The lecture teaches a structured approach ^[1]:

Adequate coverage should be from the skull base down to the C7/T1 junction. ^[1]

Four alignment lines: Anterior vertebral line, Posterior vertebral line, Spinolaminar line, Spinous process tip line. ^[1]

Why four lines? Each line traces a different anatomical boundary:

• Anterior vertebral line — traces the front of the vertebral bodies. Disruption suggests vertebral body fracture or subluxation.
• Posterior vertebral line — traces the back of the vertebral bodies (forms the anterior wall of the spinal canal). Disruption here means the spinal canal is compromised.
• Spinolaminar line — posterior wall of the spinal canal. Disruption suggests posterior element fracture or ligamentous injury.
• Spinous process tips — most posterior landmark. Widened interspinous space ("fanning") suggests posterior ligamentous disruption.

All four lines should follow a smooth lordotic curve. Any step-off or angulation is abnormal.

Destruction of inferior C5 endplate, superior C6 endplate, reduced C5/6 disc space, resulting in focal kyphosis — due to bacterial spondylodiscitis affecting C5/C6. ^[1]

Why does spondylodiscitis cause focal kyphosis? The intervertebral disc has no blood supply in adults; it relies on the vertebral endplates. Bacterial infection (usually haematogenous Staph aureus) seeds in the richly vascularised endplates and destroys the disc → loss of anterior column height → segmental kyphosis.

Oblique views facilitate assessment of foraminal narrowing secondary to decrease in disc height and uncovertebral joint hypertrophy. ^[1]

The uncovertebral joints (joints of Luschka) are unique to the cervical spine. They sit on the lateral margins of the vertebral bodies. Hypertrophy of these joints narrows the neural foramen, compressing exiting nerve roots → radiculopathy.

6 mm at C2 / < ½ vertebral body depth. 22 mm at C6 / < 1 vertebral body depth. ^[1]

Why the difference? The oesophagus and trachea lie anterior to the lower cervical spine, so normal soft tissue is thicker below C4. Increased prevertebral soft tissue swelling at any level suggests haematoma (fracture/vascular injury) or abscess (infection).

Normal cervical lordosis of 15–20 degrees. ^[1]

Loss of lordosis (straightening) may be a sign of muscle spasm, degenerative change, or ligamentous injury. Fixed kyphosis is important for surgical planning.

Midsagittal diameter of the spinal canal: Relative stenosis if < 12 mm; absolute stenosis if < 10 mm. ^[1]

Dynamic stenosis = distance from posteroinferior corner of cranial vertebra to anterosuperior edge of caudal lamina. Dynamic stenosis if < 12 mm. ^[1]

Dynamic instability if positional change > 3.5 mm or > 11° between adjacent vertebrae. ^[1]

Why dynamic views? Static X-rays may miss instability. Flexion and extension views reveal abnormal motion between segments.

ADI (atlanto-dental interval) should be < 4 mm; assess in flexion and extension views. SAC (space available for the cord) should be > 14 mm. ^[1]

Causes: rheumatoid arthritis, Down's syndrome. ^[1]

Why RA and Down syndrome? Both conditions feature ligamentous laxity:

• RA: Synovial pannus erodes the transverse ligament of C1, allowing C1 to slide forward on C2 (atlantoaxial subluxation).
• Down syndrome: Generalised ligamentous laxity predisposes to atlantoaxial instability (important for anaesthetic clearance and sports participation).

The ADI is the distance between the anterior arch of C1 and the dens. The SAC (Steel's rule of thirds: dens = ⅓, cord = ⅓, safety space = ⅓) is what's left for the spinal cord. If SAC < 14 mm, cord compression is likely.

