Neurosurgery notes/Bow hunter’s stroke

Bow hunter’s stroke

General

  • A special subset of VBI.
  • Bow hunter’s stroke (BHS): hemodynamic VBI induced by intermittent VA occlusion resulting from head rotation (ischemic sequelae range from TIA (bow hunter’s sign) to completed stroke).

Aetiology

  • May occur with forced (e.g. with chiropractic neck manipulation) or voluntary head rotation.
    • Occlusion usually involves the VA contralateral to the direction of rotation
    • Occurs at the C1–2 junction
      • Due to the immobility of the VA at this location
      • Main location
        • However, other sites have also been reported.
    • VA occlusion does not produce symptoms in most individuals due to collateral flow through the contralateral VA and/or the circle of Willis.
      • Symptomatic occlusion usually involves the dominant VA,
        • But it may also occur with non-dominant VA.
      • Most cases of BHS occur in patients with an isolated posterior circulation (incompetent posterior communicating arteries).
      • BHS has also been postulated as one possible cause of sudden infant death syndrome.

Contributing factors

  • External VA compression
    • Spondylotic bone spurs:
      • Esp in foramen transversarium
    • Tumors
    • Fibrous bands (e.g. proximal to entrance of VA into C6 foramen transversarium44) d) infectious processes e) trauma
  • Tethering of the VA
    • At the transverse foramina of C1 & C2
    • Along the sulcus arteriosus proximal to where the VA enters the dura
  • Defect in odontoid process
  • Atherosclerotic vascular disease

Diagnosis

  • General information
    • BHS should be suspected in patient with symptoms of VBI precipitated by head movement.
      • This may be very difficult to differentiate from vertigo and nausea due to vestibular dysfunction (which can also be induced by head movement)
        • Rotation of the body keeping the head motionless should not cause symptoms from vestibular symptoms and might help distinguish these conditions.
  • Dynamic cerebral angiography (DCA)
    • Significant consequences can be precipitated during DCA in patients with BHS.
    • The involved VA shows loss of flow as the head is rotated from the neutral position to the contralateral side.
    • Carotid injections demonstrate patency of P-comms and the presence of any persistent fetal anastomoses.
  • CT angiogram (CTA)
    • Same precautions as with DCA (see above).
    • Probably not the initial diagnostic study of choice.
    • If DCA is negative, CTA is not needed.
    • If DCA is positive, CTA may be helpful to demonstrate the arterial relationship to the bony anatomy.

Treatment

  • Options include:
    • Anticoagulation
    • Cervical collar: to remind patient not to turn their head
    • For VA compression at C1–2:
      • Comparison of surgical treatment for positional VA occlusion at C1–2
        • Procedure
          Advantages
          Disadvantages
          C1–2 fusion
          High success rate in eliminating symptoms
          Loss of 50–70% of neck rotation with possible discomfort
          VA decompression
          No loss of motion
          33% continue to have symptoms
      • C1–2 fusion
      • VA decompression: C1 “hemilaminectomy” via a posterior approach
      • For compression at C1–2, it is suggested that VA decompression be performed as the initial treatment.
        • This should be followed by DCA to verify maintenance of patency with head turning.
          • Patients who fail clinically or on DCA should undergo C1–2 fusion.
    • For compression at other sites:
      • Elimination of the source of compression where possible
        • Sectioning off offending fibrous band,
        • Removal of osteophytic spurs