Classification of headaches. Primary headachesOR Idiopathic headachesTHE HEADACHE IS ITSELF THE DISEASENO ORGANIC LESION IN THE BEACKGROUNDTREAT THE HEADACHE!. Secondary headachesOR Symptomatic headachesTHE HEADACHE IS ON LY A SYMPTOM OF AN OTHER UNDERLYING DISEASETREAT THE UNDERLYING DISEA
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1. Headache By
Wael Hamdy Mansy, MD
Assistant Professor of Clinical Pharmacy
King Saud University
2. Classification of headaches Primary headaches
OR Idiopathic headaches
THE HEADACHE IS ITSELF THE DISEASE
NO ORGANIC LESION IN THE BEACKGROUND
TREAT THE HEADACHE! Secondary headaches
OR Symptomatic headaches
THE HEADACHE IS ON LY A SYMPTOM OF AN OTHER UNDERLYING DISEASE
TREAT THE UNDERLYING DISEASE!
3. History and examination should clarify if Type of hedeache (1ry or 2ry).
Is any urgency?
In case of 1ry headache only the headache attacks should be treated “attack therapy, or prophylactic therapy is also necessary.
4. SECONDARY, SYMPTOMATIC HEADACHES THE HEADACHE IS A SYMPTOM OF AN UNDERLYING DISEASE, LIKE
Brain tumor, meningeal carcinomatosis
5. Primary, idiopathic headaches Tension type of headache
Other, rare types of primary headaches
6. Tension headache Renamed tension-type headaches by the International Headache Society in 1988, are the most common type of primary headaches.
The pain can radiate from the neck, back, eyes, or other muscle groups in the body.
Tension-type headaches account for nearly 90% of all headaches. Approximately 3% of the population has chronic tension-type headaches
7. Tension –type headaches can be episodic or chronic.
Episodic tension-type headaches occur 15 days a month.
Chronic tension-type headaches 15 days or more a month for at least 6 months.
Can last from minutes to days, months or even years, though a typical tension headache lasts 4-6 hs
8. Cluster headache Nicknamed "suicide headache", is a neurological disease that involves an immense degree of pain.
"Cluster" refers to the tendency of these headaches to occur periodically, with active periods interrupted by spontaneous remissions.
The cause of the disease is currently unknown. It affects approximately 0.1% of the population, and men are more commonly affected than women
9. Migraine Headache
10. Prevalence Familial
Young, healthy women; F>M: 3:1
17 – 18.2% of adult females
6 – 6.5% adult males
2-3rd decade onset… can occur sooner
Peaks ages 22-55.
½ migraine sufferers not diagnosed.
94% of patients seen in primary care settings for headache have migraines
Neurology: Migraine throughout the life cycle: Treatment through the ages
Neurology: Migraine throughout the life cycle: Treatment through the ages
Common misdiagnoses for migraine:
Sinus Headache (HA)
Referral to ENT for sinus disease and facial pain. utd online pathogen
Clinical otolaryngology and allied sciencesutd online pathogen
Clinical otolaryngology and allied sciences
12. The International Headache Society (IHS) classifies migraine headache
The IHS defines the intensity of pain with a verbal, four-point scale:
13. Migraine Definition IHS Diagnostic criteria: migraine w/o aura
HA lasting for 4-72 hrs
HA w/2+ of following:
Aggravated by routine physical activity.
During HA at least 1 of following
Phonophobia IHS criteria: Migraine/aura (3 out of 4)
One or more fully reversible aura symptoms indicates focal cerebral cortical or brainstem dysfunction.
At least one aura symptom develops gradually over more than 4 minutes.
No aura symptom lasts more than one hour.
HA follows aura w/free interval of less than one hour and may begin before or w/aura.
Utd onlineUtd online
14. Migraine mechanism Neurovascular theory.
Abnormal brainstem responses.
Calcitonin gene related peptide
Extracranial arterial vasodilation.
Extracranial neurogenic inflammation.
Decreased inhibition of central pain transmission.
15. Important role in migraine pathogenesis.
Mechanism of action in migraines not well established.
Main target of pharmacotherapy.
16. Aura Mechanism Cortical spreading depression
Self propagating wave of neuronal and glial depolarization across the cortex
Activates trigeminal afferents
Causes inflammation of pain sensitive meninges that generates HA through central/peripheral reflexes.
Alters blood-brain barrier.
Associated with a low flow state in the dural sinuses.
Vision – most common neurologic symptom
Paresthesia of lips, lower face and fingers… 2nd most common
Flickering uncolored zigzag line in center and then periphery
Motor – hand and arm on one side
Auras (visual, sensory, aphasia) – 1 hr
Lasts hours to days…
18. MIGRAINE WITH AURA DURING AURA:
19. IMPORTANT TO KNOW! MIGRAINE WITH AURA IS A RISK FACTOR FOR ISCHAEMIC STROKE
THEREFORE PATIENTS SUFFERING FROM MIGRAINE WITH AURA
SHOULD NOT SMOKE!!!
SHOULD NOT USE ORAL CONTRACEPTIVE DRUGS!!!
THE PROPROTION OF PATENT FORAMEN OVALE IN PATIENTS WITH MIGRAINE WITH AURA IS ABOUT 50-55%! (IN THE POPULATION IS ABOUT 25%).
