Migraine headache is acommon affliction andpresenting symptom in theemergency department. Itsdiagnosis is entirely clinical,and the treating physidanshould ensure precisediagnosis before commencingtherapy. Generalnon-pharmacologicalmeasures and oralmedications are usuallyeffective in relieving thesymptoms. Occasionally,patients with fixed migrainesrequire parenteral therapy.Some medications used formigraine are antiemeticagents, ergot preparations,narcotic agents,phenothiazines (particularlychlorpromazine), and newerselective serotonin agonists.

RtSU.MtLa cephalee migraineuse estun symptome de presentationet une affection que lIonrencontre couramment dansles salles d'urgence. Sondiagnostic est entierementclinique et le medecin traitantdoit s'assurer que sondiagnostic est precis avant deprescrire une therapie. Lesmesures generales nonpharmacologiques et lesmedications orales sonthabituellement efficaces poursoulager les symptomes. 11arrivera occasionnellementque certains patientssouffrant de statusmigraineux auront besoind'une therapie parenterale.Parmi les autres medicamentsutilises pour traiter lamigraine, notons lesantiemetiques, lespreparations a base d'ergot,les narcotiques et lesphenothiazines(particulierement Iachlorpromazine et lesnouveaux agonistes selectifsde la serotonine).(on Fam Phsidn 1992;38:1451-1456.

New Prescriptionsfor Migraine inthe EmergencyDepartmentPETER L. LANE, MD, FRCPC

IGRAINE HEADACHE IS A COM-

mon affliction affecting 10%to 20% of the population.1"2

ci Headache is also a frequentpresenting complaint in the

emergency department, accounting formore than 1% of all emergency depart-ment visits.3-5 Of these headaches, a signifi-cant number will be migraine headaches.

Recently, research has focused on find-ing non-narcotic alternatives for treatingmigraine in the emergency department.Because of the episodic and recurrent na-ture of the disease, a history of migraineheadache often precedes narcotic addic-tion. Indeed, many chronic daily migrainepatients seen in offices, clinics, or emergen-cy departments are addicted to their treat-ment medication.6-8 This is not to say thatpatients are abusing medications for a plea-surable sensation; rather, the patient whomight once have suffered migraine can suf-fer from daily drug withdrawal headachesdue to their addictive treatment medica-tions and require further narcotics to dullthese withdrawl headaches. Breaking thisvicious cycle is extremely difficult and oftenexpensive.* - -0 - 0 -9 * v v -9 - v v vv00 -0 - - -0 -0 0 0 0 0 0 0 0 e -0 -0 0 0

Dr Lane is an Erngency Physician in dieDepartment ofEm.egeng Medicine at Vwtoma Hospitaland is an Associate Prfessor, Department ofMedicine,Universiy of Western Ontario, London, Ont.

Diagnostic featuresWhen evaluating the patient with migraineheadache, it is essential to make a clear andprecise diagnosis (Table 19). Unfortunately,the diagnosis depends exclusively on theclinical features. There is no single investi-gation that can provide incontrovertible ev-idence of the presence of migraine. It is im-portant to have a clear definition fortreating each patient appropriately and forevaluating research into new therapies. Ifpatient populations are different, the resultswill likely be different.

Migraines vary in intensity and patternfrom patient to patient and even from epi-sode to episode within one patient. Not allfeatures listed in Table 1 need be present ineach patient on each occasion.2

The aura, present only in classic mi-graine, usually consists of bizarre visualsensations. Patients will report seeing seriesof sparkling lights in one visual field, jaggedlines, unusual colors, etc. Occasionally, pa-tients will report an aura that is entirely ol-factory or present with transient paresthe-sia or weakness. Typically, the auras last 15to 30 minutes before the onset of the head-ache. The aura is believed to be secondaryto cortical and retinal ischemia due to vaso-constriction. 10-12

Most patients will report a characteristictrigger. In the past, migraine was often at-tributed, perhaps chauvinistically, to emo-

