We studied the characteristics of headaches in 161 consecutive symptomatic patients with spontaneous dissections of the internal carotid artery (n = 135) or the vertebral artery (n = 26). For patients with internal carotid artery dissection (ICAD), the mean age was 47 years and for those with vertebral artery dissection (VAD), 40.7 years. A history of migraine was present in 18% of the ICAD group and in 23% of the VAD group. Headache was reported by 68% of the patients with ICAD and by 69% of those with VAD, and, when present, it was the initial manifestation in 47% of those with ICAD and in 33% of those with VAD. Ten percent of patients with ICAD had eye, facial, or ear pain without headache. The median interval from onset of headache to development of other neurologic manifestations was 4 days for the ICAD group and 14.5 hours for the VAD group. For all dissections, headaches typically were ipsilateral to the side of dissection. In the ICAD group, headaches were limited to the anterior head in 60% of patients and were steady in 73% and pulsating in 25%. In the VAD group, headaches were distributed posteriorly in 83% of patients and were steady in 56% and pulsating in 44%. Neck pain was present in 26% of patients with ICAD (anterolateral) and in 46% of those with VAD (posterior). The median duration of the headache in patients with VAD and ICAD was 72 hours, but headaches became prolonged, persisting for months to years, in four patients with ICAD.

Cranial nerve palsy was present in 23 of 190 consecutive adult patients (12%) with spontaneous dissection of the extracranial internal carotid artery. Ten patients (5.2%) had a syndrome of lower cranial nerve palsies (with invariable involvement of cranial nerve XII with or without additional involvement of cranial nerves XI, X, and IX), seven (3.7%) had palsy of cranial nerve V, and five (2.6%) had a syndrome of ocular motor palsies. Palsy of cranial nerve VIII and ischemic optic neuropathy occurred in one patient each. Three patients had dysgeusia without other cranial nerve involvement, presumably due to involvement of the chorda tympani nerve. Headache or face pain (often unilateral) was present in 83% of patients. Other associated manifestations were cerebral ischemic symptoms, bruits, or oculosympathetic palsy. In one patient, cranial nerve palsy was the only manifestation of internal carotid artery dissection, and in another patient, the disease presented only as a palsy of cranial nerve XII and oculosympathetic palsy. In six patients, a syndrome of hemicrania and ipsilateral cranial nerve palsy was the sole manifestation of internal carotid artery dissection. Cranial nerve palsy is not rare in internal carotid artery dissection. Compression or stretching of the nerve by the expanded artery may explain some but not all of the palsies. An alternative mechanism is likely interruption of the nutrient vessels supplying the nerve.

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