stroke
Label
Migraine Headache

DefinitionEtiologyEpidemiologyPathophysiologyClinical Manifestation
WorkupRN ManagementMedsDiagnosis and GoalsInterventionAlertsRefs
Definition:

Unilateral, bilateral or generalized often throbbing headache, which may or may not be preceded by a brief aura. The latter are usually visual but may also be sensory, motor or cognitive.

Summary of types of migraine:

1-Image-Migraine-Definition-Classification

  • Familial hemiplegic migraine (FHM):
    • Migraine with aura including motor weakness and at least one first- or second-degree relative has migraine aura including motor weakness. Autosomal dominant associated with mutation has 3 subtypes; FMH1, FMH2 and FMH3
  • Sporadic hemiplegic migraine (HM):
    • Migraine with aura including motor weakness but no first- or second-degree relative has aura including motor weakness
  • Basilar-type migraine (BTM):
    • Usually exhibit brain stem symptoms including lightheaded, vertigo, dysarthria, diplopia, ataxia and generalized weakness and decreased level of consciousness. No motor weakness
  • Retinal migraine (RM):
    • Scotoma or blindness (monocular) lasting less than an hour, with or after headaches

Ref: The International Headaches Classification (ICHD-2) (http://ihs-classification.org).

 

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Etiology:

The underlying mechanism(s) remain poorly understood, but appears to involve:

  • Neuronal hypersensitivity to physical and environmental stressors, foods and hormonal changes leading to cortical spreading depression (mitigates auras), vascular hypersensitivity and inflammation which causes throbbing focal or generalized pain
  • Genetic factors: Autosomal dominant familial hemiplegic migraine provides some evidence of a genetic link to migraine. Other forms of migraine do tend to run in families; 70% of patients have a first-degree relative with a history of migraine

 

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Epidemiology:
  • Prevalence
    • 17-19% women per year in general population
    • 6% men per year in general population
  • Male:Female ratio is 1:3
  • May begin at any age, although incidence of new-onset diminishes with age
  • Prevalence peaks at approximately 30-40 years for both sexes

 

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Pathophysiology:

Migraine Pathogenesis:

Aura:

  • Cortical spreading depression (CSD) is a self propagating wave of neuronal and glial depolarization, which spreads across the cerebral cortex and is thought to underlie migraine auras
  • CSD may spread sequentially across the cortex e.g. occipital→ parietal → frontal with ensuing sequential symptoms, i.e. visual → sensory → motor

Pain (potential mechanisms):

  1. Mediated by the trigeminovascular system; extracranial vasodilation results from stimulation of the trigeminal nerve. Neurotransmitters, such as CGRP and substance P are synthesized by ganglion cells and travel to small unmyelinated fibres around the vessels as well as the trigeminal nucleus. Stimulation of the trigeminal ganglion causes vasodilatation and enhanced plasma protein permeability and sterile inflammation. Information is then relayed to the thalamus and cortex for registering of pain. Involvement of other centers may explain the associated autonomic symptoms and affective aspects of this pain
  2. Cortical spreading depression (CSD) activates trigeminal nerve afferents, and alters blood-brain barrier permeability. The activation of trigeminal afferents by CSD in turn causes inflammatory changes in the pain-sensitive meninges that generates migraine headache through central and peripheral reflex mechanisms

 

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Clinical Manifestations:

May present with or without aura.

Migraine without aura

  • Headache for 4-72 hours
  • Location: Often unilateral, but may also be bilateral, generalized or retro-orbital
  • Quality: Tends to be, but not always, pulsatile/throbbing ±pressure or squeezing component
  • During headache patient may experience any of the following:
    • Nausea
    • Vomiting
    • Photophobia
    • Phonophobia
  • Intensity: Moderate to severe
  • Typical triggers/exacerbating factors:
    • Weather/altitude
    • Sleep disturbance (excess, deprivation or change)
    • Menses
    • Exertion
    • Certain smells, perfumes, smoke
    • Bright lights, loud noises, computer screens
    • Foods like chocolate, cheese (aged), alcohol (wine, beer), artificial sweeteners, MSG, processed meats (salami, pepperoni etc contain nitrates), nuts, citrus, some types if yeast, excess caffeine

Migraine with aura

Aura: Often develop gradually over 5-20 mins; may last for less than 60 mins. These are reversible focal neurologic symptom and includes:

  • Visual:
    • Zigzag lines, scintillating scotoma, visual field defects
  • Sensory:
    • Paraesthesia of face, arm or leg. Typically unilateral and migratory, usually spreading gradually over several minutes (Jacksonian march)
  • Motor:
    • Mild transient unilateral limb weakness or slurring of speech
  • Cognitive:
    • Transient confusion, memory disturbance, dysphasia, dysnomia

Note: There are other visual auras, but the ones listed above are the main.

