Common Headache Disorders

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Common Headache Disorders

Pei Feng Lim, BDS, MS

Scott De Rossi, DMD, MBA

Massimiliano Di Giosia, DDS

Headaches are the most prevalent neurologic disorder. It is estimated that approximately 50% of the general population have headaches during any given year and more than 90% report a lifetime history of headache. Tension‐type headache (TTH) is the most common form of primary headache, with a lifetime prevalence of about 52% compared to the lifetime prevalence of migraine of 18%. Chronic headache, defined as 15 or more headache days a month, affects 1.7–4% of the world’s adult population. Despite regional variations, headache disorders are a worldwide problem, affecting people of all ages, races, income levels, and geographic areas. Headaches are relatively rare in children but increase with age. Headache in general, and migraine specifically, increases in frequency during adolescence, particularly in women of childbearing age.

CLASSIFICATION

The International Classification of Headache disorders (ICHD‐3; Table 12‐1) classifies headaches based on specific inclusion and exclusion criteria, and is a flexible operational tool for both clinical and research application.1 In this classification there are three domains, namely primary headaches; secondary headaches; and neuropathies, facial pains, and other headache disorders. Nearly 300 different types of headaches and facial pain are described in the ICHD‐3. While some types of headaches are significantly more common than others, one must be mindful that the rate of misdiagnosis is probably equivalent to one’s knowledge (or lack thereof). Diagnostic challenges are compounded by the fact that many patients experience more than one type of headache, and that some patients are, unfortunately, unable to provide an accurate headache history, which is one of the most important aspect of the diagnostic work‐up.

DIAGNOSING HEADACHES

The diagnosis of headache is largely based on clinical symptoms and therefore an accurate history represents a crucial element of the diagnostic process. A comprehensive history needs time, interest, focus, and establishment of rapport with the patient. When to ask what question to elicit specific information is an art that is acquired by practice and improves with experience. Rather than relying on the patient to report pertinent symptoms, the clinician must possess sufficient knowledge to know what questions to ask in succession and what symptoms to explore.

Table 12‐1 ICHD‐3 (International Classification of Headache Disorders, 3rd Edition).

Source: Headache Classification Committee of the International Headache Society (IHS). The International Classification of Headache Disorders, 3rd edition. Cephalalgia, 2018;38(1):1–211.

Part I: The Primary Headaches

  1. Migraine
  2. Tension‐type headache (TTH)
  3. Trigeminal autonomic cephalalgias (TACs)
  4. Other primary headache disorders
Part II: The Secondary Headaches

  1. Headache attributed to trauma or injury to the head and/or neck
  2. Headache attributed to cranial or cervical vascular disorder
  3. Headache attributed to nonvascular intracranial disorder
  4. Headache attributed to a substance or its withdrawal
  5. Headache attributed to infection
  6. Headache attributed to disorder of homeostasis
  7. Headache or facial pain attributed to disorder of the cranium, neck, eyes, ears, nose, sinuses, teeth, mouth, or other facial or cervical structure
  8. Headache attributed to psychiatric disorder
Part III: Neuropathies and Facial Pains and Other Headaches

  1. Painful lesions of the cranial nerves and other facial pain
  2. Other headache disorders

Many patients experience more than one type of headache. Patients may distinguish various types of headaches according to location, severity, triggering factors, or associated factors. For each type of headache, the following elements need to be determined as part of the complete headache history, starting with the headache of greatest importance to the patient: (1) headache location, (2) onset, (3) precipitating factors, (4) quality, (5) intensity, (6) frequency and duration, (7) triggering factors, (8) aggravating factors, (9) relieving factors, and (10) associated factors. Ascertaining the characteristic pain quality may help distinguish one type of headache from another. For instance, while most TTHs are described as tight “band‐like” pain or pressure, migraines tend to be described as “throbbing” or “pounding.” While the pain intensity of a migraine is often rated as severe, that of a TTH is often mild or moderate. Associated factors may include photophobia or phonophobia, which is relevant for the diagnosis of migraine, or the presence of autonomic symptoms, which is relevant for the diagnosis of trigeminal autonomic cephalalgias (TACs). It is often helpful for the patient to complete a headache diary (Figure 12‐1; numerous versions are available for download as smartphone apps), as an aid to establishing a diagnosis, monitoring the headache symptoms, and/or evaluating the response to treatment.2

A table depicts headache diary.

