Migraine is a genetically influenced complex disorder characterized by episodes of moderate-to-severe headache, most often unilateral and generally associated with nausea and increased sensitivity to light and sound. The word migraine is derived from the Greek word "hemikrania" that later was converted into Latin as "hemigranea." The French translation of such a term is "migraine."[1] Migraine is a common cause of disability and loss of work. Migraine attacks are a complex brain event that unfolds over hours to days, in a recurrent matter. The most common type of migraine is without aura (75% of cases).
Migraine can be classified in subtypes, according to the headache classification committee of the International Headache Society:[2]
Genetics and Inheritance
Migraine has a strong genetic component. The risk of migraines in ill relatives is three times greater than that of relatives of non-ill subjects, but there has not been any pattern of inheritance identified.[3][4] The genetic basis of migraine is complex, and it is uncertain which loci and genes are the ones implicated in the pathogenesis; it may be based on more than one genetic source at different genomic locations acting in tandem with environmental factors to bring susceptibility and the characteristics of the disease in such individuals.[5] The identification of these genes in an individual with migraines could predict the targeted prophylactic treatment.
Familial Hemiplegic Migraine
MELAS
Melas is a syndrome of mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes.
a multisystemic disorder by maternal inheritance that can present recurrent migraine headaches.[12]
CADASIL
Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy) angiopathy by autosomal dominant inheritance, caused by mutations in the NOTCH3 gene (notch receptor 3) on chromosome 19, that can present migraine with aura (prodrome in 80%) in nearly 50% of carriers.[13]
RVCL
Retinal vasculopathy with cerebral leukodystrophy is angiopathy by C-terminal frame-shift mutations in TREX1 (three prime repair exonuclease 1) presents almost 60% of the cases.[14]
HIHRATL
Hereditary infantile hemiparesis, retinal arteriolar tortuosity, and leukoencephalopathy
HERNS
Hereditary endotheliopathy with retinopathy, nephropathy, and stroke
Triggers
Withdrawn or exposed to several factors contribute to the development of migraine headaches.[15] A retrospective study found that 76% of the patients reported triggers.[16] Some of them are probable factors that contribute, while others are only possible or unproven factors.
Migraine is highly prevalent, affecting 12% of the population, attacking up to 17% of women and 6% of men each year.[17][18][19] The adjusted prevalence of migraine is highest in North America, followed by South America, Central America, Europe, Asia, and Africa. It is ranked as the second leading cause of disability worldwide.[20] Migraine tends to run in families.[17] It is consistently the fourth or fifth most common reason for emergency visits accounting for an annual 3% of all emergency visits.[21] Its prevalence increases in puberty but continues to increase until 35 to 39 years of age, decreasing later in life, especially after menopause.[18]
At first, there was a vascular theory of migraine, which explained that the headache was produced by vasodilation and aura by vasoconstriction, but this theory is not viable anymore.[22] Nowadays, the suggestions pose that multiple primary neuronal impairments lead to a series of intracranial and extracranial changes that cause migraines.[23]
The cortical spreading depression of Leão, a propagating wave of neuronal and glial depolarization that initiates a cascade, is hypothesized to cause the aura, activate trigeminal afferents, and alter the hematoencephalic barrier permeability by activating brain matrix metalloproteinases.[24] In migraine without aura, the suggestions are that cortical depression may occur in areas where depolarization is not consciously perceived, such as the cerebellum.[25] There is activation of trigeminal afferents by neuronal pannexin-1 megachannel opening and subsequent activation of Caspase-1, followed by the release of proinflammatory mediators, activation of NF-kB (nuclear factor kappa-B), and spreading of this inflammatory signal to trigeminal nerve fibers around vessels of the pia mater.[26] This causes a series of cortical, meningeal, and brainstem events, provoking inflammation in the pain-sensitive meninges that concludes in headache through central and peripheral mechanisms.[27][28] This pathway can, therefore, explain the cortical depression (which establishes the aura) and the latter prolonged activation of trigeminal nociception (which leads to headache).
