CHAPTER 20 Headache. Christopher S. Russi. PERSPECTIVE Epidemiology. DIAGNOSTIC APPROACH Differential Considerations

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1 CHAPTER 20 Headache Christopher S. Russi PERSPECTIVE Epidemiology Up to 85% of the U.S. adult population reports significant headaches at least occasionally, and 15% does so on a regular basis. Headache as a primary complaint represents 3 to 5% of all emergency department (ED) visits. The vast majority of patients who have a primary complaint of headache do not have a serious medical cause for the problem. Tension headache accounts for approximately 50% of patients visiting the ED, another 30% have headache of unidentified origin, 10% have migraine-type pain, and 8% have headache from other potentially serious causes (e.g., tumor, glaucoma). It is estimated that less than 1% of patients who come to the ED with headache have a life-threatening organic disease. 1 These percentages can create a false sense of security, and headache is disproportionately represented in emergency medicine malpractice claims. Although still rare, the most commonly encountered life-threatening cause of severe sudden head pain is subarachnoid (SAH); approximately 20,000 potentially salvageable cases of SAH are seen in EDs each year. It is estimated that 25 to 50% of these are missed on the first presentation to a physician. 2 The other significant, potentially life-threatening causes of headache occur even less frequently. Meningitis, carbon monoxide poisoning, temporal arteritis, acute angle-closure glaucoma, intracranial (ICH), cerebral venous sinus thrombosis, and increased intracranial pressure can often be linked with specific historical elements and physical findings that facilitate their diagnosis. Pathophysiology The brain parenchyma is insensitive to pain. The pain-sensitive areas of the head include the coverings of the brain (the meninges), the blood vessels (both arteries and veins supplying the brain) and the various tissues lining the cavities within the skull. The ability of the patient to specifically localize head pain is often poor. Much of the pain associated with headache, particularly with vascular headache and migraines, is mediated through the fifth cranial nerve. Such pain may proceed back to the nucleus and then be radiated through various branches of the fifth cranial nerve to areas not directly involved. A specific inflammation in a specific structure (e.g., periapical abscess, sinusitis, or tic douloureux) is much easier to localize than the relatively diffuse pain that may be generated by tension or traction headaches. Pains in the head and neck may easily overlap. They should be thought of as a unit when complaints of headache are considered. DIAGNOSTIC APPROACH Differential Considerations The differential diagnosis of headache is complex because of the large number of potential disease entities and the diffuse nature of many types of pain in the head and neck region (Table 20-1). However, in evaluating the patient with a headache complaint, the top priority is to exclude the life-threatening causes: SAH and ICH, meningitis, encephalitis, and mass lesions. Carbon monoxide is an exogenous toxin, the effects of which may be reversible by removing the patient from the source and administering oxygen. Carbon monoxide poisoning is a rare example of a headache in which relatively simple interventions may quickly improve a critical situation. On the contrary, returning the patient to the poisoned environment without a diagnosis could be lethal. Rapid Assessment and Stabilization If the patient is in a critical or comatose state, initial stabilization, including airway management, is prioritized and, if at all possible, preceded by a neurologic examination. For purposes of the initial assessment, headache can be divided into two categories: accompanied by altered mental status and without altered mental status. Whenever a patient s mental status is impaired, brain tissue is initially assumed to be compromised. The principles of care centered on cerebral resuscitation address the seven major causes of evolving brain injury: lack of substrate (glucose, oxygen), cerebral edema, intracranial mass lesion, endogenous or exogenous toxins, metabolic alterations (fever, seizure), ischemia, or elevated intracranial pressure. Pivotal Findings History The history is the pivotal part of the workup for the patient with headache (Table 20-2). 1. The patient should be asked to describe the pattern and onset of the pain. Patients often relate having had frequent and recurrent headaches similar to the one they have on the current ED visit. A marked variation in headache pattern can signal a new or serious problem. The rate of onset of pain may have significance. Pain with rapid onset of a few seconds to minutes is more likely to be vascular in origin than pain that developed over several hours or days. However, a slow onset should not be solely 170