Headache with the features of migraine follows aura usually within 60 minutes; may begin during aura and sometime >60 minutes post aura. Less commonly headaches lack migrainous features or they may be completely absent.

Other presentations:

  • Status migrainosus: Episode lasting >72 hours
  • Chronic migraine: Occurs ≥15 days per month for more than 3 months
  • Serious complications of migraine: Both seizures and stroke have been associated with migraine

 

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Workup and Diagnosis:

History and Physical:

Enquire about pain:

  • Quality, location and frequency of headache
  • Presence of aura, triggers and exacerbating factors
  • Gradual onset; but can occur suddenly
  • Recurrence
  • Family history of migraine

 

Labs:

  • CBC, electrolytes, BUN, creatinine, LFTs, ESR

 

CT/MRI-Brain:

  • Consider if atypical presentation or persistent neurological symptoms

 

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RN/Medical Management:

Medical management depends:

  • Severity of headaches
  • Associated symptoms and medical conditions
  • Frequency, duration and impact on quality of life
  • Response to medications
  • Pregnancy

A) Treatment for acute attacks - Abortive therapy

1) Mild migraine:

  • Acetaminophen, NSAIDs and counseling with regards to potential triggers usually first course of action, along with timely institution of triptans, in early mild phase of migraine

NOTE: Use of triptans (sumatriptan) is now being considered routinely, after spectrum study demonstrated in HIS migraine sufferers, triptans (sumatriptan) was very efficacious in mild head pain, and is useful in early treatment of disabling headaches, rather than later phase of the course.

Ref: Lipton RB, Stewart WF, et al. 2000 Wolff Award. Sumatriptan for the range of headaches in migraine Sufferers. Results of the spectrum study. Headache 2000; 40: 783-91.

 

2) Moderate to severe migraine course, migraine specific therapy is recommended if no contraindications

  • Triptans and ergot derivatives should be considered for initial therapy or may be used if over the counter analgesics are ineffective
  • Antiemetics may be used at any stage
  • Medications most effective if started early in the course of the attack

 

3) Very severe migraine/ refractory cases in emergency department

  • Dopamine antagonists
  • IV Dexamethasone reduces the risk of recurrence within 72 hrs
  • IV Dihydroergotamine (DHE) - Raskin protocol (caveat: DHE is contraindicated if the patient has received triptans in the previous 24 hrs)
  • Opioids analgesics

 

B) Prophylactic treatment:

Indications include

  • Frequent >2 or more attacks per month
  • Prolonged disabling episodes
  • Contraindications or intolerance or refractory to abortive therapy
  • Frequent episodes with no well defined trigger to adopt avoidance strategies

Therapy:

Inspite the use of multiple drugs for migraine prophylaxis, many questions regarding the mechanisms of action remain unanswered and requires further research.

It has been suggested, that there are 2 main targets for migraine prevention:

  • Neuronal hyperexcitability
  • Nociceptive dysmodulation

The recommended agents for migraine prevention are as follows:

  • Antidepressants (amitriptyline)
  • Anticonvulsants (divalproex and topiramate)
  • Beta-adrenergic blockers (propranolol, timolol, and metaprolol)

Other agents may have some beneficial effect, requiring further research:

  • Methysergide
  • Fluranizine
  • Monoamine oxidase inhibitors

Factors influencing the choice of migraine prophylactic agents include consideration of comorbidities, potential adverse effects, patient's expectations or desires, compliance and cost.

