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

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

10. 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.

11. 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.

12. 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.

13. 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

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

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

16. 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

17. 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:

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

26. 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

28. “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

31. 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

32. 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.

33. 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

34. 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.

35. Common Primary Headaches
Migraine
Tension
Cluster
Chronic Daily Headache

36. 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:
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.

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

39. 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

40. 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.

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

43. 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

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

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

46. 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

47. 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

48. 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

49. 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

50. 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

51. 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

52. Triptans vs Analgesics: 2-Hour Pain Free Response73
% of Attacks 48 25 10
Cady et al Clin Ther. 2000;22:

53. 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

54. 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

55. 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/ (Imitrex) – T/SC/IN
2h Zolmitriptan / (Zomig) T/DT
2.5h Rizatriptan / (Maxalt) T/DT
1-3h Naratriptan (Amerge) T
h Almotriptan 6.25/ (Axert) T
2-4h Frovatriptan (Frova) T
1-2h Eletriptan / (Relpax) T
Tepper SJ Headache. 2001;85:

56. Stratified Therapy Behavior Modification (Avoid triggers)
Preventive Pharmacotherapy
Early treatment with specific therapy
Ergotamine/DHE
Triptan
Rescue Medication
Anti-emetics
Analgesics

60. 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

61. 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

62. 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

63. Cluster headache
Severe unilateral orbital, supraorbital and/or temporal pain, lasting 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)

64. 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

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

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

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

68. 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

69. 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.

70. 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

71. Medicines Associated with “Rebound” Headache
Acetaminophen
Caffergot
Opioids
Butalbital
Triptans
Midrin
NSAIDS

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

73. 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.