Expert Opinion on Pharmacotherapy

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Treatment of status migrainosus

Dawn A Marcus

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Pharmacotherapy, 2:4, 549-555, DOI: 10.1517/14656566.2.4.549

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 Expert Opinion on Pharmacotherapy
Marcus
Treatment of status migrainosus
Monthly Focus: Central & Peripheral Nervous Systems

Treatment of status migrainosus

Dawn A Marcus
Anesthesiology & Neurology Department, Multidisciplinary Headache Clinic,
University of Pittsburgh Medical Center, PA, USA
http://www.ashley-pub.com

Migraine episodes that persist for at least 3 days despite treatment are
Review termed status migrainosus. Traditionally, these long-lasting migraine
episodes were treated with brief in-patient hospitalisations for iv. medica-
1. Introduction tion. The full duration of disability associated with these episodes includes
both the several days of migraine and the several days of hospital stay. The
2. First-line therapy -
development of medications that specifically target the mechanism of
serotonin agents
migraine, such as dihydroergotamine and the triptans, has reduced the
3. Rescue therapy number of headache episodes that persist after initial treatment or fail to
respond to self-administered therapy.
4. Treatment in the clinic
Keywords: migraine, rescue therapy, triptan
5. Expert opinion
Bibliography Exp. Opin. Pharmacother. (2001) 2(4):549-555

1. Introduction

Status migrainosus is defined as a migraine episode that has failed to

respond to acute care therapy after 3 days. Historically, status migrainosus
has been treated with a brief in-patient hospital stay, with the use of iv.
ergotamine, antinausea medications and opioids. The development of
effective medications that patients may use at home has changed this
therapy dramatically. Most patients can manage severe migraine episodes
at home, with occasional visits to their doctor’s clinic for more recalcitrant
headache.
Chronic daily headache or chronically frequent headache needs to be
treated by withdrawal from excessive analgesic use and headache preven-
tive therapy. Only when the headache is different from the severity of
typical daily headaches or frequent headaches, should the diagnosis of
status migranosus be considered.
Status migrainosus is typically managed with a combination of acute care
medications, including migraine-specific and symptomatic medications.
The migraine-specific medications directly influence the pathophysio-
logical mechanism of migraine, while the symptomatic treatments address
symptoms like pain and nausea. First-line therapy relies on the more
effective migraine-specific therapies. These therapies target the mechanism
of migraine, which increases their therapeutic effect and minimises
unwanted side effects caused by activation of additional neural pathways.
Few studies have specifically evaluated status migrainosus. A recent review
of 146 emergency room visits for migraine revealed that 87% were success-
fully treated and discharged within 12 h [1]. Only 13% of migraineurs
needed to be hospitalised. Only one out of four patients diagnosed with
status migrainosus required hospitalisation. These data suggest that both
549
2001 © Ashley Publications Ltd. ISSN 1465-6566
550 Treatment of status migrainosus
Figure 1: Headache treatment and the serotonin (5-HT) model.
Headache
triggers
Trigger
avoidance
Central
Peripheral Dorsal
5-HT
5-HT raphe
nucleus
Migraine-specific
acute care meds:
5-HT1 agonists Headache preventive meds:
• DHE • 5-HT2 antagonists
• Triptans • Relaxation/biofeedback
increasing or excitatory effect
acute migraine and status migrainosus can be
managed without the need for hospitalisation.
2. First-line therapy - serotonin agents
Serotonin (5-HT) is critically linked to the
pathogenesis of headache. Peripheral 5-HT levels
measured in the bloodstream decrease at the onset of
headache [2] and manipulating peripheral 5-HT levels
by injecting iv. 5-HT relieves severe migraine experi-
mentally [3,4]. The essential role of 5-HT manipulation
in headache has been confirmed in rodent experi-
ments by Moskowitz and led to the development of
the neurovascular model of migraine [5].The
neurovascular model describes important interactions
between neurochemical, vascular and trigeminal
pathology during migraine. This model postulates that
migraine begins with a drop in peripheral 5-HT levels.
This decrease in peripheral 5-HT removes the inhibi-
tory drive exerted by peripheral 5-HT on the dorsal
raphe nucleus which is normally present. The dorsal
raphe nucleus then becomes susceptible to influences
by a number of poorly understood headache trigger
factors, such as medications, hormones, food
chemicals and stress. Once stimulated, the dorsal
raphe nucleus releases 5-HT, which binds to receptors
on intracranial, extracerebral vessels, like the
© Ashley Publications Ltd. All rights reserved.
Extracerebral Trigeminal
vascular
nucleus
dilation
Headache
decreasing or inhibitory effect
meningeal vessels. These vessels respond by dilating,
thereby stretching and activating the nerve fibres
surrounding them. These nerve fibres send messages
to the trigeminal system, which has pathways to the
hypothalamus (possibly causing the cravings and
sensory sensitivity associated with headache), the
cervical spinal cord (possibly resulting in ephaptic
transmission to somatic musculature causing cranial
and cervical muscle spasm) and the thalamus
(resulting in a painful sensory experience).
Knowledge of the importance of 5-HT levels for
migraine has dramatically altered therapies used to
treat migraine. The majority of migraine therapies
alter 5-HT levels, including dihydroergotamine
(DHE), the triptans, antidepressants and even relaxa-
tion/biofeedback (see Figure 1). Acute care migraine
medications act as agonists to inhibitory, autoregula-
tory 5-HT1 receptors at the dorsal raphe nucleus.
Excitation of these inhibitory receptors increases the
inhibitory drive on the dorsal raphe, acting as a
peripheral 5-HT mimic. This increased inhibition
should reduce central release of 5-HT with its coinci-
dent changes in extracerebral vascular tone,
activation of the trigeminal system and, consequently,
headache perception. Preventative headache medica-
tions, such as the antidepressants, act as antagonists
against the excitatory central 5-HT2 receptors [6,7].
Exp. Opin. Pharmacother. (2001) 2(4)
 Marcus 551

