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Migraine
- 2. Migraine
- 3. Migraine Definition โข Migraine is a complex, genetically influenced neurological disorder characterized by recurrent episodes of moderate to severe headache, often unilateral and accompanied by diverse autonomic and sensory symptoms.
- 4. Migraine Symptoms โข Headache: Throbbing, pulsating pain, typically unilateral, but can become bilateral. โข Autonomic: Nausea, vomiting, photophobia, phonophobia, dizziness, vertigo. โข Sensory: Visual auras (scintillating scotoma, fortification spectra), paresthesia, dysphasia, motor weakness. โข Psychological: Mood changes, irritability, fatigue, depression, anxiety.
- 5. Migraine Vs. Headache โข Duration: Migraine attacks last 4-72 hours, while tension headaches typically last less than 4 hours. โข Location: Migraine pain is typically unilateral, while tension headaches are often bilateral and band-like. โข Associated symptoms: Migraine has prominent autonomic and sensory features, while tension headaches do not. โข Response to treatment: Migraine responds less well to common analgesics compared to tension headaches.
- 6. Migraine Types โข Migraine with Aura: Preceded by reversible focal neurological symptoms (visual, sensory, motor, speech) before or during the headache phase. โข Migraine without Aura: No premonitory aura, just the headache and associated symptoms. โข Chronic Migraine: Headaches occur on โฅ15 days/month for โฅ3 months, with migraine features on โฅ8 days/month.
- 7. Migraine with aura โข Aura types: Visual, sensory, motor, brainstem, retinal. โข Unilat eral symptoms: Sensory auras often occur on the same side as the subsequent headache. โข Mech anisms: Cortical hyperexcitability followed by spreading depolarization wave.
- 9. Migraine
- 10. Chronic Migraine โข Increased disability: Significant burden on quality of life and productivity. โข Pathophysiology: Sensitization of trigeminal nociceptive pathways, increased cortical excitability.
- 11. Migraine Complications โข Cerebral infarction: Rare but serious, associated with prolonged aura (>72 hours) or hemiplegic migraine. โข Medication overuse headache: Chronic daily headache induced by frequent analgesic use (>15 days/month). โข Status migrainous: Incapacitating migraine lasting >72 hours, requiring hospitalization. โข Psychiatric comorbidities: Depression, anxiety, and epilepsy are more prevalent in migraineurs.
- 12. Migraine Etiology โข Genetics: Strong familial predisposition, identified susceptibility genes, polygenic inheritance.
- 13. Migraine โข Neurovascu lar theory: Cortical spreading depolarization wave, trigeminal nerve activation, cranial vasodilation. โข Serotonin and other neurotransmitters: Dysregulation of serotonin, glutamate, calcitonin gene-related peptide (CGRP) pathways. โข Environmen tal factors: Hormonal changes, stress, sleep disturbances, dietary triggers (e.g., chocolate, cheese), weather changes.
- 15. Migraine โข Hormonal: Menstruation, ovulation, pregnancy, menopause. โข Dietary: Chocolate, cheese, alcohol, caffeine, artificial sweeteners. โข Sensory: Bright lights, loud noises, strong smells. โข Environmental: Changes in temperature, barometric pressure, and sleep patterns. โข Psychological: Stress, anxiety, depression.
- 16. Migraine โข Affects 12% of the global population, 17% of women, and 6% of men. โข Second leading cause of disability worldwide. โข Onset typically in childhood or adolescence, peaks in 30s and 40s, declines with age.
- 17. Migraine
- 18. Migraine
- 19. Migraine in pregnancy โข Attacks often decrease in frequency during the second and third trimesters. โข Certain medications, including triptans, are safe for use during pregnancy. โข Hormonal changes postpartum can trigger increased attack frequency.
- 21. Migraine in children โข Most common primary headache disorder in children and adolescents. โข Symptoms similar to adults, but shorter duration and less frequent aura. โข Early diagnosis and management are crucial for preventing future disability and chronicity.