Figure 12‐1 Headache diary.

Source: American Headache Foundation.

A critical consideration in evaluating headache is ruling out an underlying structural lesion or systemic disease, such as intracranial tumor, severe infection, aneurysm, uncontrolled hypertension, or stroke (i.e., secondary headaches). The systematic SNNOOP10 is an important and useful screen for secondary headaches (Table 12‐2).3 A neurologic examination with emphasis on the gross function of the cranial nerves is essential when the history is suggestive of a secondary headache. Diagnostic imaging, such as computed tomography (CT) or magnetic resonance imaging (MRI), is useful in screening for intracranial pathology. An MRI and magnetic resonance angiography (MRA) of the brain with contrast is the diagnostic modality of choice in nonemergent cases. In the presence of a normal neurologic examination, the prevalence of vascular and neoplastic findings is low, 6.6% and 1.4%, respectively.4 In 2020, the American Headache Society recommended against the need for neuroimaging for migraines in the absence of atypical features (Table 12‐2).5

Headaches are highly comorbid with oral and facial pain. The International Classification of Orofacial Pain emphasizes three types of interactions between headaches and orofacial pain.6 First, headache patients can experience additional facial pain during headache attacks; second, headaches may be replaced by facial pain of the same quality, intensity, and duration; and third, facial pain resembling primary headaches may present in headache‐naïve patients. It is not unusual for headaches to present in the midface or dentoalveolar region, mimicking dental pain. Another important comorbidity is psychopathology, especially depression, anxiety, and somatization. Evidence from Genome‐Wide Association Study (GWAS) data suggests significant shared genetic underlying mechanisms for migraine and depression.7 The psychologic status of the patient may need to be assessed by a clinical psychologist, given the well‐demonstrated relationship between chronic head pain, poor sleep, and elevated psychosocial distress. Assessment of disability or limitation of activities, during and after a headache episode, should also be considered, especially for migraineurs. The extent of disability can be gauged using instruments such as a Migraine Disability Assessment (MIDAS) questionnaire and the Headache Impact Test (HIT‐6).8

Table 12‐2 SNNOOP10 red flags to identify secondary headache.

Source: Do TP, Remmers A, Schytz HW, et al. Red and orange flags for secondary headaches in clinical practice: SNNOOP10 list. Neurology. 2019;92(3):134–144.

Sign or Symptom
1 Systemic symptoms including fever
2 Neoplasm in history
3 Neurologic deficit or dysfunction (including decreased consciousness)
4 Onset of headache is sudden or abrupt
5 Older age (after 50 years)
6 Pattern change or recent onset of headache
7 Positional headache
8 Precipitated by sneezing, coughing, or exercise
9 Papilledema
10 Progressive headache in atypical presentations
11 Pregnancy or puerperium
12 Painful eye with autonomic features
13 Post‐traumatic onset of headache
14 Pathology of the immune system such as HIV
15 Painkiller overuse or new drug at onset of headache

PRIMARY HEADACHES

The ICHD‐3 classifies headaches into primary and secondary headaches.1 The primary headaches represent the vast majority of headaches and are defined as headaches without an underlying disease or structural cause. These headaches include migraine, TTH, TAC, and other primary headache disorders (Table 12‐1).

Migraine (ICD‐10: G43)

Migraine is more than “just a headache.” It is a complex but relatively benign neurologic disorder with head pain as one of its clinical manifestations. It is also associated with a broad spectrum of other symptoms caused by the involvement of several brain structures. There are 23 International Classification of Diseases, Tenth Revision (ICD‐10) codes for migraine diagnosis, reflecting the complexity of its subtypes.

