WHY IS MIGRAINE IMPORTANT

Transcription

1 WHY IS MIGRAINE IMPORTANT

2 Migraine is a complex disorder characterized by recurrent episodes of headache, most often unilateral and in some cases associated with visual or sensory symptoms collectively known as an aura that arise most often before the head pain but that may occur during or afterward

3 Signs and symptoms Typical symptoms of migraine include the following: Throbbing or pulsatile headache, with moderate to severe pain that intensifies with movement or physical activity Unilateral and localized pain in the frontotemporal and ocular area, but the pain may be felt anywhere around the head or neck Pain builds up over a period of 1-2 hours, progressing posteriorly and becoming diffuse Headache lasts 4-72 hours Nausea (80%) and vomiting (50%), including anorexia and food intolerance, and light-headedness Sensitivity to light and sound

4 Features of migraine aura are as follows: May precede or accompany the headache phase or may occur in isolation Usually develops over 5-20 minutes and lasts less than 60 minutes Most commonly visual but can be sensory, motor, or any combination of these Visual symptoms may be positive or negative The most common positive visual phenomenon is the scintillating scotoma, an arc or band of absent vision with a shimmering or glittering zigzag border

5 Physical findings during a migraine headache may include the following: Cranial/cervical muscle tenderness Horner syndrome (ie, relative miosis with 1-2 mm of ptosis on the same side as the headache) Conjunctival injection Tachycardia or bradycardia Hypertension or hypotension Hemisensory or hemiparetic neurologic deficits (ie, complicated migraine) Adie-type pupil (ie, poor light reactivity, with near dissociation from light)

6 Classification of migraine is as follows: Migraine without aura (formerly, common migraine) Probable migraine without aura Migraine with aura (formerly, classic migraine) Probable migraine with aura Chronic migraine Chronic migraine associated with analgesic overuse Childhood periodic syndromes that may not be precursors to or associated with migraine Complications of migraine Migrainous disorder not fulfilling above criteria

7 Migraine variants include the following: Childhood periodic syndromes Late-life migrainous accompaniments Basilar-type migraine Hemiplegic migraine Status migrainosus Ophthalmoplegic migraine Retinal migraine

8 NOT TO DO The American Headache Society released a list of 5 commonly performed tests or procedures that are not always necessary in the treatment of migraine and headache, as part of the American Board of Internal Medicine (ABIM) Foundation's Choosing Wisely campaign. The recommendations include [2, 3] : Don't perform neuroimaging studies in patients with stable headaches that meet criteria for migraine. Don't perform computed tomography imaging for headache when magnetic resonance imaging is available, except in emergency settings. Don't recommend surgical deactivation of migraine trigger points outside of a clinical trial. Don't prescribe opioid or butalbital-containing medications as first-line treatment for recurrent headache disorders. Don't recommend prolonged or frequent use of over-the-counter pain medications for headache.

9 PREVALENCE OF MIGRAINE Migraine is the 3rd most prevalent and 7th leading cause of disability worldwide. Age-standardized 1-year prevalence was 25.2% (95% CI: %; 10.6% definite, 14.6% probable migraine). Point prevalence (headache yesterday) was 2.7%. Prevalence was greater among females (31.6% vs 18.5%; OR=2.03 [95% CI: ]) and in rural areas (28.9% vs 21.7%; OR=1.45 [95% CI: ]). Prevalence peaked between years in both genders. Median frequency was 24 days/year, with a sizeable minority (6.6%) reporting >60 days/year. Headache intensity was severe in 40%. Lost productive time correlated with attack frequency. The overall mean total was 3.7 ±6.1 days/3 months, representing a loss of 6.1% of productive days, of which 2.1 ±4.0 days/3 months were lost at home and 1.4 ±4.1 days/months were lost in the work place. Disability was higher among women and in rural areas. A positive family history of headache was observed in 24.7% of probands with a possible maternal inheritance on clinical grounds in 29 of 41 families (70.7%)

10 AETIOLOGY Migraines are currently thought to be caused by dysfunction of the nerves in the brain. [10] Previously, migraines were thought to be caused by a primary problem with the blood vessels in the brain. [11] This vascular theory, which was developed in the 20th century by Wolff, suggested that the aura in migraines is caused by constriction of intracranial vessels (vessels inside the brain), and the headache itself is caused by rebound dilation of extracranial vessels (vessels just outside the brain). Dilation of these extracranial blood vessels activates the pain receptors in the surrounding nerves, causing a headache. The vascular theory is no longer accepted. [10][12] Studies have shown migraine head pain is not accompanied by extracranial vasodilation, but rather only has some mild intracranial vasodilation. [13]

11 Currently, most specialists think migraines are due to a primary problem with the nerves in the brain. [10] Auras are thought to be caused by a wave of increased activity of neurons in the cerebral cortex (a part of the brain) known as cortical spreading depression [14] followed by a period of depressed activity. [15] Some people think headaches are caused by the activation of sensory nerves which release peptides, such as serotonin, causing inflammation in arteries, dura and meninges and also cause some vasodilation. Triptans, medications which treat migraines, block serotonin receptors and constrict blood vessels. [16] People who are more susceptible to experience migraines without headache are those who have a family history of migraines, women, and women who are experiencing hormonal changes or are taking birth control pills or are prescribed hormone replacement therapy

12 targeting calcitonin gene-related peptide (CGRP), a small protein that plays a role in the initiation, transmission, and heightened sensitivity to migraine pain, might improve outcomes for patients. There are two main approaches for targeting CGRP in migraine: monoclonal antibodies given by injection to prevent attacks and small molecule, orally absorbable agents for use as acute treatment.

