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Migraine
- 1. MIGRAINE Moderated by : Dr Sujeet Gautam Presented by : Dr Dibyadip Mukherjee 1
- 2. HISTORICAL EVOLUTION ■ First described by Hippocrates ■ Later described by Greek physicianGalen : described a connection between human brain and abdomen & coined the term “hemicrania” ■ ThomasWillis : proposed the vascular theory ■ Sieveking : found a relation between epilepsy and migraine 2
- 3. What is migraine? ■ Common disabling primary headache disorder ■ Third most prevalent disorder in the world ■ Ranked third–highest cause of disability worldwide in both males and females under the age of 50 years.(Gbd 2015) ■ WHO: 19th among disorders causing disability 3
- 4. Prevalence & distribution ■ Occurs in 18 % of females & 5 % of males. ■ Highest prevalence in age group of 25-55 years (professionally active age group) ■ Male : female ratio : 3 : 1 ■ Pre puberty : similar gender distribution & overall prevalence of 4 % ■ Post puberty : increases more rapidly in girls. ■ Increase upto 40 years of age after which it declines 4
- 5. PREDISPOSING FACTORS (VULNERABILITY) ■ Patent foramen ovale ■ Mutations of the calcium channel gene in chromosome 19 ■ Mutation in the sodium channel gene ATP1A2 on chromosome 3 ■ Mutation in a sodium channel alpha subunit coding gene 5
- 7. Signs & symptoms of migraine 4 possible phases: ■ Prodrome : which occurs hours or days before the headache ■ Aura : which immediately precedes the headache ■ Headache phase ■ Postdrome : the effects experienced following the end of a migraine attack 7
- 8. Prodrome ■ Occurs in upto 70 % patients with migraine ■ May occur as early as 24 -48 hrs before the headache ■ Dopamine & serotonin are the most common neurotransmitters involved. 8
- 9. Aura ■ May or may not occur ■ Onset 30-60 minutes before headache ■ Gradual onset developing over 5 to 20 min and lasting for up to 60 minutes. ■ Characteristics : ■ Focal • Limited in time • Fully reversible • rarely observed during or after the headache phase. 9
- 10. Typical aura ■ Negative positive symptoms ■ Most common : visual auras (99%) ■ Scotoma (blind spot)photopsia (flashes of light) fortification spectrum (the arc of zig zag scintillating lights) Sensory symptoms (40-50%) (positive—pins and needles; negative—numbness) Motor: speech & language disturbances 10
- 11. Headache ■ Unilateral ■ Most commonly frontotemporal ■ Throbbing or pulsatile ■ Moderate-severe in intensity ■ Lasts 4-72 hours (2 -48 hrs in children) ■ Aggravated by physical activity ■ Note : headache may be bilateral in upto 40 % cases or may start as U/L in adults but as it reaches its peak , becomes B/L 11
- 12. Accompanying features: ■ Frequently accompanied by: ■ Nausea : 90% ■ Vomiting : 1/3rd ■ Sensitivity to light, sound, smells :patients prefer a dark and quiet room ■ Fatigue and irritability ■ Other autonomic features (blurred vision, nasal stuffiness, diarrhea, frequent urination, pallor or sweating) 12
- 13. Postdrome ■ Variable ■ The patient may feel tired or "hung over" ■ May have head pain, cognitive difficulties, GI symptoms, mood changes, weakness 13
- 15. Migraine without aura Note: migraine without aura often has a menstrual relationship 15
- 16. Migraine with aura 16 Aphasia is always regarded as a unilateral symptom; dysarthria may or may not be.