Epidemiology

The global prevalence of migraine is approximately 14.4% and it is three times more frequent in females than males.9 In children, abdominal migraine is a subtype of functional abdominal pain affecting about 13.5% of children worldwide. A high incidence of infant colic has been reported in migraineurs compared to controls.10 In females, there is a sudden increase in prevalence during puberty and a decline following menopause. Considering the high prevalence during the most productive years of a patient’s life, there is, consequently, a substantial cost to society due to decreased productivity and increased healthcare utilization. According to the 2016 Global Burden of Disease (GBD) study, migraine is the second most disabling condition in the world (second to low back pain).11 The consequential impaired functioning and decreased quality of life make migraine a debilitating neurologic disease.12 It is therefore no surprise that an increased risk of suicidal behavior has been reported in chronic migraineurs.13 About a third of migraineurs also experience auras, and female migraineurs who experience auras are more susceptible to ischemic stroke.14

Pathophysiology

Migraine is a complex neurovascular headache.15 Its etiopathophysiology is not completely understood. The phenomenon underlying the migraine pain and aura is cortical spreading depression (CSD), which is a self‐propagating neuronal and glial depolarization that spreads across the cerebral cortex. This process results in neuronal dysfunction, substantiated by recent evidence of microstructural abnormalities of the trigeminal nerve in migraineurs.16 The headache also involves recurrent activation of the trigeminocervical complex by neurotransmitters, such as neuropeptides, of which the calcitonin gene‐related peptide (CGRP) is known to be a key player, and other inflammatory mediators, which cause neurogenic inflammation and neuronal sensitization.17 Research on gut–brain interaction suggests that the gut microbiota profile also plays a role in migraine pathogenesis.18

There appears to be a genetic and familial risk, as more than half of all migraineurs report having other family members who suffer from migraine. In addition, specific mutations leading to rare causes of vascular headache have been identified.15 Hemiplegic migraine, for example, is caused by mutations in genes that encode ion channel and transport proteins. Genetic mutations cause impaired neurotransmission and cortical hyperexcitability, which result in increased susceptibility to CSD and impaired sensory processing. The gene and environment interaction has received much attention in the last decade. This epigenetic link in migraine suggests that DNA methylation of numerous genes is also involved in migraine pathogenesis.19

Migraine is a spectrum disorder. In some people, episodic migraine increases in frequency and evolves into chronic migraine, a process known as transformation. The pathophysiologic mechanisms responsible for chronification are not well understood, but likely involve genetic and epigenetic factors, neurogenic inflammation, and central sensitization. In recent years, TTH and migraine have been considered to be part of the same continuous spectrum rather than individual and distinct disease states.

Migraine, especially greater headache pain intensity and frequency, is significantly comorbid with insomnia, depression, anxiety, gastric ulcers, angina, and epilepsy.20 The comorbidity of migraine and temporomandibular disorders (TMD) is also well established.21 Individuals suffering from both TMD and migraine also had higher prevalence of bodily pain and systemic diseases.22 A prospective cohort in the Orofacial Pain: Prospective Evaluation and Risk Assessment (OPPERA) study identified migraine as a risk factor for the development of TMD.23 Therefore, prompt management of migraine may reduce the risk of developing TMD.

Clinical Features

The migraine headache is a moderate to severe, pulsating, unilateral head pain that is aggravated by routine physical activity (such as walking or climbing stairs). In addition, nausea and/or vomiting, or photophobia and phonophobia, are present. Osmophobia has been reported to increase the diagnostic sensitivity of migraine.24 The headache begins with gradual onset, reaching a peak in 2–4 hours. The pain typically lasts 4–72 hours untreated or unsuccessfully treated. Migraine may present as isolated facial pain, rendering it an important differential diagnosis for dental pain and TMD.25 Orofacial migraine is an episodic or chronic pain that presents exclusively in the orofacial region, without head pain, with the characteristics and associated features of migraine as described in the ICHD‐3.6 The three‐item ID Migraine screener is a valid and reliable screening instrument for migraine, which is especially useful in primary care and epidemiologic settings.26