Ref: Ramadan NM, Current Trends in Migraine Prophylaxis. Headache 2007;47:S52-S57)

 

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Medications:

ABORTIVE THERAPY

ANALGESICS

Including, but not limited to the following:

  • NSAIDs
    • Ibuprofen
    • Naproxen
    • Aspirin
  • Acetaminophen

Mechanism:

NSAIDs:

  • Prostaglandin are believed to be a common factor in the production of pain, fever, and inflammation
  • NSAIDs inhibit COX-1 and 2 enzymes → results in decrease formation of prostaglandin precursors

Acetaminophen

  • Analgesic action: Inhibit the synthesis of prostaglandins in the central nervous system

Dose:

Ibuprofen:

  • 200-400 mg PO every 4-6hrs; Max. 3.2 gm/24 hrs

Naproxen:

  • Initial 500-750 mg PO, an addition of 250-500 mg may be given if needed; Max. 1250 mg/24 hours

Aspirin:

  • 325-650 mg PO every 4-6 hrs; Max. 4 g/day
  • 300-600 mg rectal suppositories every 4-6 hrs; Max. 4 g/day

Acetaminophen:

  • 325-650 mg PO every 4-6 hrs or 1000 mg PO TID or QID; Max. 4 g/day
  • Note: Suppositories are used in same doses as of oral formulation.

Warning:

Increased risk of medication overuse/induced headache, if used on more than 8-10 days per month.

 

TRIPTAN AGENTS (5-HT1 receptor agonist)

  • Sumatriptan
  • Zolmitriptan
  • Naratriptan
  • Almotriptan
  • Rizatriptan
  • Frovatriptan
  • Eletriptan

Mechanism:

  • Selective serotonin agonist (5-HT1B/1D receptors)
  • Exact mechanism unknown
  • Suggested mechanism:
    • Inhibit pro-inflammatory neuropeptide release

Dose:

Sumatriptan

  • Oral: 25-50 or 100 mg; may repeat after 2 hrs not to exceed 200 mg/day
  • Intranasal: 5-20 mg; Max single dose 20 mg; may repeat after 2 hrs, Max.40 mg/24 hr
  • SC: Single dose of 6 mg; may repeat after 1 hr; Max. 12 mg/24 hrs (2 doses/24 hr)

Zolmitriptan

  • Oral: 2.5 mg; may repeat after 2 hrs; Max. 10 mg/24 hr
  • Intranasal: 2.5-5 mg dose; may repeat after 2 hrs; Max. 10 mg/24 hr
  • May decrease dose of zolmitriptan with concurrent propranalol

Naratriptan

  • Oral: 1-2.5 mg; may repeat after 4 hrs; Max. 5 mg/24 hrs
  • Mild-moderate renal impairment: Start 1 mg; Max. 2.5 mg/24 hr
  • Hepatic impairment (Child-Pugh Grade A or B): 1 mg; Max 2.5 mg/24 hours

Almotriptan

  • Oral: 6.25-12.5 mg; may repeat after 2 hrs; Max. 25 mg/24 hr
  • Renal (Clcr ≤30 mL/min) or hepatic impairment: Start 6.25 mg as a single dose; Max. 12.5 mg/24 hrs
  • Avoid use if renal impairment and concomitant CYP 3A inhibitor

Rizatriptan

  • Oral: 5-10 mg; may repeat dose after 2 hrs; Max. 30 mg/24 hr
  • Patient on Propranolol: 5 mg PO as a single dose; Max. 15 mg/24 hr

Frovatriptan

  • In Canada: 2.5 mg PO; may repeat dose after 4 hrs; Max. 5 mg/24 hr
  • In US: 2.5 mg PO; may repeat after 2 hrs; Max. 7.5 mg/24 hr

Eletriptan

  • Initial 20-40 mg PO; if headache recurs after improving, dose may be repeated after 2 hrs; (Max. single dose is 40 mg, maximum daily dose is 80 mg)

Warning:

Increased risk of medication overuse/induced headache, if used on more than 8-10 days per month.

 

ERGOT ALKALOIDS

  • Ergotamine
  • Dihydroergotamine

Mechanism:

  • Stimulates alpha-adrenergic and serotonergic (5-HT) receptors

Dose:

Ergotamine:

  • 2 mg SL; may repeat dose every 30-60 mins, Max. 6 mg/24 hrs, 10 mg/week

Dihydroergotamine (IM / IV / SC):

  • 1 mg at first sign of headache; may repeat dose hourly; Max. 6 mg/week
  • Intranasal 1 (0.5 mg) dose into each nostril; may repeat dose after 15 mins, if needed; Max. 6 sprays (3 mg)/24 hour and Max: 8 sprays (4 mg)/week

Intractable migraine (status migrainosus: >72 hrs)

  • (IV-Raskin protocol): Initial test dose of 0.5 mg over 2 minutes given after 30 minutes of premedication with IV metoclopramide
  • Subsequent dosing is titrated between the range of 0.2-1 mg every 8 hr, for 2-3 days, administered with or without metoclopramide (based on response and tolerance).
  • Maximum dose is typically 6 mg/week, but some reports suggest as much as 20 mg/week may be used

Warning:

Increased risk of medication overuse/induced headache, if used on more than 8-10 days per month.

