GC110 Paraplegia Spinal Cord Compression Transverse Myelitis Spinal Dysraphism Neuroimaging III Spinal Cord
Neuroimaging of the spinal cord encompasses MRI and CT modalities used to evaluate paraplegia, spinal cord compression, transverse myelitis, and spinal dysraphism by delineating structural, inflammatory, and congenital abnormalities affecting the cord and vertebral column.
Paraplegia, Spinal Cord Compression, Transverse Myelitis, Spinal Dysraphism & Neuroimaging of the Spinal Cord
This GC 110 lecture by Prof. Gilberto Leung is a neurosurgical overview of spinal cord disease. It covers the anatomy you need to localize a spinal cord lesion, the clinical syndromes that result from different patterns of cord injury, the major causes of myelopathy (trauma, tumour, degeneration, infection, congenital), the principles of investigation and management, and the long-term complications of spinal cord injury. It is one of the most directly-examined GC lectures in past papers — Brown-Séquard syndrome, sensory levels, sphincter dysfunction, spinal shock, and neurogenic bladder are recurrent SAQ and MCQ themes. [1]
Learning Objectives (derived from the lecture):
- Localise the level of a spinal cord lesion using motor, sensory, and autonomic findings.
- Distinguish complete from incomplete cord injury and name the incomplete cord syndromes.
- List common causes of myelopathy by aetiology and by anatomical compartment.
- Outline investigation and management principles for spinal trauma, spinal tumours, degenerative spine disease, spinal infections, and spinal dysraphism.
- Describe the long-term complications of spinal cord injury.
1. Anatomical Foundations — Why Localisation Matters
The spinal cord is organised into three functional systems. Understanding each is the key to localising a lesion and predicting the clinical picture.
The lecture distinguishes UMN and LMN lesions as the first step in motor assessment. [1]
The opening body diagrams define the distribution before discussing tone: monoplegia affects one limb, hemiplegia one side, paraplegia both lower limbs, and tetraplegia all four limbs. Distribution localises broadly; the UMN/LMN examination then narrows the site.
| Feature | UMN Lesion | LMN Lesion |
|---|---|---|
| Muscle tone | Hypertonic (spastic) | Hypotonic (flaccid) |
| Fasciculation | Not typical | May occur |
| Wasting | Disuse wasting may develop | Neurogenic wasting is more prominent |
| Tendon jerk | Hyperactive | Diminished or absent |
| Clonus | May be present | Absent |
| Plantar response | Up-going (Babinski positive) | Down-going (normal) |
These are typical patterns, not absolute rules. Immediately after acute cord injury, neurological spinal shock can temporarily make a future UMN syndrome flaccid and areflexic.
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]
- Segmental loss — a single dermatome affected (e.g., from anterior horn or nerve root damage at that level).
- 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
- Great toe/dorsum of foot: L5
The slide labels the big toe as L4; this is corrected here because the standard ISNCSCI key sensory point for L4 is the medial malleolus, while L5 is the dorsum of the foot at the third metatarsophalangeal joint. Dermatome boundaries overlap, so use the full neurological examination rather than a single point. [15]
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.
New Sphincter Dysfunction Is an Emergency
The lecture calls sphincter dysfunction a “point of no return”, but that is too absolute. New urinary retention/incontinence, bowel or sexual dysfunction, saddle sensory change, or reduced anal tone with back/radicular symptoms requires immediate specialist assessment and urgent imaging for cauda equina or cord compression. Outcome varies with cause, severity and duration; there is no universal 48-hour guarantee or irreversible threshold. [16]
The lecture's simplified level-function table: [1]
| Level | Functional Consequence |
|---|---|
| C3 or above | Breathing affected (diaphragm = C3,4,5), tetraplegia |
| C4/5 | Loss of shoulder function |
| C6 | Shoulder may function (deltoid C5 spared) |
| C7/T1 | Loss of hand dexterity |
| T1–T8 | Abdominal muscles and trunk control lost |
| Lumbosacral | Lower limb, bowel, bladder, sexual function lost |
Treat this table as a lecture mnemonic, not a precise functional prognosis. The phrenic nerve arises predominantly from C3–C5, so high cervical injury can impair ventilation and cough. Assess respiratory rate, oxygenation, cough and serial vital capacity early; ventilatory support depends on the individual neurological level and respiratory function, not a single rigid cutoff. [17]
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]
| Feature | Conus Medullaris | Cauda Equina |
|---|---|---|
| Motor | Often mixed UMN + LMN | LMN/root pattern |
| Sensory | Often bilateral, relatively symmetric saddle loss | Often asymmetric saddle/root loss |
| Bladder | Often early | May be later, but can occur at presentation |
| Pain | May be less prominent | Radicular pain is common |
| Onset | Often abrupt | Variable |
These are useful typical tendencies, not safe exclusion rules. Either syndrome with new saddle sensory change or bladder/bowel/sexual dysfunction is an emergency. [16]
The Slide Uses One Term for Two Different Syndromes
The lecture states that “spinal shock” has two meanings. Current terminology separates them: [1]
Meaning 1 — Neurological: Flaccid paralysis and areflexia for 1–2 weeks after acute cord injury. The UMN hyperreflexia appears later as the cord circuits recover from the initial "stunning."