Table 1: Migraine-specific prescription pharmacokinetics.

Medication Tmax (h) t1/2 (h) 2 h relief 4 h relief Recurrence Ref.

Fastest agents 30 - 35%
Sumatriptan sc. 0.25 2 82% 30 - 35%
Sumatriptan NS 1 2 64% 30 - 35% [11]
Fast oral agents 30 - 35%
Rizatriptan 1 - 1.5 2-3 71% 30 - 35%
Zolmitriptan 2.5 3 66% 30 - 35%
Eletriptan 2.8 4 65% (40 mg) 30 - 35% [12]
77% (80 mg)
Sumatriptan 2.5 2.5 60% 30 - 35%
Almotriptan 2.6 3.4 58% 30 - 35% [13,14]
Slower agents
DHE-45 im./sc. 1 10 73% 15% [15]
DHE-45 NS/SL 0.5 - 1 10 50%
Naratriptan 2-3 6 48% 67% 20%
Frovatriptan 2-3 26 40% 55% 15 - 20% [12]
Data from package inserts except where referenced.
DHE: Dihydroergotamine; im.: intramuscular; NS: Nasal spray; SL: Sublingual; sc.: Subcutaneous; t1/2: Half-life; Tmax: Time to
peak blood concentration.

Antagonising the action of 5-HT that has been
released by the dorsal raphe is believed to prevent
vascular dilation, trigeminal stimulation and
head ac h e. Inter es tingly, even ef f ecti ve
non-medication therapies, like relaxation, appear to
work by altering 5-HT activity. Mathew et al.
demonstrated a decrease in monoamine oxidase
levels after training in relaxation [8]. As monoamine
oxidase metabolises 5-HT, treatment with relaxation
should influence 5-HT levels in a similar manner to
treatment with antidepressants.
Both DHE and the triptans specifically target
‘migraine’ receptors. The Quality Standards Subcom-
mittee of the American Academy of Neurology
recommends triptans and DHE as first-line therapy for
the treatment of acute, moderate-to-severe migraine
[9,10]. There are several triptan medications currently
available to patients (e.g., sumatriptan, rizatriptan,
zolmitriptan and naratriptan), as well as newer
compounds currently being evaluated (e.g.,
eletriptan, frovatriptan and almotriptan). There are
some pharmacokinetic differences among the first-
line agents that is mirrored in clinical efficacy data
(Table 1). In general, those agents with the shortest
time to peak blood concentration (Tmax) have a faster
onset of clinical response. In addition, those with the
longest half-lives (t1/2) have a slower onset of action,
but a lower risk of headache recurrence. DHE, for
© Ashley Publications Ltd. All rights reserved.
example, has a very low recurrence rate and a long
half-life of the parent compound as well as active
metabolites, extending its overall duration of activity
to about 3 days. For this reason, DHE is preferred for
more longer lasting migraine attacks [10]. About one
third of triptan users report recurrence of migraine
after initially successful headache relief. The combina-
tion of triptan with non-steroidal anti-inflammatory
drugs (NSAIDs) (naproxen sodium (550 mg) or
tolfenamic acid (200 mg)) reduces recurrence by
about 60% [16,17].
2.1 Efficacy of migraine-specific 5-HT
medications in status migrainosus
There have been no controlled studies to evaluate the
efficacy of migraine-specific medications, including
DHE and the triptans, for status migrainosus.
Self-administration of DHE at home for severe
headache results in a reduction of emergency room
visits by 83% [18]. A multinational study demonstrated
superior headache quality of life scores for
migraineurs treating moderate-to-severe migraine
episodes with sc. sumatriptan [19]. At home, dosing
with sumatriptan reduces primary care visits by 32%
and emergency room visits by 85% [20]. A number of
s i mi l ar p h ar maco eco n o mi c s tu d i es ha v e
demonstrated similar reduced use of both out-patient
Exp. Opin. Pharmacother. (2001) 2(4)
552 Treatment of status migrainosus
and emergency room services when patients are
treated with migraine-specific therapy [21-24].
Similar to all acute care medications, DHE and the
triptans should be used only for infrequent, severe
migraine episodes. Daily or near daily use of either
migraine-specific or analgesic acute care medications
results in an increase of recalcitrant headache or
analgesic overuse headache [25,26]. Restricting triptan
use to permit treating a maximum of four severe
