The comorbidity between epilepsy and migraine has been well known for a century, yet it is still not fully understood; the two disorders also share some risk factors, symptoms, and preventive drug therapy. A series of clinical observations and scientific data support the hypothesis of alteration of cortical excitability as a possible mechanism underlying their pathology, with both disorders characterized by transient paroxysmal neurological disturbance. So far, the numerous pathophysiological mechanisms responsible for neuronal hyperexcitability have only been studied in familial hemiplegic migraine (FHM), but they do suggest a link between migraine and epilepsy. Several studies support the hypothesis of a clinical continuum between some types of migraine and some types of epilepsies, with possibly even a complete overlap, representing, in particular cases, headache as the sole ictal manifestation of seizures. Taking into account the data in the literature, we hypothesize that several aetiopathological noxae (either environmental or genetics), such as Na+-K+ ATPase pump impairment, converging on a common final pathway represented by neuronal membrane hyperexcitability, could manifest as either epilepsy or headache/migraine, or both. The potential implications arising from this point of view include (a) a revision of headache/migraine diagnostic criteria as the sole ictal epileptic manifestation in international classifications of both epilepsies and headache disorders; (b) the careful follow-up of patients with headache/migraine as a residual feature, taking into consideration a revised concept of "complete seizure control" to avoid mistakes due to inopportune withdrawal of antiepileptic treatment. In addition, we suggest that headache is associated with other ictal-sensitive and motor features (more than those reported); these may be highly underestimated due to impairment of consciousness during complex partial seizures with or without secondary generalization.