Canadian Family Physician VOL 38: June 1992 1451

Tabk 1. DIAGNOSTIC CRITRIA FOR MIGRAINEHEADACHE

Hedache ttacks lastig 4 to 721 (witratWl or111SVCCessfuly tretd

Headh with at lat 2 of the followig dhrocedsrls* Unilateral lcation* Pulsaing quality* Moderate or severe intensdy. Agravation by routine physial acivdy

During at lost 1 of the foHowin* Nausea or vomiting. Photophobia and phonophobia

e PIrive (sdnrilkiion or Roures). Negative (scotoma)

* lingling* Numbness* Weakness* Speech diturbance

Adaptedfom the Headache Classification Committee of the InternationalHeadache Socie!y.9

Table 2. STEPS INPREVENTIONAND EARLYTREATMENTOF MIGRAINE

1. Avoid known causativeagents

2. Treat the migraine assoon as possible

3. Remain in a dimly lit ordark room

4. Use a hot or cold com-press on the pain centeras appropriate

5. Try to relax or sleep

tional instability because it occurred mostlyin women. There is no doubt that physio-logical and emotional stress can act as trig-gers in some patients. However, there aremore common triggers, such as certainfoods, hormonal changes, medications, andweather changes.

The pain is often but not always unilat-eral. It is usually described as throbbingpain, particularly at the beginning ofthe at-tack. Almost inevitably there are associatedsymptoms, such as nausea, vomiting, pho-tophobia, and phonophobia.

Migraine headache tends to recur. Afirst diagnosis is usually made in the secondor third decade, although in retrospectmany of these patients have had childhood

headaches. Migraine headaches rarely lastbeyond the sixth or seventh decade of life.

The frequency of migraine headachescan vary considerably from patient to pa-tient; this relates to triggers to which the pa-tients might be exposed as well as the effica-cy of prophylactic medication taken. It hasbeen recommended that, in order to avoidincluding chronic daily headache patientswho do not have migraines, research stu-dies of migraine exclude those with morethan four to six headaches per month.'3

PathophysiologyEarly descriptions of migraine speculatedon a vasoconstrictive phase and a vasodila-tive phase. The vasoconstrictive phase wasassociated with relative cortical and retinalischemia resulting in aura. The vasodilativephase corresponded to the period of painand associated symptoms. More recently,angiography and cerebral blood flow stu-dies have partially confirmed these earlyspeculations. The vasodilative phase, how-ever, seems to be limited to the extracranialand meningeal vessels. There is evidencethat vasoconstriction ofcortical vessels con-tinues during the pain phase of mi-graine. 10-12

At the cellular and biochemical level,this vascular instability, particularly of arte-rioles, appears to relate to the release ofva-soactive substances from platelets.'4 Bothserotonin (5-hydroxytryptamine) and dopa-mine appear to play significant roles in thisprocess.

Newer therapies, therefore, focus on thisbasic understanding of the pathophysiology.

Some agents, such as corticosteroids,have been used to limit the "sterile inflam-matory response" seen at the arteriolar lev-el.'5 Other agents with dopamine antago-nist effects block the vasoconstrictioninduced by these vasoactive substances.

Acute therapyBy the time patients have arrived in theemergency department, they have usuallyattempted to thwart the migraine by vari-ous means (Table 2). Patients previously notdiagnosed as having migraine headachecan be an exception. In these patients, if acareful history indicates a pattern ofsimilarheadaches in the past that has not come tomedical attention, the physician might feel

1452 Canadian Family Physician VOL 38: June 1992

comfortable making a diagnosis of mi-graine and counseling the patient aboutthese simple steps for prevention and earlytreatment. The physician, however, shouldbeware of the patient presenting with a se-

vere headache of sudden onset with the as-

sociated symptoms of vomiting, photopho-bia, etc, who has never had a similarheadache in the past. Such patients requiremore intensive workup for other causes ofheadache. Such a workup usually includesa lumbar puncture and computed tomo-

graphy scan.

