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Chronic Headaches

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Last Update: July 31, 2023.

Continuing Education Activity

Chronic headache is not a single disease entity but an umbrella term that encompasses all chronic headaches. The International Headache Society defines chronic daily headaches (CDH) as "15 or more headache episodes per month for at least three months." A chronic daily headache can be divided into primary and secondary headache disorders depending upon its etiology. Primary chronic headache disorders do not have secondary organic etiology. Within the primary headache categories, a headache duration of fewer than 4 hours is labeled as a 'short headache .' More than 4 hours is known as a 'long headache.' Long headaches more commonly include chronic migraine and chronic tension headaches. There are a variety of causes and ways to manage this condition. This activity reviews the evaluation and treatment of chronic headaches and explains the role of the interprofessional team in evaluating, treating, managing, and improving care for patients with this condition.


  • Identify the etiology of chronic headaches.
  • Outline the appropriate evaluation of chronic headaches.
  • Review the management options available for chronic headaches.
  • Describe interprofessional team strategies for improving care coordination and communication to advance chronic headaches and improve outcomes.
Access free multiple choice questions on this topic.


Chronic headache is not a single disease entity but an umbrella term that encompasses all chronic headaches. The International Headache Society defines chronic daily headaches (CDH) as "15 or more headache episodes per month for at least three months."[1] Chronic headaches are not an official class in the International Classification of Headache Disorders (ICHD).[2] 

CDH is rather a descriptive term that most encompasses five subtypes of primary and secondary headaches defined by ICHD-3:

  • Chronic migraine headache
  • Chronic tension-type headache
  • Medication overuse headache (MOH)
  • Hemicrania continua
  • New daily persistent headache

A chronic daily headache can be divided into primary and secondary headache disorders depending upon its etiology. Primary chronic headache disorders do not have secondary organic etiology. Within the primary headache categories, a headache duration of fewer than 4 hours is labeled as a 'short headache .' More than 4 hours is known as a 'long headache.' Long headaches more commonly include chronic migraine and chronic tension headaches.[1] Secondary headaches can occur due to secondary causes such as medication overuse, intracranial tumors, central nervous system (CNS) infections, raised intracranial pressure, metabolic abnormalities, post-traumatic, vascular, and structural pathologies.[3] It is important to realize that chronic headaches are often caused by a multifactorial combination of the causes mentioned above and can occur along a continuum.


The International Classification of Headache Disorders (ICHD) recognizes over 200 headache disorders and divides them into three groups, which are primary, secondary, and painful cranial neuropathies.[4] The ICHD system is hierarchical, with multiple subtypes within each main headache type.

All chronic headaches meet the criteria of occurring at least 15 times a month for at least three months, but both primary and secondary chronic headaches have unique characteristics.

Primary headaches lasting more than four hours include chronic migraines, tension headaches, persistent daily headaches, and hemicrania continua. 

  • Chronic migraine has typical features of being unilateral, pulsatile, moderate to severe, and may or may not have an aura.[4] Episodic migraines may evolve into chronic migraines.
  • Chronic migraine in children and adolescents is often bilateral, and associated symptoms such as photophobia and phonophobia are often inferred from behavior.[5]
  • Chronic headaches, which are bilateral, non-pulsatile, and lack associated symptoms, are classified as chronic tension headaches.[4] Pericranial tenderness is often found on palpation.
  • A new persistent daily headache (NDPH) occurs suddenly and becomes unremitting within 24 hours of onset. Patients typically have no prior history of headaches. NDPH is rare and refractory to treatment.[6]
  • Hemicrania continua is unilateral, has autonomic symptoms, and is continuous with exacerbations. Responsiveness to indomethacin helps distinguish this form of headache.

Primary headaches lasting less than four hours include chronic cluster headaches, neuralgiform headache attacks, and primary stabbing headaches.

  • Chronic cluster headache varies from the acute form in that there are no remissions, and headaches must occur over at least one year. Headaches are unilateral in the trigeminal distribution and associated with unilateral autonomic symptoms. Patients often experience agitation during the headache.
  • The short-lasting neuralgiform headaches include short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT) and short-lasting unilateral neuralgiform headache attacks with cranial autonomic symptoms (SUNA). Both types have severe, unilateral pain associated with autonomic symptoms. In addition, SUNCT has both lacrimation and conjunctival injection. SUNA may have either but not both of those features and may be accompanied by rhinorrhea or nasal congestion.
  • Primary stabbing headaches may frequently occur throughout the day. Sharp, sudden, jabbing pain occurs in the temporal or peri-orbital regions.

