Headache
Steven A. Godwin
Daniel Eraso
THE CLINICAL CHALLENGE
Headache is the fifth most common presenting symptom to the emergency department (ED), which recorded over 4 million visits in 2014, accounting for 3% of ED encounters.1 Most headaches stem from a benign etiology, and most symptoms are self-limiting, requiring minimal workup and treatment. Such headaches are classified as primary headaches, in contrast to secondary headaches, which are manifestations of underlying disease. The clinical challenge lies in rapidly diagnosing and treating the small minority of deadly secondary headaches masquerading as benign headaches. A focused history and physical, placing emphasis on a thorough neurologic exam, can narrow the differential diagnosis and guide the subsequent workup and treatment (Table 16.1).
TABLE 16.1 Primary versus Secondary Headache | ||||||||||||
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PATHOPHYSIOLOGY
The parenchyma of the brain lacks pain receptors, and thus the sensation of headache is thought to arise from activation of sensory fibers of the meninges and large blood vessels. Activation of these sensory pathways is poorly localized and can extend to cervical and facial foci. The pathophysiology of migraine headaches has been more closely studied, and symptom activation involves the complex interaction of genetic predisposition, environmental factors, metabolic abnormalities, and hormonal influences, resulting in a cascade of neuropeptide modulation and subsequent central nervous system (CNS) activation.2 Exact mechanisms for the underlying pathophysiology of migraine have shifted over time, but current theories propose a complex interplay of neurovascular activation and neurochemical feedback loops involving serotonin, calcitonin gene-related peptide (CGRP), and other inflammatory neuropeptides involving the trigeminal nerve, the trigeminal cervical complex in the brainstem, and multiple pathways through the midbrain and cortex. Serotonin functions as both a vasoconstrictor and an inhibitor of CGRP release, whereas CGRP is implicated in vasodilation and the sterile inflammation of the meninges.
PREHOSPITAL CONCERNS
Headache management often starts in the prehospital setting, with approximately 1% of emergency medical service (EMS) transports for a primary complaint of headache; however, treatment is rarely initiated. In one study, most patients transported via EMS for headache did not receive analgesic medications (>90%), and of those who did receive medication the most common analgesic was an opioid, which is incongruent with established guidelines for headache management.3 Acetaminophen, nonsteroidal anti-inflammatory drugs (NSAIDs), triptans, or antidopaminergic medications may have a role in early symptom control.
EMS systems also play a critical role in destination decisions. For suspicion of headache associated with cerebrovascular accidents, use of a standardized stroke scale such as the Cincinnati Prehospital Stroke Scale should be routinely utilized, and patients with abnormal findings should be transferred to a stroke capable facility. Similarly, headaches secondary to traumatic injury with changes in Glasgow Coma Scale (GCS), pupillary size, or vital sign abnormalities should be transferred to appropriately capable trauma centers, because decreases in mortality have been demonstrated with evaluation at major trauma centers that have neurosurgical capabilities.
APPROACH/THE FOCUSED EXAM
Stabilization
The approach to the patient with headache will be driven largely by the history and physical, which in turn forms the differential diagnosis. Some of these patients will present in extremis, and rapid stabilization and resuscitation may be required. The patient that presents altered and vomiting, with difficulty protecting their airway may require endotracheal intubation to facilitate a safe workup and treatment. The underlying etiologies associated with the initial presentation of headache are diverse and may require both simple and complex stabilization strategies. Addressing the respiratory status and correcting hypoxemia as needed, optimizing hypotension and ensuring adequate cerebral perfusion pressure, or identifying and correcting hypoglycemia or other metabolic derangements all fall within the initial resuscitative pathway.
History
The history may identify red flag findings suggestive of a life-threatening cause of a headache, see Table 16.2.
A patient’s specific headache history can provide useful information in the workup of undifferentiated headache. Patients may report a prior history of headache similar in character, location, duration, and/or severity.
Clarifying the circumstances surrounding the onset of headache is critical. Patient presentations of severe headaches with acute onset, within seconds to minutes, are considered potentially
more ominous owing to their “thunderclap” nature and their association with subarachnoid hemorrhage (SAH). Frequently, patients will remember exactly what they were doing at the time of onset. Given the prevalence and high risk of morbidity and mortality, the preponderance of studies involving acute headache have focused mostly on SAH. A headache that develops over hours to days is less concerning for SAH. Other considerations for so-called thunderclap headache presentation include other intracranial hemorrhage, cerebral venous thrombosis (CVT), reversible cerebral vasoconstriction syndrome (RCVS), cervical artery dissection (CeAD), or, less commonly, spontaneous intracranial hypotension (SIH); see Table 16.3.
more ominous owing to their “thunderclap” nature and their association with subarachnoid hemorrhage (SAH). Frequently, patients will remember exactly what they were doing at the time of onset. Given the prevalence and high risk of morbidity and mortality, the preponderance of studies involving acute headache have focused mostly on SAH. A headache that develops over hours to days is less concerning for SAH. Other considerations for so-called thunderclap headache presentation include other intracranial hemorrhage, cerebral venous thrombosis (CVT), reversible cerebral vasoconstriction syndrome (RCVS), cervical artery dissection (CeAD), or, less commonly, spontaneous intracranial hypotension (SIH); see Table 16.3.
