Migraine overview

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Overview

Historical Perspective

Classification

Pathophysiology

Triggers

Differentiating Migraine from other Diseases

Epidemiology and Demographics

Risk Factors

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

CT

MRI

Treatment

Medical Therapy

Secondary Prevention

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Migraine is a neurological disease best known for severe headaches that are its most salient symptom.[1][2][3]. Usually migraine causes episodes of severe or moderate headache (which is often one-sided and pulsating) lasting between several hours to three days, accompanied by gastrointestinal upsets, such as nausea and vomiting, and a heightened sensitivity to bright lights (photophobia) and noise (phonophobia). Approximately one third of people who experience migraine get a preceding aura.[4] Migraines' secondary characteristics are inconsistent. Triggers precipitating a particular episode of migraine vary widely. The efficacy of the simplest treatment, applying warmth or coolness to the affected area of the head, varies between persons, sometimes worsening the migraine.[5] A particular migraine rescue drug may sometimes work and sometimes not work in the same patient. Some migraine types don't have pain or may manifest symptoms in parts of the body other than the head. Available evidence suggests that migraine pain is one symptom of several to many disorders of the serotonergic control system, a dual hormone-neurotransmitter with numerous types of receptors. Two disorders — classic migraine with aura (MA, STG) and common migraine without aura (MO, STG) — have been shown to have a genetic factor.[6] Studies on twins show that genes have a 60 to 65% influence on the development of migraine[7][8]. Additional migraine types are suspected and could be proven to be genetic. Migraine understood as several or many disorders could explain the inconsistencies, especially if a single patient has more than one genetic type. However, still other migraine types might be functionally acquired due to hormone organ disease or injury. Three quarters of adult migraine patients are female, although pre-pubertal migraine affects approximately equal numbers of boys and girls. This reveals the strong correlation to hormonal cycling and hormonal-related causes or triggers. Hormonal migraine is a likely consequence of periodically falling hormone levels causing reduction in protein biosynthesis of metabolic components including intestinal tract serotonin.

Historical Perspective

The word migraine is French in origin and comes from the Greek hemicrania, as does the Old English term megrim. Literally, hemicrania means "half (the) head".

Classification

Migraines can be divided in three different types: migraine without aura, typical migraine with aura and probable migraine without aura. Migraines are often underdiagnosed and misdiagnosed.[9][10] The diagnostic criteria for migraine include recurrent headache disorder manifesting in attacks that fulfill typical characteristics in a context of normal clinical examination that rules out other diagnoses. Migraine with aura is a recurrent disorder manifesting in attacks of reversible focal neurological symptoms that usually develop gradually over 5–20 minutes and last for less than 60 minutes.

Pathophysiology

Migraines are believed to be a neurovascular disorder[11][12] with evidence supporting its mechanisms starting within the brain and then spreading to the blood vessels.[13] Migraine begins by neuronal changes leading to the activation of the brainstem and diencephalic nuclei and subsequent dilatation of the large cranial and proximal intracranial vessels.[11] Some researchers feel neuronal mechanisms play a greater role,[14] while others feel blood vessels play the key role.[15] Others feel both are likely important.[16] High levels of the neurotransmitter serotonin, also known as 5-hydroxytryptamine, are believed to be involved.[13]

Triggers

A migraine trigger is any factor that, on exposure or withdrawal, leads to the development of an acute migraine headache. Triggers may be categorized as behavioral, environmental, infectious, dietary, chemical, or hormonal.In the medical literature, these factors are known as precipitants. Many people report that one or more dietary, physical, hormonal, emotional, or environmental factors precipitate their migraines. The most-often reported triggers include: pesticides (sprayed fruits/vegetables), perfumes or fragrances (30% of sufferers) stress, over-illumination or glare, alcohol, foods, too much or too little sleep, and weather. Some women experience migraines in conjunction with monthly menstrual cycles. Sometimes the migraine occurs with no apparent "cause". The trigger theory supposes that exposure to various environmental factors precipitates, or triggers, individual migraine episodes. Migraine patients have long been advised to try to identify personal headache triggers by looking for associations between their headaches and various suspected trigger factors. Patients are urged to keep a "headache diary" in which to note what they eat and when they get a headache, to look for correlations, and to try to avoid headache by avoiding factors they identify as triggers. Typically this advice is accompanied by a list of trigger factors.