Simple analgesics extinguish most mi-graines. These would include acetylsalicylicacid, acetaminophen, and other non-steroi-dal anti-inflammatory drugs. Again, expe-

rienced patients will have attempted thesebefore arrival; if not, they are worth trying.With more severe headaches the additionof codeine is often enough to extinguish theheadache.Many patients, however, will have ex-

hausted prevention and early treatment

measures and oral and rectal suppositorytherapy at home. Often, these headacheswill have been present for several hours.This state has been termed status migraino-sus, or fixed migraine.) "6 These patientsusually require parenteral therapy.

The simplest parenteral medicationsand often the most useful are antiemeticagents. Intramuscular injections of dimen-hydrinate, prochlorperazine, and prome-

thazine relieve the associated nausea andsome of the headache in many patients. Allof these medications are sedating and haveother important side effects.

Ergot derivatives have been the main-stay of nonanalgesic treatment in migrainefor many years. Their pharmacological ac-

tion and adverse effects were documented2000 years ago. Ergot is derived from a fun-gus (Claviceps purpurea), which grows on

grains, especially rye. It causes smoothmuscle constriction. This is particularlytrue in both the uterus and the peripheralvasculature. There is some evidence as wellthat ergotamine can also act as a partial ser-

otonin agonist in the brain. 17 Orally, its use-fulness is restricted to patients who can takeit before the onset ofpain, ie, during the va-

soconstrictive or aura phase.Some researchers have studied the use

of dihydroergotamine parenterally for mi-graine. 18"19 The marked vasoconstriction in-duced by intravenous ergot derivatives,however, limits their usefulness. Any indi-cation of pre-existing cerebral vascular dis-ease, coronary artery disease, or peripheralvascular disease is an absolute contraindi-cation to its use. Some significant adverseeffects have been recorded as a result of theuse of ergot alkaloids and ergotamine prod-ucts in patients with no known pre-existingdisease.20 22

Much of the newer work in migraineprophylaxis research focuses on the use ofphenothiazines and related compounds.Chlorpromazine (CPZ), the prototype phe-nothiazine, was initially developed 40 years

ago as a neuroleptic for use as a preanes-

thetic agent. It soon became apparent thatthe agent had significant antipsychotic ef-fects as a result of the action ofits dopamineantagonist. It is now used principally for itsantipsychotic effects. Large doses orally or

intramuscularly are common.23

Chlorpromazine has a direct antiemeticeffect at the level of the chemoreceptor trig-ger zone at the brainstem.23 It also inducessignificant cx-adrenergic blockade.2" This

Canadian Family Phlysician VOL 38 June 1992 1453

Figure- 1. PAIN ASSAELE: Padti marks the point on Me scak Mat comsponds to Me intnsi of the pain

NO PAIN UNBERABLE PAIN

I Il _1||0~~~~~10(5 1| ! 1 11

Fgure 2. RESULTS OF THE PAIN ASSESSMENT MEASUREMENT ON VISUAL ANALOG SCALE:Comparison ofchlorpromazine and meperidine groups and response to dnmg treatment

serves to decrease peripheral vascular resis-tance, and hence to decrease the tension onthe dilated meningeal and extracranial ves-sel walls. Its sedating effect is also of somebenefit in migraine. Chlorpromazine is alsoassociated with altered serotonin levels.

