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Central Cord Syndrome

Overview

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Anatomy & Pathophysiology

• Corticospinal tracts — the fibres supplying the upper extremities are located medially (closest to the central gray), while those for the lower extremities, thorax, and sacrum are located more laterally
• Spinothalamic tracts — centrally located crossing fibres
• Intramedullary decussating fibres — direct injury to these accounts for the dissociated sensory loss

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Causes / Aetiology

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Clinical Features

1. Motor weakness — upper extremities > lower extremities (disproportionately so)
2. Bladder dysfunction — urinary retention (most common)
3. Sensory disturbance — variable degree

The "MUD" Mnemonic (Rosen's EM):

Motor > sensory deficits
Upper extremities > lower extremities
Distal > proximal weakness

Additional features:

• Dissociated sensory loss: pain and temperature sensation impaired; vibration and proprioception preserved (posterior columns spared)
• Cape-like sensory deficit at cervical level — the area served by the damaged crossing spinothalamic fibres
• Spastic paraparesis or quadriparesis in more severe cases
• Bowel and bladder control usually retained in milder cases; impaired in severe ones
• Quantitative criterion: ≥10 motor score point difference (MRC scale) between upper and lower extremities

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Comparison with Other Incomplete Cord Syndromes

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Imaging

• Cervical stenosis from spondylosis
• Fracture-subluxation or sequestered disc
• Cord signal change (oedema or haemorrhage)
• No radiographic abnormality (SCIWORA) in some cases

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Management

Acute Phase:

• Spinal immobilisation and stabilisation
• Blood pressure management (MAP target ≥85 mmHg to maintain cord perfusion)
• Urinary catheterisation for retention
• Avoid steroids (no longer routinely recommended)

Surgical vs. Conservative:

• Surgery within 24 hours of traumatically induced CCS is safe and more cost-effective than delayed procedures (Rockwood and Green's Fractures in Adults, citing Chen et al.)
• Surgical decompression is indicated when imaging shows compressive pathology

Rehabilitation:

• Physical and occupational therapy targeting hand/arm function (the most impaired and slowest to recover)
• Bladder retraining
• Spasticity management

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Prognosis

• Generally good among incomplete cord syndromes
• Recovery pattern: lower extremity function tends to recover first and best; bladder function next; hand/fine motor function recovers last and least
• Elderly patients and those with more severe initial deficits have worse outcomes
• Note: Among incomplete cord syndromes, anterior cord syndrome carries the worst prognosis; central cord and Brown-Séquard have comparatively better outcomes

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Brown-Séquard Syndrome

Definition

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Anatomy & Pathophysiology

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Aetiology

• Penetrating injuries — stab wounds, gunshot wounds (most common cause)
• Blunt trauma — hyperextension, locked facets, compression fractures
• Herniated cervical disc

• Multiple sclerosis
• Spinal cord tumours (primary or metastatic)
• Spinal epidural or subdural haematoma
• Haematomyelia
• Spinal cord ischemia (e.g., vertebral artery dissection)
• Infections / inflammatory myelitis (VZV, EBV, CMV, TB, sarcoidosis)
• Posttraumatic arachnoiditis
• Spinal cord herniation

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Classic Clinical Features

1. Ipsilateral findings (same side as the lesion):

• UMN spastic paresis below the level of the lesion (corticospinal tract damage)
• Loss of vibration sense and proprioception below the level (dorsal column damage)
• Loss of discriminative (fine) touch below the level
• LMN weakness, atrophy, areflexia at the level of the lesion (anterior horn / ventral root involvement)
• Ipsilateral loss of pain & temperature at the level of the lesion (a narrow band — segmental)
• Ipsilateral Horner syndrome — if the lesion is cervical (interruption of descending sympathetic fibres)
• Ipsilateral loss of sweating below the lesion (descending autonomic fibres)
• Ipsilateral hemidiaphragm paralysis — if high cervical (UMN pathways for breathing)

2. Contralateral findings (opposite side):

• Loss of pain and temperature sensation beginning 1–2 segments below the level of the lesion (spinothalamic fibres ascend 1–2 levels before crossing, so the sensory loss level lags behind the lesion)
• Touch is relatively preserved (bilateral representation in the cord)

Key rule: Motor loss and proprioception loss are ipsilateral; pain and temperature loss is contralateral — and begins slightly below the anatomical level.

