primary headache only; skdi 4

1. HEADACHE
CAUSED BY TRACTION, DISPLACEMENT, INFLAMMATION, VASCULAR
SPASM, DISTENTION OF THE PAIN SENSITIVE STRUCTURE IN THE HEAD
OR NECK

2. 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

3. 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

4. Primary Headaches
ICHD-II. Cephalgia 2004 (Suppl 1)

5. 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

6. 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

7. MIGRAINE

8. 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.

9. 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
Activation of (Muscle spasm)
Cortex and
Thalamus
(Head pain)
Marcus, DA. Headache Simplified 2008.

10. 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.

11. 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

12. Migraine Specific Medications
Triptans
Ergots

13. Acute Treatment - Triptans
Fast onset/short duration
 Sumatriptan
 Rizatriptan
 Zomitriptan
 Almotriptan
 Eletriptan
 Treximet (Suma +
Naproxen)
Slow onset/long
duration
Naratriptan
Frovatriptan

14. 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

15. 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 2010
Loder NEJM 2010

16. 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 2010
Loder NEJM 2010

17. 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

18. Ergot Side Effects
 Nausea and vomiting (pre-treat with antiemetic)
 Coronary artery spasm, angina, MI
 Tingling, numbness, Dizziness
 Increased BP and HR
 “Ergotism”

19. 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

20. 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

21. TENSION-TYPE

22.  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.

23. Tension Type Headache
 Occurs in up to 80% of the population
Most patients treat with OTCs and do not
seek 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

24. 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

25. 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

26. 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.

27. Various precipitating factors
One half of patients with TTH identify stress
or 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

28. THERAPY
 The goals of pharmacotherapy are to relieve the headache,
reduce morbidity, and prevent complications.

29. 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

30. 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**

31. 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

32. CLUSTER & TRIGEMINAL
Tic douloureux
Baehr M, Frotscher M. Duus’ Topical Diagnosis in Neurology: Disorder Affecting the Trigeminal Nerve. Newyork:
Thieme. 2005. Page 165-7

33. 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

34. CLUSTER HEADACHE
also 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

35. 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

36. CLUSTER HEADACHE
DISTRIBUTION OF SYMPTOMS AND
SIGNS IN CLUSTER HEADACHE
PTOSIS DURING ACUTE CLUSTER
HEADACHE

37. 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.

38. CONCLUSION

40. 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

41. Thank You