The side effects ofCPZ are ofsome con-cern. Because of its ox-adrenergic blockadein some patients, it can induce postural hy-potension. In an early study of ours, an un-acceptably large proportion of patients de-veloped postural hypotension and requiredreplacement fluids in the emergency de-partment.24 This experience has led tochanges in our CPZ protocol. With the ear-ly establishment of intravenous infusionand administration of a fluid bolus, the rel-ative dehydration that some patients sufferas a result of their vomiting is treated. Inaddition, the dose ofCPZ has been reducedconsiderably from our preliminary study to0.1 mg/kg; with these changes, very fewpatients suffer postural hypotension. In asubsequent double-blind controlled trialcomparing CPZ to dimenhydrinate andmeperidine, there was no indication ofpos-tural hypotension in the CPZ group.25

Comparative studiesIn 1989, we reported on the results of adouble-blind controlled trial comparing theefficacy of intravenous CPZ with that of in-

travenous dimenhydrinate and meperi-dine.25 These agents appear to be muchmore effective when administered intrave-nously than intramuscularly. The absorp-tion of intramuscular medications is unpre-dictable. Small dose bolus therapy affordsthe physician the option of titrating the pa-tient's dose to the lowest effective dose,hence avoiding many side effects.

Pain was assessed in the study by bothvisual and verbal analog scales. The visualanalog scale (Figure 1) presents patients witha 10-cm line and asks them to mark on thepain continuum how severe their pain is.This remarkably simple instrument allowsa quantification of the pain. The verbalanalog scale allows patients to describetheir pain.23 The results of our pain assess-ment measurements are noted in Figure 2.The difference between the CPZ and mep-eridine groups is clear. This trial was highlystatistically significant. In 1990, Dell andcolleagues'8 compared the efficacy of intra-venous CPZ with that of lidocaine and di-hydroergotamine and found similar results,with CPZ being the superior agent.

At the University of Western Ontario, astudy is currently being undertaken to as-sess the efficacy of CPZ versus metoclopra-mide. Metoclopramide has been used mostcommonly as an antiemetic agent. Meto-clopramide has been evaluated as a mi-

1454 Canadian Family Physician VOI, 38: June 1992

I

graine prophylaxis when used in combina-tion with other agents, both orally andintramuscularly.26-39 A recent study fromanother center indicated its efficacy versusplacebo in migraine headache.40 The drugappears to cause fewer adverse effects thanCPZ and, if it is as effective as metoclopra-mide, would be preferable.

In addition, a new, highly selective sero-tonin receptor agonist, sumatriptan, has re-cently been approved for release in Cana-da. It certainly will add to the therapeuticoptions for migraine patients.

ConclusionThe future holds great promise for thetreatment of migraine headache in theemergency department. The agents pre-viously outlined have essentially replacednarcotic use in this patient population.Agents recently or soon to be released holdeven more promise. It is hoped that the pat-tern of habituation to narcotics in the mi-graine patient can be avoided, thus pre-venting the terrible personal and medicalcosts associated with addiction. E

Requests for reprints to: Dr Peter L. Lane,Department of Emergency Medicine, Victonra Hospi-tal, 375 South St, London, OANN6A 4G5

References1. WVaters WNE. Headache. (Clinical Epidemiology Se-

ries, vol 2). Littleton, Mass:John NVright-PSG,1986:37-9.

2. Goldstein ME, Chen TC. The epidemiology ofdisabling headache. Arch Neurol 1982;377-90.

3. Dickman RL, MasterTl'. 'I'he management ofnon-traumatic headache in a university hospitalemergency room. Headache 1979;19:391-6.

4. Leicht MJ. Non-traumatic headache in the emer-gency department. Ann Fmerg Med 1980;9:404-9.

5. Dhopesh V, Anwar R, Herring C. A retrospec-tivre assessment of emergency department patientswith complaint of headache. Headache 1979;19:37-42.

6. Edmeads JG. Migraine. Can Mled Assoc J 1988;138:107-13.

7. Kudrow L. Paradoxical effects of frequent anal-gesic use. AdvNYeurol 1982;33:335-41.

8. Mathew NT, Reuveni U, Perez K 'l'ransformedor evolutive migraine. Headache 1987;27: 102-6.

9. Headache Classification Committee, the Interna-tional Headache Society. Classification and diagnos-tic criteria for headache disorders, cranial neuralgiasand facial pain. Gephalalgia 1988;8(Suppl 7): 10-1.