Basilar invagination: odontoid prolapsing into the foramen magnum. ^[1]

Chamberlain's line: Line joining posterior hard palate to opisthion (dens should not pass). McGregor's line: Line joining posterior hard palate to most caudal point of occipital curve (dens should be < 4.5 mm above). ^[1]

Causes: congenital (achondroplasia) and acquired (rheumatoid arthritis). ^[1]

Why does this matter? The odontoid migrating upward compresses the brainstem/upper cervical cord at the foramen magnum — can be lethal or cause severe myelopathy.

The lecture shows a slide of pathological causes ^[1]. These include:

• Disc protrusion/herniation (most common acute cause)
• Osteophyte formation (most common chronic cause — cervical spondylosis)
• OPLL (ossification of posterior longitudinal ligament)
• Ligamentum flavum hypertrophy/buckling
• Facet joint hypertrophy
• Subluxation/instability

Why the cervical spine is vulnerable: The cervical canal is narrower than the lumbar canal, and the spinal cord (rather than cauda equina) runs through it. Even modest compression can cause devastating myelopathy.

Clinical features of cervical myelopathy: Numbness or sensory disturbance (fingers, upper limb); Loss of hand dexterity; Poor proprioception + spastic gait; Motor weakness and sphincteric dysfunction appear in the late stage; Pain is NOT a predominant feature. ^[1]

UMN signs below level of compression; LMN signs at the level of compression. ^[1]

Why UMN below and LMN at the level?

• At the level of cord compression, the anterior horn cells (LMN cell bodies) are directly damaged → LMN signs (wasting, fasciculations, hyporeflexia) in the corresponding myotome.
• Below the level, the descending corticospinal tracts are interrupted → UMN signs (spasticity, hyperreflexia, Babinski sign) in the limbs below.

Hoffman's sign: Involuntary finger flexor contraction due to activation of a monosynaptic stretch reflex. Positive response represents dis-inhibition of a C8 reflex, indicates lesion above C8. ^[1]

Finger escape sign: Present arms with fingers forward and palms down. Deficient adduction and/or extension of ulnar 2 or 3 fingers. ^[1]

10 second test: Number of complete cycles of movement within 10 seconds. Rhythm of movement. Difficult, slow and incomplete finger extension. Exaggerated (failure of synergy between wrist and finger). ^[1]

Inverted supinator reflex: Introduced by Babinski in 1910. Signifying lesion at C5/6 or above. Two components: Absence of contraction of brachioradialis + Hyperactive contraction of finger flexors (C8). ^[1]

Scapulohumeral reflex: Cord compression above C3 vertebral body. ^[1]

Why is the inverted supinator reflex important? It demonstrates both LMN (absent brachioradialis at C5/6 — the level of damage) and UMN (hyperreflexic C8 finger flexors — below the level) in a single reflex test. This beautifully localises a C5/6 cord lesion ^{[1] [2]}.

Long tract signs: Lower limb hyperreflexia, Clonus and upgoing Babinski, Dorsal column function (Romberg, Tandem walking), Lhermitte sign (severe demyelination and hyper-excitability of dorsal column). ^[1]

Sphincter function: Urinary frequency, Retention, Overflow incontinence, Change in bowel habit. ^[1]

Functional assessment: Japanese Orthopaedic Association (JOA) score. ^[1]

Lhermitte sign explained: An electric shock-like sensation radiating down the spine/limbs on neck flexion. It indicates dorsal column irritability — the flexion mechanically stretches an already compromised posterior cord. Classically associated with MS but also seen in cervical myelopathy.

Four scoring categories: Upper limb motor and sensory, Lower limb function, Urinary sphincter. Score from 0–17. Guide of disease severity, facilitates decision making for surgery, and monitoring of disease progression/recovery. ^[1]

The JOA score is the standard functional outcome measure for CSM. A lower score = worse function. It is used to document baseline severity, decide on surgical intervention, and track post-operative recovery.

Spinal cord ascends approximately one segment during its development. Cervical discs generally lie opposite spinal cord segments which are numbered one lower than the number of roots passing them. ^[1]

What this means: Because the cord is shorter than the vertebral column, the C5/6 disc level lies opposite the C6/7 cord segment. A disc at C5/6 compresses the C6 nerve root in the foramen (radiculopathy) and the C6/7 cord segment (myelopathy). This offset increases further down the spine.

