Management of migraine headaches for primary care physician

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Management of migraine headaches in
adults for primary care physician
MEGHANA DORESWAMY MD
NEUROLOGY AND SLEEP
MEDICINE
SEPTEMBER 6, 2015
Objectives
 Diagnostic criteria and pathophysiology of migraine
.
headache.
 Epidemiology and impact of migraine headache
 Treatment of acute migraine headache.
 Preventive therapy for migraine headaches.
What type of headache is this?
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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???
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
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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 headache
 Rebound headache
 Chronic migraine headache
 Chronic tension headache
Tension-type Headache or Migraine
Mild
Moderate
Severe
Unilateral
Bilateral
Photophobia
Nausea
Aura
Vomiting
Aggravated
by Activity
Throbbing
Pressure
Tension-Type
Migraine
© 2002 Primary Care Network
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
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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 B
B. Migraine aura fulfilling criteria B and C for one of the subforms 1.2.11.2.6
C. 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 headache
 1.2.2 Typical aura with non-migraine headache
 1.2.3 Typical aura without headache
 1.2.4 Familial hemiplegic migraine
 1.2.5 Sporadic hemiplegic migraine
 1.2.6 Basilar migraine
Retinal migraine
Diagnostic criteria:
A. At least 2 attacks fulfilling criteria B and C
B. 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 attack
C. Headache fulfilling criteria B-D for 1.1 .Migraine without aura begins
during the visual symptoms or follows them within 60 minutes
D. Normal ophthalmological examination between attacks
E. 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.
Zigzag structure
Negative scotoma. Loss of local awareness of local structure
Positive Scotoma. Additional structures
One side loss of perception.
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 months
 Not 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 households
 28 million migraineurs in the US
 Estimated annual cost of labor lost to migraine greater
than $ 13 billion per year
 Peak prevalence ages 25-55
 Often ineffectively treated.
Migraine Pain Intensity and Disability
9% Function Normally
>75% Report Severe to
Extremely Severe Pain
50
40
53%
39%
Severe
Impairment
Some
or Bed Rest Impairment
Required
Patients
(%)
30
20
10
0
Mild
Moderately
Severe
Severe
Extremely
Severe
Lipton RB et al. Headache. 2001;41:638-645.
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 education
 Avoid medication rebound headache
 Abortive therapy
 Preventive 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
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minutes of onset.
Use correct dose and formulation
Limit to 3 days per week (with exceptions)
Try drug with at least 2 headaches to see if it works before
moving on to another agent
Use drug combinations often work when a single agent
won’t work
Acute treatment options
 Specific
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Triptans
- Faster onset
Sumatriptan,
Zolmitriptan,eletriptan,
rizatriptan and almotriptan
Triptans Slower Onset
Naratriptan and Frovatriptan
-Ergotamine/DHE; Migranol
 Nonspecific
NSAIDs
 simple analgesics
 combination analgesics
 Anti-Nausea meds
Promethazine,metoclopramide,
prochloroperazine.
 Ondansetron
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Triptan therapy
As a class triptan in relation to non specific medications
 Rapid onset of relief
 Have 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 medications
 Nasal sprays- Sumatriptan, Zolmitriptan, DHE
Butarphanol
 Injectables(IM/SC/IV)- Sumatriptan, DHE, neuroleptics,
injectable NSAIDs
 Transdermal Patch- Sumatriptan 6.5 mg
 Suppositories- antiemetics,ergots, opioids.
Proven effective with more than 1 randomized control
trial
Adapted -Marmura et al, Headache 2015;55:3-20
Resistant acute migraine therapy
If acute treatment is still inadequate
 Change formulation or dosage.
 Use adjunctive therapy
 Consider addition of preventive agent
 Evaluate 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
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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?
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