Differential Diagnosis

ther conditions that can cause similar symptoms to a migraine headache include temporal arteritis, cluster headaches, acute glaucoma, meningitis and subarachnoid hemorrhage.[17] Temporal arteritis typically occurs in people over 50 years old and presents with tenderness over the temple, cluster headaches presents with one-sided nose stuffiness, tears and severe pain around the orbits, acute glaucoma is associated with vision problems, meningitis with fevers, and subaracchnoid hemorrhage with a very fast onset.[17] Tension headaches typically occur on both sides, are not pounding, and are less disabling.[17]

Epidemiology and Demographics

Migraine is widespread in the population. The majority of migraine (as it is referred to commonly) is actually mixed Headache. In the U.S., 18% of women and 6% of men report having had at least one migraine episode in the previous year[18] According to reports, 10% of people have been diagnosed with migraine and 5% have migraine but have not been diagnosed, with seriousness varying from a rare annoyance to a life-threatening and/or daily experience.

Natural History, Complications and Prognosis

Migraine with aura is associated with increased risk of subsequent stroke, a risk further amplified among females, smokers, patients on OCP and patients suffering from frequent migraine episodes. Despite the elevated risk of stroke among patients with migraine associated with aura, the incidence of stroke in this category of patients remain low particularly in young adults. Patients with migraine not associated with aura are not at an increased risk of stroke compared to the general population.[19]

Diagnosis

History and Symptoms

The signs and symptoms of migraine vary among patients. Therefore, what a patient experiences before, during and after an attack cannot be defined exactly. The four phases of a migraine attack listed below are common but not necessarily experienced by all migraine sufferers. Additionally, the phases experienced and the symptoms experienced during them can vary from one migraine attack to another in the same patient: (1) the prodrome, which occurs hours or days before the headache, (2) the aura, which immediately precedes the headache, (3) the pain phase, also known as headache phase and (4) the postdrome phase.

Physical Examination

The majority of patients with headaches complaints have a normal physical and neurological examination. Signs suggestive of a serious cause of headache, such as systemic symptoms, focal neurological signs, seizures or impairment of the level of consciousness should be ruled out.

Laboratory Findings

Migraine is a clinical diagnosis that does not require any laboratory tests. Laboratory tests can be ordered to rule out any suspected coexistent metabolic problems or to determine the baseline status of the patient before initiation of migraine therapy. When the headache is suggestive of meningitis, lumbar puncture should be done and an appropriate management of meningitis should be initiated.

CT

Neuroimaging is not necessary in patients with a clinical diagnosis of migraine. Head images such CT and MRI might be needed to rule out other suspected possible causes of headache. It is suggested to order a CT scan without contrast among patients with an unusual headache.

MRI

MRI is indicated when there is suspicion of posterior fossa lesions and cerebrospinal fluid (CSF) leak. Magnetic resonance angiography (MRA) and magnetic resonance venography (MRV) are indicated in arterial or venous lesions.

Treatment

Medical Therapy

Conventional treatment focuses on three areas: trigger avoidance, symptomatic control, and preventive drugs. Migraine sufferers usually develop their own coping mechanisms for the pain of a migraine attack. Medical therapy can be divided into two treatment regimens: non-specific treatment such as non-steroidal anti-inflammatory drug and analgesics and specific treatment such as triptans and ergot derivatives.[20] Patients who experience migraines often find that the recommended treatments are not 100% effective at preventing migraines, and sometimes may not be effective at all.

Secondary Prevention

Following treatment of an acute migraine, it is important to consider preventive measures. Preventive measures include medications such as NSAIDs, amitryptilline, devalproex, valproic acid, propranolol, timolol and topiramate among others. If the preventive measure is not effective after two to three months, the dose of the medication should be adjusted. If no improvement is noted, another first line therapy or a combination of two first line therapies should be initiated.[21][22]

Cost-Effectiveness of Therapy

Treatments are typically expensive. Periodic or unpredictable disability can cause impoverishment due to patients' inability to work enough or to hold a job at all.