Neurogenic shock — haemodynamic: Hypotension due to loss of sympathetic tone after high spinal cord injury. This may cause:
- Vasodilatation → distributive hypotension
- Bradycardia (unopposed vagal tone)
- Treatment: trauma resuscitation, judicious fluids and vasopressors according to local critical-care protocol
Why neurological spinal shock matters: Flaccidity and absent reflexes can obscure the eventual UMN pattern, so serial examinations improve prognostic accuracy. However, do not wait 1–2 weeks to classify the injury: ISNCSCI/AIS completeness is based on sacral sparing and can be documented acutely, then repeated. [15]
Why neurogenic shock matters: Hypotension with relative bradycardia supports it, but trauma patients can have simultaneous haemorrhage. Exclude haemorrhagic and other causes of shock first rather than relying on warm skin or heart rate alone. [17]
2.1 ISNCSCI/AIS — What the Classification Slide Adds
The slide reproduces the ASIA worksheet. The examination records motor and sensory levels, neurological level of injury, and whether there is sacral sparing: S4–5 light touch/pin prick, deep anal pressure, and voluntary anal contraction. [15]
| AIS grade | Meaning |
|---|---|
| A — complete | No sensory or motor function in S4–5 |
| B — sensory incomplete | Sensory but no motor function in the lowest sacral segments |
| C — motor incomplete | Motor incomplete; fewer than half of key muscles below the neurological level have grade ≥3 |
| D — motor incomplete | Motor incomplete; at least half of key muscles below the neurological level have grade ≥3 |
| E — normal | Sensory and motor examination normal after a prior deficit |
The word complete therefore has a precise sacral-sparing definition; it is not synonymous with “no movement in the legs.”
3. Incomplete Cord Syndromes — Extent of Injury
The lecture classifies spinal cord injury by extent: [1]
- Complete cord transection: complete paralysis + sensory loss below + sphincter dysfunction → poor prognosis.
- Incomplete injury: variable prognosis. Four named syndromes:
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.
Exam Trap — Sensory Level in Brown-Séquard
The contralateral pain/temperature loss starts 1–2 dermatomes below the actual lesion level because spinothalamic fibres ascend 1–2 segments before crossing. The ipsilateral posterior column loss starts at the lesion level. The 2023 SAQ asked about this discrepancy explicitly. [4]
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.
- Clinical pattern: disproportionate upper-limb weakness greater than lower-limb weakness, with variable sensory and sacral involvement.
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.
The Concentric Tract Diagram Is a Historical Teaching Model
The slide explains arm-predominant weakness by placing cervical corticospinal fibres medially and sacral fibres peripherally. Modern anatomical and pathological evidence does not support that simple concentric corticospinal somatotopy. Retain the clinical phenotype (arms more affected than legs), but understand it as the result of diffuse central cervical cord injury rather than selective destruction of a proven “medial arm-fibre” bundle. [18]
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]
That bullet reflects this lecture's table, not a universal definition. Selective posterior-column dysfunction classically causes loss of vibration and joint-position sense, sensory ataxia and a positive Romberg sign, with pain/temperature relatively preserved. Think subacute combined degeneration (B12 deficiency), tabes dorsalis, or Friedreich's ataxia as chronic causes.
