![[圖]](http://www.doctormigraine.com/wp-content/uploads/2009/10/79-four-stages-of-a-migraine.jpg)
http://www.skh.org.tw/Neuro/Migrain.htm
偏頭痛簡介
陳威宏
什麼是偏頭痛？頭痛一邊就是偏頭痛嗎？
是不是頭痛一邊就是偏頭痛？事實上「偏頭痛」一詞，在醫學上已經成為一個特定的疾病，有特別的症狀與病因，不是泛指一般半邊的頭痛。頭痛一邊的確是偏頭痛的特徵之一，但卻不是唯一的特點，有些病人會兩邊痛、後腦勺痛，甚至整個頭一起痛。
![[圖]](http://www.kmuh.org.tw/www/kmcj/images/9702/p5.jpg)
偏頭痛有哪些特徵？
就一般的了解，偏頭痛是一種原因不明、反復發生的頭痛，每次頭痛持續四至十二小時。頭痛的特徵包括：半邊頭痛，像抽痛或脹痛，伴隨心跳或脈搏跳動，痛的厲害常會噁心嘔吐，怕光怕吵；此外，走動、上下樓梯或頭晃動都會加劇頭痛。有些病人在休息睡覺後就會好了，但許多病人都需要頭痛藥的幫忙，才能解決頭痛的痛苦。
偏頭痛時為什麼會視力模糊？
上面所描述的是所謂的尋常偏頭痛，國際頭痛分類稱之為無預兆偏頭痛。但另有百分之十至二十的病人，在頭痛發生的前後會經歷到特別的神經症狀，稱之為前兆。最常發生的是所謂視覺障礙，例如複視、重疊影像、半邊偏盲，或出現盲斑、亮點、色線等的閃動、跳躍。有時候甚至出現幻覺、視覺影像扭曲變形、變大變小。另外有些人會有半邊麻木針刺等感覺，慢慢從一點擴展至半邊肢體或顏面，甚至變成無力麻痺。極少病人甚至有說不出話，類似中風的失語症，或眩暈、耳鳴、步態蹣跚等等複雜的症狀。
預兆通常持續時間不會超過一個小時，頭痛也常在預兆開始後一個小時內發生。有預兆的偏頭痛，以前稱為典型偏頭痛或複雜性偏頭痛。
偏頭痛是怎麼發生？
最近的研究發現偏頭痛是因受到內在或外在的刺激，比如壓力、睡眠不足、天候的變化或刺激性的食物等，導致神經系統失去平衡和諧的狀態，引發腦內神經傳導物質的改變，如血清素與正腎上腺素等，進而誘發一系列的疼痛流程，牽涉到腦內三叉神經與血管的交互作用，一方面三叉神經系受神經傳導物質的刺激引發疼痛的感覺，一方面血管系也引發發炎的反應，更加重腫脹與疼痛。
偏頭痛會遺傳嗎？為什麼有的人比較會偏頭痛？
至於為什麼有些人會偏頭痛?真正的原因還不清楚，不過最主要的還是體質的因素，與遺傳有關。偏頭痛患者的家族中常有類似的頭痛，據統計至少百分之七十以上的偏頭痛患者，其近親亦有人有偏頭痛的毛病，而如果父母都有偏頭痛，則生下的孩子裡，百分之八十三也有偏頭痛的困擾。另外，偏頭痛病人似乎較敏感、固執、壓抑，具完美主義傾向，對自己要求高，對環境不易妥協。而病人也常會在生活、工作上改變時，因壓力、挫折與適應不良，增加頭痛的次數與程度。
內分泌的變化也跟偏頭痛的發生有關，偏頭痛患者，女性比男性多一倍，有些婦女也注意到頭痛的發作與月經週期有關。而服用避孕藥也可能會引起頭痛，使頭痛惡化。
![[圖]](http://www.standard.com.tw/UserFiles/Image/Periodical/74/74-1.jpg)
偏頭痛怎麼治療？
偏頭痛的治療可以分為兩個層面，一是急性發作時，緩解止痛的治療；另一則為針對慢性反覆頭痛的預防治療。
偏頭痛急性發作時，大部分的患者最需要安靜與休息，因為噪音、強光都會加劇頭痛。能在安靜幽暗的房間靜躺一下，會有很大的幫助，若能入睡，醒來時頭痛大多會消失大半。如果因工作在外無法入眠，一杯濃咖啡有時可助於減緩頭痛，以手指輕按太陽穴也有助於減輕頭痛。頭痛較厲害時，一般止痛劑如阿斯匹靈、普拿疼也可止痛。另外醫生常用來治療偏頭痛的處方有加非葛(cafergot)，非類固醇消炎劑，及新一代的偏頭痛止痛藥－英明格(Imigran)。需注意的是，這類於急性發作使用的藥物需儘早，最好在預兆發生，或頭痛的初期就要趕緊服用，若在頭痛劇烈到頂點時才服藥，不僅緩不濟急，而且到這時候，病人易伴隨噁心與嘔吐，連藥都無法服用。
