral. Cortical signs = brain.
Tempo narrows aetiology: Hyperacute = vascular/trauma. Subacute = infection/inflammation. Chronic = degenerative/neoplastic/metabolic.
Cord syndrome narrows further: Anterior cord → infarct. Central cord → syringomyelia/hyperextension injury. Brown-Séquard → penetrating trauma. Dorsal cord → B12/MS/metastasis.
Surgical emergencies not to miss: Epidural abscess, epidural haematoma, metastatic compression, cauda equina syndrome, unstable fracture.
MRI is the modality of choice for non-traumatic cord compression; plain XR cannot make or exclude the diagnosis.
In trauma: always assume hypovolaemic shock before neurogenic shock. Always image the whole spine (15% non-contiguous injuries).
Red flags: cauda equina symptoms, fever/immunosuppression, cancer history, progressive neurological deficit, chronic steroid use/osteoporosis.

Active Recall - Differential Diagnosis of Spinal Cord Injuries

References

^[1] Lecture slides: GC 110. Paraplegia Spinal cord compression Transverse myelitis Spinal dysraphism Neuroimaging III Spinal Cord.pdf ^[2] Lecture slides: GC 227. Cervical Spine Pathology.pdf ^[3] Senior notes: maxim.md (Section 2.3 Approach to spine diseases) ^[6] Senior notes: Ryan Ho Neurology.pdf (Section 9.6 Spinal Trauma, p176-177) ^[8] Senior notes: Ryan Ho Fundamentals.pdf (Section 3.4.9 Paraplegia, p334-335) ^[11] Senior notes: Ryan Ho Neurology.pdf (Section 1.3 Where and What is the Lesion, p45) ^[12] Senior notes: felixlai.md (Differential diagnosis of stroke) ^[13] Senior notes: Ryan Ho Neurology.pdf (p72 — D/dx and Characteristic Presentations of sensory loss) ^[14] Senior notes: Ryan Ho Neurology.pdf (Section 6.2 Transverse Myelitis, p141) ^[15] Senior notes: Ryan Ho Respiratory.pdf (p80 — Skeletal TB / Pott disease) ^[16] Senior notes: Ryan Ho Radiology.pdf (p18 — Spinal trauma and non-traumatic cord compression imaging) ^[17] Senior notes: Ryan Ho Critical Care.pdf (p16 — Neurogenic shock) ^[18] Senior notes: felixlai.md (Differential diagnosis of LUTS — overactive bladder)

Diagnostic Criteria, Diagnostic Algorithm, and Investigations for Spinal Cord Injuries

The diagnosis of spinal cord injury is not a single "test" — it is a systematic process that answers five questions in order:

Is there a spinal cord injury? (clinical assessment — ASIA)
What is the level? (neurological examination — dermatomes/myotomes)
Is it complete or incomplete? (sacral sparing — ASIA grade)
Is it stable or unstable? (imaging — three-column theory)
What is the cause? (context + imaging + supportive investigations)

The first three are determined primarily by clinical examination. The last two require imaging. There is no single "diagnostic criterion" like the Jones Criteria for rheumatic fever — instead, the diagnosis rests on a structured clinical-radiological framework.

B. Clinical Diagnostic Assessment

The ASIA classification (IMPORTANT!) ^[3] is the internationally accepted system for classifying spinal cord injury severity. ASIA stands for American Spinal Injury Association; ISNCSCI stands for International Standards for Neurological Classification of Spinal Cord Injury.

Sensory: test pinprick and touch in each dermatome ^[6] Motor: in the 10 key motor functions listed ^[6]

The ASIA Examination systematically assesses:

Sensory examination — 28 dermatomes on each side (C2–S4/5), tested for:

Light touch (tests dorsal column-medial lemniscal pathway)
Pinprick (tests spinothalamic pathway)
Each scored 0 (absent), 1 (impaired), 2 (normal) → maximum sensory score = 112 per side per modality

Motor examination — 10 key muscles on each side (5 upper limb, 5 lower limb):

Root	Key Muscle	Action Tested
C5	Elbow flexors (biceps)	Elbow flexion
C6	Wrist extensors (ECRL, ECRB)	Wrist extension
C7	Elbow extensors (triceps)	Elbow extension
C8	Finger flexors (FDP to middle finger)	Finger flexion
T1	Small finger abductors (ADM)	Finger abduction
L2	Hip flexors (iliopsoas)	Hip flexion
L3	Knee extensors (quadriceps)	Knee extension
L4	Ankle dorsiflexors (tibialis anterior)	Ankle dorsiflexion
L5	Long toe extensors (EHL)	Great toe extension
S1	Ankle plantarflexors (gastrocnemius/soleus)	Ankle plantarflexion

Each scored 0–5 (MRC scale) → maximum motor score = 50 per side

Key definitions:

Neurological level of injury (NLI): the most caudal segment with both normal sensory AND motor function (grade ≥ 3 motor + grade 2 sensory on both modalities)
Sensory level: most caudal dermatome with normal sensation
Motor level: most caudal myotome with ≥ 3/5 power, provided the segment above is 5/5

Sacral sparing — the critical determinant of complete vs incomplete:

Test: voluntary anal contraction (motor) + S4-S5 light touch/pinprick (sensory) + deep anal pressure (sensation)
If ANY of these are present → incomplete (ASIA B–D)
If ALL absent → complete (ASIA A)

ASIA Impairment Scale ^[3]:

Grade Type Definition
A Complete No motor, No sensory, No sacral sparing
B Incomplete No motor, sensory only (preserved below level including S4-5)
C Incomplete > 50% of key muscles below the level have muscle grade < 3 (cannot raise arms or legs off bed)
D Incomplete ≥ 50% of key muscles below the level have muscle grade ≥ 3 (can raise arms or legs off bed)
E Normal Motor and sensory function are normal

Grade	Type	Definition
A	Complete	No motor, No sensory, No sacral sparing
B	Incomplete	No motor, sensory only (preserved below level including S4-5)
C	Incomplete	> 50% of key muscles below the level have muscle grade < 3 (cannot raise arms or legs off bed)
D	Incomplete	≥ 50% of key muscles below the level have muscle grade ≥ 3 (can raise arms or legs off bed)
E	Normal	Motor and sensory function are normal

ASIA C vs D — The Grade 3 Rule

The difference between C and D is whether the patient can move against gravity. Grade 3 = movement against gravity. If more than half the key muscles below the injury are weaker than grade 3, they literally cannot lift their limbs off the bed → ASIA C. If more than half can → ASIA D. This simple bedside distinction has enormous prognostic implications: ASIA D patients have a much higher chance of community ambulation.

Mechanism of injury helps determine degree of stability ^[6]:

Stable: ligament not damaged ^[6]
Unstable: ligament disrupted ^[6]

On physical examination:

"Step over spinous processes" for any tenderness, swelling or gap between spinous processes ^[6] — a palpable gap indicates rupture of interspinous ligament (i.e. unstable injury) ^[6]

Three-column theory (Denis) for thoracolumbar spine ^[3]:

Unstable fracture if 2/3 segments disrupted ^[3]
Anterior column: anterior 2/3 of vertebral body + disc + ALL
Middle column: posterior 1/3 of vertebral body + disc + PLL
Posterior column: posterior arch

You cannot definitively classify a patient as ASIA A (complete) during the spinal shock phase, because areflexia from spinal shock mimics complete injury. You must wait for the bulbocavernosus reflex to return (signalling end of spinal shock) before declaring an injury "complete" ^[3]:

	Spinal Shock	Neurogenic Shock
Bulbocavernosus reflex	Absent	Present
Motor	Flaccid paralysis	Normal

The bulbocavernosus reflex (squeeze glans penis or tug Foley catheter → look for anal wink) is the first sacral reflex to return. Once it returns, if there is still no sacral sparing, the injury is truly complete.

Don't Declare Complete Too Early

A patient in spinal shock looks like ASIA A — flaccid, areflexic, no sacral sparing. But this may be temporary. Only after the bulbocavernosus reflex returns can you reliably call it complete. This distinction matters because incomplete injuries (ASIA B–D) have far better recovery potential.

C. Imaging — The Diagnostic Workup

C1. Decision Rules: Who Needs Imaging?

Not every patient with neck pain after minor trauma needs imaging. Two validated clinical decision rules guide this:

NEXUS Mnemonic ^[2]:

N — Neuro deficit (any focal neurological deficit)
E — EtOH / intoxication (alcohol or drugs impairing assessment)
X — eXtreme distracting injury (injuries so painful they may mask spinal tenderness)
U — Unable to provide history (altered level of consciousness)
S — Spinal tenderness (midline posterior cervical tenderness)

If ALL five criteria are ABSENT → the cervical spine can be cleared clinically without imaging ^[2]. If ANY one is present → imaging is required.

The logic: NEXUS identifies patients whose clinical examination is reliable enough to exclude significant injury without radiation. If the patient is alert, sober, non-tender, neurologically intact, and has no distracting injuries, the negative predictive value is > 99%.

