Head and neck pain as a consequence of cervical artery dissection (carotid and vertebral) has been recognized for many decades. The location of the pain is variable and can involve, in isolation or in combination, any part of the head, face and neck, usually ipsilateral to the pathology; however, bilateral and diffuse headache can occur, even when the dissection is unilateral. The pain can sometimes be very localized with a predilection for the frontal, orbital, temporal and upper cervical regions. It can also simulate migraine, cluster headache or carotidynia [
31]. Horner’s syndrome; cranial-nerve palsy; tinnitus; and, rarely, cervical-root injury are the most common associated symptoms that attract attention to the secondary nature of the pain [
32••]. It has also been shown that the risk for cervical artery dissection (CAD) is doubled for any migraine [
33]. It has hence been postulated that CAD may explain the increased risk of ischemic strokes associated with migraines. The group participating with CADISP (Cervical Artery Dissection and Ischemic Stroke Patients, a multinational European network) [
34] also found both migraine with and without aura to be more frequent in patients with cervical artery dissection, as compared to healthy controls and stroke patients without a dissection. Within patients with a dissection, presence or absence of migraine did not impact the prevalence of strokes, arterial distribution, or other clinical or prognostic features [
35••]. In a separate study in the same cohort of patients, the authors found that patients with carotid artery dissection were older, more often men, more frequently had a recent infection (odds ratio of 1.59), and tended to report less often a minor neck trauma in the previous month (OR = 0.75 [0.56–1.007]) compared to patients with vertebral artery dissection. Clinically, patients with internal carotid artery dissection more often presented with headache at admission but less frequently complained of cervical pain or had cerebral ischemia than patients with vertebral artery disease. It was also noted that multiple concomitant dissections tended to cluster on the same artery type rather than involving both a vertebral and carotid artery [
36]. An important cause of dissection is fibromuscular dysplasia, which is a nonatherosclerotic, noninflammatory vascular disease that primarily affects women in the prime of their life. It commonly involves the renal, carotid, and vertebral arteries. In one of the largest cohort of fibromuscular dysplasia patients [
37], the most common clinical manifestations noted were hypertension, headaches, pulsatile tinnitus, and dizziness, but dissection, aneurysm, transient ischemic attack, and stroke also occur with a high frequency. Headaches were a common symptom (60.0 % of patients), with classical migraine-type headaches reported in 32.2 %. Severe headaches occurred weekly in 13.1 % of patients and daily in 12.5 % of patients. Since the affected population, also has one of the highest prevalence for migraine, a high index of suspicion needs to be maintained.
Once the pathology is clinically suspected, prompt confirmation of the diagnosis and commencing treatment for the underlying condition is warranted. There is class I evidence that contrast-enhanced CT angiogram, MR angiogram and catheter-based contrast angiography are all useful for diagnosis of cervical artery dissection (level of evidence: C) [
38••]. Regarding treatment , there is class IIa evidence that for patients with symptomatic cervical artery dissection, anticoagulation with intravenous heparin (dose adjusted to prolong the partial thromboplastin time to 1.5 to 2.0 times the control value) or low-molecular weight heparin (in appropriate dose) followed by warfarin [dose adjusted to achieve a target INR of 2.5 (range 2.0 to 3.0)], or oral anticoagulation without antecedent heparin, can be beneficial for 3 to 6 months, followed by antiplatelet therapy with aspirin (81–325 mg daily) or clopidogrel (75 mg daily, level of evidence: C) [
38••].
In addition, there is class IIb evidence supporting the consideration of carotid angioplasty and stenting when ischemic neurological symptoms have not responded to antithrombotic therapy after acute carotid dissection (level of evidence: C) [
38••]. The safety and effectiveness of pharmacological therapy with a b-adrenergic antagonist, angiotensin inhibitor or non-dihydropyridine calcium channel antagonist (verapamil or diltiazem) to lower blood pressure to the normal range and reduce arterial wall stress are not well established (level of evidence: C)
Independent of dissections, occurrence of headaches has been described with performance of cerebral and carotid angiogram, endovascular and surgical manipulation of the carotid and vertebral vessels.
Intracarotid or intravertebral injection of contrast induces a diffuse severe headache with a burning sensation which resolves spontaneously. The injection can also trigger a migraine attack in a person who has migraine. A very specific subtype of headache has been reported after balloon inflation or embolization of an AVM or aneurysm. It is a severe pain of abrupt onset, localized in specific areas according to the artery involved, occurring within a few seconds of the procedure and disappearing rapidly [
2]. In a recent study, frequency of headache after internal carotid stenting was 39.1 % as compared to 21.9 % angiography alone. The headache commonly arose in a short period after the procedure and was relieved in 10 minutes. In both cases headache was mild, ipsilateral, frontotemporal in location, pressing in nature, and arose frequently and resolved within 10 minutes after the procedure. Both types of headache were related to severe stenosis, however described as pressing after carotid stenting and burning after angiography [
39].