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Headache
Anatomy
- Headache is pain in various parts of the head, not confined to the area of distribution of any nerve.
- Headache is caused by distention, traction, displacement, inflammation, vascular spasm, dilation, or compression of the pain-sensitive structures in the head and neck. The pain-sensitive structures of the supratentorial space refer pain via the trigeminal nerve, which innervates the anterior scalp and face. Pain-sensitive structures in the infratentorial space refer pain via cranial nerves IX, and X, and the second and third cervical nerves;
thus, pain originating in the posterior fossa may be referred to the ear or throat, or the posterior area of the head and neck.
- Intracranial sources of head pain includes the cranial sinuses and afferent veins; the anterior and middle meningeal arteries; the trigeminal (V), glossopharyngeal (IX), and vagus (X) nerves; falx cerebri; the dura at the base of the skull; the major arteries at the base of the brain; the brain stem periaqueductal gray matter; and the sensory nuclei of the thalamus.
- Muscles frequently involved in extracranial causes of Headache include the masseter, frontalis, temporal, occipital, trapezius, sternocleidomastoid, and deep cervical muscles.
In addition, the skin, the periosteum of the skull, the subcutaneous tissues and arteries, the eyes, ears, teeth, sinuses, oropharynx, and the mucous membranes of the nasal cavity may be sources of pain.
Etiology/Risk Factors
Primary headaches are benign, usually recurrent, and have no underlying cause.
These include migraine, cluster, and tension-type headaches. Secondary headaches, on the other hand, are a symptom of underlying organic disease. Risk factors for secondary headache disorders include:
- "First or worst" headache
- Very sudden onset
- Nausea and vomiting
- Systemic illness
- Ocular findings
- History of head trauma
- History of immunodeficiency or cancer
- Increased frequency or severity
- Focal neurologic deficits, or altered mental status
- Onset after age 50, or before three
- Fever, neck stiffness, or meningeal signs
- Headache that begins with exertion or is positional
Diagnosis
History
- The most important task in evaluating a patient with headache is to identify or exclude underlying pathology based on the history and physical examination. A detailed history should be taken to include the following elements:
- Was the onset sudden, gradual, or subacute? Was the patient awakened from sleep?
Are their any precipitating or aggravating factors (e.g., activity, stress, menses/hormonal therapy, medications/medication withdrawal, foods, cough/Valsalva maneuver, environmental exposures, position changes, trauma)? Episodes of migraine are often concentrated around the menstrual period. Exposure to tyramine- or amine-containing foods, nitrates, MSG, or ethanol may precipitate a migraine; stress, whether changes, changes in sleep patterns, and caffeine withdrawal is also potential triggers.
Tension-type headaches are often stress-related. Alcohol is reported to precipitate cluster headaches. The use of cocaine is a risk factor for subarachnoid hemorrhage (SAH).
Are their any alleviating factors?
- Is there're a prodrome (e.g., visual, auditory, or olfactory aura or hallucinations; numbness, paresthesias or motor weakness; speech impairment)? An aura may proceed a migraine headache by up to an hour; patients without aura may have other symptoms suggesting the onset of a migraine, including lethargy, depression, hyperactivity, or food craving.
- Where is the pain located (e.g., unilateral or bilateral; ocular/retro-ocular; paranasal; frontal or occipital; at the vertex; in the pharynx or external auditory meatus)? What is the character of the pain (e.g., sharp, stabbing; dull, steady ache; burning; lancinating; "worst headache ever")? Tension-type headaches are described as a diffuse pressure or tightness.
Migraines are typically unilateral, with a pulsating quality. Cluster headaches are excruciating, sharp, unilateral headaches. Does the pain radiate?
- Are there any associated symptoms (e.g., fever/chills; nausea/vomiting; neck pain or stiffness; seizures; focal neurologic deficits; ataxia; speech deficit; dizziness/vertigo; visual changes or eye pain; altered mental status or transient loss of consciousness; jaw claudication; myalgias; weight loss)? Migraine headaches are frequently associated with photophobia or phonophobia. Symptoms accompanying a cluster headache include
conjunctival injection, lacrimation, rhinorrhea, ptosis, myosis, and ipsilateral forehead sweating. Suspicion should be raised for SAH when nausea and vomiting, photophobia, neck stiffness, or loss of consciousness accompanies the headache.
- What is the frequency of the pain (e.g., intermittent, chronic, seasonal)? Are the headaches increasing in frequency or severity? How long does the pain last? Cluster headaches occur once or twice daily-generally at the same time each day-and last about 30 to 90 min. The symptoms may recur for several weeks, and then the patient may
remain pain-free for months or years. Headaches that persist for more than 10 wk, without associated symptoms, are unlikely to be caused by a neoplasm.
- Is there a family history of headaches? Are there any ongoing medical problems or recent illnesses? The presence of polycystic kidney disease, Ehlers-Danlos or Marfan�s syndrome, Grave�s disease, fibromuscular dysplasia, coarctation of the aorta or abdominal aortic aneurysm, sickle cell disease, atherosclerosis, or hypertension places the patient at increased risk for SAH or unruptured aneurysm. Is there an HIV history
or risk? Are there any close contacts with similar symptoms? Patients with mild carbon monoxide poisoning may complain of nonspecific headache and flu-like symptoms; frequently, members of the same household will have the same toxic exposure and thus present with similar symptoms.
