Parisi Pasquale, Piccioli Marta, Villa Maria Pia, Buttinelli Carla, Kasteleijn-Nolst Trenité Dorothee G A
Child Neurology, Paediatric Sleep Centre & Paediatric Headache Centre, II Faculty of Medicine, La Sapienza University, Via di Grottarossa, 1035-1039, 00189 Rome, Italy.
Med Hypotheses. 2008;70(6):1150-4. doi: 10.1016/j.mehy.2007.11.013. Epub 2008 Jan 8.
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.
癫痫与偏头痛的共病现象已为人所知达一个世纪之久，但仍未被完全理解；这两种疾病还存在一些共同的危险因素、症状和预防性药物治疗方法。一系列临床观察和科学数据支持皮质兴奋性改变这一假说，认为这可能是它们病理机制的潜在原因，两种疾病均以短暂性阵发性神经功能紊乱为特征。到目前为止，导致神经元过度兴奋的众多病理生理机制仅在家族性偏瘫性偏头痛（FHM）中得到研究，但这些研究确实提示了偏头痛与癫痫之间的联系。多项研究支持某些类型的偏头痛与某些类型的癫痫之间存在临床连续体的假说，甚至可能存在完全重叠，在某些特定情况下，头痛可能是癫痫发作的唯一发作期表现。考虑到文献中的数据，我们推测，几种病因病理因素（环境因素或遗传因素），如钠钾ATP酶泵功能受损，汇聚于以神经元膜过度兴奋为代表的共同最终通路，可能表现为癫痫或头痛/偏头痛，或两者皆有。从这一观点出发可能产生的潜在影响包括：（a）在癫痫和头痛疾病的国际分类中，将头痛/偏头痛诊断标准修订为癫痫唯一的发作期表现；（b）对有头痛/偏头痛残留特征的患者进行仔细随访，同时考虑修订后的“完全癫痫控制”概念，以避免因不适当停用抗癫痫治疗而导致的错误。此外，我们认为头痛与其他发作期敏感和运动特征相关（比已报道的更多）；由于在伴有或不伴有继发性全身性发作的复杂部分性发作期间意识受损，这些特征可能被严重低估。