2 Chapter 20 / Headache 171 Table 20-1 ORGAN SYSTEM CRITICAL DIAGNOSES EMERGENT DIAGNOSES NONEMERGENT DIAGNOSES Neurologic, CNS, vessels Shunt failure Migraine, various types Traction headaches Vascular, various types Tumor or other masses Trigeminal neuralgia Subdural hematomas Post-trauma Postlumbar puncture Headaches Toxic or metabolic Carbon monoxide poisoning Mountain sickness Environmental Collagen vascular disease Temporal arteritis Eye or ENT Glaucoma or sinusitis Dental problems, temporomandibular joint disease Musculoskeletal Tension headaches Cervical strain Allergy Cluster or histamine headaches Infectious disease Bacterial meningitis, encephalitis Brain abscess Febrile headaches, non-neurologic source of infection Pulmonary or O 2 Anoxic headache Anemia Cardiovascular Hypertensive crisis Hypertension (rare) Unspecified Differential Diagnosis CNS, central nervous system; ENT, ear, nose, and throat. Effort-dependent or coital headaches Table 20-2 SYMPTOM Sudden onset of pain Worst headache of my life Near syncope or syncope Increase with jaw movement Facial pain Forehead or temporal area pain (or both) Periorbital or retroorbital pain Significant Symptoms FINDING Lightning strike or thunder clap with any decreased mentation, any positive focal finding, or intractable pain Associated with sudden onset Associated with sudden onset Clicking or snapping; pain with jaw movement Fulminant pain of the forehead and area of maxillary sinus; nasal congestion Tender temporal arteries Sudden onset with tearing POSSIBLE DIAGNOSES Temporomandibular joint disease Sinus pressure or dental infection Temporal arteritis Temporal arteritis or acute angle-closure glaucoma relied on to rule out potential life-threatening causes for headache. Almost all studies dealing with subarachnoid bleeding report that patients moved from the pain-free state to severe pain within seconds to minutes. The thunder clap or lightning strike headache is common in acute presentations of SAH but is not highly specific. If the patient with moderate or severe headache can indicate the precise activity in which he or she was engaging at the time of the onset of the headache (e.g., I was just getting up out of the chair to answer the doorbell ), the suddenness of onset should warrant consideration of SAH. Careful questioning about the onset of headache may lead to the correct diagnosis of SAH, even if the pain is improving at the time of evaluation The patient s activity at the onset of the pain may be helpful. Headaches that come on during severe exertion have a relationship to vascular bleeding, but there is enough variation to make assignment to any specific cause highly variable. The syndrome of postcoital headache is well known, but coitus is also a common time of onset for SAH. These headaches require the same evaluation on initial presentation as any other exertion-related head pain. 3. If there is a history of head trauma, the differential diagnosis and emergent causes are narrowed significantly. The considerations now focus on epidural and subdural hematoma, traumatic SAH, skull fracture, and closed-head injury (i.e., concussion and diffuse axonal injury). 4. The intensity of head pain is difficult to quantify objectively. Almost all patients who come to the ED consider their headaches to be severe. Use of a pain scale may help differentiate patients initially but has more value in monitoring their response to therapy. Rapid resolution of pain in the ED, either from time or therapy, also should not be relied on to rule out serious causes of headache. 5. The character of the pain (e.g., throbbing, steady), although sometimes helpful, may not be adequate to differentiate one type of headache from another. 6. The location of head pain is helpful when the patient can identify a specific area. It is useful to have the patient point or try to indicate the area of pain; the emergency physician can then properly examine that area. Unilateral pain is more suggestive of migraine or a localized inflammatory process in the skull (e.g., sinus) or soft tissue. 4 Occipital headaches are classically associated with hypertension. Temporal arteritis, temporomandibular joint (TMJ) disease, dental infections, and sinus infections frequently have a highly localized area of discomfort.

