Myth #1: if a headache is bilateral and/or squeezing, then it is not a migraine

Tension-type headache is the most common primary headache disorder,1 with a lifetime prevalence of 30%–78%. It is usually bilateral, non-throbbing, not associated with migrainous features, and not typically disabling.4 While migraine is generally unilateral and throbbing, it can be bilateral (40%) and can be described as pressure-like (75%).5 Furthermore, migraine can be ‘imploding’ in quality, described as bilateral tightness, stiffness, and vice-like pain with pressure squeezing in. In a prospective cross-sectional survey of 198 female patients with migraine, 31.6% of subjects described their migraine as imploding, and 10.2% described them as both imploding and exploding.6 Furthermore, although triptans do not work for pure tension-type headache, triptans are effective in patients with migraine with attacks that phenotypically resemble tension-type headache.7

A common misunderstanding among patients and clinicians alike (reinforced by simplistic cartoons perpetuated on the internet) is that migraine and tension-type headache are differentiated by whether the headache is unilateral versus bilateral. However, this is an oversimplification. Based on the ICHD-3 criteria,4 migraine and tension-type headache are differentiated based on the attack duration, headache characteristics, and associated symptoms (boxes 1 and 2). Patients with tension-type headache do not present with typical migrainous features; they cannot have nausea or vomiting and can have no more than one of photophobia or phonophobia.

The clinical distinction between tension-type headache and migraine is crucial for therapeutic reasons. There are many evidence-based treatments for migraine that are not indicated for tension-type headache, including triptans, calcitonin gene-related peptide antagonists, and chemodenervation with onabotulinumtoxinA for chronic migraine. If the migraine diagnosis is missed, patients will not receive these evidence-based treatments.8 Furthermore, if these relatively expensive treatments are used when they are not indicated, it may impact the resources available for those who need them.

Conclusion: Migraine is distinguished from tension-type headache by the headache characteristics and the presence of migrainous features. Contrary to popular belief, migraine is bilateral in 40% of cases and ‘imploding’ in over 30% of cases.

Myth #2: men are more likely to get cluster headache than migraine

Clinicians often remember from their training that cluster headache (box 3) has a male predominance, while migraine has a female predominance. However, this does not mean that men are more likely to develop cluster headache than migraine, a misunderstanding that likely contributes to men being underdiagnosed and undertreated for migraine. In our clinical experience, this also results in encountering many men with migraine who have been misdiagnosed by prior physicians with cluster headache.

Replicating many prior studies, a recent epidemiology study by Schor et al,9 found that men were more likely than women to have cluster headache between 10 and 50 years of age. In a meta-analysis of population-based studies, Fischera et al showed a lifetime cluster headache prevalence of 0.12% with an overall sex ratio of 4.3 (men to women).10 However, cluster headache is about 100 times rarer than migraine, with migraine affecting an estimated 12% of the population and over 1 billion people worldwide in 2019.1 Likely due to the influence of sex hormones, the prevalence of migraine in women is higher than in men (19.0% vs 11.2%).1 Putting this all together, due to the high prevalence of migraine and the much lower prevalence of cluster headache, existing data provide irrefutable evidence that men are more likely to suffer from migraine than cluster headache.10 11

Conclusion: Migraine affects over 1 billion people worldwide annually. Therefore, despite men being three times more likely to be affected by cluster headache than women, migraine is roughly 100 times more common among men than is cluster headache.

Myth #3: migraine with neck pain is equivalent to cervicogenic headache

It can be useful to divide patients with head and neck pain into three categories.

The first category is the population of patients with migraine or another primary headache disorder who only have neck pain before or during a headache attack and have physical exams and imaging that are not suggestive of cervical pathology. In these patients, neck pain is likely a symptom of the primary headache disorder due to central sensitization rather than a cervical pain generator.

The second category of patients is the population with no prior history of migraine or other primary headache disorder with cervical pathology on exam and/or imaging that is likely causing their headache and neck pain; these are the patients with pure cervicogenic headache. The likelihood of cervicogenic headache increases with a history of plausible inciting causes such as whiplash injuries as well as the absence of migrainous features. The age distribution of these patients likely skews older than the more well-defined age distribution of migraine.

The third category is the population of patients who straddle these first two cleanly defined groups, where cervical pain generators such as painful C2/3 facet joints might be causing a new-onset of migraine-type headache or worsening a pre-existing primary headache disorder, such as causing episodic migraine to become more frequent and turn into chronic migraine. In our experience, these patients often benefit from a combination of treatment with both migraine medications and percutaneous treatments for cervicogenic headache.

