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Migraine




          UTMB Department of
           Otolaryngology
          Grand Rounds March 2005
        Jeffrey Buyten, MD
        David C. Teller, MD
        Francis B. Quinn, MD
Prevalence
   Familial
   Young, healthy women; F>M: 3:1
    – 17 – 18.2% of adult females
    – 6 – 6.5% adult males
   2-3rd decade onset… can occur sooner
   Peaks ages 22-55.
   ½ migraine sufferers not diagnosed.
   94% pt’s seen in primary care settings for
    HA have migraines
   Common misdiagnoses
    for migraine:
    – Sinus HA
    – Stress HA


   Referral to ENT for sinus
    disease and facial pain.
   Migraineurs more likely to have
    motion sickness.
   Half of Meniere’s patients claim to
    have migrainous symptoms.
   BPPV
   $13 billion/year in lost
    productivity
   1/3 participants in
    American Migraine Study
    II missed work in prior 3
    months
Migraine Definition
   IHS criteria: Migraine/aura (3 out of 4)      IHS Diagnostic criteria: migraine w/o
     – One or more fully reversible aura           aura
        symptoms indicates focal cerebral           – HA lasting for 4-72 hrs
        cortical or brainstem dysfunction.          – HA w/2+ of following:
     – At least one aura symptom                          Unilateral
        develops gradually over more than                 Pulsating
        4 minutes.
                                                          Mod/severe intensity.
     – No aura symptom lasts more than
        one hour.                                         Aggravated by routine
     – HA follows aura w/free interval of                  physical activity.
        less than one hour and may begin            – During HA at least 1 of following
        before or w/aura.                                 N/V
                                                          Photophobia
                                                          Phonophobia

                 History, PE, Neuro exam show no other organic
                                    disease.

                              At least five attacks occur
Migraine Subtypes
            Basilar type migraine
             – Dysarthria, vertigo,
               diplopia, tinnitus,
               decreased hearing, ataxia,
               bilateral paresthesias,
               altered consciousness.
             – Simultaneous bilateral
               visual symptoms.
             – No muscular weakness.
            Retinal or ocular migraine
             – Repeated monocular
               scotomata or blindness < 1
               hr
             – Associated with or followed
               by a HA
Migraine Subtypes
   Menstrual migraine
   Hemiplegic migraine
    – Unilateral motor and
      sensory symptoms
      that may persist after
      the headache.
    – Complete recover
   Familial hemiplegic
    migraine
Migrainous vertigo
         Vertigo – sole or prevailing symptom.
         Benign paroxysmal vertigo of childhood.
         Prevalence 7-9% of pts in referral dizzy
          and migraine clinics.
         Not recognized by the IHS
         Diagnosis (proposed criteria)
           – Recurrent episodic vestibular symptoms of
             at least moderate severity.
           – One of the following:
                Current of previous history of IHS migraine.
                Migrainous symptoms during two or more
                 attacks of vertigo.
                Migraine-precipitants before vertigo in more
                 than 50% of attacks.
           – Response to migraine medications in more
             than 50% of attacks
Migraine mechanism
   Neurovascular theory.
     – Abnormal brainstem
       responses.
     – Trigemino-vascular system.
          Calcitonin gene related
           peptide
          Neurokinin A
          Substance P

