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Migraine

MedGen UID:
57451
Concept ID:
C0149931
Disease or Syndrome
Synonyms: Intermittent migraine headaches; Migraine Disorders; Migraine headache; Migraine headaches; MIGRAINE WITH OR WITHOUT AURA, SUSCEPTIBILITY TO, 1
Modes of inheritance:
Autosomal dominant inheritance
MedGen UID:
141047
Concept ID:
C0443147
Intellectual Product
Sources: HPO, OMIM, Orphanet
A mode of inheritance that is observed for traits related to a gene encoded on one of the autosomes (i.e., the human chromosomes 1-22) in which a trait manifests in heterozygotes. In the context of medical genetics, an autosomal dominant disorder is caused when a single copy of the mutant allele is present. Males and females are affected equally, and can both transmit the disorder with a risk of 50% for each child of inheriting the mutant allele.
Autosomal dominant inheritance (HPO, OMIM, Orphanet)
SNOMED CT: Migraine (37796009)
 
Genes (locations): EDNRA (4q31.22-31.23); ESR1 (6q25.1-25.2); TNF (6p21.33)
OMIM®: 157300
HPO: HP:0002076

Definition

Migraine is the most common type of chronic, episodic headache, as summarized by Featherstone (1985). One locus for migraine with or without aura (MGR1) has been identified on chromosome 4q24. Other loci for migraine have been identified on 6p21.1-p12.2 (MGR3; 607498), 14q21.2-q22.3 (MGR4; 607501), 19p13 (MGR5; 607508), 1q31 (MGR6; 607516), 15q11-q13 (MGR7; 609179), 5q21 (with or without aura, MGR8, 609570; with aura, MGR9, 609670), 17p13 (MGR10; 610208), 18q12 (MGR11; 610209), 10q22-q23 (MGR12; 611706), and the X chromosome (MGR2; 300125). Mutation in the KCNK18 gene (613655) on chromosome 10q25 causes migraine with aura (MGR13; 613656). A subtype of autosomal dominant migraine with aura (MA), familial hemiplegic migraine (FHM; see 141500), is caused by mutation in the CACNA1A gene (601011) on chromosome 19p13 (FHM1; 141500), by mutation in the ATP1A2 gene (182340) on chromosome 1q21 (FHM2; 602481), or by mutation in the SCN1A gene (182389) on chromosome 2q24 (FHM3; 609634). Another locus for FHM has been mapped to chromosome 1q31 (FHM4; see 607516). There is evidence that a polymorphism in the estrogen receptor gene (ESR1; 133430.0005) and a polymorphism in the TNF gene (191160.0004) may confer susceptibility to migraine. A polymorphism in the endothelin receptor type A gene (EDNRA; 131243.0001) may confer resistance to migraine. [from OMIM]

Clinical features

Nausea
MedGen UID:
10196
Concept ID:
C0027497
Sign or Symptom
A sensation of unease in the stomach together with an urge to vomit.
Vomiting
MedGen UID:
12124
Concept ID:
C0042963
Sign or Symptom
Forceful ejection of the contents of the stomach through the mouth by means of a series of involuntary spasmic contractions.
Photophobia
MedGen UID:
43220
Concept ID:
C0085636
Sign or Symptom
Abnormal sensitivity to light. This may occur as a manifestation of EYE DISEASES; MIGRAINE; SUBARACHNOID HEMORRHAGE; MENINGITIS; and other disorders. Photophobia may also occur in association with DEPRESSION and other MENTAL DISORDERS.
Migraine with aura
MedGen UID:
57822
Concept ID:
C0154723
Disease or Syndrome
A migraine disorder characterized by episodes that are preceded by focal neurological symptoms.
Migraine without aura
MedGen UID:
137899
Concept ID:
C0338480
Disease or Syndrome
A migraine disorder characterized by episodes that occur in the absence of preceding focal neurological symptoms.
Phonophobia
MedGen UID:
155864
Concept ID:
C0751466
Mental or Behavioral Dysfunction
A fear of sounds, which can include fear of voices, including one's own voice, in addition to other sounds.
Photophobia
MedGen UID:
43220
Concept ID:
C0085636
Sign or Symptom
Abnormal sensitivity to light. This may occur as a manifestation of EYE DISEASES; MIGRAINE; SUBARACHNOID HEMORRHAGE; MENINGITIS; and other disorders. Photophobia may also occur in association with DEPRESSION and other MENTAL DISORDERS.