- 17. Other variants Migraine with brainstem aura Hemiplegic migraine 17
- 20. Complications of migraine Status migrainosus Migraine aura trigerred seizures Persistent aura without infarction Migrainous infarction 20
- 21. Episodic syndromes a/w migraine ■ Recurrent GI disturbance – cyclic vomiting syndrome – Abdominal migraine ■ Benign paroxysmal vertigo ■ Benign paroxysmal torticollis More common in children Episodic Complete remission in between attacks Stereotypical in the individual 21
- 22. Pathogenesis ■ ACTIVATION OFTRIGEMINAL/ CERVICAL AFFERENT NEURONS ■ Vulnerability : mailnly inherited ■ Attack Initiation ■ Prodrome/Aura ■ ■ PAIN ■ Somatosensory input to the head involves pseudounipolar trigeminal and upper cervical branches 22
- 23. ■ The trigeminal nerve, which innervates the meninges, is intricately involved in migraine. ■ There is a connection between cortical spreading depression (CSD) and activation of trigeminal nerve afferents. ■ Specifically, triggering CSD leads to a long-lasting blood flow increase within the middle meningeal artery. This increase in blood flow is dependent upon trigeminal and parasympathetic activation. In addition, plasma protein leakage occurrs in the dura. ■ Central sensitization giving rise to cutaneous allodynia. ■ Peripheral sensitization in meningeal C fibres : aggravation of pain by bending over. 23
- 24. WORKUPAND INVESTIGATIONS ■ Migraine is a “Clinical Diagnosis” ■ Diagnostic investigations are performed due to following reasons : – Exclude structural and metabolic causes of headcahe – Rule out comorbid disease that could complicate headache and its treatment 24
- 25. Neuroimaging for all or not? ■ Neuroimaging is usually not necessary except ■ Onset of migraine after 5o years of age ■ Change in the pattern of previous migraine ■ First or worst severe headache ■ New onset of headache in a patient with cancer or HIV patient ■ Headache with an abnormal neurologic examination Headache with fever ■ Migraine and epilepsy ■ New daily persistent headache ■ Escalation of headache frequency/intensity in the absence of medication overuse headache ■ Posteriorly located headaches in children 25
- 26. Preferred modality 26 ■ Emergent CT examination is recommended for patients with sudden, severe, thunderclap headache or worst headache of life. ■ MRI is preferred in non urgent situations.
- 27. Other investigations ■ Visual field testing should be performed in patients with persistent visual phenomenon ■ Indications for lumber puncture include -: ■ 1. First or worst headache of a patients life ■ 2. Severe, rapid onset, recurrent headaches ■ 3. Progressive headaches ■ 4. Atypical chronic intractable headaches 27 Migraine Headache Workup Updated: Jan 30, 2018 ..medscape Author: Jasvinder Chawla, MD, MBA; Chief Editor: Helmi L Lutsep, MD
- 28. Management of migraine: Non pharmacological measures 28
- 29. Management of Migraine :Abortive therapy Specific agents 1. Triptans (5-HT agonist)- Sumatriptan : 50 -100 mg Take within 15 min of onset. Limit intake to 2 days/week Avoid in patients with HTN,IHD 2.Ergot derivatives – ergotamine 1-2 mg (nasal spray/iv) 29
- 30. Abortive therapy : nonspecific agents ■ Aspirin 900 mg ■ Acetaminophen 1000 mg ■ NSAIDS : – Naproxen – 500-1000 mg – Ibuprofen - 400 – 800 mg ■ Anti emetics by non oral route when accompanied by severe nausea / vomiting 30
- 31. Management of Migraine: Prophylactic agents Indication: ■ Frequency of attacks > 2 / month ■ Significant disability ■ Abortive therapy fails /or is used > 2/week / or is contraindicated ■ Migraine variants eg hemiplegic migraine or very long auras or attacks with a risk of permanent neurological injury 31
- 32. Drugs 1. Beta blocker- propanolol (80-240 mg/day) 2. CCB-Verapamil : 120 mg to 360mg daily 3. TCA- amitryptilline : 25 – 75mg od 4. Anticonvulsant- valproate 400-600mg bd & topiramate 50- 200 mg/day 32
- 34. 34
- 35. Interventions ■ Sphenopalatine ganglion block 35
- 36. GON BLOCK 36
- 37. PERIPHERAL NERVE STIMULATION ■ OCCIPITAL NERVE STIMULATION ■ SPHENOPALATINE GANGLION STIMULATION ■ TENS OF SUPRAORBITAL NERVE ■ NONINVASIVE VAGAL NERVE STIMULATION 37
- 38. Remember !!! ■ The history is the most important factor in establishing the diagnosis. ■ “A good headache history is never given, its taken” ■ Ask all patients to maintain a “ HEADACHE DIARY “ ■ Prophylactic treatments need atleast 2-3 weeks to have their effect … So don’t give up on a drug early. 38
- 39. "And I have learned now to live with it, learned when to expect it, how to outwit it, even how to regard it, when it does come, as more friend than lodger.We have reached a certain understanding, my migraine and I." - Joan Didion, author THANKYOU 39
Editor's Notes
- Pfo…cryptogenic stroke,decompression illness and migraine….as r-l shunt allow anp,vasoctive amines microeemboli to bypass the lungs and reach the brain.
