Migraine (VK)

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  • During activation of trigeminal sensory fibers surrounding cerebral and meningeal blood vessels, the stimulated nerve fibers release a variety of inflammatory and vasodilatory neuroactive substances, such as calcitonin gene related peptide (CGRP), substance P, NO, and cytokines.1,2
    References
    1. Bolay H., Reuter U, Dunn AK, et al. Intrinsic brain activity triggers trigeminal meningeal afferents in a migraine model. Nature Medicine. 2001;8(2):136-142.
    2. Williamson DJ, Hargreaves RJ. Neurogenic inflammation in the context of migraine. Microsc Res Tech. 2001;53(3):167-78.
  • Migraine (VK)

    1. 1. Migraine Migraine 1
    2. 2. Migraine • Characterised by episodic headache, typically unilateral, associated with vomiting and visual disturbance. • Headache may be bitemporal and generalised without focal visual or neurological disturbance. Migraine 2
    3. 3. The Headache Dilemma… Migraine Tension Sinus Treatment
    4. 4. HOW COMMON IS MIGRAINE o o o o o World- 15-20% of women 10-15% of men In India 15-20% migraine Adults-female: male ratio is 2:1 In childhood boys and girls are affected equally until puberty when predominance shifts to girls
    5. 5. Pathogenesis • ↓ cerebral blood flow at the onset of an attack in migraine with aura. During phase of attack, dilatation of extracranial arteries related to fluctuations in blood 5-ht levels. • Genetic predisposition. • Chocolate, cheese, alcohol may precipitate attack. • Episodes ↑ perimenstrually, at weekends or in women taking oral contraceptives. • Stress & anxiety may initiate an attack. Migraine 8
    6. 6. 5-HT1D Agonist 5-HT2 Antagonist Dilatation of B.V 5HT2receptor act 5-HT1D Agonist Sensory nerve discharge Trigeminal Nerve PG + kinin release NSAIDs 5-HT1D Agonist Neruogenic Inflammation (CGRP,SP release) 5-HT1D Agonist Perivascular oedmea Unknown abnormal neuronal discharge Spreading depression + Hypoperfusion Directly Aura Aura + Pain Pain
    7. 7. Release of CGRP, substance P & Inflammatory Cytokines 1 2 3 4 5 6
    8. 8. PATHOPHYSIOLOGY Vascular theoryo Intracerebral blood vessel constriction – aura o Intracranial/extra cranial blood vessel vasodilatation-headache Serotonin theoryo Decreased 5-ht levels linked with migraine o Specific 5-ht receptors found in blood vessels of brain
    9. 9. 3 4 Chemicals in the brain cause blood vessel dilation and inflammation of the surrounding tissue Changes in nerve cell activity and blood flow may result in visual disturbance, numbness or tingling, and dizziness. 5 2 Electrical impulses spread to other regions of the brain. 1 Migraine originates deep within the brain The inflammation irritates the trigeminal nerve, resulting in severe or throbbing pain
    10. 10. CLASSIFICATION o Migraine with aura o Migraine without aura o Complicated migraine
    11. 11. PHASES OF ACUTE MIGRAINE o Prodrome o Aura o Headache o Postdrome
    12. 12. PRODROME o Vague premonitory symptoms that begin from 12 to 36 hrs before the aura and headache o Symptoms include: Yawning  Excitation  Depression  Lethargy  Craving or distaste for various foods o Duration- 15-20min
    13. 13. AURA o Aura is a warning or signal before onset of headache o Symptoms include  Flashing of lights  Zig zag lines  Difficulty in focussing o Duration:15-30 min
    14. 14. HEADACHE o Headache is generally unilateral and is associated with symptoms like: o Anorexia o Nausea o Vomiting o Photophobia o Phonophobia o Tinnitus o Duration:4-72 hrs
    15. 15. POSTDROME Following headache, patient complains of o Fatigue o Depression o Severe exhaustion o Some patients feel unusually fresh o Duration: few hrs to 2 days
    16. 16. Clinical Features  Starts after puberty, continues till late midlife.  Attack may occur from a few days to several months.  Attacks may last for hours to days.  Premonitory symptoms – zig-zag lines, flashing, coloured lights, defects in visual field & dysphasias with headache.  Headache localized to frontal region & spreads to whole of one side of head – pain severe & throbbing associated with vomiting, photophobia, pallor.  Patient is shifted to a bed in darkened room. Migraine 20
    17. 17. MIGRAINE MANAGMENT Non pharmacological treatment o Identification of triggers o Meditation o Relax techniques o Psychotherapy Pharmacological treatment o Abortive treatment o Preventive treatment
    18. 18. ABORTIVE TREATMENT Non specific treatmento Aspirin o Paracetamol o Ibuprufen o diclofenac
    19. 19. ABORTIVE THERAPY Specific treatmentErgot alkaloids:-ergotamine dihydroergotamine Triptans:- sumatriptan rizatriptan Antinauseant drugs:- metaclopramide chlorpromazine Triptans work best in 1st couple of hrs of attack Ergotamine works at any time during the attack
