The migraine headache is considered a vascular headache, although the precise mechanism and etiology remain unknown. There are several known triggers some of which include food allergies, blood sugar disturbances, stress load, mechanical injury, and hormonal fluctuations. The vascular hypothesis of migraine, first proposed by Wolff, theorizes that the aura of migraine is caused by intracerebral constriction followed by extracranial vasodilation resulting in headache pain. (1)

Migraine may be classified as migraine without aura, formerly called common migraine, or migraine with aura, formerly known as classic migraine, and is based upon the presence or absence of focal neurologic symptoms prior to the onset of headache. The aura may consist of flashing lights, or zigzag lines, or may manifest as blind spots in the vision. Patients may even experience speech difficulty, tingling in the face or hands, confusion, or weakness of an arm or leg. The majority of patients suffering from classic migraine have an aura that develops 10-30 minutes prior to development of the actual headache. According to recent studies, the aura is believed to be the response to a trigger that creates a neuronal depression. This may result in as much as a 25-35 percent reduction in cerebral blood flow, and is certainly enough to cause the symptoms associated with the aura.

Auras are experienced by approximately 10 percent of migraineurs. (2) The International Headache Society has developed a classification system of migraine headaches that includes six subdivisions under the heading migraine with aura. These include the following:

    Migraine with typical aura (Aura lasting less than one hour) Migraine with prolonged aura (aura lasting more than one hour but less than one week) Familial hemiplegic migraine Basilar migraine Migraine aura without headache Migraine with acute onset aura (aura develops fully in less than 5 minutes) (3)

Migraine without aura, or common migraine, occurs in approximately 85 percent of patients. Scientists have devised one theory, which explains blood flow changes, and also biochemical changes, which may be involved in the headache process. According to this theory, migraine pain is believed to be the result of activity in the trigeminovascular system. Axons within this system originate from the trigeminal ganglia and upper cervical dorsal root. They surround cerebral blood vessels in close proximity to all vessel layers to allow for constant monitoring of the microenvironment of the vessel wall. Arteries and venous sinuses have the highest degree of trigeminal innervation. (4) Trigeminal nerves act as important initiators and promoters of tissue inflammation. When neuronal activation occurs, vasoactive neuropeptides are released which interact with dural blood vessels. The result is vasodilation and extravasation of plasma proteins, which initiates a sterile, neurogenic inflammatory response.

The inflammation sensitizes surrounding tissues and produces a hyperalgesic state that prolongs headache pain. Additionally, activation of unmyelinated C fibers of the trigeminovascular system stimulates pain-transmitting neurons within the brain stem and upper spinal cord. Activity within the trigeminovascular system is regulated by noradrenergic and, more importantly, serotonergic neurons within the brainstem. Brainstem mechanisms that lead to activation of the nociceptive trigeminovascular system may be stimulated by the cerebral cortex, thalamus, or hypothalamus in response to emotion or stress, excessive afferent stimulation (e.g., glare, noise, smells), or changes in the internal clock or environment. (5)

Serotonin is thought to be an important mediator of migraine. Of the seven classes of 5-HT receptors that have been identified, 5-HT1 receptors, presynaptic autoreceptors that modulate neurotransmitter release, and the excitatory post-synaptic 5-HT2 receptors appear to play an important role in migraine pathophysiology as well as in the beneficial effects of antimigraine therapies. (6)


World Health Organization, 2004.

  • Worldwide, migraine alone is 19th among all causes of years lived with disability (YLDs).
  • 8% of men and 18% of women experience migraine each year.

American Council for Headache Education, 1999.

    25-30 million Americans get migraines. 6% of men get migraines. 18% women suffer migraines at one time in their lifetime. 3 out of 4 migraine suffers are women.

National Headache Foundation, 1999.

    Migraines have increased 50% in the last 20 years.

Signs and Symptoms

[span class=alert]The following list does not insure the presence of this health condition. Please see the text and your healthcare professional for more information.[/span]

Migraine headaches most frequently occur in early morning hours. Approximately 60% of migraineurs also suffer from prodromal symptoms, which may last for hours or days prior to onset of headache. Prodromal symptoms may vary widely among patients, yet are usually consistent in an individual. Symptoms may manifest as psychologic symptoms such as irritability, anxiety, depression, fatigue, drowsiness or euphoria; neurologic symptoms such as photophobia, phonophobia or hyperosmia; constitutional symptoms such as diarrhea, constipation, polyuria or stiff neck; or autonomic symptoms such as thirst, yawning or food cravings. Auras are experienced by 10-15% of migraineurs. Auras generally last 10-30 minutes prior to the development of a headache and generally resemble zigzag lines in the vision, flashing lights, dark spots in the vision or tunnel vision.