An alternative (and arguably more sensitive/specific) tool:

Any high-risk factor mandating imaging? (age ≥ 65, dangerous mechanism, paraesthesia in extremities) → If yes → image
Any low-risk factor allowing safe assessment of ROM? (simple rear-end RTA, sitting in ED, ambulatory, delayed onset neck pain, no midline tenderness) → If yes → assess ROM
Can the patient actively rotate the neck 45° left and right? → If yes → no imaging needed

NEXUS vs CCR

Both are validated for "clearing the c-spine" in alert trauma patients. CCR has slightly higher sensitivity (~99.4% vs 99.0%) and specificity. In practice, many centres use NEXUS because it is simpler. Neither applies to children < 16, GCS < 15, or known vertebral disease.

C2. Imaging Modalities — Systematic Overview

Investigation – Plain X-ray ^[1]:

Readily available
Show obvious fracture and malalignment
Can miss subtle fracture
Cannot exclude ligamentous instability
Cannot exclude soft-tissue compressive lesion (e.g., haematoma)

View	What It Shows	Key Findings
AP view	Alignment, spinous process spacing	3 lines on AP should be smooth ^[6]: alignment of spinous processes, lateral margins of lateral masses/vertebral bodies
Lateral view	Most important single view	4 lines on lateral should be smooth ^[6]: anterior vertebral body line, posterior vertebral body line, spinolaminar line, spinous process tips. Fracture lines, malalignment, soft tissue swelling
Open mouth (odontoid) view	C1-C2 specifically	Odontoid fracture, C1 fracture; Rule of Spence: sum of distance between lateral masses of C1 beyond vertebral body of C2 > 7mm → transverse ligament likely disrupted → unstable injury ^[6]

C-spine lateral view: soft tissue rules ^[3]:

3×7=21 rule: prevertebral soft tissue — C1 ≤ 10mm, C3 ≤ 7mm, C7 ≤ 21mm
Soft tissue swelling may indicate nearby fracture ^[6]:
- Above C4: ≤ 1/3 vertebral body width
- Below C4: ≤ 100% vertebral body width

Why does soft tissue swelling matter? Because a vertebral fracture causes local haemorrhage and oedema → the prevertebral soft tissue space widens. This may be the only clue on a lateral X-ray when the fracture line itself is occult.

Useful plain XR findings in spinal cord lesions ^[8]:

Pedicle erosion → extradural metastases (tumour erodes the pedicle because it sits in the epidural space)
Vertebral body collapse (pathological fracture from osteoporosis or malignancy)
Narrow disc space, osteophytes, hypertrophic facet joints → spondylosis
Expansion of intervertebral foramina → neurofibroma (tumour enlarges the foramen as it grows)

Plain XR: AP + lateral views should be ordered. For C-spine, ask for open mouth view. Flexion-extension views are not useful in the acute injury period due to muscle spasm ^[16].

Limitation of Plain XR

Plain XR cannot make or exclude the diagnosis of cord compression ^[16]. A normal X-ray does NOT rule out SCI. The cord is not visible on X-ray — you can only infer cord injury from bony or alignment abnormalities. This is why CT and MRI are essential in any patient with neurological deficit.

Investigation: CT ^[1]:

Reasonably available
Still cannot show soft-tissue injury ^[1]

CT Spine ^[16]:

High sensitivity and specificity (for fractures)
T and L-S spine within scan field in patients who undergo torso CT for assessment of other injuries ^[16] — this is a practical point: if a polytrauma patient gets a CT chest/abdomen/pelvis, the spine is already in the field → reconstruct spinal images from the same data
Provides radiographic clearance when X-rays are inadequate ^[2]

What CT Shows Well	What CT Does NOT Show
Fracture lines (even subtle ones)	Ligamentous injury
Bony canal narrowing	Cord oedema / contusion
Retropulsed fragments	Disc herniation (soft tissue)
Facet joint alignment	Epidural haematoma

All injuries otherwise (i.e., not minor) → CT ± MRI (if focal neurological deficit) ^[3]

Investigation: MRI spine ^[1]:

Difficult to arrange ^[1] (takes time, limited availability)
Shows soft-tissue lesion, cord oedema ^[1]

MRI ^[16]:

For ligamentous, spinal cord and soft tissue injuries
Done when there are neurological deficits not explained by plain film or CT ^[16]
Essential if there are neurological deficits ^[2]
Useful for delineation of soft tissue injury (i.e., discoligamentous) ^[2]

For non-traumatic cord compression: MRI is the modality of choice unless contraindicated ^[16]

Contrast MRI spine: urgent if acute paraplegia ^[8]

MRI Interpretation — Basic Principles ^[2]:

Level of lesion, location
Pathoanatomy (disc, osteophyte, OPLL, flavum)
Obliteration of the CSF space (indicates significant compression — the bright CSF signal disappears around the cord)
Cord shape / cross-sectional area (cord compression causes flattening)
Intramedullary signal change (myelomalacia) — T2 hyperintensity within the cord indicates oedema or gliosis; this is a poor prognostic sign

MRI Sequence	What It Shows Best
T1-weighted	Anatomy (fat bright, CSF dark). Vertebral body marrow replacement (metastasis = dark on T1)
T2-weighted	Fluid bright (CSF, oedema bright). Cord oedema/contusion = bright signal within cord. Disc herniation well-delineated
STIR	Fat-suppressed T2 — excellent for bone marrow oedema (fractures glow bright) and ligamentous injury
T1 with gadolinium	Enhancement indicates active inflammation, infection, or tumour vascularity

Key MRI findings and their interpretation:

Finding	Interpretation	Clinical Significance
T2 hyperintensity in cord	Cord oedema / contusion	Confirms cord injury; extent correlates with severity
T1 hypointensity + T2 hyperintensity in cord	Haemorrhagic necrosis	Poor prognosis — irreversible damage
Loss of CSF signal around cord	Cord compression	Needs decompression if progressive
Disc material in canal	Disc herniation	Surgical target
T2 bright ligament signal	Ligamentous disruption	Indicates instability → may need surgical fixation
Epidural collection	Haematoma or abscess	Compressive lesion → may need urgent drainage
Vertebral body T1 low / T2 high	Metastasis, fracture (with oedema)	Check for pathological fracture

MRI is the Only Way to See the Cord

The spinal cord itself is invisible on X-ray and poorly seen on CT. MRI is the only modality that directly visualises cord contusion, oedema, haemorrhage, and compression. Any patient with neurological deficit after spinal trauma MUST get an MRI.

Myelography / CT myelography: if MRI is contraindicated or not available ^[8]

Involves intrathecal injection of contrast followed by CT scanning
Contraindicated in patients with raised intracranial pressure
Used when MRI cannot be performed (e.g., pacemaker, metallic implants, claustrophobia, patient too unstable for MRI)
Shows subarachnoid space filling defects (compression)

Modality	Indication
CTA vertebral artery	C-spine injury involving vertebral foramen — risk of vertebral artery injury ^[3]
CTA Circle of Willis	Skull base fracture involving foramen lacerum ^[3]
Spinal angiography (DSA)	Suspected vascular malformation (AVM, dural AVF)

D. Supportive Investigations

These do not diagnose the spinal cord injury itself but help identify the cause or complications:

CSF analysis: only if suspect transverse myelitis ^[8] May cause deterioration for cord compression! ^[8] — this is critically important. If there is any possibility of a compressive lesion, lumbar puncture is DANGEROUS because removing CSF below a block can cause the cord to herniate downward.

Send: R/M, cell count, C/ST, biochemistry, TB workup, viral studies, cytology ± VDRL, oligoclonal bands ^[8]

CSF Finding	Suggests
Moderate lymphocytosis, normal glucose, normal/slightly ↑protein	Transverse myelitis
Oligoclonal IgG bands	MS (↑risk of progression into MS)
Very high protein ( > 5 g/L), nodular arachnoiditis	TB arachnoiditis
Malignant cells on cytology	Leptomeningeal metastasis
Elevated WBC + low glucose + high protein + positive C/ST	Bacterial infection

NEVER LP Before Imaging in Suspected Cord Compression

If you suspect a compressive cause (tumour, abscess, haematoma), do NOT perform lumbar puncture until MRI has excluded a block. Removing CSF below a compressive lesion drops the pressure below the block relative to above it → can cause the cord to herniate further → catastrophic deterioration.

