F J Barriga1, C López de Silanes, P Gili, J A Pareja. 1. Department of Neurology, University Hospital Fundación Hospital Alcorcón, Avda. Budapest 1, Alcorcón, Madrid, Spain. fjbarriga@fhalcorcon.es
Abstract
BACKGROUND: Transient, unilateral mydriasis has been reported in migraine patients, and this has been regarded as a possible co-morbidity between migraine and Adie's tonic pupil. Mydriasis that outlasts the duration of migraine attacks is rare. METHODS: Through an eight-year period we have studied all patients referred to our neurological clinic because of migraine attack with mydriasis. All the patients underwent thorough neurologic and ophthalmologic examinations including MRI of the brain and testing of the pupil response to ocular instillation of dilute pilocarpine (0.125%). RESULTS: Seven women and two men, with a mean age of 33.8 ± 12.3 years (range: 19-52) were included. The patients presented during one hemicranial migraine attack with an ipsilateral mydriasis that persisted for a mean of three months, while migraine headaches remained with their typical episodic course. In all the patients a cholinergic supersensitivity in the symptomatic pupil was demonstrated, thus pointing to a dysfunction of the ipsilateral ganglionic parasympathetic fibers. CONCLUSIONS: Synchronous co-localization of the features suggests a pathogenic link between the pupil dysfunction and migraine, rather than a simultaneous coexistence of two independent disorders. Likely explanations include a latent Adie's pupil that could have been triggered during a particular migraine attack; a ciliar ganglionic lesion/dysfunction produced by the migrainous process; an ophthalmoplegic migraine with selective parasympathycoparesis; or an episodic ciliar ganglionitis with migrainous features. Ciliary ganglioplegic migraine is proposed as a nominal term pointing to the possible anatomic source of the migrainous-related pupil dysfunction; the pathogenesis remains unknown.
BACKGROUND: Transient, unilateral mydriasis has been reported in migrainepatients, and this has been regarded as a possible co-morbidity between migraine and Adie's tonic pupil. Mydriasis that outlasts the duration of migraine attacks is rare. METHODS: Through an eight-year period we have studied all patients referred to our neurological clinic because of migraine attack with mydriasis. All the patients underwent thorough neurologic and ophthalmologic examinations including MRI of the brain and testing of the pupil response to ocular instillation of dilute pilocarpine (0.125%). RESULTS: Seven women and two men, with a mean age of 33.8 ± 12.3 years (range: 19-52) were included. The patients presented during one hemicranial migraine attack with an ipsilateral mydriasis that persisted for a mean of three months, while migraine headaches remained with their typical episodic course. In all the patients a cholinergic supersensitivity in the symptomatic pupil was demonstrated, thus pointing to a dysfunction of the ipsilateral ganglionic parasympathetic fibers. CONCLUSIONS: Synchronous co-localization of the features suggests a pathogenic link between the pupil dysfunction and migraine, rather than a simultaneous coexistence of two independent disorders. Likely explanations include a latent Adie's pupil that could have been triggered during a particular migraine attack; a ciliar ganglionic lesion/dysfunction produced by the migrainous process; an ophthalmoplegic migraine with selective parasympathycoparesis; or an episodic ciliar ganglionitis with migrainous features. Ciliary ganglioplegic migraine is proposed as a nominal term pointing to the possible anatomic source of the migrainous-related pupil dysfunction; the pathogenesis remains unknown.