Neurosurgery notes/Intramedullary AVMs

Intramedullary AVMs

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Jul 13, 2026 07:06 PM GMT+0

General

  • Aka
    • Type II AVMs
    • “Glomus” AVM
  • True AVMs of the spinal cord parenchyma
    • Similar to cerebral AVMs

Numbers

  • Affect men and women equally
  • Mean age of presentation in 20s

Location

  • Feeding arteries are from
    • Posterior spinal artery
    • Anterior spinal artery
    • Intervening nidus
  • Drainage veins
    • Coronal venous plexus.

Classification

Diffuseness

  • Compact
  • Diffuse
  • Mixed types

Flow rate

  • High
    • Characterized by the remodelling of vessels
      • Hypertrophy of arteries,
      • Development of aneurysms
        • Rodesch et al., 2002: 31.6% incidence of arterial aneurysm
      • Development of venous pouches.
    • They are more often seen in children and patients with HHT.
    • High vascular stress → increase in intramedullary or subarachnoid haemorrhage.
    • Ischaemic myelopathy or symptoms resulting from neural compression by dilated vessels.
    • Neuropathic pain (30%).
  • Low

Natural history

  • For incidentally discovered lesions
    • Gross 2013
      • 50% of patient present with haemorrhage
      • Annual haemorrhage rate of
        • 4% no previous haemorrhage
        • 10% with previous haemorrhage

Clinical features

  • Acute haemorrhage
  • Steal phenomenon → progressive myelopathy

Radiology

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Treatment

  • Partial treatment might be better than no treatment
  • Endovascular treatment
    • Esp those fed primarily from the ASA.
    • Aims
      • Alleviate symptoms of ischaemia, mass- effect
      • Reduce risk of haemorrhage.
    • Agents
      • Onyx or NCBA glue to treat nidus
      • Coils may be used to treat venous pouches, ectasia, and aneurysms.
    • Risk
      • Inadvertent migration of embolic materials with resultant ischaemic injury due to complex angioarchitecture
    • Recanalization was significantly more likely after poly- vinyl- alcohol (PVA) particle embolization (17%) compared to Onyx or NCBA glue (0– 11%).
  • Microsurgery
    • Surgical extirpation is an effective treatment in selected cases
    • 2D angiotomography
      • Planning the surgical approach
        • Morbidity is determined mainly by the location of the malformation and the difficulty accessing it.
    • The principles of surgical excision are similar to operating on the cranial homologue but certain nuances of technique merit comment.
      • Low- flow lesions they may be advantageously approached from the venous side without the same fear of haemorrhage or congestion in the cord.
      • Excessive pial dissection may be avoided and elements of the shunt are divided ‘in- situ’ rather than attempting complete extirpation of every component of the malformation.
      • Most lesions are approached posteriorly or posterolaterally.
      • Interruption of arterial side of AVM first
    • Intraoperative neurophysiological monitoring → alterations in the motor tracts anteriorly
      • Delta waves
      • Motor evoked potentials
  • Radiosurgery
    • Indicated when microsurgery and endovascular surgery fail
    • They pose challenges not encountered with their cerebral counterparts.
      • Respiratory movements
        • Facilitated by modern image guidance systems.
      • No information about cord toxicity treatment

Outcomes

  • Gross 2013 meta analysis
    • Complete obliteration rates
      • 78% for surgery
      • 33% endovascular
    • Long-term clinical worsening
      • 12% for surgery
      • 13% for endovascular treatment
    • Complete obliteration resulted in no haemorrhages
    • Partial surgical treatment
      • The annual haemorrhage rate was 3% (95% CI: 1%-6%);
    • Partial endovascular treatment.
      • No haemorrhages were reported over 196 patient-years after — Or no one reported any rebleed
    • Long-term Aminoff- Logue scale
      • Surgery
        • Gait scores were improved or stable in 93%
        • Micturition scores the same or better in 94%.
      • Endovascular and surgical outcomes at ten years similar
  • Kalani 2016 and Hila 2003
    • Complete obliteration: 0-19% at 3 years
    • None had post-treatment hemorrhagic events.
    • If not complete obliteration, significant volume reduction was noted at 3 years

Reference