Dr Surendra Khosya, profile picture
Uploaded byDr Surendra Khosya
PPTX, PDF164,137 views

Headache ppt

1. Migraines can be classified as either primary or secondary headaches. Primary migraines include migraine without aura, migraine with aura, and tension-type headaches. Secondary migraines are caused by underlying structural or metabolic abnormalities. 2. Migraines can originate from extracranial or intracranial pain-sensitive structures. Common extracranial structures include the sinuses, eyes, ears, teeth, and blood vessels. Intracranial structures include arteries, dural veins and sinuses, and the meninges. 3. Migraines are treated either acutely to stop an attack or preventively to reduce frequency and severity. Acute treatments aim to rapidly relieve pain and associated

Embed presentation

Downloaded 5,597 times
Origins of Pain in the Head • Extra-cranial pain sensitive structures: – – – – – – – Sinuses Eyes/orbits Ears Teeth TMJ Blood vessels 5,7,9,10 cranial nerves carry pain from thes strucure • Intra-cranial pain sensitive structures: – 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 – Migraine – Cluster • SECONDARY – structural or metabolic abnormality: – Extracranial: sinusitis, otitis media, glaucoma, TMJ ds – Inracranial: SAH, vasculitis, dissection, ce ntral vein thrombosis, tumor, abscess, meningitis – Metabolic disorders: CO2 retention, CO poisoing
RED Flags • • • • • • • • New onset headache in a patient >50 y.o. Sudden, worst headache of one’s life Morning headache associated with N/V Fever, weight loss Worsens with valsalva maneuvers Focal neurologic deficits, jaw claudication Altered LOC Hx of trauma, cancer or HIV
Part 1: The primary headaches 1. Migraine 2. Tension-type headache 3. Cluster headache and other trigeminal autonomic cephalalgias 4. Other primary headaches ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
Primary Headache Types Migraine Tension Pain Throbbing, mod Pressure, t Description erate to ightness, severe, worse waxes and w/exertion wanes Associated Photo/phonoSymptoms phobia, n/v, aura Bajwa and Wootton. Up to Date 2007 None Cluster Abrupt onset, deep, continuous, excruciating, explosive Tearing, congestion, rhinorrhea, pallor, sweating
Primary Headache Types Migraine Location Duration Patient Appearance Tension Cluster 60-70% unilateral 4-72 hr Bilateral Unilateral 0.5-3 hr, many per day Resting in Remains Remains quiet dark active or active, prefers room; young prefers to hot shower, female rest male, smoker Bajwa and Wootton. Up to Date 2007 Variable
1. Migraine 1.1 Migraine without aura 1.2 Migraine with aura 1.3 Childhood periodic syndromes that are commonly precursors of migraine 1.4 Retinal migraine 1.5 Complications of migraine 1.6 Probable migraine ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
Pathophysiology • Brainstem neuronal hyperexcitability • Cortical spreading depression w/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 Cortex and Thalamus (Head pain) Marcus, DA. Headache Simplified 2008. Activation of cervical trigeminal system (Muscle spasm)
1.1 Migraine without aura A. At least 5 attacks fulfilling criteria B-D B. Headache attacks lasting 4-72 h (untreated or unsuccessfully treated) C. Headache has 2 of the following characteristics: 1. unilateral location 2. pulsating quality 3. moderate or severe pain intensity 4. aggravation by or causing avoidance of routine physical activity (eg, walking, climbing stairs) D. During headache 1 of the following: 1. nausea and/or vomiting 2. photophobia and phonophobia E. Not attributed to another disorder ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
1.1 Migraine without aura Notes • If <5 attacks but criteria B-E otherwise met, code as 1.6.1 Probable migraine without aura • When attacks occur on 15 d/mo for >3 mo, code as Notes 1.1 Migraine without aura + 1.5.1 Chronic migraine • Pulsating means varying with the heartbeat • In children: – attacks may last 1-72 h – occipital headache requires caution • In young children: – photophobia and/or phonophobia may be inferred from their behaviour 1.1 Migraine without aura ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
‘Not attributed to another disorder’ Note For all primary headaches, this criterion means: • History and physical/neurological examinations do not suggest any of the disorders listed in groups 5-12, or history and/or physical/ neurological examinations do suggest such disorder but it is ruled out by appropriate investigations, or such disorder is present but headache does not occur for the first time in close temporal relation to the disorder ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
1.2 Migraine with aura 1.2.1 1.2.2 1.2.3 1.2.4 1.2.5 1.2.6 Typical aura with migraine headache 1.2 aura with non-migraine headache TypicalMigraine with aura Typical aura without headache Familial hemiplegic migraine (FHM) Sporadic hemiplegic migraine Basilar-type migraine ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
1.2 Migraine with aura A. At least 2 attacks fulfilling criterion B 1.2 Migraine with aura B. Migraine aura fulfilling criteria B and C for one of the subforms 1.2.1-1.2.6 C. Not attributed to another disorder ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
1.2 Migraine with aura Subtypes new to classification 1.2.1 Typical aura with migraine headache • 1.2 Migraine with with headache aura most migraine auras are associated Subtypes new to classification fulfilling criteria for 1.1 Migraine without aura 1.2.2 Typical aura with non-migraine headache 1.2.3 Typical aura without headache • migraine aura is sometimes associated with a headache that does not fulfil these criteria • or occurs without headache ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