病人若經常性反覆頭痛，例如發作次數超過一週兩次，便應接受預防性治療，長期服藥，以改善頭痛體質，預防頭痛的發生。視病人的情況，醫生可以處方不同類型的藥物，如非類固醇消炎劑、乙型阻斷劑、鈣離子阻抗劑或三環抗憂鬱劑等。這些藥物處方得宜，都可以收到治療與預防的效果，不過為了確定療效避免反彈作用，可能需要治療持續兩到三個月以上。
除了藥物的治療外，生活上的調適也很重要。如養成良好的生活習慣、起居規律定時、睡眠充足而不過量、避免過勞、放鬆心情等，雖有些老生常談，卻是患者自我調養的不二法門。某些病人可能會注意到特別的誘發因素，如食物、酒類、氣溫的劇烈變動，或炎夏時進出冷氣房等，則可以自我提醒，避免類似狀況，即可預防偏頭痛。還有研究顯示，規律運動，尤其是有氧運動，如慢跑、游泳、騎自行車等，都可以改善體質而預防頭痛，值得大力提倡。
偏頭痛可以痊癒嗎？
偏頭痛的病因既然尚未確定，而且很可能是個人體質的一部分，所以基本上來說是可以治療而無法痊癒。對偏頭痛的患者來說，偏頭痛既無法痊癒，是否就成了一輩子的陰影？事實上，絕對沒有那麼悲觀，根據臨床的觀察，甚少病人會一輩子受偏頭痛的困擾，大部分的頭痛發作都在十五、六歲到三、四十歲之間，過了五十歲到六十歲，偏頭痛自然會減輕甚或消失。而在偏頭痛好發的年齡期，頭痛也不是天天來，通常都有一定的因素。若頭痛頻繁時，則是一個自然的警告，提醒自己可能因壓力、疲勞或內分泌失調等因素，應放慢腳步、放鬆情緒，讓心理與生理重新調整。在醫師的指示與治療下，自我認識並調適，如此偏頭痛不是絕症也不可怕，一定都能克服。
![[圖]](http://howtogetridofamigrainefast.com/wp-content/uploads/2014/01/how_to_get_rid_of_a_migraine_fast.jpg)
《四總穴歌》裏說“肚腹三里留，腰背委中求，頭項尋列缺，面口合谷收”，深入淺出地概括了足三里、委中、列缺、合谷4穴位的功能與主治，後世又加上內關穴，這五大要穴對全身起到了重要的保健作用。
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3.列缺。在腕橫紋上1.5寸，肱橈肌與拇長展肌腱之間。列缺穴為手太陰肺經的絡穴，又是八脈交會穴，通于奇經八脈的任脈。《四總穴歌》說：“頭項取列缺”，說明針刺按摩列缺穴，不僅善療偏頭患，而且能疏通頸項部經絡氣血，可迅速解除頸項疼痛和感冒不適症狀，每日早晚各一次，也是5-7分鐘。
![[圖]](http://images.rednet.cn/articleimage/2013/03/19/105316678.jpg)
四總穴歌
![[圖]](http://6.share.photo.xuite.net/hlele3109/16da2f3/4137234/237601761_l.jpg)
http://www.neurological.org.nz/News/Headlines-Articles/Article/Why+Migraines+Strike/
Why Migraines Strike
General Articles
For the more than 300 million people world-wide who suffer migraines, the excruciating, pulsating pain that characterizes these debilitating headaches needs no description. For those who do not, the closest analogous experience might be severe altitude sickness: nausea, acute sensitivity to light, and searing, bed-confining headache. “That no one dies of migraine seems, to someone deep into an attack, an ambiguous blessing,” wrote Joan Didion in the 1979 essay “In Bed” from her collection The White Album.