| Syndrome | Motor | Sensory | Autonomic | Classic Cause |
|---|---|---|---|---|
| Brown-Séquard | Ipsilateral UMN below | Ipsilateral PC loss; contralateral STT loss | Usually no bladder (unilateral) | Stab wound, tumour, MS |
| Central cord | Disproportionate UL > LL weakness | Variable; may include segmental upper-limb or sacral sensory findings | Variable | Hyperextension + cervical stenosis |
| Anterior cord | Bilateral UMN below | Loss pain/temp; intact proprioception/vibration | Bladder affected | Anterior spinal artery occlusion |
| Posterior cord | Mild UE weakness | Loss proprioception/vibration; intact pain/temp | Less common | B12 deficiency, tabes dorsalis |
4. Causes of Myelopathy — The Lecture Framework
The lecture classifies compressive causes by anatomical compartment: [1]
| Compartment | Causes |
|---|---|
| Extradural | Metastatic tumour, primary bone tumour, disc prolapse, osteophyte, abscess, haematoma, bone fragment |
| Intradural extramedullary | Meningioma, nerve sheath tumour (schwannoma) |
| Intradural intramedullary | Astrocytoma, ependymoma |
Also listed: arachnoid cyst, syringomyelia, AVM. [1]
Transverse myelitis: inflammatory cord lesion; compression must first be excluded with MRI. Arterial occlusion: thromboembolic occlusion of spinal arteries; iatrogenic (e.g., aortic surgery). Spinal arteriovenous fistula: cord oedema; haemorrhage. [1]
The arterial slide shows why aortic disease or surgery can injure the cord: the anterior spinal artery supplies much of the anterior cord through segmental feeders. The accompanying MRI examples emphasise that dural AV fistula may present through venous congestion and cord oedema, while vascular malformations may also bleed.
The lecture repeatedly returns to five major categories: [1]
- Spinal trauma
- Spinal tumours
- Degenerative conditions
- Infection
- Spinal dysraphism
5. Spinal Trauma — In Detail
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.
The axial MRI on the slide shows the practical consequence: haemorrhage, oedema or residual compression can extend injury after the initial impact. Spinal motion restriction, oxygenation/perfusion support and timely decompression/stabilisation aim to limit those secondary insults.
Three mechanisms: [1]
- Vertical compression (e.g., load falling onto head) → may cause a compression or burst fracture
- Hinge injury (e.g., blow to head) → flexion/extension → ligaments disrupted → unstable
- Shearing injury (e.g., fall from height) → ligaments disrupted → unstable
The pictures make ligament disruption and translation easy to recognise as instability, but the slide's “vertical compression = stable” shortcut is unsafe. A burst fracture can compromise the canal or posterior ligamentous complex and may be unstable. Classify stability from the whole injury pattern on CT, MRI when indicated, neurological findings and specialist assessment—not from mechanism or one radiograph alone.
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
- Can show some soft-tissue abnormality, but does not evaluate the cord and ligaments as well as MRI
MRI spine: [1]
- Difficult to arrange (in emergency)
- Shows soft-tissue lesion, cord oedema
- Gold standard for cord pathology
Imaging Hierarchy in Spinal Trauma
The lecture-era sequence is plain XR → CT → MRI. Current adult trauma guidance uses CT first when cervical imaging is indicated, and CT for suspected thoracic/lumbosacral injury with neurological signs. If a neurological abnormality could be due to spinal cord injury, perform MRI after CT even when CT shows no injury. Plain radiography retains a limited role in selected thoracic/lumbosacral column injury without neurological signs. [17]
From the lecture slide: [1]
- Resuscitation while preventing hypoxia and hypotension
- Spinal motion restriction and manual in-line protection during assessment/transfers
- Assume multiple injury / head injury
- Imaging studies
- Methylprednisolone(?) — note the question mark; its role is controversial
- Surgery to decompress spinal cord
- Mechanical stabilisation (e.g., anterior corpectomy + internal fixation, spinal traction)
- Prevent/Treat complications
- Rehabilitation
On methylprednisolone: The slide and 2023 SAQ preserve a historical exam association, but high-dose methylprednisolone is not a universal standard of care. The AO Spine guideline found no overall motor-score advantage; it makes only a weak option of a 24-hour infusion when started within 8 hours in selected adults, and advises against starting it after 8 hours or using a 48-hour infusion. Follow the local acute-SCI protocol and discuss risks rather than giving it reflexively. [19]
6. Spinal Tumours — In Detail
6.1 Classification & Key Features
Spinal Metastasis: [1]
- *** > 90% are extradural, located in the vertebral body***
- Commonly from breast, lung, prostate
- Commonly thoracic
- Route of spread:
- Haematogenous: arterial or venous (Batson's plexus — valveless vertebral venous plexus)
- Direct invasion: e.g., paraspinal lung cancer
- Lymphatic: along nerve root sleeves
- Subarachnoid seeding: from primary and secondary CNS neoplasms
Why Batson's plexus matters: This valveless venous plexus connects pelvic/abdominal veins to the vertebral venous system. When intra-abdominal pressure rises (coughing, straining), blood flows retrograde into the vertebral plexus, carrying tumour cells. This explains why prostate and breast cancer metastasise to the spine so frequently.
