Transcript Headaches

Headaches
J.B. Handler, M.D.
University of New England
Physician Assistant Program
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Abbreviations
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P.E.- physical exam
ETOH- alcohol
CT/CAT- computerized
axial tomography
NTG- nitroglycerin
TIA- transient ischemic
attack
PET- positron emission
tomography
N&V- nausea and vomiting
GI- gastrointestinal
SC- sub-cutaneous
EOM- extraocular
movements
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BBB- blood brain barrier
NSAID- non-steroidal antiinflammatory drug
HTN- hypertension
Hx- history
CHD- coronary heart
disease
HA- headache
ER- emergency room
ASA- acetylsalicylic acid
(aspirin)
Sx- symptoms
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Case 1
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A 33 y/o female presents with episodic,
severe throbbing headaches associated
with nausea and at times, vomiting. They
often occur during her menses or with
emotional duress. They last hours at a
time and resolve spontaneously. There
are no associated neuro Sx. NSAIDs and
ASA sometimes help if taken early.
What is the likely diagnosis?
What additional history do you want?
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Case 1
A. Migraine with aura
 B. Migraine without aura
 C. Complex migraine
 D. Migrainous neuralgia
 E. Cluster headache
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Primary Headaches
Migraine
 Tension
 Cluster
 Chronic Daily Headache
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Secondary Headaches
Post-traumatic, e.g post-concussion
 Space occupying lesions- tumors
 Headaches associated with
cerebrovascular disease
 Hypertensive encephalopathy
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A Major Primary Care
Problem
Patients present not only for the
headaches but because of the fear
of a brain tumor.
 Essential in the work-up to tell the
patient:
“By the way, you don’t have a
brain tumor”.
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History and P.E.
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Headache triggers, aura, self-treatment,
diet (food, caffeine, etoh), sleep, relation
to menses, childhood associations.
Headache history: location, onset,
frequency, duration, quality, severity,
timing, setting, aggravating/alleviating,
associated Sx.
Headache diary
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History and P.E.
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P.E: Blood pressure, examine the head,
vision, visual fields, EOM,s, funduscopic
exam (papilledema); brief neuro exam:
evaluate language, gait, motor & reflexes.
If history is characteristic, no focal neuro
findings and gait is normal, unlikely brain
tumor.
If patient still unconvinced (“no brain
tumor”), CT scan (if normal) will put most
patients at ease.
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Migraine Headaches
Images.google.com
Migraine Headaches
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2nd most common headache disorder.
Prevalence 12%: woman-18%, men-6%.
Incidence in neurologists: 40%!
Absence of aura: 80-85%
Presence of aura: 15-20%.
Onset in adolescence and early
adulthood, peak ages 30-45
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“Migraineurs”
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Infantile colic
Motion sickness with nausea and vomiting
Menstrual headaches
Headaches with physical activity including
“benign sex headaches”
Headaches post consumption of small
amounts of colored wine (e.g. Bordeau)
or liquor – not “hangover” headaches.
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“Migraineurs”
Caffeine withdrawal headaches
 Water diving headaches
 Altitude headaches
 Headaches after certain foods
(chocolate, peanuts, caffeine)
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Pathophysiology: Unclear
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End pathway- activation of afferent
sensory fibers that innervate meningeal
and/or cerebral blood vessels.
Fibers arise from the Trigeminal nerve.
Inflammatory and vascular
components.
No identifiable cause.
Migraine triggers: Physical exercise
including sex, emotional stress, lack of or
excess sleep, foods, odors, missed meals,
menstruation.
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Vasogenic Theory
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Intracranial (internal carotid)
vasoconstriction responsible for
migraine “aura”. Headache results from
rebound vasodilation and distension of
cranial vessels (external carotid) with
activation of perivascular pain fibers.
In support of theory: Vasodilation and
pulsation of extracranial vessels is
observable during headaches- ?cause or
result of headache (see neurogenic
theory, below).
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Vasogenic Theory
Vasodilators (NTG) can trigger
migraine headaches.
 Substances that cause
vasoconstriction (ergotamine) abort
the headaches.
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Neurogenic Theory
The brain activates or sensitizes
trigeminal nerve fibers within the
meninges initiating the headache via
neurogenic inflammation. The
vascular changes that occur during
the attack are the result of vascular
inflammation.
 Theory believed by most
neurologists.
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Neurogenic Theory
Symptoms such as photophobia,
phonophobia, nausea and vomiting
cannot be explained by the
vasogenic theory alone.
 Some aural symptoms like visual
hallucinations also cannot be
explained by vasoconstriction or
vasodilation alone.