Conditions with this feature

Hemifacial atrophy
MedGen UID:
8761
Concept ID:
C0015458
Disease or Syndrome
Unilateral atrophy of facial tissues, including muscles, bones and skin.
Osler hemorrhagic telangiectasia syndrome
MedGen UID:
52657
Concept ID:
C0039445
Disease or Syndrome
Hereditary hemorrhagic telangiectasia (HHT) is characterized by the presence of multiple arteriovenous malformations (AVMs) that lack intervening capillaries and result in direct connections between arteries and veins. The most common clinical manifestation is spontaneous and recurrent nosebleeds (epistaxis) beginning on average at age 12 years. Telangiectases (small AVMs) are most evident on the lips, tongue, buccal mucosa, face, chest, and fingers. The average age of onset is generally later than epistaxis, but may be during childhood. Large AVMs often cause symptoms when they occur in the lungs, liver, or brain; complications from bleeding or shunting may be sudden and catastrophic. Approximately 25% of individuals with HHT have GI bleeding, which most commonly begins after age 50 years.
Cyclical vomiting syndrome
MedGen UID:
57509
Concept ID:
C0152164
Disease or Syndrome
Cyclic vomiting syndrome is a disorder that causes recurrent episodes of nausea, vomiting, and tiredness (lethargy). This condition is diagnosed most often in young children, but it can affect people of any age.The episodes of nausea, vomiting, and lethargy last anywhere from an hour to 10 days. An affected person may vomit several times per hour, potentially leading to a dangerous loss of fluids (dehydration). Additional symptoms can include unusually pale skin (pallor), abdominal pain, diarrhea, headache, fever, and an increased sensitivity to light (photophobia) or to sound (phonophobia). In most affected people, the signs and symptoms of each attack are quite similar. These attacks can be debilitating, making it difficult for an affected person to go to work or school.Episodes of nausea, vomiting, and lethargy can occur regularly or apparently at random, or can be triggered by a variety of factors. The most common triggers are emotional excitement and infections. Other triggers can include periods without eating (fasting), temperature extremes, lack of sleep, overexertion, allergies, ingesting certain foods or alcohol, and menstruation.If the condition is not treated, episodes usually occur four to 12 times per year. Between attacks, vomiting is absent, and nausea is either absent or much reduced. However, many affected people experience other symptoms during and between episodes, including pain, lethargy, digestive disorders such as gastroesophageal reflux and irritable bowel syndrome, and fainting spells (syncope). People with cyclic vomiting syndrome are also more likely than people without the disorder to experience depression, anxiety, and panic disorder. It is unclear whether these health conditions are directly related to nausea and vomiting.Cyclic vomiting syndrome is often considered to be a variant of migraines, which are severe headaches often associated with pain, nausea, vomiting, and extreme sensitivity to light and sound. Cyclic vomiting syndrome is likely the same as or closely related to a condition called abdominal migraine, which is characterized by attacks of stomach pain and cramping. Attacks of nausea, vomiting, or abdominal pain in childhood may be replaced by migraine headaches as an affected person gets older. Many people with cyclic vomiting syndrome or abdominal migraine have a family history of migraines.Most people with cyclic vomiting syndrome have normal intelligence, although some affected people have developmental delay or intellectual disability. Autism spectrum disorders, which affect communication and social interaction, have also been associated with cyclic vomiting syndrome. Additionally, muscle weakness (myopathy) and seizures are possible. People with any of these additional features are said to have cyclic vomiting syndrome plus.
Juvenile myopathy, encephalopathy, lactic acidosis AND stroke
MedGen UID:
56485
Concept ID:
C0162671
Disease or Syndrome
MELAS syndrome, comprising mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes, is a genetically heterogeneous mitochondrial disorder with a variable clinical phenotype. The disorder is accompanied by features of central nervous system involvement, including seizures, hemiparesis, hemianopsia, cortical blindness, and episodic vomiting (Pavlakis et al., 1984; Montagna et al., 1988). Other mitochondrial encephalomyopathies include Leigh syndrome (LS; 256000), Kearns-Sayre syndrome (KSS; 530000), MERRF syndrome (545000), and Leber optic atrophy (535000).
