Frontiers of neurology and neuroscience
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Spontaneous dissection of the cervical internal carotid artery (sICAD) causes, in more than 90% of patients, carotid territory ischemia, local signs and symptoms on the side of dissection, or both, whereas the remaining sICAD remain clinically asymptomatic. Local signs and symptoms include head, facial, or neck pain, Horner syndrome, pulsatile tinnitus, and cranial nerve palsy. Head, facial, or neck pain occurs in 64-74% and is the presenting symptom in up to 58.5%, and the only manifestation in 2.2-4.5%. ⋯ About three quarters of sICAD cause ischemic events, which include ischemic stroke in 80-84%, transient ischemic attack in 15-16%, amaurosis fugax in 3%, ischemic optic neuropathy in 4%, and retinal infarct in 1%. Patients with sICAD causing ischemia show a lower prevalence of Horner syndrome and palsy of the caudal cranial nerves than patients with sICAD causing no ischemic events, whereas headache, neck pain, and pulsatile tinnitus are equally frequent in both groups. After an ischemic stroke, independency defined by a moderate Rankin scale score of 0-2 occurs in 63-90%, whereas the outcome of retinal infarct and ischemic optic neuropathy are not well known.
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The most frequent clinical manifestation of vertebral artery dissection is posterior headache or neck pain accompanied or followed by posterior circulation transient ischemic attack or stroke. Rarer clinical features include isolated headache or neck pain, cervical spinal cord ischemia and cervical root impairment. Asymptomatic vertebral artery dissections have been reported. In the case of primary intracranial vertebral artery dissection or intracranial extension of an extracranial dissection, subarachnoid hemorrhage and rarely rostral cervical spinal cord ischemia or posterior fossa mass effect may occur.