Secondary chronic daily headaches include medication overuse, CNS infection, CNS hematomas, intracranial tumor, raised intracranial pressure, low-pressure headache, vasculitis, aneurysms, and cerebrospinal fluid (CSF) leak.[2]

  • Chronic medication overuse headaches often overlap with other acute and chronic headache types. Analgesics are widely used for symptom control in migraine and tension headaches. Patients inadvertently increase headache frequency by overuse of analgesics. The ICHD further classifies this disorder based on the medications used, including NSAIDs, triptans, ergotamines, non-opioid, and opioid analgesics.[7] Withdrawal of analgesics typically worsens these headaches.
  • The remainder of the secondary chronic headache etiologies is beyond the scope of this article.


Headache disorders have a large global burden. Both acute and chronic headaches are most prevalent between the teenage years and the fifth decade.[8]

Chronic headaches occur in 1 to 4% of the entire population.[9] Approximately 39 million people in the United States and 1 billion people worldwide are affected. Of patients seen in a headache clinic, 40% are diagnosed with chronic headaches. Prevalence rates in women are 3 to 5 times higher than in men.[4]

Chronic migraines are associated with significant comorbidities, including obesity, obstructive sleep apnea, depression, chronic pain disorders, and cardiovascular disease.[10]

Chronic migraine headaches also have a prevalence of 7 to 17% in children and adolescents.[5] The prevalence is equal between boys and girls until age 12, when females predominate.

Hemicrania continua is less common than chronic migraine or tension headache. It has a 2 to 1 female to male incidence, with the peak diagnosis occurring in the third decade.

Chronic cluster headache occurs more often in men but is also experienced by women. Women often have nausea and vomiting associated with chronic cluster headaches and may be initially diagnosed with migraine headaches.[11]


Although the pathophysiology of each type of chronic headache varies, shared features include sensitization of the trigeminal system, alterations in brain structure and function, and environmental factors.[12] Most chronic headaches result from the transformation of an episodic headache disorder. 

Modifiable risk factors, including sleep disorders, obesity, and high caffeine consumption, increase the chance of headache transformation from episodic to chronic headaches.

Serotonin, which has vasoconstrictive and anti-inflammatory effects, is a therapeutic target of triptans in migraines.

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, in central pain control pathways, or by cortical projections of brainstem serotonergic nuclei.[13][14]

Calcitonin gene-related peptide is abundant in trigeminal ganglion neurons. It is released from the peripheral and central nerve terminals and secreted within the trigeminal ganglion. When released from the peripheral terminals, it initiates an increased synthesis of nitric oxide and later sensitization of trigeminal nerves.[15][16] It is a strong vasodilator of cerebral and dura mater vessels, therefore a component of neurogenic inflammation. It also mediates trigeminal pain transmission from vessels to the central nervous system.

Medication overuse headaches share much of the pathophysiology of migraine and tension headaches as functional and structural changes in the central nervous system. Changes in the serotonergic neuromodulatory system and upregulation of vasoactive and pro-inflammatory mediators also contribute.[7] The condition exhibits both functional and structural changes in the central nervous system (CNS), particularly the hippocampal periaqueductal gray area, posterior cingulate cortex thalamus, cerebellum, and orbitofrontal cortex (OFC), and the mesocorticolimbic reward system.[17][18] Also found were changes in the serotonergic neuromodulatory system, upregulation of vasoactive and pro-inflammatory mediators, increased susceptibility to cortical spreading depression, central sensitization, and an increase in nociceptive sensory fields.[19] Some studies have theorized a potential genetic risk as to the etiology of the development of MOH. One such model is the renin-angiotensin system, known to have an active role in regulating neural plasticity.[20]

Trigeminal autonomic cephalalgias, cluster headache, SUNCT, SUNA, and hemicrania continua, have complex pathogenesis. Severe pain and autonomic symptoms are attributed to the trigeminal autonomic reflex via pain-producing innervation and cranial parasympathetic activation.[21]

History and Physical

A thorough history and physical exam are indispensable in the diagnosis of chronic daily headaches. As noted above, a chronic headache should have 15 or more monthly episodes for at least three months. One should determine the frequency, intensity, and characteristics of the pain, as well as the aggravating and alleviating factors. Many headache types involve ipsilateral autonomic symptoms such as lacrimation, conjunctival injection, conjunctival edema, ptosis, miosis, nasal congestion, rhinorrhea, etc.

