Female Migraines by Biscuit350

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									              Female Migraines

Dr Muhammad El Hennawy
Ob/gyn specialist
 Rass el barr central hospital and
   dumyat specialised hospital
 Dumyatt – EGYPT
 www.geocities.com/mmhennawy
           Female with Migraines
 Prevalence of migraines
  Twenty-five percent of women
     Ten percent of women have the onset of their migraines at
    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 .
  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
 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
 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
                     Diagnostic criteria
   Headache attacks lasting 4-72 hours (from several minutes to several
   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
 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
        Common Triggers for Migraine
 Hormonal
   Menstruation, ovulation, oral contraceptive agents, hormonal replacement
 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
            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
 the character of menstrually-associated
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
 Classification of migraine by the International
 Headache Society, 1988 (with code numbers)
 1.1 Migraine without aura
  1.2 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 aura
  1.3 Ophthalmoplegic migraine
  1.4 Retinal migraine
  1.5 Childhood periodic syndromes that may be precursors
  to or associated with migraine
    1.5.1 Benign paroxysmal vertigo
    1.5.2 Alternating hemiplegia
  1.6 Complications of migraine
    1.6.1 Status migrainosus
    1.6.2 Migrainous infarction
  1.7 Migrainous disorder not fulfilling above criteria
    The cause of migraines remains unresolved
 Hormonal theory
   Estrogen cyclic withdrawal
  is 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 secretion
  reaches 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
                              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
                            Serotinin receptors
 the various families of serotonin receptors
 (5-HT1), 5-HT2 and 5-HT3 receptor subtypes
 5-HT1receptors
  5-HT1B serotinin agonist---used in acute migraine
  5-HT1D serotinin agonist --- used in acute migraine
                                                  –selective agonist –Triptan
                                        - non selective agonist—ergot 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
 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
igraine-associated nausea and vomiting.
   serotonin reuptake inhibitors (SSRIs
 Antidepressants such as tricyclic compounds and
   selective serotonin reuptake inhibitors (SSRIs) may act
   synergistically with other agents used in migraine
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..
                 dopamine antagonists
 Effective for the treatment of acute migraine include
 (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
   Characteristics of Migraine Headaches
 Migraine without aura                  Migraine with aura (classic
  (common migraine)                       migraine)
 At least five attacks per year         At least two attacks per year
 last 4 — 72 hours                      At least three of the following
 At least two of the following          One or more aura symptoms that
  symptoms:                               later subside. Aura symptoms
  Pain on one side of the head only       include: alterations in vision;
  Pulsing pain                            numbness or tingling in the face,
                                          arm, or hand on one side of the
  Moderate-to-severe intensity that       body; muscular weakness or mild
  inhibits or prohibits one’s ability     paralysis on one side of the body;
  to function                             and/or difficulty speaking or loss of
  Aggravating pain caused by              speech.
  physical activity, such as             Gradual development of at least
  climbing stairs                         one aura symptom over more than
                                          four minutes or two or more
 At least one of the following           symptoms that occur at the same
  symptoms:                               time
  Nausea and/or vomiting                 Aura symptoms that last no more
  Light sensitivity or sound              than 60 minutes
  sensitivity                            Headache that occurs
                                          simultaneously with aura
                                          symptoms or follows aura within 60
                       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
               prophylaxis                                 Treatment
 To minimize the onset and the effects of
   migraines                                        a cure has not yet been
 Non-Drug Prevention
avoiding these trigger factors                                found
Modify life style
                                                  After exclusion of visual disturbances ,
Prevention using medication
short-term rather than continuous treatment              sinusitis and dental diseases
Short ttt
 Estrogen (establishment of a stable
                                                   acute abortive measures
   estrogen state )
                                                    focuses on stopping the
  start 1 wk before expected headache during        migraine as it
    luteal phase)
Continuous ttt                                      progresses.
  also beta blockers or calcium channel
   blockers, taking continuously , the dose can    symptomatic measures
   be increased in the premenstrual or
   menstrual phase.                                 focuses on treating the
 NB: premenstrual migraine is
  considered as a part of PMTS –ttt of              symptoms that result
  PMTS to prevent it
                                                    from migraines
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 >2 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
            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.
                                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 )
    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
    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
  taking continuously , the dose can be increased in the premenstrual or menstrual phase.
 Treating underlying causes—as high blood pressure
 Stress management – bec arteries can be affected by emotional state
     non-pharmacological methods
 to control either the frequency or severity of their
 these include – biofeedback,
                  relaxation therapy
                  cognitive behavioural training
                  and lifestyle changes such as
  identifying the possible aggravating factors e.g.
  stress, alcohol, coffee, cheese and chocolate.
                 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 ?
              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.
 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
 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.
         Depot progestogen

as it also inhibits ovulation and can
 improve migraine, provided amenorrhoea
 is achieved
                      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
 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.
        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
 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
 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
                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.
   Contraindications to the use of DHE

include pregnancy, hypertension, and
 vascular disease (coronary, cerebral, and
should not be used within 24 hours of the
 serotonin analogue sumatriptan succinate
 (Imitrex), to be discussed next.
                  Symptomatic therapy
 focuses on treating the symptoms that result from migraines.
 analgesic
  For mild to moderate pain
  Acetaminophen with or without caffeine
  For moderate to severe pain
  Sumatriptan succinate (Imitrex
   DHE, dihydroergotamine mesylate;
  Agents for severe episodes
  Opioid agonists and antagonists
  neuroleptics (eg, chlorpromazine hydrochloride

   Antiemetics–used to relieve nausea and vomiting
   Sedatives
   Steroids
   Ergot-containing substances
   Serotonin agonists
     severity            last                     TTT

  mild Migraine        <2 hours          analgesics (Aspirin,
   Headache                          Acetaminophen , NSAIDS ) ,
Moderate Migraine      <4 hours           refractory to above
   Headache                           give Antiemetic , analgesics ,
                                            Triptan agents .
 Severe Migraine      4-6 hours            refractory to above
   Headache                              give Other Antiemetic ,
                                            Serotonin Agonist
                                     (Dihydroergotamine , Triptans)
Severe Refractory    6 to 72 hours        refractory to above
Migraine Headache                            Emergency ttt
status migrainosus   over 72 hours
   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
   Severe migraine
   Ergotamine plus an antiemetic, both administered by suppository
   Sumatriptan, subcutaneous injection, intranasal or oral
   Zolmitriptan, oral
   Naratriptan, oral
   Rizatriptan, oral
   DHE, intramuscular or intranasal
   Extremely severe migraine
   Ketorolac (Toradol), 60 mg intramuscularly
   DHE, intravenous, plus metoclopramide
   Dopamine antagonist
   Opioids
         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
 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.
                       Tension          migraine
  Family history                        positive
       site         Uni or bilateral   unilateral
    Character        Dull aching       Throbbing
 Nausea, vomiting       rarley         Frequently
Awaken from sleep                       Positive
Response to ergot                      Favourable

There is much overlap between symptoms of
migraine and tension headache
And many patient suffer from both
Until researchers discover a cure,
 individuals can take precautions and
 communicate their symptoms to their
 healthcare providers to find relief from
 migraine attacks.

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