Historical records suggest the condition has been with us for at least 7,000 years, yet it continues to be one of the most misunderstood, poorly recognized and inadequately treated medical disorders. Indeed, many people seek no medical care for their agonies, most likely believing that doctors can do little to help or will be downright skeptical and hostile toward them. Didion wrote “In Bed” almost three decades ago, but some physicians remain as dismissive today as they were then: “For I had no brain tumor, no eyestrain, no high blood pressure, nothing wrong with me at all: I simply had migraine headaches, and migraine headaches were, as everyone who did not have them knew, imaginary.”
Migraine is finally starting to get the attention it deserves. Some of that attention is the result of epidemiological studies revealing just how common these headaches are and how incapacitating: a World Health Organization report described migraine as one of the four most disabling chronic medical disorders. Ad¬¬ditional concern results from recognition that such headaches and their aftermaths impose an enormous cost on the economy in lost work, disability payments and health care expenses, estimated in the U.S. at $17 billion a year. But most of the growing interest comes from new discoveries in genetics, brain imaging and molecular biology. Though of very different natures, those findings seem to converge and reinforce one another, making researchers hopeful that they can get to the bottom of migraine’s causes and develop improved therapies to prevent them or halt them in their tracks.
The Ascent of Vapours
Any plausible explanation of migraine needs to account for a wide and varied set of symptoms. The frequency, duration, experience and catalysts of episodes differ greatly. Victims have, on average, one or two daylong attacks every month. But 10 percent get them weekly, 20 percent experience them for two to three days, and up to 14 percent have them more than 15 days a month. Often the pain strikes just one side of the head, but not always. Migraines in people prone to them can be set in motion by such a variety of events that they seem inescapable; alcohol, dehydration, physical exertion, menstruation, emotional stress, weather changes, seasonal changes, allergies, sleep deprivation, hunger, altitude and fluorescent lights are all cited as triggers. Migraines occur in all ages and both genders, yet women between the ages of 15 and 55 are disproportionately hit—two thirds of cases occur in this population.
Physicians over the years have proposed many reasons for why these headaches arise. Galen in ancient Greece attributed them to the ascent of vapours, or humours, from the liver to the head. Galen’s description of hemicrania—a painful disorder affecting approximately one half of the head—is indeed what we refer to as migraine today: the old word “hemicrania” eventually became “megrim” and ultimately “migraine.”
Blood flow replaced humours as the culprit in the 17th century, and this vascular hypothesis held sway, with few exceptions, until the 1980s. The accepted idea, based on the observations and inferences of several physicians, including Harold Wolff of New York–Presbyterian Hospital, was that migraine pain stems from the dilation and stretching of brain blood vessels, leading to the activation of pain-signalling neurons. Wolff thought the headache was preceded by a drop in blood flow brought about by the constriction of these same blood vessels. Fresh observations from brain scans have altered understanding of the vascular changes. It turns out that in many the pain is preceded not by a decrease in blood flow but by an increase—an increase of about 300 percent. During the headache itself, though, blood flow is not increased; in fact, circulation appears normal or even reduced. Not only has the specific understanding of blood flow changed, but so has the prevailing view of the root of migraine. Migraine is now thought to arise from a disorder of the nervous system—and likely from the most ancient part of that system, the brain stem.
Aura’s Origin
This newer insight has come mainly from studying two aspects of migraine: the aura, which precedes the pain in 30 percent of sufferers, and the headache itself. The term “aura” has been used for nearly 2,000 years to describe the sensory hallucinations immediately preceding some epileptic seizures; for 100 years or so, it has also been used to describe the onset of many mi¬¬graines. (Epilepsy may occur in people with mi¬¬graine, and vice versa; the reasons are under investigation.) The most common form of aura is a visual illusion of brilliant stars, sparks, flashes of light, lightning bolts or geometric patterns, which are often followed by dark spots in the same shape as the original bright image. For some people, the aura can include a feeling of tingling or weakness, or both, on one side of the body as well as speech impairment. Usually the aura precedes the headache, but it may start after the pain begins and persist through it.