Why thoracic: The thoracic spine is the longest segment and has the richest blood supply from intercostal arteries.
Spinal ependymoma: [1]
- Commonest primary cord tumour in adults
- Male, NF-II
- Slower growing
- Compressing (vs infiltrating) the cord → better resectability
Spinal astrocytoma: [1]
- 60% of lesions in children
- Lower grade than brain astrocytomas
- Faster growing than ependymoma
- Infiltrative → complete excision less likely
Lecture-era principles: [1]
- Steroids to reduce oedema
- 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 compartment images explain the different surgical problems: extradural metastasis compresses the cord from vertebral/epidural disease; intradural extramedullary meningioma or schwannoma displaces the cord; intramedullary ependymoma or astrocytoma expands it from within. Management therefore depends on histology, neurological status, mechanical stability, systemic disease and radiosensitivity—not compartment alone.
For suspected metastatic spinal cord compression with neurological symptoms/signs, current NICE guidance recommends dexamethasone 16 mg as soon as possible, continued while awaiting surgery or radiotherapy, and whole-spine MRI within 24 hours. Corticosteroids are not routine for every spinal tumour or for metastatic spinal disease without neurological signs. Surgery, radiotherapy and systemic treatment are individualised; modern metastatic care is not invariably “radiotherapy first” or purely palliative. [20]
The 2025 MCQ Q61 tested the emergency principle: metastatic lung cancer with pathological L1 collapse and cord compression → start steroids and obtain urgent spinal surgical consultation. [7]
The lecture lists: [1]
- Spondylosis
- Disc degeneration/prolapse
- Apophyseal (facet) joint hypertrophy
- Instability
- Spinal canal stenosis
- Myelopathy (central compression) vs Radiculopathy (lateral compression)
- Chronic progressive course with possible acute exacerbation
Clinical scenario (directly from slide 42): "Old man with degenerated spine after a fall → Central cord syndrome." [1]
This is because the cervical canal is already narrowed by spondylosis. A hyperextension injury (e.g., fall) can compress the cord between anterior degenerative change and posterior structures. The axial diagram contrasts central canal stenosis → myelopathy with foraminal narrowing → radiculopathy, while the MRI shows multilevel cervical canal narrowing.
Management
Conservative: Physiotherapy, analgesia. [1] Lecture surgical indications: [1]
- Progressive neurological deficit
- Myelopathy / Radiculopathy
- Intractable pain
- Illustrated procedures: posterior laminectomy and anterior corpectomy/decompression with fixation
Do not interpret “myelopathy/radiculopathy” as automatic surgery for every patient. Current DCM guidance recommends surgery for moderate/severe degenerative cervical myelopathy; mild DCM may receive surgery or a supervised structured rehabilitation trial, with surgery if neurological deterioration or failure to improve. Radiculopathy without myelopathy is managed according to deficit, pain, imaging and response to conservative care. [21]
Pyogenic and TB: [1]
- From adjacent foci: osteomyelitis, TB spine
- Haematogenous/lymphatic spread: epidural abscess
- Treatment principle: microbiological sampling where feasible, pathogen-directed antimicrobials, plus urgent drainage/decompression when there is neurological deficit, instability, a large/undrained collection, or failure of medical treatment [27]
TB spine (Pott's disease) deserves special mention: it begins in the anterior vertebral body (initially disc-sparing, unlike pyogenic spondylitis which starts in the disc), spreads under the anterior longitudinal ligament to adjacent vertebrae, causes disc destruction, kyphosis (Gibbus deformity), and may cause cord compression with paraplegia. The thoracic spine is most commonly affected. [8]
The lecture shows the spectrum: [1] Myelomeningocele → Meningocele → Spina bifida occulta
| Type | Definition | Neurological Deficit |
|---|---|---|
| Myelomeningocele | Spinal cord + roots protrude through bony defect in a cystic cavity lined by meninges | Significant — paraplegia, incontinence |
| Meningocele | CSF-filled cystic cavity lined with meninges but no neural tissue | Usually minimal after resection |
| Spina bifida occulta | Failure of fusion of vertebral arch only; no herniation | Usually none (5–10% of population) |
The clinical photographs add an important visual distinction: myelomeningocele contains neural tissue, whereas a meningocele contains meninges and CSF without neural tissue. Occulta may have a midline dimple, hair tuft, haemangioma or subcutaneous mass; these are clues for assessment, not proof of tethering by themselves.