Vital Signs
- Vital signs may reveal an elevated temperature or blood pressure; tachycardia; or tachypnea.
Physical Exam
- A detailed examination of the head may reveal tenderness of the scalp, temporomandibular joint (TMJ), temporal artery, or sinuses; evidence of head trauma; or disorders of the eyes, ears, nose, or teeth.
- Examine the neck for bruits, range of motion, and tenderness.
- Examination of the skin may reveal a focal cellulitis, a generalized rash, neurofibromas or caf� au lait spots, or cutaneous angiomas.
- A complete neurologic exam is essential, including level of consciousness, mental status, pupillary responses, cranial nerves, deep tendon reflexes, motor deficits and sensory function, gait, cerebellar function, and pathologic reflexes.
Differential Diagnosis
Primary Headache
- Migraine
- Tension-type
- Cluster headache
Secondary Headache
- Associated with head trauma
- Post-traumatic headache syndromes
- Associated with vascular disorders
- Infarction, transient ischemic attack (TIA), SAH, unruptured vascular malformation, arteritis, carotid or vertebral artery pain (arterial dissection, carotidynia), intracranial hematoma, venous thrombosis, acute arterial hypertension
- Associated with nonvascular intracranial disorders
- High and low CSF pressures, infection, intracranial mass, sarcoidosis, other granulomatous/inflammatory diseases
- Associated with exposure or use of substances or their withdrawal
- Associated with noncephalic infection
- Associated with metabolic disorders
- Hypoxia, hypercapnia, dialysis, hypoglycemia, hypo- or hyperthyroidism, hypoadrenalism
- Associated with facial or cranial structures
- Skull, neck, eyes, ears, nose, sinuses, teeth and jaws, mouth, TMJ joint, or other facial or cranial structures
- Paget�s disease, skull metastases, cervical arthritis, acute angle closure glaucoma, retro-orbital infection, sinusitis, dental caries
- Cranial neuralgias, nerve trunk pain, and deafferentation pain Optic neuritis, zoster (post-herpetic neuralgia), trigeminal neuralgia, glossopharyngeal neuralgia, occipital neuralgia, pain of cranial nerve origin
- Other causes of headache pain
- Idiopathic stabbing headache, external compression headache, cold stimulus headache, benign exertional headache, benign cough headache, associated with sexual activity
- High-altitude, anemia, hypotension
Evaluation
Laboratory
- A CBC may be useful in cases of suspected infection, hematologic disorders, or vasculitis.
- A CD4 count of < 500 or 200 in HIV-infected individuals increases the risk for:
- Meningitis (cryptococcal, tuberculous, syphilitic, and lymphomatous);
- Focal brain lesions (toxoplasmosis, CNS lymphoma, PML, abscess, crypotococcoma)
- Diffuse brain lesions (CMV, HSV, toxoplasmosis).
- An erythrocyte sedimentation rate (ESR) of at least 55 mm/h-and usually over 100- is seen in 90% of patients with temporal arteritis.
- A carboxyhemoglobin level is obtained if carbon monoxide poisoning is suspected.
- A lumbar puncture with analysis of the cerebrospinal fluid (CSF) is essential in the evaluation of several headache disorders:
- Meningitis-CSF may be cloudy, with elevated WBC and protein, and low glucose. Specimens should also be sent for stat Gram stain and culture, and-in specific cases-VDRL, India ink, bacterial antigens, and CSF antibody detection (for viral encephalitis).
- Subarachnoid hemorrhage-opening pressure may be increased; fluid may be bloody
or xanthochromic (discolored supernatant of centrifuged CSF, as a result of hemolysis), with increased RBC and protein, and normal glucose. (In the setting of a negative head CT, LP must still be performed to exclude small SAH not identified by CT.)
- Benign intracranial hypertension-opening pressure is elevated (above 200 mm H2O); other CSF components are normal; relief from headache with removal of fluid may be diagnostic.
Imaging
- A panorex radiograph may reveal a dental etiology in selected patients.
- A cervical spine series may be warranted in the setting of trauma or suspicion of cervical arthritis.
- Emergent neuroimaging is performed in order to identify treatable lesions (e.g., tumors, AVMs, SAH, cerebral sinus thrombosis, subdural and epidural hematomas, and hydrocephalus). Computed tomography (CT) scanning of the head without contrast is indicated when certain historical or physical "red flags" are identified in the evaluation of a new-onset headache:
- Acute onset, severe headache
- Any neurologic deficit
- History of seizures
- Ocular abnormalities including papilledema, visual impairment, or diplopia
- Persistent or frequent vomiting preceded by recurrent headaches
- Changing character of the patient�s headache
- Extremes of age (patients <3 or over 50)
- Children with neurofibromatosis
- Diabetes insipidus, HIV
- Antecedent head trauma
- Patients with signs of increased intracranial pressure (e.g., papilledema or absent venous pulsations on funduscopic exam, altered mental status, or focal neurologic deficits) should be scanned prior to having a lumbar puncture.