Peak intensity of the headache usually occurs within an hour of onset. Pain is usually unilateral and can occur anywhere on the face or head, but most often in the temple. Headaches are most often considered moderate to severe in intensity and are frequently described as throbbing, pounding, or pulsating. Activities of daily living are often affected as activity usually worsens headache pain. Patients often seek a quiet, dark place to rest, and may additionally complain of diarrhea, constipation, nausea, anorexia, vomiting, and increased sensitivity to light and sound. Headaches may last from four to seventy-two hours and patients typically suffer from a postdrome of exhaustion, scalp tenderness and recurrence of headache with sudden head movements.


  • Psychologic symptoms: irritability, anxiety, depression, fatigue, drowsiness, or euphoria
  • Constitutional symptoms: diarrhea, constipation, polyuria, stiff neck
  • Autonomic symptoms: thirst, yawning, food cravings
  • Neurologic symptoms: photophobia, phonophobia, hyperosmia
  • Auras may also occur 


  • Intense pain, usually unilateral
  • Typically peak approximately one hour after onset
  • Described as pulsating, throbbing, or pounding
  • ADLs compromised as headache generally worsens with activity
  • May be accompanied by nausea, vomiting
  • Sensitivity to light or sound
  • Diarrhea
  • May last from 4 to 72 hrs 


    Exhaustion Scalp tenderness Recurrence of headache with sudden head movements

Treatment Options


Management of migraine headaches should begin with identification and removal, if possible, of factors that consistently provoke migraine attacks. Some of these triggers may include environmental factors such as cigarette smoke, loud noise, and bright or flickering lights; psychological factors including stress, anxiety, or depression; dietary factors such as alcohol, chocolate, caffeine, or tyramine containing foods, food additives, or citrus fruit; or life-style factors such as inadequate or excessive sleep, fasting or dieting, fatigue, skipping meals, or strenuous exercise.

A higher incidence of migraine is also seen during menstruation, while generally a decrease is seen during pregnancy. A number of medications have been associated with drug-induced migraine. Some of these are cimetidine, cocaine, ethinyl estradiol, fluoxetine, histamine, hormone replacement therapy, indomethacin, mestranol, nicotine, nifedipine, nitroglycerin, oral contraceptives, and reserpine. Several mechanisms have been proposed as causing drug-induced migraine, including, vasodilation, alteration of uptake or storage of 5-HT, and altered platelet aggregation.

The use of medications in management of migraine may be targeted in two ways, either to alter the attack once it is underway (abortive therapy) or prevention of the attack altogether. Abortive therapy must begin at the onset of the attack to achieve its full potential. Once an attack is fully developed, treatment is much less likely to be effective. Medications used in abortive therapy include simple analgesics, nonsteroidal anti-inflammatory drugs, ergotamine, and 5-HT receptor agonists.

Simple analgesics, such as aspirin and acetaminophen, should be used in patients with infrequent and mild forms of migraine. Aspirin is considered the drug of choice in these patients, unless contraindicated or not tolerated. There are also combination medications, with additives such as caffeine, for increased GI absorption, bultalbital, to aid in sleep, and other narcotics for additional pain relief. These should be used with caution since rebound headache may occur when the effects wear off, leading to additional medication consumption.

Nonsteroidal anti-inflammatory drugs (NSAIDs) have been used with some success in treating migraine headaches. Inhibition of prostaglandin synthesis by NSAIDs may prevent neurogenic inflammation in the trigeminovascular system and alleviate migraine pain. (7) Those with a rapid onset of action such as ibuprofen or naproxen may be superior to those with a slower onset of action. Indomethacin should not be used due to its propensity to induce headache in many patients. The NSAIDs have not been associated with rebound headaches; however, they may cause more side effects than simple analgesics, and they are more expensive. Migraines that occur before, during, or after menstruation may respond well to NSAID therapy. The injectable drug, ketorolac, has been used in patients unable to tolerate oral therapy due to nausea and vomiting, and in patients with drug-seeking behaviors.