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Brown-Séquard Plus Syndrome

• Asymmetric hemiplegia (weaker on one side)
• Hypoalgesia more prominent on the less paretic side

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Diagnosis

• Clinical — the asymmetric pattern of ipsilateral motor/proprioceptive loss + contralateral pain/temperature loss is pathognomonic
• MRI spine — investigation of choice; shows cord signal change (T2 hyperintensity = oedema/myelomalacia), compressive lesion, or haematoma
• CT spine — for bony trauma / instability
• Sensory level examination — pin-prick testing to delineate the contralateral sensory level

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Management

Acute:

• Spinal immobilisation; maintain MAP ≥85 mmHg
• Surgical decompression if compressive aetiology (tumour, haematoma, disc, fracture)
• Treat underlying cause (antibiotics for infection, steroids for inflammatory causes, anticoagulation reversal for haematoma)

Rehabilitation:

• Physiotherapy for motor recovery
• Bladder/bowel management if autonomic involvement
• Occupational therapy

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Prognosis

• Most patients regain ambulatory capacity
• Most achieve bowel and bladder continence
• Patients with predominantly upper extremity weakness have a favourable prognosis for ambulation
• Recovery can be delayed — symptoms may appear or resolve in a delayed fashion, and BSS may co-exist with other cord syndromes

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Summary Table — Incomplete Cord Syndromes

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Neurogenic Bladder — Comprehensive 10-Mark Answer

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Normal Neural Control of Micturition (Essential Foundation)

• Parasympathetic (S2–S4, pelvic nerve): ACh → M3 receptors → detrusor contraction (voiding)
• Sympathetic (T11–L2, hypogastric nerve): NE → β3 receptors → detrusor relaxation; α1 receptors → bladder neck contraction (storage)
• Somatic (S2–S4, Onuf's nucleus, pudendal nerve): ACh → nicotinic receptors → external urethral sphincter contraction (storage)

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PART I: NEUROGENIC BLADDER (10 Marks)

Definition

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Classification — Lapides System (1970)

1. Uninhibited Neurogenic Bladder

• Lesion: Cortex / corticoregulatory tract (suprapontine)
• Causes: CVA, brain tumour, Parkinson's disease, multiple sclerosis, dementia
• Mechanism: Loss of cortical inhibition → sacral micturition reflex overactive
• Features: Frequency, urgency, urge incontinence; voiding often incomplete; sensation intact or reduced; small-capacity bladder with normal/strong contractions
• Cystometry: Low-volume involuntary detrusor contractions; normal compliance

2. Reflex Neurogenic Bladder (Automatic Bladder)

• Lesion: Complete suprasacral spinal cord (above sacral segments, below pons)
• Causes: Traumatic spinal cord injury, transverse myelitis, advanced MS
• Mechanism: Spinal cord transection severs both sensory and motor pathways to/from brain; sacral reflex arc intact but disconnected from higher centres
• Features: No bladder sensation; no voluntary voiding; reflex (involuntary) voiding at low volumes; detrusor-sphincter dyssynergia (DSD); incontinence
• Cystometry: Detrusor overactivity (hyperreflexia); DSD on EMG

3. Autonomous Neurogenic Bladder

• Lesion: Complete destruction of sacral cord (S2–S4) or sacral nerve roots / pelvic nerves
• Causes: Spina bifida, conus medullaris tumour, pelvic surgery, trauma
• Mechanism: Complete motor AND sensory separation of the bladder from the sacral cord → loss of both reflex and voluntary control
• Features: No sensation; no voluntary or reflex voiding; bladder becomes flaccid/large; overflow incontinence; large post-void residual
• Cystometry: Detrusor areflexia; large capacity; low pressure; high compliance initially, may reduce with chronicity

4. Sensory Neurogenic Bladder

• Lesion: Afferent (sensory) fibres from bladder to spinal cord
• Causes: Diabetes mellitus (most common), tabes dorsalis, pernicious anaemia
• Mechanism: Loss of afferent stretch sensation → no urge to void → progressive overdistension
• Features: Insidious — gradual loss of urge sensation; bladder enlarges progressively; overflow incontinence in late stages; motor function intact initially
• Cystometry: Large capacity; flat, high-compliance filling curve; no sensation at normal fill volumes; large residual

5. Motor Paralytic Bladder (Motor Neurogenic Bladder)

• Lesion: Efferent (motor/parasympathetic) fibres from sacral cord to bladder
• Causes: Pelvic surgery, trauma, herpes zoster
• Mechanism: Detrusor motor denervation → inability to contract despite intact sensation
• Features: Urinary retention with painful distension; sensation preserved; inability to initiate voiding; may progress to overflow incontinence
• Cystometry: Normal filling; no voluntary detrusor contraction; large residual