In migraine with aura, the headache is preceded or accompanied by one or more fully reversible aura symptoms. An aura is a unilateral, stereotyped, sensory, motor, visual, speech, brainstem, or retinal focal neurologic symptom. The aura symptoms usually develop gradually and last minutes. Visual aura is the most common. Sensory aura such as paresthesia follow a cortical somatotopic pattern and may involve the face, lips, and tongue. Rarely, focal motor weakness may occur. Prodromal symptoms such as fatigue, poor concentration, and neck stiffness may begin hours to a few days before a migraine. These symptoms should not be confused with aura symptoms. What was previously misconstrued as migraine triggers, such as eating chocolate and bright light, is now known to be prodromal symptoms warning of the impending migraine. These symptoms announce the arrival of the migraine and precede the head pain. Patients should be taught to recognize these prodromal symptoms so that abortive medications can be administered early in the migraine attack for maximum efficacy. Similarly, postdromal symptoms, such as fatigue or mood change, may last hours or a few days following the migraine.

Migraines occurring at least 15 days per month for more than 3 months fulfill the criteria for chronic migraine, although patients with 8 or more migraine days per month are similarly disabled.27 Data from the Chronic Migraine Epidemiology and Outcomes (CaMEO) study suggests that the presence of noncephalic pain (pain in the face, neck, back, arms, legs, chest, abdomen, and other locations) may identify episodic migraineurs who are at risk of chronicity.28 The American Academy of Neurology recommends neuroimaging only for migraine with atypical headache patterns or neurologic signs.29

Management

The management of migraine includes patient education, in addition to pharmacologic and nonpharmacologic strategies. The patient needs to be educated about the diagnosis, etiology, trigger avoidance (if applicable), and management strategies. Generally, pharmacotherapy is divided into prophylactic or preventative therapy, and acute or abortive therapy.

Patients experiencing four or more migraine headache days per month, patients whose migraines significantly interfere with daily routine despite acute treatment, and patients in whom acute treatment is contraindicated, has failed, or is overused (defined as use in 10 or more days per month) are candidates for prophylactic therapy.30 First‐line migraine preventatives (Table 12‐3) include anticonvulsants (such as topiramate, which is the only US Food and Drug Administration (FDA)‐approved oral chronic migraine preventative), β‐adrenergic receptor blockers (metoprolol, propranolol, and timolol), frovatriptan, and onabotulinum toxin A. Second‐line therapy includes amitriptyline, venlafaxine, atenolol, and nadolol. The oral prophylactics must be taken daily and usually have a 2–6‐week period before an effect is observed. Onabotulinum toxin A is FDA approved for the management of chronic migraine and is injected every 3 months via the PREEMPT protocol using a total of 155 units into 31 injection sites.31 Onabotulinum toxin A acts via blocking the release of pro‐inflammatory and excitatory neurotransmitters and reducing the pronociceptive ion channels on the afferent neurons. Monoclonal antibodies (MABs) targeting the CGRP receptor (such as erenumab, fremanezumab, and galcanezumab) have been recently approved by the FDA for the prevention of migraine.32 CGRP pathway blockers are the first mechanism‐specific migraine treatment. The CGRP MABs are injected subcutaneously monthly and are devoid of drug interaction concerns. The most common adverse effects are injection site discomfort, constipation, and hypertension. They are indicated upon failure of at least two oral preventatives or inadequate response to at least two quarterly injections of onabotulinum toxin A.30 A reasonable goal for preventative therapy is a 50% reduction in migraine headache days, a significant decrease in migraine duration or pain intensity, improved response to acute treatment, reduction in migraine‐related disability, or improvement in quality of life.

Table 12‐3 Migraine preventative medications listed in order of most established efficacy.