Episodic ataxia type 2
MedGen UID:
314039
Concept ID:
C1720416
Disease or Syndrome
Episodic ataxia type 2 (EA2) is characterized by paroxysmal attacks of ataxia, vertigo, and nausea typically lasting minutes to days in duration. Attacks can be associated with dysarthria, diplopia, tinnitus, dystonia, hemiplegia, and headache. About 50% of individuals with EA2 have migraine headaches. Onset is typically in childhood or early adolescence (age range 2-32 years). Frequency of attacks can range from once or twice a year to three or four times a week. Attacks can be triggered by stress, exertion, caffeine, alcohol, fever, heat, and phenytoin; they can be stopped or decreased in frequency and severity by administration of acetazolamide or 4-aminopyridine. Between attacks, individuals may initially be asymptomatic but commonly develop interictal findings that can include nystagmus, pursuit and saccade alterations, and ataxia.
Dystonia 9
MedGen UID:
371427
Concept ID:
C1832855
Disease or Syndrome
The phenotypic spectrum of glucose transporter type 1 deficiency syndrome (Glut1 DS) is now known to be a continuum that includes the classic phenotype as well as paroxysmal exercise-induced dyskinesia and epilepsy (previously known as dystonia 18 [DYT18]) and paroxysmal choreoathetosis with spasticity (previously known as dystonia 9 [DYT9]), atypical childhood absence epilepsy, myoclonic astatic epilepsy, and paroxysmal non-epileptic findings including intermittent ataxia, choreoathetosis, dystonia, and alternating hemiplegia. The classic phenotype is characterized by infantile-onset seizures, delayed neurologic development, acquired microcephaly, and complex movement disorders. Seizures in classic early-onset Glut1 DS begin before age six months. Several seizure types occur: generalized tonic or clonic, focal, myoclonic, atypical absence, atonic, and unclassified. In some infants, apneic episodes and abnormal episodic eye-head movements similar to opsoclonus may precede the onset of seizures. The frequency, severity, and type of seizures vary among affected individuals and are not related to disease severity. Cognitive impairment, ranging from learning disabilities to severe intellectual disability, is typical. The complex movement disorder, characterized by ataxia, dystonia, and chorea, may occur in any combination and may be continuous, paroxysmal, or continual with fluctuations in severity influenced by environmental factors such as fasting or with infectious stress. Symptoms often improve substantially when a ketogenic diet is started.
Hereditary hemorrhagic telangiectasia type 2
MedGen UID:
324960
Concept ID:
C1838163
Disease or Syndrome
Hereditary hemorrhagic telangiectasia (HHT) is characterized by the presence of multiple arteriovenous malformations (AVMs) that lack intervening capillaries and result in direct connections between arteries and veins. The most common clinical manifestation is spontaneous and recurrent nosebleeds (epistaxis) beginning on average at age 12 years. Telangiectases (small AVMs) are most evident on the lips, tongue, buccal mucosa, face, chest, and fingers. The average age of onset is generally later than epistaxis, but may be during childhood. Large AVMs often cause symptoms when they occur in the lungs, liver, or brain; complications from bleeding or shunting may be sudden and catastrophic. Approximately 25% of individuals with HHT have GI bleeding, which most commonly begins after age 50 years.
Sensory ataxic neuropathy, dysarthria, and ophthalmoparesis
MedGen UID:
375302
Concept ID:
C1843851
Disease or Syndrome