 

ANTIEMETICS

  • Metoclopramide
  • Prochlorperazine
  • Chlorpromazine
  • Haloperidol

Mechanism:

Metoclopramide

  • Blocks dopamine and serotonin receptors in chemoreceptor trigger zone of the CNS
  • Enhances the response to acetylcholine of tissue in upper GI tract

Prochlorperazine/chlorpromazine/haloperidol

  • Blocks postsynaptic mesolimbic dopaminergic receptors in the brain
  • Exhibits a strong alpha-adrenergic and anticholinergic blocking effect
  • Depresses the release of hypothalamic and hypophyseal hormones

Dose:

Metoclopramide:

  • 10-20 mg PO, IM or IV

Prochlorperazine

  • Oral: 5-10 mg 3-4 times/day prn; Max. 40 mg/day
  • IM: 5-10 mg every 3-4hrs as needed; Max. 40 mg/day
  • IV: 2.5-10 mg; Max. 10 mg/dose or 40 mg/day
  • Rectal: 25 mg BID or as needed

Chlorpromazine:

  • Oral: 10-25 mg; may repeat dose after 4-6 hrs as needed
  • IM: 25 mg (1 mL). If no hypotension occurs, give 25 to 50 mg every 3-4 hrs, until vomiting stops; then switch to oral dosage
  • Rectal: One 100 mg suppository every 6-8 hrs. In some patients, half this dose will do

Haloperidol:

  • 0.5-2 mg IM or IV

 

ANALGESIC, OPOID

  • Tramadol
  • Codeine
  • Acetaminophen + codeine
  • Oxycodone
  • Acetaminophen + oxycodone

Mechanism:

  • Not fully understood
  • Binds to mu opioid receptors in the CNS
  • Tramadol: Inhibits serotonin and norepinephrine reuptake in the CNS

Dose:

Tramadol

  • Immediate release: 25-100 mg PO every 4-6 hrs Max. 400 mg/day
  • Extended release: 100 mg PO daily; titrate every 5 days, as needed; Max. 300 mg/day

Codeine

  • Oral: 30 mg every 4-6 hrs; usual range 15-120 every 4-6 hrs.
    • Prior exposure may require higher initial dose
  • Controlled release: 50-300 every 12 hrs; should only be considered in chronic or continuous pain, higher doses are used in opioid tolerant patients
  • IM/SC: 30 mg every 4-6 hrs; prior exposure require higher doses. Usual dose 15-120 mg
  • Note: Dose adjustment required in renal/hepatic impairment.

Oxycodone

  • Oral: 5-15 mg every 4-6 hrs; range 5-20 mg/dose
  • Controlled release: 10 mg every 12hrs; with concurrent CNS depressants decrease dose by 1/3 to 1/2

Warning:

Increased risk of medication overuse/induced headache, if used on more than 8-10 days per month.

 

CORTICOSTEROID

  • Dexamethasone

Mechanism:

Glucocorticoids decrease inflammation through multiple mechanisms, including

  • Stabilization of leukocyte lysosomal membranes
  • Inhibition of macrophage accumulation
  • Reduction of capillary permeability

Dose:

Dexamethasone

  • 8-24 mg IV for abortive therapy in ER phase.