3 172 PART I Fundamental Clinical Concepts / Section Two Cardinal Presentations Meningitis, encephalitis, SAH, and even severe migraine, although intense in nature, are usually more diffuse in their localization. 7. Exacerbating or alleviating factors may be important. Patients whose headaches rapidly improve when they are removed from their environment or recur each time they are exposed to a particular environment (e.g., basement workshop) may have carbon monoxide poisoning. Most other severe causes of head pain are not rapidly relieved or improved when patients get to the ED. Headaches on awakening are typically described with brain tumors. Intracranial infections, dental infections, and other regional causes of head pain tend not to be improved or alleviated before therapy is given. 8. Associated symptoms and risk factors may relate to the severity of headache but rarely point to the specific causes (Box 20-1). Nausea and vomiting are completely nonspecific. Migraine headaches, increased intracranial pressure, temporal arteritis, and glaucoma can all manifest with severe nausea and vomiting, as can some systemic viral infections with headache. Such factors may point toward the intensity of the discomfort but are not specific in establishing the diagnosis. Immunocompromised patients are at risk for unusual infectious causes of headache. Toxoplasmosis, cryptococcal meningitis, and abscess are very rare but may be seen in patients with a history of HIV or another immunocompromised state. This subset of patients may have serious central nervous system infection without typical signs or symptoms of systemic illness (e.g., fever and meningismus). 9. A prior history of headache, although helpful, does not rule out current serious problems. It is extremely helpful, however, to know that the patient has had a workup for severe disease. Previous ED and outpatient visits and computed tomography (CT), magnetic resonance imaging, and other forms of testing can provide support for or help rule out a specific diagnosis. Patients with migraine, cluster, and tension headaches tend to have a stereotypical recurrent pattern. Adherence to these patterns is also helpful in deciding the degree to which a patient s symptoms are pursued. Physical Examination Physical findings associated with various forms of headache are listed in Table Ancillary Testing The vast majority of headache patients do not require additional testing (Table 20-4). The most common and consequential mistake made by emergency physicians in the workup of the headache patient is believing that a single CT scan clears the patient of the possibility of SAH or other serious intracranial disease. Brain CT can miss 6 to 8% of patients with SAH, especially patients with minor (grade I) SAH, who are most treatable. 5,6 The sensitivity of CT for identifying SAH is reduced by nearly 10% for symptom onset greater than 12 hours and by almost 20% at 3 to 5 days. The basic approach to integrating CT and lumbar puncture in the assessment of headache is outlined in Figure Obtaining cerebrospinal fluid should not delay antimicrobial treatment if intracranial infection is suggested. Intravenous antibiotics are given before lumbar puncture. Abnormal mental status, signs of increased intracranial pressure, papilledema, focal findings on neurologic examination, or any other indication suggestive of a focal intracranial mass lesion requires CT before lumbar puncture. BOX 20-1 Risk Factors Associated with Potentially Catastrophic Illness 1. Carbon monoxide poisoning a. Breathing in enclosed or confined spaces with engine exhaust or ventilation of heating equipment b. Multiple family members with the same symptoms c. Pattern of recurrence in one setting (where the exposure is occurring), relief when not in that setting d. Wintertime and working around machinery or equipment producing carbon monoxide (e.g., furnaces) 2. Meningitis, encephalitis, abscess a. History of sinus or ear infection or recent surgical procedure b. Immunocompromised state c. General debilitation with decreased immunologic system function d. Acute febrile illness any type e. Extremes of age f. Impacted living conditions (e.g., military barracks, college dormitories) g. Lack of primary immunizations 3. Temporal arteritis a. Age >50 b. Females more often than males (4 : 1) c. History of other collagen vascular diseases (e.g., systemic lupus) d. Previous chronic meningitis e. Previous chronic illness such as tuberculosis, parasitic or fungal infection 4. Glaucoma sudden angle-closure a. Not associated with any usual or customary headache pattern b. History of previous glaucoma c. Age >30 d. History of pain increasing in a dark environment 5. Increased intracranial pressure a. History of previous benign intracranial hypertension b. Presence of a cerebrospinal fluid shunt c. History of congenital brain or skull abnormalities 6. Cerebral venous sinus thrombosis 7. Intracranial (ICH) a. (SAH) i. Sudden severe pain; worst headache of life ii. Acute severe pain after sexual intercourse or straining (i.e., heavy lifting) iii. History of SAH or cerebral aneurysm iv. History of polycystic kidney disease v. Family history of subarachnoid vi. Hypertension severe vii. Previous vascular lesions in other areas of the body viii. Young and middle-aged b. Subdural hematoma (SDH) i. History of alcohol dependency with or without trauma ii. Current use of anticoagulants c. Epidural hematoma (EDH) i. Traumatic injury ii. Lucid mentation followed by acute altered mentation or somnolence iii. Anisocoria on physical examination DIFFERENTIAL CONSIDERATIONS Certain historical and physical findings can help determine whether the patient s condition warrants further investigation. Indications of patients at higher risk for serious causes of headache who are candidates for more comprehensive evaluation include (1) sudden onset of headache, (2) patient description of the headache as the worst ever, (3) altered mental status, (4) meningismus, (5) unexplained fever, (6) focal neurologic