20. Is there a relationship between aura and patent foramen ovale ?
Paradoxic emboli theory is not likely
Shunting of venous blood to the arterial side could be the reason ? no breakdown of certain neurotransmitters (5HT) in the lung!
Comorbidity could be also an explanation.
However, closure of patent foramen ovale decreases the frequency of migraine attacks.
BUT! Migraine is a benign disease. Please do not indicate closure of patent foramen ovale just because of migraine with aura!
21. Migraine Subtypes Basilar type migraine
Dysarthria, vertigo, diplopia, tinnitus, decreased hearing, ataxia, bilateral paresthesias, altered consciousness.
Simultaneous bilateral visual symptoms.
No muscular weakness.
Retinal or ocular migraine
Repeated monocular scotomata or blindness < 1 hr
Associated with or followed by a HA
Utd onlineUtd online
22. Migraine Subtypes Menstrual migraine
Unilateral motor and sensory symptoms that may persist after the headache.
Familial hemiplegic migraine
23. Migrainous vertigo Vertigo – sole or prevailing symptom.
Benign paroxysmal vertigo of childhood.
Prevalence 7-9% of pts in referral dizzy and migraine clinics.
Not recognized by the IHS
Diagnosis (proposed criteria)
Recurrent episodic vestibular symptoms of at least moderate severity.
One of the following:
Current of previous history of IHS migraine.
Migrainous symptoms during two or more attacks of vertigo.
Migraine-precipitants before vertigo in more than 50% of attacks.
Response to migraine medications in more than 50% of attacks Utd onlineUtd online
24. Clinical manifestations
Lateralized in severe attacks – 60-70%
Bifrontal/global HA – 30%
Gradual onset with crescendo pattern.
Limits activity due to its intensity.
Worsened by rapid head motion, sneezing, straining, constant motion or exertion.
Focal facial pain, cutaneous allodynia, GI dysfunction, facial flushing, lacrimation, rhinorrhea, nasal congestion and vertigo…
25. Precipitating factors
26. Treatment Abortive
27. Abortive Therapy Reduces headache recurrence.
Alleviation of symptoms.
Selective - triptans
Nonselective – ergots
28. Abortive care strategies Stepped
Start with lower level drugs, then switch to more specific drugs if symptoms persist or worsen.
Analgesics – Tylenol, NSAIDs…
Vasoconstrictors – sympathomimetics…
Opioids (try to avoid) - Butorphanol
Triptans – sumatriptan (oral, SQ, nasal), naratriptan, rizatripatan, zomatriptan.
Limited by patient compliance.
Adjusts treatment according to symptom intensity.
Mild – analgesics, NSAIDs
Moderate – analgesic plus caffeine/sympathomimetic
Severe – opioids, triptans, ergots…
Severe sx treatment limited due to concomitant GI sx’s.
Bases treatment on intensity and time of attacks.
HA diary reviewed with patient.
Medication plan and backup plans.
29. Preventive therapy Consider if pt has more than 3-4 episodes/month.
Reduces frequency by 40 – 60%.
Breakthrough headaches easier to abort.
Calcium channel blockers
30. Botox 51% migraineurs treated had complete prophylaxis for 4.1 months.
38% had prophylaxis for 2.7 months.
Randomized trial showed significant improvement in headache frequency with multiple treatments.
31. Conclusions Migraine is common but unrecognized.
Keep migraine and its variants in the differential diagnosis.
33. References Landy, S. Migraine throughout the Life Cycle: Treatment through the Ages. Neurology. 2004; 62 (5) Supplement 2: S2-S8.
Bailey, BJ. Head and Neck Surgery – Otolaryngology 3rd Edition. 2001. Pgs. 221-235.
Bajwa, ZH, Sabahat, A. Pathophysiology, Clinical Manifestations, and Diagnosis of Migraine in Adults. Up To Date online. 2005.
Lipton, RB, Stewart, WF, Liberman, JN. Self-awareness of migraine: Interpreting the labels that headache sufferers apply to their headaches. Neurology. 2002; 58(9) Supplement 6: S21-S26.
Cady, RK, Schreiber, CP. Sinus headache or migraine?: Considerations in making a differential diagnosis. Neurology. 2002; 58 (9) Supplement 6: S10-S14.
Perry, BF, Login, IS, Kountakis, SE. Nonrhinologic headache in a tertiary rhinology practice. Otolaryngology – Head and Neck Surg 2004; 130: 449-452.
Daudia, AT, Jones, NS. Facial migraine in a rhinological setting. Clinical Otolaryngology and Allied Sciences. 2002; 27(6): 521-525.
Spierings, EL. Migraine mechanism and management. Otolarynogol Clin N Am 36 (2003): 1063 – 1078.
Avnon, y, Nitzan, M, Sprecher, E, Rogowski, Z, and Yarnitsky, D. Different patterns of parasympathetic activation in uni- and bilateral migraineurs. Brain. 2003; 126: 1660-1670.
Stroud, RH, Bailey, BJ, Quinn, FB. Headache and Facial Pain. Dr. Quinn’s Online Textbook of Otolaryngology Grand Rounds Archive. 2001. http://www.utmb.edu/otoref/Grnds/HA-facial-pain-2001-0131/HA-facial-pain-2001.doc
Ondo, WG, Vuong KD, Derman, HS. Botulinum toxin A for chronic daily headache: a randomized, placebo-controlled, parallel design study. Cephalalgia 2004 (24): 60-65.