MEGHANA DORESWAMY MDNEUROLOGY AND SLEEP

MEDICINESEPTEMBER 6, 2015

Management of migraine headaches in adults for primary care physician

Objectives

Diagnostic criteria and pathophysiology of migraine headache.

Epidemiology and impact of migraine headacheTreatment of acute migraine headache.Preventive therapy for migraine headaches.

.

A 32-year-old male presents with worsening headache

He has had headaches since 23, they have always been under and around eyes

He has a history of sinus trouble Headaches are associated with

photophobia/osmophobia/occasional loss of appetite

Pain is a dull pulsing pain, better with sleeping.

Diagnosis???

What type of headache is this?

Migraine vs. Sinus headache

Studies show that about 85% of people with self described sinus headaches actually have migraine headaches.

Sinus problems, like many other things trigger migraine headaches

Bottom line– the majority of headaches severe enough to cause a person to seek medical attention are Migraines

45% of migraine patients report sinus symptoms including rhinorrhea, nasal congestion and lacrimation.

Case 2

A 36 yr female presents with worsening headaches.

Started 2 years ago, occurred 2x per month, associated with N/V/photophobia/phonophobia

She has constant, background, holocephalic headache associated with continuous photophobia for three months, rated 6/10

Exacerbations- 4x /week, severe throbbing with worsened photophobia, phonophobia and nausea, last up to 24 hrs

Sumatriptan 100 mg has not been effective

Diagnosis?

Cluster headacheRebound headacheChronic migraine headacheChronic tension headache

Tension-Type Migraine

Mild

Moderate

Severe

Unilateral

Bilateral

Photophobia

Nausea

Throbbing

Pressure

Aura

Vomiting

Aggravated by Activity

© 2002 Primary Care Network

Tension-type Headache or Migraine

Dilemma in diagnosis of migraine headaches

Visual aura only 15-20% of migraineurs

Head pain can be non-throbbing in ~40% of patients

Head pain can be bilateral in ~ 43% of patients

Sinus pain and pressure, stuffiness, rhinorrhea & weather association is often present in up to 97% of migraine attacks

Neck pain is often present in up to 75% of migraine attacks

Migraine without aura

Diagnostic criteria:A. At least 5 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 characteristics:

unilateral location pulsating quality moderate or severe pain intensity aggravation by or causing avoidance of routine physical activity (eg,

walking or climbing stairs) D. During headache at least one of the following:

nausea and/or vomiting photophobia and phonophobia

Not attributed to another disorder ICHS classification

Migraine with Aura

Diagnostic criteria:A. At least 2 attacks fulfilling criterion BB. Migraine aura fulfilling criteria B and C for one of the subforms 1.2.1-1.2.6C. Not attributed to another disorder.

Note:History and physical and neurological examinations do not suggest any of secondary disorders , or history and/or physical and/or neurological examinations do suggest such disorder but it is ruled out by appropriate investigations, or such disorder is present but attacks do not occur for the first time in close temporal relation to the disorder.

Migraine aura subforms

1.2.1 Typical aura with migraine headache1.2.2 Typical aura with non-migraine headache1.2.3 Typical aura without headache1.2.4 Familial hemiplegic migraine1.2.5 Sporadic hemiplegic migraine1.2.6 Basilar migraine

Retinal migraine

Diagnostic criteria:A. At least 2 attacks fulfilling criteria B and CB. Fully reversible monocular positive and/or negative visual phenomena (eg, scintillations, scotomata or blindness) confirmed by examination during an attack or (after proper instruction) by the patient's drawing of a monocular field defect during an attackC. Headache fulfilling criteria B-D for 1.1 .Migraine without aura begins during the visual symptoms or follows them within 60 minutesD. Normal ophthalmological examination between attacksE. Not attributed to another disorder.

Comment:Some patients who complain of monocular visual disturbance in fact have hemianopia. Other causes of transient monocular blindness (amaurosis fugax), such as optic neuropathy or carotid dissection, must be excluded.

Negative scotoma. Loss of local awareness of local structure

Positive Scotoma. Additional structures One side loss of perception.

Zigzag structure

Phases of migraine

Chronic migraine headaches

Migraine headache occurring on 15 or more days per month for more than 3 months in the absence of medication overuse.

Diagnostic criteria:Headache fulfilling criteria C and D for  Migraine

without aura on ≥15 days/month for >3 monthsNot attributed to another disorder.

Figure 2. One-year period prevalence of migraine by age and sex adjusted for demographics.

R. B. Lipton et al. Neurology 2007;68:343-349

©2007 by Lippincott Williams & Wilkins

Figure 3. One-year period prevalence of migraine by sex and household income.

R. B. Lipton et al. Neurology 2007;68:343-349

©2007 by Lippincott Williams & Wilkins

Prevalence of primary headache types in waiting room

Migraine Burden in U.S.

Migraineur in one in four households28 million migraineurs in the USEstimated annual cost of labor lost to migraine

greater than $ 13 billion per yearPeak prevalence ages 25-55 Often ineffectively treated.

