Practice pearls diagnosis and prophylaxis of migraine

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  • Clinicaly possible : Episodic + 1Clinicaly probable: Episodic +2Clinically definite: Episodic + 3 or more
  • Progression may be aconsequence of the underlying mechanisms thatgenerate the migraine attacks itself (eg, CSD), a hypothesis supportedby the increase in lesions with attack frequency.
  • progression refers to increases in attack frequencyover time leading to CM, which characterizes clinicalprogression. A less discussed form of migraineprogression may be defined in terms of physiologicalprogression, where migraine leads to changes in thecentral nervous system which manifest themselvesthrough alterations in nociceptive thresholds (allodynia)and alterations in pain pathways (eg, centralsensitization). Finally, an even less discussed form ofprogression takes the form of definitive lesionsClinical - Evolution from Episodic to Chronic MigraineProgression from Peripheral to Central Sensitization Cutaneous Allodynia (pain induced by an innocuous stimulus)
  • white matter lesionsincreased with attack frequency, possibly demonstratingprogression of the disease. This study showed adose–response effect, in that the number of lesionsincreased with migraine attacks frequency, even after
  • Fifty-six SD rats were divided into seven groups randomlywith each group consisting of eight rats.
  • Practice pearls diagnosis and prophylaxis of migraine

    1. 1. Practice Pearls :Diagnosis & Prophylaxis of Migraine Prof. A.V. SRINIVASAN, MD, DM, Ph.D,DSc(HON) F.A.A.N, F.I.A.N. Emeritus Professor The Tamilnadu Dr. M.G.R. Medical University Former Head Institute of Neurology, Madras Medical College Adjunct Prof. IIT Madras
    2. 2. IHS Guidelines Diagnosis of MigrainePresence of two or more Presence of one or more Head related symptoms Non headache symptoms1. Moderate to severe Pain 1. Aura2. Pain on one side of head 2. Nausea during headache3. Throbbing Pulsating 3. Photophobia, Phonophob headache ia during headache4. Headache exacerbated by routine activities
    3. 3. How to approach the patient with a headache ?
    4. 4. Patients presents with complaint of a headache Diagnosis Algorithm Critical first steps : • Detailed history • Focused physical examination • Focused neurological examination • BP, Ocular/Fundus Examination Worrisome Headache: Red Flags – “SNOOP”” no Meets criteria for Consider secondary headache disorder Specialty primary headache no consultation indicated disorder? Migraine Cluster Headache yes Tension-type Headache Other headaches - sinus
    5. 5. SNOOP• Systemic Symptoms such as fever or weight loss or Secondary Risk factors as HIV or systemic cancer• Neurologic Symptoms or abnormal signs such as confusion, impaired alertness, papilloedema, asymmetry, motor weakness, nuchal rigidity, visual disturbance other than aura, dysphasia• Onset Sudden, abrupt, split-seconds to minutes, rapid onset of headache• Older New headache onset in an older patient or a progressively worsening headache in a middle-aged patient (>50 years of age)• Progression Previous headache history-A major change in attack frequency, severity, or clinical features; a first headache pattern or different headache unlike any experienced before
    6. 6. Simplifying history taking for migraine diagnosis Sensitivity to light &/or sound Unilateral or bilateral Stomach uneasiness Pulsating or throbbing headache Episodic headache Connected with Triggers
    7. 7. Migraine: Triggers Migraines occur in response to stimuli in up to 85% of patients Common triggers related to : • Environment (weather changes, smoke, bright lights, certain smells) • Emotions (stress, anxiety, crying) • Change in sleep pattern • Diet (cheese, red wine, chocolate, nitrates) • Skipping meals • Estrogen (menstrual cycle)
    8. 8. Detailed History•Characteristics of the headache•Assess functional impairment•Past medical history•Family history of migraines•Current medications and previous medications for headache (Rx and over-the-counter)•Social history•Review of systems – to rule out systemic illness
    9. 9. IHS Classification System: Primary Headache Diagnosis of migraine currently based on International Headache Society (IHS) classification Primary headache is headache not caused by another disorder Migraine and tension-type account for 75%-90% of primary headache
    10. 10. Migraine Episodic, throbbing, usually unilateral headache May be preceded by visual, sensory or speech disturbances and also accompanied by nausea, vomiting Tends to be disruptive, a significant loss in quality of life and inability to perform their daily activities Migraine is a heterogeneous disorder - attacks vary in their frequency, duration, severity and number of associated symptoms Duration : 4 – 72 hrs (average 24 hrs.)
    11. 11. Tension headaches • Band-like, bilateral • Tightness/pressure/dull ache • Radiates to neck and shoulders • Mild to moderate • Not aggravated by movement • 30 min to several days
    12. 12. Tension Headache vs Migraine
    13. 13. Cluster headache• Rare condition that can be acute or chronic in nature• Characterized by 1-3 short-lived i.e. 15min – 3hrs (avg. 45 min) attacks of peri-orbital pain• Occurs in clusters for 2-3 months, followed by pain-free interval of one year• Attack often associated with red tearing eyes, nasal stuffiness and ptosis.