Test	Purpose
Vitamin B12	Rule out subacute combined degeneration ^[8]
FBC, CRP, ESR	Infection (abscess, spondylodiscitis), malignancy
RFT, LFT	Baseline; renal function for contrast imaging
Calcium, phosphate, ALP	Metastatic bone disease, osteoporosis
Coagulation profile	If haematoma suspected; anticoagulant use
Blood cultures	If epidural abscess/spondylodiscitis suspected
Tumour markers (PSA, etc.)	If metastatic disease suspected
NMO-IgG (anti-AQP4 Ab)	If longitudinally extensive transverse myelitis (≥ 3 segments) → NMO spectrum disorder
ANA, anti-Ro, anti-La	SLE, Sjögren's as cause of myelitis
HIV antibody, VDRL	Infective/inflammatory causes of myelopathy
TSH	Hypothyroidism can cause myelopathy (rare)

Test	Purpose	Interpretation
Nerve conduction study (NCS)	Differentiate cord (central) from peripheral nerve lesion	Normal NCS with UMN signs = cord lesion. Abnormal NCS = peripheral neuropathy/radiculopathy
Somatosensory evoked potentials (SSEP)	Assess dorsal column conduction	Delayed or absent cortical potentials confirm cord conduction block; useful for intraoperative monitoring
Motor evoked potentials (MEP)	Assess corticospinal tract conduction	Useful intraoperatively to monitor motor pathways during spinal surgery
EMG	Assess denervation in muscles	Confirms LMN involvement at specific levels; differentiates from NMJ or myopathic disease

Assess neurogenic bladder function (detrusor pressure, sphincter coordination)
Important for long-term management of bladder in established SCI
Shows detrusor sphincter dyssynergia (DSD) in suprasacral lesions

Scenario	Imaging	Rationale
High energy trauma	CT whole spine	High sensitivity for fractures ^[16]
Patient at risk of fractures (e.g., ankylosing spondylitis)	CT whole spine	Rigid spine fractures easily; may be missed clinically ^[16]
Focal neurological deficits	CT + MRI (essential)	CT for bony; MRI essential if there are neurological deficits ^[2]^[16]
Minor injury, alert, NEXUS-negative	No imaging needed	Clinical clearance is safe
Minor injury, NEXUS-positive	Full C-spine XR (AP + lateral + open mouth view) or CT	Screening for fracture ^[3]
Non-traumatic progressive myelopathy	MRI — modality of choice	Plain XR cannot make or exclude dx of cord compression ^[16]
Suspected transverse myelitis (after MRI excludes compression)	MRI + CSF analysis	Demonstrate cord inflammation without compression
Suspected vascular lesion	MR angiography or DSA	Map AVM/AVF for treatment planning

Clinical evaluation: aim to localise and delineate lesion ^[8]:

History ^[8]:

Weakness, sensory loss, sphincter disturbance, pain
Temporal course and spatial distribution
Mechanism (high / low energy trauma; motor vehicle accident, fall from height, fall from level ground) ^[2]
Time of injury ^[2]
Delay in diagnosis (risk factors for missed SCI): unconscious, head injury, alcohol, multiple distracting injuries ^[2]

Physical Examination ^[8]:

Motor: segmental weakness according to myotome
Sensory: sensory level according to dermatome
Cerebellar: for MS and Friedreich's ataxia
Signs of cord compression: saddle anaesthesia, anal tone, perianal sensation ^[19]
DRE: anal reflex, bulbocavernosus reflex (BCR, S2-4) ^[19]
LL neurological examination ^[19]

Investigations ^[8]:

Plain XR spine
Contrast MRI spine: urgent if acute paraplegia
Myelography / CT myelography: if MRI is C/I or N/A
CSF analysis: only if suspect transverse myelitis (may cause deterioration for cord compression!)
Vitamin B12 for subacute combined degeneration

Investigations for cervical spine pathology: X-rays (AP/lateral, oblique views for foraminal narrowing), CT scan, MRI scan (confirm nerve root/cord compression), NCV/EMG ^[2]

In unconscious or intubated patients, clinical clearance is impossible. The approach:

Maintain immobilisation (hard collar + logroll precautions)
CT cervical spine — if normal:
- Some centres accept CT-only clearance in obtunded patients (high sensitivity > 99%)
- Others require MRI within 48–72 hours to exclude occult ligamentous injury
If CT abnormal → MRI
If MRI abnormal → neurosurgical consultation

Spinal cord injury: sensory level, motor deficits, anal tone should be assessed as part of head injury assessment ^[3]. Always assume spinal injury in an unconscious trauma patient until proven otherwise.

High Yield Summary — Diagnosis of SCI

ASIA/ISNCSCI is the gold standard for classifying SCI: tests 28 dermatomes (pinprick + light touch) and 10 key muscles bilaterally. Sacral sparing (S4-5 sensation or voluntary anal contraction) distinguishes complete (ASIA A) from incomplete (ASIA B-D).
Cannot declare complete until spinal shock resolves — wait for bulbocavernosus reflex to return.
NEXUS criteria clear the c-spine clinically: N (neuro deficit), E (EtOH), X (extreme distracting injury), U (unable to provide history), S (spinal tenderness). All 5 absent → no imaging needed.
Three imaging modalities: Plain XR (readily available but misses subtle fractures and cannot see the cord); CT (high sensitivity for fractures but cannot show soft tissue); MRI (shows cord, ligaments, disc — essential with neurological deficit, but harder to arrange).
Plain XR cannot make or exclude cord compression — MRI is mandatory if neurological deficit present.
CSF analysis only if transverse myelitis suspected AND MRI excludes compression first — LP with a compressive lesion risks catastrophic deterioration.
CT whole spine for all significant trauma — 15% have non-contiguous injuries.
Three-column theory: ≥ 2/3 columns disrupted = unstable.
MRI key findings: T2 cord hyperintensity = oedema/contusion; T1 hypointensity = haemorrhagic necrosis (poor prognosis); loss of CSF signal = compression; ligament bright on T2/STIR = disruption.
Supportive blood tests: B12, NMO-IgG, ANA, HIV, VDRL to identify non-traumatic causes.

Active Recall - Diagnosis of Spinal Cord Injuries

References

Management of Spinal Cord Injuries

Management of SCI follows a time-critical, phased approach. The fundamental principle is that you cannot reverse primary injury, but you CAN prevent secondary injury. Every minute of ongoing cord compression, ischaemia, or instability allows the secondary cascade (oedema, excitotoxicity, apoptosis) to extend the zone of damage. The management framework therefore moves through:

Resuscitation (keep the patient alive — ABCDE)
Protection (prevent further cord damage — immobilisation)
Decompression (relieve ongoing cord compression — surgery)
Stabilisation (restore spinal alignment and prevent future instability)
Prevention of complications (DVT, pressure sores, bladder, etc.)
Rehabilitation (maximise functional recovery)

Principles of Management: Resuscitation (NB: spinal shock); Collar & log roll to protect spine; Assume multiple injury / head injury; Imaging studies; Methylprednisolone(?); Surgery to decompress spinal cord; Mechanical stabilisation; Prevent/Treat complications; Rehabilitation ^[1]

Phase 1: Pre-Hospital and Emergency Department — Resuscitation and Protection

A. ABCDE Approach

ABCDE before any P/E ^[6]. The entire point is to keep the patient alive first. A dead patient has no spinal cord to save.

Jaw thrust when C-spine injury IS a concern (eg. trauma) ^[20] — never head-tilt chin-lift in a suspected C-spine injury because extending the neck can worsen cervical cord compression
If airway is not maintainable with basic manoeuvres → rapid sequence intubation (RSI) with manual in-line stabilisation (MILS) — this means one person holds the head and neck perfectly still while another intubates
High cervical injuries (above C3-5) may cause respiratory arrest → immediate intubation and mechanical ventilation is life-saving ^[8]

Why? The phrenic nerve (C3, 4, 5) innervates the diaphragm. Lesions above C3 eliminate all spontaneous breathing. Lesions C3-5 may partially preserve diaphragmatic function but patients often need ventilatory support.

Diaphragmatic breathing if C5 or below (loss of control of intercostal muscles) ^[8]
Paradoxical ventilation if intercostal muscles are paralysed ^[6]
High-flow O₂ (15 L/min via non-rebreather mask) for all trauma patients
Monitor SpO₂ continuously — target SpO₂ > 92%
Consider mechanical ventilation for:
- High cervical SCI with respiratory insufficiency
- Flail chest or associated thoracic injuries
- Fatigue from isolated diaphragmatic breathing

Neurogenic shock management ^[1]^[8]:

Cause: sympathetic signal disruption ^[8]
Presentation: vasodilatation → hypotension, bradycardia, warm, flushed skin ^[8]
Treat with IV fluids and vasopressors/inotropes ^[1]

Step	Intervention	Rationale
1	IV crystalloid bolus (e.g., Ringer's lactate or 0.9% NaCl)	Expand intravascular volume to compensate for relative hypovolaemia from venous pooling
2	Vasopressors (noradrenaline first-line, or phenylephrine) if fluid-refractory	Restore vascular tone lost from sympathetic disruption — noradrenaline provides both α₁ (vasoconstriction) and β₁ (cardiac inotropy)
3	Atropine for symptomatic bradycardia	Block excessive vagal tone that is now unopposed
4	Target MAP ≥ 85 mmHg for 5–7 days	Current AO Spine/AANS guidelines recommend augmented MAP to optimise cord perfusion pressure — the cord, like the brain, needs adequate perfusion to minimise secondary ischaemic injury

Hypovolaemic Before Neurogenic

In polytrauma, always assume hypovolaemic shock first and actively search for bleeding (chest, abdomen, pelvis, long bones). Neurogenic shock is a diagnosis of exclusion. The classic trap: you assume the bradycardia is neurogenic, give vasopressors, and miss an intra-abdominal haemorrhage. If in doubt, resuscitate for blood loss AND neurogenic shock simultaneously.