Aura appears to stem from cortical spreading depression—a kind of “brainstorm” anticipated as the cause of migraine in the writings of 19th-century physician Edward Lieving. Although biologist Aristides Leão first reported the phenomenon in animals in 1944, it was experimentally linked to migraine only recently. In more technical terms, cortical spreading depression is a wave of intense nerve cell activity that spreads through an unusually large swath of the cortex (the furrowed, outer layer of the brain), especially the areas that control vision. This hyperexcitable phase is followed by a wave of widespread, and relatively prolonged, neuronal inhibition. During this inhibitory phase, the neurons are in a state of “suspended animation,” during which they cannot be excited.
Neuronal activity is controlled by a carefully synchronized flow of sodium, potassium and calcium ions across the nerve cell membrane through channels and pumps. The pumps keep resting cells high in potassium and low in sodium and calcium. A neuron “fires,” releasing neurotransmitters, when the inward flow of sodium and calcium through opened channels depolarizes the membrane—that is, when the inside of the cell becomes positively charged relative to the outside. Normally, cells then briefly hyperpolarize: they become strongly negative on the inside relative to the outside by allowing potassium ions to rush out. Hyperpolarization closes the sodium and calcium channels and returns the neurons to their resting state soon after firing. But neurons can remain excessively hyperpolarized, or inhibited, for a long time following intense stimulations. The phases of hyperexcitability followed by inhibition that characterize cortical spreading depression can explain the changes in blood flow that have been documented to occur before migraine pain sets in. When neurons are active and firing, they require a great deal of energy and, thus, blood—just what investigators see during brain scans of patients experiencing aura. But afterward, during inhibition, the quiet neurons need less blood.
Various other observations support the idea that cortical spreading depression underlies aura. When recorded by advanced imaging technology, the timing of the depolarizing wave dovetails neatly with descriptions of aura. The electrical wave travels across the cortex at a rate of two to three millimeters a minute, and the visual illusions that accompany aura are exactly those that would arise from an activation spreading across the cortical fields at just that rate. The suite of sensations that aura can entail—visual, sensory, motor—suggest that corresponding areas of the cortex are affected in sequence as the “storm” crosses them. The dark spots that patients experience after the bright hallucinations are consistent with neuronal inhibition in the regions of the visual cortex that have just experienced the hyperexcitability.
Genetic studies have offered a clue to why cortical spreading depression occurs in some migraine sufferers. Nearly all migraine is thought to be a common complex polygenetic disorder—in the same camp as diabetes, cancer, autism, hypertension and many other disorders. Such diseases run in families. Identical twins are much more likely to share migraine than fraternal twins are, indicating a strong genetic component. But the disease is clearly not caused by a single genetic mutation; rather a person apparently becomes susceptible by inheriting mutations in a number of genes, each probably making a small contribution. Nongenetic components operate as well, because even identical twins are “discordant” for the disorder: sometimes one twin will suffer from migraine, and the other will not.
Investigators do not know which genes increase susceptibility to migraine and its aura in the general population, but studies of people affected by a rare form of the disorder, called familial hemiplegic migraine, indicate that flaws in neuronal ion channels and pumps cause the aura and pain in these patients. Notably, three genes have been shown to carry mutations that individually are potent enough to cause the disease—and all three encode neuronal ion channels and pumps. What is more, the genes are altered by mutations that increase the excitability of nerve cells, presumably by altering the properties of the encoded ion channels and pumps. These findings strongly support the idea that migraine could be a channelopathy, a newly recognized type of disease that arises from disturbances in ion transport systems—a known cause of ailments such as cardiac arrhythmia and seizures.
It is not clear whether malfunctioning ion pumps and channels are the only means by which aura can be produced. Nor is it clear that the common forms of migraine involve perturbations in the three genes implicated in familial hemiplegic migraine. But the genetic insights remain very exciting because they suggest a relation between cortical spreading depression and ion channel problems, one that could prove crucial to designing new medications.
