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Headaches in Headaches in Primary CarePrimary Care
Steve Cobb MD
Residency Program Director
ESJH Family Medicine Residency
Headaches in Headaches in Primary CarePrimary Care
Steve Cobb MD
Residency Program Director
ESJH Family Medicine Residency
Headaches in Headaches in Primary Care – ObjectivesPrimary Care – Objectives
Use IHS criteria to diagnose common primary headache syndromes.
Treat common primary headaches.Recognize symptoms and signs associated
with secondary and worrisome headaches
Why Us?Why Us?
Family Physicians and Internists– Headache is the second most common pain
complaint seen in primary care– 63% of migraineurs see their PCP alone for
care– 18M patients visit PCPs per year for HA– Over 1,000 visits to the OU FMC annually
Case 1Case 1
26 year old female presents with CC of headache x 6 months. Headaches occur everyday, are usually unilateral, but not always. They often improve with Midrin, but sometimes she misses work when it fails. Sometimes she is nauseated enough that she vomits. Physical exam, including vital signs, fundoscopic, and neurologic exams are normal today.
Strategy for Headache Strategy for Headache Evaluation and TreatmentEvaluation and Treatment
1. Ensure this is a benign primary Headache disorder.
2. Determine the type. 3. Determine treatment goals and prioritize and
communicate them clearly. 4. Arrange for periodic review and oversight. 5. Know when to refer and to whom.
Clinical Approach to Clinical Approach to Headache Headache
How many headache types are there?Headache history for each typePhysical ExamDifferential DiagnosisIndications for NeuroimagingClassification Treatment
HistoryHistory
Age of onsetFrequencyCharacterAura or prodromeNeurologic symptomsPrecipitating factorsPMHx/Meds/Trauma/Procedures
Migraine auraMigraine aura
Visual disturbances confined to one field– phosphenes, eg, sparks, flashes, geometric forms – scotoma, area of diminished vision moving across visual field– scintillating scotoma, flickering spectrum at margin of scotoma
Sensory: unilateral paresthesias and/or numbnessWeakness, or more commonly a sense of limb
heaviness: unilateralSpeech: dysphasia
Migraine Aura: Scintillating Scotoma
Reprinted with permission from Fisher CM. Late-life (migrainous) scintillating zigzags without headache: one person’s 27-year experience. Headache. 1999;39:391-397.
PhysicalPhysical
BP, fundoscopy, temporal and scalp area palpation
Neuro Exam
Indications for NeuroimagingIndications for Neuroimaging
Abnormal neurologic findings
Confusion, somnolence Post-traumatic An isolated severe
headache Abrupt onset, or onset
during exercise Pain severe enough to
disturb sleep
Age less than 5 years Onset in late life Family history of
aneurysm or polycystic kidney disease
Consistently localized head pain
Progressively worsening
““SNOOP”SNOOP” Systemic symptoms-fever, weight loss, stiff neck, rash
Secondary risk factors-HIV, cancer, coagulopathy
Neurologic symptoms or signs-confusion, change in alertness or LOC
Onset is sudden-abrupt or split second onset
Older age at onset-new or progressive headache, first at age>50
Previous Headache history-first/worst headache, different progressive type, change in clinical features
Strategy for Headache Strategy for Headache Evaluation and TreatmentEvaluation and Treatment
1. Ensure this is a benign primary Headache disorder.
2. Determine the type. 3. Determine treatment goals and prioritize and
communicate them clearly. 4. Arrange for periodic review and oversight. 5. Know when to refer and to whom.
Make the diagnosisMake the diagnosis Pearls Pearls
Use a validated screening tool– ID Migraine TM
Listen (3 minute rule)Make a follow up appointment specifically
to discuss headache and do a careful neurologic exam
Headache diariesNeuro-imaging is seldom necessary
Make the Diagnosis Make the Diagnosis International Headache Society International Headache Society
ClassificationClassification Primary
– Migraine– Tension type– Cluster– “Miscellaneous
headache not associated with structural lesion”
Secondary– Increased (or decreased)
intracranial pressure– Vascular disorders
(Temporal arteritis)– Substance associated– Infection– Metabolic disorder– Trauma– Neuralgias– Associated with other
diseases of the cranium
Differential Diagnosis - PearlsDifferential Diagnosis - Pearls 90% of HA’s are Primary HA’s Life-threatening causes are rare Evaluate carefully for Secondary and life-
threatening HA’s– If exam is normal, then neuroimaging is usually normal– If history supports intracranial bleed and CT is normal, LP
Once you R/O Secondary HA….. Determine what type(s) of primary headache your
patient has.
