Spine

Spinal cord blood supply and injury syndromes

Cord vascular anatomy, acute SCI steroid management, central cord and cauda equina syndromes

19 questions 4 source pages

Images appear with the first question taken from each source page — tap a question to open it.

Q1What are the vertical arteries supplying the spinal cord?▸

Q2What are the segmental and radicular arteries of the spinal cord?▸

Segmental arteries: CS from VA, TS from posterior intercostal artery, LS from lumbar and iliac artery
Enter via intervertebral foramen and divide into posterior and anterior radicular arteries
Follow the anterior and posterior rami of each nerve root; anastomose with the ASA and PSA

Q3What is the artery of Adamkiewicz?▸

A segmental medullary artery coming directly off the segmental artery to anastomose with ASA/PSA
From left posterior intercostal artery; 60% left
T9-L2, supplies lower 2/3 of spinal cord; joins the ASA

Q4Describe the venous drainage of the spinal cord.▸

Anterolateral and posterolateral spinal veins (x4); 1 anterior median vein and 1 posterior median spinal vein
Drain into radicular veins --> internal vertebral venous plexus
--> external vertebral venous plexus
--> ascending lumbar veins and azygous system (right side)

Q5What is the rationale for methylprednisolone in acute spinal cord injury?▸

Prevent secondary injury to the cord due to ischaemia, lipid peroxidation and free radicals
Increase microcirculation, decrease inflammation and cell death

Q6What did the NASCIS I-III studies show?▸

NASCIS I: high vs low dose MP - no difference (dose)
NASCIS II: MP vs naloxone vs placebo - no difference; posthoc high dose MP within 8hr improved 5 motor points
NASCIS III: examined timing

Q7What are the criticisms of the NASCIS evidence?▸

Q8What is the dosage of methylprednisolone if used?▸

Q9What do guidelines recommend regarding steroids for acute SCI?▸

NICE - do not recommend it
2013 AANS - methylprednisolone should not be used for acute SCI
AO Spine 2017: suggest not offering 24hr high dose MPSS if presenting >8hrs
Suggest 24hr infusion MPSS be offered within 8 hours (30mg/kg loading then 5.4mg/kg/hr)

Q10What is the pathoanatomy behind central cord syndrome?▸

Pre-existing narrowing of the spinal canal (congenital or secondary to OA), usually after a flexion/extension neck injury
A/P force distributes the greatest damaging effect on the central cord (anterior osteophytes, posterior thickened ligamentum flavum)
Concentrated stress in the middle of the cord + the water-shed circulation between anterior and posterior horns -> ischemic insult to the central part of the SC
Stasis of axoplasmic flow and/or Wallerian degeneration of the corticospinal tracts

Q11Why is the deficit UL >> LL and what is dissociative anaesthesia?▸

Lamination of the lateral corticospinal (motor) and spinothalamic (sensory) tracts: sacral segments are the most lateral, with lumbar, thoracic and cervical components arranged somatotopically, proceeding medially toward the central canal
UL >> LL is much more pronounced in motor than sensory
Dissociative anaesthesia: pain and light touch affected, deep touch and proprioception not affected

Q12What is the typical recovery pattern in central cord syndrome?▸

Q13When is surgery indicated in central cord syndrome?▸

Early surgery if associated with a large disc protrusion, fracture or instability
STASCIS 2012 and 2021 (Lancet) suggest surgical decompression within 24hrs
Samuel Spine 2015: delay surgery is associated with reduced mortality
Michael Fehlings 2017 – suggest within 24hrs
HKU paper 2022 (Spine J): surgery beyond the acute post-injury period failed to improve outcomes; clinical (AMS >61) and radiological (length of stenosis >3.9cm) factors were prognosticative of neurological recovery rates

Q14What did Anderson Neurosurgery 2015 conclude about the timing of surgery in central cord syndrome?▸

Systematic review: insufficient evidence to give a clear recommendation for early surgery (<24hrs)
It is preferable to operate during the first hospital admission and <2 weeks after injury

Q15What is cauda equina syndrome (CES)?▸

Clinical syndrome from compression of the terminal spinal nerve roots in the lumbosacral spine
Features: 1. bowel and bladder dysfunction, 2. saddle anaesthesia, 3. bilateral leg pain, 4. lower extremity sensorimotor changes
Presentation can be acute or insidious
Acute CES is an orthopaedic emergency warranting urgent MRI and surgery

Q16What is the pattern of bladder dysfunction in cord compression versus cauda equina syndrome?▸

Cord compression: reflex arc intact, lack of voluntary control -> bladder spasm, high pressure, incontinence
Cauda equina: impaired reflex arc -> flaccid bladder, urinary retention, sphincter leakage, overflow incontinence

Q17What is the timing of surgery in acute cauda equina syndrome?▸

Controversial - studies quote <24h, 24-48h or within 48h
Todd et al 2016 (Br J Neurosurg): CESS bilateral radiculopathy, CESI urinary difficulties, CESR retention with overflow, CESC absent perianal sensation/lax anus
Urgency: S admit/observe, I emergency, R - <12hr emergency, >12hr next acute list, C next acute list
Kumar et al 2021 (Eur Spine J): within 48h
BASS: decompressive surgery should be undertaken at the earliest opportunity, balancing duration of pre-existing symptoms and night-time morbidity
Do not wait for CESR or CESC - outcomes are poor despite surgery; if safe, operate as an emergency

Q18How would you perform a decompression for cauda equina syndrome?▸

Prone patient; II to identify the level of decompression
Posterior midline approach through the inter-nervous plane between erector spinae; subperiosteal dissection to lamina
Laminotomy of the cranial lamina above the ligamentum flavum; resect ligamentum flavum proximal to distal, then undercut the distal lamina
Decompress laterally until the lateral edge of the dura is identified and the nerve root can be retracted to access the disc

Q19What is the clinical vignette of cauda equina syndrome shown?▸

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