The term "primary headache" includes all forms of migraine, tension-type, and cluster headaches. There is considerable clinical overlap in primary headache syndromes, and it has been suggested that they share a pathophysiology and represent different ends of a clinical spectrum. 7
MIGRAINE Epidemiology Migraine headaches are common, with onset usually in the early teens or even younger. Prevalence is estimated at approximately 5 percent for males and 15 to 17 percent for females.2 Prevalence peaks in both sexes at around 40 years of age and then gradually declines.
Pathophysiology Early theories postulated abnormal vasculature as the root cause of migraine headaches, with vasoconstriction being responsible for the aura and rebound vasodilatation the cause of the pounding headache. It now seems clear that migraines are a primary response of brain tissue to some trigger, while the disordered activity of blood vessels is secondary.
Auras are thought to be due to primary neuronal dysfunction. The neurologic symptoms of auras are believed to result from a slowly spreading wave of neuronal hypoactivity traveling across brain tissue. There is a corresponding decrease in local blood flow where neuronal activity is reduced. This reduction in blood flow does not follow vascular territories, which makes it unlikely to be vasospastic in origin. 9
Pain-sensitive intracranial structures, such as blood vessels and the dural matter, are largely supplied by sensory axons of the trigeminal ganglion in the supratentorium, while the upper cervical roots innervate the posterior fossa. Animal models suggest that the headache of migraine is related to activation of these sensory axons, leading to the release of various peptides. This causes sterile neurogenic inflammation in pain-sensitive arteries, the dura, and meningial tissues, and promotes local vasodilatation. The release of these peptides and the resulting inflammation and plasma extravasation can be blocked by sumatriptan, a selective agonist of 5-HT1D (serotonin) receptors, as well as by ergots, indomethacin, and others. Sumatriptan also has direct vasoconstricting effects. Both mechanisms may explain its efficacy at revealing migraine headache. The neurophysiologic pathways linking auras and headaches are still poorly understood.
What actually triggers these complex mechanisms for migraines? Enhanced excitability of occipital cortex neurons in migraine patients has been proposed as a possible trigger, but no clear answer has yet emerged.9
Clinical Features Migraine without aura accounts for about 80 percent of migraines. The headache generally is slow in onset and lasts from 4 to 72 h. It is typically unilateral and pulsating, and worsened by physical activity. Nausea, vomiting, and photo- or phonophobia frequently accompany the headache. 3 The scalp may or may not be tender. These features, however, are not entirely sensitive (migraines need not be unilateral or pulsating) or specific (the same features can be present in tension-type headaches).7 Suspicion should be raised when a patient presents with a "migraine" that is significantly different from prior headaches. The headache in migraine with aura is similar but is preceded or accompanied by an aura that develops gradually over minutes, lasts no more than 60 min, and is fully reversible.
Visual auras are the commonest, usually consisting of scintillating scotomata (i.e., dark spots) or flashing lights, but virtually any neurologic symptom or sign can occur. Other "typical" auras include hemiparesthesia, hemiparesis, aphasia, or other speech difficulties. Rarer types of aura include those with brainstem symptoms (basilar migraine), those lasting longer than 60 min (migraine with prolonged aura), and aura without accompanying headache (migraine aura without headache). Auras should be distinguished from migraine prodromes, which occur many hours prior to the headache and can consist of lethargy, hyperactivity, yawning, depression, food craving, polyuria, or fluid retention. 9
Other, less common forms of migraine include ophthalmoplegic migraine, in which headache overlaps with paresis of one or more of cranial nerves III, IV, and VI, or retinal migraine, with sudden monocular scotoma or blindness associated with headache. Childhood periodic syndromes (previously known as migraine equivalents) are ill-defined childhood syndromes thought to be associated with migraine, in which symptoms such as abdominal pain or vomiting are prominent while headache may be absent.3 Rarely, migrainous infarction may occur (previously called complicated migraine), characterized by an aura lasting more than 7 days or neuroimaging evidence of cerebral infarction.3
Clearly, in a patient who presents with a focal neurologic deficit and headache, migraine of any sort must be a diagnosis of exclusion unless the patient has a clear history of previous similar migraines, including the neurologic deficit, and normal results of prior investigations. Given that they rarely last more than 60 min, the aura and deficits would be expected to resolve in migraine patients prior to discharge from the ED.
Treatment Advances in the understanding of the pathophysiology of migraine have been paralleled by much improved ED treatment options for severe migraine. Yet, while an impressive array of medications has been studied and virtually every route of administration has been tried, there remains a wide spectrum of clinical practice and no clear consensus on the best therapy. This reflects the fact that, to date, no migraine treatment has been shown to be superior in all respects. 14
Physicians choosing a medication should consider several factors besides efficacy in relieving headache in the ED, including the ability to abort migraine (i.e., prevent recurrence after relief of symptoms), contraindications, relief of other symptoms, side effects, cost, ease of administration, and time to return to normal activities. Patients should also be asked about their previous experience with a drug and whether they are willing to accept the same treatment again. Unfortunately, many migraine studies do not adequately assess these outcomes and suffer from other limitations.
At present, several effective options are available for the ED management of acute severe migraine headache, based on a review of ED randomized controlled trials (RCTs) and consensus guidelines prepared by the Canadian Headache Society.2 Dihydroergotamine (DHE), a 5-HT1D (serotonin) receptor agonist, is highly effective in relieving headaches and is an appropriate first-line therapy for migraine. 2!5 However, DHE causes vomiting in a significant proportion of patients, probably due to its affinity for other serotonin and dopamine receptors. Patients should therefore be pretreated with an antiemetic, such as metoclopramide or prochlorperazine. 2 Sumatriptan, a more selective 5-HT1D agonist than DHE, is effective in relieving headache in the ED and causes less nausea and vomiting. —I6 However, ED-based studies have shown that subcutaneous sumatriptan results in frequent but short-lived minor adverse effects (e.g., sensations of heat, tingling, chest discomfort, and injection site reactions), is more costly, and has a higher 24-h recurrence rate than DHE.16 While sumatriptan may still be useful for migraines unresponsive to other medications, it should not be given within 24 h of the administration of DHE or other ergots, since both cause vasoconstriction. 2
Other migraine drugs studied in ED-based RCTs and shown to be effective include metoclopramide, 17 chlorpromazine,15!8 prochlorperazine,17 and ketorolac.18 Table 219-4 summarizes dosing, contraindications and precautions for each drug. Regardless of medication chosen, patients should be placed in a darkened, quiet area in order to lessen the associated phono- and photophobic symptoms. Given that patients may have been vomiting and had poor oral intake for hours or days prior to their arrival in the ED, intravenous rehydration is also frequently of benefit. 2
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