There are a wide variety of acute treatments available for migraine.(Table 12)  A further listing of abortive and symptomatic therapies for migraine is adapted from Baumel.²³⁷ (Tables 13 & 14) 

Table 12.          Drugs Used for Acute Migraine Therapy

TRADE NAME (MANUFACTURER)	COMPOSITION	ROUTE AND DOSE
Cafergot tablets and suppositories (Novartis)	1 mg ergotamine tartrate 100 mg caffeine 2 mg ergotamine tartrate 100 mg caffeine	Orally: 2 tablets at onset; 1 additional tablet every 30 min if needed to maximum 6/attack, 10/wk   Rectally: 1 suppository at onset, second in 1 hr if needed; maximum 2/attack, 4/wk
Ergotamine Tartrate (Sandoz)	1.0 mg ergotamine tartrate	2 tablets orally at onset, 1/30 min to maximum 6/attack, 10/wk
D.H.E. 45 injection	1.0 mg/ml dihydroergotamine	1 ml IM at onset, repeat every hour to total of 3 ml if needed; may be given IV 0.5 mg or 1.0 mg every 8 hrs
Ergonovine Maleate tablets	0.2 mg ergonovine maleate	1 tablet at onset, 1 every hour to 6/attack
Wigraine tablets and suppositories (Organon)	1.0 mg ergotamine tartrate 100 mg caffeine 0.1 mg belladonna 130 mg phenacetin	1 tablet at onset, 1 every hour to 6/attack 1-2 tablets or suppositories at onset with 1-2 after 15 min to maximum of 6/attack or 12/wk
Stadol NS (Bristol-Myers Squibb)	1.0 mg butorphanol tartrate spray	1.0 mg at onset; 1.0 mg in 60 - 90 min

 

 

Table 13.          Abortive therapy for migraine

Drug	Route of administration	Dosage
Serotinin-receptor agonists Dihydroergotamine	IM, SC, IV	0.5-1.0 mL
Ergotamine derivatives Ergotamine and caffeine*	PO	2 tablets, repeat in 1 h if necessary; limit, 4 per attack
Ergotamine*	Sublingual	1 tablet (let dissolve), may repeat in 30 min; limit, 2 per attack
Ergotamine and caffeine*	Suppository	½-1 suppository, repeat in 1 h if necessary; limit, 2 doses
Sympathomimetic agents
Isometheptene, acetaminophen, dichloralphenazone	PO	2 capsules, may repeat in 1 h; limit, 3 times per wk
Corticosteroids
Dexamethasone	PO†   IM†	2-6 mg, may repeat in 3 h if necessary 4 mg
All NSAIDs Mixed barbiturate analgesics (see Table 9)
*                                  Wait 3 days between dosing with ergotamine in  patients with frequent migraine or daily headache. †                                  For protracted migraine. IM                               Intramuscular. SC                               Subcutaneous. PO                               Oral. NSAIDs           Nonsteroidal anti-inflammatory drugs

 

 

Table 14.          Symptomatic therapy for migraine

Drug	Route of administration	Dosage
NSAIDs Naproxen	PO	550-750 mg with repeat in 1-2 h; limit, 3 times per wk
Meclofenamate	PO	100-200 mg with repeat in 1-2 h; limit, 3 times per wk
Flurbiprofen	PO	50-100 mg with repeat in 1-2 h; limit, 3 times per wk
Ibuprofen	PO	200-300 mg with repeat in 1-2h; limit, 3 times per wk
Mixed barbiturate analgesics
Butalbital, aspirin or acetaminophen, and caffeine; butalbital and acetaminophen	PO	1-2 tablets q4-6h; limit, 4 tablets per day up to twice per wk
Narcotics (codeine-containing compounds, oxycodone, propoxyphene, meperidine)	PO	sparingly and infrequently, if at all, in patients with chronic headaches
Antiemetics*
Promethazine	PO, IM	50-125mg/d
Prochlorperazine	PO Suppository IM/IV	1-25 mg/d 2.5-25 mg/d 5-10 mg/d
Trimethobenzamide	PO Suppository	250 mg/d 200 mg/d
Metoclopramide	PO IM IV	5-10 mg/d 10 mg/d 5-10 mg (diluted
Dimenhydrinate	PO	50 mg
*          Given 10-20 minutes before ingestion of oral abortive migraine medication.

 

 

As pointed out by Silberstein and Lipton, the choice of acute treatment depends upon the severity and frequency of headaches, the pattern of associated symptoms, comorbid illnesses, and the patient’s treatment response profile.  The simplest treatment is with non-prescription or prescription analgesics.  Many individuals find headache relief with compounds such as aspirin or acetaminophen either alone or in combination with caffeine.  Butalbitol, a short-acting barbiturate is often added to the combination of simple analgesics and caffeine.  The combination of acetaminophen, isometheptene,  a sympathomimetic; and dichloralphenazone, a chloral hydrate derivative, is also safe and effective in headache treatment.^245,246  When simple analgesics fail, consideration may be given to combination with more potentially habit forming medication.  Combinations are available with codeine.  The nausea is often effectively treated with prochloperazine.

More potent narcotic analgesics such as propoxyphene, meperidine, morphine, hydromophone, and oxycodone are available alone and in combination.  However, because of medication overuse and rebound, these agents should be used sparingly and only for patients who experience infrequent headaches.¹⁴  Further discussion about the use of opioids and transnasal opioids are discussed by Silberstein and Lipton.⁹

Headaches similar to migraine can be triggered by serotonergic drugs such as reserpine and m-chloralphenalpiprazine (serotonergic agonist).^37,38  Two agents effective in the acute treatment of migraine, sumatriptan,^247-249  a serotonin analogue, and dihydroergotamine (DHE),^250,251 an ergot derivative.  These agents block the development of neurogenically induced inflammation in rat dura mater.  This in turn blocks the release of neuropeptides including substance P and calcitonin gene-related peptide, preventing neurogenic inflammation.⁹  The NSAIDs may also block neurogenic inflammation; the mechanism of this action, however, is less certain.

Ergotamine and DHE can be used to treat moderate to severe migraine.²⁵²   It was once the mainstay of acute therapy. It was once said that "if a headache does not respond to ergotamine tartrate, it is not true migraine."²⁵³   This agent, derived from Claviceps purpurea, a fungus that grows in rye and other grains, is the major compound effective as a specific agent in an acute migraine attack.  Ergotamine is one of the naturally occurring alkaloids in crude ergot; all the ergot alkaloids are derivatives of lysergic acid.²⁵⁴  Ergotamine has as one of its major pharmacologic properties the ability to produce a peripheral vasoconstriction and, in higher doses, damages capillary endothelium.  Inasmuch as ergotamine is neither sedative nor analgesic and other forms of pain are not relieved by the drug, its action is believed to directly related to the pathophysiology of migraine.  In the classic experiments of Graham and Wolff,²⁵⁵ the intensity of pain was directly related to the amplitude of the temporal artery pulsation, and both decline in response to intravenous ergotamine tartrate. (Fig 13) 

Figure 13. Relation of amplitude of pulsations of temporal artery to intensity of headache after administration of ergotamine tartrate. The sharp decrease in the amplitude of pulsation following injection of ergotamine closely paralleled the rapid decrease in intensity of headache. Representative sections of photographic record are inserted. The average amplitude of pulsations for any given minute before and after administration of ergotamine was ascertained by measuring individual pulsations from the photographic record. The points on the heavy black line (lower half) represent these averages, expressed as percentages. Initial or "control" amplitude was taken as 100%. (Dalessio DJ: Wolff's Headache and Other Head Pain, 3rd ed. New York, Oxford)