Common Primary HeadachesCommon Primary Headaches
MigraineTensionClusterChronic Daily Headache
Migraine - EpidemiologyMigraine - Epidemiology
25 – 30 Million sufferers in the U.S.One year prevalence
– Women – 18%– Men – 6%
Many Still Undiagnosed – 14.6MLipton et al Headache 2001;41:638-645.
– Women – 49%– Men – 59%
2
Migraine: Diagnostic Criteria
At least 5 attacks that include• Headache lasting 4 to 72 hours• At least 2 of the following:
— Unilateral location— Pulsating quality— Moderate to severe intensity (inhibits or prohibits
daily activity)— Aggravated by climbing stairs or similar activity
• At least 1 of the following:— Nausea and/or vomiting— Photophobia and/or phonophobia
• Not attributable to other causes
Headache Classification Committee of the InternationalHeadache Society. Cephalalgia. 1988.
2 of these
1 of these
Make The Make The DiagnosisDiagnosis
Migraine - PathophysiologyMigraine - Pathophysiology
– The Neurovascular Theory = Vasodilatation may be secondary to Neurogenic Inflammation
Trigeminal Nerve Activation Dural Blood Vessel Dilation AND Inflammation
– 5HT 1B1D Receptors - Where Triptans Work 1B Cranial Blood Vessel Constriction 1D Inhibits Neurogenic Inflammation
CGRP: calcitonin gene-related peptide
NK: neurokinin A
SP: substance P
CGRPNKSP
5-HT1F5-HT1D
5-HT1B
Blood vessel
Trigeminal nerve
MOA of triptans
CONSTRICTION
INHIBITION
Adapted from Goadsby et al. Neurol Clin. 1997.
Proposed Mechanism of Action
Central ActivationCentral Activation
Periaqueductal Grey AreaTrigeminal Nucleus CaudalisCranial nerve stimulated by abnormal
signaling centrally
Strategy for Headache Strategy for Headache Evaluation and TreatmentEvaluation and Treatment
1. Ensure this is a benign primary Headache disorder.
2. Determine the type. 3. Determine treatment goals and prioritize
and communicate them clearly. 4. Arrange for periodic review and oversight. 5. Know when to refer and to whom.
Treatment GoalsTreatment Goals
Eliminate Pain and other associated symptoms
Preserve/Restore functionPrevention (reduce number and intensity of
headaches).
Migraine - TreatmentMigraine - Treatment
Non-pharmacologic effortsMedsTreat concomitant mood disordersFollow-up and re-evaluation
Migraine- Associated triggersMigraine- Associated triggers
-Menstruation, pregnancy, menopause-Hormonal contraceptives or hormone replacement therapy
-Intense or strenuous activity/exercise
-Sleeping too much/too little/jet lag
-Fasting/missing meals
-Bright or flickering lights
-Excessive or repetitive noises
Odors/fragrances/tobacco smoke
-Weather/seasonal changes
-High altitudes -Medications -Stress/stress letdown
Migraine Triggers - DietaryMigraine Triggers - Dietary
Probably: Monosodium
glutamate (MSG) (soy sauce, meat tenderizers, seasoned salt)
Alcoholic beverages (wine, beer, whiskey, etc.)
Possibly: Ripened cheeses (cheddar,
ernmenthaler, stilton, brie, camembert)
Sausage, bologna, salami, pepperoni, summer sausage, hot dogs, pizza
Herring (pickled or dried) Any food pickled, fermented,
or marinated Broad beans, lima beans,
fava beans, snow peas Caffeinated beverages (tea,
coffee, cola, etc.) Aspartame/phenylalanine-
containing foods or beverages
Non-pharmacologicNon-pharmacologic
Grade A Evidence– Relaxation Therapy– Thermal Biofeedback– Cognitive behavioral
therapy
Grade B Evidence– Behavioral therapy
with medication
Grade C Evidence– Hypnosis– Acupuncture– TENS Unit– Cervical spine
manipulation– Occlusal Adjustment– Hyperbaric O2
Pharmacologic Treatment Pharmacologic Treatment Episodic MigraineEpisodic Migraine
Prophylactic– Antiepileptics– Antidepressants– B-Blockers– CCB– NSAIDS– Serotonin Agonists– Vitamins and Herbs
Abortive– Specific
Triptans Ergots
– General Antiemetics NSAIDS Opioids Barbiturates Corticosteroids*
EvidenceEvidence
Prophylaxis– Level A
Depakote (Topamax) Sansert Propranolol
– Level B Tegretol Gabitrol Other B-blockers Verapamil Feverfew, B2, Mg
Abortive– Level A
Triptans Intra-nasal DHE
– Level B Exedrine in non-
disabling migraines Caffeine Corticosteroids in status
migranosis
Two Migraine Abortive Agents
Ergots• Acts on 5-HT1A, 1B, 1D,
1F, 2A and 2C receptors, also DA1 and DA2
• Relieves headache; can be taken during aura to abort attack
• Vomiting is a side effect of ergotamine (less with DHE)
Triptans• 5-HT1D and 1B receptor
agonists
• Relieves headache & associated symptoms
• May produce “triptan sensations” as side effects, eg, tightness in the chest and jaw
Triptans vs Analgesics:Triptans vs Analgesics:2-Hour Pain Free Response2-Hour Pain Free Response
0
10
20
30
40
50
60
70
80
Mild Moderate
Non-Triptan
Triptan
% of Attacks
25
73
10
48
Cady et al Clin Ther. 2000;22:1035-1048.