- Acute migraine attacks occur in the context of an individual’s inherent level of vulnerability. The greater the vulnerability or lower the threshold, the more frequent attacks occur. Attacks are initiated when internal or environmental triggers are of sufficient intensity to activate a series of events which culminate in the generation of a migraine headache. We are all too familiar with the clinical phases of a migraine attack. Many migraineurs experience vague vegetative or affective symptoms as much as 24 hours prior to the onset of a migraine attack. This phase is called the prodrome and should not be confused with the aura phase. The aura phase consists of focal neurological symptoms that persist up to one hour. Symptoms may include visual, sensory, or language disturbance as well as symptoms localizing to the brainstem. Within an hour of resolution of the aura symptoms, the typical migraine headache usually appears with its unilateral throbbing pain and associated nausea, vomiting, photophobia, or phonophobia. Without treatment, the headache may persist for up to 72 hours before ending in a resolution phase often characterized by deep sleep. For up to twenty-four hours after the spontaneous throbbing has resolved, many patients may experience malaise, fatigue, and transient return of the head pain in a similar location for a few seconds or minutes following coughing, sudden head movement, or valsalva movements. This phase is sometimes called the migraine hangover.
- Paraesthesias are often cheiroaural :starts in hand Migrates upto arm and jumps to involve the face,lips and tongue
- Usually enters the resolution phase with sleep
- Attacks fulfilling criteria for 1.2.1 Migraine with typical aura and criterion B below No headache accompanies or follows the aura within 60 minutes.
- One or a few migraine attacks may be difficult to distinguish from symptomatic migraine-like attacks. Furthermore, the nature of a single or a few attacks may be difficult to understand. Therefore, at least five attacks are required. Individuals who otherwise meet criteria for 1.1 Migraine without aura but have had fewer than five attacks should be coded 1.5.1 Probable migraine without aura. When the patient falls asleep during migraine and wakes up without it, duration of the attack is reckoned until the time of awakening. In children and adolescents (aged under 18 years), attacks may last 2-72 hours (the evidence for untreated durations of less than two hours in children has not been substantiated). Migraine without aura often has a menstrual relationship
- Many patients who have migraine attacks with aura also have attacks without aura; they should be coded as both 1.2 Migraine with a ura and 1.1 Migraine without aura. Visual aura is the most common type of aura, occurring in over 90% of patients with 1.2 Migraine with aura, at least in some attacks. It often presents as a fortification spectrum: a zigzag figure near the point of fixation that may gradually spread right or left and assume a laterally convex shape with an angulated scintillating edge, leaving absolute or variable degrees of relative scotoma in its wake. In other cases, scotoma without positive phenomena may occur; this is often perceived as being of acute onset but, on scrutiny, usually enlarges gradually. In children and adolescents, less typical bilateral visual symptoms occur that may represent an aura. A visual aura rating scale with high specificity and sensitivity has been developed and validated. Next in frequency are sensory disturbances, in the form of pins and needles moving slowly from the point of origin and affecting a greater or smaller part of one side of the body, face and/or tongue. Numbness may occur in its wake, but numbness may also be the only symptom. Less frequent are speech disturbances, usually aphasic but often hard to categorize. Patients with aura symptoms arising from the brainstem are coded as 1.2.2 Migraine with brainstem aura, but they almost always have additional typical aura symptoms. When the aura includes motor weakness, the disorder should be coded as 1.2.3 Hemiplegic migraine or one of its subforms. 1.2.3 Hemiplegic migraine is classified as a separate subtype because of genetic and pathophysiological differences from 1.2.1 Migraine with typical aura. Patients with 1.2.3 Hemiplegic migraine often have brainstem symptoms in addition. Migraine aura is sometimes associated with a headache that does not fulfil criteria for 1.1 Migraine without aura, but this is still regarded as migraine headache because of its relation to the aura. In other cases, migraine aura may occur without headache. In the absence of headache fulfilling criteria for 1.1 Migraine without aura, the precise diagnosis of aura and its distinction from mimics that may signal serious disease (eg, transient ischaemic attack) becomes more difficult and often requires investigation. When aura occurs for the first time after age 40, when symptoms are exclusively negative (eg, hemianopia) or when aura is prolonged or very short, other causes, particularly transient ischaemic attacks, should be ruled out.