migraine episodes per month reduces the risk for the
development of medication overuse headache and
does not increase medical costs or healthcare utilisa-
tion [27].
3. Rescue therapy
Rescue therapy is used when patients fail to achieve
adequate relief from first-line therapy or patients
cannot use the migraine-specific medications. This
would include patients with uncontrolled hyperten-
sion, cardiovascular disease or significant risk factors
for cardiovascular disease. Particularly severe
migraine episodes, such as status migrainosus, often
require the combination of symptomatic therapy with
migraine-specific medications. Most of these
therapies, however, can be administered by the
patient at home and will eliminate the need for office
or in-patient care.
3.1 Analgesics
Analgesics are effective for mild-to-moderate
headache. Aspirin and NSAIDs are more effective for
migraine than acetaminophen with or without
codeine [28-30]. The addition of caffeine increases
analgesic effect and absorption when using a caffeine
dose of at least 60 mg [31]. For example, the addition
of caffeine (100 mg) to NSAIDs increases analgesic
effect by 250% [32]. Lipton et al. demonstrated
effective headache relief in 59% using a combination
of aspirin-acetaminophen-caffeine, compared with
relief in 33% in the placebo group [33]. These
headaches, however, were not as severe as the typical
attack of status migranosus and patients who
commonly vomited or had severe or disabling
migraine were excluded from the study. Therefore,
analgesics are typically used as adjunctive therapy for
status migrainosus.
© Ashley Publications Ltd. All rights reserved.
3.2 Anti-emetic medications
Prochlorperazine (25 mg rectal suppository (PR), 10
mg im., or 10 mg iv.) is effective for migraine [34], and
more effective than metoclopramide [35] or ketoralac
[36]. Jones et al. compared emergency room treatment
of severe migraine with either prochlorperazine (10
mg im.) or metoclopramide (10 mg im.). Relief
occurred in 67% with prochlorperazine, 34% with
metoclopramide and 16% with placebo [37]. Despite
good early relief, rescue analgesics were required
after 60 minutes for 80% in both active treatment
groups.
3.3 Opioids
Status migrainosus may require treatment with
adjunctive opioids when migraine-specific therapy
has failed to adequately relieve the headache, or in
patients who cannot use triptans or ergotamines. A
variety of opioids may be helpful, such as
butorphanol NS, hydromorphone (2 mg po. or 3 mg
PR), or morphine (15 - 30 mg po. or 30 mg PR). Acute
therapy with opioids is often associated with sedation,
which may prolong the duration of headache-related
disability.
3.4 Steroids
Tapering oral doses of steroids over 4 days (e.g.,
prednisone 80 mg initially, reduced by 20 mg each
day or dexamethasone 8 mg initially, reduced by 2 mg
each day) is reported to be beneficial in clinical
practice [38]. Intravenous steroids have also been
reported effective for refractory headache [39].
4. Treatment in the clinic
When patients have failed to control their headaches
with medications at home, or nausea and vomiting
prohibits the use of oral medications, injectable
medication may be necessary. Injectable migraine-
specific therapy, such as sumatriptan or DHE, is more
effective than symptomatic therapy. Diener reported a
comparative trial between iv. analgesic and sc.
sumatriptan for acute migraine [40]. After 2 hours, 76%
in the sumatriptan group were pain-free, compared to
44% with analgesics and 14% with placebo. The
sumatriptan group was also able to return to work
about 4 h faster than the other groups.
Sumatriptan (6 mg sc.) is the first choice for patients
requiring office management of status migranosus.
This may be repeated if ineffective after 1 h. For
Exp. Opin. Pharmacother. (2001) 2(4)
 Marcus 553
Figure 2: Treatment of status migrainosus.
DHE: Dihydroergotamine; im.: Intramuscular; NS: Nasal spray; NSAID: Non-steroidal anti-inflammatory drug; PO: Per os (by
mouth); SL: Sublingual; sc.: Subcutaneous; rx: Prescription.