From Aura to Ache
At the same time that researchers have been making headway in understanding the relation between aura and cortical spreading depression, they have been probing the source of migraine pain—the headache that is felt in those who experience aura as well as those who do not. The immediate source of the pain itself is obvious. Although most regions of the brain do not register or transmit pain signals, a network of nerves called the trigeminal nerve system does. These neurons carry pain signals from the membranes that surround the brain, called the meninges, as well as from the blood vessels that infuse the membranes. Pain is relayed through the trigeminal network to an area called the trigeminal nucleus in the brain stem and, from there, can be conveyed up through the thalamus to the sensory cortex, which is involved in our awareness of pain and other senses. What first activates the trigeminal nerves in migraine, however, is under debate. There are essentially two schools of thought:
Some researchers contend that cortical spreading depression directly stimulates the trigeminal nerves. As the wave of hyperexcitability travels across the cortex, it brings about the release of neurotransmitters, such as glutamate and nitric oxide, as well as of ions. These chemicals serve as messengers that induce the trigeminal nerves to transmit pain signals. Researchers have observed in animals that cortical spreading depression does indeed activate the trigeminal nerves in this way. That pathway to pain could even explain what happens in patients who do not experience aura. According to this view, cortical spreading depression might occur in areas of the cortex whose activation produces no outward symptoms before the onset of pain. Or spreading depression might occur in subcortical regions in certain people and stimulate the trigeminal nerves. In this case, although patients may not experience aura, the basic physiology would be the same as in those who do. Good evidence supports this hypothesis. Spreading depression can be evoked in laboratory animals in subcortical regions. Moreover, the changes in cerebral blood flow that reflect the phases of cortical excitation and subsequent inhibition in migraine sufferers with aura have also been seen in people who experience migraine without aura; those patients, too, show a large increase in blood flow followed by normal or reduced flow. This finding raises the possibility that cortical spreading depression is fundamental to migraine but that only in some instances does it give rise to visual symptoms recognized as aura. Instead the process might generate less obvious symptoms, such as fatigue or difficulty concentrating. The finding may also explain why many people who experience aura will at times undergo attacks without it.
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※ 編輯: ott 時間: 2017-12-18 19:16:33
Other investigators place the root of migraine pain not in cortical or subcortical spreading depression but in the brain stem—Grand Central Station for information passing to and from the body and the brain. It is also home to the control center for alertness, perception of light and noise, cerebral blood flow, respiration, sleep-wake cycles, cardiovascular function and, as described earlier, pain sensitivity.
Positron-emission tomography has revealed that three clusters of cells, or nuclei, in the brain stem—the locus coeruleus, raphe nucleus and periaqueductal gray—are active during and after migraine. According to this hypothesis, abnormal activity in those nuclei could induce pain in two ways. The nuclei normally inhibit trigeminal neurons within the trigeminal nucleus, continuously saying, in effect, “don’t fire.” The nuclei’s misbehavior could impair this ability and thus allow the trigeminal neurons to fire even when the meninges send no pain signals. In that situation, the trigeminal nucleus would relay pain messages to the sensory cortex in the absence of incoming pain signals from the meninges or blood vessels. The three nuclei might also trigger spreading depression.
Researchers have noted that if one were to alter a part of the brain stem so as to bring about other symptoms of migraine as well, including aura, the place to do it would be these three nuclei. One of their most important functions is to control the flow of sensory information—such as light, noise, smell and pain—that reaches the sensory cortex. Occasional dysfunction in these clusters of cells could therefore explain why migraine sufferers may experience sensitivity to light, sound and odours. In addition, the activity of these cells is modulated by the behavioural and emotional state of the individual—factors that can trigger mi¬¬graines. These brain stem areas receive input from only two areas of the cortex, the limbic and paralimbic cortices, regions that regulate arousal, attention and mood. Through its connection with the brain stem, the limbic cortex affects the functioning of the rest of the cortex—a fact that might explain how emotional and psychological stress could catalyze mi¬¬graines, why mood fluctuates during migraine, and why there is an association between mi¬¬graine and depression and anxiety disorders, both of which occur more commonly in mi¬¬graine sufferers than in others.
