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Migraine Overview PowerPoint Presentation

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Description : Check out this medical PowerPoint presentation titled "Migraine Overview” by David Watson, MD.

This medical PowerPoint presentation is about migraine, a neurological condition that affects millions of people worldwide. It is characterized by recurrent headaches that can be moderate to severe in intensity and are often accompanied by other symptoms such as nausea, vomiting, and sensitivity to light and sound.

Migraines are believed to be caused by changes in the brain and its interactions with the bodys nervous and vascular systems. These changes can be triggered by a variety of factors, including stress, certain foods, hormonal changes, and changes in sleep patterns.

There are two main types of migraines-migraine with aura and migraine without aura. Migraine with aura is characterized by the presence of visual or other sensory disturbances that typically occur before the headache, while migraine without aura does not have these pre-headache symptoms.

Treatment for migraines can include medication, lifestyle changes, and other therapies such as acupuncture or cognitive-behavioral therapy. While migraines can be a chronic condition, with proper treatment and management, many people are able to manage their symptoms and live a full, active life.

Tags : migraine, Neurology, Neurology PowerPoint presentation

Published on : Jun 07, 2023 | Views : 888 | Downloads : 0

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Slide 1-

Migraine Overview David Watson, MD Director, WVU Headache Center
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EPIDEMIOLOGY AND IMPACT Resolving barriers to care requires several interventions Migraine is a common, often disabling disease of the nervous system The burden of migraine is greatest for the most severely affected people Despite improvements, migraine remains underdiagnosed and undertreated
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There are currently 36 million people with migraine age 12+ in the United States 27 million female 9 million male MIGRAINE PREVALENCE (American Migraine Study II) Lipton RB et al. Headache. 2001. Nearly 1 in 4 households has at least 1 person with migraine Migraine prevalence peaks between the ages of 25–55
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MIGRAINE IS MORE COMMON THAN ASTHMA AND DIABETES COMBINED Data from the Centers for Disease Control & Prevention, US Census Bureau, and the Arthritis Foundation. Hauser & Kuland, Hauser et al., Epilepsia 1993. 1% 7% 6% 7% 13% 0% 5% 10% 15% 20% Migraine Osteoarthritis Diabetes Asthma Rheumatoid Arthritis Epilepsy 0.5%
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ONE-YEAR PREVALENCE OF COMMON HEADACHE DISORDERS Lipton RB et al. Headache. 2001; Schwartz BS et al. JAMA. 1998; Scher AI et al. Headache. 1998. Female Male
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AGE- AND GENDER-SPECIFIC PREVALENCE OF MIGRAINE Migraine Prevalence (%) Age (Years) Lipton RB et al. Headache. 2001.
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BURDEN OF MIGRAINE Individual burden Hu HX et al. Arch Intern Med. 1999. Stewart WF et al. Cephalalgia. 1996. Societal burden Direct costs $2.5 billion per year Indirect costs $13-31 billion per year Absenteeism Reduced effectiveness Burden disproportionately distributed 51% females with migraine 93% of work loss due to migraine 38% males with migraine 85% work loss due to migraine
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WHAT IS MIGRAINE? Disorder characterized by episodic attacks of head pain and associated symptoms, such as nausea, sensitivity to light, sound, or intolerance to head movement Inherited tendency Neurobiologically based, common clinical problem
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GENETIC BASIS Twin studies: MZ > DZ Ion channelopathy – Familial hemiplegic migraine 1A subunit of the P/Q voltage-gated Ca2+ channel on chromosome 19 (~50% of cases) Mutation in gene ATP1A2 (encodes alpha2 subunit of Na+/K+ pump) results in loss of function of single ATP1A2 allele (chromosome 1) Linked to regular migraine Genetically heterogeneous EXCITATION SOUND
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SENSITIVE BRAIN People with Migraine have altered neuro-physiologic responses between attacks Stabbing headache (“ice-pick” pains) Enhanced sensory processing visual auditory
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TRIGGERING MIGRAINE Episodes may recur regularly as if initiated by an internal clock located in the hypothalamus Attacks may originate in the nervous system in response to stress or excessive afferent stimulation, such as flickering light or noise Some triggers act primarily on the cranial blood vessels; craniovascular afferents may then excite central pathways For many patients no factor can be identified