POLG-related disorders comprise a continuum of overlapping phenotypes that were clinically defined long before their molecular basis was known. Most affected individuals have some, but not all, of the features of a given phenotype; nonetheless, the following nomenclature can assist the clinician in diagnosis and management. Onset of the POLG-related disorders ranges from infancy to late adulthood. Alpers-Huttenlocher syndrome (AHS), one of the most severe phenotypes, is characterized by childhood-onset progressive and ultimately severe encephalopathy with intractable epilepsy and hepatic failure. Childhood myocerebrohepatopathy spectrum (MCHS) presents between the first few months of life and about age three years with developmental delay or dementia, lactic acidosis, and a myopathy with failure to thrive. Other findings can include liver failure, renal tubular acidosis, pancreatitis, cyclic vomiting, and hearing loss. Myoclonic epilepsy myopathy sensory ataxia (MEMSA) now describes the spectrum of disorders with epilepsy, myopathy, and ataxia without ophthalmoplegia. MEMSA now includes the disorders previously described as spinocerebellar ataxia with epilepsy (SCAE). The ataxia neuropathy spectrum (ANS) includes the phenotypes previously referred to as mitochondrial recessive ataxia syndrome (MIRAS) and sensory ataxia neuropathy dysarthria and ophthalmoplegia (SANDO). About 90% of persons in the ANS have ataxia and neuropathy as core features. Approximately two thirds develop seizures and almost one half develop ophthalmoplegia; clinical myopathy is rare. Autosomal recessive progressive external ophthalmoplegia (arPEO) is characterized by progressive weakness of the extraocular eye muscles resulting in ptosis and ophthalmoparesis (or paresis of the extraocular muscles) without associated systemic involvement; however, caution is advised because many individuals with apparently isolated arPEO at the onset develop other manifestations of POLG-related disorders over years or decades. Of note, in the ANS spectrum the neuropathy commonly precedes the onset of PEO by years to decades. Autosomal dominant progressive external ophthalmoplegia (adPEO) typically includes a generalized myopathy and often variable degrees of sensorineural hearing loss, axonal neuropathy, ataxia, depression, parkinsonism, hypogonadism, and cataracts (in what has been called "chronic progressive external ophthalmoplegia plus," or "CPEO+").
PHACE syndrome
MedGen UID:
376231
Concept ID:
C1847874
Disease or Syndrome
PHACE is an acronym for a neurocutaneous syndrome encompassing the following features: posterior fossa brain malformations, hemangiomas of the face (large or complex), arterial anomalies, cardiac anomalies, and eye abnormalities. The association is referred to as PHACES when ventral developmental defects, such as sternal clefting or supraumbilical raphe, are present (summary by Bracken et al., 2011).
Mitochondrial DNA depletion syndrome 7 (hepatocerebral type)
MedGen UID:
338613
Concept ID:
C1849096
Disease or Syndrome
Infantile-onset spinocerebellar ataxia (IOSCA) is a severe, progressive neurodegenerative disorder characterized by normal development until age one year, followed by onset of ataxia, muscle hypotonia, loss of deep-tendon reflexes, and athetosis. Ophthalmoplegia and sensorineural deafness develop by age seven years. By adolescence, affected individuals are profoundly deaf and no longer ambulatory; sensory axonal neuropathy, optic atrophy, autonomic nervous system dysfunction, and hypergonadotropic hypogonadism in females become evident. Epilepsy can develop into a serious and often fatal encephalopathy: myoclonic jerks or focal clonic seizures that progress to epilepsia partialis continua followed by status epilepticus with loss of consciousness.
Hereditary hemorrhagic telangiectasia type 4
MedGen UID:
341824
Concept ID:
C1857688
Disease or Syndrome
Hereditary hemorrhagic telangiectasia (HHT) is characterized by the presence of multiple arteriovenous malformations (AVMs) that lack intervening capillaries and result in direct connections between arteries and veins. The most common clinical manifestation is spontaneous and recurrent nosebleeds (epistaxis) beginning on average at age 12 years. Telangiectases (small AVMs) are most evident on the lips, tongue, buccal mucosa, face, chest, and fingers. The average age of onset is generally later than epistaxis, but may be during childhood. Large AVMs often cause symptoms when they occur in the lungs, liver, or brain; complications from bleeding or shunting may be sudden and catastrophic. Approximately 25% of individuals with HHT have GI bleeding, which most commonly begins after age 50 years.
Angiomatosis, diffuse corticomeningeal, of Divry and Van Bogaert
MedGen UID:
347234
Concept ID:
C1859783
Disease or Syndrome
Vasculopathy, retinal, with cerebral leukodystrophy
MedGen UID:
348124
Concept ID:
C1860518
Disease or Syndrome