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Complications of Neurogenic Bladder

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Management

• Clean Intermittent Catheterisation (CIC) — gold standard for emptying in areflexic bladder
• Antimuscarinics (oxybutynin, tolterodine) — for detrusor overactivity/hyperreflexia
• Alpha-blockers — for smooth sphincter dyssynergia
• Botulinum toxin — intravesical for refractory detrusor overactivity
• Neuromodulation (sacral nerve stimulation, PTNS) — for overactive bladder
• Surgical — bladder augmentation (enterocystoplasty), Mitrofanoff procedure, urinary diversion, artificial urinary sphincter
• Urodynamic surveillance — essential; high-risk patients (SCI, spina bifida) need regular video-urodynamics to monitor pressures and prevent upper tract damage

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PART II: AUTOMATIC BLADDER (Reflex Neurogenic Bladder) — 10 Marks

Definition

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Anatomical Basis

• The pontine micturition centre (PMC) normally coordinates detrusor contraction with sphincter relaxation
• A suprasacral lesion disconnects this coordination centre from the sacral reflex arc
• The sacral cord (S2–S4) and the spinal micturition reflex arc remain intact
• Both afferent (stretch) signals from the bladder and efferent (motor) parasympathetic signals to the detrusor are preserved within the sacral cord
• However, both ascending afferent signals to the brain and descending inhibitory signals from the cortex/PMC are severed

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Phases After Spinal Cord Injury

Phase 1 — Spinal Shock (days to weeks)

• Immediately after cord transection, all spinal reflexes below the lesion are suppressed (spinal shock)
• Bladder becomes atonic, flaccid, and overfills
• Overflow incontinence occurs with no reflex voiding
• Management: indwelling catheter or CIC to prevent bladder overdistension and damage

Phase 2 — Recovery / Automatic Bladder (weeks to months)

• As spinal shock resolves, the sacral micturition reflex gradually re-establishes
• Bladder becomes hyperreflexic — empties automatically at low volumes by spinal reflex
• Detrusor overactivity (hyperreflexia) develops
• Bladder capacity is reduced
• Voiding is unannounced, involuntary, incomplete — significant residual urine

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Clinical Features

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Urodynamic Findings (Cystometry)

• Reduced bladder capacity (voids at low volumes)
• Uninhibited/involuntary detrusor contractions (neurogenic detrusor overactivity)
• Detrusor-sphincter dyssynergia (simultaneous detrusor contraction + external sphincter contraction)
• High detrusor pressures (risk of upper tract damage if sustained >40 cmH₂O)
• No voluntary augmentation of voiding

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Causes

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Management of Automatic Bladder

Important: Reflex bladder emptying and abdominal straining (Valsalva voiding) are NOT recommended because they generate high intradetrusor pressures that damage the upper urinary tract. — Smith & Tanagho's General Urology

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PART III: COMPARISON OF ALL TYPES OF NEUROGENIC BLADDER

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Key Principles to Remember

1. Lesion above sacral cord (suprasacral) → Detrusor hyperreflexia + DSD (UMN pattern) — automatic / reflex bladder
2. Lesion at sacral cord or below (infrapontine LMN) → Detrusor areflexia — autonomous/flaccid bladder
3. Lesion above pons (suprapontine) → Detrusor hyperreflexia but synergic sphincter — uninhibited bladder
4. Storage pressure >40 cmH₂O is the critical threshold above which renal damage occurs — urodynamic monitoring is mandatory
5. Automatic (reflex) bladder is the most important exam type — represents the post-spinal shock stage of complete suprasacral SCI

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Lumbar Fusion Surgeries and Approaches — 10 Marks Each

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PART I: LUMBAR SPINAL FUSION — OVERVIEW (10 Marks)

Definition

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Principles of Fusion

1. Instrumentation — provides immediate mechanical stability (pedicle screws + rods, plates) while biological fusion occurs
2. Bone grafting — provides the biological substrate for osseous union

Graft Types

Metalwork provides temporary support only until uninterrupted osseous union is achieved. — Grainger & Allison's

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Indications for Lumbar Fusion

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Goals of Lumbar Fusion

1. Decompression of neural structures (spinal cord, nerve roots)
2. Stabilisation of the motion segment — reduce pain from abnormal movement
3. Restoration of disc height and foraminal height
4. Restoration of sagittal alignment (lumbar lordosis)
5. Prevention of progression of deformity

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Types of Lumbar Fusion by Location of Graft Placement