TABLE 16.2 Red Flags by History Onset: Sudden or “Thunderclap,” Associated with Trauma | |
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The headache location can likewise narrow the differential. Unilateral headaches with associated phonophobia or photophobia are suggestive of migraine headache, whereas discrete focal head pain can indicate giant cell arteritis (GCA), temporomandibular joint dysfunction, occipital neuralgia, or sinus headaches.
Understanding the duration of the pain can also assist in identifying a diagnosis. Those patients with persistent cephalgia over weeks to months are unlikely to represent an acute process but may have equally concerning underlying pathology, such as chronic subdural hemorrhage, or malignancy.
Clarifying exacerbating or alleviating factors can be helpful. Stress, sleep disorders, food, alcohol, hormonal changes, visual and olfactory stimuli, weather changes, heat, and sexual activity may all be triggers for acute migraines. Positional triggers for the onset of headache may indicate the presence of intracranial hypertension or intracranial hypotension. Geographical headaches can alert the clinician to inquire further to unmask environmental concerns for carbon monoxide poisoning. Visual changes or eye pain can be associated with GCA or acute angle closure glaucoma.
Physical Exam
Vital Signs
The physical exam starts with the evaluation of vital signs, with particular attention paid to temperature and blood pressure. Headaches can develop as a nonspecific manifestation of an acute viral illness with associated fever; however, intracranial infections such as meningitis, encephalitis, and
intracranial abscess must be considered. Posterior reversible encephalopathy syndrome, intracranial hemorrhage, stroke, herniation, and preeclampsia may all present with hypertension. Hypoxia or anemia may also manifest with tachycardia and headache.
intracranial abscess must be considered. Posterior reversible encephalopathy syndrome, intracranial hemorrhage, stroke, herniation, and preeclampsia may all present with hypertension. Hypoxia or anemia may also manifest with tachycardia and headache.
TABLE 16.3 Dangerous Causes of Secondary Headache | |
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Neurologic Exam
The complete neurologic exam is outlined in Chapter 2: The Neurologic Examination. The focused neurologic exam in a patient with a complaint of headache should include a mental status exam, motor and sensory exams, gait evaluation, and cranial nerve exam. Nonfocal changes in mental status can be seen in infections or metabolic derangements. Focal neurologic deficits are associated with intracranial pathology such as stroke, intracranial hemorrhage, or more benign etiologies such as hemiplegic migraine. Cranial nerves II to VIII are particularly pertinent to the patient presenting with headache. Evaluation of cranial nerve II includes evaluation of visual fields to localize lesions in the optic tract versus cortical lesions. Fundoscopy is performed to assess for signs of papilledema. Abnormalities in extraocular movements can indicate space occupying lesions that affect cranial nerves III, IV, or VI. Aneurysmal compression of the superficial parasympathetic fibers of cranial nerve III from the posterior communicating artery can cause pupillary dilation manifesting as anisocoria.
Head and Neck
Headache associated with stiff or painful neck movements can reflect inflammation of the meninges and can be seen in meningitis and SAH. Tenderness to palpation along the temporal arteries is concerning for GCA. Palpation lateral to the occipital protuberance may reproduce pain originating from occipital neuralgia. Frontal or maxillary tenderness may represent sinusitis. Acute otitis media can cause headache, and mastoid tenderness is commonly seen in mastoiditis.
Eye
Visual acuity should be checked and documented in all patients presenting with headache and vision changes. In patients presenting with a history consistent with acute angle glaucoma, intraocular pressures should be measured. A fundoscopic exam should be performed to evaluate for papilledema secondary to increased intracranial pressure (ICP), as seen in idiopathic intracranial hypertension (IIH), intracranial hemorrhage, or mass lesions. Alternately, bedside ultrasound has been used to measure optic sheath diameter, with measurements >5 mm concerning for elevated ICP (Figure 16.1).
PRIMARY HEADACHES
Primary headaches are biologic disorders of the brain that result in activation of the cerebrovascular pain pathways and include migraine, tension-type, and cluster headache. In contrast, secondary headaches result from underlying medical conditions such as vascular, infectious, anatomic, or metabolic abnormalities.
Migraine headache is the most common headache presentation seen in the ED. More common in females, migraine headaches usually peak in middle age, and then gradually decline in prevalence. The typical presentation is a moderate to severe headache that is unilateral, pulsatile, and often associated with nausea, vomiting, photophobia, and/or phonophobia.4 A patient may be able to identify migraine triggers such as stress, sleep deprivations, association with menstrual cycle, caffeine, and others. Migraine with aura is a headache preceded by distinct neurologic symptoms that are fully reversible usually after only a few minutes. Typical aura symptoms include visual and/or sensory changes but can also include motor dysfunction or speech abnormalities.