10. O'Brien MDI. Cerebral blood flow changes inmigraine. Headache 1971; 10:139-43.

11. Skinhoj E,. HeXmodynamic stuldies writh the brainduring migraline. Arch Neural 973;29:95-8.

12. Edmeads J. Cerebral blood flowv in migraine.Headache 1977; 17: 148-52.

13. Tfelt-Hansen P, Olesen J. Methodological as-pects of drug trials in migraine. Neuroepidemiology1985;4(4):204-26.

14. Friedman AP. Overiew of migraine. Adv Neurol1982;33:1-15.

15. Gallagher DO. Emergency treatment of intrac-table migraine. Headache 1986;26:74-5.

16. CouchJR, Diamond S. Status migrainosus:causative and therapeutic aspects. Headache 1983;23:94-101.

17. Faciullacci M, Franchi G, Sicuteri F. Ergota-mine and methysergide as serotonin partial ago-nists in migraine. Headache 1976;16:185-8.

18. Dell R, Montoya D, Shuaib A, Lee MA.A comparative trial of three agents in the treat-ment of acute migraine headache. Ann Fmerg Med1990; 19: 1079-82.

19. Raskin NH. Repetitive intravenous dihydroer-gotamine as therapy for intractable migraine. Neu-rology 1986;36(7):995-7.

20. Diamond S, MedinaJL. Current thoughts onmigraine. Headache 1980;20:208- 12.

21. Carter JB. Cardiac manifestations following er-gotamine tartrate therapy for migraine. JAAIA1940; 114:2291-2.

22. Taylor GJ, Cohen B. Ergonovine-induced coro-nary artery spasm and myocardial infarction afternormal delivery. Obstet Gynecol 1985;66:821-2.

23. Kalant H, Roschlau WVHE, Sellers EM4. Principleof medical phannacology. 4th ed. Toronto, Ont: Uni-versity of Toronto Press, 1985.

24. Lane PL, Ross R. Intravenous chlorpromazine:preliminary results of acute migraine. Headache1985;25:302-4.

25. Lane PL, McLellan BA, Baggoley CJ. Compar-ative efficacy of chlorpromazine and meperidineand dimenhydrinate in migraine headache. AnnE'merg Med 1989; 18:360-5.

26. Johnson ES, Ratcliffe DM, WVilkinson M. Na-proxen sodium in the treatment of migraine. Ce-phalalgia 1985;5(1):5-10.

27. Peatfield RC, Petty RG, Rose FC. Doubleblind comparison of mefenamic acid and acetami-nophen (paracetamol) in migraine. Cephalalgia1983;3(2): 129-34.

28. TIfelt-Hansen P, Jensen K, Vendsborg P,Lauritzen M, OlesenJ. Chlormezanone in thetreatment of migraine attacks: a double blindcomparison with diazepam and placebo.Cephalalgia 1982;2(4):205- 10.

29. Tfelt-Hansen P, OlesenJ. Paracetamol (aceta-minophen) versus acetylsalicyclic acid in migraine.F'ur .Aeurol 1980; 19(3): 163-5.

30. Tfelt-Hansen P, Olesen J, Aebelholt-Krabbe A,Melgaard B, Veilis B. A double blind study ofmetoclopramide in the treatment of migraine at-tacks. _7 NeurolANeurosurg Psychiatry 1980;43(4):369-71.

31. Tokola RA. The effect of metoclopramide andprochlorperazine on the absorption of effervescentparacetamol in migraine. Cephalalgia1988;8(3): 139-47.

32. Volans GN. Mligraine and drug absorption. ClinPharmacokinet 1 978;3(4):3 13-8.

33. Ross-Lee L, Heazlewood V, TyrerJH, EadieMJ. Aspirin treatment of migraine attacks: plasmadrug level data. G,ephalaigia 982;2(l):9- 14.

