Transcript Headache - Angelfire

Headaches in
Primary Care
Steve Cobb MD
Residency Program Director
ESJH Family Medicine Residency
Headaches in
Primary Care
Steve Cobb MD
Residency Program Director
ESJH Family Medicine Residency
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
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 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.
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
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.
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
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 lifethreatening 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%
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 International
Headache Society. Cephalalgia. 1988.
2 of these
Make The
Diagnosis
1 of these
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
Proposed Mechanism of Action
Trigeminal
nerve
INHIBITION
5-HT1D
5-HT1F
CGRP
NK
SP
MOA of triptans
5-HT1B
CONSTRICTION
Blood vessel
CGRP: calcitonin gene-related peptide
NK: neurokinin A
SP: substance P
Adapted from Goadsby et al. Neurol Clin. 1997.
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.
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/tobac
co 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/phenylalaninecontaining foods or beverages






Non-pharmacologic

Grade A Evidence
Grade C Evidence
– Relaxation Therapy
– Hypnosis
– Thermal Biofeedback
– Acupuncture
– Cognitive behavioral
– TENS Unit
therapy


Grade B Evidence
– Behavioral therapy
with medication
– Cervical spine
manipulation
– Occlusal Adjustment
– Hyperbaric O2
Pharmacologic Treatment
Episodic Migraine
Prophylactic
– Antiepileptics
Abortive
– Specific
– Antidepressants

– B-Blockers

– CCB
– NSAIDS
Triptans
Ergots
– General


– Serotonin Agonists

– Vitamins and Herbs


Antiemetics
NSAIDS
Opioids
Barbiturates
Corticosteroids*
Evidence

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 nondisabling migraines
Caffeine
Corticosteroids in status
migranosis
Two Migraine Abortive Agents
Ergots
Triptans
• 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)
• 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:
2-Hour Pain Free Response
80
70
73
60
% of
Attacks
50
48
40
30
20
25
10
10
0
Mild
Moderate
Cady et al Clin Ther. 2000;22:1035-1048.
Non-Triptan
Triptan
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 proinflammatory 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 Triptans
Abortive Therapy – Selective 5-HT 1B/1D receptor agonists
Tmax
Triptan
Dose
Formulations
Sumatriptan 25/50/100 (Imitrex) – 1991
2h
Zolmitriptan 2.5/5
(Zomig) - 1997
2.5h Rizatriptan
5/10
(Maxalt)
1-3h Naratriptan
2.5
(Amerge)
1.5-3.8h Almotriptan 6.25/12.5
(Axert)
2-4h Frovatriptan
2.5
(Frova)
1-2h Eletriptan
20/40
(Relpax)
T/SC/IN
T/DT
T/DT
T
T
T
T
2.5h
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
Efficacy of Eletriptan:
Comprehensive Relief at 2 Hours
Placebo
Headache response, %
80
60
Pain-free response, %
40
Relief of Nausea, %
40
20
30
20
10
0
40
20
60
80
20 20
40
Relief of Photophobia, %
60
80
40
60
Relief of Phonophobia, %
80
Sumatriptan was blinded using encapsulation. Encapsulated sumatriptan was bioequivalent to commercial tablets.
*P<.001 vs placebo.
Adapted from Mathew et al. Headache. 2003.
Efficacy of Eletriptan:
Comprehensive Relief at 2 Hours
Placebo
Sumatriptan 100 mg
Headache response, %
80
60 *
Pain-free response, %
40
Relief of Nausea, %
40
30
*
20
*
20
10
0
40
20
60
80
20 20
40
Relief of Photophobia, %
*
60
80
40
*
60
Relief of Phonophobia, %
80
Sumatriptan was blinded using encapsulation. Encapsulated sumatriptan was bioequivalent to commercial tablets.
*P<.001 vs placebo. †P<.05 vs sumatriptan.
Adapted from Mathew et al. Headache. 2003.
Efficacy of Eletriptan:
Comprehensive Relief at 2 Hours
Placebo
Sumatriptan 100 mg
Eletriptan 40 mg
Headache response, %
80
*†
60 *
Pain-free response, %
*†
40
Relief of Nausea, %
40
20
*
30
†
*
*
80
20
10
0
40
20
60
20 20
40
Relief of Photophobia, %
*†
* 60
80
40
60
*
*†
Relief of Phonophobia, %
80
Sumatriptan was blinded using encapsulation. Encapsulated sumatriptan was bioequivalent to commercial tablets.
*P<.001 vs placebo. †P<.05 vs sumatriptan.
Adapted from Mathew et al. Headache. 2003.
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
headache
At least 10 previous headache
D.
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:
A.
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
Both of the following:
1.
2.
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.
a.
b.
Overuse may lead to
rebound headaches.
Frequent butalbital use
can also result in
dependency
Frequent headache may
require preventive
medications
a.
b.
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
- Lacrimation
- Nasal congestion
- Forehead/facial sweating

- Miosis
- Ptosis
- Eyelid edema
- 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
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
– O2
– Injectable triptans
– Injectable ergotamines

Preventive
– Steroids
– Verapamil
– AED’s
Chronic Daily Headache
1.
2.
Headache 15 or more days per month
Includes different headache types
CDH – Transformed migraine
Transformed migraine (chronic migraine) with or without medication
overuse
1.
2.
3.
4.
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
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 Headache
Taper medications which may
be causing rebound
a.
b.
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 longacting 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.
– 302-2661

OU Neurology
– 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.