Montagna Pasquale
Department of Neurological Sciences, University of Bologna Medical School, Via Ugo Foscolo, 7, 40123 Bologna, Italy.
J Headache Pain. 2008 Apr;9(2):57-69. doi: 10.1007/s10194-008-0026-x. Epub 2008 Mar 15.
The primary headaches, migraine with (MA) and without aura (MO) and cluster headache, all carry a substantial genetic liability. Familial hemiplegic migraine (FHM), an autosomal dominant mendelian disorder classified as a subtype of MA, is due to mutations in genes encoding neural channel subunits. MA/MO are considered multifactorial genetic disorders, and FHM has been proposed as a model for migraine aetiology. However, a review of the genetic studies suggests that the FHM genes are not involved in the typical migraines and that FHM should be considered as a syndromic migraine rather than a subtype of MA. Adopting the concept of syndromic migraine could be useful in understanding migraine pathogenesis. We hypothesise that epigenetic mechanisms play an important role in headache pathogenesis. A behavioural model is proposed, whereby the primary headaches are construed as behaviours, not symptoms, evolutionarily conserved for their adaptive value and engendered out of a genetic repertoire by a network of pattern generators present in the brain and signalling homeostatic imbalance. This behavioural model could be incorporated into migraine genetic research.
原发性头痛，即伴（MA）或不伴先兆（MO）的偏头痛以及丛集性头痛，均具有显著的遗传易感性。家族性偏瘫性偏头痛（FHM）是一种常染色体显性孟德尔疾病，被归类为MA的一种亚型，它是由编码神经通道亚基的基因突变所致。MA/MO被认为是多因素遗传疾病，FHM已被提议作为偏头痛病因学的一个模型。然而，对遗传学研究的一项综述表明，FHM基因并不参与典型偏头痛的发病过程，FHM应被视为一种综合征性偏头痛，而非MA的一个亚型。采用综合征性偏头痛这一概念可能有助于理解偏头痛的发病机制。我们推测表观遗传机制在头痛发病过程中起重要作用。我们提出了一个行为模型，据此原发性头痛被视为行为而非症状，因其适应性价值而在进化过程中得以保留，并由大脑中存在的模式发生器网络从基因库中产生，该网络发出内环境稳态失衡的信号。这个行为模型可以纳入偏头痛遗传学研究。