GCS assessment
Pupillary examination
ASIA neurological examination (as described in diagnostic section)
Note: flaccid limbs + sensory level + AROU + lax anal tone + priapism = spinal cord injury until proven otherwise ^[6]

Full log-roll examination of the spine — "step over spinous processes" for any tenderness, swelling or gap ^[6]
Temperature monitoring — patients with high SCI are poikilothermic (cannot thermoregulate below the lesion) → cover with warming blankets
Look for associated injuries — assume multiple injury / head injury ^[1]

Collar & log roll to protect spine ^[1]

Method	Description	Purpose
Rigid cervical collar (e.g., Philadelphia, Aspen)	Circumferential device around neck	Limits cervical flexion/extension/rotation to prevent further cord damage
Log-roll technique	Patient rolled as a unit (head, trunk, pelvis aligned) by ≥ 4 people	Prevents spinal rotation/flexion during transfers and examination
Spinal board	Rigid flat board for transport	Prevents spinal flexion during pre-hospital transport; remove as soon as possible (pressure sore risk)
Sandbags + tape	Placed either side of head and taped across forehead to the board	Additional immobilisation of the head/neck

Extreme caution in transportation of patient in those likely to have spinal cord injury ^[6]

Why immobilise? An unstable fracture means the vertebral column cannot hold its alignment. Any movement (even routine nursing care) can cause further displacement → further cord compression → secondary neurological injury ^[1]. Immobilisation buys time until definitive imaging and treatment.

Phase 2: Medical Management

Management — Medical ^[6]:

ABC support
Prophylaxis for DVT, stress ulcers, AROU (urinary catheter)
Analgesics

As detailed above: IV fluids + vasopressors, target MAP ≥ 85 mmHg × 5-7 days.

SCI patients have one of the highest rates of DVT/PE of any patient population (prevalence up to 80% without prophylaxis). Why? Loss of lower limb muscle pump + immobility + hypercoagulable state from trauma.

Modality	Details	Timing
Mechanical	Intermittent pneumatic compression (IPC) devices, graduated compression stockings	Start immediately
Pharmacological	Low-molecular-weight heparin (LMWH, e.g., enoxaparin 40 mg SC daily)	Start within 24–72 hours once haemostasis confirmed (no ongoing haemorrhage)
Duration	Continue for 2–3 months post-injury or until fully ambulatory	Extended prophylaxis because SCI patients remain at risk for months

VTE is the Leading Preventable Cause of Death in SCI

Without prophylaxis, DVT occurs in up to 80% and fatal PE in up to 5% of SCI patients. Mechanical prophylaxis starts day 1; pharmacological prophylaxis as soon as safely possible. This is one of the most important medical interventions in SCI management.

SCI patients are at high risk of stress-related mucosal disease (Curling-type ulceration) due to unopposed vagal stimulation to the stomach (particularly in high thoracic/cervical injuries where sympathetic innervation to the gut is lost).

Agent	Details
Proton pump inhibitor (PPI)	e.g., omeprazole 40 mg IV/PO daily — first-line
H₂-receptor antagonist	e.g., ranitidine 50 mg IV TDS — alternative
Duration	Continue until patient is eating and mobile

Prophylaxis for AROU (urinary catheter) ^[6]

Neurogenic bladder is universal in acute SCI — the patient cannot sense bladder fullness (loss of afferent sensation) and cannot voluntarily initiate micturition (loss of descending control to sacral micturition centre). An over-distended bladder risks:

Detrusor muscle damage (myogenic stretch injury)
Vesicoureteric reflux → hydronephrosis → renal damage
UTI

Phase	Catheter Type	Rationale
Acute (spinal shock)	Indwelling Foley catheter (14-18 Fr)	Continuous drainage during haemodynamic instability and immobility; allows accurate urine output monitoring
Subacute/chronic	Intermittent clean catheterisation (ICC)	Lower infection risk than indwelling; promotes bladder cycling; gold standard for long-term neurogenic bladder

Contraindications to urethral catheterisation ^[21]:

Absolute: urethral injury (blood at urethral meatus, high-riding prostate on DRE — typically associated with pelvic trauma)
Relative: urethral stricture, recent urological surgery

If urethral catheterisation fails or is contraindicated → suprapubic catheterisation (SPC) ^[21].

Neurogenic bowel → ileus initially, then constipation
Regular bowel programme: scheduled glycerine suppositories, digital stimulation, stool softeners (docusate), adequate fibre intake
Prevent faecal impaction (a common trigger for autonomic dysreflexia in chronic SCI)

Analgesics ^[6] — SCI pain is multifactorial:

Pain Type	Agent	Rationale
Nociceptive (bone, soft tissue)	Paracetamol, NSAIDs (if no C/I), opioids for severe pain	Standard WHO analgesic ladder
Neuropathic (burning, shooting, below-level)	Pregabalin or gabapentin (first-line); amitriptyline or duloxetine (second-line)	Modulate hyperexcitable dorsal horn neurons; gabapentinoids bind α₂δ subunit of voltage-gated Ca²⁺ channels → reduce excitatory neurotransmitter release
Spasticity-related	Baclofen (oral or intrathecal), tizanidine, diazepam	See spasticity section below

High SCI (C3-C5) patients require:

Early intubation if respiratory compromise
Assisted cough techniques (quad cough — manual abdominal thrust synchronised with cough effort)
Incentive spirometry and chest physiotherapy
Tracheostomy if prolonged mechanical ventilation expected (facilitates weaning, bronchial toileting)
Monitor vital capacity serially — a declining VC in a cervical SCI patient may indicate ascending oedema or deterioration

Impaired thermoregulation ^[8] — patients become poikilothermic below the lesion
Active warming/cooling measures as needed
Avoid hypothermia (worsens coagulopathy in polytrauma) and hyperthermia (worsens secondary injury)

Methylprednisolone is associated with higher risk of morbidity and complications and should NOT be used. ^[6]

Methylprednisolone(?) ^[1] — the question mark in the lecture slides is deliberate.

The story: The NASCIS-II trial (1990) suggested that high-dose methylprednisolone (30 mg/kg bolus then 5.4 mg/kg/hr for 23 hours) within 8 hours of non-penetrating SCI improved motor recovery. This led to widespread use for decades ^[21].

The problem: Subsequent analysis and further trials (NASCIS-III, multiple Cochrane reviews) showed:

The original NASCIS-II benefit was a post-hoc subgroup analysis (not pre-specified), making it statistically questionable
Increased complications: wound infections, pneumonia, sepsis, GI haemorrhage, hyperglycaemia, avascular necrosis
No mortality benefit
No improvement in long-term neurological outcomes in well-designed replications

Current guideline (AO Spine 2017, AANS/CNS 2013, updated 2024): Routine use of methylprednisolone in acute SCI is NOT recommended. It may be considered as an option (not a standard) within 8 hours for non-penetrating SCI, but the risks likely outweigh the benefits.

Methylprednisolone — Do NOT Use

This is a classic exam point. The answer expected is: methylprednisolone should NOT be used in acute SCI because it increases morbidity (infection, GI bleed, hyperglycaemia) without proven neurological benefit. The NASCIS-II trial had significant methodological flaws. If asked about it, state the controversy and the current consensus against routine use.

Steroid Setting	Recommendation	Evidence
Acute traumatic SCI	NOT recommended	NASCIS trials methodologically flawed; ↑ complications without proven benefit ^[6]
Acute cord compression from metastasis	High-dose dexamethasone (e.g., 16 mg/day)	Reduces vasogenic oedema around tumour; buys time before definitive RT/surgery ^[8]
Transverse myelitis	IV methylprednisolone 1 g daily × 3-5 days	Treats the underlying inflammatory/autoimmune process ^[8]

Note the critical distinction: steroids are not recommended for traumatic SCI but are indicated for inflammatory myelopathy and metastatic cord compression — these are different diseases with different pathophysiology.

Phase 3: Surgical Management

Surgical treatment in unstable injuries ^[6]:

Indication	Rationale
Unstable fracture (≥ 2/3 columns disrupted)	Spinal column cannot hold alignment → ongoing risk of secondary cord injury from movement
Surgical decompression if a patient with normal cord function or incomplete cord lesion progressively deteriorates ^[6]	Progressive deficit = ongoing compression → decompression can halt or reverse decline
Progressive neurological deficit ^[1]	The cord is being squeezed NOW → remove the compression before it becomes irreversible
Myelopathy / Radiculopathy ^[1]	Persistent cord or root compression causing functional deficit
Intractable pain ^[1]	Structural cause of pain (e.g., nerve root compression, instability) amenable to surgical correction
Spinal cord compression from haematoma, abscess, or disc	These are surgical emergencies — the compressive lesion must be evacuated

Principles of Management — Surgical treatment if: Progressive neurological deficit; Myelopathy / Radiculopathy; Intractable pain ^[1]

Three goals of surgery ^[6]:

Decompression of spinal cord — relieve external pressure on the cord
Reduction of fractures or dislocation — restore normal alignment
Fixation of unstable spinal elements — prevent future displacement

