The lecture distinguishes UMN and LMN lesions as the first step in motor assessment. ^[1]

Why this matters from first principles: The corticospinal tract (upper motor neuron) crosses at the medullary pyramids and descends in the lateral column of the cord. When a lesion hits the cord, you get:

• LMN signs at the level of the lesion — because the anterior horn cells at that segment are destroyed directly.
• UMN signs below the level of the lesion — because the descending corticospinal tract fibres are interrupted for all segments below.

"Diseases can cause LMN lesion at that level and UMN lesions at levels below." ^[1]

This is a critical exam concept: a C5 lesion may cause flaccid weakness of the deltoid/biceps (LMN at C5) but spastic weakness of the hand intrinsics and lower limbs (UMN below C5).

Two major ascending tracts to know:

• Posterior column (uncrossed): proprioception, fine touch, pressure (vibration)
• Lateral spinothalamic tract (crossed): pain, temperature ^[1]

Why "crossed" vs "uncrossed" matters: The spinothalamic tract crosses within 1–2 segments of entry (anterior white commissure). The posterior columns ascend ipsilaterally and cross only in the medulla. This is why a hemisection (Brown-Séquard) gives ipsilateral posterior column loss and contralateral spinothalamic loss.

Two types of sensory loss in cord disease: ^[1]

1. Segmental loss — a single dermatome affected (e.g., from anterior horn or nerve root damage at that level).
2. Ascending long-tract loss — loss of sensation from all levels below the lesion → this creates the sensory level.

Key dermatome landmarks (high-yield for exam):

• Shoulder: C5
• Nipple: T4
• Umbilicus: T10
• Groin: L1
• Knee: L3/4
• Big toe: L4 ^[1]

Bladder and bowel dysfunction is a hallmark of spinal cord disease. ^[1]

• Acutely: painless urinary retention (the detrusor is atonic in spinal shock).
• Later: neurogenic bladder develops (detrusor overactivity ± detrusor-sphincter dyssynergia depending on the level).
• Bowel: lax anal tone on PR examination.

The lecture's simplified level-function table: ^[1]

Why C3 is the critical threshold: The phrenic nerve (C3,4,5) innervates the diaphragm. A lesion at C3 or above denervates the diaphragm → respiratory arrest → need for mechanical ventilation.

The lecture diagram shows three zones: ^[1]

• Above the conus → pure UMN lesion
• At the conus → mixed UMN + LMN (the cord and emerging roots are both damaged)
• Cauda equina → pure LMN lesion

Saddle anaesthesia (S2–S5 dermatomes — perineum, inner thighs, perianal region) is a classic finding in both conus and cauda equina lesions but is highlighted in the lecture as a key exam finding. ^[1]

Ipsilateral UMN weakness + ipsilateral posterior column loss (proprioception, vibration) + contralateral spinothalamic loss (pain, temperature) below the lesion. ^[1]

This is the most-tested syndrome in past papers. The 2023 SAQ directly asked about the motor and sensory distribution in thoracic hemitransection. ^[4]

Why the pattern: The corticospinal tract has already crossed (at the medulla), so it is ipsilateral. The posterior column hasn't crossed yet, so it is ipsilateral. The spinothalamic tract has already crossed (in the cord, 1–2 segments above), so the loss is contralateral and begins about 2 dermatomes below the lesion.

The lecture highlights: ^[1]

• Segmental loss: decussating secondary sensory neurons affected → bilateral upper limb pain/numbness at the level of lesion.
• Anterior horn cell involvement at the level → LMN weakness of hands/arms.
• Long tract signs: medial motor fibres (upper limb) are more affected than lateral fibres (lower limb) → upper limb weakness > lower limb weakness = "sacral sparing."

Classic clinical scenario (directly from the lecture): "Old man with degenerated spine after a fall → Central cord syndrome." ^[1] This is a hyperextension injury in a patient with pre-existing cervical spondylosis (narrow canal). The cord is "pinched" centrally.

Paraplegia + spinothalamic loss (pain/temperature) + intact posterior column (proprioception/vibration). ^[1]

Why: The anterior spinal artery supplies the anterior 2/3 of the cord (corticospinal tracts + spinothalamic tracts + anterior horn cells). The posterior columns are supplied by the posterior spinal arteries and are spared. Causes include anterior spinal artery occlusion, aortic surgery, aortic dissection. ^[5]

Pain and paraesthesia in upper limb and trunk + mild upper extremity paraparesis. ^[1]

This is rare. The posterior columns are selectively affected. Think subacute combined degeneration (B12 deficiency), tabes dorsalis, or Friedreich's ataxia as chronic causes.

The lecture classifies compressive causes by anatomical compartment: ^[1]

Also listed: arachnoid cyst, syringomyelia, AVM. ^[1]

Transverse myelitis: diagnosis by exclusion; LP shows high CSF protein. Arterial occlusion: thromboembolic occlusion of spinal arteries; iatrogenic (e.g., aortic surgery). Spinal arteriovenous fistula: cord oedema; haemorrhage. ^[1]

The lecture repeatedly returns to five major categories: ^[1]

1. Spinal trauma
2. Spinal tumours
3. Degenerative conditions
4. Infection
5. Spinal dysraphism

Primary neurological injury: complete or incomplete cord injury at the time of impact. Secondary neurological injury: instability from bony/ligamentous injuries → delayed neurological deterioration. Haematoma can also cause secondary compression. ^[1]

Why this distinction matters: You can prevent secondary injury by immobilisation, early imaging, and surgical stabilisation. This is the rationale for the collar and log-roll.