A. Posterolateral Fusion (PLF) — Intertransverse Fusion

• Bone graft placed between transverse processes and/or facet joints
• Combined with decompressive laminectomy and discectomy
• Does not enter the disc space
• Provides fusion of posterior column elements
• Facilitated by pedicle screws + rod construct
• Advantage: simpler; less neural retraction
• Disadvantage: no anterior column support; lower fusion rates than interbody techniques

B. Interbody Fusion

• Disc is removed and interbody cage + graft placed directly between vertebral bodies
• Restores disc height, foraminal height, and load-sharing at anterior column
• Higher fusion rates than PLF alone
• Multiple approaches (covered in detail in Part II)

C. 360° / Circumferential Fusion

• Combination of anterior interbody fusion + posterior instrumentation (pedicle screws + rods + posterolateral bone grafting)
• Provides maximum stability
• Indicated for severe instability, high-grade spondylolisthesis, revision surgery
• Higher fusion rates but more operative morbidity (two approaches)

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Instrumentation

• Provide three-column fixation (anterior, middle, posterior columns)
• Rigid, strong, well-tolerated
• Risk: screw malposition → nerve root injury
• Other fixation options: translaminar screws, transfacet screws, hooks, wires

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Complications of Lumbar Fusion

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PART II: APPROACHES FOR LUMBAR FUSION (10 Marks)

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1. PLIF — Posterior Lumbar Interbody Fusion

1. Patient prone; midline incision
2. Bilateral laminectomy / laminotomy
3. Bilateral facetectomy (partial or complete)
4. Retraction of dural sac and nerve roots bilaterally
5. Total discectomy; removal of cartilaginous end plates
6. Bone graft / cage packed into disc space bilaterally
7. Pedicle screw + rod fixation

• Direct visualisation of neural elements
• Single posterior incision
• Bilateral interbody support
• Good fusion rates — better than PLF alone for spondylolisthesis

• Extensive bilateral muscle stripping
• Significant dural retraction → risk of nerve root injury, dural tear
• High blood loss
• Epidural scar formation

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2. TLIF — Transforaminal Lumbar Interbody Fusion

1. Patient prone; midline or paramedian incision
2. Unilateral facetectomy on symptomatic side
3. Approach through the intervertebral foramen (Kambin's triangle) — avoids the dural sac
4. Discectomy via unilateral corridor
5. Curved/crescent-shaped cage inserted across the disc space
6. Bone graft + bilateral pedicle screw-rod construct

• Less dural retraction than PLIF (unilateral approach)
• Single posterior incision — avoids anterior approach morbidity
• Lower risk to neural elements
• Can be done as MIS-TLIF (minimally invasive)
• Preserves contralateral musculature

• Unilateral disc clearance — less complete than bilateral PLIF
• Risk of cage migration
• Less restoration of lordosis than ALIF

MIS-TLIF uses tubular retractors and fluoroscopic guidance, minimising muscle damage and blood loss. — Miller's Anesthesia

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3. ALIF — Anterior Lumbar Interbody Fusion

1. Patient supine; left paramedian or midline abdominal incision (or laparoscopic)
2. Retroperitoneal dissection → mobilisation of aorta, IVC, iliac vessels
3. Complete discectomy via anterior disc space
4. Large cage (lordotic) + graft placed with full endplate coverage
5. Anterior plate/screws OR supplemented with posterior pedicle screws

• Largest cage footprint → best endplate coverage, highest fusion rate
• Maximal restoration of disc height and lumbar lordosis
• No posterior muscle dissection — posterior musculature preserved
• Excellent deformity correction
• Access to L4–L5 and L5–S1 (difficult to reach from other approaches)

• Risk of retrograde ejaculation (superior hypogastric plexus injury) — 1–5%
• Risk of vascular injury (aorta, IVC, iliac vessels)
• Requires vascular/access surgeon collaboration
• Cannot address posterior neural compression directly
• Bowel and urological complications

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4. LLIF / XLIF — Lateral (Extreme) Lumbar Interbody Fusion (Direct Lateral Interbody Fusion — DLIF)

1. Patient in lateral decubitus position
2. Small flank incision; retroperitoneal dissection
3. Blunt dilation through psoas muscle under intraoperative neuromonitoring (EMG) to avoid lumbar plexus
4. Large wide cage placed at disc space under fluoroscopic guidance
5. Can be supplemented with lateral plate or posterior pedicle screws

• Minimally invasive — minimal blood loss
• Large cage footprint → strong endplate contact, good fusion
• Avoids posterior muscle stripping and anterior vascular structures
• Can address T12–L4 levels efficiently (multiple levels in one position)
• Good for coronal deformity correction (adult degenerative scoliosis)