4 Chapter 20 / Headache 173 Table 20-3 SIGN FINDING POSSIBLE DIAGNOSES General appearance Alteration of mental status nonfocal Meningitis, encephalitis Anoxia Alterations of mental status with focal findings Intraparenchymal bleed Tentorial herniation Stroke Severe nausea, vomiting Acute angle-closure glaucoma Vital signs Hypertension with normal heart rate or bradycardia Tachycardia Fever Tentorial herniation Intraparenchymal bleed Anoxia, anemia Febrile headache Exertional or coital headaches Febrile headaches Meningitis, encephalitis HEENT Tender temporal arteries Temporal arteritis Fundi loss of spontaneous venous pulsations or presence of papilledema Pivotal Findings on Physical Examination Subhyaloid Acute red eye (severe ciliary flushing) and poorly reactive pupils Enlarged pupil with third nerve palsy Mass lesions Acute angle-closure glaucoma Tentorial pressure cone Mass effect (i.e., subdural or epidural hematoma, tumor, intraparenchymal ) Neurologic Lateralized motor or sensory deficit Stroke (rare) Subdural hematoma, epidural hematoma, hemiplegic or anesthetic migraine (rare) Acute cerebellar ataxia Acute cerebellar Acute cerebellitis (mostly children) Chemical intoxication various types CSF, cerebrospinal fluid; HEENT, head, eyes, ears, nose, and throat. Table 20-4 Diagnostic Adjuncts in Headache Assessment TEST FINDING DIAGNOSIS Erythrocyte sedimentation rate (ESR) Significant elevation Temporal arteritis ECG Nonspecific ST-T wave changes CBC Severe anemia Anoxia CT head Increased ventricular size Blood in subarachnoid space Blood in epidural or subdural space Epidural or subdural hematoma Bleeding into parenchyma of brain Intraparenchymal Areas of poor vascular flow Pale infarct Structural, mass lesion Traction headache secondary to mass effect Lumbar puncture and CSF analysis Increased pressure Pseudotumor cerebri Mass lesions Shunt failure Increased protein Tumor or other structural lesions Increased RBCs Increased WBCs Infection Positive Gram s stain Infection Decreased glucose Infection CBC, complete blood count; CSF, cerebrospinal fluid; CT, computed tomography; ECG, electrocardiogram; RBC, red blood cell; WBC, white blood cell.

5 174 PART I Fundamental Clinical Concepts / Section Two Cardinal Presentations Table 20-5 Causes and Differentiation of Potentially Catastrophic Illness Manifesting with Nontraumatic Headache DISEASE ENTITIES PAIN HISTORY ASSOCIATED SYMPTOMS SUPPORT HISTORY PREVALENCE PHYSICAL EXAMINATION USEFUL TESTS ATYPICAL OR IMPORTANT ASPECTS Carbon monoxide poisoning Usually gradual, subtle, dull, nonfocal throbbing pain May wax and wane as individual leaves and enters the involved area of carbon monoxide; throbbing may vary considerably Exposure to engine exhaust, old or defective heating systems, most common in winter months Rare No focal neurologic findings May need cognitive testing Carbon monoxide level, cognitive testing May improve on the way to the hospital Occurs in groups, may involve entire families or groups of people exposed to the carbon monoxide Sudden onset, thunder clap or lightning strike, severe throbbing Whenever altered mental status is present, the outcome is decidedly worse History of polycystic kidney disease. History of chronic hypertension Uncommon Frequently decreased mentation meningismus, increased blood pressure, decreased pulse, decreased spontaneous venous pulsations, rarely subhyaloid CT, lumbar puncture If CT positive, immediate involvement of neurosurgery; if CT negative, lumbar puncture Meningitis, encephalitis, abscess Gradual as general symptoms increase, headache increases nonfocal Decreased mentation prominent, irritability prominent With abscess, focal neurologic findings may be present Recent infection Recent facial or dental surgery or other ENT surgery Uncommon Fever late in course, decreased spontaneous venous pulsations CT, lumbar puncture When such infection suspected, treat Do not delay antibiotics and steroids while awaiting laboratory results Temporal arteritis Often pain developing over a few hours from mild to severe Virtually always focal in nature Decreased vision, nausea, vomiting intense may confuse diagnosis Age over 50 Other collagen vascular diseases or inflammatory diseases Uncommon Tender temporal arteries Sedimentation rate Usually unrelated and rapidly progressive Acute angle-closure glaucoma Sudden in onset Nausea, vomiting, decreased vision History of glaucoma History of pain going into dark area Rare Steamy cornea Midposition pupil poorly reactive Acute red eye Measurement of intraocular pressure Rapid intervention with medications required if no relief, immediate surgery may be required Increased intracranial pressure syndromes Gradual, dull, nonfocal Vomiting, decreased mentation History of CSF shunt or other congenital brain or skull abnormality Uncommon Papilledema; loss of spontaneous venous pulsations CT, shunt function study; if normal, lumbar puncture Shunt failure or other cause of significant increased CSF pressure requires involvement of neurosurgery CSF, cerebrospinal fluid; CT, computed tomography; ENT, ear, nose, and throat.