Retinal vasculopathy with cerebral leukodystrophy is an adult-onset autosomal dominant disorder involving the microvessels of the brain and resulting in central nervous system degeneration with progressive loss of vision, stroke, motor impairment, and cognitive decline. Death occurs in most patients 5 to 10 years after onset. A subset of affected individuals have systemic vascular involvement evidenced by Raynaud's phenomenon, micronodular cirrhosis, and glomerular dysfunction (summary by Richards et al., 2007).
Stormorken syndrome
MedGen UID:
350028
Concept ID:
C1861451
Disease or Syndrome
Stormorken syndrome is an autosomal dominant disorder characterized by mild bleeding tendency due to platelet dysfunction, thrombocytopenia, anemia, asplenia, tubular aggregate myopathy, congenital miosis, and ichthyosis. Additional features may include headache or recurrent stroke-like episodes (summary by Misceo et al., 2014).
Phosphoglycerate kinase 1 deficiency
MedGen UID:
410166
Concept ID:
C1970848
Disease or Syndrome
Phosphoglycerate kinase-1 deficiency is an X-linked recessive condition with a highly variable clinical phenotype that includes hemolytic anemia, myopathy, and neurologic involvement. Patients can express 1, 2, or all 3 of these manifestations (Shirakawa et al., 2006).
Episodic ataxia, type 6
MedGen UID:
390739
Concept ID:
C2675211
Disease or Syndrome
The hereditary ataxias are a group of genetic disorders characterized by slowly progressive incoordination of gait and often associated with poor coordination of hands, speech, and eye movements. Frequently, atrophy of the cerebellum occurs. In this GeneReview the hereditary ataxias are categorized by mode of inheritance and gene (or chromosome locus) in which pathogenic variants occur.
Periodic fever, menstrual cycle-dependent
MedGen UID:
766332
Concept ID:
C3553418
Disease or Syndrome
Women show menstrual cycle-dependent physiologic changes in relation to sex hormone levels. Because ovulation triggers a significant change in the hormonal milieu that is similar to local inflammation, a 0.5 to 1.0 degree Celsius increase in basal body temperature after ovulation is commonly associated with progesterone secretion and is believed to be triggered by the induction of several inflammatory cytokines. Rare menstrual cycle-dependent febrile episodes have been reported, some of which have shown a luteal-phase-dependent pattern (summary by Jiang et al., 2012).
Peroxisome biogenesis disorder 14B
MedGen UID:
766969
Concept ID:
C3554055
Disease or Syndrome
PBD14B is an autosomal recessive peroxisome biogenesis disorder characterized clinically by mild intellectual disability, congenital cataracts, progressive hearing loss, and polyneuropathy (Ebberink et al., 2012), all of which had been observed in patients with mild peroxisomal biogenesis disorders (e.g., Kelley et al., 1986; Poll-The et al., 1987). Additionally, recurrent migraine-like episodes following mental stress or physical exertion, not a common feature in peroxisome disorders, was reported. Thoms and Gartner (2012) classified the disorder described by Ebberink et al. (2012) in their patient as a mild 'Zellweger syndrome (214100) spectrum' (ZSS) disorder. See PBD1B (601539) for a phenotypic description and discussion of genetic heterogeneity of less severe phenotypes on the Zellweger syndrome spectrum. See PBD9B (614879) for another atypical peroxisome biogenesis disorder.
Idiopathic basal ganglia calcification 5
MedGen UID:
815975
Concept ID:
C3809645
Disease or Syndrome
Primary familial brain calcification (PFBC) is a neurodegenerative disorder with characteristic calcium deposits in the basal ganglia and other brain areas visualized on neuroimaging. Most affected individuals are in good health during childhood and young adulthood and typically present in the fourth to fifth decade with a gradually progressive movement disorder and neuropsychiatric symptoms. The movement disorder first manifests as clumsiness, fatigability, unsteady gait, slow or slurred speech, dysphagia, involuntary movements, or muscle cramping. Neuropsychiatric symptoms, often the first or most prominent manifestations, range from mild difficulty with concentration and memory to changes in personality and/or behavior, to psychosis and dementia. Seizures of various types occur frequently, some individuals experience chronic headache and vertigo; urinary urgency or incontinence may be present.