References

  1. "NINDS Migraine Information Page". National Institute of Neurological Disorders and Stroke, National Institutes of Health. Retrieved 2007-06-25. 
  2. "Advances in Migraine Prophylaxis: Current State of the Art and Future Prospects" (PDF). National Headache Foundation (CME monograph). Retrieved 2007-06-25. 
  3. "Migraine: diagnosis, management, and new treatment options, Gallagher RM, Cutrer FM, University of Medicine and Dentistry of New Jersey, School of Medicine, Stratford, USA". The American Journal of Managed Care, PMID: 11859906. Retrieved 2007-06-25. 
  4. "Guidelines for all healthcare professionals in the diagnosis and management of migraine, tension-type, cluster and medication-overuse headache, Jan 2007,British Association for the Study of Headache" (PDF). Retrieved 2007-06-25. 
  5. The Essential Book of Herbal Medicine (also known as Out of the Earth) by Simon Y. Mills, Viking Arkana, 1994(1991). Mills is former president of the UK licensed medical herbalists association. Mills' point is the traditional classification of migraines into "hot" and "cold" types, meaning that one's migraine type is determined by whether one's pain is reduced by hot/warm versus cold water.
  6. Ogilvie AD, Russell MB, Dhall P, et al. "Altered allelic distributions of the serotonin transporter gene in migraine without aura and migraine with aura." Cephalalgia. 1998 Jan;18(1):23-6. PMID 9601620
  7. Ulrich V, Gervil M, Kyvik KO, Olesen J, Russell MB (1999). "The inheritance of migraine with aura estimated by means of structural equation modelling". Journal of Medical Genetics. 36 (3): 225–7. PMC 1734315Freely accessible. PMID 10204850. Retrieved 2012-08-30. 
  8. Gervil M, Ulrich V, Kaprio J, Olesen J, Russell MB (1999). "The relative role of genetic and environmental factors in migraine without aura". Neurology. 53 (5): 995–9. PMID 10496258. Retrieved 2012-08-30. 
  9. Lipton RB, Stewart WF, Celentano DD, Reed ML (1992). "Undiagnosed migraine headaches. A comparison of symptom-based and reported physician diagnosis". Arch. Intern. Med. 152 (6): 1273–8. PMID 1599358. 
  10. Schreiber CP, Hutchinson S, Webster CJ, Ames M, Richardson MS, Powers C (2004). "Prevalence of migraine in patients with a history of self-reported or physician-diagnosed "sinus" headache". Arch. Intern. Med. 164 (16): 1769–72. PMID 15364670. doi:10.1001/archinte.164.16.1769. 
  11. 11.0 11.1 Goadsby PJ, Lipton RB, Ferrari MD (2002). "Migraine--current understanding and treatment.". N Engl J Med. 346 (4): 257–70. PMID 11807151. doi:10.1056/NEJMra010917. 
  12. Bartleson JD, Cutrer FM (May 2010). "Migraine update. Diagnosis and treatment". Minn Med. 93 (5): 36–41. PMID 20572569. 
  13. 13.0 13.1 The Headaches Chp. 29, Pg. 276
  14. Goadsby, PJ (January 2009). "The vascular theory of migraine – a great story wrecked by the facts". Brain : a journal of neurology. 132 (Pt 1): 6–7. PMID 19098031. doi:10.1093/brain/awn321. 
  15. Brennan, KC (June 2010). "An update on the blood vessel in migraine". Current Opinion in Neurology. 23 (3): 266–74. PMID 20216215. doi:10.1097/WCO.0b013e32833821c1. 
  16. Dodick, DW (April 2008). "Examining the essence of migraine – is it the blood vessel or the brain? A debate". Headache. 48 (4): 661–7. PMID 18377395. doi:10.1111/j.1526-4610.2008.01079.x. 
  17. 17.0 17.1 17.2 Gilmore B, Michael M (2011). "Treatment of acute migraine headache.". Am Fam Physician. 83 (3): 271–80. PMID 21302868. 
  18. . Silberstein S. "Migraine". Lancet 2004;363:381-391
  19. Kurth T, Chabriat H, Bousser MG (2012). "Migraine and stroke: a complex association with clinical implications.". Lancet Neurol. 11 (1): 92–100. PMID 22172624. doi:10.1016/S1474-4422(11)70266-6. 
  20. Lanteri-Minet M, Valade D, Geraud G, Lucas C, Donnet A (2014). "Revised French guidelines for the diagnosis and management of migraine in adults and children.". J Headache Pain. 15 (1): 2. PMID 24400971. doi:10.1186/1129-2377-15-2. 
  21. Silberstein SD, Holland S, Freitag F, Dodick DW, Argoff C, Ashman E; et al. (2012). "Evidence-based guideline update: pharmacologic treatment for episodic migraine prevention in adults: report of the Quality Standards Subcommittee of the American Academy of Neurology and the American Headache Society.". Neurology. 78 (17): 1337–45. PMC 3335452Freely accessible. PMID 22529202. doi:10.1212/WNL.0b013e3182535d20. 
  22. Modi S, Lowder DM (2006). "Medications for migraine prophylaxis.". Am Fam Physician. 73 (1): 72–8. PMID 16417067. 

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