Headache

Perspective

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 hemorrhage (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 hemorrhage (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.

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.

Table 20-1

Differential Diagnosis

CNS, central nervous system; ENT, ear, nose, and throat.

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).

Table 20-2

Significant Symptoms

SYMPTOM	FINDING	POSSIBLE DIAGNOSES
Sudden onset of pain	Lightning strike or thunder clap with any decreased mentation, any positive focal finding, or intractable pain	Subarachnoid hemorrhage
“Worst headache of my life”	Associated with sudden onset	Subarachnoid hemorrhage
Near syncope or syncope	Associated with sudden onset	Subarachnoid hemorrhage
Increase with jaw movement	Clicking or snapping; pain with jaw movement	Temporomandibular joint disease
Facial pain	Fulminant pain of the forehead and area of maxillary sinus; nasal congestion	Sinus pressure or dental infection
Forehead or temporal area pain (or both)	Tender temporal arteries	Temporal arteritis
Periorbital or retro-orbital pain	Sudden onset with tearing	Temporal arteritis or acute angle-closure glaucoma

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 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.³

2. 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. 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).