偏头痛发病机制的脑功能影像学研究

偏头痛是一种具有多种神经系统和非神经系统表现的综合征，表现为一侧或双侧发作性、搏动性的剧烈头痛。发作时常伴有众多植物神经系统症状，如恶心、呕吐、面色苍白、心率加快、呼吸增快、胃肠道功能紊乱等。部分患者在头痛发作前常有视物模糊、闪光、偏盲、偏侧面部麻木、言语困难、偏侧肢体麻木或轻偏瘫等先兆表现，历时数分钟或半小时。世界卫生组织指出严重的偏头痛将与瘫痪一同位居人类疾病致残率之首，但其发病机制目前尚存在许多疑问。各国学者就此提出了多种学说。     

偏头痛发病机制研究进展

综述近年来偏头痛发病机制研究 ,包括三叉神经血管假说 ,三叉神经炎性反应学说 ,皮质扩散抑制假说 ,5 羟色胺、一氧化氮、镁、遗传与偏头痛相关性机制的阐明 ,并介绍了偏头痛共发病     

偏头痛发病机制的研究进展

偏头痛是一种临床常见的慢性神经血管性疾患,年患病率女性为3．3％～32．6％,男性为0．7％～16．1％。世界卫生组织发布的2001年世界卫生报告将常见疾病按健康寿命损失年进行排列,偏头痛位列前20位。本病反复发作迁延难愈,其发病机制至今尚未完全阐明。     

镁和偏头痛发病机制的研究

目的　了解镁与偏头痛发病机制的关系。方法　检测偏头痛发作患者及健康对照组手术后或肿瘤疼痛（ 疼痛组） 患者血清镁和红细胞镁水平,同时给予偏头痛患者静脉注射潘南金（ Ｄ Ｌ门冬氨酸钾镁） 并观察其反应。结果　偏头痛患者较健康对照组及疼痛组血清镁和红细胞镁均明显降低。经潘南金治疗后具有较低血清镁（ ＜ ０ ．７６ ｍ ｍｏｌ／ Ｌ） 及红细胞镁（ ＜１３５ ｍ ｍｏｌ／ Ｌ） 水平的偏头痛患者症状缓解较血清镁（ ≥０７６ ｍ ｍｏｌ／ Ｌ） 及红细胞镁（ ≥１３５ ｍ ｍｏｌ／ Ｌ） 水平较高的偏头痛患者缓解明显。结论　血液中镁的浓度对偏头痛发作起着重要作用,并参与发病机制。通过补充镁可缓解偏头痛发作的疼痛。     

偏头痛发病机制的研究进展

偏头痛是一种常见的原发性头痛,其发病机制至今尚未完全阐明,近年来的研究认为由于大脑神经元兴奋性增加降低了诱发偏头痛的阈值,皮质扩散抑制活动触发先兆产生,然后三叉神经系统被激活释放血管活性肽类物质导致血管扩张和中枢致敏,再加上中枢疼痛调节系统功能异常,从而引发头痛,而导水管周围灰质进行性受损则可能是延长头痛发作时间,并使发作性偏头痛转变成慢性偏头痛的原因。     

氧化应激参与偏头痛发病机制的研究进展

氧化应激是活性氧物质(reactive oxygen species,ROS)、活性氮物质(reactive nitrogen species,RNS)在体内合成及代谢失衡,导致组织中ROS、RNS水平增高,引起组织损伤的一种状态。氧化应激对机体发挥作用的关键物质是过氧化物(superoxide,SO)及其与一氧化氮反应的产物-过氧亚硝酸盐(peroxynitrite,PN)。     

偏头痛发病机制及外科治疗现状

偏头痛是一种慢性进行性疾病,确切的发病机制目前尚不清楚,可能和血管、神经、遗传、感染等因素有关.世界卫生组织(WHO)将偏头痛看做与四肢瘫痪、痴呆等同样严重的致残性疾病.所以,一旦诊断成立就应积极治疗.在临床工作中,以头痛作为就诊原因者极为多见,头痛的治疗是临床一大难题.目前,偏头痛通常都用药物治疗,虽可缓解疼痛,但是部分患者由于药物副作用或其他原因而导致依从性较差.外科治疗偏头痛技术的出现,使部分不能耐受药物的患者可以得到有效的治疗.     

