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SUNCT in Multiple Sclerosis

SUNCT (short-lasting unilateral neuralgiform headache with conjunctival injection and tearing) describes a relatively new nosological entity in the group of trigeminal autonomic cephalalgias. First proposed by Sjaastad et al. in 1989 (1), it represents a rare condition with brief, unilateral attacks of pain typically in orbital or temporal area, accompanied by ipsilateral autonomic manifestations. The attacks usually last 5–240 s (2) and are stabbing and burning in character. The predominant autonomic features are conjunctival injection and lacrimation, although sweating of the forehead and rhinorrhoea are also common. The condition favours males, with a male/female ratio varying according to different authors from 2 : 1 to 8.5 : 1 (3, 4). The diagnostic criteria (5) have been agreed by the IHC classification (6). Although many cases reveal no apparent structural causes on imaging studies, SUNCT has been reported secondary to structural lesions in the posterior fossa. Previously associated pathologies include vascular malformations at the cerebellopontine angle (7, 8), brainstem infarction (9), congenital bone malformations of the posterior skull (10, 11), prolactinoma (12, 13), trauma (14), and HIV infection (15). Although there have been no former reports on SUNCT in multiple sclerosis (MS), trigeminal involvement caused by MS on magnetic resonance imaging (MRI) has been reported mainly in association with trigeminal neuralgia (TN) or painless paraesthesia in the distribution of the fifth nerve (16). In addition, the coexistence of cluster headache and MS has been reported (17). Pathogenetic mechanisms of SUNCT remain unclear. A neurovascular aetiology has been suggested with involvement of the trigemino-vascular system (2, 7). The activation of the trigeminalautonomic reflex and release of vaso-neuroactive substances (vasoactive intestinal peptide, substance P, calcitonin gene-related peptide) are thought to mediate both pain and autonomic phenomena in SUNCT (2). Many SUNCT cases are relatively refractory to drug treatment. Drugs used for treatment of TN such as carbamazepine (7, 18), lamotrigine (18) and gabapentin (19–22) have been reported to be effective in some cases. Clinical reports on TN transforming into SUNCT (23) and cases of TN with marked autonomic features (24) have raised discussions whether SUNCT should be considered as a variation of TN with concomitant autonomic features or as a separate nosological entity. Nevertheless, the hallmark for distinction between these disorders appears to be the degree of cranial autonomic activation, not merely its presence. Here, we present a case of SUNCT in a 42-year-old man with progressive relapsing MS.