 Extracranial arterial vasodilation.
    – Temporal
    – Pulsing pain.
 Extracranial neurogenic
  inflammation.
 Decreased inhibition of central
  pain transmission.
    – Endogenous opioids.
   Important role in
    migraine
    pathogenesis.
   Mechanism of action
    in migraines not well
    established.
   Main target of
    pharmacotherapy.
Aura Mechanism
   Cortical spreading depression
     – Self propagating wave of neuronal and glial depolarization across the
        cortex
           Activates trigeminal afferents
               – Causes inflammation of pain sensitive meninges that generates
                 HA through central/peripheral reflexes.
           Alters blood-brain barrier.
     – Associated with a low flow state in the dural sinuses.
   Auras
    – Vision – most common
      neurologic symptom
    – Paresthesia of lips, lower
      face and fingers… 2nd most
      common
    – Typical aura
        Flickering uncolored
         zigzag line in center and
         then periphery
        Motor – hand and arm on
         one side
        Auras (visual, sensory,
         aphasia) – 1 hr
   Prodrome
    – Lasts hours to days…
Clinical manifestations
               Clinical manifestations
                 – Lateralized in severe attacks –
                   60-70%
                 – Bifrontal/global HA – 30%
                 – Gradual onset with crescendo
                   pattern.
                 – Limits activity due to its
                   intensity.
                 – Worsened by rapid head
                   motion, sneezing, straining,
                   constant motion or exertion.
                 – Focal facial pain, cutaneous
                   allodynia, GI dysfunction,
                   facial flushing, lacrimation,
                   rhinorrhea, nasal congestion
                   and vertigo…
Precipitating factors
stress
head and neck infection
head trauma/surgery
aged cheese
dairy
red wine
nuts
shellfish
caffeine withdrawal
vasodilators
perfumes/strong odors
irregular diet/sleep
light
Treatment
 Abortive
  –   Stepped
  –   Stratified
  –   Staged
 Preventive
Abortive Therapy
   Reduces headache recurrence.
   Alleviation of symptoms.
   Analgesics
    – Tylenol, opioids…
   Antiphlogistics
    – NSAIDs
   Vasoconstrictors
    – Caffeine
    – Sympathomimetics
    – Serotoninergics
         Selective - triptans
         Nonselective – ergots
   Metoclopramide
Abortive care strategies
   Stepped
     – Start with lower level drugs, then switch to more specific drugs if
       symptoms persist or worsen.
             Analgesics – Tylenol, NSAIDs…
             Vasoconstrictors – sympathomimetics…
             Opioids (try to avoid) - Butorphanol
             Triptans – sumatriptan (oral, SQ, nasal), naratriptan, rizatripatan,
              zomatriptan.
     – Limited by patient compliance.
   Stratified
     – Adjusts treatment according to symptom intensity.
             Mild – analgesics, NSAIDs
             Moderate – analgesic plus caffeine/sympathomimetic
             Severe – opioids, triptans, ergots…
     – Severe sx treatment limited due to concomitant GI sx’s.
   Staged
     –   Bases treatment on intensity and time of attacks.
     –   HA diary reviewed with patient.
     –   Medication plan and backup plans.
Preventive therapy
   Consider if pt has more than 3-4
    episodes/month.
   Reduces frequency by 40 – 60%.
   Breakthrough headaches easier to abort.
   Beta blockers
   Amitriptyline
   Calcium channel blockers
   Lifestyle modification.
   Biofeedback.
Botox
51% migraineurs treated
  had complete prophylaxis
  for 4.1 months.
38% had prophylaxis for 2.7
  months.
Randomized trial showed
  significant improvement
  in headache frequency
  with multiple treatments.
Conclusions
 Migraine is common but unrecognized.
 Keep migraine and its variants in the
 differential diagnosis.
References
1.    Landy, S. Migraine throughout the Life Cycle: Treatment through the Ages. Neurology. 2004; 62
      (5) Supplement 2: S2-S8.
2.    Bailey, BJ. Head and Neck Surgery – Otolaryngology 3rd Edition. 2001. Pgs. 221-235.
3.    Bajwa, ZH, Sabahat, A. Pathophysiology, Clinical Manifestations, and Diagnosis of Migraine in
      Adults. Up To Date online. 2005.
4.    Lipton, RB, Stewart, WF, Liberman, JN. Self-awareness of migraine: Interpreting the labels that
      headache sufferers apply to their headaches. Neurology. 2002; 58(9) Supplement 6: S21-S26.
5.    Cady, RK, Schreiber, CP. Sinus headache or migraine?: Considerations in making a differential
      diagnosis. Neurology. 2002; 58 (9) Supplement 6: S10-S14.
6.    Perry, BF, Login, IS, Kountakis, SE. Nonrhinologic headache in a tertiary rhinology practice.
      Otolaryngology – Head and Neck Surg 2004; 130: 449-452.
7.    Daudia, AT, Jones, NS. Facial migraine in a rhinological setting. Clinical Otolaryngology and
      Allied Sciences. 2002; 27(6): 521-525.
8.    Spierings, EL. Migraine mechanism and management. Otolarynogol Clin N Am 36 (2003): 1063
      – 1078.
9.    Avnon, y, Nitzan, M, Sprecher, E, Rogowski, Z, and Yarnitsky, D. Different patterns of
      parasympathetic activation in uni- and bilateral migraineurs. Brain. 2003; 126: 1660-1670.
10.   Stroud, RH, Bailey, BJ, Quinn, FB. Headache and Facial Pain. Dr. Quinn’s Online Textbook of
      Otolaryngology Grand Rounds Archive. 2001.
      http://www.utmb.edu/otoref/Grnds/HA-facial-pain-2001-0131/HA-facial-pain-2001.doc
11.   Ondo, WG, Vuong KD, Derman, HS. Botulinum toxin A for chronic daily headache: a
      randomized, placebo-controlled, parallel design study. Cephalalgia 2004 (24): 60-65.

