Migraine treatment

Migraine treatment may be either prophylactic (preventive) or abortive (rescue). Prevention is better than cure, so the ideal treatment goal is to prevent migraine attacks. Because migraine is an exceedingly complex condition, there are various preventive treatments which have their effect by disrupting different links in the chain of events that occur during a migraine attack. As rescue treatments also target and disrupt different processes occurring during migraine, these are summarized, with their relative merits and demerits.

Preventive treatment

Preventive treatments can be sub-divided into non-drug treatments, and treatment with medication. Non-drug treatment, when possible, is preferable because of the high incidence of unpleasant or debilitating side-effects that occur with migraine preventive drugs.

Non-drug preventive treatment

Because of the complexity of migraine, no preventive treatment modality is effective for all migraine sufferers. However in FDA trials the Nociceptive Trigeminal Inhibition Tension Suppression System (NTI-tss) had been proven to provide a 77% reduction of Migrain events in 82% of subjects tested. [1]Practical Neurology Oct. 2005[2] The origin of the pain must be determined in each individual, and each contributory factor must be addressed. Most migraine sufferers have a combination of two or more of the following: a) vascular pain (pain originating in the arteries of the scalp)[3] , b) muscular pain (pain originating from the jaw and neck muscles)[4][5][6][7] , c) pain or abnormal sensitivity of the skin of the scalp (known as cutaneous allodynia)[8] , and hypersensitivity of the brain to incoming pain messages[9]

Surgical preventive procedures

Chronic daily headache is a major worldwide health problem that affects 3–5% of the population and results in substantial disability. Advances in the medical management of headache disorders have meant that a substantial proportion of patients can be effectively treated with medical treatments. However, a significant proportion of these patients are intractable to drug treatment.[10] The successful use of surgical procedures for the treatment of migraine is becoming more frequently reported in the medical literature, particularly for those patients who do not respond to medication. There is resistance in some quarters the concept of surgery for migraine, on the grounds that it is unnecessarily invasive. On the contrary, others argue that to undergo a relatively minor and minimally invasive once-off surgical procedure is not as invasive as having to permanently take chronic medication, which in many people has unpleasant or intolerable side effects, or is ineffective. The answer to this conundrum lies however in informed consent - the patient must be advised of all the possibilities, and of all the pros and cons of each option, so that an informed choice can be made. In some instances, patients opt for the drug route, and only take the surgical option when the medication has not had the desired effect. For others, the thought of being on chronic medication is anathema.

Arterial pain

There is abundant irrefutable physiological, experimental, pharmacological, and clinical evidence that in many migraine sufferers the pain originates in painfully dilated extracranial terminal branches of the external carotid artery. That vasodilatation is an important factor in migraine is further confirmed by the fact that the most widely used migraine rescue medications, the ergots, the triptans, and the promising newer drugs, the gepants, possess one significant common denominator: they all potently constrict abnormally dilated extracranial arteries while simultaneously reducing or eliminating migraine pain. Furthermore, to date all migraine-provoking agents have had vasodilating properties.[3]

Arterial surgery

In patients where the pain has been positively diagnosed to originate from the scalp arteries (the terminal branches of the external carotid artery), the preventive treatment of choice is surgical cauterization of the responsible arteries – known as the Shevel Procedure.[11]

Details of the Procedure

In order to pinpoint the position of the relevant arteries, a three-dimensional CT scan is done, which allows accurate visualization of the course of each artery. This is necessary, as the course of the arteries varies from person to person, and even from side to side in the same individual. During surgery, the position of the artery is further verified by means of a Doppler Flowmeter, with which one can hear the blood flowing through the vessel. Use of the three-dimensional CT scan and the Doppler Flowmeter allows the surgeon to make use of the smallest possible incision, so the procedure is minimally invasive. The most common vessels involved in the pain of migraine are the terminal branches of the external carotid artery, and in particular, the superficial temporal artery and its frontal branch, and the occipital artery, but the maxillary, posterior auricular, supra-orbital, and supra-trochlear branches may also be involved. These vessels are subcutaneous (just under the skin) and the small incisions required to access them and the minimally invasive nature of the procedure means that the surgery can be done in a day facility. As these vessels have no connection with the arterial supply to the brain, the Shevel Procedure is exceedingly safe with no unpleasant side effects. The cosmetic effect is excellent as most of the incisions are within the hairline.[11]

When is arterial surgery indicated?

Arterial surgery is only indicated once there is positive confirmation that the arteries are indeed the source of pain. Some migraine sufferers have a visibly distended artery on the temple during an attack, which confirms that the arteries are involved. The distention usually subsides as the pain is controlled by vasoconstrictor drugs (ergots or triptans).[12] In some, this artery is always visible, but it is only when it becomes distended during an attack that it becomes important for diagnosis. Patients who take triptans or ergots for relief of migraine pain are also prime candidates for arterial surgery. The reason for this is that the action of these drugs is to constrict the painfully dilated branches of the external carotid artery - the same arteries that are targeted by the surgery. The purpose of the surgery is to provide a permanent 'triptan or ergot effect'. Most of these arteries are in the scalp and are readily accessible to minimally invasive surgery. This treatment modality is of particular value in: 1) patients who have not responded to preventive drug therapy, 2) patients who are unable to use drug therapy because they experience unacceptable side effects, 3) patients who have to make too frequent use of abortive drugs such as the triptans or ergots, and 4) patients who would prefer not to be on permanent medication. Included in this category are those with Chronic Daily Headache (headache on more than 15 days per month) and patients with what is known as "refractory headache" - headache that has not benefited from any other form of treatment. Elliot Shevel, a South African surgeon, showed that patients with chronic migraine experienced a significant reduction in pain levels and significant improvement in their quality of life following the surgery.[11]

Muscle surgery - trigger site release

Trigger site release was first described by a plastic surgeon, Dr Bahaman Guyuron.[13] The theory is that trigger sites (TSs) exist where sensory nerves are being compressed by a surrounding muscle. The nerve becomes inflamed, and a cascade of events is initiated, triggering migraine headaches. Thus far, three muscle trigger areas where the nerve passes through a muscle have been identified as surgical candidates – where the a) greater occipital nerve pierces through the semispinalis capitis muscle, b) the zygomaticotemporal nerve passes through the temporalis muscle, and c) the supraorbital/supratrochlear nerves pass through the glabellar muscle group (the corrugator supercilii, depressor supercilii, and procerus muscles).[14][15][16] Several large series of studies have been conducted to evaluate the efficacy of surgical obliteration of trigger points. Almost all demonstrated more than 90% response in a carefully selected group of patients who have a positive response to Botox therapy, with at least 50% improvement to complete resolution of migraine pain.