Ergotamine has been used for years as a treatment for migraine, and as theories of the pathophysiology of migraine have changed, so have proposed mechanisms of action for ergotamine and its derivatives. Currently, it is believed that antimigraine action occurs as a result of stimulation of presynaptic 5HT1 receptors. Ergotamine is available as an oral tablet, a sublingual tablet, and a suppository. (8) Dihydroergotamine (DHE) is the injectable form and is usually used in emergency rooms; however, it can be safely administered in the home. Intravenous administration is the fastest way to achieve therapeutic drug concentrations and may be preferred by some patients, especially in severe attacks. Oral ergotamine has poor bioavailability, mostly due to extensive first-pass metabolism. Dose and route of administration should be tailored to each patient to achieve safe and effective treatment. Frequent dosing, or exceeding maximum dosage guidelines, may lead to increased side effects and ergotamine dependency.

5-HT1 receptor agonists have emerged as effective treatments against migraine headaches. The first to be introduced, sumatriptan, is available as a subcutaneous injection, and now in oral form as well as intranasal spray. Three additional agents in the same class, zolmitriptan, naratriptan, and rizatriptan have been approved since 1997. These agents have vasocostrictive effects as well as releasing tachykinins, which block neurogenic plasma protein extravasation and inflammation. The efficacy of oral and subcutaneous dosage forms seems to be comparable; however, the subcutaneous dosage form has a faster onset of action.

Prophylactic therapy for migraine should be considered if:

    Attacks occur more than 2-3 times per month Attacks are severe or prolonged and produce profound impairment Symptomatic therapies have failed Patients cannot cope with attacks Headaches come in a predictable pattern

The daily administration of medications, such as beta-blockers, tricyclic antidepressants, anticonvulsants, NSAIDs, and 5-HT antagonists, may reduce the frequency and severity of migraine attacks and increase responsiveness to symptomatic migraine therapies. (9) Because most prophylactic drugs have demonstrated similar efficacy in published trials, the selection of an agent should be based on its side effect profile and comorbid conditions of the patient. (10)

Nutritional Supplementation


Magnesium’s role in the pathogenesis of migraine headaches has been clearly established in numerous clinical and experimental studies. However, the precise role of how and why low levels of magnesium increase the risk of migraines remains to be discovered. Possible mechanisms include the following: magnesium levels affect serotonin receptors, the synthesis and release of nitric oxide, NMDA receptors, and numerous other migraine-related receptors and neurotransmitters. Current evidence suggests that up to 50% of patients have lowered levels of ionized magnesium during an acute migraine attack. Infusion of magnesium often results in rapid and sustained relief in such patients. Two double-blind studies suggest that chronic oral magnesium supplementation may also reduce the frequency of migraine headaches. Because magnesium has an excellent safety profile and is cost effective, despite the lack of definitive studies, the authors of this review suggest that a trial of oral magnesium supplementation can be recommended to a majority of migraine sufferers. They also note that refractory patients may sometimes benefit from intravenous infusions of magnesium sulfate. (11)

Examples of studies reporting on the relationship between magnesium and migraine headaches include the following: Patients with migraines have low brain magnesium levels (12) and in a study of 3,000 women, 80 percent responded well to magnesium supplementation. (13) Magnesium was also found to be effective in the prophylaxis of menstrual migraines. In a double-blind trial, women taking 360 mg/day of magnesium for two months reported a reduction in the number of days with headaches in addition to overall improvement in premenstrual complaints. (14) In addition to reducing the incidence of menstrual migraines, the authors of this study suggest that low levels of magnesium could actually act as a trigger to induce migraine headaches.

Vitamin B2

High-dose riboflavin therapy has proven to be remarkably effective in the treatment of migraine headaches. In an open study, 55 patients took 400 mg of vitamin B2 daily for three months. Riboflavin was far superior to placebo in reducing the frequency of migraine attacks and the number of days with headache. The number of patients who improved by at least 50% (responders) was 59% for riboflavin compared to 15% for the placebo patients. At this high dosage level, only two patients reported minor side effects of diarrhea and excess urination. (15) A previous pilot study that utilized 400 mg/day of riboflavin with 49 patients suffering from migraine had similar beneficial therapeutic effects. (16) The results of these studies suggest that high-dose riboflavin could thus be an effective, low-cost prophylactic treatment of migraine with no significant side effects. A open study conducted in 2004 found that 400 mg of riboflavin reduced the average frequency of migraines from 4 per 2 months to 2 per 3 to 6 months. (17)