Based on the ICHD-3 criteria, neck pain is not part of the criteria for migraine, nor does it distinguish migraine from cervicogenic headache (box 4) or other headache disorders. If a pain practitioner encounters a patient with headache and neck pain with unrevealing imaging studies, without inciting cervical cause, and/or who does not respond to cervical interventions, a migraine history should be taken (including assessing for presence of photophobia, phonophobia and nausea with headaches and whether the neck pain is only present at the beginning of or during a headache attack). If the patient meets ICHD-3 criteria for migraine, the clinician should consider the possibility that the patient’s neck pain is a migraine symptom.

Pain doctors might not realize that in many patients with migraine, neck pain can occur as a migraine symptom, even in the absence of cervical pathology. Epidemiological and cross-sectional studies have found a high rate of cervical symptoms among patients with migraine, but these studies are unable to answer ‘chicken and egg’ questions of causation. Among patients with migraine, population-based studies have reported a neck pain prevalence in upwards of 75% of adult patients,12 and provide evidence that neck pain is more frequently associated with migraine than is nausea. Al-Khazali et al, in a recent meta-analysis,13 showed that 77% of patients with migraine in clinic-based studies reported neck pain, compared with only 23% of non-headache controls. The odds ratio (OR) of neck pain in patients with migraine was 11.5 (95% CI 5.8 to 22.4) compared with non-headache controls; the OR in chronic migraine was 2.04 (95% CI 1.3 to 3.3) compared with episodic migraine.13 Anarte-Lazo et al, in another meta-analysis,14 found a greater range of rotation reduction (by cervical flexion-rotation test) in cervicogenic headache than in migraine. Migraine also displayed a reduced cervical range of motion versus asymptomatic individuals.14 However, the clinical validity of the cervical flexion-rotation test has been questioned.15

Pain practitioners should recognize that cervical symptoms are highly prevalent among patients with migraine, and that the pain practitioner’s task is to use history, exam, imaging, clinical reasoning, and appropriate use of diagnostic injections and other procedures to tease apart which of the aforementioned categories to place a given patient into. Neck pain and migraine both involve activation of the trigeminocervical complex (TCC). While conflicting data exist, neck pain may result from migraine-related central sensitization, cervical pain generators, and local inflammation-related peripheral sensitization.16 17 There is likely a bidirectional relationship between migraine and neck pain. Given the high prevalence of migraine (over 1 billion people worldwide), its heritability, and its typical onset in the first four decades of life, one of the common causes of neck pain is often likely migraine, especially in patients without cervical pathology. Conversely, neck pain can also reflect the underlying upper cervical pathology. True cervicogenic headache, with prevalence ranging from 0.4% to 4%, often benefits from cervical spine interventions, such as medial branch blocks and radiofrequency ablations.18 19 In short, pain practitioners need to know that episodic neck pain may be a norm among people with migraine, and is likely more often an accompanying symptom of migraine than its cause.

Conclusion: Neck pain and reduced range of motion may present in both migraine and cervicogenic headache. Recognizing that such clinical nuance exists is critical in reaching the correct diagnosis and deciding subsequent treatment.

Myth #4: migraine is just a headache and is not serious

While migraine may not be deadly, its seriousness is due to the disability that it causes and the effects it has on the lives of patients and their families. Migraine is the second leading cause of years lived with disability for ages 15–49 worldwide.1 Migraine’s disability is beyond headache alone. People with migraine experience numerous non-headache symptoms, including nausea, vomiting, photophobia, and phonophobia. Some experience aura before or during an attack, characterized by reversible neurological symptoms, including visual changes, sensory, language, brainstem, or motor symptoms. They also often experience various prodromal (or premonitory) and postdromal symptoms before and after the headache that contribute to migraine disability. These symptoms can impact the ability to carry out daily activities leading to reduced productivity and decreased quality of life. Underdiagnosis, social stigma, and lack of appropriate care further exacerbate the overall impact.20 21

Migraine has negative impacts not only on patients but also on their family members, activities, and relationships. The burden of migraine on the patient’s family was greater among those with chronic migraine than among people with episodic migraine. Migraine has also been linked to an increased risk of depression, anxiety, stroke, and cardiovascular disease. Migraine with aura conveys an increased risk of ischemic stroke, hemorrhagic stroke, and cardiovascular disease.22 While the correlation between the frequency of migraine attacks and the risk of stroke exists, there are no data indicating that migraine prophylaxis decreases the risk of a migrainous infarct.

