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Female Migraines

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Title: Female Migraines


1
Female Migraines
  • Dr Muhammad El Hennawy
  • Ob/gyn specialist
  • Rass el barr central hospital and
  • dumyat specialised hospital
  • Dumyatt EGYPT
  • www.geocities.com/mmhennawy

2
Female with Migraines
  • Prevalence of migraines
  • Twenty-five percent of women
  • Ten percent of women have the onset of
    their migraines at menarche
  • 1.5 to 15 of women suffer from migraine
    only with the menses
  • 60 present migraine at other times in
    the menstrual cycle
  • Gender --70 percent of all migraine sufferers are
    women
  • Women are three times more likely to
    experience migraine headaches than men
  • Age --variable
  • Socioeconomic Groups are found among various
    socioeconomic groups .

3
In many women, migraine headaches are clearly
linked to estrogen levels
  • at the menarche the incidence rises because it is
    clearly linked to estrogen levels
  • before menses attacks may be precipitated by
    falling estrogen levels (premenstrual migraine)
  • menstruation-associated migraine The falling
    estradiol level rather than the absolute level
    provides the trigger for migraine (menstrual
    migraine)
  • ovulation or mid cycle migraine is infrequent
  • during pregnancy symptoms usually improve
    temporary when there are noncyclic high levels of
    estrogen at first trimester , Absence of migraine
    noted in second third trimesters of pregnancy.
  • during lactation Decreased estrogen production
    may trigger an exacerbation of migraine and make
    lactation difficult
  • Birt control pills make headache worse specially
    in week off , stop pills may give some relief
  • in the climacteric phase Decreased estrogen
    production may trigger an exacerbation of
    migraine
  • after menopause when estrogen levels are
    noncyclic and low, there may be an improvement in
    migraine

4
migraine
  • It is a type of a vascular headache
  • Of unknown aetiology
  • In which final step of pathology of pain is
    constriction (producing the neurological symptoms
    of the prodroma and the aura) followed by
    diltation of one or more of branches of carotid
    artery or vertebrobasilar arteries
  • Leading to stimulation of pain nerve endings
    surrounding artery by stretching -- producing
    the headache). Pain is prolonged by surrounding
    muscle contraction

5
Diagnostic criteria
  • Headache attacks lasting 4-72 hours (from several
    minutes to several days).
  • Headache has at least two of the following four
  • Unilateral location (on one side of the head only
    )
  • Pulsating quality
  • Moderate or severe intensity (inhibits or
    prohibits daily activities).
  • Aggravation by walking stairs or similar routine
    physical activity.
  • During headache at least one of the following
    accompaniments
  • Nausea and/or vomiting
  • photophobia and phonophobia
  • It could be triggering an attack by the types of
    food they choose to eat during this time include
    red wine, some types of cheese, caffeine and the
    flavour enhancer monosodium glutamate.
  • Other headache types not suggested or confirmed--
    No evidence of Organic Headache.
  • in premenstrual or menstrual migraine, It is
    not usually preceded by (aura) visual , sensory
    and speech disturbances as classic migraine ,
    also it is familial

6
NB
  • It is necessary to assume that headache is
    physical in origin until sufficient time and
    repeated examination has excluded an organic
    origin
  • The only sign of migraine can be seen is
    dilatation of external carotid arteryon one side
    recognised by visible pulsation in superficial
    temporal artery
  • Pain is temporary relieved by compression of
    common carotid artery and return op pain with
    increase of severity when compression is released

7
Common Triggers for Migraine
  • Hormonal
  • Menstruation, ovulation, oral contraceptive
    agents, hormonal replacement therapy
  • Dietary
  • nitrite-laden meat, monosodium glutamate,
    aspartame, chocolate, aged cheese, missing a meal
  • Beverages Caffeinated beverages, beers, wines
    (especially red wine )
  • Psychological
  • Stress, post-stress (weekends or vacation),
    anxiety, worry, depression
  • Environmental
  • Glare, flashing lights, visual stimulation,
    fluorescent lighting, odors , weather changes,
    high altitude
  • Sleep-related
  • Lack of sleep, excessive sleep
  • Drugs
  • Nitroglycerin, histamine, reserpine,
    hydralazine, ranitidine, estrogen
  • Miscellaneous
  • Head trauma, physical exertion, fatigue