Recent clinical studies

Etiology

Pezzini A, Busto G, Zedde M, Gamba M, Zini A, Poli L, Caria F, De Giuli V, Simone AM, Pascarella R, Padovani A, Padroni M, Gasparotti R, Colagrande S, Fainardi E
Stroke 2018 Mar;49(3):573-578. Epub 2018 Feb 19 doi: 10.1161/STROKEAHA.118.020554. PMID: 29459398
Izquierdo-Casas J, Comas-Basté O, Latorre-Moratalla ML, Lorente-Gascón M, Duelo A, Vidal-Carou MC, Soler-Singla L
J Physiol Biochem 2018 Feb;74(1):93-99. Epub 2017 Jun 17 doi: 10.1007/s13105-017-0571-3. PMID: 28624934
Florencio LL, de Oliveira AS, Carvalho GF, Dach F, Bigal ME, Fernández-de-Las-Peñas C, Bevilaqua-Grossi D
J Manipulative Physiol Ther 2017 May;40(4):250-254. Epub 2017 Apr 6 doi: 10.1016/j.jmpt.2017.02.006. PMID: 28390711
Muehlberger T, Wormald JCR, Hachach-Haram N, Mosahebi A
J Plast Reconstr Aesthet Surg 2017 Jul;70(7):914-921. Epub 2017 Mar 7 doi: 10.1016/j.bjps.2017.02.009. PMID: 28359726
Aupiais C, Wanin S, Romanello S, Spiri D, Moretti R, Boizeau P, Massano D, Zuccotti GV, Crichiutti G, Kanagarajah L, Houdouin V, Alberti C, Titomanlio L
Headache 2017 Apr;57(4):612-624. Epub 2017 Feb 4 doi: 10.1111/head.13032. PMID: 28160287

Diagnosis

Siirtola P, Koskimäki H, Mönttinen H, Röning J
Sensors (Basel) 2018 Apr 28;18(5) doi: 10.3390/s18051374. PMID: 29710791Free PMC Article
Ren C, Liu J, Zhou J, Liang H, Wang Y, Sun Y, Ma B, Yin Y
Biochem Biophys Res Commun 2018 Feb 5;496(2):267-273. Epub 2017 Dec 30 doi: 10.1016/j.bbrc.2017.11.203. PMID: 29294327
Gunes A, Karadag AS, Yazgan S, Celik HU, Simsek A
Clin Exp Optom 2018 Jan;101(1):109-115. Epub 2017 Sep 20 doi: 10.1111/cxo.12585. PMID: 28940251
Izquierdo-Casas J, Comas-Basté O, Latorre-Moratalla ML, Lorente-Gascón M, Duelo A, Vidal-Carou MC, Soler-Singla L
J Physiol Biochem 2018 Feb;74(1):93-99. Epub 2017 Jun 17 doi: 10.1007/s13105-017-0571-3. PMID: 28624934
Florencio LL, de Oliveira AS, Carvalho GF, Dach F, Bigal ME, Fernández-de-Las-Peñas C, Bevilaqua-Grossi D
J Manipulative Physiol Ther 2017 May;40(4):250-254. Epub 2017 Apr 6 doi: 10.1016/j.jmpt.2017.02.006. PMID: 28390711

Therapy

Pezzini A, Busto G, Zedde M, Gamba M, Zini A, Poli L, Caria F, De Giuli V, Simone AM, Pascarella R, Padovani A, Padroni M, Gasparotti R, Colagrande S, Fainardi E
Stroke 2018 Mar;49(3):573-578. Epub 2018 Feb 19 doi: 10.1161/STROKEAHA.118.020554. PMID: 29459398
Allais G, Chiarle G, Sinigaglia S, Benedetto C
Expert Opin Pharmacother 2018 Feb;19(2):123-136. Epub 2017 Dec 12 doi: 10.1080/14656566.2017.1414182. PMID: 29212383
Razeghi Jahromi S, Abolhasani M, Ghorbani Z, Sadre-Jahani S, Alizadeh Z, Talebpour M, Meysamie A, Togha M
Obes Surg 2018 Jan;28(1):87-96. doi: 10.1007/s11695-017-2793-4. PMID: 28685361
Witteveen H, van den Berg P, Vermeulen G
J Headache Pain 2017 Dec;18(1):45. Epub 2017 Apr 17 doi: 10.1186/s10194-017-0752-z. PMID: 28417308Free PMC Article
Aupiais C, Wanin S, Romanello S, Spiri D, Moretti R, Boizeau P, Massano D, Zuccotti GV, Crichiutti G, Kanagarajah L, Houdouin V, Alberti C, Titomanlio L
Headache 2017 Apr;57(4):612-624. Epub 2017 Feb 4 doi: 10.1111/head.13032. PMID: 28160287