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Serotonin
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Serotonin (5-HT), a neurotransmitter
which activates pain fibers is also
involved. Headaches are initiated by the
release of peptides and
neurotransmitters at trigeminal nerve
branches, leading to inflammation and
vasodilation of meningeal and dural blood
vessels.
Drugs that are agonists for serotonin
receptors (5-hydroxy tryptamine analogs)
abort the headaches when taken early.
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Serotonin: Confusion
In spinal cord serotonin inhibits pain
pathways via release of enkephalin.
 In brainstem serotonin chemically
activates/inflames painfibers of
trigeminal nerve which innervate
meninges and dura, contributing to
migraine headache.
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Aura
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Migraine with aura: transient (15-30”)
episodes of focal neurologic
dysfunction that appear before the
headache phase begins. These include:
Expanding scotoma (blind spot) with
scintillating margin (visual
hallucinations- stars, sparks and zigzags
of light), visual field defects, unilateral
paresthesias, numbness, weakness,
dysphasia.
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Aura
Some aural symptoms suggest
decreased blood flow in the
distribution of the internal carotid
artery, mimicking TIA’s (lecture to
follow on 9/4).
 Uncommonly involve distribution of
basilar artery: Vertigo, ataxia,
tinnitus, hearing loss.
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Scintillating Scotoma
Images.google.com
Migraine Aura
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Some of the symptoms may be explained
by bloodflow, while others (visual
hallucinations) cannot.
Aura is contributed to by activation of a
wave of electrical activity that spreads
throughout the brain, depressing
cortical activity and resulting in visual
disturbance; initiated by the CNS.
“Spreading depression of Lao” seen on
PET scans.
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Headache Phase
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Headaches can be lateralized to one
side or generalized. Usually throbbing
(moderate to severe) and worse with
physical activity. Develop gradually and
last several hours.
Associated symptoms: nausea,
photophobia, phonophobia.
Headache spectrum varies and is a
continuum that might include aura,
lateralization, varying length, etc.
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Complex Migraine
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Prolonged aura with neurologic
deficits lasting 1 hour up to a week.
Uncommon.
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Rarely, there are permanent neuro deficits
consistent with a localized stroke in the
distribution of the internal carotid artery, but:
Neuro-imaging or angiography do not
show occlusion or fixed stenosis of the
intracerebral vessels.
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Case 1 (continued)
Diagnosis: Migraine without aura.
 How would you manage this patients
acute episodes?
 What preventive measures would be
useful?
 When are prophylactic medications
indicated?
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Rules of Therapy
Treat early
 Treat aggressively until headache is
gone. This may require more than
one dose of meds.
 Consider pros and cons of oral vs.
parenteral forms of medications.
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N&V, absorption, onset of action, etc.
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Prevention and Abortive
Treatment
Prevention: avoid migraine triggers
if identifiable (foods, additives,
caffeine, strong smells, response to
stress, sleep cycles).
 Bed rest in a dark room
 Mild attacks: ASA, NSAIDS
effective if taken early. May need to
be combined with other meds.
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Abortive Treatment: Older
Meds
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Ergotamine: Potent serotonin agonist and
vasoconstrictor- Caution in patients
with HTN, Hx of CAD or stroke.
Cafergot-Ergotamine 1mg and caffeine
100mg.
Ergot drugs are less selective/safe than
the newer agents (tryptans).
Avoid opiates (exception: patient in ED)
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Migraine and the Seven
Tryptans
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Newer agents that are a big advance in
the treatment of migraine headaches.
5-HT1 receptor agonists- high affinity for
serotonin receptors in trigeminal nerve
branches with additional vasoconstrictive
effects (see below): Sumatriptan
(Imitrex), Zolmitriptan (Zomig) and
others; similar efficacy.
These agents have few side-effects and
are very safe; avoid in patients with
CHD.
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Serotonin: More Confusion
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Why should a serotonin agonist abort migraines?
5-HT1 receptors are the predominant serotonin
receptors in the CNS. Many of them function as
presynaptic autoreceptors whose activation
inhibits the release of serotonin and related
neurotransmitters that cause vasodilation,
inflammation and pain.
Activation of these receptors in pial/dural vessels
leads to vasoconstriction.
Activation of these receptors in the brain stem
may inhibit further activation of trigeminal
neurons responsible for migraine attacks.
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Migraine Treatment
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For mild/moderate HA, oral tryptan ok.
For acute, severe headache, consider
alternative route. Injected (auto-injector)
sub-cutaneous sumatriptan is most
effective in aborting the HA at a cost
($100-$200).
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Oral meds often poorly absorbed
Intra-nasal sumatriptan an alternative but
less predictable depending on absorbtion.
Repeat dosing of the tryptans until HA
gone or maximal daily dose taken.
