Female Migraines

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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

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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 .

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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

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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

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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

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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

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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

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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

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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

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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

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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

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• 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

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• 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

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• 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

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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..

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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).

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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

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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

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• 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

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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

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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.

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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

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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.

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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 ?

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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.

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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

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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.

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Depot progestogen

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

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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.

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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

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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

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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.

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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.

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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

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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

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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.

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

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• 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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• thank you