Details of the procedures

Patients have to be screened preoperatively with a full neurological examination, and subsequent Botox injection. A positive response to Botox has been an accurate predictor of a successful outcome. Single or multiple TSs may be treated. Migraine headaches can start in one area depending on their corresponding trigger site and spread to the rest of the head. It is important to identify the initial trigger sites rather than address all the areas of pain, after the inflammation involves the entire trigeminal tree. Forehead migraine headaches: In the glabellar area the supra-orbital and supra-trochlear nerves are skeletonized by resecting the corrugator and depressor supercilii muscle using an endoscopic approach similar that of used for cosmetic forehead lift. Temporal migraine headaches: The temporal area, where the zygomaticotemporal branch of trigeminal nerve passes through the temporalis muscle, is addressed using a similar endoscopic approach but involves removing a segment of the nerve rather than transecting the muscle. This results in a slight sensory defect over temporal skin area, but cross-innervation from other sensory nerves helps to limit the damage. Occipital migraine headaches: The posterior neck area where the greater occipital nerve passes through the semispinalis capitis muscle is addressed with an open surgical approach with resection of a small segment of the semispinalis muscle and shielding the nerves with a subcutaneous adipose flap.[15]

A further trigger point, not involving muscles, has been identified in the nose of patients who have significant nasal septum deviation with enlargement of the turbinates.[15] The nasal trigger points where enlarged turbinates are in contact with the nasal septum are addressed with a septoplasty and a turbinectomy.

When is muscle surgery with trigger point release indicated?

Trigger point release is only carried out for patients who respond favorably to intramuscular injections of Botulinum toxin. This removes the guesswork, as the surgery is only carried out when a positive diagnosis has been made.

Patent foramen ovale closure

There is significant evidence that a link exists between migraine with aura and the presence of a patent foramen ovale (PFO), a hole between the upper chambers (the atria) of the heart.[17] It is estimated that 20-25% of the general population in the United States has a PFO.[18][18][19][19] Medical research studies have shown that migraineurs are twice as likely as the general population to have a PFO,[17][18] that over 50% of sufferers of migraine with aura have a PFO,[17] that patients with a PFO are 5.1 times more likely to suffer from migraines and 3.2 times more likely to have migraines with aura than the general population,[17] and that patients with migraine with aura are much more likely to have a large opening than the general PFO population.[17][19][20] There is however some controversy, as some have shown a link,[21] while others have failed to demonstrate a link.[22]

Details of the procedure

A catheter is advanced up to the hole in the heart after it is inserted in a vein in the leg. Through the catheter, a device is then placed which blocks the hole between the left and right atria of the heart. There are a number of different devices being used or tested, the Coherex FlatStent PFO Closure System,[23] the CardioSEAL,[24] and the AMPLATZER PFO Occluder device.[25]

Migraine frequency and severity has been shown to be reduced if the hole (PFO) is patched surgically.[26] It has been suggested that there is an advantage to non-pharmacological migraine relief - "in contrast to drugs, PFO closure appears highly effective against migraines and usually has no side effects".[27] Because PFO closure continues to prove successful, new devices are being produced to make the surgery easier to perform and less invasive. Some studies, however, have emphasized caution in relating PFO closure surgeries to migraines, stating that the favorable studies have been poorly designed retrospective studies and that insufficient evidence exists to justify the dangerous procedure.[28][29] There have however been reports of short-term increases in migraine frequency and intensity following the surgery.[25][30][31]

Nerve stimulation

Occipital nerve stimulation (ONS)

Published reports from open-label studies have demonstrated possible efficacy of ONS in a variety of primary headache disorders, including chronic migraine.[10][32] ONS for the treatment of medically intractable headaches was introduced by Weiner and Reed [33] ONS is typically performed with the equipment normally used for spinal cord stimulation (SCS), which includes electrodes and their leads, anchors to fasten the leads to connective tissue, and the implantable pulse generator (IPG).

Details of the procedure

Electrodes are placed subcutaneously (under the skin) superficial to the cervical muscle fascia, transverse to the affected occipital nerve trunk at the level of C1, usually using fluoroscopic guidance. The standard procedure is typically performed in two stages. The first stage, carried out under local anesthesia with sedation, is used to test the stimulation and determine optimal placement of electrodes. The second part, which involves insertion of the rest of the ONS system, is carried out under general anesthesia. However, a recent report of a small case series described successful placement of ONS systems entirely under general anesthesia while still achieving the desired occipital region stimulation.[34]

When is ONS indicated?

A stimulation trial can be performed before the permanent implantation, with the view to improving selection of the candidates for a permanent stimulation. The procedure involves inserting percutaneous (through the skin) leads into the epidural space and externally powering them for 5–7 days. If the trial is successful in terms of significant pain improvement, the patient is offered a permanent implantation. However, in primary headache syndromes, unlike in neuropathic pain, there can be a considerable delay of several weeks to months before the response emerges and therefore the utility of a stimulation trial in selecting patients for permanent implantation remains questionable for now.[32]

Non-surgical preventive treatments

Muscle relaxation

The involvement of the pericranial muscles in migraine has been well documented,[4][35][36][37] and muscle relaxation techniques have been used successfully to prevent migraine.

Intra-oral appliances

Intra-oral appliance are designed to relax the pericranial muscles, which have been reported to be tender in 100% of migraine sufferers during an attack.[4] There are a number of different designs, which have been reported to be effective in many migraine sufferers.[38][39][40][41][42]

Biofeedback

Biofeedback is the process of gaining greater awareness of many physiological functions primarily using instruments that provide information on the activity of those same systems, with a goal of being able to manipulate them at will.[43][44] Some of the processes that can be controlled include brainwaves, muscle tone, skin conductance, heart rate and pain perception.[45] Biofeedback to induce muscle relaxation is widely used in migraine prevention.[46][47]

Botulinum Toxin (Botox)

OnabotulinumtoxinA (trade name Botox) received FDA approval for treatment of chronic migraines (occurring more than 15 days per month) in 2010. The toxin is injected into the muscles of head and neck. Approval followed evidence presented to the agency from two studies funded by Allergan, Inc. showing a very slight improvement in incidence of chronic migraines for migraine sufferers undergoing the Botox treatment.[48][49] Since then, several randomized control trials have shown Botulinum Toxin Type A to improve headache symptoms and quality of life when used prophylactically for patients with chronic migraine[50]

Drug preventive treatment

Preventive drugs are used to reduce the frequency, duration, and severity of migraine attacks. Because of frequent unpleasant and sometimes debilitating side effects, preventive drugs are only prescribed for those migraineurs whose quality of life is significantly adversely affected. The most commonly prescribed drugs for migraine prevention are beta-blockers, antidepressants, and anticonvulsants. The drugs are started at a low dose, which is gradually increased until therapeutic effects develop, the ceiling dose for the chosen drug is reached, or side effects become intolerable.