Migraine Pain Intensity and Disability

0

10

20

30

40

50

Mild ModeratelySevere

Severe ExtremelySevere

>75% Report Severe to Extremely Severe Pain

Lipton RB et al. Headache. 2001;41:638-645.

Patients

(%)

39%

Some Impairment

9% Function Normally

53%

Severe Impairment or Bed Rest

Required

Pathophysiology of migraine headache

Harold G Wolff, a pioneer of the vascular theory of migraine, proposed that the neurological symptoms of the migraine aura were caused by cerebral vasoconstriction, and the headache by vasodilatation.

This had been replaced by cortical spreading depression theory of Leao(neural theory)

Most recent theory- migraine neurovascular phenomenon

Pathophysiology of migraine headache

Pathophysiology of migraine headache

Genetic predisposition to migraine headaches

The concordance for migraines is higher in monozygotic than dizygotic twins.

The first three types of familial hemiplegic migraine (FHM) are channelopathies. FHM1 is caused by mutations in the CACNA1A gene, FHM2 by mutations in the ATP1A2 gene, and FHM3 by mutations in the SCN1A gene. Mutations in the PRRT2 gene also cause some cases of familial hemiplegic migraine

Genetic basis is more complex- and increases individuals susceptibility to migraine headaches

Environmental factors

Principles of migraine management

Life style management- with patient educationAvoid medication rebound headacheAbortive therapyPreventive therapy.

Lifestyle Management

Sleep 8 hours consistent schedule Eat 3 regular meals (or more) per day Drink lots of fluids Get Aerobic exercise regularly Limit caffeine (or better yet avoid completely) Identify your triggers Keep a headache diary Manage stress Use correct posture and pause during repetitive

activities

Acute (abortive) migraine treatment principles

Treat early, while headache is building, within 15-30 minutes of onset.

Use correct dose and formulationLimit to 3 days per week (with exceptions)Try drug with at least 2 headaches to see if it

works before moving on to another agentUse drug combinations often work when a single

agent won’t work

Acute treatment options

Nonspecific NSAIDs simple analgesics combination analgesics Anti-Nausea meds

Promethazine,metoclopramide, prochloroperazine.

Ondansetron

Specific Triptans

- Faster onsetSumatriptan, Zolmitriptan,eletriptan, rizatriptan and almotriptanTriptans Slower Onset Naratriptan and Frovatriptan

-Ergotamine/DHE; Migranol

Triptan therapy

As a class triptan in relation to non specific medicationsRapid onset of reliefHave higher efficacy .Favorable side effect

Adverse effects- flushing, chest pain.Contraindicated in patients with coronary artery disease, angina, patients with hemiplegic or basilar migraines, severe uncontrolled hypertension.

Formulations

Oral therapies- Most medicationsNasal sprays- Sumatriptan, Zolmitriptan, DHE ButarphanolInjectables(IM/SC/IV)- Sumatriptan, DHE,

neuroleptics, injectable NSAIDsTransdermal Patch- Sumatriptan 6.5 mgSuppositories- antiemetics,ergots, opioids.

Adapted -Marmura et al, Headache 2015;55:3-20

Proven effective with more than 1 randomized control trial

Resistant acute migraine therapy

If acute treatment is still inadequate

Change formulation or dosage.Use adjunctive therapyConsider addition of preventive agentEvaluate for medication overuse, excessive caffeine

use.Reconsider diagnosis.

Mechanism of action of migraine medications

When to start migraine preventive therapy

Migraine significantly interferes with patient’s routine despite acute Rx

Frequent headaches> or = 2/ week.Acute therapy is ineffective, contraindicated or

ineffective.Patient preference.

Principles of preventive therapy

In order for preventive meds to be most effective, limit acute meds to 3 days per week

Make sure to use an appropriate dose At least a 2 month trial at a proper dose is required Goal is to decrease headache freq by 50% Evaluate headache therapy(use headache log), attempt to

lower and discontinue therapy when well controlled. Assess for coexisting conditions.

AAN/AHS guideline for migraine prophylaxis

AAN/AHS guideline for migraine prophylaxis

Nonpharmacologic Treatments

Biofeedback Relaxation therapy Cognitive Behavioral Therapy Acupressure Acupuncture Physical Therapy Chiropractic treatment

Additional Treatment Measures

Occipital Nerve Stimulators

TENS units

Transcranial Magnetic Stimulator

Special Diets

Botox Injections- Approved by FDA in Oct 2010. Approved for chronic migraine (migraine headaches more than 15 days/ month)31 injection sites in forehead, temples, shoulders and neck

Emerging therapy in migraine management

Monoclonal antibodies (mAbs) targeting calcitonin gene-related peptide (CGRP) and its receptor.

5-HT1F receptor agonist lasmiditan and glial cell modulator ibudilast.

Neuro-modulation for migraine headache- sphenopalatine ganglion stimulation, trigeminal nerve stimulation and transcutaneous vagus nerve stimulation.

Questions?