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Severe Intractable Migraine
Headaches
Usually treated in the ED with
injectable dihydroergotamine and
effective hours into an attack.
Essential to pre-treat with antinauseant/emetic agent like
metoclopramide.
 Injectable narcotic, often
Meperidine, combined with an antiemetic (ED only).
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Severe Intractable
Headaches
Indomethacin, a very potent NSAID,
may be useful in preventing relapse
of the acute headache.
 Steroids (glucocorticoids)- used
infrequently but effectiveshort
course.
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Note: systemic steroids (glucocorticoids
like prednisone) are not benign drugs.
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Migraine Prophylaxis
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Indications:
HA’s limit work or daily activity 3 or
more days/month.
 Sx of the HA are severe or prolonged
 Previous migraines were associated
with a complication (complex
migraine, stroke).
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Treatment is empirical- meds were
discovered serendipitously.
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Migraine Prophylaxis
Beta adrenergic blockers:
propranolol, metoprolol and others
that cross the BBB
 Tricyclic antidepressants:
amitriptylene, nortriptylene, others
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Migraine Prophylaxis
Calcium channel blockers:
verapamil, others.
 Anticonvulsants: gabapentin,
valproic acid, topiramate
(Topamax)
 Botulinum toxin type A- local
injection into scalp
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Tension Headaches
Most common type of headache,
females>males, usually begin in the
3rd decade.
 Pathophysiology: poorly understoodvascular, muscular, myofascial.
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Tension Headaches
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Clinical features: Episodic and chronic
forms; tight, pressure bilaterally,
mild/mod pain (minutes-days), do not
worsen with physical exertion, no
nausea or vomiting or other neuro
sx. Associations: Poor concentration,
stress, fatigue, noise, glare, depression.
Treatment: Acetaminophen, NSAIDS.
Meds for migraine may also be effective
but are not 1st line.
Prevention: relaxation techniques,
biofeedback.
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Case 2
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A 40 y/o man presents with recurrent
episodes of severe pain involving the left
eye and surrounding face, accompanied
by marked tearing and nasal congestion.
Episodes last 15-20” and recur 6-8 times
daily (last 3 days). He gets some relief
from NSAIDS.
What is your diagnosis?
Treatment?
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Cluster Headaches
Aka: Migrainous neuralgia.
 Much less common than migraine
or tension HA’s.
 Male 6x> female, 3rd-6th decade
 Pathogeneses: Poorly understood;
likely vascular with activation of
trigeminal-vascular system.
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Cluster Headaches
Images.google.com
Cluster Headaches
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Clinical features: Recurrent episodes
of intense unilateral orbital,
supraorbital, or temporal head pain
along with ipsilateral partial cervical
sympathetic paralysis (conjunctival
injection, lacrimation, rhinorrhea, nasal
congestion, eyelid edema, loss of facial
sweating); last 15” to 2 hrs and recur
daily for days to weeks.
Triggers: ETOH, stress, glare, foods.
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Treatment
100% O2 x 15”- very effective for
long duration (1-2 hrs) HA’s
 Indomethacin- excellent for
recurrent short duration HA’s (15”).
 Ergotamine tartrate (oral, rectal
suppository, injection).
 Sumatriptan, Zolmitriptan.
 Prophylaxis: Verapamil, Ergotamine.
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Chronic Daily Headache
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Any headache occurring > 15 days/month
for at least 1 month. Often develops over
time in a patient with intermittent HA’s.
Includes tension, cluster, migraine, and
other vascular headaches.
Patients often end up being treated in
“headache specialty clinics”.
Medication overuse, especially multiple
meds, is the most common contributing
factor, and withdrawal of meds often
improves the symptoms.
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Intracranial Mass Lesions
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A variety of neoplasms (benign
and malignant) can cause
headaches related to
displacement of vascular
structures.
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Intracranial Mass Lesions
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Symptoms: usually dull bifrontal or
occipital headaches that begin in the
a.m., are worsened by exertion or
postural changes and may be
associated with N & V.
Clues: new onset HA’s in patients >45
y.o. Usually associated with other
neurologic findings, focal or diffuse
(generalized disturbance of cerebral
function).
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Pathology, Diagnosis and
Rx
50% gliomas, remainder are
meningiomas, astrocytomas,
acoustic neuromas, others.
 Signs: Neuro defects, papilledema,
personality changes, intellectual
decline, seizures and emotional
lability.
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Pathology, Diagnosis and Rx
Dangers: Brain Hernation through
tentorial hiatus due to incrased
pressure, leading to stupor and
coma often followed by death.
 Diagnosis: CT or MRI scans will
detect and localize the tumors.
 Treatment: Depends on the
pathology.
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