    14. 14. Comparison of Most Common Primary HeadachesCHARACTERISTIC MIGRAINE TENSION CLUSTERAge of onset 25 to 55 years 30 to 50 years 20 to 40 years Unilateral (but may be Unilateral, orbital,Location Bilateral bilateral) supraorbital, temporalDuration of episode 4 to 72 hrs 30 min to 7 days 15 to 180 minSeverity Moderate to severe Mild to moderate Extremely severeType Pulsating, throbbing Pressing, tightening but not Boring, searing pulsatingPattern 1 to 2 attacks per month <180 attacks per year (or 1 to 8 attacks per day <15 attacks per month) separated by pain- free periodsAssociated Nausea, vomiting, Either photophobia or Conjunctival injectionsymptoms photophobia, phonophobia, but not both, Lacrimation phonophobia (2 of no nausea or vomiting Forehead/facial swelling these) Nasal congestion Rhinorrhea Ptosis Miosis Eyelid edema
    15. 15. MIGRAINE MAY OFTEN BE MISDIAGNOSED As SINUS HEADACHE – SIMILAR DISTRIBUTION OF PAIN – MIGRAINES CAN BE SEASONAL – WITHDRAWAL FROM DECONGESTANTS CAN PRECIPITATE MIGRAINES
    16. 16. Sinus-related headache may also confuse the diagnosis of migraine Parameters Sinus headacheMigraine Face Pain + - Infection + - Upper Respiratory Problems + - Fever, purulent discharge and postnasal drip + - Pale or pink nasal mucosa + +/- Significant sinus fluid levels + -
    17. 17. Performing the physical exam• PE should include vital signs, a complete neurologic exam (including funduscopic exam), CV, head, and neck exam• A complete neurologic examination is essential
    18. 18. Performing the neurological examination• mental status • sensation• level of consciousness • pathologic reflexes (e.g.• cranial nerve testing Babinskis sign)• pupillary responses • cerebellar function and gait• funduscopic exam testing• motor strength testing • signs of meningeal irritation (Kernigs and• deep tendon reflexes Brudzinskis signs).
    19. 19. Fundoscopic exam • Papilledema
    20. 20. IHS Classification System: Secondary Disorders Secondary headache disorders are a symptom of another disease A common type of secondary headache is called rebound headache - the result of overuse of analgesic medications (MOH) Another type is sinus headache - sometimes incorrectly diagnosed when condition is really migraine
    21. 21. Treat the migraine attack, Prevent the disorder
    22. 22. Principles of PreventionFactors Influencing Medication Choice AE Profile Migraine Type Coexisting Relative Drug Conditions Efficacy Patient Preference
    23. 23. Acute Therapy: Pros and Cons POSITIVES: – Rapid onset of action – Ideal for occasional migraine NEGATIVES: – Doesn’t address frequency of attacks or impact on quality of life – If not taken at onset, less effective – Acute therapies not always effective – Undesirable side effects – Frequent use can cause medication overuse headache (“rebound” headache)
    24. 24. MIGRAINE PROPHYLAXISAim of pharmacologic prophylaxis in migraine:1. reducing the number of migraine days per month,2. reducing headache pain and associated symptoms,3. shortening individual attacks,4. improving the effect of acute medication,5. preventing medication-overuse headache
    25. 25. Preventive Therapy: Advantages• Reduces frequency of migraines, so that the patients can live more normal & productive life• Reduces use of acute medications – and possible “rebound” headache• Reduces overutilization of medical resources, including: • Emergency room visits • Physician office visits
    26. 26. Candidates for migraine prevention US-Guidelines for the use of preventive medication • Recommendations are based on 1. headache days per month experienced by migraine patients 2. Level of attack-related impairment caused by the headachesMigraine prevalence, disease burden, and the need for preventive therapy,Lipton et al. Neurology 2007;68;343-349
    27. 27. Candidates for migraine prevention US-Guidelines for the use of preventive medication • II. Prevention should be considered: – Patients with 4 or 5 migraine days per month with normal functioning, – 3 migraine days with some impairment, or – 2 migraine days with severe impairment.Migraine prevalence, disease burden, and the need for preventive therapy,Lipton et al. Neurology 2007;68;343-349
    28. 28. Guidelines for migraine prophylaxis Successful therapyA migraine prophylaxis is considered successful ifthe frequency of migraine attacks per month isdecreased atleast by 50% within 3 months Evers S et al. Eur J Neurol 2006;13:560-572
    29. 29. Guidelines for migraine prophylaxis Duration of therapy• Preventive therapy to be continued for atleast 1 year Peterlin BL. Headache 2008;48: 805-819• Preventive therapy needs to be taken everyday because it requires dose- titration and may take several months to achieve the desired effect.• Therapy from 6 to 12 months may be required, before evaluation of efficacy Freitag FG. Clinical Therapeutics 2007; 29: 939-949• A full therapeutic trial can take 2 – 6 months Silberstein SD. Trends in Pharmacological Sciences 2006; 27: 410-415
    30. 30. Potential Mechanisms of preventive medication Silberstein SD. Trends in Pharmacological Sciences 2006; 27: 410-415
    31. 31. Prophylactic Treatment Of Migraine Assess factors that may trigger migraine First-line treatment: - Calcium channel blockers (flunarizine) Reinforce education and lifestyle management - Beta-blockers Consider other therapies (biofeedback, relaxation) - Anti-epileptic drugs – (Divalproex & Topiramate) Screen for depression and generalized anxiety yes Successful ?* Continue treatment for 6- no 12 months, then reassess Try combination Successful ?* yes Continue treatment for 6- 12 months, then reassess no * A migraine prophylaxis is considered successful if theRefer to Neurologist or Headache Specialist frequency of migraine attacks per month is decreased atleast by 50% within 3 months.