Beta-blockers

The beta-blocker, propranalol's effectiveness in headache treatment was a chance finding in patients receiving the drug for angina (chest pain due to a lack of blood to the heart muscle).[51] The beta-blockers that are used in migraine treatment are propranolol, nadolol, timolol, metoprolol, and atenolol.[52]

Beta blockers adverse reactions

Adverse drug reactions (ADRs) associated with the use of beta blockers include: nausea, diarrhea, bronchospasm, dyspnea, cold extremities, exacerbation of Raynaud's syndrome, bradycardia, hypotension, heart failure, heart block, fatigue, dizziness, alopecia (hair loss), abnormal vision, hallucinations, insomnia, nightmares, sexual dysfunction, erectile dysfunction and/or alteration of glucose and lipid metabolism. Due to the high penetration across the blood–brain barrier, lipophilic beta blockers, such as propranolol and metoprolol, are more likely than other, less lipophilic, beta blockers to cause sleep disturbances, such as insomnia and vivid dreams and nightmares.[53]

Antidepressants

Amitriptyline has been more frequently studied of the antidepressants and is the only antidepressant with fairly consistent support for efficacy in migraine prevention. The method of headache prevention with antidepressants is uncertain, but does not result from treating masked depression.[52]

Amitriptyline adverse reactions

The main two side effects that occur from taking amitriptyline are drowsiness and a dry mouth. Other common side effects of using amitriptyline are mostly due to its anticholinergic activity, including: weight gain, changes in appetite, muscle stiffness, nausea, constipation, nervousness, dizziness, blurred vision, urinary retention, and changes in sexual function. Some rare side effects include seizures, tinnitus, hypotension, mania, psychosis, sleep paralysis, hypnagogic or hypnopompic hallucinations related to sleep paralysis, heart block, arrhythmias, lip and mouth ulcers, extrapyramidal symptoms, depression, tingling pain or numbness in the feet or hands, yellowing of the eyes or skin, pain or difficulty passing urine, confusion, abnormal production of milk in females, breast enlargement in both males and females, fever with increased sweating, and suicidal thoughts.[54]

Anticonvulsants

Anticonvulsant medication is commonly prescribed for migraine prevention, because they have been shown in placebo-controlled double-blind trials to be effective in some migraine sufferers.

Valproate acid

Placebo controlled trials of both divalproex sodium and sodium valproate have shown them to be significantly better than placebo at reducing headache frequency.[55][56][57][58]

Valproate adverse reactions

Nausea, vomiting, and gastrointestinal disturbances are the most common side-effects of valproate therapy, and are slightly less common with divalproex sodium than with sodium valproate.[52] The results of a study on the long-term safety of divalproex sodium showed premature discontinuation of the drug in 36% of patients because of either drug intolerance or ineffectivity of the drug.[59]

Topiramate

Topiramate has been approved by the FDA for prevention of migraine. Studies have shown that it provides significant reductions in the frequency of migraine episodes in patients with 3-12 headaches a month[60]

Topiramate adverse reactions

Adverse reactions related to topiramate treatment occurred in 82.5% of 328 subjects who took part in an extensive trial covering 46 different centres. Most commonly reported were paresthesia (28.8%), upper respiratory tract infection (13.8%, and fatigue (11.9%)[61]

Rescue treatment

The two main methods of rescue treatment are trigger avoidance, and acute symptomatic control with medication.[62] Medications are more effective if used earlier in an attack.[62] A serious potential problem with the frequent use of medications is the possible development of medication overuse headache, in which the headaches become more severe and more frequent.[63] This may occur with triptans, ergotamines, and analgesics, especially narcotic analgesics.[63][64]

Analgesics

Recommended initial treatment for those with mild to moderate symptoms are simple analgesics such as non-steroidal anti-inflammatory drugs (NSAIDs) or the combination of acetaminophen (paracetamol), acetylsalicylic acid, and caffeine.[65] A number of NSAIDs have been shown to be effective. Ibuprofen provides effective pain relief in about 50%.[66] Diclofenac has been found effective.[67]

Non-steroidal anti-inflammatory drugs (NSAIDS)

A number of NSAIDs have evidence to support their use. Ibuprofen has been found to provide effective pain relief in about 50% of migraine attacks.[66]

NSAIDS adverse reactions

The widespread use of NSAIDs has meant that the adverse effects of these drugs have become increasingly prevalent. The two main adverse drug reactions (ADRs) associated with NSAIDs relate to gastrointestinal (GI) effects and renal effects of the agents. These effects are dose-dependent, and in many cases severe enough to pose the risk of ulcer perforation, upper gastrointestinal bleeding, and death, limiting the use of NSAID therapy. An estimated 10-20% of NSAID patient’s experience dyspepsia, and NSAID-associated upper gastrointestinal adverse events are estimated to result in 103,000 hospitalizations and 16,500 deaths per year in the United States, and represent 43% of drug-related emergency visits. Many of these events are avoidable; a review of physician visits and prescriptions estimated that unnecessary prescriptions for NSAIDs were written in 42% of visits.[68]

Acetylsalicylic acid

Acetylsalicylic acid(Aspirin) can relieve moderate to severe migraine pain, with an effectiveness similar to the triptans.[69] Ketorolac is available in an intravenous formulation.[65]

Acetylsalicylic acid adverse reactions

Aspirin should not be taken by people who have salicylate intolerance[70][71] or a more generalized drug intolerance to NSAIDs, and caution should be exercised in those with asthma or NSAID-precipitated bronchospasm. Owing to its effect on the stomach lining, manufacturers recommend people with peptic ulcers, mild diabetes, or gastritis seek medical advice before using aspirin.[72][73] Use of aspirin during dengue fever is not recommended owing to increased bleeding tendency.[74] People with kidney disease, hyperuricemia, or gout should not take aspirin because it inhibits the kidneys' ability to excrete uric acid, and thus may exacerbate these conditions.