- 22. Migraine phases โข Prodrome: Early warning signs occurring hours or days before the headache. โข Aura: Reversible focal neurological symptoms preceding or accompanying the headache (25% of cases). โข Headache: The hallmark feature, characterized by throbbing, unilateral pain, often accompanied by autonomic and sensory symptoms. โข Postdrome: A period of lingering fatigue, difficulty concentrating, and mood changes after the headache subsides.
- 23. Migraine
- 24. Prodrome phase โข Etiology: Increased hypothalamic activity, activation of trigeminal nociceptive pathways, and neurotransmitter fluctuations (dopamine, serotonin).
- 25. Prodrome phase symptoms โข Symptoms: Yawning, neck stiffness, mood changes (irritability, depression), fatigue, food cravings, light sensitivity.
- 26. Prodrome phase
- 27. Migraine
- 32. Aura Phase โข Mechanisms: Cortical hyperexcitabili ty followed by a spreading depolarization wave across the cortex. Decreased Neural Depolarization: Contrary to traditional views, recent research suggests that the aura may reflect a decrease in neuronal depolarization, leading to temporary dysfunction
- 33. Aura Phase symptoms โข Symptoms: Visual (scintillating scotoma, fortification spectra), sensory (tingling, numbness), motor (weakness), speech disturbances, retinal (visual field defects).
- 35. Aura Phase- decreased neural depolarization Decreased Neural Depolarization: Contrary to traditional views, recent research suggests that the aura may reflect a decrease in neuronal depolarization, leading to temporary dysfunction
- 36. Migraine โ headache phase โข Etiology: Trigeminal nerve activation, cranial vasodilation, release of inflammatory neuropeptides (CGRP), meningeal inflammation. โข Mechanisms: The trigeminal vascular pathway plays a central role, with activation of nociceptive neurons leading to vasodilation and subsequent pain.the
- 37. Migraine โ headache phase โข CGRP: This neuropeptide contributes to vasodilation, meningeal inflammation, and sensitization of trigeminal nociceptive neurons, making it a key target for migraine therapy.
- 38. Migraine Treatment โข Acute Treatment: Aims to abort or alleviate ongoing attacks. โข Preventive Treatment: Focuses on reducing attack frequency and severity.
- 39. CGRP receptor blockers โข Novel class of drugs targeting calcitonin gene- related peptide (CGRP), a key mediator in migraine pathophysiology. โข Examples: Gepants (e.g., rimegepant, atogepant) โข Advantages: High efficacy, specificity, and favorable safety profile.
- 41. 5HT1 B vs. 5HT1F Agonists โข 5HT1B agonists: Cause vasoconstriction, but can have cardiovascular side effects (e.g., sumatriptan). โข 5HT1F agonists: Preferentially activates trigeminal nociceptive pathways, leading to vasoconstriction without cardiovascular effects (e.g., Lasmiditan). โข Future research may focus on selective 5HT1F agonists for improved efficacy and tolerability.
- 42. Prophylaxis treatment โข Aim to reduce attack frequency and severity by 50% or more. โข Options: Beta- blockers, calcium channel blockers, antidepressants (amitriptyline), anticonvulsants (topiramate), CGRP monoclonal antibodies (e.g., Erenumab). โข Choice depends on individual patient profile, comorbidities, and response to previous treatments.
- 43. Non-pharmacologic treatment โข Behavioral therapy: Cognitive- behavioral therapy (CBT) can help manage stress, identify triggers, and develop coping strategies. โข Biofeedback: Teaches patients to recognize and modify physiological responses associated with migraine, promoting self- management. โข Lifestyle modifications: Regular sleep schedule, balanced diet, regular exercise, stress management techniques. โข Neuromodulator y therapies: Botox injections, transcranial magnetic stimulation (TMS) are emerging options for refractory cases.
- 44. Migraine