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THE NEUROVASCULAR THEORY Goadsby PJ et al. N Engl J Med. 2002.
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THE NEUROVASCULAR THEORY Referred pain from dura mater and blood vessels Peripheral neural processing Neurogenic plasma protein extravasation (PPE) Neuropeptides Central neural processing Migraine is a neurovascular pain syndrome
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CUTANEOUS ALLODYNIA Burstein R et al. Brain. 2000. 1-Peripheral Trigeminal Sensitization 2-Central Trigeminal Sensitization 3-Forehead Allodynia 4-Thalamic Sensitization 5-Extracephalic Allodynia 1 4 2
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CLINICAL PRESENTATION OF HEADACHES Secondary Infection Hemorrhage Increased ICP Brain tumor Primary Migraine Tension-type (TTH) Cluster Other (eg, benign cough headache)
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WORRISOME HEADACHE RED FLAGS“SNOOP” Older: new onset and progressive headache, especially in middle-age >50 (giant cell arteritis) Systemic symptoms (fever, weight loss) or Secondary risk factors (HIV, systemic cancer) Neurologic symptoms or abnormal signs (confusion, impaired alertness, or consciousness) Onset: sudden, abrupt, or split-second Previous headache history: first headache or different (change in attack frequency, severity, or clinical features)
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A. At least five attacks fulfilling criteria B–D B. Headache attacks lasting 4-72 hours (untreated or unsuccessfully treated) C. Headache has at least two of the following four characteristics: 1. unilateral location 2. pulsating quality 3. moderate or severe pain intensity 4. aggravation by or causing avoidance of routine physical activity (e.g. walking or climbing stairs) D. During headache at least one of the following: 1. nausea and/or vomiting 2. photophobia and phonophobia E. Not better accounted for by another ICHD-3 diagnosis ICHD-3 Beta Diagnostic Criteria Migraine without Aura
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IHS MIGRAINE AND TENSION-TYPE HEADACHE 5 attacks lasting 4–72 h 2 of the following 4 Unilateral Pulsating Moderate or severe intensity Aggravation by routine physical activity 1 of the following Nausea and/or vomiting Photophobia and phonophobia Not attributable to another disorder Migraine Tension 10 attacks lasting 30 min–7 days 2 of the following 4 Bilateral Pressing/tightening (Not pulsating) Mild or moderate intensity Not aggravated by routine physical activity No nausea or vomiting One or neither photophobia or phonophobia Not attributable to another disorder
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IMPORTANT DIAGNOSTIC CONSIDERATIONS Recurring moderate-to-severe headache is migraine until proven otherwise Russell MB et al. Cephalalgia. 1996. Pryse-Phillips WEM et al. Can Med Assoc J. 1997. No single criterion necessary nor sufficient for diagnosis 15% of patients have a neurological aura IHS criteria do not require GI symptoms Vomiting occurs in < 1/3 of patients 41% of migraine patients report bilateral pain 50% of the time, pain is non-pulsating
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UNDIAGNOSED MIGRAINE SUFFERERS OFTEN RECEIVE OTHER MEDICAL DIAGNOSES Lipton RB et al. Headache. 2001.
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DIAGNOSIS TESTINGCT AND MRI Consensus expert opinion MRI is more sensitive Role of CT or MRI in patients with nonmigraine headache is unclear In patients with recurrent migraine, neither CT nor MRI is warranted except in cases with: Recent substantial change in headache pattern History of seizures Focal neurologic symptoms or signs Report of Quality Standards Subcommittee of AAN. Neurology. 1994.
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STRATEGIES FOR MIGRAINE TREATMENT Preemptive treatment Migraine trigger time-limited and predictable Preventive treatment Decrease in migraine frequency warranted Acute treatment To stop pain and prevent progression Silberstein SD, Goadsby PJ. Cephalalgia. 2002.
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ACUTE MIGRAINE MEDICATIONS Nonspecific NSAIDs Combination analgesics Opioids? Neuroleptics/antiemetics Corticosteroids Specific Ergotamine/DHE Triptans CGRP antibodies?
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ACUTE TREATMENT PRINCIPLES Early intervention Use correct dose and formulation Use a maximum of 2–3 days/week     Use preventive therapy in selected patients  Stratified care Silberstein SD. Neurology. 2000; Lipton RB, et al. JAMA. 2000.
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TRIPTANS As a class, relative to nonspecific therapies, triptans provide Rapid onset of action High efficacy Favorable side effect profile Adverse events and contraindications Selective 5-HT1B/1D/1F agonists Silberstein SD. Neurology. 2000.
