Headaches

1
Headaches

• J.B. Handler, M.D.
• University of New England
• Physician Assistant Program

2
Abbreviations

• P.E.- physical exam
• ETOH- alcohol
• CT/CAT- computerized axial tomography
• NTG- nitroglycerin
• TIA- transient ischemic attack
• PET- positron emission tomography
• NV- 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?

4
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 dont 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.

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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 TIAs (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
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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.
• NV, 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
  effective?short course.
• Note systemic steroids (glucocorticoids like
  prednisone) are not benign drugs.

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Migraine Prophylaxis

• Indications
• HAs 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, femalesgtmales,
  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 HAs.
• Male 6xgt female, 3rd-6th decade
• Pathogeneses Poorly understood likely vascular
  with activation of trigeminal-vascular system.

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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) HAs
• Indomethacin- excellent for recurrent short
  duration HAs (15).
• Ergotamine tartrate (oral, rectal suppository,
  injection).
• Sumatriptan, Zolmitriptan.
• Prophylaxis Verapamil, Ergotamine.

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Chronic Daily Headache

• Any headache occurring gt 15 days/month for at
  least 1 month. Often develops over time in a
  patient with intermittent HAs.
• 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 HAs in patients gt45 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.