- Contrast-enhanced head CT should be considered in patients with a history of immunodeficiency or malignancy (after a negative noncontrast CT).
- Magnetic resonance imaging (MRI) of the brain may be preferable to CT in cases in which the posterior fossa must be specifically evaluated but is generally not as readily available as CT.
Treatment
Primary Headache
Secondary Headache
- Patients treated with any of the previously mentioned medications may experience relief from their headache, despite having significant intracranial pathology as a cause of their pain. Thus, response to therapy should not be used to distinguish primary from secondary causes of headache.
- Treatment of secondary headache varies by etiology. Treatment of primarily neurologic diagnoses will be described here. Management of neurosurgical, infectious, and other causes is explained elsewhere.
- Giant-Cell Arteritis
- Giant-cell arteritis (temporal arteritis) is typically seen in patients over age 50 (with a peak incidence in the 70s). The headache is usually in the temporal region (but may occur anywhere) and variously described as continuous or intermittent, throbbing or steady, boring, or aching. Associated symptoms include jaw claudication
(virtually pathognomonic, when present), amaurosis, malaise, anorexia, weight loss,
myalgias, arthralgias, fever, neuropathies, TIAs, and stroke. Patients often complain of scalp tenderness, and examination may reveal a tender, indurated, warm, temporal artery with reduced or absent pulse. If the diagnosis of temporal arteritis is suspected, treatment with prednisone (1 mg/kg) should be initiated; improvement in headache should be observed within 48 h. Intravenous methylprednisolone, 250 mg q6h, is recommended for patients with associated visual loss. Temporal artery biopsy should be accomplished within 72 h of initiating treatment; however, immediate treatment with steroids may prevent complications and should not be delayed pending confirmation of the diagnosis.
- Benign Intracranial Hypertension
- Benign intracranial hypertension (pseudotumor cerebri) refers to a diffuse increase in intracranial pressure, producing a diffuse headache, papilledema, and visual changes. MRI or CT scanning reveals slit-like ventricles. Acetazolamide, with or without a diuretic, may be sufficient for mild cases. Otherwise, prednisone may be
indicated. Refractory cases may require intermittent lumbar puncture or lumboperitoneal shunting. Maintaining intracranial pressure at relatively normal levels helps to protect against irreversible vision loss. The disease process is generally self-limited and resolves within several months.
- Trigeminal Neuralgia
- Trigeminal neuralgia is described as unilateral jabs of lightning-like pain confined to the areas of the face supplied by the second and third divisions of the trigeminal nerve. Attacks may be precipitated by tactile or mechanical stimulation (e.g., brushing the teeth), and last seconds to minutes. Oral carbamazepine is highly effective for remission of symptoms (often within 24 h) but cannot be loaded; the initial dose is
100 mg PO BID, increased every 2 days by 100-mg increments (max. dose, 1.2 to 2 g/day). An acute attack may be aborted with intravenous phenytoin, 250 mg, and the patient discharged on 300 mg PO at bedtime. Alternatively, parenteral narcotics may be required.
- Post-Traumatic Headache
- Patients may experience headache within hours to days following trauma-in the setting of a normal neurologic exam and CT scan-which may last for several weeks.
When post-traumatic headache is associated with other nonspecific symptoms (e.g., dizziness, vertigo, nausea and vomiting, difficulty with concentration, and labile mood swings), the symptom complex is referred to as post-traumatic headache syndrome. NSAIDs are generally used as first-line therapy, with the addition of
sedatives, physiotherapy, psychotherapy, and-as a last resort-narcotics, if necessary. Symptoms generally resolve within months.
- Post-Lumbar Puncture Headache
- Post-lumbar puncture headache is caused by leakage of CSF through the defect in the dura caused by the spinal needle. The pain is aggravated by sitting or standing and relieved with recumbency. Associated symptoms include orthostatic lightheadedness, tinnitus, photophobia, anorexia, nausea, and vomiting. The incidence of post-lumbar puncture headache is reduced by use of a small-gauge spinal needle, as well as minimizing the amount of CSF removed; however, bed rest and increased fluid intake immediately following the procedure have not been shown to
influence the course or duration of symptoms. Treatment includes rest and analgesics, and symptoms are generally self-limited. For more severe cases, caffeine (500 mg in 1 L of normal saline administered over 1 h) may be effective. The dose may be repeated once, if necessary. Finally, in persistent cases, consultation with anesthesiology for an autologous epidural "blood patch" may be warranted.
Disposition
- Most patients who present to the ED with headache can be discharged home after adequate pain relief has been achieved.
- Patients with status migrainosus-or any patient whose pain is not adequately controlled in the ED-should be admitted.
- Patients with documented visual loss and suspected temporal arteritis should be admitted for intravenous steroid therapy.
- Any patient with new-onset headache should have close follow-up with his/her primary care provider (PCP) or the appropriate specialist. Patients with migraine or cluster headaches should be encouraged to follow-up with their PCPs for consideration of prophylaxis.
- All patients should receive instructions on appropriate use of discharge medications
and explicit return precautions.
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