MRI — basic interpretation: Level of lesion, location; Pathoanatomy (disc, osteophyte, OPLL, flavum); Obliteration of CSF space; Cord shape/cross-sectional area; Intramedullary signal change (myelomalacia). ^[1]

Myelomalacia = T2 hyperintense signal within the cord on MRI, representing gliosis/necrosis from chronic compression. This is an ominous sign — it suggests irreversible cord damage and poorer surgical outcomes.

Plain CT scan to delineate OPLL. Dynamic X-rays to diagnose atlantoaxial subluxation in RA. Important to rule out other pathological process. ^[1]

Ectopic calcification as a cause of cord compression. Much more common in Asian vs non-Asian populations (up to 2–4%). Male predominance, affects younger population. More commonly affects cervical than thoracic spine. ^[1]

High prevalence of cervical spine involvement. Formation of retroodontoid pannus. Synovial inflammation predisposes to cervical instability: Atlantoaxial subluxation (C1/2), Subaxial subluxation, Vertical subluxation (basilar invagination). Use of RA medications reduces the incidence of cervical involvement. ^[1]

Why RA affects the cervical spine: The C1/C2 articulation has extensive synovial tissue. RA pannus erodes the transverse ligament and dens, causing instability. Modern DMARDs (especially biologics) have significantly reduced the incidence of severe cervical involvement.

Progressively deteriorating disorder: 75% deteriorate in a stepwise fashion, 20% deteriorate slowly and steadily, 5% have rapid onset with a stable plateau. At present, no good conservative treatment options. ^[1]

Progressive neurologic deficit; Significantly impaired ADL (JOA score); Compatible imaging findings. ^[1]

All three should be present. Imaging alone (e.g. cord compression on MRI) without clinical correlation is not an automatic indication for surgery.

General considerations: Fixed kyphotic deformities favour anterior approach. Disc protrusions better treated with anterior technique. Infolding/thickening of ligamentum flavum better treated with posterior technique. 3 level pathology or more favours posterior approach. Fusion is indicated if subluxation or instability. Laminoplasty patients may experience more post-op axial neck pain. ^[1]

Examples of procedures:

• Anterior: ACDF (Anterior Cervical Discectomy and Fusion), Corpectomy
• Posterior: Laminoplasty (open-door technique preserves posterior elements), Laminectomy ± fusion

Anterior surgery: Esophageal injury (intra-op or late due to implant), Vertebral artery injury, Airway compromise, Pseudoarthrosis (failed fusion), Adjacent level degeneration. ^[1]

Posterior surgery: Post-op kyphosis, Axial symptoms (shoulder and neck pain), C5 nerve root paresis. ^[1]

C5 palsy after posterior surgery is a well-known complication — the C5 root is tethered and short; posterior decompression allows the cord to drift backward, stretching C5 preferentially. Patients develop deltoid weakness post-operatively.

Cervical myelopathy (symptoms may overlap — myeloradiculopathy); Peripheral nerve compression; Shoulder pathology. ^[1]

X-rays (AP/lateral, Oblique views for foraminal narrowing); CT scan; MRI scan (confirm nerve root/cord compression); NCV/EMG. ^[1]

NCV/EMG helps differentiate cervical radiculopathy from peripheral nerve entrapment (e.g. carpal tunnel, cubital tunnel). In radiculopathy, the sensory nerve action potential is preserved (because the lesion is proximal to the dorsal root ganglion), whereas in peripheral neuropathy it is reduced.