A thorough medication reconciliation, including over-the-counter analgesics, is essential. Patients with medication-overuse headaches often have a primary headache disorder, and they frequently use pain medications.[22] Medication classes may include non-steroidal anti-inflammatory drugs (NSAIDs), triptans, ergotamines, opioids, or a combination of multiple analgesics. Key historical features include morning headaches, the onset of headaches when medication is delayed, and relief when medication is taken.[23]

Comorbidities, sleep history, and a family history of headaches should also be noted. A secondary headache disorder should be excluded from the history and examination. 

Recognition of headache "red flags" is critical in identifying secondary headaches and ordering additional diagnostic testing. Those "red flags" include:

  • Age above 50
  • A significant change in prior headache pattern
  • Severe, "thunderclap" headache
  • Systemic illness signs such as fever
  • Known illness which increases the risk for secondary headaches such as cancer or HIV
  • Neurologic symptoms 
  • Headaches associated with Valsalva maneuvers[24]

Physical exam findings concerning secondary headache causes include focal neurological deficits, papilledema, bitemporal hemianopia, homonymous hemianopia, decreased visual acuity, or increased pain with the Valsalva method.

Primary chronic headaches often lack physical findings but may have autonomic activation or muscle tenderness in the occipital or cervical regions.


Further evaluation may not be warranted in a straightforward chronic primary headache disorder. Still, many clinicians will advise baseline laboratory testing and brain imaging to exclude the secondary treatable causes.

The necessary information that has to be gathered consists of these simple questions:

  • Demographic features of the patient: age, gender, race, profession
  • When did the headache start?
  • Where does it hurt? Location, irradiation.
  • What is the intensity of the pain?
  • How is the pain? Which are the qualitative characteristics of the pain?
  • How long does the pain last?
  • At which moment of the day does the pain appear?
  • How has it evolved since it started?
  • What is the frequency of appearance?
  • What are the triggering situations?
  • Simultaneous symptoms?
  • Is it related to sleep?
  • How does it get better or worse?
  • Which medications do you take to make it better? What is the frequency of this medication?

Laboratory workup includes a complete blood count to look for infection. Erythrocyte sedimentation rate (ESR) is increased in giant cell arteritis and other vasculitides. A metabolic panel looks for metabolic causes of headaches and endocrine testings to look for pituitary gland abnormalities.

Magnetic resonance imaging (MRI) of the brain is the imaging modality of choice.[25] A contrast study is often recommended to increase the sensitivity and specificity to detect structural abnormalities. A need for vascular imaging is based on the differential diagnosis. Further studies may be warranted depending upon the underlying cause. These may include positron emission tomography (PET) scan, magnetic resonance spectroscopy (MRS), and/or biopsy. A lumbar puncture may be required if there is suspicion of a CNS infection or idiopathic intracranial hypertension.

Medication Overuse Headache by Drug Class and Duration of Headache

  • Ergotamine--> ten days/month for over three months
  • Triptan--> ten days/month for over three months
  • ASA-->15 days/month for over three months
  • NSAIDs-->15 days/month for >3 months
  • Acetaminophen/paracetamol-->15 days/month for over three months
  • Opioids--> ten days/month for over three months
  • Combination analgesics--> ten days/month for over three months
  • Multiple drug classes--> ten days/month for over three months[22]

Treatment / Management

Treatment and management of chronic headache disorders depend upon the underlying etiology and may require an interprofessional approach.

The patient should maintain a headache journal documenting their headache episodes and any accompanying triggers. If found, stressors should be avoided or minimized. 