• Limited to L1–L4 (cannot reach L4–L5 easily; cannot reach L5–S1 due to iliac crest)
• Risk of lumbar plexus / genitofemoral nerve injury → thigh numbness, hip flexor weakness (most common complication)
• Requires neuromonitoring
• Peritoneal contents injury (occult)

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5. OLIF — Oblique Lumbar Interbody Fusion (ATP approach)

1. Patient lateral or supine with roll; oblique flank incision
2. Retroperitoneal approach in the corridor between the great vessels anteriorly and the psoas posteriorly
3. Avoids traversing the psoas (unlike XLIF)
4. Cage inserted obliquely
5. Supplemented with posterior fixation

• Avoids psoas → lower risk of lumbar plexus injury vs. XLIF
• Can access L5–S1 (unlike XLIF)
• Minimally invasive
• Applicable for L2–S1

• Risk of sympathetic plexus, ureter, vascular injury
• Technically demanding anatomy
• Less familiar approach

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6. PLF — Posterolateral (Intertransverse) Fusion

• Bone graft placed between transverse processes and facets (outside the disc space)
• Combined with pedicle screw-rod instrumentation
• Simpler; no interbody work
• Lower fusion rates compared to interbody techniques
• Indicated where interbody access not needed or not possible

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Summary Comparison of Approaches

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Key Principles for Exam

1. TLIF is the most commonly performed interbody fusion today — unilateral transforaminal approach, less neural retraction than PLIF
2. ALIF gives the best lordosis correction and cage footprint — used especially at L5–S1
3. XLIF/LLIF cannot reach L5–S1 due to the iliac crest — limited to L1–L4
4. Pedicle screws + rods = gold standard instrumentation; three-column fixation
5. Pseudoarthrosis = failed fusion — most common indication for revision surgery
6. Adjacent segment disease = degeneration above/below fused levels — long-term complication of any fusion

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Visual Guide to Lumbar Interbody Fusion Approaches

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All Approaches — Trajectories at a Glance

Panel A (axial CT): White arrows show entry corridors — OLIF and XLIF approach laterally/obliquely, TLIF through the foramen, PLIF from the direct posterior midline. Panel B: 3D view of a tubular retractor docked at the lateral facet for a minimally invasive approach.

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All Approaches — Schematic Diagram from Textbook

(Miller's Review of Orthopaedics, modified from Mobbs et al., 2015)

• ALIF = anterior (12 o'clock)
• OLIF = oblique anterolateral
• LLIF/XLIF = true lateral (3 or 9 o'clock)
• TLIF = oblique posterior through foramen
• PLIF = direct posterior bilateral

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TLIF vs MIS-TLIF (Transforaminal LIF)

(a) MIS-TLIF: Tubular retractor angled obliquely through the foramen — minimal muscle disruption. (b) Open TLIF: Wide midline incision with bilateral paraspinal muscle retraction. Note how MIS-TLIF avoids the spinal canal, accessing the disc through Kambin's triangle.

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TLIF vs PLIF vs MIS-TLIF — Postoperative Imaging Comparison

Rows 1–2 (TLIF/MIS-TLIF): Postoperative axial MRI (column E) shows preserved multifidus muscle bulk (dark, healthy signal). Row 3 (PLIF): Axial MRI shows significant multifidus atrophy and fatty infiltration (bright signal) due to bilateral muscle stripping — key disadvantage of PLIF over TLIF.

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ALIF — Postoperative Radiograph (L5–S1)

ALIF at L5–S1: Two large oval cages placed side-by-side in the disc space from the anterior approach. The wide cage footprint covering the ring apophysis (strongest endplate zone) is the hallmark of ALIF — maximising fusion surface area and lordosis correction.

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Summary — Approach Corridors

1. All approaches together — the textbook schematic (Miller's Review of Orthopaedics) showing ALIF, OLIF, LLIF, TLIF, and PLIF trajectories in both axial and 3D views
2. All approaches on CT — axial CT with overlaid arrows labelling OLIF, XLIF, TLIF, and PLIF corridors
3. TLIF / MIS-TLIF — illustrated axial diagram comparing open vs minimally invasive transforaminal approach
4. TLIF vs PLIF comparison — postoperative X-rays + MRI showing muscle atrophy difference between PLIF and TLIF
5. ALIF — AP radiograph showing two large interbody cages at L5–S1 after anterior approach

• Search for different/clearer images for any specific approach
• Find intraoperative photos instead of X-rays
• Generate a labelled diagram illustrating each approach