Acetaminophen (Paracetamol)

Paracetamol (also known as acetaminophen), either alone or in combination with metoclopramide (an anti-nausea drug), is another effective treatment with a low risk of adverse effects.[75] In pregnancy acetaminophen and metoclopramide are deemed safe as are NSAIDs until the third trimester.[65]

Acetaminophen (Paracetamol) adverse reactions

In recommended doses, the side effects of paracetamol are mild to non-existent.[76] In contrast to aspirin, it is not a blood thinner (and thus may be used in patients where coagulation is a concern), and it does not cause gastric irritation.[77] Compared to Ibuprofen—which can have adverse effects that include diarrhea, vomiting, and abdominal pain—paracetamol is well tolerated with fewer side effects.[78] Prolonged daily use increases the risk of upper gastrointestinal complications such as stomach bleeding,[79] and may cause kidney or liver damage.[77][80] Paracetamol is metabolized by the liver and is hepatotoxic; side effects may be more likely in chronic alcoholics or patients with liver damage.[76][81]

Until 2010 paracetamol was believed safe in pregnancy (as it does not affect the closure of the fetal ductus arteriosus as NSAIDs can[82]). However, in a study published in October 2010 it has been linked to infertility in the adult life of the unborn.[83] Like NSAIDs and unlike opioid analgesics, paracetamol has not been found to cause euphoria or alter mood although recent research shows some evidence that paracetamol can ease psychological pain.[84] Unlike aspirin, it is safe for children, as paracetamol is not associated with a risk of Reye's syndrome in children with viral illnesses.[85] Paracetamol use for fever in the first year of life was associated with an increase in the incidence of asthmatic symptoms at 6–7 years, and that paracetamol use, both in the first year of life and in children aged 6–7 years, was associated with an increased incidence of rhinoconjunctivitis and eczema.[86] The authors acknowledged that their "findings might have been due to confounding by indication", i.e., that the association may not be causal but rather due to the disease being treated with paracetamol, and emphasized that further research is needed. Furthermore, a number of editorials, comments, correspondence, and their replies have been published in The Lancet concerning the methodology and conclusions of this study.[87][88][89][90][91][92][93] The UK regulatory body the Medicines and Healthcare products Regulatory Agency, also reviewed this research and published a number of concerns over data interpretation, and offer the following advice for healthcare professionals, parents, and care-givers: "The results of this new study do not necessitate any change to the current guidance for use in children. Paracetamol remains a safe and appropriate choice of analgesic in children. There is insufficient evidence from this research to change guidance regarding the use of antipyretics in children. "[94] Chronic users of paracetamol may have a higher risk of developing blood cancer.[95]

Triptans

Triptans such as sumatriptan are effective for both pain and nausea in up to 75% of migraineurs.[96] They are the initially recommended treatments for those with moderate to severe pain or those with milder symptoms who do not respond to simple analgesics.[65] The different forms available include oral, injectable, nasal spray, and oral dissolving tablets. In general, all the triptans appear equally effective, with similar side effects. However, individuals may respond better to specific ones.[65]

Triptans - adverse reactions

Most side effects are mild, such as flushing; however, rare cases of myocardial ischemia have occurred. They are thus not recommended for people with cardiovascular disease.[65] They are not addictive, but they are an exceedingly potent cause of medication overuse headaches if used more than 10 days per month.[97]

Ergots

Ergotamine and dihydroergotamine (DHE) are older medications still prescribed for migraines, the latter in nasal spray and injectable forms. They appear equally effective to the triptans,[98] are less expensive,[99] and experience adverse effects that typically are benign.[100] In the most debilitating cases, such as those with status migrainosus, they appear to be the most effective treatment option.[100]

Ergots adverse reactions

The most common adverse effects are nausea, vomiting, abdominal pain, generalized weakness, tiredness, malaise, paresthesia, coldness, muscle pains, diarrhea, and chest tightness. These are less common with DHE than with ergotamine tartrate.[101]

Other

Intravenous metoclopramide or intranasal lidocaine are other potential options.[65] Metoclopramide is the recommended treatment for those who present to the emergency department.[65] A single dose of intravenous dexamethasone, when added to standard treatment of a migraine attack, is associated with a 26% decrease in headache recurrence in the following 72 hours.[102] Spinal manipulation for treating an ongoing migraine headache is not supported by evidence.[103] It is recommended that opioids and barbiturates not be used.[65]