- Originally the terms basilar artery migraine or basilar migraine were used but, since involvement of the basilar artery is unlikely, the term migraine with brainstem aura is preferred. Dysarthria should be distinguished from aphasia. Vertigo does not embrace and should be distinguished from dizziness. This criterion is not fulfilled by sensations of ear fullness. Diplopia does not embrace (or exclude) blurred vision. The Glasgow Coma Scale (GCS) score may have been assessed during admission; alternatively, deficits clearly described by the patient allow GCS estimation. When motor symptoms are present, code as 1.2.3 Hemiplegic migraine. The term plegic means paralysis in most languages, but most attacks are characterized by motor weakness. Motor symptoms generally last less than 72 hours but, in some patients, motor weakness may persist for weeks.
- Retinal migraine is an extremely rare cause of transient monocular visual loss. Cases of permanent monocular visual loss associated with migraine have been described. Appropriate investigations are required to exclude other causes of transient monocular blindness.
- On ≥8 days/month for >3 months, fulfilling any of the following2: criteria C and D for 1.1 Migraine without aura criteria B and C for 1.2 Migraine with aura believed by the patient to be migraine at onset and relieved by a triptan or ergot derivative The most common cause of symptoms suggestive of chronic migraine is medication overuse, as defined under 8.2 Medication-overuse headache. Around 50% of patients apparently with 1.3 Chronic migrainerevert to an episodic migraine type after drug withdrawal; such patients are in a sense wrongly diagnosed as 1.3 Chronic migraine. Equally, many patients apparently overusing medication do not improve after drug withdrawal; the diagnosis of 8.2 Medication-overuse headache may be inappropriate for these (assuming that chronicity induced by drug overuse is always reversible). For these reasons, and because of the general rule to apply all relevant diagnoses, patients meeting criteria for 1.3 Chronic migraine and for 8.2 Medication-overuse headache should be coded for both. After drug withdrawal, migraine will either revert to an episodic type or remain chronic, and should be re-diagnosed accordingly; in the latter case, the diagnosis of 8.2 Medication-overuse headache may be rescinded.
- Occurring in a patient with 1.2 Migraine with aura, and during or within 1 hour after an attack of migraine with aura Typical of the previous attacks except for duration and severity
- At least five attacks of intense nausea and vomiting, fulfilling criteria B and C Stereotypical in the individual patient and recurring with predictable periodicity All of the following: nausea and vomiting occur at least four times per hour attacks last for ≥1 hour, up to 10 days attacks occur ≥1 week apart Complete freedom from symptoms between attacks Not attributed to another disorder1. Cyclic vomiting syndrome is typically a self-limiting episodic condition occurring in childhood, with periods of complete normality between episodes. The cyclic nature is the hallmark, and attacks are predictable. At least five attacks of abdominal pain, fulfilling criteria B–D Pain has at least two of the following three characteristics: midline location, periumbilical or poorly localized dull or “just sore” quality moderate or severe intensity At least two of the following four associated symptoms or signs: anorexia nausea vomiting pallor Attacks last 2-72 hours when untreated or unsuccessfully treated Complete freedom from symptoms between attacks Not attributed to another disorder1. Vertigo1 occurring without warning, maximal at onset and resolving spontaneously after minutes to hours without loss of consciousness At least one of the following five associated symptoms or signs: nystagmus ataxia vomiting pallor fearfulness Normal neurological examination an ilt of the head to either side, with or without slight rotation, remitting spontaneously after minutes to days At least one of the following five associated symptoms or signs: pallor irritability malaise vomiting ataxia2 Normal neurological examination between attacks
- Migraine should be regarded as neurovascular headache. Vulnerability is inherited This corresponds to the rate of the spreading oligemia that has been observed in studies of cerebral blood flow during aura (2,3). A positron emission tomography (PET) study of spontaneous migraine demonstrated a spreading, bilateral oligemia, which establishes that the phenomenon exists in migraine sufferers (4). It is interesting that headache starts when blood flow is still reduced (3), making it unlikely that vasodilatation is a cause of pain More likely, it is evoked by aberrant firing of neurons and related cellular elements characteristic of cortical spreading depression. Vascular changes follow changes in neuronal activity during the visual aura. It may be that in patients who experience the aura, the neurophysiological events which result in the visual or sensory symptoms also result in activation of trigeminal/cervical nociceptive
