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Primary headache types and management gate02.pptx
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- 2. HEADACHE CAUSED BY TRACTION,DISPLACEMENT, INFLAMMATION, VASCULAR SPASM, DISTENTION OF THE PAIN SENSITIVE STRUCTURE IN THE HEAD OR NECK
- 3. Origins of Painin 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
- 4. 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
- 5. Primary Headaches ICHD-II. Cephalgia2004 (Suppl 1)
- 6. Primary Headache Types MigraineTension 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
- 7. Primary Headache Types MigraineTension 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
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- 9. Pathophysiology Brainstem neuronalhyperexcitability Cortical spreading depression with aura Abnormalities of 5-HT, CGRP, NE, DA, GABA, glutamate, NO, and endorphins Trigeminal Activation Marcus, DA. Headache Simplified 2008.
- 10. Presymptomatic hyperexcitabilty increasesbrain 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.
- 11. Migraine Migraine headachesare 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.
- 12. TEMPORAL PATTERN OFHEADACHE 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
- 13. International Headache Society-Diagnostic Criteria A. At least 5 attacks fulfilling criteria B–D B. Headache attacks lasting 4–72 hours (when untreated or unsuccessfully treated) C. Headache has at least 2 of the following 4 characteristics: 1.Unilateral location 2.Pulsating quality 3.Moderate or severe pain intensity 4.Aggravation by or causing avoidance of routing physical activity (e.g., walking or climbing stairs) D. During headache at least 1 of the following: 1.Nausea and/or vomiting 2.Photophobia and phonophobia E. Not better accounted for by another ICHD-3 diagnosis 1.1 Migraine without aura
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- 15. Acute Treatment -Triptans Fast onset/short duration Sumatriptan Rizatriptan Zomitriptan Almotriptan Eletriptan Treximet (Suma + Naproxen) Slow onset/long duration Naratriptan Frovatriptan
- 16. 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
- 17. 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
- 18. 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
- 19. 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
- 20. Ergot Side Effects Nausea and vomiting (pre-treat with antiemetic) Coronary artery spasm, angina, MI Tingling, numbness, Dizziness Increased BP and HR “Ergotism”
- 21. Choosing Acute Rx EarlyN/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
- 22. Indications for aPreventive 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
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- 24. TTH isthe 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.
- 25. Tension Type Headache Occursin 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
- 26. 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
- 27. 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
- 28. Pathophysiology Pathogenesis ofTTH 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.
- 29. Various precipitating factors Onehalf 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
- 30. THERAPY The goalsof pharmacotherapy are to relieve the headache, reduce morbidity, and prevent complications.
- 31. Acute Treatment (EpisodicTTH) 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
- 32. Preventive Treatment (ChronicTTH) 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**
- 33. Patient Education Advise thepatient 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
- 34. CLUSTER & TRIGEMINAL Ticdouloureux Baehr M, Frotscher M. Duus’ Topical Diagnosis in Neurology: Disorder Affecting the Trigeminal Nerve. Newyork: Thieme. 2005. Page 165-7
- 35. TRIGEMINAL NEURALGIA • AFACIAL 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
- 36. CLUSTER HEADACHE also knownas 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
- 37. CLUSTER HEADACHE BRIEFATTACKS 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
- 38. CLUSTER HEADACHE DISTRIBUTION OFSYMPTOMS AND SIGNS IN CLUSTER HEADACHE PTOSIS DURING ACUTE CLUSTER HEADACHE
- 39. CLUSTER HEADACHE Theattacks 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.
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- 42. 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
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