References

  1. ↑ Practical Neurology Oct. 2005
  2. ↑ p
  3. 1 2 Shevel E (2011). "The Extracranial Vascular Theory of Migraine – A Great Story Confirmed by the Facts". Headache. 51 (3): 409–417. PMID 21352215. doi:10.1111/j.1526-4610.2011.01844.x.
  4. 1 2 3 Tfelt-Hansen P; Lous I; Olesen J. (1981). "Prevalence and significance of muscle tenderness during common migraine attacks". Headache. 21 (2): 49–54. PMID 7239900. doi:10.1111/j.1526-4610.1981.hed2102049.x.
  5. ↑ Jensen K, Bulow P, Hansen H (1985). "Experimental toothclenching in common migraine". Cephalalgia. 5 (4): 245–251. PMID 4084979. doi:10.1046/j.1468-2982.1985.0504245.x.
  6. ↑ Fernández-de-Las-Peñas C; Cuadrado ML; Arendt-Nielsen L; Pareja JA. (2008). "Side-to-side differences in pressure pain thresholds and pericranial muscle tenderness in strictly unilateral migraine". Eur J Neurol. 15 (2): 162–8. PMID 18093151. doi:10.1111/j.1468-1331.2007.02020.x.
  7. ↑ Fernández-de-Las-Peñas C, Cuadrado ML, Pareja JA (2006). "Myofascial trigger points, neck mobility and forward head posture in unilateral migraine". Cephalalgia. 26 (9): 1061–70. PMID 16919056. doi:10.1111/j.1468-2982.2006.01162.x.
  8. ↑ Burstein R, Cutrer MF, Yarnitsky D (2000). "The development of cutaneous allodynia during a migraine attack". Brain. 123: 1703–9. PMID 10908199. doi:10.1093/brain/123.8.1703.
  9. ↑ Strassman AM, Raymond SA, Burstein R (1996). "Sensitization of meningeal sensory neurons and the origin of headaches". Nature. 384 (6609): 560–4. Bibcode:1996Natur.384..560S. PMID 8955268. doi:10.1038/384560a0.
  10. 1 2 Lambru G; Matharu MS. (2012). "Occipital nerve stimulation in primary headache syndromes". Ther Adv Neurol Disord. 5 (1): 57–67. PMC 3251898 Freely accessible. PMID 22276076. doi:10.1177/1756285611420903.
  11. 1 2 3 Shevel E (2007). "Vascular Surgery for Chronic Migraine". Therapy. 4 (4): 451–456. doi:10.2217/14750708.4.4.451.
  12. ↑ Graham JR, Wolff HG (1938). "Mechanism of migraine headache and action of ergotamine tartrate". Arch Neurol Psychiatry. 39: 737–763. doi:10.1001/archneurpsyc.1938.02270040093005.
  13. ↑ Guyuron B; Varghai A; Michelow BJ; Thomas T; Davis J. (2000). "Corrugator supercilii muscle resection and migraine headaches". Plast Reconstr Surg. 106 (2): 429–34. PMID 10946944. doi:10.1097/00006534-200008000-00030.
  14. ↑ Mosser, W.; Guyuron, B.; Janis, E.; Rohrich, J. (Feb 2004). "The Anatomy of the Greater Occipital Nerve: Implications for the Etiology of Migraine Headaches". Plastic and Reconstructive Surgery. 113 (2): 693–697; discussion 697–700. ISSN 0032-1052. PMID 14758238. doi:10.1097/01.PRS.0000101502.22727.5D.
  15. 1 2 3 Guyuron, B. K.; Kriegler, J. S.; Davis, J.; Amini, S. B. (Jan 2005). "Comprehensive surgical treatment of migraine headaches". Plastic and Reconstructive Surgery. 115 (1): 1–9. PMID 15622223. doi:10.1097/01.PRS.0000145631.20901.84.
  16. ↑ Poggi, T.; Grizzell, E.; Helmer, D. (Jul 2008). "Confirmation of Surgical Decompression to Relieve Migraine Headaches". Plastic and Reconstructive Surgery. 122 (1): 115–122; discussion 122–4. ISSN 0032-1052. PMID 18594393. doi:10.1097/PRS.0b013e31817742da.
  17. 1 2 3 4 5 Schwedt, T. J. (2009). "The Migraine Association with Cardiac Anomalies, Cardiovascular Disease, and Stroke". Neurologic Clinics. 27 (2): 513–523. PMC 2696390 Freely accessible. PMID 19289229. doi:10.1016/j.ncl.2008.11.006.
  18. 1 2 3 Waters, Jen (31 Jul 2007). "Easing Migraines.; Drugs, surgery help some; heart defect role studied". Washington Times. Washington, D.C. pp. B01.
  19. 1 2 3 Post, M. C.; Luermans, J.; Plokker, H.; Budts, W. (Jan 2007). "Patent foramen ovale and migraine". Catheterization and Cardiovascular Interventions. 69 (1): 9–9. ISSN 1522-1946. PMID 17143907. doi:10.1002/ccd.20931.
  20. ↑ Wilmshurst, T.; Pearson, J.; Nightingale, S.; Walsh, P.; Morrison, L. (Nov 2004). "Inheritance of persistent foramen ovale and atrial septal defects and the relation to familial migraine with aura". Heart (British Cardiac Society). 90 (11): 1315–1320. ISSN 1355-6037. PMC 1768524 Freely accessible. PMID 15486131. doi:10.1136/hrt.2003.025700.
  21. ↑ Rigatelli G; Cardaioli P; Giordan M; Dell'Avvocata F; Braggion G; Chianaglia M; Roncon L. (2009). "Transcatheter interatrial shunt closure as a cure for migraine: can it be justified by paradoxical embolism-risk-driven criteria?". Am J Med Sci. 337 (3): 179–81. PMID 19301452. doi:10.1097/maj.0b013e31818599a7.
  22. ↑ Garg P; Servoss SJ; Wu JC; Bajwa ZH; Selim MH; Dineen A; Kuntz RE; Cook EF; Mauri L. (2010). "Lack of association between migraine headache and patent foramen ovale: results of a case-control study". Circulation. 121 (12): 1406–12. PMID 20231534. doi:10.1161/CIRCULATIONAHA.109.895110.
  23. ↑ Collins, Lois M. (October 3, 2007). "Utah company's new stent may help repair heart defects". Deseret News. Salt Lake City, Utah, United States. pp. E1.
  24. ↑ "Patent Foramen Ovale". Cleveland Clinic. Cleveland Clinic. August 2009.
  25. 1 2 Sharifi, M.; Dehghani, M.; Mehdipour, M.; Al-Bustami, O.; Emrani, F.; Burks, J. (Jun 2005). "Intense Migraines Secondary to Percutaneous Closure of Atrial Septal Defects". Journal of Interventional Cardiology. 18 (3): 181–183. ISSN 0896-4327. PMID 15966922. doi:10.1111/j.1540-8183.2005.04068.x.
  26. ↑ Schwerzmann, M.; Wiher, S.; Nedeltchev, K.; Mattle, H. P.; Wahl, A.; Seiler, C.; Meier, B.; Windecker, S. (Apr 2004). "Percutaneous closure of patent foramen ovale reduces the frequency of migraine attacks". Neurology. 62 (8): 1399–1401. ISSN 0028-3878. PMID 15111681. doi:10.1212/01.WNL.0000120677.64217.A9.
