Etiology and Pathogenesis

The pathophysiology of headache is not fully understood. The blood vessels and meninges sense pain but refer it to the anterior or posterior scalp, explaining why pain from multiple etiologies and locations can feel similar.

The mechanism of migraine pain has been studied most extensively. Cortical spreading depression, which is associated with aura, is a rapid depolarization of neurons followed by prolonged hyperpolarization, which propagates as a wave through brain. This leads to release of ions, prostaglandins, and amino acids that irritate axon collateral nociceptors in the pia and dura mater. These nociceptors activate trigeminal and parasympathetic pain afferents in meningeal vessels, causing meningeal artery dilatation and activation of the trigeminal ganglion and then the trigeminal nucleus caudalis. The messages cross in the brainstem and continue to the ventroposterior thalamus, causing the sensation of pain (Figure 75-1).

Figure 75-1 Pathophysiology of migraine.

Figure 75-2 Migraine prodromes.

Clinical Presentation

Headaches have a wide variety of causes. Although many headaches are caused by primary headache syndromes, most commonly migraine and tension-type headache, an extensive history and physical examination must guide the differential diagnosis. Relevant elements of the history are listed in Table 75-1. The physical examination should include vital signs and general and neurological examinations, including visualization of the fundus. Table 75-2 outlines characteristics of many primary and secondary headaches, the recommended workup, and treatment where applicable.

Table 75-1 Headache History

Description of the headache	Location and Radiation	Quality of pain
	Severity and school absence	Frequency and duration of attacks
	Pattern over time	Time of day and day of week
	Awaken patient from sleep
Triggers and exacerbating factors	Stress at home and school	Food (MSG, caffeine, alcohol)
	Sleep changes	Valsalva maneuver, cough, sneeze
	Posture (recumbent, upright)
Alleviating factors	Medication: clarify frequency and duration	Sleep
Associated symptoms	Nausea or vomiting	Photo- or phonophobia
	Weakness	Sensory changes
	Visual symptoms	Lacrimation or rhinorrhea
	Ptosis, pupillary changes	Pulsatile tinnitus
Other	Allergic symptoms	Snoring or teeth grinding
Other	Blurred vision	Family history

MSG, monosodium glutamate.

Table 75-2 Differential Diagnosis and Evaluation of Headaches by Cause

Evaluation and Management

See Table 75-2 for workup based on specific to etiology. Indications for imaging are summarized here. Generally, magnetic resonance imaging (MRI) is preferred because it provides more detail, but CT is appropriate when looking for bony changes or bleeding or in emergent situations when MRI is not available. MR angiogram (MRA) and MR venogram (MRV) are sometimes important to obtain with MRI of the brain.

• Acute-onset, severe headache should be imaged emergently. The American Academy of Neurology Practice Parameter recommends imaging for any headache of less than 1 month’s duration.

• Alteration of consciousness

• Symptoms or examination findings that suggest focal brain pathology (the brain and arteries should be imaged with MRI and MRA)

• Symptoms or examination findings that suggest increased intracranial pressure (ICP) (the brain and veins should be imaged with MRI and MRV)

• Comorbid seizures

• Change in headache quality, frequency, or severity

• Consider for any recurrent headache in which there is no family history of headache

Imaging is necessary before lumbar puncture if a patient has an abnormal physical examination result to ensure that it is safe to perform lumbar puncture (no signs of herniation nor significant edema). Indications for lumbar puncture (with opening pressure) include:

• Acute-onset, severe headache (looking for subarachnoid hemorrhage; the first and last tubes should be collected for a cell count to aid interpretation)

Only gold members can continue reading. Log In or Register to continue