Limited evidence for use of neck collar and bedrest. Physical therapy: Traction, ROM exercises, Strength training and stretching. Medications: NSAIDs, Neuroleptics, Steroids. Epidural steroid injections. Up to 90% of patients have good response to conservative treatment measures. ^[1]

Indications: Persistent symptoms despite conservative management; Neurological deficits. Treatment options: Anterior — ACDF, artificial disc replacement; Posterior — posterior cervical foraminotomy. ^[1]

21 yo male, dived into shallow end of swimming pool headfirst, sudden onset neck pain, unable to move immediately. ^[1]

This is a classic axial loading/compression mechanism — the most common cause of cervical burst fractures and complete spinal cord injury in young adults.

Bimodal distribution: Young adults — High energy trauma; Old adults — Low energy trauma, Osteoporotic bone, Pre-existing spinal stenosis. ^[1]

Why bimodal? Young patients sustain high-energy injuries (diving, MVA, falls from height) that fracture normal bone. Elderly patients have pre-existing spondylosis/stenosis so even a minor fall can cause cord injury (often central cord syndrome from hyperextension).

Polytrauma involves injuries to the spine in up to 30% of cases. Multiple spinal fractures occur in 3–5%. Examine and X-ray the whole spine. ^[1]

Continue immobilization until clinical and radiological clearance: Cervical spine immobilization, Spine board, Log roll. ^[1]

A — Airway maintenance AND cervical spine protection; B — Breathing; C — Circulation; D — Disability (motor/sensory exam); E — Exposure (log-roll, per-rectal exam). ^[1]

Why is C-spine protection part of "A"? Because any airway manoeuvre (jaw thrust, intubation) risks further cervical injury. In-line stabilisation must be maintained during airway management.

Trauma series: CXR, AP pelvis, Lateral cervical spine. Polytrauma CT. ^[1]

NEXUS criteria to clear the cervical spine. ^[1]

The NEXUS (National Emergency X-Radiography Utilization Study) criteria allow clinical clearance of the cervical spine without imaging if ALL five criteria are met:

1. No midline cervical tenderness
2. No focal neurological deficit
3. Normal alertness
4. No intoxication
5. No painful distracting injury

If any one criterion is not met → image the cervical spine.

Rigid collar (correct size); Sand-bags and tape; Skull traction. ^[1]

Skull traction (Gardner-Wells tongs or halo ring) is used for reducible cervical fracture-dislocations. The weight is gradually increased under fluoroscopic guidance to reduce the subluxation before definitive fixation.

High/low energy trauma (MVA, fall from height, fall from level ground); Time of injury; Delay in diagnosis (unconscious, head injury, alcohol, multiple distracting injuries). ^[1]

Head to Toe: Head/chest wounds and cervical injury (relates to mechanism); Spine: Bruising, Tenderness, Stepping, Restricted movement. ^[1]

Stepping = palpable gap/step between spinous processes on posterior palpation → suggests ligamentous disruption or facet dislocation.

Sensory: Dermatome landmarks. Motor: Full ROM. Reflexes/Sphincter. ^[1]

The neurological exam in SCI must be documented using the ASIA (American Spinal Injury Association) chart:

Motor level: Lowest myotome with a grade of at least 3 on manual muscle testing. Sensory level: Most caudal normally innervated dermatome for both pin prick and light touch. Neurological level of injury: Most caudal segment with normal sensory and antigravity motor function (MMT ≥ 3) on both sides. ^[1]

Period of temporary loss of function after injury (hours to days). Flaccid paralysis below level of lesion. Areflexia. Loss of bowel/bladder control. Spinal shock is over if bulbocavernosus and/or anal wink reflex has returned. Assess for motor and sensory function only after spinal shock is over. ^[1]

Bulbocavernosus reflex: Squeezing the glans penis (or pulling on a Foley catheter) → anal sphincter contraction. Its return signals the end of spinal shock. Only then can you determine if the injury is complete or incomplete.

Complete injury — poor prognosis: No motor or sensory recovery, including sacral roots, distal to the site of injury and at the end of spinal shock. Incomplete injury — good prognosis: Degree of sparing, Speed of recovery. ^[1]

The key distinction: A complete injury (ASIA A) has NO sacral sparing (no perianal sensation, no voluntary anal contraction, no motor function below the level). If there is ANY sacral sparing, the injury is incomplete and prognosis is significantly better.