  27. ↑ Harder, B. (19 February 2005). "Against the Migraine". Science News. Society for Science & the Public. 167 (8): 119–120. ISSN 0036-8423. JSTOR 4016110. doi:10.2307/4016110.
  28. ↑ Schürks, M.; Diener, C. (Jan 2009). "Closure of patent foramen ovale in the prevention of migraine: not enough evidence in favor". Nature Clinical Practice Neurology. 5 (1): 22–23. ISSN 1745-834X. PMID 19048002. doi:10.1038/ncpneuro0971.
  29. ↑ Sarens, T.; Herroelen, L.; Van Deyk, K.; Budts, W. (Jan 2009). "Patent foramen ovale closure and migraine: Are we following the wrong pathway?". Journal of Neurology. 256 (1): 143–144. ISSN 0340-5354. PMID 19172218. doi:10.1007/s00415-009-0126-9.
  30. ↑ Bhindi, R.; Ormerod, O. (Apr 2008). "Rebound increase in migraines following PFO closure". Catheterization and Cardiovascular Interventions. 71 (5): 719. ISSN 1522-1946. PMID 18360874. doi:10.1002/ccd.21394.
  31. ↑ Wilmshurst, T.; Nightingale, S.; Walsh, P.; Morrison, L. (Sep 2005). "Clopidogrel reduces migraine with aura after transcatheter closure of persistent foramen ovale and atrial septal defects". Heart. 91 (9): 1173–1175. ISSN 1355-6037. PMC 1769061 Freely accessible. PMID 16103551. doi:10.1136/hrt.2004.047746.
  32. 1 2 Joel R Saper; David W Dodick; Stephen D Silberstein; Sally McCarville; Mark Sun; Peter J Goadsby (2011). "Occipital nerve stimulation for the treatment of intractable chronic migraine headache: ONSTIM feasibility study". Cephalalgia. 31 (3): 271–285. PMC 3057439 Freely accessible. PMID 20861241. doi:10.1177/0333102410381142.
  33. ↑ Weiner RL, Reed KL (1999). "Peripheral neurostimulation for control of intractable occipital neuralgia.". Neuromodulation. 2 (3): 217–21. PMID 22151211. doi:10.1046/j.1525-1403.1999.00217.x.
  34. ↑ Trentman TL, Zimmerman RS, Dodick DW, Dormer CL, Vargas BB (2010). "Occipital nerve stimulator placement under general anesthesia: initial experience with 5 cases and review of the literature". J Neurosurg Anesthesiol. 22 (2): 158–62. PMID 19816202. doi:10.1097/ANA.0b013e3181c04693.
  35. ↑ Jensen K, Bulow P, Hansen H (1985). "Experimental toothclenching in common migraine". Cephalalgia. 5 (4): 245–251. PMID 4084979. doi:10.1046/j.1468-2982.1985.0504245.x.
  36. ↑ Fernández-de-Las-Peñas C; Cuadrado ML; Arendt-Nielsen L; Pareja JA. (2008). "Side-to-side differences in pressure pain thresholds and pericranial muscle tenderness in strictly unilateral migraine". Eur J Neurol. 15 (2): 162–8. PMID 18093151. doi:10.1111/j.1468-1331.2007.02020.x.
  37. ↑ Fernández-de-Las-Peñas C, Cuadrado ML, Pareja JA (2006). "Myofascial trigger points, neck mobility and forward head posture in unilateral migraine". Cephalalgia. 26 (9): 1061–70. PMID 16919056. doi:10.1111/j.1468-2982.2006.01162.x.
  38. ↑ Lapeer GL (1988). "Reduction of the painful sequelae of migraine headache by use of the occlusal diagnostic splint: an hypothesis". Cranio. 6 (1): 82–6. PMID 3282687.
  39. ↑ Quayle AA, Gray RJ, Metcalfe RJ, Guthrie E, Wastell D (1990). "Soft occlusal splint therapy in the treatment of migraine and other headaches". J Dent. 18 (3): 123–9. PMID 2401762. doi:10.1016/0300-5712(90)90048-J.
  40. ↑ Lamey PJ, Barclay SC (1987). "Clinical effectiveness of occlusal splint therapy in patients with classical migraine". Scott Med J. 32 (1): 11–2. PMID 3563468.
  41. ↑ Shevel E (2005). "Craniomandibular muscles, intraoral orthoses and migraine". Expert Rev Neurother. 5 (3): 371–377. PMID 15938670. doi:10.1586/14737175.5.3.371.
  42. ↑ Shankland WE 2nd (2001). "Migraine and tension-type headache reduction through pericranial muscular suppression: a preliminary report". Cranio. 19 (4): 269–78. PMID 11725851.
  43. ↑ Durand, Vincent Mark; Barlow, David (2009). Abnormal psychology: an integrative approach. Belmont, CA: Wadsworth Cengage Learning. pp. 331. ISBN 0-495-09556-7.
  44. ↑ "What is biofeedback?". Association for Applied Psychophysiology and Biofeedback. 2008-05-18. Retrieved 2010-02-22.
  45. ↑ deCharms RC, Maeda F, Glover GH, et al. (December 2005). "Control over brain activation and pain learned by using real-time functional MRI". Proc. Natl. Acad. Sci. U.S.A. 102 (51): 18626–31. Bibcode:2005PNAS..10218626D. PMC 1311906 Freely accessible. PMID 16352728. doi:10.1073/pnas.0505210102.
  46. ↑ Vasudeva S, Claggett AL, Tietjen GE, McGrady AV (2003). "Biofeedback-assisted relaxation in migraine headache: relationship to cerebral blood flow velocity in the middle cerebral artery". Headache. 43 (3): 245–50. PMID 12603643. doi:10.1046/j.1526-4610.2003.03048.x.
  47. ↑ McGrady A; Wauquier A; McNeil A; Gerard G. (1994). "Effect of biofeedback-assisted relaxation on migraine headache and changes in cerebral blood flow velocity in the middle cerebral artery". Headache. 34 (7): 424–8. PMID 7928327. doi:10.1111/j.1526-4610.1994.hed3407424.x.
  48. ↑ Walsh, Sandy (October 15, 2010). "FDA approves Botox to treat chronic migraine". FDA Press Releases. Retrieved 2010-10-15.
  49. ↑ Watkins, Tom (October 15, 2010). "FDA approves Botox as migraine preventative". CNN (US).
  50. ↑ Dodick, DW; Turkel, CC; DeGryse, RE; Aurora, SK; Silberstein, SD; Lipton, RB; Diener, HC; Brin, MF; PREEMPT Chronic Migraine Study, Group (June 2010). "OnabotulinumtoxinA for treatment of chronic migraine: pooled results from the double-blind, randomized, placebo-controlled phases of the PREEMPT clinical program". Headache. 50 (6): 921–36. PMID 20487038. doi:10.1111/j.1526-4610.2010.01678.x.
  51. ↑ Rabkin R; Stables DP; Levin NW; Suzman MM. (1966). "The prophylactic value of propranolol in angina pectoris". Am J Cardiol. 18 (3): 370–83. PMID 4958813. doi:10.1016/0002-9149(66)90056-7.