Chronic Migraine

  • Chronic migraine treatment should begin with setting the expectation that headache frequency and severity will decrease, but headaches will not be eliminated.
  • The patient should be counseled that high caffeine intake, sleep deprivation, overuse of analgesics, and comorbid conditions can worsen chronic migraines.
  • Prophylactic pharmacologic treatment should be used. First-line therapy includes beta-blockers, anticonvulsants, and antidepressants. The most commonly used medications are propranolol, topiramate, and amitriptyline.[26]
  • Botulinum toxin A is a Food and Drug Administration (FDA) approved treatment for chronic migraines and is considered second-line therapy.
  • Monoclonal antibodies that target calcitonin gene-related peptide (CGRP) are the newest development in chronic migraine treatment. Erenumab, fremanezumab, and galcanezumab are approved for chronic migraines, which have failed to respond to other treatments.[26]
  • Triptans, steroids, NSAIDs, and opioids are often used to abort acute episodes, but routine use of these medications increases the risk of developing a medication-overuse headache.
  • Patients may also benefit from psychological counseling if anxiety or depression is present.
  • Manual medicine, such as spinal manipulation and trigger point treatment, may be used as complementary or alternative therapy.[27]
  • In drug-resistant cases, invasive procedures such as sphenopalatine ganglion and occipital nerve blockades may be tried with variable results. Deep brain stimulation (DBS) is also used in some treatment-resistant cases.[28][29] 

Chronic Tension Headache

  • Amitriptyline, a tricyclic antidepressant, is recommended as the first-line treatment for chronic tension headaches.
  • Amitriptyline, in addition to inhibiting serotonin and noradrenaline reuptake, also reduces tenderness in pericranial muscles.
  • Tricyclic antidepressants increase the risk for cardiac arrhythmia, and patients should be screened for cardiovascular disorders before initiating therapy. In addition, patients over 40 should undergo an ECG.
  • Anticonvulsants, such as topiramate and gabapentin, can be considered second-line treatment.
  • Addressing the potential musculoskeletal causes of tension headaches, treatment with physical therapy, acupuncture, trigger point injections, spinal manipulation, or muscle relaxants may be beneficial.[30]
  • Behavioral therapy, including cognitive-behavioral therapy, biofeedback, and relaxation techniques, is particularly helpful for patients with coexisting anxiety or depression.

Medication Overuse Headache

  • Patient education about the potential for overuse of analgesic medication to lead to headache progression is key. Include the use of over-the-counter analgesics in the discussion.
  • The physician initiates a preventative medication while simultaneously assisting the patient in discontinuing the causative drug.
  • Patients may experience withdrawal symptoms of nausea and anxiety for 2 to 10 days when the analgesic medication is discontinued.
  • There is no consensus on the most appropriate medication for bridge therapy following discontinuation of the offending drug. Long-acting NSAIDs, prednisone, dihydroergotamine, and antiemetics are options.[31] The medication should not be from the same class as the offending medication.
  • Medications that may be effective for prophylaxis include topiramate, amitryptiline, valproic acid, and beta-blockers. The choice of medication should be based upon comorbidities and the primary headache disorder.[32]

Chronic Autonomic Cephalgia

  • Indomethacin is the drug of choice for paroxysmal hemicrania, hemicrania continua, primary stabbing headache, hypnic headache, and Valsalva-induced headaches (e.g., cough headache, exercise headache).
  • Verapamil is the drug of choice for the prevention of chronic cluster headaches. However, Verapamil requires titration to become effective, and glucocorticoids or dihydroergotamine can be used for exacerbations.
  • Chronic cluster headaches not responsive to pharmacologic therapy can be treated with a non-invasive vagus nerve stimulator or sphenopalatine ganglion microstimulator.[11]
  • First-line prophylactic therapy for chronic SUNCT and SUNA is lamotrigine. Topiramate and gabapentin are alternatives.[33]

Differential Diagnosis

  • Medication-overuse headache 
  • Brain neoplasm 
  • Chronic infections (e.g., CNS tuberculosis)
  • Chronic sinusitis
  • Cervical spine-related pain
  • CNS vasculitis
  • Temporomandibular joint pathologies
  • Idiopathic intracranial hypertension
  • Chronic hydrocephalus
  • Cerebral aneurysms
  • Chronic paroxysmal hemicrania
  • Dissection syndromes
  • Encephalitis
  • Subarachnoid/intracranial hemorrhage
  • Meningitis
  • Temporal/giant cell arteritis

Treatment Planning

Table Icon


Table 1. Acute therapy for migraine *Adverse effects in this section pertain to all triptans unless specified.

