Headaches in Primary Care Steve Cobb MD Residency Program Director ESJH Family Medicine Residency Brother at Medford

Headaches in Primary Care Steve Cobb MD Residency Program Director ESJH Family Medicine Residency Brother at Medford

Headaches in Primary 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 To keep you from getting a headache.

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 Why isn’t this a problem for neurologists? Medical Director CPN – Neurology referral problems. Bimodal population of mild and very severe At annual AHS meeting, over half of the attendees self reported migraines. I’m a convert. I used to hate to see this CC on the schedule.

Case 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 Evaluation 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. Longstanding vs. new. Normal neuro exam. Is it worrisome? Is it migraine? Migraine, Tension, Cluster, Complicated/Mixed Communicate what they are. Limit narcs and sedative/hypnotics If weird or not better, punt

Clinical Approach to Headache How many headache types are there? Headache history for each type Physical Exam Differential Diagnosis Indications for Neuroimaging Classification Treatment

History Age of onset Frequency Character Aura or prodrome Neurologic symptoms Precipitating factors PMHx/Meds/Trauma/Procedures

Migraine 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 numbness Weakness, or more commonly a sense of limb heaviness: unilateral Speech: dysphasia

Migraine Aura: Scintillating Scotoma Slide to remind me to remind you of what you already know : 90% Migraine is without aura Reprinted with permission from Fisher CM. Late-life (migrainous) scintillating zigzags without headache: one person’s 27-year experience. Headache. 1999;39:391-397.

                                                            

Physical BP, fundoscopy, temporal and scalp area palpation Neuro Exam

Indications 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” 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 Evaluation 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. Longstanding vs. new. Normal neuro exam. Is it worrisome? Is it migraine? Migraine, Tension, Cluster, Complicated/Mixed Communicate what they are. Limit narcs and sedative/hypnotics If weird or not better, punt

Make the diagnosis 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 diaries Neuro-imaging is seldom necessary Since so many patients suffer without being diagnosed or by being misdiagnosed, what can we do better. Listen well, at least once. 3 minute rule. Don’t accept previous dx. Take a hx for each H/a type. Self prompted ROS, or nurse-driven.

Make the Diagnosis International Headache Society Classification 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 - 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 Headaches Migraine Tension Cluster Chronic Daily Headache

Migraine - Epidemiology 25 – 30 Million sufferers in the U.S. One year prevalence Women – 18% Men – 6% Many Still Undiagnosed – 14.6M Lipton et al Headache 2001;41:638-645. Women – 49% Men – 59% …whether we want to hear it or not! Misdiagnosis and Missed diagnoses are felt to be a big problem for all of who treat H/A, not just us FP’s, etc.

Great slide, older data. Shows we’re getting better at making the dx.

Make The Diagnosis S evere U nilateral L ocation T hrobbing A ctivity 2 of these L ocation Make The Diagnosis T hrobbing A ctivity Critical elements of IHS diagnostic criteria. Episodic. Lasts 4-72 hours. 5 similar attacks 2 of first: Unilat location N ausea 1 of these S ensory

Migraine - 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 Primary etiology is more akin to seizure than chronic pain or vascular models.

Central Activation Periaqueductal Grey Area Trigeminal Nucleus Caudalis Cranial nerve stimulated by abnormal signaling centrally

Strategy for Headache Evaluation 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. Longstanding vs. new. Normal neuro exam. Is it worrisome? Is it migraine? Migraine, Tension, Cluster, Complicated/Mixed Communicate what they are. Limit narcs and sedative/hypnotics If weird or not better, punt

Treatment Goals Eliminate Pain and other associated symptoms Preserve/Restore function Prevention (reduce number and intensity of headaches).