How do Triptans Work?
Selective 5-Hydroxytryptamine 1B/1Receptor Agonist (5-HT 1B/1D)
Two Theories Activation of 5HT1 receptors on cranial blood vessels
leads to vasoconstriction Activation of 5HT1 receptors on sensory nerve endings
in the trigeminal system results in inhibition of pro-inflammatory neuropeptide release
Triptan Treatment Pearls
• Acute Treatment (Abortive) for Patients with Diagnosed Migraine with and without Aura
• Do Not Use as Diagnostic Agent
• 18 years of age?
• Do not use Triptans and Ergotamines/DHE within 24 hours of each other.
• Triptans with Propanolol– Ergots + Propanolol = risk of severe vasoconstriction– Frovatriptan + Propanolol = hypotension/AV Block
Comparative TriptansAbortive Therapy – Selective 5-HT 1B/1D receptor agonists
Tmax Triptan Dose Formulations
2.5h Sumatriptan 25/50/100 (Imitrex) – 1991 T/SC/IN
2h Zolmitriptan 2.5/5 (Zomig) - 1997 T/DT
2.5h Rizatriptan 5/10 (Maxalt) T/DT
1-3h Naratriptan 2.5 (Amerge) T
1.5-3.8h Almotriptan 6.25/12.5 (Axert) T
2-4h Frovatriptan 2.5 (Frova) T
1-2h Eletriptan 20/40 (Relpax) T
Tepper SJ Headache. 2001;85:959-970
Stratified TherapyStratified Therapy
Behavior Modification (Avoid triggers)Preventive PharmacotherapyEarly treatment with specific therapy
– Ergotamine/DHE– Triptan
Rescue Medication– Anti-emetics– Analgesics
20
Efficacy of Eletriptan: Comprehensive Relief at 2 Hours
Relief of Photophobia, %
Headache response, %
Relief of Nausea, %
Relief of Phonophobia, %
Pain-free response, %
Placebo
0
20
40
60
4030
80
2010
40
60
80
80
40
60
80
Adapted from Mathew et al. Headache. 2003.
Sumatriptan was blinded using encapsulation. Encapsulated sumatriptan was bioequivalent to commercial tablets.
60
20 20
2040
*P<.001 vs placebo.
21
Efficacy of Eletriptan: Comprehensive Relief at 2 Hours
Relief of Photophobia, %
Headache response, %
Relief of Nausea, %
Relief of Phonophobia, %
Pain-free response, %
Placebo
0
20
40
60
4030
80
2010
40
60
80
80
40
60
80
Adapted from Mathew et al. Headache. 2003.
Sumatriptan was blinded using encapsulation. Encapsulated sumatriptan was bioequivalent to commercial tablets.
60*
*
*
* *
*P<.001 vs placebo. †P<.05 vs sumatriptan.
Sumatriptan 100 mg
20 20
2040
22
Efficacy of Eletriptan: Comprehensive Relief at 2 Hours
Relief of Photophobia, %
Headache response, %
Relief of Nausea, %
Relief of Phonophobia, %
Pain-free response, %
Placebo
0
20
40
60
4030
80
2010
40
60
80
80
40
60
80
Adapted from Mathew et al. Headache. 2003.
Sumatriptan was blinded using encapsulation. Encapsulated sumatriptan was bioequivalent to commercial tablets.
60
*†
*†
*†*†
*†
*
*
*
* *
*P<.001 vs placebo. †P<.05 vs sumatriptan.