    32. 32. Techniques in Regional Anesthesia and Pain Management 2009;13:20-27.
    33. 33. Migraine activity starts in the Cortex
    34. 34. Cortical spreading depression (CSD) amain culprit behind migraine attacks Patients with migraine exhibit high cortical excitability Cortical hyperexcitability Frequency of migraine Attacks National Headache Foundation Migraine Prevention Summit Proceedings 2006
    35. 35. Migraine - A Channelopathy Genetic mutations leads to defective Na+ and Ca++ channels which are linked to migraine Widely used drugs for migraine prevention work by inhibiting the function of one or both of these ion channels(Na+, Ca2+)**Cohen et al ,Medical Hypotheses (2005) 65, 114–122
    36. 36. To prevent CSDIts necessary to block both the channels: Na+ and Ca++
    37. 37. Na + and Ca2+ current inhibition by FlunarizineConcentration-dependent effects of FLN on I Na Concentration-dependent effects of FLN on I Ca Q.Ye,etal., Chinese Medical Journal 2011;124(17):2649-2655
    38. 38. Flunarizine
    39. 39. Beta-blockers compared with Placebo • Early studies can be criticized from a methodological point of view • Propranolol, nadolol, timolol, metoprolol and atenolol have shown better efficacy than placebo in RCT • Some trials failed to show a significant prophylactic effect of propranolol • Two RCT have not shown any effect in the acute treatment of attacks
    40. 40. Beta-blockers compared with Placebo • Early studies can be criticized from a methodological point of view • Propranolol, nadolol, timolol, metoprolol and atenolol have shown better efficacy than placebo in RCT • Some trials failed to show a significant prophylactic effect of propranolol • Two RCT have not shown any effect in the acute treatment of attacks
    41. 41. Beta-blockers: side effects • Propranolol 80-0-80 mg – With side effects 35 % – Without side effects 48 % • Most commonly reported – Fatigue 18 % – Dizziness 2% – Nausea 6% – Sleep disturbances 4% – Depression 4% – Abnormal dreaming 2%
    42. 42. Flunarizine vs Propranolol Post Treatment Benefits 90 80 % of respondents 70 60 50 40 30 N = 45 0 Flunarizine Propranolol % of patients with very good or excellent response in terms of global evaluation after 45 days of drug withdrawal Bordini CA et al. Arquivos de Neuro-Psiquiatria 1997; 55 :536-541.
    43. 43. Antiepileptic drugs side effects Drug Dose Common ContraindicationsValproic acid 500-1800 Tiredness, cognitive deficits, dizziness, hepatic disease or mg upset stomach significant hepatic nausea, vomiting, hair loss, weight dysfunction, gain, depression, tremor, pancreatitis, childbearing hepatitis (test of liver function potential, pregnancy necessary during treatment)Topiramate 25-100 mg Paresthesia, Dizziness, Asthenia, Weight childbearing Decrease, Somnolence, Difficulty with potential, pregnancy Memory, Depression, Difficulty with Concentration/Attention, Anxiety, Taste Perversion, Upper Respiratory Tract Infection, Suicidal thinking, diabetes, kidney stonesEFNS guidelines on the drug treatment of migraine. European Journal of Neurology 2009, 16, 968-981
    44. 44. Migraine progression - Consequence of CSD - Headache 2008;48:7-15)44
    45. 45. 3 Types of Migraine Progression Clinical Increase in attack frequency Migraine Physiological/Progression Alterations in pain pathways functional Anatomical Neurological damage 45
    46. 46. Anatomical progression - Neurological damage in Migraine • Neuroimaging findings of a large- scale population-based study showed that silent brain damage is more frequent in migraineurs, compared with control subjects. • Migraine is associated with white matter lesions. • Clinical studies reported that migraine is a risk factor for ischemic stroke in younger women.Reference: Headache 2008;48:1044-1055 46
    47. 47. Study details Journal of Headache Pain (2011) 12:47–53 Official journal of European Headache Federation • Study results • Flunarizine reduced – Number of CSD waves – Amplitude of CSD waves – Duration of CSD waves Flunarizine a potent CSD inhibitor FLN does not only prevent the migraine disorder but also may reduce complications of migraine like neurological damage
    48. 48. Prevent theprogression from Episodic toChronic Migraine Start Early Effective Migraine Prophylaxis
    49. 49. Thank you

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