Conclusion: Migraine is a debilitating disease with serious sequela for patients and their families. It is crucial for physicians and the public alike to understand that migraine is a leading cause of disability worldwide so that patients with migraine seek medical treatment and providers deliver the appropriate diagnosis and treatments. It is also important for policymakers to recognize that migraine is a disabling disease that is treatable and deserving of resources.

Myth #5: sinus headaches are caused by allergies

In an observational study, Schreiber et al found that 88% of patients with a ‘sinus headache’ history fulfill the International Headache Society migraine or migrainous criteria.23 ‘Sinus headache’, which may feel like an infection in the sinuses, can often be migraine with nasal symptoms (eg, rhinorrhea). According to the American Academy of Otolaryngology—Head and Neck Surgery guidelines, rhinosinusitis is defined as symptomatic inflammation of the paranasal sinuses and nasal cavity that can be classified by duration as acute (<4 weeks) or chronic (>12 weeks).24 Sinus inflammation, which may be due to allergy or infection, can cause pressure, pain, and discomfort in the face. They often report sinus pressure, sinus pain, and nasal congestion. However, nasal obstruction or facial pain without purulent nasal drainage is not consistent with rhinosinusitis. In another observational study, Kari et al showed that 82% of patients with ‘sinus headache’ with negative findings on nasal endoscopy or sinus computer tomography had significant head pain reduction with triptan use.25 The ICHD-3 defines diagnostic criteria for headache attributed to rhinosinusitis: any headache phenotype is allowed, but there must be clinical, nasal endoscopic, or imaging evidence of paranasal sinus infection/inflammation, as well as evidence of causation.4 In rare instances, isolated sphenoid sinusitis can present with atypical and noncharacteristic headache, which is most commonly in the vertex but can be anywhere in the craniofacial region and may be associated with cranial nerve involvement. While the presentation of headaches secondary to sinus disease may overlap with primary headache disorders, it is important to evaluate for the possibility of migraine.

However, it is important not to oversimplify all sinus headache as migraine. Positive migraine histories apparently do not obviate the need for a thorough otolaryngologic evaluation, including nasal endoscopy or sinus computer tomography, especially in patients with persistent sinus pain. In the case where headache is associated with mucosal contact points, nasal surgery may be needed.

Conclusion: Rather than caused by allergy or rhinitis, nearly 90% of patients with ‘sinus headache’ meet migraine criteria.

Myth #6: response to occipital nerve block is specific for occipital neuralgia

The response to occipital nerve block (ONB) is required but insufficient to diagnose occipital neuralgia. Per ICHD-3, occipital neuralgia is defined by headache presentation and exam findings, along with the response to ONB (box 5). Many pain providers may conflate occipital headache with occipital neuralgia.26 Occipital headache can be a symptom of many primary and secondary headache disorders, and the effect of an ONB is not limited to occipital headache. For example, for those with occipital headache who respond to ONB but have migrainous symptoms, the most likely diagnosis is migraine. That said, having a migraine diagnosis does not negate the possibility of concurrent occipital nerve compression or inflammation. The convergence of sensory input from both cervical and trigeminal fibers in the TCC provides the rationale for the use of ONBs in the treatment of various headache disorders, not just occipital neuralgia.27 Typically, ONB leads to increased pressure pain thresholds in the trigeminal distribution, inhibiting central sensitization in the TCC.28

The majority of evidence for ONBs is for use in migraine. In a narrative review of peripheral nerve blocks for headache management, 11/12 randomized controlled trials (RCTs) showed ONBs reduced migraine intensity, frequency, and duration compared with placebo, with no difference with or without steroid use.29 Two RCTs show the benefit of ONBs with steroids in cluster headache and another one in cervicogenic headache. In contrast, the evidence is limited to observational studies in occipital neuralgia, as well as in status migrainosus, prolonged aura, and post-dural puncture headache.

Conclusion: ONB has evidence of efficacy for treating migraine, CH, and cervicogenic headache, and as such, response to ONB is not diagnostic of occipital neuralgia. According to the ICHD-3, response to ONB is necessary but insufficient to diagnose occipital neuralgia.