8
Types of female migraines
  • 1 - without relation to menstruation
  • a - classic migraine (with
    aura)
  • b common migraine(without aura)
  • 2 - with relation to menstruation
  • ( Menstrually associated migraines (MAM))
  • (usually migraine without aura )
  • a - premenstrual migraine 2 to 7 days
    before the onset of menses ,it considered as a
    part of PMTS
  • b - menstrual migraine when 90 of all
    attacks occur between the two days before and
    the last day of their menstrual periods. occurs
    regularly, each month

9
the character of menstrually-associated migraine
  • tends to differ from other migraines
  • it lasts longer
  • generally more resistant to treatment
  • more likely to reoccur.
  • But this is not true?
  • they have a better chance to prevent or treat
    it

10
Classification of migraine by the International
Headache Society, 1988 (with code numbers)
  • 1.1 Migraine without aura1.2 Migraine with
    aura   1.2.1 Migraine with typical aura   1.2.2
    Migraine with prolonged aura   1.2.3 Familial
    hemiplegic migraine   1.2.4 Basilar
    migraine   1.2.5 Migraine aura without
    headache   1.2.6 Migraine with acute onset
    aura1.3 Ophthalmoplegic migraine1.4 Retinal
    migraine1.5 Childhood periodic syndromes that
    may be precursors to or associated with
    migraine   1.5.1 Benign paroxysmal
    vertigo   1.5.2 Alternating hemiplegia1.6
    Complications of migraine   1.6.1 Status
    migrainosus   1.6.2 Migrainous infarction1.7
    Migrainous disorder not fulfilling above criteria

11
The cause of migraines remains unresolved
  • Hormonal theory
  • Estrogen cyclic withdrawalis thought to
    be the trigger for the migrainous attack ,is
    accompanied by a decrease in central opioid tone,
    dopamine-receptor hypersensitivity, and an
    increase in cerebral vasoreactivity to serotonin
  • Estradiol vasodilates small-diameter cerebral
    vessels in healthy women.
  • Prostaglandin secretionreaches maximal
    concentrations at the time of menstruation in
    response to the withdrawal of estradiol and
    progesterone. Prostaglandins increase uterine
    contractions, causing the pain of dysmenorrhea.
    The prostaglandin F2-alpha (PGF2-alpha) is
    thought to stimulate the intense vasospasm and
    vasoconstriction that cause necrotic ischemia of
    the endometrium Prostaglandins inhibit
    norepinephrine release in the central nervous
    system and antagonize electrical and morphine
    analgesia PGF2-alpha may induce intracerebral
    vasoconstriction, and PGE1 may cause dilation of
    external carotid arteries. Prostaglandins
    sensitize pain receptors and increase neurogenic
    inflammation
  • Traditional theory the veins and arteries outside
    of the skull expand and the veins and arteries
    inside the skull contract, causing pressure and
    pain
  • Central theory an attack is initiated by low
    magnesium levels in the body that eventually
    create abnormal electrical activity and a
    disturbance in the hormone called serotonin in
    the brain.
  • Neurogenic theory
  • reaction between the nerves and arteries that
    control the face, eyes, nose, mouth, and jaws
    (the trigeminovascular system).
  • Unifying theory a disturbance in the electrical
    activity in the brain, which causes changes in
    the brain stem and the trigeminovascular system

12
  • decrease
    estrogen (cyclic)
  • decrease magnesium
    increase prostaglandin E
  • disturbance in electrical activity
  • Decrease Vitamin B2 decrease serotinin in
    brain

  • vasodiltation of cerebral artery
  • Decrease pain threshold in periarterial nerve
    ending
  • stimulation of pain nerve
    ending surrounding artery
  • pain of migraine


13
  • Serotinin receptors
  • the various families of serotonin receptors
  • (5-HT1), 5-HT2 and 5-HT3 receptor subtypes
  • 5-HT1receptors
  • 5-HT1A
  • 5-HT1B serotinin agonist---used in acute
    migraine
  • 5-HT1D serotinin agonist --- used in acute
    migraine

  • selective agonist Triptan
    -
    non selective agonistergot alkaloid
  • Selective 5-HT1F agonist -- under
    development
  • 5-HT2 receptors
  • 5-HT2 serotinin receptor antagonist
    ---propranolol ,methylsergide
  • 5-HT3 receptors
  • 5-HT3 serotinin receptor antagonist----
    metoclopramide

