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Headaches

J.B. Handler, M.D.University of New EnglandPhysician Assistant Program

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Abbreviations 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

BBB- blood brain barrier NSAID- non-steroidal anti-

inflammatory 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 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. 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. 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.

Migraine Headaches

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Migraine Headaches

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” 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 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 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 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 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.

Scintillating Scotoma

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Migraine Aura 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 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 Prolonged aura with neurologic

deficits lasting 1 hour up to a week. Uncommon. 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. 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

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 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 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 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). 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 anti-nauseant/emetic agent like metoclopramide.

Injectable narcotic, often Meperidine, combined with an anti-emetic (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 effectiveshort course. Note: systemic steroids (glucocorticoids

like prednisone) are not benign drugs.

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Migraine Prophylaxis 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).

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 understood- vascular, muscular, myofascial.

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Tension Headaches 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 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.

Cluster Headaches

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Cluster Headaches

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 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

A variety of neoplasms (benign and malignant) can cause headaches related to displacement of vascular structures.

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Intracranial Mass Lesions 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.