Vitamin D, Calcium

Two studies report that a combination of vitamin D and calcium were effective in reducing the frequency and duration of migraine attacks. One was a case study of two postmenopausal women who developed frequent and excruciating migraine headaches (one following estrogen replacement therapy and the other following a stroke). These women were treated with combination vitamin D and calcium. This therapeutic supplementation resulted in a dramatic reduction in the frequency and duration of their migraine headaches. (18)

The second study is a report of two premenopausal women with a history of premenstrual syndrome coupled with menstrually-related migraines. Each woman was treated with a combination of vitamin D and elemental calcium for late luteal phase symptoms of PMS. Within 2 months of therapy, both women experienced fewer migraines and PMS symptoms. (19) The results of these two small case studies suggest that vitamin D and calcium therapy should receive consideration as a possible treatment of migraine headaches.

Herbal Supplementation


Feverfew has gained immense popularity because of its effectiveness in relieving migraine headaches. (20) It can take time for this herb to work, so staying on it for a minimum of a month is recommended for proper activity. It is also used for inflammatory conditions such as rheumatoid arthritis, (21) relaxing smooth muscle in the uterus, (22) inhibiting platelet aggregation and blood clotting, (23) , (24) and fever. (25) The flowers from the plant have been used as a vermifuge. Feverfew has also been used as a natural insecticide. (26)

Feverfew reportedly inhibits the manufacture of inflammatory mediators such as leukotrienes, prostaglandins and thromboxanes. (27) , (28) Feverfew may influence the initial stages of the inflammation process in contrast to the action of aspirin and nonsteroidal anti-inflammatory drugs (NSAID). Clinical trials in the treatment of rheumatoid arthritis have been inconclusive. Authors have speculated that a higher dosage of feverfew is needed to interfere with arachidonate-mediated inflammation. (29)

Several clinical studies have reported the efficacy of feverfew in the prevention of migraine headaches. (30) , (31) , (32) Feverfew exhibits several pharmacological actions that may be implicated in migraine prophylaxis, including inhibition of histamine secretion, (33) inhibition of granular secretion, platelet aggregation and arachidonate mediated responses, (34) , (35) and inhibition of vascular smooth muscle contractility. (36) Also, excess serotonin (5HT) release from platelets has been implicated as one of the primary mechanisms in the pathogenesis of migraines, which may explain some of feverfew’s prophylactic activity in migraine headaches. (37)


In Ayurvedic medicine (traditional Indian medicine), turmeric rhizome has been used for centuries internally as a tonic for the stomach and liver and as a blood purifier, and externally in the treatment and prevention of skin diseases and in arthritic complaints. (38) The laboratory and clinical research indicates that turmeric and its phenolics have unique antioxidant and anti-inflammatory properties. (39) The anti-inflammatory strength of turmeric is comparable to steroidal drugs such as indomethacin. (40) Turmeric has been reported to be anti-rheumatic, anti-inflammatory and antioxidant. (41) Curcuminoids reportedly inhibit enzymes which participate in the synthesis of inflammatory substances (leukotrienes and prostaglandins) derived from arachidonic acid, and it is claimed they are comparable in activity to the NSAID. (42) In a double-blind study of individuals with rheumatoid arthritis, curcumin produced significant improvement in all subjects. (43) Turmeric is also claimed to inhibit platelet aggregation. (44) Many of these pharmacological factors contribute to the supportive use of turmeric in migraine headaches. (45)

Curcumin reportedly has a similar action to that of aspirin and aspirin-like anti-inflammatory agents. (46) However, an advantage of curcumin over aspirin is claimed, since curcumin, unlike aspirin, is reported to selectively inhibit synthesis of inflammatory prostaglandins but does not affect the synthesis of prostacyclin. (47) Curcumin may be preferable for individuals who are prone to vascular thrombosis and require anti-inflammatory and/or anti-arthritic therapy.