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HOW DO SPECIFIC MEDICATIONS WORK? Trigeminovascular Antimigraine Targets Hargreaves RJ et al. Can J Neurol Sci. 1999. (Modified)
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TRIPTANS:TREATMENT CHOICES Are there differences between the triptans? If one triptan fails, will another triptan work? Zolmitriptan Tablet & melt (2.5, 5 mg) Nasal spray (5 mg) Rizatriptan Tablet & melt (5, 10 mg) Naratriptan Tablet (1, 2.5 mg) Almotriptan Tablet (6.25, 12.5 mg) Frovatriptan Tablet (2.5 mg) Sumatriptan Tablet (25, 50, 100 mg) Injection (3, 4, 6 mg) Nasal spray (5, 20 mg) Breath Powered Nasal Ferrari MD et al. Lancet. 2001. Eletriptan Tablet (20, 40 mg)
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ROUTES OF ADMINISTRATION Suppositories: antiemetics, ergots, opioids Oral therapies: most medications Nasal sprays: sumatriptan, DHE, zolmitriptan Injectable (SL, IM, IV) sumatriptan, DHE, injectable NSAIDs, neuroleptics
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TREAT MIGRAINE WHEN PAIN IS MILD P<0.02* vs. placebo Moderate or Severe Mild Mild headache: N=40 sumatriptan; N=6 placebo Moderate/severe headache: N=130 sumatriptan; N=36 placebo Cady RK et al. Headache. 2000 % of Attacks Pain Free *post-hoc analysis
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PRESENCE OF CUTANEOUS ALLODYNIA PREDICTS TRIPTAN EFFICACY % of patients achieving pain-free Burstein R et al. Headache. 2002. (abstract; preliminary analysis) Triptans lead to a reduction in pain intensity, but only 20% achieved pain-free status Triptans relieve throbbing in all patients, regardless of presence of allodynia at time of treatment n=20 10
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TREATING WITHIN 15 MIN OF PAIN ONSET IMPROVES PAIN-FREE RATES <15 min onset of pain 2 11 20 16 6 19 43 57 0 10 20 30 40 50 60 30 60 90 120 Zolmitriptan 2.5 mg tablet Placebo Pain-free Response (% patients) Time post-treatment (min) *p<0.01 vs placebo;**p<0.0001 vs placebo 15 25* 43** 14 18 <4 H of onset of pain Klapper et al. Neurology. 2002. (abstract;)
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REBOUND Rebound: Recurring headache induced by repetitive and chronic overuse of acute headache medication Prevention: Limit frequency and dose of medications Treatment: Withdrawal and washout of overused medication; consider using preventives Capobianco DJ et al. Headache. 2001.
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NON-DRUG SYMPTOM MANAGEMENT Quiet/White noise Dim Light (NO SCREENS!) Cool Temp Fluids Ignore? Setting Expectations – when will you return to class
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HEADACHE TREATMENT: OPIOIDS AND BUTALBITAL Opioids Danger of abuse: restrict use Major concerns are overuse, drug-induced headache, and withdrawal No controlled studies have established their efficacy in migraine Use should be limited and carefully monitored Butalbital Combination Analgesics Silberstein SD et al. Wolff’s Headache And Other Head Pain. 2001. WHO USES THEM…?
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GUIDELINES: WHEN TO USE PREVENTIVE MANAGEMENT Uncommon migraine conditions Silberstein SD et al. Wolff’s Headache And Other Head Pain. 2001. Migraine significantly interferes with patient’s daily routine, despite acute Rx Acute medications contraindicated, ineffective, intolerable AEs, or overused Frequent headache (3 attacks per month?) Patient preference
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GOALS OF PREVENTIVE TREATMENT Silberstein SD et al. Headache in Clinical Practice. 2nd ed. 2002. Decrease attack frequency (by 50%), intensity, and duration Improve responsiveness to acute Rx Improve function and decrease disability
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PREVENTIVE MEDICATIONS:DRUG CLASSES Ca2+-Channel blockers Silberstein SD. Cephalalgia. 1997. Antiepileptics Antidepressants -Blockers NSAIDs 5-HT antagonists Other Vitamins Minerals Herbs Angiotensin antagonists Neurotoxins
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NONPHARMACOLOGIC TREATMENT:POTENTIAL INDICATIONS Goslin RE et al. Behavioral and Physical Treatments for Migraine Headache. 1999. Patient preference Poor tolerance, response, or contraindications to drug therapy Pregnancy, planned pregnancy, or nursing History of overuse Significant life stress or deficient stress-coping skills
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NONPHARMACOLOGIC TREATMENTS Insufficient evidence to recommend: GRADE C Acupuncture TENS Cervical manipulation Occlusal adjustment Hyperbaric oxygen Hypnosis Goslin RE et al. Behavioral and Physical Treatments for Migraine Headache. 1999. Effective: GRADE A Relaxation training Thermal biofeedback with relaxation training EMG biofeedback Cognitive behavioral therapy The benefits of behavioral therapy (eg, biofeedback, relaxation) are in addition to preventive drug therapy (eg, propranolol, amitriptyline): GRADE B
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Questions?