Canadian Family Physician \01, 38: June 1992 1455

Good_ f..Xw:f !:health

I.((_ ~~throughcleanlwaterUSC Canadasponsored

village taps andF. --1 weUs helpAfican

BCPrvncial Office hlrntpituSC "J;?" #201 -4351 FraserSt. chilren tap into aVancouver, B.C. Iefbeftr

CSanad OnariPrvincial OfficOttSawas P.O. Box 2303, Staf_tnKIP 581 N2N6M2 4 IC

My contribution $ is enclosed.KS)'I Name: (otd chqu" are welome) CanadaAddress:_ Unitarian Service

Committee of Canada

(Please print and indcate Apt. No. and Posml Code) Building tomsrrow.Today--Registration number 006 4758 09 10 JFounded by Dr. Lode Hischmenova. C.C.L

-

Rgsulo nu- O-S 09 10- - -

in 1915

34. Tfelt-Hansen P, Olesen J. Effervescentmetoclopramide and aspirin (Migravess)versus effervescent aspirin or placebo formigraine attacks. a double-blind study. Ce-phalalgia 1984;4(2): 107-11.

35. Tokola RA, Kangasniemi P, NeuvonenPJ, Tokola 0. Tolfenamic acid, metoclo-pramide, caffeine and their combinationsin the treatment of migraine attacks. Cepha-lalgia 1984;4(4):253-63.

36. Tokola RA, Neuvonen PJ. Effects of mi-graine attack and metoclopramide on theabsorption of tolfenamic acid. Br] ClinPhannacol 1984;17(l):67-75.

37. Hakkarainen H, ParantainenJ, GothoniG, Vapaatalo H. Tolfenamic acid and caf-feine: a useful combination in migraine. Ce-phalalgia 1982;2(4):173-7.

38. Tokola RA, Anttila VJ, Neuvonen PJ.The effect of metoclopramide on the ab-sorption of tolfenamic acid. IntJ Clin Phar-macol Ther Toxicol 1982;20(10):465-8.

39. Pfaffenrath V, Reiter M. MedikamentoseTherapie der Migraine (Drug therapy ofmigraine). Wen Med Wochenschr 1988;138(23-24):591-9.

40. Tek DS, McClellan DS, OlshakerJS,Allen CL, Arthur DC. A prospectivedouble-blind study of metoclopramide hy-drochloride for the control of migraine inthe emergency department. Ann Emerg Med1990; 19:1083-7.

5Anaproxg DS 550 mgMAnaproxg 275 mg(naproxen sodium)Indications:Relief of mild to moderately severe pain, accompanied byinflammation such as musculoskeletal trauma, post-dental extraction, relief of post-partum cramping anddysmenorrhea.Contraindications:Anaprox and Anaprox DS (naproxen sodium) are contrain-dicated in patients, with active ulcers or active inflam-matory diseases of the gastrointestinal tract. They arealso contraindicated in patients who have shown hyper-sensitivity to it or to naproxen. Since cross-sensitivityhas been demonstrated, Anaprox or Anaprox DS shouldnot be given to patients in whom ASA or other non-steroidal anti-inflammatory drugs induce the syndromeof asthma, rhinitis, or uticaria. Sometimes severe andoccasionally fatal anaphylactic reactions have occurredin such individuals.Warnings:Peptic ulceration, perforation and gastrointestinal bleed-ing, sometimes severe and occasionally fatal, have beenreported during therapy with non-steroidal anti-inflam-matory drugs (NSAID's) including Anaprox and AnaproxDS. Anaprox and Anaprox DS should be given underclose medical supervision to patients prone to gastroin-testinal tract irritation particularly those with a history ofpeptic ulcer, diverticulosis or other inflammatory dis-eases of the gastrointestinal tract.