Three mechanisms: ^[1]

• Vertical compression (e.g., load falling onto head) → burst fracture → ligaments intact → stable
• Hinge injury (e.g., blow to head) → flexion/extension → ligaments disrupted → unstable
• Shearing injury (e.g., fall from height) → ligaments disrupted → unstable

The key concept: ligamentous integrity determines stability. If ligaments are intact, the injury is mechanically stable (even if there's a fracture). If ligaments are disrupted, the injury is unstable and the cord is at risk of further damage with any movement.

Plain X-ray: ^[1]

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

CT spine: ^[1]

• Reasonably available
• Better for bony detail
• Still cannot show soft-tissue injury

MRI spine: ^[1]

• Difficult to arrange (in emergency)
• Shows soft-tissue lesion, cord oedema
• Gold standard for cord pathology

From the lecture slide: ^[1]

1. Resuscitation (NB: spinal shock — treat hypotension with fluids + vasopressors)
2. Collar & log roll to protect spine
3. Assume multiple injury / head injury
4. Imaging studies
5. Methylprednisolone(?) — note the question mark; its role is controversial
6. Surgery to decompress spinal cord
7. Mechanical stabilisation (e.g., anterior corpectomy + internal fixation, spinal traction)
8. Prevent/Treat complications
9. Rehabilitation

On methylprednisolone: The 2023 SAQ asked to "name one medication that could potentially improve functional recovery in spinal cord injury" — the expected answer is methylprednisolone, even though current evidence is weak and many centres no longer use it routinely. The lecture flags it with a "?" to signal controversy but it remains the standard exam answer. ^{[1] [4]}

Principles: ^[1]

• Steroids to reduce oedema (dexamethasone is standard)
• Surgical resection within safety limit
• Intraoperative monitoring with MEP and SSEP
• Adjuvant radiotherapy for some
• For metastasis:
  • Primarily ERT (external radiation therapy)
  • Surgery for pain, instability, or lesions resistant to RT
  • Palliative in nature

The 2025 MCQ Q61 tested this: a patient with metastatic lung cancer with pathological L1 collapse and cord compression → the correct answer was "Start high-dose steroids and arrange urgent orthopaedic consultation for decompressive surgery." ^[7]

Very complex pathophysiology. Variable presentations depending on level and completeness of injury. ^[1]

• Lack awareness of bladder filling
• Loss of sphincter control
• Detrusor overactivity & detrusor-sphincter dyssynergia
• Urinary incontinence, UTI, calculi, reflux nephropathy
• Also constipation & sexual dysfunction

Why reflux nephropathy: High-pressure detrusor contractions against a closed sphincter (dyssynergia) → vesicoureteral reflux → hydronephrosis → renal damage. This is a major cause of morbidity and mortality in chronic spinal cord injury.

The 2023 SAQ asked for two delayed complications of neurogenic bladder — expected answers: UTI/recurrent infections and reflux nephropathy/renal failure/calculi. ^[4]

Lesion above T5/6. Late problem. ^[1] Trigger: e.g., full bladder → sympathetic response → vasoconstriction → hypertension. Vagal bradycardia occurs (baroreceptor-mediated above the lesion). Also: poor body temperature control. ^[1]

Mechanism from first principles: Below the lesion, the cord is intact but disconnected from brainstem modulation. A noxious stimulus (full bladder, constipation, skin irritation) triggers a massive sympathetic reflex arc within the isolated cord segments below the lesion. Above the lesion, the brain detects the hypertension via baroreceptors and sends vagal (parasympathetic) signals → bradycardia, flushing, sweating above the level. But the vagal signal cannot reach below the lesion to counteract the sympathetic surge → sustained hypertension below.

Why T5/6 threshold: The splanchnic sympathetic outflow (major contributor to vascular tone) exits at T5–T12. If the lesion is above T5/6, the majority of sympathetic outflow is "disconnected" from brainstem control → more severe autonomic dysreflexia.

Spastic muscle tone → limb deformity → immobility → difficult nursing care → difficult rehabilitation → pressure sores and sepsis. ^[1]

Pressure sores (decubitus ulcers) occur over bony prominences (sacrum, heels, ischial tuberosities) because the patient cannot feel pressure and cannot shift weight. They are a major source of sepsis and mortality. Prevention: regular turning, pressure-relief mattresses, skin inspection.

1. Q: A man with lower limb weakness, spasticity, bilateral Babinski sign, no upper limb symptoms. Where is the lesion?

   • Answer: Thoracic spinal cord (2023 MCQ Q11) ^[11]

2. Q: Middle-aged obese man: acute back pain, urinary incontinence, buttock numbness, bilateral LL weakness after heavy lifting. Most likely diagnosis?

   • Answer: Cauda equina syndrome (2021 MCQ Q70) ^[12]

3. Q: MRI shows longitudinally extensive transverse myelitis C5–T4. Which antibody?

   • Answer: Anti-aquaporin-4 antibodies (NMO) (2025 MCQ Q84) ^[7]

4. Q: Metastatic lung cancer with L1 collapse and cord compression. Most appropriate initial management?

   • Answer: High-dose steroids + urgent surgical consultation (2025 MCQ Q61) ^[7]

5. Describe the motor and sensory distribution in thoracic hemitransection (Brown-Séquard).
6. What is the most likely abnormal PR finding in spinal cord injury? → Lax anal tone
7. How is micturition affected acutely? → Painless urinary retention
8. Name one medication for functional recovery in SCI. → Methylprednisolone
9. Name two delayed complications of neurogenic bladder. → UTI/recurrent infections; reflux nephropathy/renal calculi/renal failure

10. Demonstrate examination of a patient with suspected spinal cord injury. Focus on: sensory level (pinprick), motor power in key myotomes, tone, reflexes, plantar response, PR (anal tone), and bladder (palpate for retention).