Prognosis

Izquierdo-Casas J, Comas-Basté O, Latorre-Moratalla ML, Lorente-Gascón M, Duelo A, Vidal-Carou MC, Soler-Singla L
J Physiol Biochem 2018 Feb;74(1):93-99. Epub 2017 Jun 17 doi: 10.1007/s13105-017-0571-3. PMID: 28624934
Witteveen H, van den Berg P, Vermeulen G
J Headache Pain 2017 Dec;18(1):45. Epub 2017 Apr 17 doi: 10.1186/s10194-017-0752-z. PMID: 28417308Free PMC Article
Florencio LL, de Oliveira AS, Carvalho GF, Dach F, Bigal ME, Fernández-de-Las-Peñas C, Bevilaqua-Grossi D
J Manipulative Physiol Ther 2017 May;40(4):250-254. Epub 2017 Apr 6 doi: 10.1016/j.jmpt.2017.02.006. PMID: 28390711
Galioto R, O'Leary KC, Thomas JG, Demos K, Lipton RB, Gunstad J, Pavlović JM, Roth J, Rathier L, Bond DS
J Headache Pain 2017 Dec;18(1):41. Epub 2017 Mar 29 doi: 10.1186/s10194-017-0748-8. PMID: 28357702Free PMC Article
Kokonyei G, Szabo E, Kocsel N, Edes A, Eszlari N, Pap D, Magyar M, Kovacs D, Zsombok T, Elliott R, Anderson IM, William Deakin JF, Bagdy G, Juhasz G
Psychol Health 2016 Dec;31(12):1481-1497. Epub 2016 Sep 28 doi: 10.1080/08870446.2016.1235166. PMID: 27616579Free PMC Article

Clinical prediction guides

Gunes A, Karadag AS, Yazgan S, Celik HU, Simsek A
Clin Exp Optom 2018 Jan;101(1):109-115. Epub 2017 Sep 20 doi: 10.1111/cxo.12585. PMID: 28940251
Razeghi Jahromi S, Abolhasani M, Ghorbani Z, Sadre-Jahani S, Alizadeh Z, Talebpour M, Meysamie A, Togha M
Obes Surg 2018 Jan;28(1):87-96. doi: 10.1007/s11695-017-2793-4. PMID: 28685361
Izquierdo-Casas J, Comas-Basté O, Latorre-Moratalla ML, Lorente-Gascón M, Duelo A, Vidal-Carou MC, Soler-Singla L
J Physiol Biochem 2018 Feb;74(1):93-99. Epub 2017 Jun 17 doi: 10.1007/s13105-017-0571-3. PMID: 28624934
Lo Buono V, Bonanno L, Corallo F, Pisani LR, Lo Presti R, Grugno R, Di Lorenzo G, Bramanti P, Marino S
J Headache Pain 2017 Dec;18(1):72. Epub 2017 Jul 20 doi: 10.1186/s10194-017-0782-6. PMID: 28730563Free PMC Article
Muehlberger T, Wormald JCR, Hachach-Haram N, Mosahebi A
J Plast Reconstr Aesthet Surg 2017 Jul;70(7):914-921. Epub 2017 Mar 7 doi: 10.1016/j.bjps.2017.02.009. PMID: 28359726

Recent systematic reviews

Lan L, Zhang X, Li X, Rong X, Peng Y
J Headache Pain 2017 Aug 22;18(1):86. doi: 10.1186/s10194-017-0792-4. PMID: 28831756Free PMC Article
Hou M, Xing H, Cai Y, Li B, Wang X, Li P, Hu X, Chen J
J Headache Pain 2017 Dec;18(1):42. Epub 2017 Apr 7 doi: 10.1186/s10194-017-0750-1. PMID: 28389966Free PMC Article
He A, Song D, Zhang L, Li C
J Headache Pain 2017 Dec;18(1):26. Epub 2017 Feb 20 doi: 10.1186/s10194-017-0720-7. PMID: 28220376Free PMC Article
Cai X, Shi X, Zhang X, Zhang A, Zheng M, Fang Y
J Headache Pain 2017 Dec;18(1):13. Epub 2017 Feb 2 doi: 10.1186/s10194-017-0725-2. PMID: 28150221Free PMC Article
Thorlund K, Toor K, Wu P, Chan K, Druyts E, Ramos E, Bhambri R, Donnet A, Stark R, Goadsby PJ
Cephalalgia 2017 Sep;37(10):965-978. Epub 2016 Aug 12 doi: 10.1177/0333102416660552. PMID: 27521843

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