14
  • The 5-HT1B receptors are postsynaptic receptors
    on blood
  • vessels. Intracranial blood vessels have a rich
    supply of these
  • receptors. They are also, to a small degree, in
    the coronary
  • arteries, which accounts for the reason selective
    serotonin
  • receptor agonists are contraindicated in patients
    with occlusive
  • coronary artery disease.
  • The 5-HT1D receptors, on the other hand, are
    presynaptic
  • receptors on the trigeminal nerve endings.
    Stimulation causes a
  • reduction in the release of vasoactive
    polypeptides, such as
  • calcitonin gene-related peptide (CGRP) and
    substance P, and,
  • hence, a reduction in the degree of neurogenic
    inflammation.
  • The excitatory 5-HT2 receptors are also important
    in the
  • pathogenesis of migraine. Preventive medications,
    such as
  • methysergide and propranolol, are 5-HT2 receptor
    antagonists.
  • The 5-HT3 family of receptors is also relevant in
    migraine
  • pharmacotherapy. The nausea and vomiting
    associated with
  • migraine may be partly due to stimulation of
    5-HT3 receptors in
  • the nausea and vomiting center of the brain stem.
    5-HT3
  • antagonists such as metoclopramide can provide
    relief of

15
serotonin reuptake inhibitors (SSRIs
  • Antidepressants such as tricyclic compounds and
    selective serotonin reuptake inhibitors (SSRIs)
    may act synergistically with other agents used
    in migraine prophylaxis.
  • The combination of a tricyclic antidepressant,
    particularly amitriptyline, and a beta blocker is
    a very practical approach in patients with
    frequent headaches,
  • especially if migraine is associated with
    depression,
  • stress, anxiety and sleep problems.
  • An antidepressant and a beta blocker are also
    commonly used in patients with refractory
    headache disorders..

16
dopamine antagonists
  • Effective for the treatment of acute migraine
    include chlorpromazine
  • (Thorazine), 12.5 mg
  • prochlorperazine, 5 to 10 mg
  • metoclopramide, 5 mg with DHE
  • and droperidol (Inapsine), 2.5
  • These agents serve as alternatives to 5-HT1
    agonists in
  • patients who present to the emergency department
    for the
  • treatment of migraine. They are good choices
    for patients in whom the triptans are
    contraindicated. Intravenous diphenhydramine (50
    mg) may also be useful in the emergency
    department setting, as may intravenous valproate
    (300 to 500mg).

17
Characteristics of Migraine Headaches
  • Migraine without aura (common migraine)
  • At least five attacks per year
  • last 4 72 hours
  • At least two of the following symptoms
  • Pain on one side of the head only
  • Pulsing pain
  • Moderate-to-severe intensity that inhibits
    or prohibits ones ability to function
  • Aggravating pain caused by physical activity,
    such as climbing stairs
  • At least one of the following symptoms
  • Nausea and/or vomiting
  • Light sensitivity or sound sensitivity
  • Migraine with aura (classic migraine)
  • At least two attacks per year
  • At least three of the following symptoms
  • One or more aura symptoms that later subside.
    Aura symptoms include alterations in vision
    numbness or tingling in the face, arm, or hand on
    one side of the body muscular weakness or mild
    paralysis on one side of the body and/or
    difficulty speaking or loss of speech.
  • Gradual development of at least one aura symptom
    over more than four minutes or two or more
    symptoms that occur at the same time
  • Aura symptoms that last no more than 60 minutes
  • Headache that occurs simultaneously with aura
    symptoms or follows aura within 60 minutes

18
Migraine Phases
  • Prodrome it occurs within hours or up to days
    before a migraine attack. Many physical and
    psychological symptoms are associated with
    prodrome. These symptoms may vary between
    individuals, but they usually remain consistent
    for an individual.
  • Aura ( or - ) it develops 5 20 minutes before
    a migraine attack and lasts no longer than an
    hour. Aura symptoms usually effect the senses,
    especially sight, but they can also effect muscle
    strength.
  • Migraine headacheSymptoms that distinguish
    migraines from other headaches, include
  • Headache on one side of the head
    (unilateral), behind the eyes (retrorbital), or
    around the eyes (periorbital)
  • Pain intensity that is moderate to markedly
    severe and worsened by physical activity
  • Some migraines may develop on both of sides
    of the head and then shift to one side of the
    head. In other individuals, the pain may develop
    on one side of the head and then become more
    generalized.
  • Postdrome (headache termination) While migraines
    subside during the postdrome phase, individuals
    will experience the following symptoms Fatigue
    ,Irritability,Impaired concentration ,Scalp
    tenderness Mood changes

