26^th European Neurology Congress

Sterile inflammatory changes due to the release of neuropeptides, i.e. calcitonin gene related peptide (CGRP), neurokinin A and substance P in trigeminovascular system of brain stem is the likely mechanism of acute migraine attack. Recurrent attack of migraine sensitizes central and peripheral nervous system leading to chronicity. Although there are no structural changes occurs in brain stem but PET study proved several areas are activated during migraine attack like red nucleus (RN), substantia nigra (SN), dorsal raphe nucleus (DRN), periaqueductal grey (PAG) and locus caeruleus (LC). Pain initiated or caused by a primary lesion or dysfunction of brain including brainstem and spinal cord is called as central pain syndrome. As brainstem dysfunction also occurs in migraine it is likely that migraine can also produce central neuropathic pain. Sixteen cases of migraine have shown the features of central pain syndrome contralateral to the frequent hemicranial side and five

cases independent of headache side. Risk factors for developing neuropathic pain are same as that of migraine with nociceptive pain on the aff ected body parts like sprain or strain in ligament tendon and muscles. Majority of those cases has predominant limb and trunk pain (n=17) rather than headache. All the cases are of migraine without aura. They are all diagnosed by the criteria laid down by the international classification of headache disorders (ICHD 3 beta). Central neuropathic are diagnosed by criteria laid down by group of expert from the neurologic and pain community. The mechanism behind reduction of

headache after developing neuropathic pain is not known. Migraine and neuropathic pain management both are necessary for best outcome.