TREATMENT OF STATUS MIGRAINOSUS

No contraindications Contraindications to

to DHE and triptans DHE and triptans

Maximally severe Not peak severity Rescue therapy

If ineffective,
Sumatriptan sc. Triptan PO or NS
office management
DHE im. DHE NS or SL
with injectable

symptomatic rx

If effective, If ineffective, If ineffective, If effective, If ineffective,

redose triptan or add symptomatic follow maximally send home with inpatient rx

DHE if needed rescue rx severe algorithm symptomatic rx symptomatic rx

If headache recurs If effective, If ineffective,

within 24 h, rx next headache inpatient rx

redose DHE or with triptan or DHE DHE Q8h and

triptan with NSAID plus rescue med symptomatic rx

patients who have failed to achieve benefit from 5. Expert opinion

triptans used to treat earlier headache episodes, DHE
may be used. Fewer side effects and equal efficacy are
seen when DHE is adminstered im. rather than iv.,
which typically requires premedication with prochlor-
perazine or metoclopramide (10 mg im.). DHE may be
repeated after 1 and 2 h if patients fail to achieve
headache relief. When patients have used maximum
doses of triptans or ergotamines earlier in the day to
treat the particular headache episode, injections may
not be used. If patients cannot use sumatriptan, or
DHE, they may need additional rescue medications.
These would include iv. hydration, ketorolac, opioids
(such as injectable hydromorphone) or anti-emetics
(such as prochlorperazine or chlorpromazine). After
patients have received triptan or DHE in the clinic, in
addition to rescue medications, they should be
discharged to home. If the headache continues
unchanged after several hours, they may require
hospitalisation. This rarely occurs for most patients
since the widespread use of both DHE and the
triptans. Patients who are hospitalised are typically
treated with DHE iv. injections every 8 h (0.5 mg with
10 mg metoclopramide) and opioids as needed over a
2 - 3 day period.
© Ashley Publications Ltd. All rights reserved.
Status migrainosus can usually be effectively managed
by patients with the combination of migraine-specific
and symptomatic medications. The use of migraine-
specific medications has limited the need for clinic or
emergency room treatment as well as in-patient
hospitalisations. The ability of migraine patients to
manage headache effectively generally avoids the
prolonged disability associated with status migrai-
nosus (Figure 2).
Once patients have successfully managed their
headache episode, effective medications should be
reviewed so that medications may be provided to the
patient to keep at home to self-administer for
subsequent headache episodes. If patients treat
headaches earlier in their course, rather than waiting
until the headache is maximally severe, relief is more
complete and quicker and disability will be
minimised.
Current migraine therapy has been demonstrated in
both clinical and pharmacoeconomic studies to
reduce pain, disability and costs associated with
migraine. Future studies are warranted to evaluate the
specific incidence of status migrainosus. Specifically,
Exp. Opin. Pharmacother. (2001) 2(4)
554 Treatment of status migrainosus
studies should investigate whether the use of
effective, migraine-specific medications results in a
reduction in the number of migraine episodes that
persist for more than 3 days.
Bibliography
Papers of special note have been highlighted as:
• of interest
•• of considerable interest
1. BIGAL M, BORDINI CA, SPECIALI JG: Headache in an
emergency room in Brazil. Sao Paulo Med. J. (2000)
118:58-62.
2. ANTHONY M, HINTERBERGER H, LANCE JW: Plasma
serotonin in migraine and stress. Arch. Neurol. (1967)
16:544-552.
3. KIMBALL RW, FRIEDMAN AP, VALLEJO E: Effect of
serotonin in migraine patients. Neurology (1960)
10:107-111.
4. GOADSBY PJ, LANCE JW: Physiopathology of migraine.
Revue du Praticien (1990) 40:389-393.
5. MARCUS DA: Serotonin and its role in headache
pathogenesis and treatment. Clin. J. Pain (1993)
9:159-167.