Decreasing and managing stress may also play a key role in relieving and preventing migraine headaches. The herb kava has been used for centuries by South Pacific natives. The root is used in the preparation of a recreational beverage known by a variety of local names (kava, yaqona, awa) and occupies a prominent position in the social, ceremonial, and daily life of Pacific island peoples as coffee or tea does in the Western cultures. In European phytomedicine, kava has long been used as a safe, effective treatment for mild anxiety states, nervous tension, muscular tension, and mild insomnia. (48) , (49) Studies have reported that kava preparations compare favorably to benzodiazepines in controlling symptoms of anxiety and minor depression, while increasing vigilance, sociability, memory, and reaction time. (50) , (51) Reports are conflicting as to whether kava’s anti-anxiety actions are GABA mediated. (52) , (53) Kavalactones appear to act on the limbic system, in particular the amygdala complex – the primitive part of the brain that is the center of the emotional being and basic survival functions. (54) It is thought that kava may promote relaxation, sleep, and rest by altering the way in which the limbic system modulates emotional processes. Tolerance does not seem to develop with kava use. (55) , (56)

Evening Primrose

Evening primrose oil (EPO) is rich in gamma-linolenic acid which is an omega-6 fatty acid. (57) , (58) Omega-6 fatty acids reportedly reduce the arachidonic acid cascade and decrease inflammation through inhibiting the formation of inflammatory mediators in this process. Fatty acids are an important part of normal homeostasis. The human body can produce all but two fatty acids - omega-3 and omega-6 fatty acids. Both must be obtained through the diet or by the use of supplements. Obtaining a balance of these two fatty acids is essential. Essential fatty acids are needed for building cell membranes and are precursors for production of hormones and prostaglandins. Modern diets tend to be lacking in quality sources of fatty acids.

Diabetics who do not convert linoleic acid to gamma-linolenic acid will need a quality source of GLA. (59) , (60) This is said to be essential for proper nerve function and for the prevention of diabetic neuropathy. (61) , (62) Evening primrose oil was reported to be beneficial in effecting the course of diabetic neuropathy by decreasing microvascular problems associated with hyperinsulinemia. (63)


Gymnema is a rain forest vine found in Central and Southern India which has a long tradition in the treatment and management of diabetes. The Indian name is Gurmar, which means “sugar destroyer." Its use has been documented in Ayurvedic medical texts for over 2000 years in the treatment of “sweet" urine. Gymnema is gaining popularity with clinicians utilizing natural therapy protocols in the management of diabetes, hyperinsulinemia and impaired glucose tolerance. The leaves of gymnema are thought to increase insulin secretion, and several studies report control of hyperglycemia in moderately diabetic laboratory animals. (64) , (65) A decrease in body weight was also reported. Gymnema reportedly produced blood glucose homeostasis and increased the activity of the enzymes involved in the utilization of glucose by insulin dependent pathways. (66)

Human studies have reported a significant reduction in blood glucose during therapy with gymnema. (67) , (68) A reduction in glycosylated hemoglobin and glycosylated plasma proteins has also been reported, with a reduction in conventional drug dosage. In studies patients with diabetes were able to discontinue conventional drugs and maintain their blood glucose homeostasis with gymnema alone. (69) Researchers suggest that beta cells may be regenerated and/or repaired in Type 2 diabetics on gymnema supplementation. (70) They support their claim by the appearance of increased endogenous insulin levels in the serum of individuals after gymnema supplementation. Other studies report that gymnemic acids suppress the elevation of blood glucose levels by inhibiting glucose uptake in the intestine. (71)

Gymnema has also been reported to selectively suppress the neural responses to sweet taste stimuli. (72) , (73) , (74) Because gymnema leaf powder has an anesthetizing effect on the taste buds which can last for several hours, some researchers feel that gymnema may be a potential agent in weight reduction and sweet cravings. (75) A recent study reports significant serum cholesterol lowering effects of gymnema. (76) Gymnema may potentially be used in athletes to develop a higher ratio of lean muscle mass to body fat. This may be due to the reported increase of insulin output associated with long-term use of gymnema. Increased insulin output and utilization encourages the uptake of amino acids into muscle tissue.

Bitter Melon

Bitter melon or karela fruit has long been used in South American and the Orient as not only a food but also as a febrifuge, abortifacient, emmenagogue, vermifue, anti-viral, emetic, anthelminitic and antidiabetic agent among other uses. (77) Recent studies have focused on the beneficial properties of the fruit in diabetes and hyperinsulinemia, HIV viral infection and certain cancers. (78) , (79)

Bitter melon has been reported to significantly improve glucose tolerance in humans. (80) , (81) The currently accepted hypotheses regarding hypoglycaemic activity is claimed to be mediated through an insulin secretagogue effect or through an influence on enzymes involved in glucose metabolism. (82) Research indicates that molecules with insulin-like bioactivity may be present in bitter melon seeds. (83) A few studies suggest that the hypoglycemic mechanism of action of bitter melon could be partly attributed to increased glucose utilization in the liver rather than an insulin secretion effect. (84) A recent laboratory study reported a significant reduction of fasting blood glucose levels observed in diabetic rats, but no hypoglycaemic activity in the treated normal rats. (85) Bitter melon also showed considerable lowering of serum cholesterol and triglycerides in the treated diabetic group. There was a significant improvement in hepatic glycogen level in treated diabetic rats, with a return of close to normal levels after the treatment with bitter melon. There have been negative reports as to the ability of bitter melon extracts to lower blood sugar levels in laboratory animals. (86) , (87) It is recommended that a standardized extract of bitter melon always be used.


