- Criteria for clinical diagnosis requires 2 or more of the following:
- Motor or sensory symptoms or both, occurring bilaterally in the same event
- Diplopia: ischemia of upper brainstem (midbrain) near ocular nuclei
- Dysarthria: ischemia of lower brainstem
- Homonymous hemianopsia: ischemia of occipital cortex (NB: this is binocular, in contrast to amaurosis fugax which is monocular)
- Symptoms
- Due to inadequate blood flow through the posterior cerebral circulation (vertebral arteries, basilar artery and their branches).
- Mnemonic 5D
- “Drop attack”
- Diplopia
- Dysarthria
- Defect (visual field)
- Dizziness
- Predicting the site of the lesion based only on clinical evaluation is very unreliable.
- VBI may be suspected
- In a patient with transient episodes of “dizziness” (vertigo that is otherwise unexplained, e.g. absence of orthostatic hypotension or benign positional vertigo) that are initiated by positional changes.
- Aetiology
- Hemodynamic insufficiency (may be the most common etiology), including:
- Subclavian steal: reversed flow in VA due to proximal stenosis of subclavian artery
- Stenosis of both VAs or of one VA where the other is hypofunctional (e.g. hypoplastic, occluded, or terminates in PICA) causing reduced distal flow in face of inadequate collaterals (see below)
- Embolism from ulcerations
- Atherosclerotic occlusion of brainstem perforators
- Vertebrobasilar hypoplasia: reported as a possible etiology for cerebellar stroke.
- Compression of the VA at the C1–2 level with:
- Head turning (see below)
- Os odontoideum
- Anterior atlantoaxial subluxation: e.g. in rheumatoid arthritis
- With rotatory atlantoaxial subluxation
- Natural history
- No clinical study accurately defines the natural history.
- Stroke rate is 22–35% over 5 years, or 4.5–7% per year
- Risk of stroke after first VBI-TIA has been estimated as 22% for first year.
- Evaluation
- Four-vessel angiography,
- Sometimes with provocative maneuvers (see e.g. Bow hunter’s stroke).
- CTA
- Treatment
- Anticoagulation Main
- Alternatives include
- Anti-platelet drugs such as ASA (efficacy of either remains unproven35,37).
- Surgical treatment includes:
- Vertebral endarterectomy
- Transposition of VA to ICA (with or without carotid endarterectomy, with or without saphenous vein patch graft) or to thyrocervical trunk or to subclavian artery
- Bypass grafting (e.g. occipital artery to PICA)
- C1–2 posterior arthrodesis may prevent potentially life-threatening stroke in cases of os odontoideum