Drug Class Examples
Anticonvulsants Topiramate, valproate sodium, divalproex sodium
Beta‐adrenergic blockers metoprolol, propranolol, timolol
Onabotulinum toxin Onabotulinum toxin A
Calcitonin gene‐related peptide monoclonal antibodies (CGRP MABs) Erenumab, fremanezumab, galcanezumab
Triptans Frovatriptan
Antidepressants Amitriptyline, venlafaxine

Episodic migraine can often be managed with abortive therapy alone. While most individual attacks are successfully managed with oral agents, parenteral drugs may be necessary when nausea and/or vomiting accompany the attacks. Abortive agents for migraine (Table 12‐4) include the nonsteroidal anti‐inflammatory drugs (NSAIDs), ergotamine derivatives, the triptans (5‐HT1B/1D/1F agonists), opioids, and the gepants (CGRP receptor antagonists). Ergotamine and its derivatives are nonselective 5‐hydroxytryptamine (5‐HT1) receptor agonists, whereas the triptans are selective 5‐HT1 receptor agonists. Triptans are available in oral, nasal, and parenteral formulations, and in combination with NSAIDs. They are contraindicated in ischemic vascular conditions, uncontrolled hypertension, and other significant cardiovascular disease. A novel selective 5‐HT1F receptor agonist, lasmiditan, is devoid of vasoconstrictor properties.33 Lasmiditan acts presynaptically to block the release of pro‐nociceptive neurotransmitters, and therefore has a high positive response rate. It is also a more specific agonist, resulting in fewer side effects, most commonly dizziness. Novel CGRP receptor antagonists, the gepants (such as ubrogepant and rimegepant), have also been recently approved by the FDA for the acute treatment of migraine.34 The gepants do not have a vasoconstrictor effect either. The blockage of the CGRP pathway in the form of both abortive agents and prophylaxis has blurred the line in the concept of acute versus preventative therapy. It is noteworthy that the presence of cutaneous allodynia increases the likelihood of poor response to treatment for all oral abortive agents, urging the need for prompt administration at migraine onset and the use of intranasal and injectable agents (due to faster onset compared with oral agents).35 It is also noteworthy that frequent use of migraine‐abortive medications may cause medication‐overuse headaches (defined as the use of abortive medication for 10–15 days per month and that the abortive is causing the increase in headaches).

Table 12‐4 Migraine‐abortive medications (listed in order of most established efficacy).

Drug Class Examples
Nonsteroidal anti‐inflammatory drugs (NSAIDs) Aspirin, ibuprofen, diclofenac, naproxen
Ergot alkaloids Dihydroergotamine, ergotamine
Triptans (5HT receptor agonists) Almotriptan, eletriptan, frovatriptan, naratriptan, rizatriptan, sumatriptan, zolmitriptan, lasmiditan
Gepants (calcitonin gene‐related peptide [CGRP] receptor antagonists) Ubrogepant, rimegepant
Opioids Butorphanol

Nonpharmacologic management plays an important role in the management of migraine. This includes biobehavioral therapies such as relaxation training, biofeedback, cognitive behavioral therapy, mindfulness and meditation, and other forms of complementary and alternative therapies such as acupuncture treatment.36 These modalities are important for patients in whom pharmacologic management is contraindicated and for those who prefer nonpharmacologic management. In addition, when combined with pharmacotherapy, they may enhance the clinical therapeutic outcome or permit a reduction in the amount of medications used. Pericranial nerve blocks, including occipital nerve blocks and sphenopalatine ganglion blocks, have been investigated for both migraine abortion and prevention.37 They are associated with few contraindications, good safety, and are generally well tolerated. Percutaneous implantation of neurostimulators and surgical decompression procedures have also received much attention despite the lack of well‐designed clinical trials. Neuromodulation approaches such as single‐pulse transcranial magnetic stimulation, noninvasive vagus nerve stimulation, and external trigeminal nerve stimulation have been approved by the FDA for migraine treatment.38 Last but not least, adequate management of migraine comorbidities is integral to the success of migraine management. Comorbid depression, anxiety, insomnia, and widespread pain (including TMD) should be identified and their management prioritized.

Tension‐Type Headache (ICD‐10: G44.2)

Epidemiology

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Nov 28, 2021 | Posted by in General Dentistry | Comments Off on Common Headache Disorders

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