Table Icon


Table 2. Preventive therapy for migraine[48].


The prognosis of chronic headaches is variable. Anxiety and mood disorders, elevated stress levels, insufficient sleep, poor headache management, and low socioeconomic status are the primary prognostic characteristics—patients with higher expectations for treatment display a better prognosis for decreased headache intensity and frequency. No specific age group has an improved response to treatment. Incidence at an older age generally correlates to less severe symptoms. Employed patients responded better to treatment than those patients on medical leave.[9] Exercise, prophylactic medication regimen compliance, and cessation of overused medications tend to lead to a favorable prognosis.[1]


  • Mood disorders
  • Decreased quality of life
  • Suicide
  • Unemployment
  • Progressive neurological deficits
  • Vision loss
  • Seizures
  • Drowsiness
  • Medication adverse effects

Deterrence and Patient Education

Patients should be educated to become more aware of their headache symptoms and triggers. Interventions should be clearly explained to patients.  

The role of over-the-counter analgesics in medication overuse headaches must be explained to patients. Patients with all types of primary headaches have the potential to overuse analgesics. They should be counseled on the potential for frequent use of these medications to worsen the intensity and frequency of headaches.

Enhancing Healthcare Team Outcomes

Management of patients with chronic headaches will require the efforts of an interprofessional healthcare team. The interprofessional care provided to the patient must use an integrated care pathway combined with an evidence-based approach to planning and evaluating all joint activities. Primary care clinicians (MDs, DOs, NPs, and PAs) obtain the assistance of an internist, a neurologist, or a headache specialist if there's any doubt about the diagnosis. Nurses and psychologists can assist team management by teaching lifestyle changes, mental health supervision, drug overuse detoxification, and medication use recommendations.

Pharmacists can aid the team in checking for appropriate dosing and determining drug interactions, especially if the patient is treated for chronic migraines. Nursing must coordinate activities between the various disciplines and often serve as initial contact points for patients and other team members. All interprofessional team members must document any changes in patient status as they observe them and notify the appropriate other parties on the healthcare team so additional diagnostic and/or therapeutic measures can occur if necessary. Open communication among team members is crucial to optimal patient care.

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 for a good result. [Level 5]

