Carotidynia

Carotidynia describes pain arising from the cervical carotid artery resulting in unilateral neck pain that frequently radiates to the ipsilateral face and ear and sometimes to the head. Facial pain is a common primary symptom and carotid artery tenderness and overlying soft tissue swelling are the major physical findings. Raskin (1988) reports that there are two forms of this disorder: an acute form that results in a monophasic illness usually lasting for a week or two and tending not to recur; and a chronic recurring form that appears to be a variant of migraine and is responsive to antimigraine measures. Both forms are common and are highly responsive to the administration of corticosteroids.
Acute carotidynia has been most accurately described in Roseman’s 1967 report. There were 33 patients affected, without apparent sexual predilection, with an age range of 15 to 78 years. Seven patients had evidence of a concurrent upper respiratory infection. Seven patients had a history of migraine. In three patients, bilateral pain was reported and three other patients experienced multiple (two, three, and four) attacks. In 17 patients neck pain was aggravated by head and neck motion, swallowing, coughing, chewing, yawning, or sneezing. The character of the pain was reported as stabbing, throbbing, or dull and continuous. The duration of the syndrome ranged from 5 days to 4 months (average, 12 days). Although Roseman found that corticosteroids at very low dosages were not helpful, Bank (1978) found that in 12 patients moderate dosages of prednisone (30 mg) given for 2 days and tapered over the next 4 days rendered all 12 pain-free within 24 hours and without carotid artery tenderness within 3 to 4 days, without exception. Others (Sanders, 1962) have found that the acute syndrome is steroid-responsive as well. Raskin (1988) begins treatment with 60 mg prednisone or 24 mg triamcinolone daily for 7 days and then tapers the dosage over the next 7 days. Feit (1982) has found that triamcinolone is superior to prednisone in the treatment of this disorder. Raskin (1988) found that several patients with incomplete responses to prednisone improved dramatically when triamcinolone was substituted.
Of course, acute carotid pain in the absence of other neurologic findings may also rarely be the major manifestation of temporal arteritis (Sanders, 1962), spontaneous carotid dissection (Mokri et al, 1986; Hart and Easton, 1983), and carotid atherosclerosis or dysplasia. Acute neck pain may also result from thyroiditis and careful examination of the neck should identify the anatomic source of tenderness. MRI of the neck has proven highly sensitive in the diagnosis of structural disease of the carotid arteries, so that this imaging study should be considered if there is no other explanation.
Chronic, recurring carotidynia has also been termed facial migraine (Raskin, 1988). Lovshin (1960) recorded 100 such cases and was the first to appreciate the relationship to migraine. Most of his patients were women in the fourth and fifth decades. He observed that the carotid artery was almost always tender during a migraine attack and that the absence of headache should not deter the diagnosis of this migraine variant. Raskin and Prusiner (1977) reintroduced the concept of the chronic carotidynia syndrome as a form of migraine in their description of 8 patients evaluated over 6 years. The patients were women, aged 37 to 77 years with pain located at the jaw or neck. The patients experienced continuous, dull pain with superimposed throbbing or pounding episodically once to several times weekly; each exacerbation lasted minutes to hours. Occasionally, sharp, ice pick-like jabs were also reported. They believe that the primary mechanism of the recurring carotidynia syndrome is that of migraine, with a secondary vascular phenomena focused upon the carotid artery instead of the more commonly involved superficial temporal artery. Carotidynia is by far the most common cause of recurring facial pain in association with the findings of carotid tenderness and soft tissue swelling. According to Raskin (1988) dental trauma has proven to be fairly common precipitant of the syndrome. A differential of this syndrome should include temporal arteritis as well as unruptured cervical carotid aneurysm.
Additional considerations with ipsilateral neck pain in the region of the carotid artery near its bifurcation include thyroiditis, migraine, aneurysm of the carotid system, and neck neoplasms (Cannon, 1994).


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