13 Differential diagnosis of headaches Tension headache New daily persistent headache Cluster headache Migraine mild to moderate dull or aching pain severe pain moderate to severe pain duration of 30 minutes to several hours duration of at least four hours daily duration of 30 minutes to 3 hours duration of 4 hours to 3 days Occur in periods of 15 days a month for three months may happen multiple times in a day for months periodic occurrence; several per month to several per year located as tightness or pressure across head located on one or both sides of head located one side of head focused at eye or temple located on one or both sides of head consistent pain pain describable as sharp or stabbing pulsating or throbbing pain no nausea or vomiting no aura no aura auras nausea, perhaps with vomiting uncommonly, light sensitivity or noise sensitivity may be accompanied by running nose, tears, and drooping eyelid, often only on one side sensitivity to movement, light, and noise exacerbated by regular use of acetaminophen or NSA IDS may exist with tension headache [20

14

15 Management Pharmacologic agents used for the treatment of migraine can be classified as abortive (ie, for alleviating the acute phase) or prophylactic (ie, preventive). Acute/abortive medications Acute treatment aims to reverse, or at least stop the progression of, a headache. It is most effective when given within 15 minutes of pain onset and when pain is mild. [4] Abortive medications include the following: Selective serotonin receptor (5-hydroxytryptamine 1, or 5-HT1) agonists (triptans) Ergot alkaloids (eg, ergotamine, dihydroergotamine [DHE]) Analgesics Nonsteroidal anti-inflammatory drugs (NSAIDs) Combination products Antiemetics

16 Preventive/prophylactic medications The following may be considered indications for prophylactic migraine therapy: Frequency of migraine attacks is greater than 2 per month Duration of individual attacks is longer than 24 hours The headaches cause major disruptions in the patient's lifestyle, with significant disability that lasts 3 or more days Abortive therapy fails or is overused Symptomatic medications are contraindicated or ineffective Use of abortive medications more than twice a week Migraine variants such as hemiplegic migraine or rare headache attacks producing profound disruption or risk of permanent neurologic injury [5]

17 Prophylactic medications include the following: Antiepileptic drugs Beta blockers Tricyclic antidepressants Calcium channel blockers Selective serotonin reuptake inhibitors (SSRIs) NSAIDs Serotonin antagonists Botulinum toxin Other measures Treatment of migraine may also include the following: Reduction of migraine triggers (eg, lack of sleep, fatigue, stress, certain foods) Nonpharmacologic therapy (eg, biofeedback, cognitive-behavioral therapy) Integrative medicine (eg, butterbur, riboflavin, magnesium, feverfew, coenzyme Q10)

18 AVOID COMPLICATIONS COMPLICATED MIGRAINE STATUS MIGRAINOSUS MEDICATION OVERUSE HEADACHE MIXED HEADACHES MIGRAINOUS INFARCTS

19 In cases of status migrainosus, aggressive therapy is warranted, including the following 5 components: Rehydration Analgesics (eg, ketorolac, naproxen, or indomethacin; ideally, narcotics should be avoided) Specific antimigraine medications (eg, triptans, valproate, or dihydroergotamine) Antiemetics (eg, prochlorperazine or metoclopramide) Sedatives (eg, diphenhydramine or a benzodiazepine) Steroids

20 MIGRANOUS INFARCTS Migrainous infarction is a term that was originally coined by the International Headache Society to describe strokes which occur in the setting of a migraine attack. The word infarction, as used in this term, has the same meaning as the word stroke. Thus, this condition is also known as "migraineinduced stroke".

21 migrainous infarction mostly occurs in the posterior circulation, and in younger women with a history of migraine with aura. Acute ischemic lesions were often multiple and located in distinct arterial territories. As there were no overlapping ischemic lesions, hemodynamic compromise during the development of migraine is unlikely the cause of infarction The prevalence of a patent foramen ovale was high (64.7%)

22 MI is diagnosed when one or more aura symptoms last longer than 60 minutes, and neuroradiological studies demonstrate ischemic stroke that potentially explains the symptoms.