The chasteberry tree finds its origins in the Mediterranean. Its fruit is harvested and dried for medicinal purposes. It has a long folk history of use in women’s health and in hormonal regulation. Chasteberry has been recommended for use in mild to moderate female complaints, especially in endometriosis, menopause, and PMS symptoms. The actual activity of the constituents of chasteberry is not fully established at this time. Studies have reported it to have significant effect on the pituitary. (88) , (89) Studies point to a progesterone-like component and effect. (90) , (91) Studies report that vitex stimulates luteinizing hormone (LH) and inhibits follicle stimulating hormone (FSH). (92) , (93) Because of this activity, vitex has been recommended for a variety of female complaints, such as PMS, amenorrhea, menopausal symptoms, endometriosis, and hyperprolactinemia. (94) , (95) , (96) Several studies have reported beneficial effects of vitex on female-related disorders. (97) , (98) Several clinical studies have reported beneficial results with using chasteberry in treating women with infertility associated with corpus luteum deficiency. (99)

Black Cohosh

Black cohosh rhizome has been shown to have phytoestrogenic properties. (100) The isoflavone formononetin has been reported to have estrogenic activity in laboratory rats. (101) Formononetin was reported to act as a competitor with estrogen in binding to uterine cells ex vivo. Clinical studies have reported positive effects on menopausal and post-menopausal complaints when using standardized extracts of black cohosh. (102) , (103)

The triterpenoid 27-deoxyactein has also been reported to produce estrogen-like effects in humans. (104) In a controlled study, black cohosh tablets, standardized to 1mg of 27-deoxyactein, were given to 110 female patients in a university gynecological clinic. Patients received 2 tablets twice daily for 2 months. Half the patients took the black cohosh tablet, and half took a placebo. At the end of the required treatment period, both groups were tested for luteinizing hormone (LH) and follicle stimulating hormone (FSH) levels, as increases in LH levels have been found in menopausal individuals complaining of hot flashes. There was no significant effect on the FSH serum concentration in either group. This study reported positive effects that black cohosh has on LH suppression in menopausal women, with an estrogen-like manner. It should be noted, however, that naturally occurring estrogen in the body also affects the release of FSH through receptor binding; so even though black cohosh has estrogenic properties in the body, it does not have the exact pharmacology as naturally occurring estrogen.

Also, the constituent cimicifugoside is reported to affect the hypothalamus-pituitary system, producing a hormonal balancing effect in the female reproductive system. (105) The hypothalamus and pituitary glands control many aspects of human biochemistry, including hormonal release and regulation.


Iris versicolor

Typical Dosage: 6X or 6C, 30X or 30CHeadache starts with blurred vision; Sharp, throbbing pain mostly located above the eyes; Especially on the right side

Lachesis mutus

Typical Dosage: 6CCongestive headaches; Especially left-sided; Menopausal headaches; Worse from heat and alcohol

Natrum muriaticum

Typical Dosage: 6X or 6C, 30X or 30CPounding in the head; Especially in the morning; Worse from moving the eyes or head

Spigelia anthelmia

Typical Dosage: 6X or 6C, 30X or 30CIntense, neuralgic pain above left eye or left side of head; Worse from noise and in the morning

Thuja occidentalis

Typical Dosage: 6X or 6C, 30X or 30CBoring; Pressing pain; Especially left-sided

Acupuncture & Acupressure

Wang treated 60 cases of migraine with acupuncture. The acupoints selected for treatment were Bai Hui (Du 20), Shang Xing (Du 23), Feng Chi (GB 20), Tai Yang (Extra 2), Tai Zhong (Sp 3), and Lie Que (Lu 7). Gentle and slow twirling manipulation was used and the needles were retained for 20 minutes. The procedure was performed once a day, and 10 sessions constituted one course of treatment. After 1-3 courses of treatment, 32 cases recovered, 17 cases improved, and the remaining 11 cases did not respond to the treatment, with a total effective rate of 95% (the effective rate was 94.1% for those with a less-than-3-year illness history, 86.7% for those with an illness history between 4 and 10 years, and 71.4% for those with an illness history longer than 11 years). (106)

