title: Allodynia in migraine: frequent random association or unavoidable consequence?
abstract: Allodynia, the perception of pain induced by a non-painful stimulus, is frequently associated with migraine, especially when chronic, and mainly in the aura subtype. Among migraineurs, allodynia is thought to be caused by the headache and the activation of nociceptors with the development of central sensitization in subjects with an altered regulation of the central nociceptive pathway. The persistence of pain sensation seems to be able to induce central sensitization in the caudal nucleus of the trigeminal nerve by lowering the neuronal pain threshold. Different pathogenetic mechanisms may be involved and genetic, environmental and psychological elements should be considered. The complaint of allodynia is more frequent during the headache attack (acute allodynia) than in-between attacks (interictal allodynia). Acute allodynia is generally referred to the painful region but may diffuse to other areas, cephalic or even extracephalic. Extracephalic allodynia could not be mediated by nucleus caudalis as its neurons do not express whole-body receptive fields. The likely mechanism is thalamic sensitization. This symptom must be carefully assessed because it may be as annoying and limiting in daily activities as pain itself, and because its presence seems to reduce the efficacy of drugs used for migraine attacks. Instrumental measures may be applied, and clinical questionnaires to assess the presence of allodynic symptoms have also been developed and validated. All these aspects will be discussed.
authors.affiliation: Luigi Sacco Headache Centre, Clinic of Neurology, Milan, Italy. carlo.lovati@tiscalinet.it
authors.forename: Carlo
authors.initials: C
authors.lastname: Lovati
authors.forename: Domenico
authors.initials: D
authors.lastname: D'Amico
authors.forename: Pierluigi
authors.initials: P
authors.lastname: Bertora
mesh_terms: D000818:Animals; D002490:Central Nervous System / Q000503:physiopathology; D013181:Cortical Spreading Depression / Q000502:physiology; D006801:Humans; D006941:Hyperesthesia / Q000150:complications* / Q000378:metabolism / Q000473:pathology; D008881:Migraine Disorders / Q000150:complications* / Q000473:pathology; D017288:Pain Threshold / Q000502:physiology*; D014276:Trigeminal Nerve / Q000503:physiopathology