Bilateral facet dislocation: Flexion-distraction injury; Bony and ligamentous instability; Associated with significant neurological deficit; Require emergent treatment via reduction, decompression, and surgical fusion. ^[1]

Flexion teardrop fracture: Results from flexion and axial loading; Triangular bony fragment over anteroinferior body; ± Posterior displacement of vertebral body with canal compromise. ^[1]

Bilateral facet dislocation typically results in > 50% anterolisthesis on lateral X-ray and is highly associated with spinal cord injury. It is a surgical emergency.

Flexion teardrop fracture is the most unstable cervical fracture — the small "teardrop" fragment at the anteroinferior corner of the vertebral body belies the massive ligamentous disruption posteriorly.

Primary and secondary injury. Maximal damage occurs at the time of injury (primary). Inappropriate or delayed management can result in further oedema and cord damage (secondary injury) which is preventable. ^[1]

Minimizing secondary injury: Proper transfer; Steroid; Decompress; Stabilise. ^[1]

NASCIS: Methylprednisolone given within 8 hours of injury had better motor and sensory function at 6 weeks and 6 months. Higher rates of wound infection, pneumonia, sepsis so overall benefit is questionable. ^[1]

Structural: Instability; Decompression: Neurological deficit, Lack of improvement/deteriorating neurology; Polytrauma: To facilitate mobilization and rehabilitation. ^[1]

Respiratory problems: Respiratory muscle paralysis (Abdominal/intercostals T1–T12, Diaphragm C3–C5, Accessory muscles above C3); Decreased cough effort; Direct chest injuries; Autonomic dysfunction. ^[1]

DVT: Mechanical prophylaxis via sequential compression device; Anticoagulation prophylaxis within 72 hours of injury. ^[1]

Pressure sores: Turning every two hours; Padding of at-risk areas; Frequent skin inspection. ^[1]

Functional goals by level of spinal cord injury. ^[1]

Multiple team approach. Develop the functions which remain normal. Compensate for those that have been lost. ^[1]

The multidisciplinary team includes: orthopaedic/neurosurgery, rehabilitation medicine, physiotherapy, occupational therapy, speech therapy, clinical psychology, social work, nursing, and urology.

For OSCE: Be able to demonstrate:

1. Hoffman's sign — flick DIP of middle finger
2. Finger escape sign — hands outstretched, watch ulnar fingers drift
3. 10-second test — open/close fists rapidly
4. Spurling's test — extension + ipsilateral rotation + axial compression
5. Inverted supinator reflex — tap brachioradialis → finger flexion, no elbow flexion
6. Bulbocavernosus reflex — for SCI assessment

"A 65-year-old front seat passenger complained of acute neck pain and bilateral hand paraesthesia and weakness after a head-on collision accident. Physical examination of the lower limbs power and sensation was normal. Which of the following is suggestive of the diagnosis of central cord syndrome?"

A. Degenerative cervical spondylosis on X-ray B. Elevated right hemidiaphragm C. Left eye miosis and ptosis D. Loss of anal tone

Answer: A. Central cord syndrome is a hyperextension injury in a degenerative cervical spine ^[1]. Degenerative spondylosis narrows the canal, predisposing to central cord injury. Option B suggests phrenic nerve injury (C3-5), not central cord. Option C is Horner syndrome (sympathetic chain, not cord). Option D suggests complete cord injury, not the incomplete pattern of central cord syndrome ^[7].

"A 40-year-old man sustained a whiplash injury in a car crash. Which of the following findings suggests a high risk of respiratory compromise?"