Zhan, et al. treated 35 cases of migraine with acupuncture on the bilateral acupoint Lie Que (Lu 7). The needles were inserted obliquely 0.5-1 cun (1.65-3.3cm) deep. The reducing method was used to provide strong stimulation, and the needles were retained for 30 minutes. The results: 18 cases recovered, 9 cases significantly improved, 5 cases improved, and the remaining 3 cases did not respond to the treatment, with a total effective rate of 91.4%. (107)

Blood-pricking therapy
Ye treated 50 cases of migraine with blood-pricking therapy. The acupoints treated were Tai Yang (Extra 2), Tou Wei (St 8), Han Yan (GB 4), Xuan Lu (GB 5), Xuan Li (GB 6), Qu Bin (GB 7). 1-2 points on the affected side were treated in each session. Gentle patting was applied to cause local hyperemia. Subcutaneous vein was rapidly pricked with a prismatic needle to bleed about 1-2ml. The procedure was conducted once every 2-3 days, and seven sessions constituted one course of treatment. The results: 40 cases recovered, 5 cases significantly improved, 3 cases improved, and the remaining 2 cases did not respond to the treatment, with a total effective rate of 96%. (108)

Acupuncture combined with acupoint injection therapy
Weng treated 130 cases of migraine with acupuncture and liquid-acupuncture on Jen Ying (St 9), Feng Chi (GB 20), Tai Yang (Extra 2), Tou Wei (St 8), Wai Guan (SJ 5), and Di Wu Hui (GB 42). The uniform reinforcing-reduction method was used, and the needles were retained for 30 minutes. After the needles had been withdrawn, Vitamin B12 was injected at both sides of Jen Ying (St 9) (0.25mg each side). The treatment was repeated once a day or every other day, and 10 days constituted one course of treatment. The study reported a total effective rate of 93.8%. (109)

Mild Moxibustion therapy
Zhu, et al. treated 62 cases of senile obstinate migraine with mild moxibustion on Zu San Li (St 36), Chi Hai (Ren 6), San Yin Jiao (Sp 6), Tai Xi (K 3), and Shen Shu (UB 23). During remission, 2-4 of the above-mentioned points were selected each time for moxibustion (3 cones for each acupoint), and when a migraine attack is under way, acupuncture treated was applied on Ah Shi point, Feng Chi (GB 20), Tou Wei (St 8), and Shuai Gu (GB 8). The acupuncture treatment was repeated daily, and 10 sessions constituted one course of treatment. After 4-6 courses of treatment, 7 cases recovered, 28 cases significantly improved, 17 cases improved, and the remaining 10 cases did not respond to the treatment, with a total effective rate of 83.9%. (110)

Otopoint plaster therapy
Wang treated 13 cases of menstrual migraine with otopoint plaster therapy. Points of the liver, gallbladder, forehead, and Tai Yang (Extra 2) were selected for Shao Yang headache. Points of the liver, spleen, stomach, and eye were selected for Yang Ming headache. And Shen Men (H 7), and point related to the subcortical system, sympathetic nerve, endocrine, and the kidney were treated for both types of headaches. 3-5 days before menstruation, Wang Bu Liu Xing (Vaccaria) seed was plastered onto the above points every other day till the end of the menstrual cycle. One menstrual period comprised one course of treatment. The study reported satisfactory therapeutic effect in all 13 cases. (111)

Traditional Chinese Medicine


Extensive information regarding the treatment of this health condition using Traditional Chinese Medicine is available through the link above.

Clinical Lab Assessment

Some of the following laboratory testing can provide information necessary for diagnosis and treatment. In addition, the tests listed may also give insight to functional metabolism and functional nutrient status in the body.

Allergy and Food Sensitivity Response Assessment

The severity of allergic response correlates with an increase in stress levels. (112) Allergies may have considerable impact on inflammatory processes. Elevated histamine increases susceptibility to migraines, thus possibly implicating allergic response in migraines. (113) Direct correlation of impaired digestion or food allergic response is controversial, though some case studies manifest improvements on food elimination diets.


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