Extracranial dissection is easily diagnosed by ultrasound

Vertebral Artery Dissection (VAD) –43% of are spontaneous in nature –31% are associated with cervical spine manipulation –16% from trivial trauma –10% from major trauma Haldeman et al. Spine. 1999; 15: 24:

VAD Relatively rare. ( =34 studies, 762 pts of VAD- JNNP,2008) Presenting symptoms: –Unilateral posterior headache Pain may radiate to neck and face –Dysarthria –Dysphagia –Ataxia –Double vision –Limb or trunk numbness (Caplan et al.1985)

VAD Anatomical level: Segment III (petrous level) From the superior of C2 foramen to the dura, most of the spontaneous dissected region. Can extended to segment IV(upstream) with neurological s/s. Most injured rotated point.

Segment I: Rises from the Subclavian artery to the transverse foramen of C6

Segment II: Within the transverse foramina from C6-C2 (the most massage injured level)

Segment IV: From the dura into the cranium

Vertebral Artery Dissection Presenting Findings and Predictors of Outcome V1= 20% V2 =35% V3 =34% V4= 11% (Stroke, 2006) Younger age+ Low NIHSS score => are good prognostic outcome

VAD Diagnosis is same as in carotid dissection. Treatment includes early anticoagulation or followed by anti-platelet therapy.

Account for 20 % of stroke younger than 45 yrs old % of extracranial carotid, 15% of extracranial VA. Trauma, respiratory infection, underlying arteriopathy played some roles in etiology. Local pain, headache, and ipsilateral Horner’s- s/s of Triad. Hours before retina or cerebral stroke. Prognosis is much better in extracranial than intracranial dissection. Recurrence is rare. SAH can be happened in intracranial dissection sometimes. Anti-platelet or anti-coagulation equally.