The anterior structures are most innervated by the ophthalmic division of the trigeminal nerve, which could explain the pain in the anterior region of the head. There is a convergence of fibers from the upper cervical roots which originate the trigeminal nerve neurons along with the trigeminal ganglion and the trigeminal nerve at the trigeminal nucleus caudalis which can explain the anterior to the posterior distribution of pain, from where the fibers ascend to the thalamus and the sensory cortex.[29]
Neurogenic inflammation, which is based on vasodilation, edema, and plasma protein extravasation, results from nociceptor activation; in this case, the trigeminal system. It is associated with the release of substance P, calcitonin gene-related peptide, and neurokinin a; all vasoactive neuropeptides liberated by trigeminal ganglion stimulation.[30] Elevated levels of these neuropeptides have been found in the spinal fluid of chronic migraine patients.[31][32] Neurogenic inflammation can lead to sensitization, which is the process in which neurons tend to become more responsive to stimulation. This can explain some clinical symptoms of the pain and the conversion from episodic migraine to a chronic one.[33]
Serotonin, released from the brainstem serotonergic nuclei, may play a role in migraine; however, the exact role of its mechanisms remains a matter of controversy. Most likely, serotonin levels are low between attacks because it may cause a deficiency in the serotonin pain inhibition system, therefore helping the activation of the trigeminal system. It could mediate by acting directly over the cranial vessels, or in central pain control pathways, or by cortical projections of brainstem serotonergic nuclei.[34][35]
Calcitonin gene-related peptide is abundant in trigeminal ganglion neurons. It is released from the peripheral nerve and central nerve terminals as well as secreted within the trigeminal ganglion. When released from the peripheral terminals, it initiates an increased synthesis of nitric oxide and latter sensitization of trigeminal nerves.[36][37] It is a strong vasodilator of cerebral and dura mater vessels, therefore a component of neurogenic inflammation, and it also mediates trigeminal pain transmission from vessels to the central nervous system.
Migraine attacks occur through four phases:[38]
The diagnosis of migraine is based on patient history, physical examination, and fulfillment of the diagnostic criteria. The necessary information that has to be gathered consists of these simple questions:
The International Classification of Headache Disorders (ICHD-3) describes these diagnostic criteria.[2]
B1. Migraine without aura:
B1a. Headache attacks lasting 4 to 72 hours (untreated or unsuccessfully treated)
B1b. Headache has at least two of the following characteristics:
B1c. During headache at least one of the following:
B2. Migraine with aura:
B2a. One or more of the following fully reversible aura symptoms:
B2b. At least two of the following characteristics:
C. On eight days or more per month for more than three months, fulfilling any of the following:
D. Not better accounted for by another ICHD-3 diagnosis
The ICHD-3 criteria for migraine without aura are:
The ICHD-3 criteria for migraine with aura are:
The ICHD-3 criteria for chronic migraine are:
Neuroimaging (computed tomographic scan, magnetic resonance imaging, magnetic resonance angiography, or magnetic resonance venography) is indicated in the following cases:[43][44]
The commonly used acronym “SNOOP” can be used to aid in the determination of neuroimaging indications:
Cerebrospinal fluid analysis and electroencephalogram are not typically performed unless seizure activity of infectious etiology has to be excluded.
Treatment options are based on the onset scenarios: acute or chronic.
The following should be considered in a patient with migraine:
Tension-type headache is usually bilateral, lasting 30 minutes to 7 days. The patient feels pressure or tightness but remains active. There are no associated symptoms.
Cluster headache is unilateral and had a sudden start around the eye or temple. It progresses in intensity within minutes to an excruciating continuous deep pain. It lasts 15 minutes to 3 hours. Associated symptoms include lacrimation and redness of the eye, rhinorrhea, pallor, sweating, Horner syndrome, agitation, and focal neurologic symptoms. It can easily be provoked by alcohol.
A migraine is a chronic condition that can revert to episodic migraine in 26% to 70% of the patients. Prolonged remissions are common; however, some patients have a pattern of leaving and returning to chronic states. The severity and frequency of attacks can diminish with age.[61] Episodes increase during puberty but continue to climb until 35 to 39 years of age, decreasing later in life, especially after menopause.[18]
Management of a migraine patient will require the efforts of an interprofessional team. The interprofessional care provided to the patient must use an integrated care pathway combined with an evidence-based approach to planning and evaluation of all joint activities. Primary care physicians must be assessed by an internist, a neurologist, or a headache specialist if there's any doubt about the diagnosis. Nurses and psychologists can be helpful in lifestyle changes, mental health supervision, drug overuse detoxification, and medication use recommendations.
Pharmacists can aid in determining drug interactions, especially if the patient is treated for chronic migraines. An interprofessional team that provides an integrated approach to patient care can help achieve the best possible outcomes. Collaboration, shared decision making, and communication are crucial elements for a good result.
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