Transient Horner’s syndrome as sign of intrapetrous carotid dissection in a migrainous patient

We report the case of a patient that, during a migraine attack presented a transient Horner’s syndrome (HS), secondary to a spontaneous intrapetrous carotid artery dissection (IPCAD). Migraine is a common disorder with a pathophysiology that is incompletely understood. Migraine is considered a functional disorder of the brain, however, there are evidences linking migraine to the vascular system [1]. Endothelial dysfunction, altered vascular reactivity and hypercoagulability are reported in patients with migraine [2]. Migraine with aura seems to increase the risk of ischemic stroke [3] with unclear mechanisms. One link may be cervical artery dissection (CAD), since the association between M and CAD has been suggested [4]. Among CAD, spontaneous IPCAD is a rare occurrence, by far rarer than extracranial dissection, probably related to the anatomic localization that determinate the immobility of the petrous carotid portion fixed in the carotid canal [4]. A 36-year-old female presented with a moderate headache associated with 2-mm left ptosis and 2-mm anisocoria (left pupil smaller) without other neurological signs. The degree of anisocoria was enhanced in dim light, while visual fields and tonometry were normal. She had a positive family history for migraine without aura (MO). Past medical history was unremarkable. The patient did not present any cerebrovascular risk factor. When she was 17 years old, she started suffering from MO (ICHD-II criteria, [5]). The attacks were characterized by moderate, rarely severe, pulsating pain, aggravated by efforts. The pain was usually localized unilaterally in the periorbital right or left region and lasted 6–8 h. She reported nausea, rarely vomiting, phono and photophobia during the attacks. NSAIDs showed a good response. The attack associated with HS did not differ from the usual ones; pain was moderate, pulsating, localized in left fronto-temporal region and associated with phono and photophobia. Brain MRI with gadolinium and neck MRI with fat suppression were reported as negative; intracranial angio-MRI evidenced IPCAD on the left side (Fig. 1a, c). No etiological or predisposing factors to the dissection were disclosed, in particular, no clinical signs of Marfan’s syndrome were present. An occasional precipitating factor could have been the cough, secondary to a pharyngitis presented by the patient few days before hospital admittance. Routine blood counts, blood chemistry, coagulation studies, chest X-ray, electrocardiogram, transthoracic echocardiography and ophthalmology assessment were negative. A patent foramen ovale was excluded by a negative transcranial Doppler sonography with bubble test. Therapy with ASA was started; the subjective and neurological symptoms including HS disappeared in 48 h. A follow-up a month later evidenced a recanalization of the left carotid artery (Fig. 1b, d) and the patient was asymptomatic. The mechanisms by which migraine increase the risk of ischemic stroke could be resumed in the following points: (1) migraine may directly cause an ischemic stroke F. Maggioni (&) C. Disco G. Zanchin Department of Neurosciences, Headache Center, University of Padua, Via Giustiniani 5, 35128 Padua, Italy e-mail: ferdinando.maggioni@unipd.it