Procedure	What It Does	When It's Used
Anterior corpectomy + fusion	Remove the vertebral body (corpectomy — from Latin corpus = body + Greek ektomē = cutting out) and replace with a cage/graft; stabilise with anterior plate	Anterior compression (burst fracture retropulsed fragments, disc herniation, tumour involving vertebral body); anterior corpectomy shown in lecture slides ^[1]
Posterior laminectomy	Remove lamina (the posterior arch of the vertebra — the "roof" of the canal) to decompress the cord from behind	Posterior compression, multilevel stenosis; useful when compression is from ligamentum flavum or posterior elements
Posterior laminoplasty	"Hinge open" the lamina rather than remove it — creates more space while preserving posterior elements	Multilevel cervical stenosis (particularly in OPLL or spondylosis) — preserves some posterior stability
Posterior instrumented fusion	Pedicle screws + rods to hold vertebrae in alignment	Unstable fractures, post-laminectomy instability, fracture-dislocations
Combined anterior-posterior (360°) fusion	Both approaches in one or staged operations	Severe instability (e.g., 3-column injury, fracture-dislocation with anterior + posterior disruption)
Closed reduction + traction	Skull tongs (e.g., Gardner-Wells) or halo ring with traction weights	Cervical facet dislocations — attempt closed reduction before open surgery if no disc herniation on MRI

Timing of surgery — The Debate:

Current evidence (STASCIS trial, 2012; AO Spine guidelines) supports early surgery (within 24 hours) for acute traumatic SCI with ongoing compression:

Earlier decompression → better neurological outcomes in incomplete SCI (ASIA B, C, D)
Reduced duration of ICU stay and complications
For complete SCI (ASIA A), the benefit is less clear but early stabilisation still prevents complications and facilitates rehabilitation

The latest AO Spine consensus (2024) recommends decompression within 24 hours whenever safely feasible, particularly for incomplete injuries.

Non-surgical immobilisation only in stable injuries ^[6]:

Orthosis	Indication	Details
Rigid cervical collar (e.g., Philadelphia, Miami J)	Stable cervical fractures, post-operative C-spine	Limits flexion/extension but does NOT fully immobilise
Halo vest	Unstable upper cervical fractures (e.g., odontoid type II in elderly), some C1 fractures	Most effective external cervical immobilisation; pins screwed into skull attached to vest
TLSO (thoracolumbar-sacral orthosis)	Stable thoracolumbar fractures (e.g., compression fractures with < 50% height loss, intact posterior ligaments)	Limits thoracolumbar motion; various types (Jewett, CASH, custom-moulded)

Use: 2-3 months after injury to facilitate healing ^[6] Problems: pressure sores, weakening of muscles, soft tissue contractures, ↓pulmonary function, chronic pain syndrome ^[6]

Phase 4: Management by Specific Cause

Not all SCI is traumatic. The management differs significantly depending on the aetiology:

Principles of Management — Spinal Tumours ^[1]:

Steroids to reduce oedema

Surgical resection within safety limit

Intraoperative monitoring with motor evoked potential (MEP) and somatosensory evoked potential (SSEP)

Adjuvant radiotherapy for some

For Metastasis ^[1]:

Primarily ERT (external beam radiotherapy)

Surgery for pain, instability, or lesions resistant to RT

Palliative in nature

Tumour Type	Primary Treatment	Adjuncts
Intradural extramedullary (schwannoma, meningioma)	Surgical excision (often curative)	Intraoperative MEP/SSEP monitoring
Intramedullary (ependymoma)	Surgical excision (discrete tumours)	± Adjuvant RT if incomplete resection
Intramedullary (astrocytoma)	Biopsy + debulking (indistinct borders)	± Adjuvant RT/chemo
Extradural metastasis	Primarily ERT; surgery if pain/instability/RT-resistant	Steroids (dexamethasone) to reduce oedema

Conservative management: Physiotherapy, Analgesia ^[1] Surgical treatment if: Progressive neurological deficit; Myelopathy / Radiculopathy; Intractable pain ^[1]

Approach	When	Options
Conservative	Mild myelopathy, stable symptoms, no progressive deficit	Physiotherapy, cervical collar, NSAIDs, activity modification
Surgical	Progressive deficit, moderate-severe myelopathy, intractable radiculopathy	Anterior cervical discectomy and fusion (ACDF), anterior corpectomy, posterior laminoplasty/laminectomy ± fusion

TB spine: anti-TB treatment (2HRZE / 9HR±E) ± surgery if neurological deficit or significant deformity ^[15]
Epidural abscess: urgent surgical drainage + IV antibiotics (empiric: flucloxacillin + third-gen cephalosporin; adjust based on C/ST)

IV methylprednisolone 1 g IV over 1 hour daily × 3-5 days ^[8]
If refractory → plasma exchange (PLEX)
Treat underlying cause (NMO → rituximab; MS → disease-modifying therapy; SLE → immunosuppression)

Complication	Prevention	Management
DVT/PE	LMWH + IPC + compression stockings (start day 1)	Therapeutic anticoagulation; IVC filter if anticoagulation contraindicated
Pressure sores	2-hourly turning, pressure-relieving mattress, skin inspection, adequate nutrition	Wound care, debridement, flap surgery for Grade III-IV ulcers
UTI	Intermittent catheterisation (lower infection risk than indwelling), aseptic technique	Antibiotics based on C/ST; NOT prophylactic antibiotics
Respiratory	Chest physiotherapy, assisted cough, incentive spirometry, early mobilisation	Antibiotics for pneumonia; ventilatory support as needed
Stress ulcers	PPI prophylaxis	Endoscopy if GI bleeding
Spasticity	Early physiotherapy, stretching, positioning	Baclofen (oral → intrathecal pump if severe); tizanidine; botulinum toxin for focal spasticity; diazepam
Contractures	Range-of-motion exercises, positioning, splinting	Surgical release if fixed
Autonomic dysreflexia	Identify and manage triggers (full bladder, constipation, skin issues)	Sit patient upright, loosen clothing, identify/remove trigger, sublingual nifedipine or GTN paste for severe HTN
Neurogenic bladder	ICC programme, anticholinergics for overactive detrusor	Long-term: ICC, suprapubic catheter, surgical options (augmentation cystoplasty, continent diversion)
Neuropathic pain	Early gabapentin/pregabalin	Combination therapy; TENS; psychology
Impaired thermoregulation ^[8]	Environmental temperature awareness, layered clothing	Active warming/cooling as needed
Depression/psychological	Early psychological assessment and support	CBT, SSRIs, peer support groups
Heterotopic ossification	NSAIDs (indomethacin) prophylaxis in high-risk	Excision if functionally limiting

Rehabilitation ^[1] is arguably the most important long-term intervention. The goals are:

Maximise residual function — train the patient to use whatever neurological function remains
Prevent secondary complications — pressure sores, contractures, UTI, psychological decline
Reintegrate into society — vocational rehabilitation, community support, assistive devices

Discipline	Role
Physiotherapy	Strengthening exercises, transfer training, gait re-education (for incomplete injuries), respiratory physiotherapy
Occupational therapy	Activities of daily living (ADLs), assistive devices, wheelchair skills, home modifications
Speech therapy	If high cervical injury with ventilator → communication aids
Psychology	Adjustment counselling, depression screening, coping strategies
Social work	Housing, financial support, community reintegration
Vocational rehabilitation	Return to work assessment and support
Urology	Neurogenic bladder programme (ICC training)
Orthotics	Braces, splints, standing frames

Prognosis ^[6]:

Complete injury: recovery rare
Incomplete injury: difficult to predict
- Most recovery occurs ≤ 6 months, many can eventually walk with aids
- Depends on level and extent of injury
- Loss of sphincter function is a poor prognostic factor

ASIA Grade	Prognosis
A (Complete)	Very poor for motor recovery below the level; < 5% convert to useful motor function
B (Sensory only)	~30% recover some useful motor function
C (Motor < 3)	~75% will eventually walk (with aids)
D (Motor ≥ 3)	Majority achieve community ambulation

Complete injury — prognosis is generally poor. Incomplete injury — prognosis highly variable. Long-term issues with dysreflexia, neurogenic bladder, spasticity, contracture, and skin problems ^[1]

High Yield Summary — Management of SCI

ABCDE first — jaw thrust (NOT head-tilt chin-lift) for airway in suspected C-spine injury. C3-5 injuries threaten the diaphragm.
Immobilise immediately: collar + log roll. Unstable spine = any movement worsens secondary injury.
Neurogenic shock: IV fluids + vasopressors (noradrenaline), target MAP ≥ 85 mmHg for 5-7 days. Always rule out hypovolaemic shock first.
Medical prophylaxis: DVT (LMWH + IPC), stress ulcers (PPI), AROU (urinary catheter), analgesics.
Methylprednisolone is NOT recommended for acute traumatic SCI — increases infection, GI bleed, hyperglycaemia without proven neurological benefit. BUT steroids ARE used for metastatic cord compression (dexamethasone) and transverse myelitis (IV methylprednisolone).
Surgery for: unstable fractures, progressive neurological deterioration, myelopathy/radiculopathy, intractable pain. Aim: decompression + reduction + fixation. Early surgery (within 24 hours) preferred for incomplete injuries.
Non-surgical immobilisation for stable injuries: spinal orthosis for 2-3 months. Problems: pressure sores, muscle weakness, contractures, decreased pulmonary function.
Tumours: primary → surgical resection ± adjuvant RT; metastasis → primarily ERT, surgery if pain/instability/RT-resistant.
Rehabilitation is lifelong: PT, OT, bladder programme (ICC), psychological support, vocational rehab.
Prognosis: Complete (ASIA A) → recovery rare. Incomplete → most recovery within 6 months. Loss of sphincter function is a poor prognostic factor.