Review Questions


Murinova N, Krashin D. Chronic daily headache. Phys Med Rehabil Clin N Am. 2015 May;26(2):375-89. [PubMed: 25952071]
Sheeler RD, Garza I, Vargas BB, O'Neil AE. Chronic Daily Headache: Ten Steps for Primary Care Providers to Regain Control. Headache. 2016 Nov;56(10):1675-1684. [PubMed: 27552176]
Yancey JR, Sheridan R, Koren KG. Chronic daily headache: diagnosis and management. Am Fam Physician. 2014 Apr 15;89(8):642-8. [PubMed: 24784123]
Headache Classification Committee of the International Headache Society (IHS) The International Classification of Headache Disorders, 3rd edition. Cephalalgia. 2018 Jan;38(1):1-211. [PubMed: 29368949]
Özge A, Faedda N, Abu-Arafeh I, Gelfand AA, Goadsby PJ, Cuvellier JC, Valeriani M, Sergeev A, Barlow K, Uludüz D, Yalın OÖ, Lipton RB, Rapoport A, Guidetti V. Experts' opinion about the primary headache diagnostic criteria of the ICHD-3rd edition beta in children and adolescents. J Headache Pain. 2017 Nov 23;18(1):109. [PMC free article: PMC5745373] [PubMed: 29285570]
Yamani N, Olesen J. New daily persistent headache: a systematic review on an enigmatic disorder. J Headache Pain. 2019 Jul 15;20(1):80. [PMC free article: PMC6734284] [PubMed: 31307396]
Vandenbussche N, Laterza D, Lisicki M, Lloyd J, Lupi C, Tischler H, Toom K, Vandervorst F, Quintana S, Paemeleire K, Katsarava Z. Medication-overuse headache: a widely recognized entity amidst ongoing debate. J Headache Pain. 2018 Jul 13;19(1):50. [PMC free article: PMC6043466] [PubMed: 30003412]
Stovner LJ, Al Jumah M, Birbeck GL, Gururaj G, Jensen R, Katsarava Z, Queiroz LP, Scher AI, Tekle-Haimanot R, Wang SJ, Steiner TJ. The methodology of population surveys of headache prevalence, burden and cost: principles and recommendations from the Global Campaign against Headache. J Headache Pain. 2014 Jan 27;15(1):5. [PMC free article: PMC3907133] [PubMed: 24467862]
Probyn K, Bowers H, Caldwell F, Mistry D, Underwood M, Matharu M, Pincus T., CHESS Team. Prognostic factors for chronic headache: A systematic review. Neurology. 2017 Jul 18;89(3):291-301. [PMC free article: PMC5513814] [PubMed: 28615422]
Diener HC, Solbach K, Holle D, Gaul C. Integrated care for chronic migraine patients: epidemiology, burden, diagnosis and treatment options. Clin Med (Lond). 2015 Aug;15(4):344-50. [PMC free article: PMC4952796] [PubMed: 26407383]
Wei DY, Khalil M, Goadsby PJ. Managing cluster headache. Pract Neurol. 2019 Dec;19(6):521-528. [PMC free article: PMC6902063] [PubMed: 31278205]
Su M, Yu S. Chronic migraine: A process of dysmodulation and sensitization. Mol Pain. 2018 Jan-Dec;14:1744806918767697. [PMC free article: PMC5900816] [PubMed: 29642749]
Deen M, Christensen CE, Hougaard A, Hansen HD, Knudsen GM, Ashina M. Serotonergic mechanisms in the migraine brain - a systematic review. Cephalalgia. 2017 Mar;37(3):251-264. [PubMed: 27013238]
Deen M, Hansen HD, Hougaard A, Nørgaard M, Eiberg H, Lehel S, Ashina M, Knudsen GM. High brain serotonin levels in migraine between attacks: A 5-HT4 receptor binding PET study. Neuroimage Clin. 2018;18:97-102. [PMC free article: PMC5790018] [PubMed: 29387527]
Iyengar S, Johnson KW, Ossipov MH, Aurora SK. CGRP and the Trigeminal System in Migraine. Headache. 2019 May;59(5):659-681. [PMC free article: PMC6593989] [PubMed: 30982963]
Edvinsson L. Role of CGRP in Migraine. Handb Exp Pharmacol. 2019;255:121-130. [PubMed: 30725283]
Schwedt TJ, Chong CD. Medication Overuse Headache: Pathophysiological Insights from Structural and Functional Brain MRI Research. Headache. 2017 Jul;57(7):1173-1178. [PubMed: 28160280]
Lai TH, Wang SJ. Neuroimaging Findings in Patients with Medication Overuse Headache. Curr Pain Headache Rep. 2018 Jan 16;22(1):1. [PubMed: 29340793]
Srikiatkhachorn A, Tarasub N, Govitrapong P. Effect of chronic analgesic exposure on the central serotonin system: a possible mechanism of analgesic abuse headache. Headache. 2000 May;40(5):343-50. [PubMed: 10849027]