Tension-type headaches account for most headaches in the general population, although symptoms are usually mild enough for home treatment without further workup. Various studies approximate 50% lifetime prevalence, with women affected more than men. Tension-type headaches are usually mild to moderate, bilateral, pressure or bandlike tightening that is not pulsatile or throbbing, and without nausea, vomiting, photophobia, or phonophobia. Tension-type headaches are not typically exacerbated by exertion, whereas migraine headaches usually exhibit this association.
 Figure 16.1: Ocular ultrasound with measurements of optic nerve sheath diameter (ONSD) at 3 mm posterior to retina. A, Normal measurement of 3 mm. B, Abnormal measurement of 6.2 mm. Images courtesy of Thomas Cook, MD; and from McAdams BH, Ellis KB. Does this thyroid nodule need to be biopsied? In: Bornemann P, ed. Ultrasound for Primary Care. Wolters Kluwer; 2021. Figure 3.5. |
Trigeminal autonomic cephalagias are a group of headache disorders that include cluster headaches, paroxysmal hemicrania, and hemicrania continua. Cluster headaches are typically severe, acute in onset, unilateral sharp or stabbing periorbital pain, with associated ipsilateral autonomic symptoms, including lacrimation, ptosis, miosis, eyelid edema, nasal congestion, and/or facial/forehead anhidrosis. These headaches are more common in males in the 20- to 40-year age range and usually last for 15 minutes to 3 hours. They typically recur over weeks to months over a defined period of time. Headaches in paroxysmal hemicrania are similar in character to cluster headaches but shorter in duration. Hemicrania continua is a similar headache that lasts for >3 months. Both paroxysmal hemicrania and hemicrania continua typically respond to indomethacin.
Other primary headache disorders include headaches associated with cough, exercise, sexual activity, cold stimulus (“brain freeze”), as well as primary stabbing headaches, nummular headaches, hypnic headaches, and new daily persistent headaches.
MANAGEMENT
Once a presumptive primary headache disorder is diagnosed and dangerous secondary causes are ruled out, treatment should be administered targeting pain and associated symptoms (Table 16.4).5 As most primary headaches presenting to the ED are accompanied by nausea and vomiting with decreased oral intake, IV fluid replacement is often indicated. Antidopaminergic medications such as prochlorperazine, promethazine, droperidol, and haloperidol are thought to treat the underlying etiology of migraine headaches and have additional antiemetic and sedative effects. Extrapyramidal side effects of antidopaminergic medications, including akathisia and dystonia, occur at rates 10% to 45%, thus coadministration of diphenhydramine is recommended. All of these medications are known to prolong the QT interval, although the clinical significance is less clear. Metoclopramide also has antidopaminergic properties in addition to serotonin reception antagonism.
NSAID medications are frequently given in conjunction with antidopaminergic medications, commonly ketorolac. Acetaminophen can be administered by mouth or intravenously. Sumatriptan or dihydroergotamine can be administered either parenterally or intranasally. Corticosteroids such as dexamethasone have a greater effect on preventing headache recurrence than on the acute management of symptoms and should be considered an adjunct to standard therapy. Regional anesthesia may be useful, such as in sphenopalatine nerve blocks for migraine or occipital nerve blocks for occipital neuralgia.
In patients presenting to the ED with severe migraine, a reasonable initial approach could include intravenous NSAIDs (eg, ketorolac), an antidopaminergic antiemetic (eg, metoclopramide, prochlorperazine), diphenhydramine, and intravenous hydration. An alternate approach administering subcutaneous sumatriptan would circumvent the resource requirements of intravenous access. In view of the ongoing opioid crisis of misuse and abuse, multiple national and
international organizing committees recommend against the use of opioid medications in favor of the above nonopioid options.6
international organizing committees recommend against the use of opioid medications in favor of the above nonopioid options.6
TABLE 16.4 Primary Headache Treatment | ||||||||||||||||||||||||||||||||||||||||||||
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SUBARACHNOID HEMORRHAGE
EPIDEMIOLOGY
With potential mortality >50%, SAH is a condition that requires rapid diagnosis, and even when managed appropriately, up to 50% of survivors have long-term neurologic deficits.7 SAH accounts for approximately 1% of all patients presenting to the ED with headache; however, this number increases to upward of 10% in those patients presenting with acute onset “thunderclap” headaches.10 Ruptured aneurysm is the underlying etiology of nontraumatic SAH in 70% to 80% of cases, and other causes include arteriovenous malformations, angiomas, and neoplasm. Risk factors include age (predominantly 40-60 years old), hypertension, smoking history, and sympathomimetic drug use, as well as family histories of aneurysm in first-degree relatives, autosomal dominant polycystic kidney disease, Marfan syndrome, and Ehlers-Danlos syndrome.
PRESENTATION
The classic presentation of SAH is a sudden onset “thunderclap” headache that is often described as the worst in the patient’s life and that peaks within seconds or minutes, although a subset of patients may present with worsening headache over an hour. Patients complaining of a headache that is historically different in quality or severity should also prompt investigation of SAH. The headache is often exertional or associated with Valsalva, micturition, or sexual intercourse. Other commonly associated symptoms include nausea and vomiting, neck stiffness, meningismus, focal neurologic deficits, or seizure.
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