19
  • Treatment
  • a cure has not yet been found
  • After exclusion of visual disturbances ,
    sinusitis and dental diseases
  • acute abortive measures focuses on stopping the
    migraine as it progresses.
  • symptomatic measures focuses on treating the
    symptoms that result from migraines
  • prophylaxis
  • To minimize the onset and the effects of
    migraines
  • Non-Drug Prevention
  • avoiding these trigger factors
  • Modify life style
  • Prevention using medication
  • short-term rather than continuous treatment
  • Short ttt
  • Estrogen (establishment of a stable estrogen
    state )
  • NSAIDs
  • start 1 wk before expected headache during
    luteal phase)
  • Continuous ttt
  • also beta blockers or calcium channel
    blockers, taking continuously , the dose can be
    increased in the premenstrual or menstrual phase.
  • NB premenstrual migraine is considered as a
    part of PMTS ttt of PMTS to prevent it

20
Indications of prophylactic drugs
  • A - Consider in any patient desiring Migraine
    prophylaxis
  • B - Headache frequency
  • Two or more Headaches monthly
  • Absolutely indicated for 2 Headache days per
    week
  • C - Headache duration
  • Prolonged Headaches gt2 days with
    Disability
  • D - Headache response to Migraine Abortive
    Treatment
  • Refractory to current abortive agents
  • Intolerance to abortive agents
  • Overuse of abortive agents
  • Protocol
  • Effective prophylaxis reduces Headache
    frequency by 50
  • Trial of prophylactic agent for 2-3 months
  • Keep Headache diary
  • Start prophylaxis at low dose and gradually
    increase

21
Migraine prophylaxis
  • the treatments used for the prophylaxis of
    non-menstrual related migraine are used, with the
    additional of hormonal therapy
  • short-term prophylaxis (Intermittent Prophylaxis
    ) -- when the association between migraine and
    menses has been confirmed with prospective
    records kept with a diary for a minimum of three
    cycles ---start 1 wk before expected headache
    during luteal phase)
  • long-term prophylaxis (Daily Prophylaxis) ---
    when migraine occur at menses and also occur in
    the non-menstrual period -- taking drugs
    continuously , but the dose should be increased
    in the premenstrual or menstrual phase.

22
Migraine prophylaxis
  • To minimize the onset and the effects of
    migraines
  • Non-Drug Prevention
  • avoiding these trigger factors (Foods ,
    Medications , Hormonal Factors , Lifestyle
    Factors , Environmental Changes )could reduce the
    frequency of migraine attacks by half.
  • individuals should exercise, get plenty of
    sleep, form regular sleeping habits,
  • avoid missing meals, and discontinue smoking.
  • Individuals may also find that relaxation, and
    stress management help to prevent migraines.
  • Prevention using medication (prophylactic
    treatment)
  • is only recommended in individuals when
  • Migraines occur twice a month, producing
    disability that lasts three days or longer
  • Medication that treats symptoms or tries to
    stop an attack are not best for patients or are
    not working
  • Pattern of migraine attacks are predictable,
    such as premenstrual and menstrual migraines
  • Drugs--- short-term rather than continuous
    treatment
  • Estrogen (establishment of a stable estrogen
    state )
  • NSAIDs
  • start 1 wk before expected headache during
    luteal phase)
  • Depot progestogen
  • continuous oral contraceptive
  • Triptans have also been studied for use in
    short-term prophylaxis. In an open-label trial,
    sumatriptan proved to be effective
  • also Beta-blockers (Most commonly used.
    Approximately 60 80 effective in reducing
    attacks by 50.) Calcium Channel Blockers ,
    Serotonin Antagonists , Tricyclic Antidepressants
    , Anticonvulsants , Monoamine Oxidase Inhibitors
    (MAOIs) , Selective Serotonin-reuptake Inhibitors
    (SSRIs) , Alpha-adrenergic Blockers

23
non-pharmacological methods
  • to control either the frequency or severity of
    their migraines,
  • these include biofeedback,
  • relaxation therapy
  • hypnosis,
  • meditation,
  • osteopathy,
  • acupuncture,
  • cognitive behavioural
    training
  • and lifestyle changes
    such as identifying the possible
    aggravating factors e.g. stress, alcohol, coffee,
    cheese and chocolate.

24
the Migraine Diet
  • Women who suffer ,she must follow a migraine diet
  • She may find that they feel better by eating five
    or six small meals at regular three-hour
    intervals.
  • limiting caffeine
  • avoiding red wine, some types of cheese,
    caffeine and the flavour enhancer monosodium
    glutamate.
  • vitamin (B2 ,B6 ,E )and mineral
    (magnesium)supplements both before and during
    menstruation ?