Current prevention advice: Everyone capable of becoming pregnant should take 400 micrograms folic acid daily. After a previous neural-tube-defect-affected pregnancy, CDC advises 4,000 micrograms daily from 1 month before conception through the first 3 months, under clinician guidance. This replaces the slide-era risk multipliers and percentage reduction, which should not be used for counselling. [22]
Associations: Hydrocephalus, Chiari type II malformation. [9]
9.1 Tethered Cord Syndrome
Common in spina bifida occulta. [1] Anchoring of lower end of spinal cord by:
- Fatty filum terminale
- Lipoma Low-lying conus medullaris Cord under tension as spine lengthens during growth [1]
Clinical features: [1]
- Progressive neurological deficit
- Lower limb LMN deficit
- Sphincter dysfunction
- Pain
- Scoliosis and foot deformity
- Clinical deterioration at growth spurt (because the spine grows but the cord is tethered)
Management: [1]
- Early detection with MRI
- Urodynamic studies
- Lecture recommendation: surgical untethering before deterioration
Current practice is more individualised. Evaluate evolving pain, motor/sensory change, orthopaedic deformity and bladder/bowel function; MRI defines anatomy and urodynamics can detect hostile bladder change. Spina Bifida Association guidance centres on symptomatic tethered cord and longitudinal clinical/urological surveillance, with untethering decisions made by a specialist multidisciplinary team rather than blanket prophylactic surgery for every low conus or fatty filum. [23]
The lecture says “diagnosis by exclusion” and “LP shows high CSF protein.” [1]
The safe modern formulation is an acute/subacute inflammatory myelopathy syndrome. Obtain urgent spinal MRI to exclude compression and characterise the cord lesion. Then investigate the cause with brain MRI, CSF (cells, protein, oligoclonal bands and infection testing as appropriate) and targeted blood tests including AQP4-IgG and MOG-IgG. Raised CSF protein may occur but is nonspecific and is neither required nor diagnostic. [24]
Aetiology:
- Idiopathic
- Demyelinating disease (most common): MS, NMOSD, ADEM
- Infection: HSV, enterovirus, syphilis
- Autoimmune: SLE, RA, AS
- Paraneoplastic
Key exam pearl — NMOSD vs MS: [10]
- NMOSD (anti-aquaporin-4 antibody positive) → longitudinally extensive transverse myelitis (≥3 vertebral segments) + bilateral optic neuritis
- MS → typically short-segment (< 2 vertebral segments), partial cord lesions
The 2025 MCQ Q84 tested this directly: patient with longitudinally extensive transverse myelitis (C5–T4) → the answer was anti-aquaporin-4 antibodies (NMO). [7]
Management: High-dose IV corticosteroid is a common first-line acute treatment once infection/other mimics are considered; exact regimen is protocol- and patient-specific. Plasma exchange is considered for severe disease or inadequate steroid response, while antimicrobial or disease-specific therapy treats an identified cause. [24]
11. Long-Term Complications of Spinal Cord Injury
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 neural-control diagram also shows why no single bladder pattern can be predicted from “SCI” alone: suprasacral, sacral/root and incomplete lesions disrupt different parts of detrusor–sphincter coordination. Measure post-void residual, use renal imaging/urodynamics in high-risk patients, and individualise bladder-emptying and pressure-control strategies with urology rather than assuming all patients have detrusor overactivity. [25]
The 2023 SAQ asked for two delayed complications of neurogenic bladder — expected answers: UTI/recurrent infections and reflux nephropathy/renal failure/calculi. [4]
Typically a lesion at or above T6; may occur at lower levels but is less common. 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 the T6 threshold: The splanchnic sympathetic outflow is a major contributor to vascular tone. With a lesion at or above T6, descending control cannot adequately restrain the large sympathetic response below the injury, making autonomic dysreflexia more likely and more severe.