Migraine - Treatment Non-pharmacologic efforts Meds Treat concomitant mood disorders Follow-up and re-evaluation

Migraine- 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 - 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-pharmacologic Grade A Evidence Grade B Evidence Grade C 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 Episodic Migraine Prophylactic Antiepileptics Antidepressants B-Blockers CCB NSAIDS Serotonin Agonists Vitamins and Herbs Abortive Specific Triptans Ergots General Antiemetics NSAIDS Opioids Barbiturates Corticosteroids* Prophylactics. Depakote – A, topamax less weight gain Tegretol, Gabitrol – B Elavil – A, Prozac – B Propranolol – A, other B-blockers B (lopressor and BBB) Verapamil-B ASA, ketoprofen, naprosyn – B Sansert – A, but… feverfew, B2, Mg – B Abortive. triptans –all A only intranasal DHE A caffeine combos work Exedrine only studied in non-disabling migraines Corticosteroids may work as adjunct in Status migrainosis and in w/d of meds causing CDH

Evidence Prophylaxis Abortive Level A Level A Level B Level B 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 Illustrate specific VS. general

Triptans vs Analgesics: 2-Hour Pain Free Response 73 % of Attacks 48 25 10 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

Abortive Therapy – Selective 5-HT 1B/1D receptor agonists Comparative Triptans Abortive 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 Therapy Behavior Modification (Avoid triggers) Preventive Pharmacotherapy Early treatment with specific therapy Ergotamine/DHE Triptan Rescue Medication Anti-emetics Analgesics

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 Prophylaxis is controversial Vasculopaths CYP3A4 Inhibitors

EpisodicTension-type headache 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 Headaches lasting from 30 minutes to 7 days At least two of the following pain characteristics: Pressing or tightening (nonpulsating) quality Mild to moderate intensity (nonprohibitive) Bilateral location No aggravation from walking stairs or similar routine activities D. Both of the following: No nausea or vomiting Photophobia and phonophobia absent, or only one is present

Treatment –Tension type headache Acute headaches may respond to aspirin, acetaminophen, or combinations with caffeine; NSAIDs; isometheptene combinations; butalbital combinations; and muscle relaxants. Overuse may lead to rebound headaches. Frequent butalbital use can also result in dependency Frequent headache may require preventive medications Tricyclic medications are generally more effective than SSRIs Other migraine preventatives (see chapter migraine) may be helpful especially when tension-type and migraine are both present

Cluster headache Severe 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: Individual Attacks Day Time 90 Minute Attack in Late Evening Night Time Two Attacks Disturbing Sleep Typical Seasonal Patterns in Episodic Cluster Headache (IHS 3.1.2) 1997 1998 1999 2000

Note: Attacks daily or almost daily for more than one year Episodic Cluster Headache Evolving to Chronic Cluster (IHS 3.1.3.2) 1998 1999 2000 Note: Attacks for more than 1 year with remission lasting less than 14 days Chronic Cluster Headache Unremitting from Onset (IHS 3.1.3.1) 1999 2000 Note: Attacks daily or almost daily for more than one year

Treatment - Cluster Acute Preventive O2 Injectable triptans Injectable ergotamines Preventive Steroids Verapamil AED’s

Chronic Daily Headache Headache 15 or more days per month Includes different headache types

CDH – Transformed migraine Transformed migraine (chronic migraine) with or without medication overuse Previous history of intermittent migraine usually by age 20-30 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). In 20%, sudden transformation which may be triggered by head or neck trauma, flulike illness, aseptic meningitis, and operations, and medical illnesses. Migraine characteristics to a significant degree intermittently or continuously

CDH –Hemicrania Continua Hemicrania continua with or without medication overuse Rare entity with constant, unilateral pain of variable intensity. Painful exacerbations associated with ptosis, lacrimation, and nasal stuffiness. Responds dramatically to indomethacin.

Chronic Daily Headache Taper medications which may be causing rebound The headaches may get worse before improving which may not occur before three to six weeks 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 “Rebound” Headache Acetaminophen Caffergot Opioids Butalbital Triptans Midrin NSAIDS

Referral Wayne Wasemiller, M.D. OU Neurology 302-2661 Marc Lenarts, M.D. Jim Couch, M.D. Call 271-3635 ext 0 Call chief resident on call

Case 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.