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
- 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
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 |