Finally, the spontaneous, pacemakerlike activity of the raphe nucleus neurons—crucial to regulating pain pathways, circadian rhythms and sleep-wake cycles—depends on the perfect working of ion channels in neurons of that region and on the neurons’ release of the neurotransmitters norepinephrine and serotonin into other brain areas. Such neurotransmission may be an ancient mechanism that is perturbed in migraine: experiments in the roundworm Caenorhabditis elegans have revealed that two genes very like those mutated in familial hemiplegic migraine are critical regulators of serotonin release. This finding opens the possibility that mutations in ion channels may lead to aberrant function in these brain stem areas and perhaps, as a result, to hyperexcitability in the cortical areas they influence.
The question then becomes, Does pain typically arise from the intrinsic hyperexcitability of cortical neurons (which leads to cortical spreading depression, activation of meningeal trigeminal pain fibers and the pain of a migraine)? Or does some glitch in brain stem activity incite the pain (by directly rendering the trigeminal neurons spontaneously active or by facilitating cortical spreading depression, or both)? The latter scenario is more convincing to some researchers because the pivotal control exerted by the brain stem over so many aspects of our experience could explain the varied symptoms of migraine.
What the Future May Hold
At the moment, only a few drugs can prevent migraine. All of them were developed for other diseases, including hypertension, depression and epilepsy. Because they are not specific to migraine, it will come as no surprise that they work in only 50 percent of patients—and, in them, only 50 percent of the time—and induce a range of side effects, some potentially serious.
Recent research on the mechanism of these antihypertensive, antiepileptic and antidepressant drugs has demonstrated that one of their effects is to inhibit cortical spreading depression. The drugs’ ability to prevent migraine with and without aura therefore supports the school of thought that cortical spreading depression contributes to both kinds of attacks. Using this observation as a starting point, investigators have come up with novel drugs that specifically inhibit cortical spreading depression. Those drugs are now being tested in migraine sufferers with and without aura. They work by preventing gap junctions, a form of ion channel, from opening, thereby halting the flow of calcium between brain cells.
The medicines prescribed for use during an attack have been as problematic as the ones used preventively. Triptans, as this class of drug is called, constrict blood vessels throughout the body, including coronary arteries, seriously limiting their use. These treatments were developed based on the mistaken idea that blood vessel dilation caused the pain and thus constriction was necessary to alleviate it. It now appears that triptans ease migraine by interrupting the release of messenger molecules, specifically calcitonin gene–related peptide, from trigeminal nerves that feed signals into the trigeminal nucleus. The interruption blocks those trigeminal nerves from communicating with the brain stem’s pain-transmitting network of neurons. It is also possible that triptans prevent such communication by operating in the thalamus and the periaqueductal gray matter of the midbrain.
The new understanding of triptan activity has opened up possibilities for drug development, including a focus on calcitonin gene–related peptide. Several medicines that block the action of that pain-producing neurotransmitter are in clinical trials, and they appear not to constrict arteries. In addition, researchers are devising therapies that target other trigeminal neurotransmitters, such as glutamate and nitric oxide, in a further effort to interrupt the communication between trigeminal nerves innervating the meninges and the trigeminal nucleus in the brain stem. These compounds will be the first specifically designed to combat migraine during an attack by targeting neurons without constricting blood vessels.
Researchers have also examined nonpharmaceutical approaches. A handheld device that transmits brief pulses of magnetic stimulation is being evaluated, for example, for the treatment of migraine with and without aura. The premise is that this technology, called transcranial magnetic stimulation, or TMS, may interrupt cortical spreading depression and possibly prevent pain from arising or progressing.
For millions of people, these developments mark a breakthrough—not only in terms of relief from pain if all goes well but also in regard to attitudes about migraine. Scientists and physicians are finally coming to see migraine for the complex, biologically fascinating process it is and to recognize its powerfully debilitating effects. The disorder is “imaginary” no longer.
David W. Dodick and J. Jay Gargus share a deep interest in understanding and ameliorating migraine. Dodick, a professor of neurology at the Mayo Clinic’s Arizona campus and a Fellow of the Royal College of Physicians (Canada), received his medical degree at Dalhousie University in Halifax, Nova Scotia. He studies the central nervous system abnormalities behind migraine and other forms of headache; he is the President-elect of the American Headache Society. Gargus, professor of physiology, biophysics and human genetics at the University of California, Irvine, received his medical degree and doctorate at Yale University. He is studying the genetic underpinnings of migraine and other ion channel disorders.
This report was first published in Scientific American.
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