Active Recall - Management of Spinal Cord Injuries

References

^[1] Lecture slides: GC 110. Paraplegia Spinal cord compression Transverse myelitis Spinal dysraphism Neuroimaging III Spinal Cord.pdf ^[6] Senior notes: Ryan Ho Neurology.pdf (Section 9.6 Spinal Trauma, p176-177) ^[8] Senior notes: Ryan Ho Fundamentals.pdf (Section 3.4.9 Paraplegia, p334-335) and Ryan Ho Neurology.pdf (Section 9.1, p168-169) ^[15] Senior notes: Ryan Ho Respiratory.pdf (p80 — TB spondylitis management) ^[16] Senior notes: Ryan Ho Radiology.pdf (p18 — Spinal trauma imaging) ^[20] Senior notes: Ryan Ho Critical Care.pdf (p7 — Airway management) ^[21] Senior notes: felixlai.md (Neurogenic shock management; Foley catheter indications/contraindications)

Complications of Spinal Cord Injuries

Complications of SCI are the major drivers of morbidity, mortality, and healthcare cost in the long term. Many patients survive the initial injury but then die or suffer significantly from preventable complications. The key principle is: the paralysed body doesn't stop having physiological needs — it just loses the ability to signal, regulate, and protect itself. Every complication below can be traced back to the loss of motor, sensory, or autonomic function.

The complications can be organised by timing (acute vs. chronic) and by system.

Long-term issues with dysreflexia, neurogenic bladder, spasticity, contracture, and skin problems ^[1]

A. Acute / Early Complications

Neurogenic (spinal) shock in SCI down to T1 ^[8]:

Cause: sympathetic signal disruption ^[8]
Presentation: vasodilatation → hypotension, bradycardia, warm, flushed skin ^[8]
Diaphragmatic breathing if C5 or below (loss of control of intercostal muscles) ^[8]
Respiratory arrest if above C3 (loss of control of diaphragm) ^[8]

Why it happens: The sympathetic chain exits the cord from T1–L2. Any cervical or upper thoracic SCI disrupts this entire outflow → the body cannot constrict its blood vessels or increase heart rate → profound vasodilatory hypotension with paradoxical bradycardia (because the vagus nerve, which exits the brainstem and is NOT affected by the spinal injury, is now unopposed).

Why it's dangerous: Hypotension reduces cord perfusion → worsens secondary ischaemic injury. Bradycardia can progress to cardiac arrest in high cervical lesions.

Management: IV fluids and vasopressors/inotropes ^[1]. Target MAP ≥ 85 mmHg.

Neurogenic vs Hypovolaemic Shock — Again

In polytrauma, neurogenic and hypovolaemic shock often coexist. A warm, bradycardic, hypotensive patient who is also bleeding from a pelvic fracture needs BOTH volume resuscitation and vasopressors. Never assume one diagnosis exclusively.

The most common cause of death in acute SCI, particularly for cervical injuries.

Level	Respiratory Impact	Mechanism
Above C3	Respiratory arrest	Loss of phrenic nerve (C3-5) → no diaphragm function → apnoea
C3-C5	Diaphragmatic breathing only, ↓vital capacity	Partial/complete phrenic nerve injury; intercostals paralysed
C5-T6	Paradoxical ventilation ^[6], impaired cough	Intercostal muscles paralysed → cannot stabilise chest wall during inspiration; abdominal muscles paralysed → cannot generate adequate cough pressure for secretion clearance
Below T6	Mild restriction	Loss of abdominal muscle tone reduces forced expiration and cough

Specific respiratory complications:

Atelectasis and pneumonia: the combination of poor cough, retained secretions, and immobility creates a perfect environment for lung collapse and lower respiratory tract infections. Pneumonia is the leading cause of death in both acute and chronic SCI.
Pulmonary embolism: from DVT (see below) — a massive PE is a sudden, catastrophic complication.
Ventilator dependence: high cervical SCI patients may require lifelong mechanical ventilation or diaphragmatic pacing.

Prevention: chest physiotherapy, assisted cough techniques (quad cough), incentive spirometry, early mobilisation where possible, suctioning of secretions, VTE prophylaxis.

SCI patients have the highest rate of DVT of any hospitalised population — up to 80% without prophylaxis.

Why? Virchow's triad is perfectly fulfilled:

Stasis: paralysed lower limbs → no calf muscle pump → blood pools in deep veins
Endothelial injury: trauma, surgery, catheterisation
Hypercoagulability: trauma-induced coagulopathy with elevated tissue factor and reduced fibrinolysis

Clinical problem: the patient cannot feel leg swelling or pain (sensory loss below the level) → DVT is often clinically silent until it presents as massive PE.

Prevention: LMWH + intermittent pneumatic compression + compression stockings from day 1. Continue for 2-3 months.

Spinal injury and operation are recognised causes of paralytic ileus ^[22].

Why? Acute SCI disrupts the autonomic innervation of the gut. The sympathetic (T5-L2) and parasympathetic (vagus for proximal gut, S2-4 for distal gut) inputs are both affected to varying degrees. In the acute phase, there is a generalised loss of coordinated peristalsis → the gut becomes atonic.

Clinical features: abdominal distension, absent bowel sounds, vomiting, inability to tolerate oral feeds.

Management: NPO, nasogastric tube drainage, IV fluids, correction of electrolytes (especially K⁺ and Mg²⁺). Usually resolves within days as autonomic reflexes partially recover.

Risk: a distended gut elevates the diaphragm → further compromises the already-limited respiratory function in a cervical SCI patient. This is a vicious cycle.

Anogenital issues: spastic or paralytic bladder, incontinence ± constipation and sexual dysfunction ^[8]

In the acute phase (during spinal shock), the detrusor muscle is areflexic — it cannot contract. The patient cannot sense bladder fullness (loss of afferent S2-4 pathways) and cannot voluntarily initiate voiding (loss of descending control). The result is painless AROU.

Why painless? Because the afferent sensory fibres from the bladder (travelling via S2-4) are also disrupted → the patient has no urge to void and no suprapubic discomfort. This contrasts with mechanical obstruction (e.g., BPH) where the patient is in significant pain because the sensory pathways are intact.

Management: indwelling urethral catheter in the acute phase → transition to intermittent clean catheterisation (ICC) once stable.

High SCI causes unopposed vagal (parasympathetic) stimulation to the stomach → excessive gastric acid secretion → stress-related mucosal damage.

Prevention: PPI (omeprazole) or H₂-blocker from day 1.

B. Subacute Complications (Days to Weeks)

Others: pressure sores ^[8]

One of the most devastating and costly complications of SCI. Prevalence: 25–60% of SCI patients will develop a pressure ulcer at some point.

Why? Three factors converge:

Loss of sensation: the patient cannot feel the pain of prolonged pressure on a bony prominence → no reflexive repositioning
Immobility: cannot shift weight, roll, or adjust position
Autonomic dysfunction: impaired vasomotor control below the lesion → poor microcirculation → tissue is more vulnerable to ischaemic damage from external pressure

Common sites: sacrum, ischial tuberosities (sitting), greater trochanters, heels, occiput (lying on hard spinal board).

Pathophysiology: sustained pressure > capillary closing pressure (~32 mmHg) → local tissue ischaemia → necrosis → ulceration → secondary infection → osteomyelitis → sepsis → death.

Grading (NPUAP/EPUAP):

Stage	Description
I	Non-blanchable erythema of intact skin
II	Partial-thickness skin loss (blister or shallow ulcer)
III	Full-thickness skin loss (subcutaneous fat visible, bone/tendon NOT exposed)
IV	Full-thickness tissue loss with exposed bone, tendon, or muscle

Prevention (far easier than treatment):

2-hourly turning/repositioning
Pressure-relieving mattress (alternating air pressure)
Regular skin inspection (especially over bony prominences)
Adequate nutrition (protein, vitamin C, zinc for wound healing)
Weight shifts every 15–30 minutes when seated in wheelchair

Treatment: offloading, wound debridement, moist wound dressings, VAC therapy, flap surgery for Grade III-IV ulcers, antibiotics if infected.

Pressure Ulcers Kill

Pressure ulcers are not trivial. They are a major cause of sepsis, prolonged hospitalisation, and death in SCI patients. Prevention is a core nursing and medical responsibility. A stage IV sacral ulcer with osteomyelitis can take months to heal and may require multiple surgeries.

Spasticity ^[1] — this is a hallmark late complication of UMN-type SCI.

Pathophysiology: After spinal shock resolves (1-2 weeks), the loss of descending inhibitory input from the cortex and brainstem (reticulospinal, vestibulospinal pathways) results in anterior horn cells becoming hyperexcitable → exaggerated stretch reflexes → velocity-dependent increase in muscle tone.

Think of it this way: normally, the brain sends "calm down" signals to spinal motor neurons. When those signals are cut off, the motor neurons fire excessively in response to even minimal stretch stimuli.