 

PROPHYLACTIC THERAPY

BETA-ADRENERGIC RECEPTOR BLOCKERS

  • Cardioselective
    • Atenolol
    • Metoprolol
  • Non-Cardioselective
    • Nadolol
    • Propranolol
    • Timolol

Mechanism:

  • Decrease heart rate and cardiac output
  • Decrease renin release
  • Actual mechanism of migraine prophylaxis unknown

Dose:

Cardioselective:

Atenolol

  • Initial 12.5-25 mg PO daily; may gradually increase to 100 mg/day in divided doses

Metoprolol

  • Initial 25-50 mg PO BID; may increase 100-200mg/day
  • Max. ~300mg/day

Non-Cardioselective:

Nadolol:

  • Initial 40 mg PO daily; usual 40-120 mg daily; may increase to ~240-320 mg/day

Propranolol:

  • Conventional tablets: Start 40-80 mg PO daily in 2-3 divided doses; may increase by 20-40 mg/dose every 3-4 weeks; Max. 160-240 mg/day in divided doses
  • Extended-release capsules: Start 80 mg PO daily, usual 160-240 mg/day

Timolol:

  • Start 20 mg PO BID; may increase gradually every 7 days; usual dose 20-40 mg PO BID, Max dose is 60 mg/day

 

TRICYCLIC ANTI-DEPRESSANTS

  • Amitriptyline
  • Nortriptyline
  • Desipramine

Mechanisms:

  • Inhibits the presynaptic reuptake of neurotransmitters → increases synaptic serotonin and/or norepinephrine → potentiates its effect
  • Also has significant anticholinergic properties

Dose:

Amitriptyline/Nortriptyline/Desipramine

  • Start 10-25 mg PO at bedtime; may increase gradually by 10-20 mg increments weekly as needed; usual maintenance dose 50-75 mg/day at bedtime; Max dose: ~150 mg at bedtime

 

ANTICONVULSANTS

  • Valproate/divalproex
  • Topiramate

Mechanisms:

  • Exact mechanism is not known, but suggestions include:
    • Increased availability of GABA → resulting in seizure activity suppression, decreased manic episodes and decreased frequency of migraine headaches

Dose:

Valproate/divalproex:

  • 250 mg/day PO BID; titrate dose based on patient response; Max. 1500 mg/day

Topiramate:

  • 25 mg PO daily for 1 week; then increase weekly by 25 mg/day until at 50 mg BID
    • Doses >100 mg/day have shown no additional benefit.
  • Renal:
    • Administer 50% dose and titrate more slowly if ClCr <70 mL/minute/1.73 m2

SELECTIVE CALCIUM CHANNEL ANTAGONIST

  • Flunarizine

Mechanism:

  • Mediated through blockade of calcium channels
  • Also have antihistamine properties (histamine H1 receptors inhibition)

Dose:

Flunarizine

  • 5-10 mg PO daily, to minimize the side effects allow 2 medication free days in a week

Maintenance Therapy:

  • Same effective daily dose for 5 days and then 2 days of medicine free interval every week

Note: Discontinued if no improvement after 2 months.

 

SEROTONIN AND HISTAMINE ANTAGONIST

  • Pizotifen

Mechanism:

  • Is not fully known, in migraine
  • It is a competitive serotonin antagonist with antihistamine
  • Weak anticholinergic properties

Dose:

Pizotifen

  • Start 0.5 mg PO daily at night, increased gradually to maintenance dose of 1.5 mg/day in 3 divided doses; Max. 6 mg/day

Note: May take ~4 weeks to reach its maximum effect.

 

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Diagnosis and Goals:

Diagnosis:

  • Acute pain related to headache
  • Ineffective coping related to chronic and/or disabling pain
  • Sleep pattern disturbance related to pain
  • Anxiety related to lack of knowledge of etiology and treatment of headache and uncertainty of recurrence of headache
  • Hopelessness related to chronic pain, alteration of lifestyle and ineffective treatment modalities

Goals:

  • Relieve pain and associated symptoms such as nausea/vomiting
  • Prevent recurrent attacks by explaining the patient to continue with preventative treatment. The client will also understand triggering events and will use positive coping strategies to deal with chronic pain

 

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Nursing Intervention:

Controlling pain:

  • Use of pharmacological agents should not be delayed in an acute attack
  • Advise rest once headache is relieved to recover from fatigue of the pain
  • Non pharmacological intervention in early phase should include following:
    • Advise to rest/lie down and attempt to sleep
    • Avoid various stimuli - Lights (e.g. sunlight, computer screens), noises (e.g. TV, radio)
    • Provide quite, dark environment and decrease movement (elevate head of bed to 300)
  • Symptomatic treatment as prescribed to comfort patient for nausea/vomiting
  • Explain the reason for, and proper use of medication, as well as adverse effects
  • If attacks are preceded by auras, ask patient to take preventive measures (reduced exposure to sensory stimuli if possible) and/or use abortive therapy (NSAIDs/triptans) at that time