  52. 1 2 3 Silberstein SD, Saper JR, Freitag FG (2001). "Migraine: Diagnosis and Treatment". Wolff’s Headache and other head pain. New York: Oxford University Press. pp. 176–198.
  53. ↑ Cruickshank JM (2010). "Beta-blockers and heart failure". Indian Heart J. 62 (2): 101–10. PMID 21180298.
  54. ↑ "Amitriptyline: Side Effects, Dosage, Uses". healthline.com.
  55. ↑ Klapper J (1997). "Divalproex sodium in migraine prophylaxis: a dose-controlled study". Cephalalgia. 17 (2): 103–8. PMID 9137847. doi:10.1046/j.1468-2982.1997.1702103.x.
  56. ↑ Mathew NT, Saper JR, Silberstein SD, Rankin L, Markley HG, Solomon S, Rapoport AM, Silber CJ, Deaton RL (1995). "Migraine prophylaxis with divalproex". Arch Neurol. 52 (3): 281–6. PMID 7872882. doi:10.1001/archneur.1995.00540270077022.
  57. ↑ Hering R, Kuritzky A (1992). "Sodium valproate in the prophylactic treatment of migraine: a double-blind study versus placebo". Cephalalgia. 12 (2): 81–4. PMID 1576648. doi:10.1046/j.1468-2982.1992.1202081.x.
  58. ↑ Jensen R; Brinck T; Olesen J. (1994). "Sodium valproate has a prophylactic effect in migraine without aura: a triple-blind, placebo-controlled crossover study". Neurology. 44 (4): 647–51. PMID 8164818. doi:10.1212/wnl.44.4.647.
  59. ↑ Silberstein SD, Collins SD (1999). "Safety of divalproex sodium in migraine prophylaxis: an open-label, long-term study. Long-term Safety of Depakote in Headache Prophylaxis Study Group". Headache. 39 (9): 633–43. PMID 11284461. doi:10.1046/j.1526-4610.1999.3909633.x.
  60. ↑ Mathew NT (2006). "The prophylactic treatment of chronic daily headache". Headache. 46 (10): 1552–64. PMID 17115988. doi:10.1111/j.1526-4610.2006.00621.x.
  61. ↑ Silberstein SD, Lipton RB, Dodick DW, Freitag FG, Ramadan N, Mathew N, Brandes JL, Bigal M, Saper J, Ascher S, Jordan DM, Greenberg SJ, Hulihan J; Topiramate Chronic Migraine Study Group (2007). "Efficacy and safety of topiramate for the treatment of chronic migraine: a randomized, double-blind, placebo-controlled trial". Headache. 47 (2): 170–80. PMID 17300356. doi:10.1111/j.1526-4610.2006.00684.x.
  62. 1 2 Bartleson JD, Cutrer FM (2010). "Migraine update. Diagnosis and treatment". Minn Med. 93 (5): 36–41. PMID 20572569.
  63. 1 2 Headache Classification Subcommittee of the International Headache Society (2004). "The International Classification of Headache Disorders: 2nd edition". Cephalalgia. 24 (Suppl 1): 9–160. PMID 14979299. doi:10.1111/j.1468-2982.2004.00653.x. as PDF Archived 2010-03-31 at the Wayback Machine.
  64. ↑ "Sumatriptan (oral route of administration) for acute migraine attacks in adults". Reviews. doi:10.1002/14651858.CD008615.pub2.
  65. 1 2 3 4 5 6 7 8 9 Gilmore, B; Michael, M (2011-02-01). "Treatment of acute migraine headache.". American family physician. 83 (3): 271–80. PMID 21302868.
  66. 1 2 Rabbie, Roy; Derry, Sheena; Moore, R. Andrew (2013-04-30). "Ibuprofen with or without an antiemetic for acute migraine headaches in adults". The Cochrane Database of Systematic Reviews (4): CD008039. ISSN 1469-493X. PMID 23633348. doi:10.1002/14651858.CD008039.pub3.
  67. ↑ Derry, Sheena; Rabbie, Roy; Moore, R. Andrew (2013-04-30). "Diclofenac with or without an antiemetic for acute migraine headaches in adults". The Cochrane Database of Systematic Reviews (4): CD008783. ISSN 1469-493X. PMID 23633360. doi:10.1002/14651858.CD008783.pub3.
  68. ↑ Green, Ga (2001). "Understanding NSAIDs: from aspirin to COX-2". Clinical cornerstone. 3 (5): 50–60. ISSN 1098-3597. PMID 11464731. doi:10.1016/S1098-3597(01)90069-9.
  69. ↑ Kirthi, Varo; Derry, Sheena; Moore, R. Andrew (2013-04-30). "Aspirin with or without an antiemetic for acute migraine headaches in adults". The Cochrane Database of Systematic Reviews (4): CD008041. ISSN 1469-493X. PMID 23633350. doi:10.1002/14651858.CD008041.pub3.
  70. ↑ Raithel M, Baenkler HW, Naegel A, et al. (September 2005). "Significance of salicylate intolerance in diseases of the lower gastrointestinal tract" (PDF). J. Physiol. Pharmacol. 56 Suppl 5: 89–102. PMID 16247191.
  71. ↑ Senna GE, Andri G, Dama AR, Mezzelani P, Andri L (1995). "Tolerability of imidazole salycilate in aspirin-sensitive patients". Allergy Proc. 16 (5): 251–4. PMID 8566739. doi:10.2500/108854195778702675.
  72. ↑ "PDR Guide to Over the Counter (OTC) Drugs". Archived from the original on 10 April 2008. Retrieved 28 April 2008.
  73. ↑ Frank B. Livingstone. (1985). Frequencies of hemoglobin variants: thalassemia, the glucose-6-phosphate dehydrogenase deficiency, G6PD variants, and ovalocytosis in human populations. Oxford University Press. ISBN 0-19-503634-4. Retrieved 7 May 2011.
  74. ↑ "Dengue and Dengue Hemorrhagic Fever: Information for Health Care Practitioners". Archived from the original on 17 March 2008. Retrieved 28 April 2008.
  75. ↑ Derry S, Moore RA, McQuay HJ (2010). Moore, Maura, ed. "Paracetamol (acetaminophen) with or without an antiemetic for acute migraine headaches in adults". Cochrane Database Syst Rev. 11 (11): CD008040. PMID 21069700. doi:10.1002/14651858.CD008040.pub2.
  76. 1 2 Hughes, John (2008). Pain Management: From Basics to Clinical Practice. Elsevier Health Sciences. ISBN 9780443103360.
  77. 1 2 Sarg, Michael; Ann D Gross; Roberta Altman (2007). The Cancer Dictionary. Infobase Publishing. ISBN 978081606 4113.
  78. ↑ Ebrahimi, Sedigheh; Soheil Ashkani Esfahani; Hamid Reza Ghaffarian; Mahsima Khoshneviszade (2010). "Comparison of efficacy and safety of acetaminophen and ibuprofen administration as single dose to reduce fever in children.". Iranian Journal of Pediatrics. 20 (4): 500–501.