Di Lorenzo C, Coppola G, Currà A, Grieco G, Santorelli FM, Lepre C, Porretta E, Pascale E, Pierelli F. Cortical response to somatosensory stimulation in medication overuse headache patients is influenced by angiotensin converting enzyme (ACE) I/D genetic polymorphism. Cephalalgia. 2012 Dec;32(16):1189-97. [PubMed: 23053304]
Wei DY, Yuan Ong JJ, Goadsby PJ. Cluster Headache: Epidemiology, Pathophysiology, Clinical Features, and Diagnosis. Ann Indian Acad Neurol. 2018 Apr;21(Suppl 1):S3-S8. [PMC free article: PMC5909131] [PubMed: 29720812]
Headache Classification Committee of the International Headache Society (IHS). The International Classification of Headache Disorders, 3rd edition (beta version). Cephalalgia. 2013 Jul;33(9):629-808. [PubMed: 23771276]
Micieli A, Robblee J. Medication-overuse headache. CMAJ. 2018 Mar 12;190(10):E296. [PMC free article: PMC5849449] [PubMed: 29530871]
Lee VME, Ang LL, Soon DTL, Ong JJY, Loh VWK. The adult patient with headache. Singapore Med J. 2018 Aug;59(8):399-406. [PMC free article: PMC6109828] [PubMed: 30175370]
Loder E, Weizenbaum E, Frishberg B, Silberstein S., American Headache Society Choosing Wisely Task Force. Choosing wisely in headache medicine: the American Headache Society's list of five things physicians and patients should question. Headache. 2013 Nov-Dec;53(10):1651-9. [PubMed: 24266337]
Agostoni EC, Barbanti P, Calabresi P, Colombo B, Cortelli P, Frediani F, Geppetti P, Grazzi L, Leone M, Martelletti P, Pini LA, Prudenzano MP, Sarchielli P, Tedeschi G, Russo A., Italian chronic migraine group. Current and emerging evidence-based treatment options in chronic migraine: a narrative review. J Headache Pain. 2019 Aug 30;20(1):92. [PMC free article: PMC6734211] [PubMed: 31470791]
Whalen J, Yao S, Leder A. A Short Review of the Treatment of Headaches Using Osteopathic Manipulative Treatment. Curr Pain Headache Rep. 2018 Oct 05;22(12):82. [PubMed: 30291550]
Vyas DB, Ho AL, Dadey DY, Pendharkar AV, Sussman ES, Cowan R, Halpern CH. Deep Brain Stimulation for Chronic Cluster Headache: A Review. Neuromodulation. 2019 Jun;22(4):388-397. [PubMed: 30303584]
Leone M. Deep brain stimulation in headache. Lancet Neurol. 2006 Oct;5(10):873-7. [PubMed: 16987734]
Linde K, Allais G, Brinkhaus B, Manheimer E, Vickers A, White AR. Acupuncture for tension-type headache. Cochrane Database Syst Rev. 2009 Jan 21;(1):CD007587. [PMC free article: PMC3099266] [PubMed: 19160338]
Boes CJ, Black DF, Dodick DW. Pathophysiology and management of transformed migraine and medication overuse headache. Semin Neurol. 2006 Apr;26(2):232-41. [PubMed: 16628534]
Tassorelli C, Jensen R, Allena M, De Icco R, Sances G, Katsarava Z, Lainez M, Leston J, Fadic R, Spadafora S, Pagani M, Nappi G., the COMOESTAS Consortium. A consensus protocol for the management of medication-overuse headache: Evaluation in a multicentric, multinational study. Cephalalgia. 2014 Aug;34(9):645-655. [PubMed: 24558185]
Baraldi C, Pellesi L, Guerzoni S, Cainazzo MM, Pini LA. Therapeutical approaches to paroxysmal hemicrania, hemicrania continua and short lasting unilateral neuralgiform headache attacks: a critical appraisal. J Headache Pain. 2017 Dec;18(1):71. [PMC free article: PMC5519518] [PubMed: 28730562]
Biglione B, Gitin A, Gorelick PB, Hennekens C. Aspirin in the Treatment and Prevention of Migraine Headaches: Possible Additional Clinical Options for Primary Healthcare Providers. Am J Med. 2020 Apr;133(4):412-416. [PubMed: 31712099]
Lipton RB, Munjal S, Brand-Schieber E, Tepper SJ, Dodick DW. Efficacy, Tolerability, and Safety of DFN-15 (Celecoxib Oral Solution, 25 mg/mL) in the Acute Treatment of Episodic Migraine: A Randomized, Double-Blind, Placebo-Controlled Study. Headache. 2020 Jan;60(1):58-70. [PMC free article: PMC7003821] [PubMed: 31647577]
Wiffen PJ, Knaggs R, Derry S, Cole P, Phillips T, Moore RA. Paracetamol (acetaminophen) with or without codeine or dihydrocodeine for neuropathic pain in adults. Cochrane Database Syst Rev. 2016 Dec 27;12(12):CD012227. [PMC free article: PMC6463878] [PubMed: 28027389]