25
A healthy lifestyle
  • a helpful preventive measure.
  • Physical activities and exercise may be valuable
    in decreasing stress in addition to contributing
    to fitness and well-being.
  • Early identification and monitoring of the signs
    of physical and psychological stress, such as
    tight neck muscles or an anxious feeling, will
    lead to early intervention and possible
    prevention of migraine
  • get plenty of sleep
  • discontinue smoking.

26
Estrogen
  • Because menstrual migraine can be triggered by
    falling estrogen levels that are either
    endogenously or exogenously induced (by week-off
    oral contraceptive or hormonal replacement
    therapy),
  • prevention can be attempted by providing a more
    stable estrogen state Percutaneous estrogen in
    gel form applied for 7 days, beginning at least 2
    days before the expected migraine, has been shown
    to decrease the frequency and severity of
    menstrual migraine The estradiol cutaneous patch
    may be less effective than gel but is used in
    many headache clinics, either alone or in
    combination with a small dose (20 mg) of
    methyltestosterone
  • the birth control pill If used continuously (no
    break), it may also occasionally be effective

27
NSAIDs
  • Prostaglandins may play a role in the initial
    vasoconstriction phase of migraine and in the
    pain and sensitization to the pain of headache
    and of dysmenorrhea, if present. Nonsteroidal
    anti-inflammatory drugs (NSAIDs) are valuable
    both for prophylaxis of menstrual migraine and
    for analgesia the agents inhibit prostaglandin
    synthesis and block neurogenic inflammation.
    Naproxen has been used effectively for
    prophylaxis (Typically, the drugs are started 7
    days before the expected menses. Effective doses
    vary, but naproxen, 550 mg twice a day
    ketoprofen (Orudis), 75 mg three times a day (or
    extended-release form Oruvail, 200 mg once a
    day) ibuprofen, 300 mg two or three times a day
    or mefenamic acid (Ponstel), 250 mg two or three
    times a day, may be helpful for prophylaxis If
    one class of NSAID is not effective, another
    should be tried.

28
Depot progestogen
  • as it also inhibits ovulation and can improve
    migraine, provided amenorrhoea is achieved

29
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30
Abortive therapy
  • the treatment of acute menstrual migraine is
    currently similar to any other type of acute
    migraine
  • focuses on stopping the migraine as it
    progresses.
  • The earlier the treatment is given,the better the
    result
  • All drugs should be considered on basis of
    therapeutic trial because responses of each
    individual women vary
  • Rest in dark , quiet room
  • Analgesic
  • antiemetic drugs-- Dopamine antagonist
    antiemetics, such as metoclopramide and
    prochlorperazine, are effective, even if nausea
    is not prominent.
  • Vasoconstrictor drugs (if prolonged , severe
    attack)
  • caffeine (cerebral vessels vasoconstrictor)
  • 5-HT1 agonists
  • a class of new drugs called Triptans
  • a class of old drugs eg ergot alkaloid
    agents
  • all work by cerebral vasoconstriction
  • Acute migraine headaches are self-limited and
    respond well to placebos, so many therapies are
    effective.

31
5-HT1D receptor agonist (serotonin analogue )
  • An old class of drugs -- The ergot derivatives--
    ergotamine tartrate and Dihydroergotamine (DHE)
  • A new class of drugs --a selective 5-HT1D
    receptor agonist --- Triptans-- Stimulation of
    the 5-HT1D (serotonin )receptors can inhibit
    release of vasodilatory peptides such as CGRP and
    substance P and can block neurogenic inflammation
    ,thus induce vasoconstriction of extracerebral
    blood vessels and also reduce neurogenic
    inflammation .
  • can abort migraine pain in about 70 of patients

32
Triptans
  • Triptans can be divided into 2 groups
  • Group I fast onset, relatively high headache
    response and pain free rates at 2 hours
    sumatriptan (Imitrex, Imigran), zolmitriptan
    (Zomig, Zomigon, Ascotop), rizatriptan (Maxalt),
    almotriptan (Axert, Almogran), and eletriptan
    (Relpax).
  • Group II slower onset and lower efficacy rates.
    naratriptan (Amerge, Naramig) and frovatriptan.
  • Precautions NOT to be given to pregnant or
    lactating women.
  • Contraindicated in  Ischemic heart disease,
    Prinzmetal angina Uncontrolled hypertension
    Decreased arterial flow, Raynaud's disease
    Impaired hepatic function Ingestion of any
    ergotamine-containing medication. within 24 hours
    (DHE, methysergide, ergotamine tartrate etc). MAO
    inhibitor use within 2 weeks Hypersensitivity to
    sumatriptan Basilar or hemiplegic migraine Age
    over 50, particularly males Cerebrovascular
    disease