  79. ↑ García Rodríguez LA, Hernández-Díaz S (December 15, 2000). "The risk of upper gastrointestinal complications associated with nonsteroidal anti-inflammatory drugs, glucocorticoids, acetaminophen, and combinations of these agents". Arthritis Research & Therapy. 3 (2): 98–101. PMC 128885 Freely accessible. PMID 11178116. doi:10.1186/ar146.
  80. ↑ "Painkillers 'cause kidney damage'". BBC News. November 23, 2003. Retrieved March 27, 2010.
  81. ↑ Dukes, MNG; Jeffrey K Aronson (2000). Meyler's Side Effects of Drugs, Vol XIV. Elsevier. ISBN 9780444500939.
  82. ↑ Rudolph AM (1981). "Effects of aspirin and acetaminophen in pregnancy and in the newborn". Arch. Intern. Med. 141 (3 Spec No): 358–63. PMID 7469626. doi:10.1001/archinte.141.3.358.
  83. ↑ Leffers, H; et al. (2010). "Intrauterine exposure to mild analgesics is a risk factor for development of male reproductive disorders in human and rat". Human Reproduction. 25 (1): 235–244. doi:10.1093/humrep/deq382.
  84. ↑ "Could Tylenol Ease Emotional Pain?". Evergreen Magazine. Retrieved 17 August 2014.
  85. ↑ Lesko SM, Mitchell AA (1999). "The safety of acetaminophen and ibuprofen among children younger than two years old". Pediatrics. 104 (4): e39. PMID 10506264. doi:10.1542/peds.104.4.e39.
  86. ↑ Beasley, Richard; Clayton, Tadd; Crane, Julian; von Mutius, Erika; Lai, Christopher; Montefort, Stephen; Stewart, Alistair (2008). "Association between paracetamol use in infancy and childhood, and risk of asthma, rhino conjunctivitis, and eczema in children aged 6–7 years: analysis from Phase Three of the ISAAC programme". The Lancet. 372 (9643): 1039–1048. PMID 18805332. doi:10.1016/S0140-6736(08)61445-2.
  87. ↑ The Lancet (2008). "Asthma: still more questions than answers". The Lancet. 372 (9643): 1009–1009. doi:10.1016/S0140-6736(08)61414-2.
  88. ↑ Barr, R. G. (2008). "Does paracetamol cause asthma in children? Time to remove the guesswork". The Lancet. 372 (9643): 1011–1012. PMID 18805311. doi:10.1016/S0140-6736(08)61417-8.
  89. ↑ Lawyer, A. B. (2009). "Paracetamol as a risk factor for allergic disorders". The Lancet. 373 (9658): 121–121. doi:10.1016/S0140-6736(09)60032-5.
  90. ↑ Lowe, A.; Abramson, M.; Dharmage, S.; Allen, K. (2009). "Paracetamol as a risk factor for allergic disorders". The Lancet. 373 (9658): 120–120. doi:10.1016/S0140-6736(09)60030-1.
  91. ↑ Lawrence, J.; Moore, E.; Port, L.; Danchin, M.; Connell, T. (2009). "Paracetamol as a risk factor for allergic disorders". The Lancet. 373 (9658): 119–119. doi:10.1016/S0140-6736(09)60029-5.
  92. ↑ Singh, M. (2009). "Paracetamol as a risk factor for allergic disorders". The Lancet. 373 (9658): 119–119. doi:10.1016/S0140-6736(09)60028-3.
  93. ↑ Beasley, R.; Clayton, T.; Crane, J.; Von Mutius, E.; Lai, C. K. (2009). "Paracetamol as a risk factor for allergic disorders – Authors' reply". The Lancet. 373 (9658): 120–121. doi:10.1016/S0140-6736(09)60031-3.
  94. ↑ Medicines and Healthcare products Regulatory Agency; Commission on Human Medicines (2008). "Paracetamol use in infancy: no strong evidence for asthma link". Drug Safety Update. 2 (4): 9. Retrieved May 1, 2009.
  95. ↑ Roland B. Walter; Filippo Milano; Theodore M. Brasky; Emily White (2011). "Long-Term Use of Acetaminophen, Aspirin, and Other Nonsteroidal Anti-Inflammatory Drugs and Risk of Hematologic Malignancies: Results From the Prospective Vitamins and Lifestyle (VITAL) Study". Journal of Clinical Oncology. 29 (17): 2424–31. PMC 3107756 Freely accessible. PMID 21555699. doi:10.1200/JCO.2011.34.6346.
  96. ↑ Johnston MM, Rapoport AM (August 2010). "Triptans for the management of migraine". Drugs. 70 (12): 1505–18. PMID 20687618. doi:10.2165/11537990-000000000-00000.
  97. ↑ Tepper Stewart J., S. J.; Tepper, Deborah E. (April 2010). "Breaking the cycle of medication overuse headache". Cleveland Clinic Journal of Medicine. 77 (4): 236–42. PMID 20360117. doi:10.3949/ccjm.77a.09147.
  98. ↑ Kelley, NE; Tepper, DE (January 2012). "Rescue therapy for acute migraine, part 1: triptans, dihydroergotamine, and magnesium.". Headache. 52 (1): 114–28. PMID 22211870. doi:10.1111/j.1526-4610.2011.02062.x.
  99. ↑ al.], ed. Jes Olesen, ... [et (2006). The headaches. (3. ed.). Philadelphia: Lippincott Williams & Wilkins. p. 516. ISBN 9780781754002.
  100. 1 2 Morren, JA; Galvez-Jimenez, N (December 2010). "Where is dihydroergotamine mesylate in the changing landscape of migraine therapy?". Expert opinion on pharmacotherapy. 11 (18): 3085–93. PMID 21080856. doi:10.1517/14656566.2010.533839.
  101. ↑ Silberstein SD, Young WB (1995). "Safety and efficacy of ergotamine tartrate and dihydroergotamine in the treatment of migraine and status migrainosus. Working Panel of the Headache and Facial Pain Section of the American Academy of Neurology". Neurology. 45 (3 Pt 1): 577–84. PMID 7898722. doi:10.1212/wnl.45.3.577.
  102. ↑ Colman I, Friedman BW, Brown MD, et al. (June 2008). "Parenteral dexamethasone for acute severe migraine headache: meta-analysis of randomized controlled trials for preventing recurrence". BMJ. 336 (7657): 1359–61. PMC 2427093 Freely accessible. PMID 18541610. doi:10.1136/bmj.39566.806725.BE.
  103. ↑ Posadzki, P; Ernst, E (June 2011). "Spinal manipulations for the treatment of migraine: a systematic review of randomized clinical trials.". Cephalalgia : an international journal of headache. 31 (8): 964–70. PMID 21511952. doi:10.1177/0333102411405226.
This article is issued from Wikipedia. The text is licensed under Creative Commons - Attribution - Sharealike. Additional terms may apply for the media files.