Derry CJ, Derry S, Moore RA. Sumatriptan (all routes of administration) for acute migraine attacks in adults - overview of Cochrane reviews. Cochrane Database Syst Rev. 2014 May 28;2014(5):CD009108. [PMC free article: PMC6469574] [PubMed: 24865446]
Derry CJ, Derry S, Moore RA. Sumatriptan (intranasal route of administration) for acute migraine attacks in adults. Cochrane Database Syst Rev. 2012 Feb 15;2012(2):CD009663. [PMC free article: PMC4164476] [PubMed: 22336867]
Havanka H, Dahlöf C, Pop PH, Diener HC, Winter P, Whitehouse H, Hassani H. Efficacy of naratriptan tablets in the acute treatment of migraine: a dose-ranging study. Naratriptan S2WB2004 Study Group. Clin Ther. 2000 Aug;22(8):970-80. [PubMed: 10972633]
Rapoport AM, Ramadan NM, Adelman JU, Mathew NT, Elkind AH, Kudrow DB, Earl NL. Optimizing the dose of zolmitriptan (Zomig, 311C90) for the acute treatment of migraine. A multicenter, double-blind, placebo-controlled, dose range-finding study. The 017 Clinical Trial Study Group. Neurology. 1997 Nov;49(5):1210-8. [PubMed: 9371896]
Goadsby PJ, Zanchin G, Geraud G, de Klippel N, Diaz-Insa S, Gobel H, Cunha L, Ivanoff N, Falques M, Fortea J. Early vs. non-early intervention in acute migraine-'Act when Mild (AwM)'. A double-blind, placebo-controlled trial of almotriptan. Cephalalgia. 2008 Apr;28(4):383-91. [PubMed: 18294251]
Smith LA, Oldman AD, McQuay HJ, Moore RA. Eletriptan for acute migraine. Cochrane Database Syst Rev. 2001;(3):CD003224. [PubMed: 11687056]
Kelley NE, Tepper DE. Rescue therapy for acute migraine, part 2: neuroleptics, antihistamines, and others. Headache. 2012 Feb;52(2):292-306. [PubMed: 22309235]
Croop R, Goadsby PJ, Stock DA, Conway CM, Forshaw M, Stock EG, Coric V, Lipton RB. Efficacy, safety, and tolerability of rimegepant orally disintegrating tablet for the acute treatment of migraine: a randomised, phase 3, double-blind, placebo-controlled trial. Lancet. 2019 Aug 31;394(10200):737-745. [PubMed: 31311674]
Lipton RB, Dodick DW, Ailani J, Lu K, Finnegan M, Szegedi A, Trugman JM. Effect of Ubrogepant vs Placebo on Pain and the Most Bothersome Associated Symptom in the Acute Treatment of Migraine: The ACHIEVE II Randomized Clinical Trial. JAMA. 2019 Nov 19;322(19):1887-1898. [PMC free article: PMC6865323] [PubMed: 31742631]
Goadsby PJ, Wietecha LA, Dennehy EB, Kuca B, Case MG, Aurora SK, Gaul C. Phase 3 randomized, placebo-controlled, double-blind study of lasmiditan for acute treatment of migraine. Brain. 2019 Jul 01;142(7):1894-1904. [PMC free article: PMC6620826] [PubMed: 31132795]
Smith TR, Winner P, Aurora SK, Jeleva M, Hocevar-Trnka J, Shrewsbury SB. STOP 301: A Phase 3, open-label study of safety, tolerability, and exploratory efficacy of INP104, Precision Olfactory Delivery (POD® ) of dihydroergotamine mesylate, over 24/52 weeks in acute treatment of migraine attacks in adult patients. Headache. 2021 Sep;61(8):1214-1226. [PMC free article: PMC9292844] [PubMed: 34363701]
Modi S, Lowder DM. Medications for migraine prophylaxis. Am Fam Physician. 2006 Jan 01;73(1):72-8. [PubMed: 16417067]
Pringsheim T, Davenport WJ, Becker WJ. Prophylaxis of migraine headache. CMAJ. 2010 Apr 20;182(7):E269-76. [PMC free article: PMC2855933] [PubMed: 20159899]
Markley HG. Verapamil and migraine prophylaxis: mechanisms and efficacy. Am J Med. 1991 May 17;90(5A):48S-53S. [PubMed: 2039020]

Disclosure: Christie Murphy declares no relevant financial relationships with ineligible companies.

Disclosure: Sajid Hameed declares no relevant financial relationships with ineligible companies.

Copyright © 2024, StatPearls Publishing LLC.

This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ), which permits others to distribute the work, provided that the article is not altered or used commercially. You are not required to obtain permission to distribute this article, provided that you credit the author and journal.

Bookshelf ID: NBK559083PMID: 32644509


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