Promoting positive coping:

  • Determine and explain to the patient potential triggers that should be avoided
  • Develop a strategy to overcome the acute phase prior to the severe headache
  • After taking a detail account of events help patient to recognize specific events which may lead to headache
  • Patient should have clear knowledge of early onset headache symptoms
  • Inform patient of proper nutrition, including avoiding hunger, rest and relaxation, and avoid stress and overexertion to better cope with headaches. Daily exercise and socializing can be encouraged as this can help decrease the recurrence of headache
  • Determine and develop strategies to solve issues arising in social or work situation which may lead to stress, exertion and headaches. The nurse can suggest alternative ways of handling pain of headache through practices such as relaxation, meditation, yoga and self-hypnosis. Massage and moist hot packs can assist a client with a tension-type headache
  • Review, verbalize and strengthen coping mechanisms

Promoting home and community based care:

  • Teach proper administration of medication, techniques
    • Self-injection of sumatriptan given subcutaneously with auto injector
    • Inhalation of ergotamine (ergostat) through metered-dose inhaler
  • Advise NSAIDs to be taken with food to avoid GI upset, gastritis, and possible ulcer formation
  • Report immediately if numbness, coldness, paraesthesia, and pain of extremities occur with ergot derivatives
  • Chest pain, wheezing, flushing with triptan agents should be reported to the physician
  • Beta-adrenergic blockers and calcium channel blockers may cause hypotension. Advise patient of this and if indicated to rise slowly from the sitting or lying position to avoid orthostatic hypotension
  • Teach patient never to exceed prescribed dosage, and not to discontinue beta-blockers abruptly
  • Patients who have alcohol-induced headaches should avoid or minimize alcohol consumption
  • - Dietary counseling may be beneficial for patients whose headaches are triggered by food. Food rich in tyramine (e.g. aged cheese, red wine, liver, chocolate, excessive caffeine, monosodium glutamate), may trigger migraines
  • Teach patient how to perform relaxation techniques to reduce stress

Outcomes:

  • Have fewer episodes, with less severity
  • Is able to use coping mechanisms with benefit

 

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Nursing Alerts:
  • Vasoconstrictors and 5HT-agonists used to abort vascular headaches are contraindicated in patients with uncontrolled hypertension, coronary artery disease, and peripheral vascular disease
  • Use of simple analgesics <15 days/month and ergots or triptans or opioids or combination analgesics <10 days/month is recommended

 

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References:

Core Resources:

  • Brust JCM (2007) Current Diagnosis and Treatment (Neurology) (2nd ed.) New York: McGraw Hill
  • Compendium of Pharmaceuticals and Specialties (CPS). Canadian Pharmacist association. Toronto: Webcom Inc. 2012
  • Day RA, Paul P, Williams B, et al (eds). Brunner & Suddarth's Textbook of Canadian Medical-Surgical Nursing. 2nd ed. Philadelphia: Lippincott Williams and Wilkins; 2010
  • Dirksen, S., Lewis, S., & Collier, I., Heitkemper, M., O'Brien, P., & Bucher, L. (2010). Medical- Surgical Nursing in Canada: Assessment and management of clinical problems (2nd ed.). Toronto: Mosby Elsevier
  • Foster C, Mistry NF, Peddi PF, Sharma S, eds. The Washington Manual of Medical Therapeutics. 33rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2010
  • Gray J, ed. Therapeutic Choices. Canadian Pharmacists Association. 6th ed. Toronto: Webcom Inc. 2011
  • Katzung BG, Masters SB, Trevor AJ, eds. Basic and Clinical Pharmacology. 11th ed. New York: McGraw-Hill; 2009
  • Longo D, Fauci A, Kasper D, et al (eds). Harrison's Principles of Internal Medicine. 18th ed. New York: McGraw-Hill; 2011
  • McPhee SJ, Papadakis MA, eds. Current Medical Diagnosis & Treatment. 49th ed. New York: McGraw-Hill; 2010
  • Pagana KD, Pagana TJ eds. Mosby's Diagnostic and Laboratory Test Reference. 9th ed. St. Louis: Elsevier-Mosby; 2009
  • Rowland LP et al. (2010) Merritt's Neurology (9th ed.) Philadelphia: Lippincoot Williams and Wilkins
  • Skidmore-Roth L. ed. Mosby's drug guide for nurses. 9th ed. St. Louis: Elsevier-Mosby; 2011
  • Skidmore-Roth L, ed. Mosby's nursing drug reference. 24th ed. St. Louis: Elsevier-Mosby; 2011

