Headache
Headache is a common complaint in emergency practice. The differential diagnosis ranges from benign self-limiting conditions to life-threatening emergencies. The clinical challenge is to provide relief to those patients who suffer from primary headache syndromes (the majority) but detect those headaches that are due to potentially fatal or permanently disabling causes.
COMMON CAUSES OF HEADACHE
Tension headache*
Migraine headache*
Cluster headache*
Sinusitis*
Trauma/posttrauma
LESS COMMON CAUSES OF HEADACHE NOT TO BE MISSED
Subarachnoid hemorrhage (SAH)*/cerebellar hemorrhage*
Meningitis* or encephalitis
Brain tumor/mass effect
Acute narrow-angle glaucoma
Thromboembolic cerebrovascular accident
Temporal arteritis*
Carbon monoxide poisoning
OTHER CAUSES OF HEADACHE
Benign intracranial hypertension
Uveitis
Hypoglycemia
Trigeminal neuralgia
Central venous sinus thrombosis
HISTORY
Headache caused by tension is frequently bilateral, is described as “band-like,” commonly occurs at the end of the day, and is often relieved with rest.
Migraine headaches are usually unilateral but commonly alternate sides. Attacks of migraine or vascular headache are often preceded by or associated with nausea, vomiting, or an aura, which includes scintillating scotomata, loss of the peripheral field of vision, and other disturbances of visual perception. Occasionally, patients with migraine report associated neurologic deficits, including hemiparesis and cranial neuropathies. These phenomena are attributed to cerebral vasospasm with resulting ischemia and generally improve without residual deficit.
The cluster headache is a form of vascular headache that usually localizes to the periorbital area, occurs in “clusters” every few weeks to months, and may be accompanied by unilateral tearing and conjunctival injection and occasional visual disturbances.
Patients with headaches secondary to sinusitis may report pain over or surrounding the involved sinus and may complain of purulent nasal discharge or symptoms of a recent upper respiratory tract infection.
The headache associated with subarachnoid hemorrhage is classically described as sudden onset and the “worst headache of one’s life” and may be associated with neck aching or stiffness or an initial loss of consciousness.
Meningitis/encephalitis produces dull, constant headaches, as do brain tumors; the latter are occasionally associated with the report of headaches on awakening, which may accompany specific progressive neurologic signs or symptoms.
Patients with cerebellar hemorrhage generally have a history of hypertension or are noted to be hypertensive at presentation; they experience a sudden-onset, severe, occipital headache associated with nausea, vomiting, and inability to walk or stand. Some patients report vertiginous symptoms as well.
PHYSICAL EXAMINATION
Photophobia is a common finding in patients with vascular headaches and meningitis; tension headaches also may be associated with photophobia.
Percussion tenderness over the involved sinus and a decrease in sinus transillumination are often noted in sinusitis.
Neck stiffness may accompany SAH and meningitis, and both of these disorders may cause fever and an abnormal mental status.
Signs of increased intracranial pressure from subarachnoid or intracerebral hemorrhage, purulent meningitis, or brain tumor may be detected on funduscopy.
Focal neurologic deficits may be detected in patients with brain tumors, migraine, subarachnoid or intracerebral hemorrhage, and, rarely, meningoencephalitis.
Uveitis causes an acutely red and painful eye with a characteristic ciliary or perilimbal flush; narrow-angle glaucoma may be associated with corneal clouding, decreased visual acuity, and, most distinctively, increased intraocular pressure on tonometry.
Patients with cerebellar hemorrhage are typically nauseous, vomiting, and unable to stand or walk without assistance. In addition, paresis of conjugate ipsilateral gaze, ipsilateral sixth nerve weakness, and forced conjugate deviation of the eyes are occasional accompanying signs. Although the mental status of such patients may initially be normal, it may rapidly deteriorate.
EMERGENCY DIAGNOSTIC TESTS
A complete blood count often reveals a leukocytosis in patients with meningitis, often with an increase in polymorphonuclear and band forms.
Sinus roentgenograms or sinus computed tomography (CT) may demonstrate mucosal thickening, opacification, and/or air-fluid levels in the affected sinus or sinuses.
In 90% to 95% of patients with SAH, the CT scan of the brain will reveal evidence of bleeding. If SAH is likely but the CT scan is negative, a lumbar puncture must be performed to exclude a hemorrhage.
When meningitis or encephalitis is suspected, a lumbar puncture must be performed.
A CT scan of the head should be obtained prior to lumbar puncture in patients with an abnormal mental status, evidence of increased intracranial pressure, immunocompromised or focal neurologic deficits.
CLINICAL REMINDERS
Perform a lumbar puncture in any patient suspected of having meningitis. If immunocompromised, clinical signs of focality or increased intracranial pressure are noted, obtain a noncontrast CT first.
If SAH is suspected, CT alone is not adequate to exclude hemorrhage. CT must be followed by lumbar puncture to definitely exclude SAH.
SPECIFIC DISORDERS
Tension Headache
Tension headache is the most common cause of headache but must be diagnosed
by exclusion. Patients often report a “band-like” tightness about the head that is often worse toward the day’s end, especially in the setting of stress at work or home. Headaches typically occur posteriorly, cervically, or temporally, where muscle spasm may be prominent and palpable. The physical examination and laboratory studies are normal. Occasionally, a trigger point may be elicited on examination of the occipital area or neck. Patients usually find relief from mild analgesics, including acetaminophen or NSAIDs. Social or psychological consultation may be required if headaches become persistent or severe.
Migraine Headache
Migraine headaches are a form of vascular headache, which result from cerebral vasospasm followed by vasodilation. Although a variety of factors, including food (nuts, coffee, chocolate), alcohol, and stress have been implicated as precipitants, the causal role of these agents in migraine remains unclear. It is the dilatory phase that is responsible for the headache and toward which acute pharmacotherapy is directed; prophylactic therapy is aimed at both phases. The vasospastic phase is occasionally accompanied by neurologic deficits, and it is this pathophysiologic event that is responsible for the prodrome.
Diagnosis
Patients with migraine headache typically report unilateral discomfort, the side of which may alternate with each episode. The migrainous prodrome in its classic form includes nausea, vomiting, and a visual or perceptual aura that may include “lightning-like” images, scintillating scotomata, or loss of the peripheral field of vision, all of which usually disappear with the onset of the headache. The headache itself is quite severe, often throbbing, and associated with profound photophobia.
Despite the severity of symptoms, the physical examination usually is unrevealing. Rarely, patients have true focal neurologic deficits accompanying the aura or headache (complex migraine), which usually improve and disappear as vasospasm subsides. Very rarely, a patient with a history of migraine headache may present with an isolated neurologic deficit without headache; aura may be noted in these patients and is important diagnostically.
Diagnostic Tests
The diagnosis of migraine headache cannot be confirmed or excluded with any laboratory test; all basic studies typically are normal.
Treatment
In the acute phase, patients appear quite ill and require prompt treatment. During the aura or prodromal period or immediately after the onset of headache, patients may be treated with one of the following regimens to abort the onset of headache.Related posts:
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