Clinical features: increased muscle tone (clasp-knife pattern), hyperreflexia, clonus, flexor or extensor spasms (often painful), muscle contractures if left untreated.

Double-edged sword: some degree of spasticity can be useful — it maintains muscle bulk (preventing atrophy), aids venous return (reducing DVT risk), and can be used functionally for standing/transfers. But excessive spasticity causes pain, interferes with function, causes contractures, and triggers autonomic dysreflexia.

Management:

Physiotherapy: stretching, range-of-motion exercises, standing programmes
Oral medications: baclofen (GABA-B agonist — reduces presynaptic excitatory neurotransmitter release), tizanidine (α₂-agonist — reduces spinal excitatory interneuron activity), diazepam (GABA-A agonist — general CNS depression)
Focal: botulinum toxin injections for localised problematic spasticity
Intrathecal baclofen pump: for severe, diffuse, refractory spasticity — delivers baclofen directly to the CSF around the spinal cord at much lower doses than oral (avoids systemic side effects like sedation)
Surgical: tendon lengthening, neurectomy (rarely needed)

Contracture ^[1] — fixed shortening of muscles, tendons, or joint capsules.

Why? Immobility + spasticity → muscles held in shortened position for prolonged periods → fibrosis and permanent shortening of soft tissues → the joint becomes fixed in one position.

Common patterns: hip flexion, knee flexion, ankle equinus (plantarflexion), wrist flexion.

Prevention: daily range-of-motion exercises, proper positioning, splinting, stretching programmes.

Treatment: serial casting, dynamic splinting, surgical release if fixed.

C. Chronic / Late Complications

Autonomic dysreflexia (if lesion at or above T6) due to episodic autonomic fluctuation ^[8]

This is a medical emergency unique to SCI patients with lesions at or above T6.

Mechanism (from first principles) ^[8]:

A noxious stimulus below the level of injury (most commonly a full bladder, constipation, skin pressure, UTI, ingrown toenail)
Afferent signals travel to the spinal cord and trigger a massive reflex sympathetic discharge below the lesion → widespread vasoconstriction below the injury level → ↑↑BP
The brain detects the hypertension via intact carotid/aortic baroreceptors → sends strong vagal reflex → bradycardia and attempted vasodilation above the lesion
But the inhibitory sympathetic signals from the brain CANNOT pass through the damaged cord → the vasoconstriction below the lesion continues unchecked → BP keeps rising

S/S: paroxysmal HTN, throbbing headache, excessive sweating, flushing of skin, bradycardia, anxiety etc ^[8]

Why is it dangerous? Systolic BP can exceed 250–300 mmHg → risk of seizures, intracranial haemorrhage, retinal detachment, cardiac arrhythmia, myocardial infarction, death.

Why ≥ T6? Because the major splanchnic vascular bed (supplied by the greater splanchnic nerve from T5-T9) is the largest capacitance vessel system in the body. If the lesion is above T6, this entire bed participates in the unopposed sympathetic vasoconstriction → massive rise in BP. Lesions below T6 do not produce enough vasoconstriction to overwhelm the compensatory vasodilation above.

Emergency management:

Sit the patient upright (uses gravity to lower BP)
Loosen any tight clothing or constrictive devices
Identify and remove the trigger:
- Check the bladder (blocked catheter? → flush or replace; no catheter? → catheterise)
- Check the bowels (faecal impaction? → digital disimpaction with anaesthetic gel)
- Check the skin (pressure ulcer, ingrown toenail, tight clothing)
Pharmacological BP control if trigger cannot be immediately identified or BP remains dangerously high:
- Sublingual nifedipine (10 mg) — calcium channel blocker → rapid vasodilation
- GTN paste (2% topical) — direct smooth muscle relaxant
- IV hydralazine or labetalol for refractory cases

Autonomic Dysreflexia — The Full Bladder is the Commonest Trigger

In any SCI patient (T6 or above) who suddenly develops headache + hypertension + sweating above the lesion + bradycardia → think autonomic dysreflexia immediately. The first thing to check is the urinary catheter — is it blocked? Is the bag full? Is there a kink? 85% of episodes are triggered by bladder or bowel distension.

Anogenital issues: spastic or paralytic bladder ^[8]

This is one of the most functionally significant and dangerous long-term complications.

The two patterns (depending on level of lesion):

Type	Lesion Level	Mechanism	Bladder Behaviour	Consequence
Spastic (reflex/UMN) bladder	Suprasacral (above S2)	Loss of cortical inhibition → reflex arc intact → involuntary detrusor contractions	Small-capacity, overactive bladder with uninhibited contractions; detrusor sphincter dyssynergia (DSD) — detrusor and sphincter contract simultaneously	↑↑urinary tract pressure → upper tract damage (hydronephrosis, renal failure) ^[8]
Paralytic (areflexic/LMN) bladder	Sacral (S2-4) or cauda equina	Destruction of the reflex arc → detrusor cannot contract at all	Large-capacity, flaccid bladder that fills passively and overflows	Overflow incontinence, UTI, bladder stones

Detrusor sphincter dyssynergia (DSD) is the most dangerous pattern ^[8]:

Cause: spinal cord injury, pontine stroke
Mechanism: interruption of descending control by pontine micturition centre → failure of detrusor-sphincter coordination → synchronous contraction of both detrusor and sphincters
Consequence: ↑↑urinary tract pressure → upper tract damage

Long-term complications of neurogenic bladder:

Recurrent UTIs (the most common complication of SCI overall): stagnant urine + instrumentation + impaired immune responses below the lesion
Bladder stones (stagnant, alkaline urine + catheter as nidus)
Hydronephrosis and renal failure (from high-pressure DSD or chronic reflux)
Squamous cell carcinoma of the bladder: chronic irritation from indwelling catheter → squamous metaplasia → SCC (16-20× risk) ^[10]

Management: intermittent clean catheterisation (gold standard), anticholinergics (oxybutynin) for overactive detrusor, alpha-blockers for sphincter relaxation in DSD, botulinum toxin injection into detrusor, augmentation cystoplasty for refractory cases, regular surveillance for bladder cancer in long-term catheter users.

Patients with spinal cord injuries who have long-term indwelling catheters have a 16-20× risk of developing SCC in the bladder (NOT UCC because of chronic irritation by catheter in bladder) ^[10]

Loss of autonomic and voluntary control of defecation. Two patterns mirror the bladder:

Suprasacral (reflex) bowel: intact reflex arc → stool held by spastic sphincter → responds to rectal stimulation (suppositories, digital stimulation)
Sacral (areflexic) bowel: flaccid sphincter → faecal incontinence, no reflex defecation

Complications: constipation (commonest), faecal impaction (trigger for autonomic dysreflexia), bowel obstruction, megacolon, haemorrhoids.

Management: scheduled bowel programme (same time every day/every other day), digital stimulation or glycerine suppositories, adequate fluid/fibre, stool softeners (docusate), prokinetics (metoclopramide if needed).

Sexual dysfunction ^[8]

Function	Innervation	Impact of SCI
Erection	Parasympathetic S2-4 (reflex erection) + Psychogenic erection (T11-L2 sympathetic)	Suprasacral lesion: reflex erection preserved (S2-4 arc intact) but psychogenic erection lost. Sacral lesion: both lost.
Ejaculation	Sympathetic T11-L2	Often impaired in both suprasacral and sacral lesions → male infertility
Female arousal/orgasm	Parasympathetic S2-4	Often impaired but pregnancy is possible

Management: PDE5 inhibitors (sildenafil — "Viagra") for erectile dysfunction; electroejaculation or vibratory stimulation for fertility; psychological support and counselling.

Impaired thermoregulation ^[8]

Why? Thermoregulation depends on:

Cutaneous vasodilation/vasoconstriction (sympathetic T1-L2 control)
Sweating (sympathetic cholinergic fibres)
Shivering (motor — requires functioning skeletal muscles)

All three are disrupted below the lesion → the patient becomes poikilothermic below the injury level (body temperature drifts with environmental temperature).

Clinical significance: patients are at risk of both hypothermia (in cold environments — cannot shiver or vasoconstrict) and hyperthermia (in hot environments — cannot sweat or vasodilate). Hyperthermia can worsen secondary cord injury in the acute phase.

Present in 60-80% of SCI patients. Two major types:

Type	Description	Mechanism
Nociceptive (musculoskeletal)	Shoulder pain (from wheelchair propulsion), back pain, overuse syndromes	Mechanical stress on functioning joints that compensate for paralysed ones
Neuropathic (central/below-level)	Burning, shooting, electric-shock pain below the lesion; often diffuse and constant	Reorganisation of dorsal horn circuits after deafferentation → spontaneous ectopic firing of pain pathways; central sensitisation
Neuropathic (at-level)	Band-like burning at the sensory level	Damaged dorsal root entry zone → abnormal signal generation

Management: pregabalin/gabapentin (first-line for neuropathic), amitriptyline/duloxetine, TENS, intrathecal drug delivery, psychological approaches (CBT), exercise.

Formation of mature lamellar bone in soft tissues (usually around paralysed joints — hip, knee, elbow).

Why? The exact mechanism is unclear, but involves aberrant mesenchymal stem cell differentiation in response to local inflammation + neurogenic signalling disruption. Incidence: 10-53% of SCI patients.