- CSD IS TRIGERRED WHEN ENHANCED CORTICAL ACTIVITY COINCIDES WITH OTHER TRIGERRING FACTORS The most important structures that register pain in the head are the large cranial vessels, proximal cerebral vessels and dural arteries and the large veins and venous sinuses Migraine is a primary brain disorder most likely involving an ion channel in the aminergic brain stem nuclei (), a form of neurovascular headache in which neural events result in dilation of blood vessels aggravating the pain and resulting in further nerve activation. It involves dysfunction of brain-stem pathways that normally modulate sensory input. The key pathway for the pain is the trigeminovascular input from the meningeal vessels. These nerves pass through the trigeminal ganglion and synapses on second-order neurons in the trigeminocervical complex, which then project through the quintothalamic tract and, after decussating in the brain stem, form synapses with neurons in the thalamus. A reflex connection exists between neurons in the pons in the superior salivatory nucleus, which results in a cranial parasympathetic outflow that is mediated through the pterygopalatine, otic, and carotid ganglia. This trigeminal-autonomic reflex is present in normal persons but is expressed most strongly in patients with trigeminal-autonomic cephalgias, such as cluster headache and paroxysmal hemicrania. It may also be active in migraine. Most migraine patients exhibit cutaneous allodynia inside and outside their pain- referred areas during migraine attacks. Burstein and colleagues studied the development of cutaneous allodynia in migraine by measuring the pain thresholds in the head and forearms of a patient at several points during the migraine attack (1, 2, and 4 hours after onset) and compared the pain thresholds in the absence of an attack. This study demonstrated that a few minutes after the initial activation of the patient’s peripheral nociceptors, these became sensitized and mediated the symptoms of cranial hypersensitivity. The barrage of impulses then activated second-order neurons and initiated their sensitization, mediating the development of cutaneous allodynia on the ipsilateral head. The sensitized second-order neurons activated and eventually sensitized third-order neurons leading to allodynia on the patients contralateral head and forearms by the two-hour point, a full hour after the initial allodynia on the ipsilateral head. The authors concluded that this progression of symptoms calls for the early use of antimigraine drugs that target peripheral nociceptors before central sensitization occurs. CSD is a well defined wave of neuronal excitation in the cortical grey matter that spreads from its site of origin at the rate of 2- 6mm/min ∗This cellular depolarization causes the primary cortical phenomenon aura phase, in turn, it activates trigeminal fibers causing headache. 9 Cutaneous Allodynia ∗ Secondary pain pathways of the trigeminophthalamic system become sensitized during a migraine attack. 10
- BALANCED LIFE WITH LESS HIGHS AND LOWS NEED TO KNOW THE TRIGGERS
- Status migranosus…intravenous valproate or ergotamine
- B blocker and valproate : very good combo in resistant migraine
- 1-2 g magnesium over 20 mins Magnesium sulphate 500mg or magnesium oxide 5oomg od
- Migraine headache is frequently concomitant with gastrointestinal symptoms, including nausea, vomiting, diarrhea, constipation, Moreover, infantile colic has been known as an early-life expression of migraine headache, with a maternal history of migraine predisposing to an approximately 2.6 times higher likelihood of colic than controls (3). Moreover, intestinal microbiota have been found to directly alter neurotransmitter levels, indicating the possibility of established communication between bacteria and neurons (12). Metabolites from gut mi- crobiota promote production of 5-hydroxytryptamine by intestinal epithelial cells and levels of serotonin are lower in the blood of germ-free animals compared with normal controls. bioactive peptides, amino acids, 4 probiotics (Lactobacillus acidophilus, L. bulgaricus, Enterococcus faecium, and Bifidobacterium bifidum) 90 days/ 12 weeks
- DT,ONSET,ENDING,SEVERITY,TRIGGERS.