Autonomic Dysreflexia — Immediate Actions
This is a potentially life-threatening hypertensive emergency. Sit the patient upright, loosen tight clothing/devices, repeat blood pressure frequently, and search for/remove the trigger—first the bladder (blocked catheter/retention), then bowel impaction and skin/other noxious stimuli. If hypertension persists, follow the emergency protocol for a rapid-onset, short-acting antihypertensive and urgent medical review. [26]
Spastic muscle tone → limb deformity → immobility → difficult nursing care → difficult rehabilitation → pressure injuries and sepsis. [1]
The photograph shows an advanced pressure injury over a bony prominence. Reduced sensation, immobility, moisture, shear and poor tissue tolerance all contribute. Prevention includes an individual pressure-relief/repositioning plan, appropriate mattress/cushion, daily skin inspection, nutrition and prompt management of moisture or equipment pressure.
From GC Emergency Radiology: "Acute myelopathy — emergency diagnosis and treatment to prevent permanent neurologic dysfunction. Cord compression from spinal metastases, traumatic insults, or acute disc prolapse. MRI — modality of choice for imaging spinal cord." [6]
| Modality | Strengths | Limitations |
|---|---|---|
| Plain XR | Readily available; shows gross fracture/malalignment | Misses subtle fracture; cannot assess ligaments or soft tissue |
| CT | Rapid; excellent fracture, alignment and canal-bone detail; may show gross soft-tissue abnormality | Does not characterise cord, oedema and ligaments as well as MRI |
| MRI | Shows cord oedema, compression, intramedullary lesions, ligaments, discs | Difficult to arrange emergently; longer scanning time; CI in some patients |
When to image depends on context: For adult trauma, CT is usually first when cervical imaging is indicated or when thoracolumbar injury has neurological signs, followed by MRI for an attributable neurological abnormality even if CT is normal. For non-traumatic suspected cord compression or inflammatory myelopathy, urgent MRI is the key test; suspected metastatic spinal cord compression with neurological signs needs whole-spine MRI within 24 hours. [17] [20]
MRI sequences:
- T1: Anatomy. Cord/bone detail.
- T2: Highlights fluid, oedema, cord signal change (myelopathy appears as T2 hyperintensity within the cord).
- STIR: Suppresses fat signal; excellent for bone marrow oedema and ligamentous injury.
- Post-gadolinium T1: Enhancing lesions (tumour, abscess, active inflammation).
| Trap | Correct Approach |
|---|---|
| Calling cardiovascular collapse “spinal shock” | Use neurological spinal shock for transient flaccid areflexia and neurogenic shock for loss of sympathetic tone; always exclude haemorrhage in trauma |
| Saying Brown-Séquard has contralateral weakness | Weakness is ipsilateral (corticospinal tract has already crossed at medulla) |
| Waiting for spinal shock to resolve before classifying completeness | Perform ISNCSCI/AIS using sacral sparing now, then repeat serially |
| Treating sphincter dysfunction as either benign or invariably irreversible | New bladder/bowel/sexual dysfunction or saddle sensory loss requires immediate CES/cord-compression assessment; outcome is not determined by one rigid time cutoff |
| Treating conus vs cauda features as absolute | Conus is often mixed and symmetric; cauda often LMN/asymmetric, but overlap is substantial and both can be emergencies |
| Saying XR or CT excludes cord injury | CT is first-line in many adult trauma pathways; MRI is needed for attributable neurological abnormality and is the key test for non-traumatic cord pathology |
| Forgetting NF-II associations | Meningioma, schwannoma, AND ependymoma all associated with NF-II |
High Yield Summary
- Acute paraplegia with a sensory level or new sphincter/saddle change is an emergency. Protect the spine in trauma, assess breathing/perfusion, and obtain cause-appropriate urgent imaging and specialist input.