• This review describes a model for the role of 5-HT in
migraine that incorporates both experimental and clinical
data.
6. SANDERS-BUSH E, BREEDING M, KNOTH K, TSUTSUMI M:
Sertraline-induced desensitzation of the serotonin
5HT-2 receptor transmembrane signaling system.
Psychopharmacology (Berl) (1989) 99:64-69.
7. PAPP M, KLIMEK V, WILLNER P: Effects of imipramine
on serotonergic and beta-adrenergic receptor binding
in a realistic animal model of depression. Psychophar-
macology (Berl) (1994) 144:309-314.
8. MATHEW RC, HO BT, KRALIK P, CLAGHORN JL:
Biochemical basis for biofeedback treatment of
migraine: a hypothesis. Headache (1979) 19:290-293.
9. SILBERSTEIN SD: Practice parameter: evidence-based
guidelines for migraine headache (an evidence-based
review). Neurology (2000) 55:754-763.
•• A comprehensive review of recommendations for the
treatment of migraine.
10. TFELT-HANSEN P, SAXENA PR, DAHLOF C et al.: Ergota-
mine in the acute treatment of migraine: a review and
European consensus. Brain (2000) 123:9-18.
• European consensus statement on acute management of
migraine.
11. MOORE KH, HUSSEY EK, SHAW S et al.: Safety,
tolerability and pharmacokinetics of sumatriptan in
healthy subjects following ascending single intranasal
doses and multiple intranasal doses. Cephalalgia (1997)
17:541-550.
12. Presentations European Neurological Society Meeting.
Lisbon, Portugal (1999).
© Ashley Publications Ltd. All rights reserved.
13. CABARROCAS X, SALVA M: Pharmacokinetic and
metabolic data on almotriptan, a new migraine drug.
Cephalalgia (1997) 17:422.
14. SPIERINGS EL, GOMEZ-MANCILLA B, GROSZ DE et al.:
Oral almotriptan vs. oral sumatriptan in a double-
blind, randomized, parallel-group study in migraine
patients. Headache (2000) 40:433.
15. WINNER P, RICALDE O, LEFORCE B et al.: A double-blind
study of sc. dihydroergotamine versus sc. sumatiptan
in the treatment of acute migraine. Arch. Neurol. (1996)
53:180-184.
16. KRYMCHANTOWSKI AV: Naproxen sodium decreases
recurrence when used with sumatriptan. Headache
Quarterly (1999) 10:297-299.
17. KRYMCHANTOWSKI AV, ADRIANO M, FERNANDES D:
Tolfenamic acid decreases migraine recurrence when
used with sumatriptan. Cephalalgia (1999) 19:186-187.
18. KLAPPER JA, STANTON J: Clinical experience with
patient administered subcutaneous dihyddroergota-
mine mesylate in refractory headaches. Headache
(1992) 32:21-23.
19. DAHLOF C, BOUCHARD J, CORTELLI P et al.: A multina-
tional investigation of the impact of subcutaneous
sumatriptan. II: Health-related quality of life. Pharma-
coeconomics (1997) 11(Suppl. 1):24-34.
20. LOFLAND JH, JOHNSON NE, BATENHORST AJ, NASH DB:
Changes in resource use and outcome for patients
with migraine treated with sumatriptan: a managed
care perspective. Arch. Int. Med. (1999) 159:857-868.
•• A study of the economic impact of sumatriptan administered
to a community-based sample of migraineurs.
21. COHEN JA, BEALL DG, MILLER DW et al.: Subcutaneous
sumatriptan for the treatment of migraine:
humanistic, economic, and clinical consequences.
Fam. Med. (1996) 28:171-177.
22. LEGG RF, SCLAR DA, NEMEC NL et al.: Cost-effectiveness
of sumatriptan in a managed care population. Am. J.
Manag. Care (1997) 3:117-122.
23. COHEN JA, BEALL D, BECK A et al.: Sumatriptan
treatment for migraine in a health maintenance
organization: economic, humanistic, and clinical
outcomes. Clin. Ther. (1999) 21:190-204.
24. BIDDLE AK, SHIH YC, KWONG WJ: Cost-benefit analysis
of sumatriptan tablets versus usual therapy for
treatment of migraine. Pharmacotherapy (2000)
20:1356-1364.
25. GAIST D, TSIROPOULOS I, SINDRUP SH et al.: Inappro-
priate use of sumatriptan: population based register
and interview study. Br. Med. J. (1998) 16:1352-1353.
26. GOADSBY PJ: Sumatriptan is not the only analgesic
used inappropriately. Br. Med. J. (1998) 317:1016.
27. GOLDFARB SD, DUNCAN BS, DANS PE, SLOAN AS: HMO
direct cots and health care resources use after
implementation of a monthly limit on sumatriptan.
Am. J. Health Syst. Pharm. (1999) 56:2206-2210.
Exp. Opin. Pharmacother. (2001) 2(4)