A. Bilateral hand numbness and clumsiness B. Loss of cervical lordosis C. Raised diaphragm on chest radiograph D. Systemic hypotension and bradycardia

Answer: C. A raised hemidiaphragm indicates phrenic nerve palsy (C3-C5) — directly threatening respiratory function ^[1]. Bilateral hand numbness (option A) suggests central cord syndrome but does NOT indicate respiratory compromise. Loss of lordosis (B) is non-specific. Hypotension/bradycardia (D) is neurogenic shock — cardiovascular, not respiratory ^[9].

"A man with lower limb weakness, spasticity and bilateral Babinski sign, without any upper limb symptoms or signs." Location options include: Cervical spinal cord, Thoracic spinal cord, etc.

Answer: J. Thoracic spinal cord. UMN signs (spasticity, Babinski) in the lower limbs WITHOUT upper limb involvement localises the lesion to the thoracic cord. If the cervical cord were affected, upper limb signs would be expected ^[10].

"A 20-year-old man sustained a fall from height. Imaging studies showed hemitransection of thoracic spinal cord." (a) Distribution of motor weakness? (b) Distribution/modalities of sensory loss? (c) Where is the sensory level if loss from T10 downward? (d) Most likely abnormal finding on PR exam in SCI? (e) How is micturition affected acutely? (f) Name one medication for functional recovery? (g) Two delayed complications of neurogenic bladder?

Answers:

• (a) Ipsilateral motor weakness below the level of lesion (UMN pattern: spasticity, weakness in ipsilateral lower limb)
• (b) Ipsilateral loss of proprioception and vibration below the level; Contralateral loss of pain and temperature 1-2 levels below the lesion (Brown-Séquard pattern)
• (c) T8 or T9 — the contralateral pain/temp loss starts 1-2 segments below the lesion because the spinothalamic tract crosses 1-2 levels above entry
• (d) Loss of anal tone (lax anal sphincter)
• (e) Urinary retention (during spinal shock, the detrusor is areflexic → bladder cannot contract)
• (f) Methylprednisolone (NASCIS protocol)
• (g) UTI (recurrent), Renal calculi / Hydronephrosis / Renal failure ^[8]

"A 23-year-old man is carried in after diving head first into a river. He is speaking and his airway is open but he cannot walk or move his arms or legs. What is the first thing you must do?"

A. Examine him for other injuries B. Give him a tetanus vaccination C. Immobilise the cervical spine D. Place an intravenous line

Answer: C. In the ATLS primary survey, Airway with C-spine protection is step 1 ^[1]. The airway is open, so the next priority is cervical spine immobilisation to prevent secondary injury. This directly mirrors the lecture's emergency management teaching ^[11].

"A 70-year-old lady presented with a 6-month history of hand clumsiness and difficulty in using chopsticks. MRI of cervical spine showed cervical myelopathy. Which of the following is NOT a common symptom of cervical myelopathy?"

A. Gait instability B. Neck pain C. Sphincter disturbances D. Upper limb numbness

Answer: B. Neck pain. The lecture explicitly states "Pain is not a predominant feature" of cervical myelopathy ^[1]. Gait instability (spastic gait), sphincter disturbance (late stage), and upper limb numbness (early symptom) are all common features ^[12].

"A 70-year-old man with chronic neck pain sustains a fall on level ground, causing hyperextension. Plain X-rays show multiple osteophytes and narrowing of spinal canal. MRI shows T2 hyperintense signals within cervical spinal cord. What is MOST LIKELY present on clinical examination?"

A. Clumsy hand movement B. Foot drop C. Loss of proprioception in lower limbs D. Urinary retention

Answer: A. Clumsy hand movement. This is a classic central cord syndrome presentation — elderly patient with pre-existing spondylosis, hyperextension injury, T2 signal change (myelomalacia/oedema) in the cord. Arms are affected more than legs with loss of hand dexterity being the hallmark ^[1]. Foot drop (B) is a peripheral nerve/L5 root finding. Proprioception loss (C) would suggest posterior cord or dorsal column pathology. Urinary retention (D) is a late-stage finding, not the most likely ^[12].