Clinical features: joint swelling, reduced ROM, warmth (can mimic DVT); if severe, complete ankylosis of the joint.

Diagnosis: elevated serum ALP (early), triple-phase bone scan (sensitive early), plain XR (once mature).

Prevention: NSAIDs (indomethacin), early mobilisation, low-dose radiation in high-risk patients.

Treatment: physiotherapy to maintain ROM; surgical excision once the bone is mature (wait ≥ 12-18 months — premature surgery leads to recurrence).

Why? Wolff's law — bone remodels in response to mechanical load. Paralysed limbs bear no weight → osteoclastic resorption exceeds osteoblastic formation → rapid bone loss below the level of injury (up to 40% bone mineral density loss in the first 2 years).

Consequence: fragility fractures from minimal trauma (transfers, physiotherapy). These fractures may go unrecognised because the patient cannot feel pain.

Prevention: standing programmes (standing frame), bisphosphonates (limited evidence in SCI), calcium and vitamin D supplementation, denosumab.

A late complication in 3-4% of SCI patients. A fluid-filled cavity (syrinx) develops within the injured cord, usually at or above the level of injury, and gradually expands.

Clinical features: progressive ascending neurological deficit (pain, weakness, sensory loss) months to years after the original injury — often presenting as a new "central cord syndrome" pattern.

Why? Altered CSF dynamics from arachnoid adhesions at the injury site → fluid is driven into the central canal → progressive cavitation.

Diagnosis: MRI — shows an intramedullary cystic cavity.

Management: observation for small/stable syrinx; surgical drainage (syringoperitoneal or syringopleural shunt) or untethering of scar tissue for progressive symptomatic syrinx.

System	Acute	Subacute/Chronic
Cardiovascular	Neurogenic shock (hypotension + bradycardia)	Autonomic dysreflexia (paroxysmal HTN); DVT/PE (ongoing risk)
Respiratory	Respiratory failure, aspiration, atelectasis	Pneumonia (leading cause of death), ventilator dependence
Urological	AROU (painless)	Neurogenic bladder (spastic or paralytic), UTI, stones, SCC of bladder (16-20× risk with long-term catheter), hydronephrosis, renal failure
GI	Paralytic ileus, stress ulceration	Neurogenic bowel, constipation, faecal impaction
Musculoskeletal	—	Spasticity, contractures, heterotopic ossification, osteoporosis, pathological fractures
Skin	—	Pressure ulcers
Neurological	Spinal shock, secondary neurological injury	Neuropathic pain, post-traumatic syringomyelia
Metabolic/Autonomic	Impaired thermoregulation	Impaired thermoregulation (chronic), metabolic syndrome, increased cardiovascular risk
Sexual/Reproductive	Priapism (acute)	Sexual dysfunction, infertility
Psychological	Acute stress reaction	Depression (very common), PTSD, adjustment disorder, suicide risk

Complete cord transection: Complete paralysis & sensory loss below; Sphincter dysfunction; Poor functional prognosis ^[1]

Incomplete injury: Prognosis variable ^[1]

Sphincter dysfunction — a point of no return ^[1]

High Yield Summary — Complications of SCI

Respiratory failure is the #1 killer in acute cervical SCI. C3-5 controls the diaphragm. Pneumonia is the leading cause of death in both acute and chronic phases.
DVT/PE: highest risk of any hospitalised population. Start LMWH + IPC from day 1. Silent because patients cannot feel leg swelling.
Neurogenic shock: hypotension + bradycardia + warm skin from sympathetic disruption (T1-L2). Treat with IV fluids + vasopressors. Always exclude hypovolaemia first.
Autonomic dysreflexia: lesion ≥ T6. Noxious stimulus below lesion → massive reflex sympathetic discharge → severe HTN + bradycardia + headache + sweating above lesion. Commonest trigger = full bladder. Sit up, find and remove trigger, sublingual nifedipine if severe. Medical emergency — can cause stroke/death.
Neurogenic bladder: suprasacral = spastic (DSD → high-pressure → upper tract damage); sacral = paralytic (overflow incontinence). ICC is the gold standard. Long-term catheter → 16-20× risk of SCC (not UCC).
Pressure ulcers: loss of sensation + immobility + poor circulation. Sacrum, ischial tuberosities, heels. Prevention: 2-hourly turning, pressure-relieving mattress, nutrition. Stage IV → osteomyelitis → sepsis → death.
Spasticity + contractures: from loss of descending inhibition (UMN). Treat with physiotherapy, baclofen, tizanidine, botulinum toxin, intrathecal baclofen pump.
Impaired thermoregulation: poikilothermia below the lesion. Risk of both hypothermia and hyperthermia.
Neuropathic pain: present in 60-80%. Pregabalin/gabapentin first-line.
Post-traumatic syringomyelia: ascending deficit months-years later. MRI diagnosis. Surgery if progressive.
Depression: very common. Screen early, treat aggressively. Suicide risk is elevated in SCI populations.
Sphincter dysfunction is a point of no return — once established, it has the worst prognosis for recovery.

Active Recall - Complications of Spinal Cord Injuries

References

^[1] Lecture slides: GC 110. Paraplegia Spinal cord compression Transverse myelitis Spinal dysraphism Neuroimaging III Spinal Cord.pdf ^[6] Senior notes: Ryan Ho Neurology.pdf (Section 9.6 Spinal Trauma, p176-177) ^[8] Senior notes: Ryan Ho Fundamentals.pdf (Section 3.4.9 Paraplegia, p334-335) and Ryan Ho Neurology.pdf (Section 9.1, p168-169) ^[10] Senior notes: felixlai.md (Section on bladder cancer risk factors — SCC in SCI patients) ^[22] Senior notes: Ryan Ho GI.pdf (p141 — Paralytic ileus causes including spinal injury)

Spinal Cord Injuries

1. Definition

2. Epidemiology

2.1 Global and Hong Kong Context

2.2 Age and Sex Distribution

2.3 Common Causes

2.4 Site of Injury

3. Risk Factors

4. Anatomy and Function of the Spinal Cord

4.1 Vertebral Column

4.2 Three-Column Theory (Denis Classification)

4.3 Spinal Cord Internal Anatomy

4.4 Blood Supply

4.5 Key Dermatome Landmarks

4.6 Key Myotome Landmarks (ASIA Motor Testing)

4.7 The Phrenic Nerve (C3, C4, C5)

5. Etiology (Focus on Hong Kong)

5.1 Traumatic SCI (Most Common)

5.2 Non-Traumatic SCI

6. Pathophysiology

6.1 Primary Injury Mechanisms

6.2 Secondary Injury Cascade

6.3 Spinal Shock — Two Meanings

6.4 Why Does SCI Above T6 Cause Autonomic Dysreflexia (Later)?

7. Classification

7.1 By Completeness — ASIA Classification (IMPORTANT!) [1][3][6]

7.2 By Level

7.3 By Spinal Cord Syndrome — Clinical Patterns

Complete Cord Syndrome

Anterior Cord Syndrome

Dorsal Cord Syndrome (Posterior Cord)

Brown-Séquard Syndrome (Cord Hemisection)

Central Cord Syndrome

Conus Medullaris Syndrome

Cauda Equina Syndrome

7.4 AO Classification of Cervical Spine Fractures [3]

Upper Cervical (C0–C2)

Subaxial (C3–C7)

7.5 Stability Assessment

8. Clinical Features

8.1 Symptoms

A. Motor Symptoms

B. Sensory Symptoms

C. Autonomic and Visceral Symptoms

D. Pain

8.2 Signs

A. Motor Signs

B. Sensory Signs

C. Autonomic and Other Signs

8.3 Clinical Scenario (From Lecture Slides)

9. Special Considerations

9.1 Neurogenic Bladder in SCI

9.2 SCI in the Context of Head Injury

9.3 Long-Term Issues [1]

10. Summary of Clinical Approach

Active Recall - Spinal Cord Injuries

References

Overview: The Clinical Problem

Step 1: Is This a Spinal Cord Lesion? — Localising the Problem

Step 2: Differential Diagnosis by Tempo of Onset

A. Acute Onset (Minutes to Hours)

B. Subacute Onset (Days to Weeks)

C. Chronic/Insidious Onset (Weeks to Months to Years)

Step 3: Differential by Cord Syndrome Pattern

Step 4: "Don't Miss" Diagnoses (Surgical Emergencies)

Step 5: Diagnostic Differentiation by Context

In the Trauma Setting

In the Non-Trauma Setting

Differential Diagnosis Algorithm

Summary Table: Key Differentiating Features

The Neurogenic Shock vs Other Causes of Shock — A Critical DDx in Trauma

Special DDx: Overactive Bladder / Neurogenic Bladder

Active Recall - Differential Diagnosis of Spinal Cord Injuries

A. Diagnostic Framework — What Are We Trying to Answer?

B. Clinical Diagnostic Assessment

B1. The ASIA / ISNCSCI Examination — The Gold Standard for Classifying SCI

B2. Determining Stability — Clinical Signs

B3. Determining Completeness — Spinal Shock Caveat

C. Imaging — The Diagnostic Workup

C1. Decision Rules: Who Needs Imaging?