Patients taking any NSAID including this drug shouldbe instructed to contact a physician immediately if theyexperience symptoms or signs suggestive of peptic ulcer-ation or gastrointestinal bleeding. These reactions canoccur without warning at any time during the treatment.Elderly, frail and debilitated patients appear to be athigher risk from a variety of adverse reactions fromNSAIDs. For such patients, consideration should be

given to a starting dose lower than usual. The safetyof Anaprox and Anaprox DS in pregnancy and lactationhas not been established and its use is therefore notrecommended.

Precautions:Anaprox or Anaprox DS (naproxen sodium) should notbe used concomitantly with the related drug Naprosyng(naproxen) since they circulate in plasma as thenaproxen anion.

GI. system: If peptic ulceration is suspected or con-firmed, or if gastrointestinal bleeding or perforation occursAnaprox or Anaprox DS should be discontinued, andappropriate treatment instituted. Renaleffects: Patientswith impaired renal function, extracellular volume deple-tion, sodium restrictions, heart failure, liver dysfunction,those taking diuretics, and the elderly, are at greater riskof developing overt renal decompensation. Assessmentof renal function in these patients before and duringtherapy is recommended. Naproxen sodium and its metab-olites are eliminated primarily by the kidneys, and there-fore, a reduction in daily dosage should be anticipated toavoid the possibility of drug accumulation in patientswith significantly impaired renal function. Naproxensodium should not be used chronically in patients havingbaseline creatinine clearance less than 20 ml/minute.

Peripheral edema has been observed, consequently,patients with compromised cardiac function should bekept under observation when taking Anaprox or AnaproxDS. Each Anaprox tablet contains approximately 25mgof sodium and each Anaprox DS tablet contains approxi-mately 50mg of sodium. This should be considered inpatients whose overall intake of sodium must be mark-edly restricted. As with other drugs used in the elderly orthose with impaired liver function it is prudent to use thelowest effective dose. Severe hepatic reactions includ-ing jaundice and cases of fatal hepatitis have beenreported with NSAIDs. The prescriber should be alert tothe fact that the anti-inflammatory, analgesic and antipy-retic effects of Anaprox or Anaprox DS (naproxen sodium)may mask the usual signs of infection. Periodic liverfunction tests and ophthalmic studies are recommended

for patients on chronic therapy. Caution should be exer-cised by patients whose activities require alertness ifthey experience drowsiness, dizziness, vertigo or depres-sion during therapy with the drug. The naproxen anionmay displace other albumin-bound drugs from their bind-ing sites and may lead to drug interactions or interferewith certain laboratory tests. See product monograph forspecific examples. The safety and efficacy of this drug inchildren has not been established and its use in childrenis therefore not recommended.Adverse reactions:Adverse reactions which occur in >1% of patientsinclude:

G.I.: heartburn, constipation, abdominal pain, nausea,diarrhea, dyspepsia, stomatitis and diverticulitis.

CNS: headache, dizziness, drowsiness, light-headed-ness, vertigo, depression and fatigue.

Skin: pruritus, ecchymoses, skin eruptions, sweatingand purpura.

CVS: dyspnea, peripheral edema and palpitations.Special Senses: tinnitus and hearing disturbances.Others: thirst.For additional adverse reactions please refer to the

product monograph.Availability:Anaproxg is available in OVAL-SHAPED, BLUE film-coated tablets of 275mg in bottles of 100, 500 and1000 tablets.

Anaprox" DS is available in OVAL-SHAPED, BLUEfilm-coated tablets of 550mg in bottles of 100 tablets.Dosage:AnaproxO 275mg: Two tablets (550mg) followed byone tablet (275 mg) every 6 - 8 hours as required.Anaprox" DS: One tablet (550 mg) twice daily.Maximum daily dose: 1375mg.Product monograph available on request.

Is SYTEXSyntex Inc* Mississauga, Ont./Montreal, Que.*Reg. user of all ® trademarks. M

1456 Canadian Family Physician VOL 38: June 1992