    20. 20. Management  Avoid dietary and other precipitants.  Maintain a diary of attacks.  Stop oral contraceptives.  Soluble Aspirin (600-900 mg) or Paracetamol (1 Gm) with or without Metoclopramide as antiemetic.  Ergotamine tartarate, 0.5-1.0 mg sublingually may abort headache if taken as soon as visual symptoms are felt. No More than 12 mg in a week. Excessive use may lead to vasospasm & paradoxical headache. Contraindicated in pregnancy, IHD & peripheral vascular disorders. Migraine 25
    21. 21. …Management • Serotonin agonist-triptans – Sumatriptan for acute attacks of migraine (100 mg). No more than 300 mg per 24 hours or Inj. Sumatriptan 6 mg SC. Not more than 2 injections per 24 hours. Highly efficacious. • Prophylaxis if attacks occur weekly: Propranolol : 40-80 mg 8 hrly. Pizotifen : 1.5-3 mg at night. • Amitriptyline : 25-100 mg at night. Migraine 26
    22. 22. Migraine & Oral Contraceptives C/I migraine if there is typical aura, focal features or if it is severe and lasts for more than 72 hrs despite treatment with ergotamine. Migraine 28
    23. 23. Acute Migraine Attack • It appears to begin in serotonergic (5-HT) and noradrenergic neurons in the brain. These monoamines affect cerebral & extracerebral vasculature and cause release of vasoactive substances such as H, PGs, neuropeptides involved in pain, i.e. neurogenic inflammation can be inhibited by antimigraine drugs. • Migraine aura of visual or sensory disturbance originates in occipital or sensory cortex. • Throbbing headache is due to dilatation of vessels – sensitive arteries outside the brain. Migraine 29
    24. 24. Triggering Factors Avoidance • Stress – exertion, anxiety, excitement, fatigue, anger. • Foods containing vasoactive amines – chocolate, cheese. • Bright lights, loud noise. • Food Allergy. • Hypoglycemia. • Menstruation and oral contraceptives. Migraine 30
    25. 25. Treatment – Stepped Approach • Aspirin 600 mg oral dispersible (soluble) as early as possible. • Alternatives are Paracetamol, Ibuprofen, Naproxen. • Metoclopramide or Domperidone (dopamine agonists) – antiemetics that promote gastric emptying & enhance absorption of analgesic. • Efficient use of analgesic & antiemetic is adequate for majority of attacks. Migraine 31
    26. 26. Stepped Treatment  Severe migraine attacks should be treated with triptans – Sumatriptan. Headache may return in 6-36h in 1/3rd patients. Use second dose.  Ergotamine 1-2 mg used if other treatments failed, but not within 12h of the last dose.  Do not give triptans until 24h have elapsed after stopping ergotamine. Migraine 32
    27. 27. Triptans  Selectively stimulate 5-HT 1B/1D – receptors found in cranial blood vessels – vasoconstriction. -Sumatriptan. -Rizatriptan. -Almotriptan. -Naratriptan. -Zolmitriptan. Migraine 33
    28. 28. SUMATRIPTAN • • • • Rapid oral absorption. 84% presystemic elimination. SC bioavailability 96%. Oral 50-100 mg, maximum 300 mg in 24h, Repeat 2h. • Intranasal 20 mg, maximum 40 mg in 24h, Repeat 1h. • SC 6 mg, 12 mg in 24h, Repeat 1h. Migraine 34
    29. 29. Sumatriptan - ADRs • • • • Malaise, fatigue, dizziness, vertigo, sedation. N,V. Feelings of chest pressure, tightness and pain. Cardiac arrhythmias, MI. Migraine 35
    30. 30. Sumatriptan – C/I  Prophylaxis of migraine  MI  IHD  Variant angina  Uncontrolled HT  Concomitant ergotamine  Within 2 wks after stopping MAOIs Migraine 36
    31. 31. RIZATRIPTAN • C/I: HT, IHD, Prinzmetal’s angina, Lactation, Within 2 wks of MAOIs, Within 24 hrs of treatment with another 5-HT agonist or ergotamine. Tab. Rizact 5 mg Rs 30/- 10 mg Rs 50/Migraine 37
    32. 32. ERGOTAMINE  Partial agonist at α-adrenoceptors (vasoconstrictor).  Partial agonist at serotonergic receptors.  Constricts all peripheral arteries.  Effect persists for 24h, repeated doses cause cumulative toxicity.  Tablets 1 mg crushed before swallowing.  Initially 1-2 mg, maximum 4 mg in 24h.  Not more than 8 tablets in a week.  Rectal suppositories of 2 mg preferred. Migraine 38
    33. 33. …ERGOTAMINE  CONTRAINDICATIONS: Vascular & Valvular disease. Pregnancy. -Collagen diseases. -Prophylaxis.  ADRs: -Muscle cramps. -Stiffness. -Tiredness. -N,V,D.  ERGOTISM: Severe peripheral vasoconstriction, hypertension, gangrene of extremities, anginal pain. Migraine 39
    34. 34. Drug Prophylaxis • More than 2 attacks per month. • Propranolol, Atenolol, Metoprolol. • Verapamil, Flunarizine. • Pizotifen, Cyproheptidine. • Amytriptyline. • Methysergide. Migraine 40
    35. 35. THANK YOU Migraine 41

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