月经性偏头痛的发病机制及防治

月经性偏头痛是一种与卵巢周期变化有关的特殊类型偏头痛,占女性偏头痛的60％,主要与雌激素水平、前列腺素和遗传因素等有关。本文主要对其发病机制及防治的研究进展作阐述。     

慢性偏头痛的病理生理及发病机制

偏头痛是常见的特发性慢性神经血管功能障碍疾病。其中慢性偏头痛是偏头痛最常见的致残并发症,其中约有8%的患者由发作性偏头痛转化而来。慢性偏头痛患者中,约26%的患者病情可在两年得到缓解。其病理生理及发病机制尚未明确,本文从下行疼痛调节网的功能障碍、三叉神经和自主神经系统的改变、丘脑对中枢敏化的影响、药物造成的中枢敏化和预防几方面论述了慢性偏头痛的基本发病机制,为缓解偏头痛慢性化进程、临床药物的靶向研发提供方向。     

偏头痛发病机理的研究进展

本文综述了近年来在偏头痛发病机理研究方面的新进展,不仅介绍了两大经典学说—血管源学说和神经源学说的新成果,也阐述了偏头痛发病机理的新理论,如高钾诱导的血管痉挛假说、低镁学说、免疫学理论、植物神经功能紊乱学说等,旨在这一基础上进一步促进该病的临床研究。     

Current views on the pathogenesis of migraine aura

The pathogenesis of migraine aura, like migraine, remains unclear. The probable cause of migraine aura may be cortical spreading depression (CSD) and cerebral hypoperfusion. Ion changes, activation of the trigeminal nerve and release of neuropeptides seem to be secondary to CSD during an attack of migraine aura. There are many hypotheses of migraine pathogenesis. The focal symptoms during migraine aura may be due to transient constriction of a cerebral artery and headache can result from a sterile inflammatory reaction around the walls of dilated cranial vessels. The development of aura makes a vascular origin a remote possibility, while a primary disturbance of cortical neuron function, probably CSD and activation of the trigeminovascular system, is a more reasonable explanation.     

Migraine-update--current concepts of migraine pathogenesis]

The pathophysiology of migraine still remains unclear. However, abundant evidence in support of the view that migraine as an illness of the central nervous system has been accumulated. First, the hyperexitability in the brain is recognized even in the stage between attacks in migraineurs according to findings of transcranial magnetic stimulation techniques, MRI-BOLD studies or 31P SPECT examinations. Second, cortical spreading depression originating in the occipital cortex is more likely to be related to the aura. Third, sensitization of the trigeminal nerve system is substantially involved in process of headache pain in migraine. Fourth, clonic dysfunction of the priaqueductal gray matter in the brain stem may underlie the migraine pathogenesis. Thus, current concept of susceptibility of migraine is attributed to certain dysfunction of the deep brain structures such as the brain stem rather than the blood vessels in the brain or dura mater.     

The role of gamma-aminobutyric acid in migraine pathogenesis

Migraine is one of the most common forms of primary headaches; it affects nearly 10% of the population in developed countries. All major CNS neurotransmitter systems are implicated in migraine pathogenesis, indicating the polyneurochemical nature of the nosology. This review is focused on the role of gamma-aminobutyric acid (GABA) and its receptors in the neurobiology of migraine. The report describes evidence for the existence of a cause-effect relationship between impaired GABA metabolism and development of the disease. It summarizes data on the distribution of GABA-A and GABA-B receptors in the trigeminovascular system and on the contribution of GABA to the modulation of nociceptive neurotransmission in the trigemino-thalamo-cortical pathway. As well, it provides detailed information on the mechanisms that underlie GABA-ergic inhibition at the peripheral, spinal, and suprasegmental levels. In the end, we discuss the pharmacodynamics of some GABA-positive drugs that are used for prophylactic and acute treatments of migraine, as well as other primary headaches.     

Inflammation and excitotoxicity: role in migraine pathogenesis

Neurological Sciences - The pathogenesis of migraine is still unclear, but much evidence suggests a role of inflammation in pain generation. Calcitonin gene related peptide, nitric oxide and...     

肉毒毒素镇痛机制与偏头痛发病机制的相关性

肉毒毒素-A(BTX-A)是一种麻痹性的神经毒素.1998年,Binder等[1]发现在使用BTX-A除皱美容的同时,患者的偏头痛得以缓解,而首先报道了BTX-A临床治疗偏头痛的可能.最近,美国食品及药品管理局(Food and Drug Administration,FDA)批准其用于慢性偏头痛的预防治疗.为此,探究和了解BTX-A的镇痛机制及其与偏头痛病理生理的相关性就具有重要的意义.