- Localise level and extent: UMN signs below with possible LMN signs at the level; classify completeness by sacral sparing (AIS), not by leg movement alone.
- Brown-Séquard: ipsilateral corticospinal/posterior-column loss with contralateral pain/temperature loss below. Central cord: arms more weak than legs; the old concentric tract diagram is not accepted anatomy.
- Compressive compartments: extradural (metastasis, disc, abscess, haematoma), intradural extramedullary (meningioma, schwannoma), intramedullary (ependymoma, astrocytoma).
- Imaging: CT leads many adult trauma pathways; MRI evaluates cord, ligaments and soft-tissue compression and is urgent after trauma CT when a neurological abnormality is attributable to SCI.
- Transverse myelitis: MRI excludes compression and characterises the lesion; CSF protein alone is nonspecific. Test for causes including AQP4-IgG/MOG-IgG when appropriate.
- Long-term care: protect renal function in neurogenic bladder; recognise autonomic dysreflexia (usually ≥T6) and treat triggers immediately; prevent contractures and pressure injuries.
- Tethered cord: low/tethered conus plus progressive neurological, orthopaedic or urological dysfunction requires specialist surveillance and individualised surgical assessment.
Active Recall - Lecture Notes
[1] Lecture slides: GC 110. Paraplegia Spinal cord compression Transverse myelitis Spinal dysraphism Neuroimaging III Spinal Cord.pdf [2] Senior notes: Maksim Medicine Notes.pdf (Neurology section — Spastic paraparesis, Transverse myelitis) [3] Senior notes: Ryan Ho Fundamentals.pdf (Ch 3.4.9 Paraplegia, p334–335) [4] Past papers: 2023 Fourth Summative SAQ.pdf (Question 8) [5] Senior notes: Block A - Sudden severe chest pain_ acute myocardial infarction; aortic dissection.pdf (Aortic dissection complications — paraplegia from anterior spinal artery involvement) [6] Lecture slides: GC 013. Emergency radiology.pdf (Acute Myelopathy section) [7] Past papers: 2025 Fourth Summative MCQ.pdf (Questions 61, 84) [8] Senior notes: Ryan Ho Respiratory.pdf (TB spondylitis / Pott's disease, p80) [9] Senior notes: Adrian Lui Pediatrics Notes.pdf (Spinal Dysraphism, p130) [10] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf (NMO / Transverse myelitis section, p1273) [15] American Spinal Injury Association — International Standards for Neurological Classification of Spinal Cord Injury (ISNCSCI), revised 2019 [16] NICE NG127 — Suspected cauda equina syndrome: immediate referral criteria [17] NICE NG41 — Spinal injury: assessment and initial management [18] Shakil et al. — Traumatic central cord syndrome: neurologic recovery after surgical management (2023) [19] AO Spine — Guideline on methylprednisolone sodium succinate in acute spinal cord injury [20] NICE NG234 — Spinal metastases and metastatic spinal cord compression [21] AO Spine — Clinical practice guideline for degenerative cervical myelopathy [22] CDC — Folic acid and neural-tube-defect prevention [23] Spina Bifida Association — Neurosurgery guideline [24] NINDS — Transverse myelitis [25] NICE CG148 — Urinary incontinence in neurological disease [26] Paralyzed Veterans of America — Autonomic dysreflexia and other autonomic dysfunctions guideline [27] Infectious Diseases Society of America — Native vertebral osteomyelitis guideline
GC109 Headache And Loss Of Consciousness Acute Stroke, Subarachnoid Haemorrhage And Vascular Malformation
Acute stroke involves sudden neurological deficit from cerebral ischemia or hemorrhage, subarachnoid haemorrhage is bleeding into the subarachnoid space typically from a ruptured aneurysm, and vascular malformations are abnormal collections of blood vessels that can cause hemorrhage or seizures.
GC111 Raised Intracranial Pressure And Hydrocephalus
Raised intracranial pressure is an elevation of pressure within the cranial cavity above normal (> 20 mmHg), often caused by mass lesions, cerebral edema, or hydrocephalus—a pathological accumulation of cerebrospinal fluid within the ventricular system due to impaired production, flow, or absorption.