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Migraine

  • 1. Migraine  UTMB Department of Otolaryngology  Grand Rounds March 2005  Jeffrey Buyten, MD  David C. Teller, MD  Francis B. Quinn, MD
  • 2. Prevalence  Familial  Young, healthy women; F>M: 3:1 – 17 – 18.2% of adult females – 6 – 6.5% adult males  2-3rd decade onset… can occur sooner  Peaks ages 22-55.  ½ migraine sufferers not diagnosed.  94% pt’s seen in primary care settings for HA have migraines
  • 3. Common misdiagnoses for migraine: – Sinus HA – Stress HA  Referral to ENT for sinus disease and facial pain.
  • 4. Migraineurs more likely to have motion sickness.  Half of Meniere’s patients claim to have migrainous symptoms.  BPPV
  • 5. $13 billion/year in lost productivity  1/3 participants in American Migraine Study II missed work in prior 3 months
  • 6. Migraine Definition  IHS criteria: Migraine/aura (3 out of 4)  IHS Diagnostic criteria: migraine w/o – One or more fully reversible aura aura symptoms indicates focal cerebral – HA lasting for 4-72 hrs cortical or brainstem dysfunction. – HA w/2+ of following: – At least one aura symptom  Unilateral develops gradually over more than  Pulsating 4 minutes.  Mod/severe intensity. – No aura symptom lasts more than one hour.  Aggravated by routine – HA follows aura w/free interval of physical activity. less than one hour and may begin – During HA at least 1 of following before or w/aura.  N/V  Photophobia  Phonophobia History, PE, Neuro exam show no other organic disease. At least five attacks occur
  • 7. Migraine Subtypes  Basilar type migraine – Dysarthria, vertigo, diplopia, tinnitus, decreased hearing, ataxia, bilateral paresthesias, altered consciousness. – Simultaneous bilateral visual symptoms. – No muscular weakness.  Retinal or ocular migraine – Repeated monocular scotomata or blindness < 1 hr – Associated with or followed by a HA
  • 8. Migraine Subtypes  Menstrual migraine  Hemiplegic migraine – Unilateral motor and sensory symptoms that may persist after the headache. – Complete recover  Familial hemiplegic migraine
  • 9. Migrainous vertigo  Vertigo – sole or prevailing symptom.  Benign paroxysmal vertigo of childhood.  Prevalence 7-9% of pts in referral dizzy and migraine clinics.  Not recognized by the IHS  Diagnosis (proposed criteria) – Recurrent episodic vestibular symptoms of at least moderate severity. – One of the following:  Current of previous history of IHS migraine.  Migrainous symptoms during two or more attacks of vertigo.  Migraine-precipitants before vertigo in more than 50% of attacks. – Response to migraine medications in more than 50% of attacks
  • 10. Migraine mechanism  Neurovascular theory. – Abnormal brainstem responses. – Trigemino-vascular system.  Calcitonin gene related peptide  Neurokinin A  Substance P  Extracranial arterial vasodilation. – Temporal – Pulsing pain.  Extracranial neurogenic inflammation.  Decreased inhibition of central pain transmission. – Endogenous opioids.
  • 11. Important role in migraine pathogenesis.  Mechanism of action in migraines not well established.  Main target of pharmacotherapy.
  • 12. Aura Mechanism  Cortical spreading depression – Self propagating wave of neuronal and glial depolarization across the cortex  Activates trigeminal afferents – Causes inflammation of pain sensitive meninges that generates HA through central/peripheral reflexes.  Alters blood-brain barrier. – Associated with a low flow state in the dural sinuses.
  • 13. Auras – Vision – most common neurologic symptom – Paresthesia of lips, lower face and fingers… 2nd most common – Typical aura  Flickering uncolored zigzag line in center and then periphery  Motor – hand and arm on one side  Auras (visual, sensory, aphasia) – 1 hr  Prodrome – Lasts hours to days…
  • 14. Clinical manifestations  Clinical manifestations – Lateralized in severe attacks – 60-70% – Bifrontal/global HA – 30% – Gradual onset with crescendo pattern. – Limits activity due to its intensity. – Worsened by rapid head motion, sneezing, straining, constant motion or exertion. – Focal facial pain, cutaneous allodynia, GI dysfunction, facial flushing, lacrimation, rhinorrhea, nasal congestion and vertigo…