6 Initial assessment: history and physical Suspicion of CO poisoning: check CO level and administer O 2 CT +: treat underlying condition Blood/abscess/ tumor: notify neurosurgery Decreased mentation Focal neurologic finding or meningismis Figure Initial assessment and treatment of headache. CO, carbon monoxide; O 2, oxygen; CT, computed tomography; LP, lumbar puncture. CT LP + blood: treat subarachnoid If meningitis suggested, there should be no unreasonable delay. Do not wait for test results to start empirical antibiotic therapy. LP may be performed immediately if the patient has no focal neurologic findings and normal funduscopic examination. CT : LP LP + infection: treat infection appropriately LP : treat as a basic pain problem, anticipate post-lp headache deficit on examination, (7) symptoms refractory to appropriate treatment or worsening despite treatment, (8) onset of headache during exertion, or (9) history of human immunodeficiency virus (HIV) infection or immunosuppression. Patients with a headache that is similar in location and intensity to an established history of recurrent headache (e.g., migraine) or Chapter 20 / Headache 175 of minor severity and gradual onset (e.g., typical tension headache); with normal neurologic examination findings including mental status; with absence of fever or meningismus; and showing improvement with appropriate treatment generally require no laboratory testing or imaging. Sequential evaluation of the patient s condition and response to therapy and assessment of ancillary data will confirm a working diagnosis or trigger a reconsideration of alternatives, including more serious conditions (Table 20-5). 7 MANAGEMENT Empirical Headache, although a frequent chief complaint, is a nonspecific symptom, and the speed and intensity of the initial evaluation and treatment are guided by the initial presentation (described earlier) and, particularly, the patient s mental status. Pain should be mitigated as soon as possible. The pain medication of choice depends on the working diagnosis of the patient s headache. If migraine is suspected, parenteral therapy is directed accordingly (see Chapter 103). For nonspecific mild to moderate headache, oral nonsteroidal anti-inflammatory medication is appropriate, in analgesic doses. Opioids generally are not first-line management for any type of headache pain, except when ICH (including SAH) is thought to be present, conditions for which opioid analgesia is effective and beneficial. Specific Specific management for headache is described in Chapter 103. The challenge in emergency medicine, however, is to eliminate life-threatening causes of headache and to treat the patient s pain. DISPOSITION Most patients with headache are discharged from the ED with appropriate analgesia and follow-up, unless evaluation has determined a serious underlying condition. The references for this chapter can be found online by accessing the accompanying Expert Consult website.

7 References 1. Barton CW: Evaluation and treatment of headache patients in the emergency department: A survey. Headache 1994; 34: Mayer PL, et al: Misdiagnosis of symptomatic cerebral aneurysm: Prevalence and correlation with outcome at four institutions. Stroke 1996; 27: Day JW, Raskin NH: Thunderclap headache: Symptom of unruptured cerebral aneurysm. Lancet 1986; 2: Olesen J, Lipton RB: Migraine classification and diagnosis: International Headache Society criteria. Neurology 1994; 44(Suppl 4):S6. 5. Edlow J, Caplan L: Avoiding pitfalls in the diagnosis of subarachnoid. N Engl J Med 2000; 342: McCormack RF, Hutson A: Can computed tomography angiography of the brain replace lumbar puncture in the evaluation of acute-onset Chapter 20 / Headache 175.e1 headache after a negative noncontrast cranial computed tomography scan? Acad Emerg Med 2010; 17: Edmeads J: Emergency management of headache. Headache 1988; 28: Silberstein SD: Evaluation and emergency treatment of headache. Headache 1992; 32: Byyny RL, et al: Sensitivity of noncontrast cranial computed tomography for the emergency department diagnosis of subarachnoid. Ann Emerg Med 2008; 51: Perry JJ, et al: Is the combination of negative computed tomography result and negative lumbar puncture result sufficient to rule out subarachnoid? Ann Emerg Med 2008; 51: