HEADACHE

CAUSED BY TRACTION, DISPLACEMENT, INFLAMMATION, VASCULAR

SPASM, DISTENTION OF THE PAIN SENSITIVE STRUCTURE IN THE HEAD

OR NECK

Origins of Pain in the Head(Pain-Sensitive)

EXTRA-CRANIAL

Sinuses

Eyes/orbits

Ears

Teeth

TMJ

Blood vessels

5,7,9,10 cranial nerves

carry pain from these

structure

INTRA-CRANIAL

Arteries of circle of willis

and proximal dural

arteries,

Dural Venous sinuses,

veins

Meninges

Dura

Classification of Headaches

PRIMARY

NO structural or

metabolic

abnormality:

Tension Type

Migraine

Cluster

Other Primary

Headaches

SECONDARY

Structural or metabolic abnormality: Extracranial: sinusitis,

otitis media, glaucoma, TMJ ds

Inracranial: SAH, vasculitis, dissection, central vein thrombosis, tumor, abscess, meningitis

Metabolic disorders: CO2 retention, CO poisoing

Primary HeadachesICHD-II. Cephalgia 2004 (Suppl 1)

Primary Headache Types

Migraine Tension Cluster

Pain

Description

Throbbing,

moderate to

severe, worse

w/exertion

Pressure,

tightness,

waxes and

wanes

Abrupt onset,

deep,

continuous,

excruciating,

explosive

Associated

Symptoms

Photo/phono-

phobia, n/v, aura

None Tearing,

congestion,

rhinorrhea,

pallor, sweating

Bajwa and Wootton. Up to Date 2007

Primary Headache Types

Migraine Tension Cluster

Location 60-70%

unilateral

Bilateral Unilateral

Duration 4-72 hr Variable 0.5-3 hr,

many per day

Patient

Appearance

Resting in

quiet dark

room; young

female

Remains

active or

prefers to

rest

Remains

active, prefers

hot shower,

male, smoker

Bajwa and Wootton. Up to Date 2007

MIGRAINE

Pathophysiology

Brainstem neuronal hyperexcitability

Cortical spreading depression with aura

Abnormalities of 5-HT, CGRP, NE, DA, GABA, glutamate, NO, and endorphins

Trigeminal Activation

Marcus, DA. Headache Simplified 2008.

Presymptomatic hyperexcitabilty increases brain stem response to triggers

Release of Neurotransmitters

(5-HT, NE, DA, GABA, Glutamate, NO, CGRP, Substance P, Estrogen)

Neurotransmitters activate the Trigeminal Nucleus

Dilation of

Meningeal

blood vessels

(Throbbing)

Activation of

Area Postrema

(N/V)

Activation of

Hypothalamus(Hypersensitivity)

Activation of

cervical

trigeminal

system

(Muscle spasm)Activation of

Cortex and

Thalamus

(Head pain)

Marcus, DA. Headache Simplified 2008.

Migraine

Migraine headaches are frequently relieved by

Darkness,

Sleep,

Vomiting,

Pressing On The Ipsilateral Temporal Artery,

And Their Frequency Is Often Diminished During Pregnancy.

Post lumbar-puncture headaches are typically relieved

by recumbency, whereas headaches caused by intracranial mass lesions may be less severe with the

patient standing.

TEMPORAL PATTERN OF HEADACHE

Headaches from mass lesions are commonly maximal on awakening, as are sinus headaches. Headaches from mass lesions, however, increase in severity over time.

Cluster headaches frequently awaken patients from sleep; they often recur at the same time each day or night.

Tension headaches can develop whenever stressful situations occur and are often maximal at the end of a workday.

Migraine headaches are episodic and may be worse during menses

Roppper A, Brown,H. Adams and Victor’s Principles of Neurology: Common Type of Headache. United States of America: McGraw-Hill. 2005. Page 148-9

Migraine Specific MedicationsTriptans

Ergots

Acute Treatment - Triptans

Fast onset/short duration

Sumatriptan

Rizatriptan

Zomitriptan

Almotriptan

Eletriptan

Treximet (Suma + Naproxen)

Slow onset/long

duration

Naratriptan

Frovatriptan

Acute Treatment - Triptans

Reasonable first choice for patients with moderate to severe disability from migraines

Limit use to 2-3 days per week

Patients who fail one triptan often respond to another

Do not use one triptan within 24 hours of another

Acute Treatment - Triptans

Mechanism of action

5HT-1B/1D agonists

Inhibit release of CGRP & substance P

Inhibit activation of the trigeminal nerve

Inhibit vasodilation in the meninges

Precautions

Ischemic heart dz or stroke

High risk for CAD

Pregnancy

Hemiplegic or basilar migraine

Ergots

Johnston et al Drugs 2010Loder NEJM 2010

Triptan Side Effects

Flushing, feeling or warmth

Chest pressure or heaviness

Throat tightness

Paresthesias

Dizziness, fatigue, drowsiness

Nausea

Intolerable taste with nasal formulations

Johnston et al Drugs 2010Loder NEJM 2010

Acute Treatment – Ergots

Mechanism of Action Constrict peripheral and cranial blood vessels

Bind to 5HT, NE, DA, alpha and beta receptors

Contraindications and precautions CAD or CVD (or high risk), uncontrolled HTN

Hemiplegic or basilar migraine

Pregnancy (category X) and breast feeding

Drugs metabolized by CYP3A4, triptans

Ergot Side Effects

Nausea and vomiting (pre-treat with antiemetic)

Coronary artery spasm, angina, MI

Tingling, numbness, Dizziness

Increased BP and HR

“Ergotism”

Choosing Acute Rx

Early N/V

Nasal triptans

Sumatriptan SubQ

Sensitive to SE

Naratriptan

Frovatriptan

Almotriptan

Recurrence

Nara, Frova, Almotriptan

Ergots

Triptan + NSAID

Rapid Onset

Sumatriptan SubQ

Nasal Triptans

DHE nasal or IM

Indications for a Preventive Agent

Migraine-related disability > 3d/month

Migraines last over 48 hours

Acute treatments are contraindicated, ineffective, or overused

Migraines cause profound disability or prolonged aura

Patient preference

TENSION-TYPE

TTH is the most common type of headache, and it is classified

as episodic (ETTH) or chronic (CTTH). It had various ill-

defined names in the past including tension headache, stress

headache, muscle contraction headache, psychomyogenic

headache, ordinary headache, and psychogenic headache.

Tension Type Headache

Occurs in up to 80% of the population

Most patients treat with OTCs and do notseek medical attention

Pathophysiology unclear Theory of increased muscle tension is unproven

Pain characteristics Bandlike, bilateral Extends form forehead to sides of temples Involves posterior neck muscles in cape-like distribution

Episodic tension-type headache

At least 10 previous headaches fulfilling the following criteria; number of days with such headache fewer than 15 per month

Headaches lasting from 30 minutes to 7 days

At least 2 of the following pain characteristics:

Pressing/tightening (no npulsating) quality

Mild or moderate intensity (may inhibit but does not prohibit activities)

Bilateral location

No aggravation from climbing stairs or similar routine physical activity

Both of the following:

No nausea or vomiting

Photophobia and phonophobia absent or only one present

Secondary headache types not suggested or confirmed

Chronic tension-type headache

Average headache frequency of more than 15 days per month for more than 6 months fulfilling the following criteria

At least 2 of the following pain characteristics: Pressing/tightening (nonpulsating) quality Mild or moderate intensity (may inhibit but does not prohibit activities) Bilateral location No aggravation from climbing stairs or similar routine physical activity

Both of the following: No vomiting No more than one of the following: nausea, photophobia, or

phonophobia

Secondary headache types not suggested or confirmed

Pathophysiology

Pathogenesis of TTH is complex and multifactorial, with contributions from both central and peripheral factors.

In the past, various mechanisms including vascular, muscular, and psychogenic factors were suggested.

The more likely cause of these headaches is believed now to be abnormal neuronal sensitivity and pain facilitation, not abnormal muscle contraction.

Various precipitating factors

One half of patients with TTH identify stressor hunger as a precipitating factor.

Stress - Usually occurs in the afternoon after long stressful work hours

Sleep deprivation

Uncomfortable stressful position and/or bad posture

THERAPY

The goals of pharmacotherapy are to relieve the headache,

reduce morbidity, and prevent complications.

Acute Treatment (Episodic TTH)

First line: OTC analgesics (APAP, NSAIDs)

Second line: ASA+APAP+caffeine, butalbital containing

products

High risk of rebound headaches

Limit acute treatment to 2-3 days per week

Preventive Treatment (Chronic TTH)

Non-Pharmacologic

Proper sleep hygiene

Stress management

Acupuncture

Biofeedback

Physical therapy

Pharmacologic

TCAs (best efficacy)

SSRIs (better

tolerated)

**Consider for patients with >15 headaches per month**

Patient Education

Advise the patient to take the following actions:

Avoid stressful situations if possible

Maintain a regular sleep schedule

Exercise regularly

Eat balanced meals

Avoid uncomfortable stressful positions and bad posture

Avoid eyestrain

Try biofeedback and relaxation techniques

CLUSTER & TRIGEMINAL

Tic douloureux

Baehr M, Frotscher M. Duus’ Topical Diagnosis in Neurology: Disorder Affecting the Trigeminal Nerve. Newyork:

Thieme. 2005. Page 165-7

TRIGEMINAL NEURALGIA

• A FACIAL PAIN SYNDROME OF UNKNOWN

CAUSE THAT DEVELOPS IN MIDDLE TO LATE

LIFE

• THE TRIGEMINAL ROOTS CLOSE TO SOME

VASCULAR STRUCTURE

• PAIN USUALLY 5-2, 5-3 BRANCHES

• CHARACTERISTICALLY

• LIGHTNINGLIKE MOMENTARY JABS OF

EXCRUCIATIONG PAIN OCCUR AND

APONTANEOUSLY ABATE

CLUSTER HEADACHEalso known as BingHorton syndrome, erythroprosopalgia, and histamine headache

MEN>WOMEN

MEAN AGE ONSET AT 25 YEARS

A CLUSTER OF BRIEF VERY SEVERE, UNILATERAL, SONSTANT NONTHROBBING HEADACHES THAT LAST FROM A FEW MINUTES-LESS THAN 2 HOURS

ALWAYS UNILATERAL, SAME SIDE, COMMONLY OCCUR AT NIGHT, RECUR DAILY, SAME TIME A DAY FOR A CLUSTER PERIOD OF WEEKS TO MONTHS

PATOPHYSIOLOGY IS UNCLEAR

MRI FUNCTIONAL ACTIVATION OF THE IPSILATERAL HYPOTHALAMIC GRAY

CLUSTER HEADACHE

BRIEF ATTACKS OF PAIN OCCURS MAINLY AT NIGHT INCLUDING DURING SLEEP (IN DISTINCTION TO TRIGEMINAL NEURALGIA)

BEGIN AS A BURNING SENSATION OVER THE LATERAL ASPECT OF THE NOSE OR A PRESSURE BEHIND THE EYES

IPSILATERAL CONJUNCTIVAL INJECTION

NASAL STUFFINESS

THESE ATTACKS ARE ACCOMPANIED BY FACIAL ERYTHEMA, LACRIMATION, WATERY NASAL SECRETION, AND OFTEN HORNER SYNDROME AS WELL.

EPISODES ARE OFTEN PRECIPITATED BY THE USE OF ALCOHOL OR VASODILATING DRUGD

CLUSTER HEADACHE

DISTRIBUTION OF SYMPTOMS AND

SIGNS IN CLUSTER HEADACHE

PTOSIS DURING ACUTE CLUSTER

HEADACHE

CLUSTER HEADACHE

The attacks occur repeatedly in periods (clusters)

characteristically lasting a week or more, separated by

headache-free intervals of at least two weeks’ duration.

Its treatment is empirical, with oxygen, triptanes, or other

medications.

CONCLUSION

Roppper A, Brown,H. Adams and Victor’s Principles of Neurology: Common Type of Headache. United States of

America: McGraw-Hill. 2005. Page 148-9

Thank You