 

Online Pharmacological Resources:

  • e-therapeutics
  • Lexicomp
  • RxList
  • Epocrates Online

 

Journals/Clinical Trials:

  • Andersson, PG, Hinge, HH, Johansen, O, et al. Double-blind study of naproxen vs placebo in the treatment of acute migraine attacks. Cephalalgia 1989; 9:29
  • Cady R, Lipton RB, Hall C, et al. Treatment of mild headache in disabled migraine suffers Results of the Spectrum Study. Headache 2000; 40: 792-797
  • Colman I et al. Parenteral dexamethasone for acute severe migraine headache: Meta-analysis of randomised controlled trials for preventing recurrence. BMJ 2008 Jun 14; 336:1359
  • Diener HC, Barbanti P, Dahlöf C, et al. BI 44370 TA, an oral CGRP antagonist for the treatment of acute migraine attacks: results from a phase II study. J.Cephalalgia. 2011 Apr; 31(5):573-84. Epub 2010 Dec 20
  • Dahlof, C, Bjorkman, R. Diclofenac-K (50 and 100 mg) and placebo in the acute treatment of migraine. Cephalalgia 1993; 13:117
  • Evans RW. Treating migraine in the emergency department. BMJ 2008 Jun 14; 336:1320
  • Havanka-Kanniainen, H. Treatment of acute migraine attack: ibuprofen and placebo compared. Headache 1989; 29:507
  • Hewitt DJ, Aurora SK, Dodick DW, Randomized controlled trial of the CGRP receptor antagonist MK-3207 in the acute treatment of migraine. Cephalalgia. 2011 Apr; 31(6):712-22 Phase II b
  • Kellstein, DE, Lipton, RB, Geetha, R, et al. Evaluation of a novel solubilized formulation of ibuprofen in the treatment of migraine headache: a randomized, double-blind, placebo-controlled, dose-ranging study. Cephalalgia 2000; 20:233
  • Lipton RB, Stewart WF, Cady R. et al. 2000 Wolff Award. Sumatriptan for the range of headaches in migraine Sufferers. Results of the spectrum study. Headache 2000; 40: 783-91
  • Massiou, H, Serrurier, D, Lasserre, O, Bousser, MG. Effectiveness of oral diclofenac in the acute treatment of common migraine attacks: a double-blind study versus placebo. Cephalalgia 1991; 11:59
  • Nestvold, K, Kloster, R, Partinen, M, Sulkava,R. Treatment of acute migraine attack: naproxen and placebo compared. Cephalalgia 1985; 5:115
  • Ramadan NM, Current Trends in Migraine Prophylaxis. Headache 2007;47:S52-S57
  • Rose FC, et al. Pathogenesis of migraine. Journal of the Royal Society of Medicine.1991 84: 519-521
  • Shaunak S, Wilkins A, Pilling J B, Dick D J Pericardial, retroperitoneal, and pleural fibrosis induced by pergolide J Neurol Neurosurg Psychiatry 1999;66:79-81
  • Singhal AB, Cerebral Vasoconstriction Syndromes. Top Stroke Rehabil 2004; 11:1-6
  • The Diclofenac-K/Sumatriptan Migraine Study Group.Bussone G, Grazzi L, D'Amico D et al. Acute treatment of migraine attacks: efficacy and safety of a nonsteroidal anti-inflammatory drug, diclofenac-potassium, in comparison to oral sumatriptan and placebo Cephalalgia 1999; 4: 232-240
  • Welch, KM. Drug therapy of migraine. N Engl J Med 1993; 329:1476. Kloster, R, Nestvold, K, Vilming, ST. A double-blind study of ibuprofen versus placebo in the treatment of acute migraine attacks. Cephalalgia 1992; 12:169

 

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Reviewers

EXPERT REVIEWER:
Lucian Sitwell, MD, FRCPC, Lecturer, University of Ottawa, The Ottawa Hospital-Riverside Campus, ON Canada
.......................................... NURSING REVIEWER:
Suzette Mahabeer, RN, MScN, Nursing Faculty - McMaster University, Hamilton, ON Canada

 
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