28. PETERS BH, FRAIM CJ, MASEL BE: Comparison of 650 mg
aspirin and 1,000 mg acetaminophen with each other
and with placebo in moderately severe headache. Am.
J. Med. (1983) 76:36-42.
29. BOUREAU F, JOUBERT JM, LASSERE V, PRUM B,
DELECOEIULLERIE G: Double-blind comparison of an
acetaminophen 400 mg-codiene 25 mg combination
versus aspirin 1000 mg and placebo in acute migraine
attack. Cephalagia (1994) 14:156-161.
30. HAMALAINEN ML, HOPPU K, VALKEILA E, SANTAVUORI
P: Ibuprofen or acetaminophen for the acute
treatment of migraine in children: a double-blind,
randomized, placebo-controlled, crossover study.
Neurology (1997) 48:103-107.
31. DALESSIO DJ: Caffeine as an analgesic adjuvant: review
of the evidence. Headache (1994) 34(Suppl. 1):10-12.
32. FORBES JA, BEAVER WT, JONES KF et al.: Effect of
caffeine on ibuprofen analgesic in postoperative oral
surgery pain. Clin. Pharmacol. Ther. (1991) 49:674-684.
33. LIPTON R, STEWART WF, RYAN RE, Jr., SAPER J, SILBER-
STEIN S, SHEFTELL F: Efficacy and safety of acetamino-
phen, aspirin, and caffeine in alleviating migraine
headache pain: 3 double-blind, randomized, placebo-
controlled trials. Arch. Neurology (1998) 55:210-217.
34. JONES EB, GONZALEZ ER, BOGGS JG, GRILLO JA,
ELSWICK RK: Safety and efficacy of rectal prochlor-
perazine for the treatment of migraine in the
emergency department. Ann. Emerg. Med. (1994)
24:237-241.
35. COPPOLA M, YEALY DM, LEIBOLD RA: Randomized,
placebo-controlled evaluation of prochlorperazine
© Ashley Publications Ltd. All rights reserved.
Marcus 555
versus metoclopramide for emergency department
treatment of migraine headache. Ann. Emerg. Med.
(1995) 26:541-546.
36. SEIM MB, MARCH JA, DUNN KA: Intravenous ketorolac
versus intravenous prochloperaine for the treatment
of migraine headache. Acad. Emerg. Med. (1998)
5:573-576.
37. JONES J, PACK S, CHUN E: Intramuscular prochlopera-
zine versus metochlopramide as single agent therapy
for the treatment of acute migraine headache. Am. J.
Emerg. Med. (1996) 14:262-264.
38. VON SEGGERN RL, ADELMAN JU: Practice and
economics cost considerations in headache treatment.
Part 2: acute migraine treatment. Headache (1996)
36:493-502.
39. SAADAH HA: Abortive migraine therapy in the office
with dexamethasone and prochlorperazine. Headache
(1994) 34:366-370.
40. DIENER HC (ASASUMAMIG STUDY GROUP): Efficacy and
safety of intravenous acetylsalicylic acid lysinate
compared to subcutaneous sumatriptan and
parenteral placebo in the acute treatment of migraine.
A double-blind, double-dummy, randomized,
multicenter, parallel group study. Cephalalgia (1999)
19:581-588.
Dawn A Marcus
Pain Evaluation & Treatment Institute, 4601 Baum Boulevard,
Pittsburgh, PA 15213, USA
Tel.: +1 412 578 3100;
E-mail: dawnpainmd@yahoo.com
Exp. Opin. Pharmacother. (2001) 2(4)