  • 15. Precipitating factors stress head and neck infection head trauma/surgery aged cheese dairy red wine nuts shellfish caffeine withdrawal vasodilators perfumes/strong odors irregular diet/sleep light
  • 16. Treatment  Abortive – Stepped – Stratified – Staged  Preventive
  • 17. Abortive Therapy  Reduces headache recurrence.  Alleviation of symptoms.  Analgesics – Tylenol, opioids…  Antiphlogistics – NSAIDs  Vasoconstrictors – Caffeine – Sympathomimetics – Serotoninergics  Selective - triptans  Nonselective – ergots  Metoclopramide
  • 18. Abortive care strategies  Stepped – Start with lower level drugs, then switch to more specific drugs if symptoms persist or worsen.  Analgesics – Tylenol, NSAIDs…  Vasoconstrictors – sympathomimetics…  Opioids (try to avoid) - Butorphanol  Triptans – sumatriptan (oral, SQ, nasal), naratriptan, rizatripatan, zomatriptan. – Limited by patient compliance.  Stratified – Adjusts treatment according to symptom intensity.  Mild – analgesics, NSAIDs  Moderate – analgesic plus caffeine/sympathomimetic  Severe – opioids, triptans, ergots… – Severe sx treatment limited due to concomitant GI sx’s.  Staged – Bases treatment on intensity and time of attacks. – HA diary reviewed with patient. – Medication plan and backup plans.
  • 19. Preventive therapy  Consider if pt has more than 3-4 episodes/month.  Reduces frequency by 40 – 60%.  Breakthrough headaches easier to abort.  Beta blockers  Amitriptyline  Calcium channel blockers  Lifestyle modification.  Biofeedback.
  • 20. Botox 51% migraineurs treated had complete prophylaxis for 4.1 months. 38% had prophylaxis for 2.7 months. Randomized trial showed significant improvement in headache frequency with multiple treatments.
  • 21. Conclusions  Migraine is common but unrecognized.  Keep migraine and its variants in the differential diagnosis.
  • 22.
  • 23. References 1. Landy, S. Migraine throughout the Life Cycle: Treatment through the Ages. Neurology. 2004; 62 (5) Supplement 2: S2-S8. 2. Bailey, BJ. Head and Neck Surgery – Otolaryngology 3rd Edition. 2001. Pgs. 221-235. 3. Bajwa, ZH, Sabahat, A. Pathophysiology, Clinical Manifestations, and Diagnosis of Migraine in Adults. Up To Date online. 2005. 4. Lipton, RB, Stewart, WF, Liberman, JN. Self-awareness of migraine: Interpreting the labels that headache sufferers apply to their headaches. Neurology. 2002; 58(9) Supplement 6: S21-S26. 5. Cady, RK, Schreiber, CP. Sinus headache or migraine?: Considerations in making a differential diagnosis. Neurology. 2002; 58 (9) Supplement 6: S10-S14. 6. Perry, BF, Login, IS, Kountakis, SE. Nonrhinologic headache in a tertiary rhinology practice. Otolaryngology – Head and Neck Surg 2004; 130: 449-452. 7. Daudia, AT, Jones, NS. Facial migraine in a rhinological setting. Clinical Otolaryngology and Allied Sciences. 2002; 27(6): 521-525. 8. Spierings, EL. Migraine mechanism and management. Otolarynogol Clin N Am 36 (2003): 1063 – 1078. 9. Avnon, y, Nitzan, M, Sprecher, E, Rogowski, Z, and Yarnitsky, D. Different patterns of parasympathetic activation in uni- and bilateral migraineurs. Brain. 2003; 126: 1660-1670. 10. Stroud, RH, Bailey, BJ, Quinn, FB. Headache and Facial Pain. Dr. Quinn’s Online Textbook of Otolaryngology Grand Rounds Archive. 2001. http://www.utmb.edu/otoref/Grnds/HA-facial-pain-2001-0131/HA-facial-pain-2001.doc 11. Ondo, WG, Vuong KD, Derman, HS. Botulinum toxin A for chronic daily headache: a randomized, placebo-controlled, parallel design study. Cephalalgia 2004 (24): 60-65.

Editor's Notes

  1. Neurology: Migraine throughout the life cycle: Treatment through the ages Bailey’s
  2. utd online pathogen Clinical otolaryngology and allied sciences
  3. Neurology: Migraine throughout the life cycle: Treatment through the ages
  4. Utd online
  5. Utd online
  6. Utd online