Sumatriptan 100 mgEletriptan 40 mg
20 20
2040
Triptans• Prophylaxis• Cluster HA• Hemiplegic or Basilar Migraine• Pts with Known or Suspected Ischemic Heart Disease• Pts with Neurovascular Syndromes – CVA /TIA• Pts with ASPVD• Pts with Uncontrolled HTN• Pts with Severe Hepatic Impairment• Pts who have used another 5-HT1 agonist /DHE/Methysergide
within 24 hrs• With meds that are potent CYP3A4 Inhibitors• Pregnancy Category C
EpisodicTension-type EpisodicTension-type headacheheadache
A. At least 10 previous headache episodes fulfilling criteria B through D; number of days with such headaches: less than 180 per year or 15 per month
B. Headaches lasting from 30 minutes to 7 days
C. At least two of the following pain characteristics:
1. Pressing or tightening (nonpulsating) quality
2. Mild to moderate intensity (nonprohibitive)
3. Bilateral location 4. No aggravation from walking stairs
or similar routine activities
D. Both of the following: 1. No nausea or vomiting
2. Photophobia and phonophobia absent, or
only one is present
Treatment –Tension type Treatment –Tension type headacheheadache
Acute headaches may respond to aspirin, acetaminophen, or combinations with caffeine; NSAIDs; isometheptene combinations; butalbital combinations; and muscle relaxants.
a. Overuse may lead to rebound headaches.
b. Frequent butalbital use can also result in dependency
Frequent headache may require preventive medications
a. Tricyclic medications are generally more effective than SSRIs
b. Other migraine preventatives (see chapter migraine) may be helpful especially when tension-type and migraine are both present
Cluster headacheCluster headacheSevere unilateral orbital, supraorbital
and/or temporal pain, lasting 15-180 min.Headache accompanied by at least 1 of
the following signs ipsilateral with the pain: - Conjunctival injection - Miosis- Lacrimation - Ptosis- Nasal congestion - Eyelid edema- Forehead/facial sweating - Rhinorrhea
Attack frequency: q.o.d. to 8 per day.International Headache Society Diagnostic Criteria. Cephalalgia 1988; 8(suppl 7)
Typical Temporal Patterns in Cluster Headache: Typical Temporal Patterns in Cluster Headache: Individual AttacksIndividual Attacks
Typical Seasonal Patterns in Episodic Cluster Headache (IHS 3.1.2)1997
Day Time90 Minute Attack in Late Evening
Night TimeTwo Attacks Disturbing Sleep
1998
1999
2000
Episodic Cluster Headache Episodic Cluster Headache Evolving to Chronic Cluster (IHS 3.1.3.2)Evolving to Chronic Cluster (IHS 3.1.3.2)
Chronic Cluster Headache Unremitting from Onset (IHS 3.1.3.1)
Note: Attacks for more than 1 year with remission lasting less than 14 days
Note: Attacks daily or almost daily for more than one year
1998
1999
2000
1999
2000
Treatment - ClusterTreatment - Cluster
Acute– O2– Injectable triptans– Injectable ergotamines
Preventive– Steroids– Verapamil– AED’s
Chronic Daily HeadacheChronic Daily Headache
1. Headache 15 or more days per month
2. Includes different headache types
CDH – Transformed migraineCDH – Transformed migraine
Transformed migraine (chronic migraine) with or without medication overuse
1. Previous history of intermittent migraine usually by age 20-30
2. In 80%, gradual transformation from episodic to CDH which may be associated with analgesic overuse and psychological factors (depression, anxiety, abnormal personality profile, and home or work stress).
3. In 20%, sudden transformation which may be triggered by head or neck trauma, flulike illness, aseptic meningitis, and operations, and medical illnesses.
4. Migraine characteristics to a significant degree intermittently or
continuously
CDH –Hemicrania ContinuaCDH –Hemicrania Continua
Hemicrania continua with or without medication overuse
1. Rare entity with constant, unilateral pain of variable intensity.
2. Painful exacerbations associated with ptosis, lacrimation, and nasal stuffiness.
3. Responds dramatically to indomethacin.
Chronic Daily HeadacheChronic Daily Headache
Taper medications which may be causing rebound
a. The headaches may get worse before improving which may not occur before three to six weeks
b. For outpatients, headaches may lessen with the transitional use of a tapering dose of prednisone (60 mg for 2 days, 40 mg for 2 days, and 20 mg for 2 days) for 6 days or the combination of tizanidine and a long-acting NSAID
Inpatient Detox may be required
a. Fluids
b. Steroids
c. Reglan
d. DHE-45
e. Phenobarbitol
Medicines Associated with Medicines Associated with “Rebound” Headache“Rebound” Headache
AcetaminophenCaffergotOpioidsButalbitalTriptansMidrinNSAIDS
ReferralReferral
Wayne Wasemiller, M.D.– 302-2661
OU Neurology– Marc Lenarts, M.D.– Jim Couch, M.D.
Call 271-3635 ext 0 Call chief resident on call
Case 1Case 1
26 year old female presents with CC of headache x 6 months. Headaches occur everyday, are usually unilateral, but not always. They often improve with Midrin, but sometimes she misses work when it fails. Sometimes she is nauseated enough that she vomits. Physical exam, including vital signs, fundoscopic, and neurologic exams are normal today.