33
Ergot derivatives
  • The ergot derivatives can be effective for both
    prophylaxis and treatment of menstrual migraine
  • DHE is a serotonin receptor agonist with
    strong binding at the 5-HT1 receptor subtypes.
    Stimulation of these receptors constricts
    cerebral blood vessels, thus relieving headache.
  • Methylergonovine maleate (Methergine), 0.4 mg
    orally followed by 0.2 mg three times a day for 2
    days, may provide prophylaxis
  • Dihydroergotamine (DHE) mesylate DHE is a
    serotonin receptor agonist with strong binding at
    the 5-HT1 receptor subtypes. Stimulation of these
    receptors constricts cerebral blood vessels, thus
    relieving headache. (D.H.E.) is used for acute
    moderate to severe pain it is given parenterally
    (1 mg subcutaneously or intramuscularly or 0.5 mg
    intravenously), up to a maximum of 3 mg over 24
    hours Metoclopramide (Maxolon, Octamide PFS,
    Reglan), 10 mg intravenously, can be given before
    DHE to provide relief from any associated nausea
    and vomiting.

34
Contraindications to the use of DHE
  • include pregnancy, hypertension, and vascular
    disease (coronary, cerebral, and peripheral).
  • should not be used within 24 hours of the
    serotonin analogue sumatriptan succinate
    (Imitrex), to be discussed next.

35
Symptomatic therapy
  • focuses on treating the symptoms that result from
    migraines.
  • analgesic
  • For mild to moderate pain Acetaminophen with
    or without caffeine
  • NSAIDs
  • For moderate to severe painNSAIDsSumatriptan
    succinate (Imitrex
  • DHE, dihydroergotamine mesylate
  • Agents for severe episodesOpioid agonists
    and antagonists
  • narcotics
  • neuroleptics (eg, chlorpromazine
    hydrochloride
  • Antiemeticsused to relieve nausea and vomiting
  • Sedatives
  • Steroids
  • Ergot-containing substances
  • Serotonin agonists

36
severity
37
  • Mild migraine
  • Simple analgesics
  • NSAIDs
  • Isometheptene (Midrin, etc.)
  • Metoclopramide (Reglan) may be added to reduce
    nausea and enhance drug absorption
  • Moderately severe migraine
  • NSAIDs
  • Isometheptene
  • Ergotamine, oral or intranasal
  • Sumpatriptan (Imitrex), oral or intranasal
  • Zolmitriptan (Zomig), oral
  • Naratriptan (Amerge), oral
  • Rizatriptan (Maxalt), oral
  • DHE, intranasal
  • With oral agents, metoclopramide may be added to
    reduce nausea and enhance drug absorption
  • Severe migraine
  • Ergotamine plus an antiemetic, both administered
    by suppository
  • Sumatriptan, subcutaneous injection, intranasal
    or oral
  • Zolmitriptan, oral

38
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39
resistant menstrual migraine
  • These include the antiestrogen tamoxifen citrate
    (Nolvadex), 5 to 15 mg a day for seven to
    fourteen days at 10 mg. per day
  • the dopaminergic agent bromocryptine mesylate
    (Parlodel), 2.5 to 5 mg a day
  • the androgen derivative danazol (Danocrine), 200
    to 600 mg a day
  • The serotonin reuptake inhibitor fluoxetine
    hydrochloride (Prozac) has been used selectively
    in the luteal phase of the cycle in women with
    PMS.
  • For the most severe cases of menstrual migraine
    and PMS, gonadotropin-releasing hormone (Gn-RH)
    agonists with estrogen and progestin replacement
    may be considered
  • Oophorectomy -- by inducing a hypoestrogenic
    state, could be instrumental in controlling the
    worst premenstrual and menstrual migraine attacks
    in some women.

40
  • There is much overlap between symptoms of
    migraine and tension headache
  • And many patient suffer from both

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42
  • Until researchers discover a cure, individuals
    can take precautions and communicate their
    symptoms to their healthcare providers to find
    relief from migraine attacks.

43
  • thank you
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