Research & Innovation (R&I), Corso Stati Uniti, 4, 35127, Padova, Italy.
University of Padova, Padova, Italy.
Neurol Sci. 2022 Nov;43(11):6299-6304. doi: 10.1007/s10072-022-06241-2. Epub 2022 Jul 16.
The pathogenesis of migraine, as well as cluster headache (CH), is yet a debated question. In this review, we discuss the possible role of tyrosine and tryptophan metabolism in the pathogenesis of primary headaches, including the abnormalities in the synthesis of neurotransmitters. High level of dopamine, low level of norepinephrine, and very elevated levels of octopamine and synephrine were found in the plasma of episodic migraine without aura. We hypothesize that the imbalance between the levels of neurotransmitters and elusive amines synthesis is due to a metabolic shift directing tyrosine toward increased decarboxylase and reduced hydroxylase enzyme activities, favored by a state of neuronal hyperexcitability and a reduced mitochondrial activity. In addition, we present biochemical studies performed in chronic migraine (CM) and chronic tension-type headache patients (CTTH) to verify if the same anomalies are present in these primary headaches and, if so, their possible role in the chronicity process of CM and CTTH. The results show that important abnormalities of tyrosine-related metabolites are present only in CM patients while tryptamine plasma levels were found significantly lower in both CM and CTTH patients. Because of this, we propose that migraine and, possibly, CH attacks derive from neurotransmitter and neuromodulator metabolic abnormalities in a hyperexcitable and hypoenergetic brain that spread from the frontal lobe, downstream, resulting in abnormally activated nuclei of the pain matrix. The low tryptamine plasma levels found in CM and CTTH patients suggest that these two primary chronic headaches are characterized by a common insufficient serotoninergic control of the pain threshold.
偏头痛和丛集性头痛(CH)的发病机制仍存在争议。在这篇综述中,我们讨论了色氨酸和酪氨酸代谢在原发性头痛发病机制中的可能作用,包括神经递质合成的异常。在无先兆的发作性偏头痛患者的血浆中发现多巴胺水平升高、去甲肾上腺素水平降低、章鱼胺和辛弗林水平非常升高。我们假设,神经递质和隐匿胺合成之间的失衡是由于代谢转移导致酪氨酸向增加的脱羧酶和减少的羟化酶活性方向发展,这是由神经元过度兴奋和线粒体活性降低的状态所促成的。此外,我们还介绍了在慢性偏头痛(CM)和慢性紧张型头痛(CTTH)患者中进行的生化研究,以验证这些原发性头痛中是否存在相同的异常,如果存在,它们在 CM 和 CTTH 的慢性过程中的可能作用。结果表明,只有在 CM 患者中存在与酪氨酸相关的代谢物的重要异常,而在 CM 和 CTTH 患者中均发现色胺血浆水平显著降低。因此,我们提出偏头痛,可能还有 CH 发作,是由过度兴奋和能量不足的大脑中的神经递质和神经调质代谢异常引起的,这些异常从额叶向下游扩散,导致疼痛矩阵中异常激活的核。在 CM 和 CTTH 患者中发现的低色胺血浆水平表明,这两种原发性慢性头痛的特征是疼痛阈值的共同缺乏血清素能控制。