23

24 WOMEN WITH MIGRAINE CHILD BEARING AGE PREGNANT OC PILLS MENSTRUAL IRREGULARITIES

25 CO MORBIDITIES EPILEPSY DEPRESSION ANXIETY WEIGHT GAIN OBSTRUCTIVE AIRWAY DISEASE

26 CHILDHOOD MIGRAINE EPISODIC VOMITING ABDOMEN PAIN FAMILY HISTORY OF MIGRAINE

27 Recognized childhood syndromes assumed to be pathophysiologically related to migraine include the following: Benign paroxysmal vertigo of childhood Abdominal migraine Cyclic vomiting of childhood Acute confusional migraine (acute confusional state) Paroxysmal torticollis Infant colic (epidemiologic association with migraine)

28 Infants may present with only episodic head banging Preschool children often have episodes involving an ill appearance, abdominal pain, vomiting, and the need to go to sleep; they may exhibit pain by irritability, crying, rocking, or seeking a dark room in which to sleep Children aged 5-10 years typically have bifrontal, bitemporal, or retro-orbital headache; nausea; abdominal cramping; vomiting; photophobia; phonophobia; a need to sleep; migraine facies; tearing, swollen nasal passages; thirst; edema; excessive sweating; increased urination; or diarrhea Older children may experience increasing headache intensity and duration; a pulsating or throbbing character to the headache; and a shift to a unilateral, temporal location

29 Measures that may be helpful for managing acute attacks include the following: Advising the child to lie down in a cool, dark, quiet room during the attack and go to sleep Providing simple analgesics (eg, acetaminophen or ibuprofen); in some cases, stronger agents (eg, butalbital) may be necessary Applying ice or pressure to the affected artery Using nonpharmacologic treatment modalities such as selfrelaxation, biofeedback, and self-hypnosis Employing specific pharmacologic abortive therapies for acute attacks (ie, ergot preparations or triptans) Analgesic and abortive therapies are for occasional acute attacks and should not be used frequently (frequent use may result in rebound headaches).

30 Possible medications for migraine prophylaxis include the following: Amitriptyline Propranolol Selective serotonin reuptake inhibitors Anticonvulsants (eg, gabapentin, valproate, and topiramate) Riboflavin Tricyclic antidepressants The agents that seem to be the most effective for prophylaxis in children are those that block the serotonin 5-HT2 receptor, such as the following: Beta blockers Cyproheptadine Methysergide

31 CADASIL

32 The American Headache Society recommends using "SSNOOP", a mnemonic to remember the red flags for identifying a secondary headache: [22] Systemic symptoms (fever or weight loss) Systemic disease (HIV infection, malignancy) Neurologic symptoms or signs Onset sudden (thunderclap headache) Onset after age 40 years Previous headache history (first, worst, or different headache)

33 REAL EMERGENCY Emergency phone call 26yrs female presented with acute headaches with vomiting not relieved with migranil,action 500,saridon History dates back So called new onset headaches Relief of symptoms

34 CURABLE TREATABLE

35 Management of pediatric migraine has the following 3 facets: Educate patients and parents concerning migraine triggers Formulate a plan of treatment for the acute attacks Consider prophylaxis for patients with frequent migraines Treatment of mild, infrequent attacks consists primarily of rest, trigger avoidance, and stress reduction. Education regarding migraine triggers includes the following: Explaining the disease to the child and the parents Encouraging parents to maintain a regular bedtime and strict meal schedules for the child and to avoid overloading the child s schedule with activities Helping the child recognize and avoid precipitating triggers to the extent possible, while maintaining realistic expectations (ie, migraine frequency may be reduced, but headaches will not be entirely eliminated) Helping the child keep a headache diary to record unique triggers and features of attacks

36 PRESCRIPTION ERRORS MIGRANIL PAIN KILLERS SIBELIUM-acute treatment Subordinate prescription

37

38 Papilledema Severe headache following head trauma Inability to move a limb Change in personality, consciousness, or mental status Headache triggered by cough, exertion or while engaged in sexual intercourse hypertension (pseudo (from inside the tumor brain) and causes cerebri), meningitis papilledema. Brain bleeds (intracranial hemorrhage, subdura l hematoma, epidural hematoma), posttraumatic headache Arteriovenous malformation, collagen vascular disease, intracranial mass lesion Trauma can cause bleeding in the brain or shake the nerves, causing a posttraumatic headache Other red flag symptoms include: [6][22][23][25] Central nervous system infection, intracranial bleed, mass Mass lesion, subarachnoid hemorrhage lumbar puncture Neuroimaging of brain, skull, and possibly cervical spine Focal neurological signs indicate Neuroimaging, blood something is pushing tests for collagen against nerves in the vascular diseases brain responsible for one part of the body Change in mental status indicates a global infection or inflammation of the brain, or a large bleed compressing the brainstem where the consciousness centers lie Blood tests, lumbar puncture, neuroimaging Coughing and exertion increases the intra cranial pressure, which may cause a vessel to burst, causing a subarachnoid hemorrhage. A mass Neuroimaging, lesion already lumbar puncture increases intracranial pressure, so an