1.2.1 Typical aura with migraine headache A. At least 2 attacks fulfilling criteria B–D B. Aura consisting of 1 of the following, but no motor weakness: 1. fully reversible visual symptoms including positive and/or negative features 2. fully reversible sensory symptoms including positive and/or negative features 3. fully reversible dysphasic speech disturbance 1.2.1 Typical aura with migraine headache ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
1.2.1 Typical aura with migraine headache C. At least two of the following: 1. homonymous visual symptoms and/or unilateral sensory symptoms 2. at least one aura symptom develops gradually over 5 min and/or different aura symptoms occur in succession over 5 min 3. each symptom lasts 5 and 60 min D. Headache fulfilling criteria B-D for 1.1 Migraine without aura begins during the aura or follows aura within 60 min E. Not attributed to another disorder 1.2.1 Typical aura with migraine headache ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
1.2.2 Typical aura with non-migraine headache As 1.2.1 except: D. Headache that does not fulfil criteria B-D for 1.1 Migraine without aura begins during the aura or follows aura within 60 min ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
1.2.3 Typical aura without headache 1.2.3 Typical aura without headache As 1.2.1 except: D. Headache does not occur during aura nor follow aura within 60 min ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
1.2.4 Familial hemiplegic migraine (FHM) A. At least 2 attacks fulfilling criteria B and C B. Aura consisting of fully reversible motor weakness and 1 of: 1. fully reversible visual symptoms including positive and/or negative features 2. fully reversible sensory symptoms including positive and/or negative features 3. fully reversible dysphasic speech disturbance ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
1.2.6 Basilar-type migraine As 1.2.1 except: B. Aura consisting of 2 of the following fully reversible symptoms, but no motor weakness: 1. dysarthria; 2. vertigo; 3. tinnitus; 4. hypacusia; 5. diplopia; 6. visual symptoms simultaneously in both temporal and nasal fields of both eyes; 7. ataxia; 8. decreased level of consciousness; 9. simultaneously bilateral paraesthesias C. At least one of the following: 1. at least one one aura symptom develops gradually over 5 min and/or different aura symptoms occur in succession over 5 min 2. each aura symptom lasts 5 and 60 min ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
1.3 Childhood periodic syndromes that are commonly precursors of migraine 1.3.1 Cyclical vomiting 1.3.2 Abdominal migraine 1.3.3 Benign paroxysmal vertigo of childhood ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
1.3.2 Abdominal migraine A. At least 5 attacks fulfilling criteria B-D B. Attacks of abdominal pain lasting 1-72 h C. Abdominal pain has all of the following characteristics: 1. midline location, periumbilical or poorly localised 2. dull or “just sore” quality 3. moderate or severe intensity D. During abdominal pain 2 of the following: 1. anorexia; 2. nausea; 3. vomiting; 4. pallor E. Not attributed to another disorder ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
Types of Migraine Treatment • Acute – Taken during an attack – Reduces pain, associated symptoms and disability and stops progression • Preventive – Taken daily for months to years – Reduces frequency, severity, and duration – Used in addition to acute treatments .
Acute Treatment Principles • Treat attacks rapidly and consistently • Tailor treatment to the patient and the sx • Minimize adverse events and cost • Limit to 3 days per week or less
Antiemetics • Prevent and treat nausea • Improve GI motility • Enhance absorption of other anti-migraine medications • Limited RCT to support their use in migraine
Phenothiazines • Promethazine (Phenergan) – Available PO, IM, PR – Dose = 25-50 mg Q6H PRN – Blocks dopamine and histamine receptors • Prochlorperazine (Compazine) – Available PO, IM, IV, PR – Dose = 5-10 mg Q6H PRN – Blocks dopamine receptors • SE = sedation, dizziness, dystonic rxn
Migraine Specific Medications Triptans 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 Johnston et al Drugs 2010 Loder NEJM 2010 Precautions • Ischemic heart dz or stroke • High risk for CAD • Pregnancy • Hemiplegic or basilar migraine • Ergots • Use w/ SSRIs?
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
Triptan Comparison Drug Tmax (h) T1/2 (h) Metabolism Sumatriptan 50 &100 mg tablets 2.5 2 MAO-A Sumatriptan 20 mg nasal 1 2 Sumatriptan 6 mg subQ 0.16-0.2 2 Zolmitriptan 2.5 mg tab 2 3 Zolmitriptan 2.5 mg ODT 3.3 2.5-3 Zolmitriptan 5 mg nasal 4 2.82 Rizatriptan 10 mg tab 1.2 2 Rizatriptan 10 mg ODT 1.6-2.5 2 Naratriptan 2-3 5-6 P450, 50% unchanged Almotriptan 1.4-3.8 3.2-3.7 MAO-A, 3A4, and 2D6 Frovatriptan 2-4 26 Mostly unchanged Eletriptan 1-2 3.6-5.5 3A4 2D6 and MAO-A MAO-A
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 Recurrence • Nasal triptans • Sumatriptan SubQ • ODT triptans? • Nara, Frova, Almotriptan • Ergots • Triptan + NSAID Sensitive to SE Rapid Onset • Naratriptan • Frovatriptan • Almotriptan • 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
Beta Blockers • FDA approved for migraine prevention – Propranolol (Inderal) 60-240 mg PO once daily for ER or divided BID or TID for IR – Timolol (Blocadren) 10-30 mg PO daily in 2 divided doses • Limited evidence for migraine prevention – Nadolol (Corgard) 20-240 mg PO once daily – Atenolol (Tenormin) 50-150 mg PO daily or divided BID – Metoprolol (Lotensin, Toprol XL) 100-200 mg daily or divided BID for IR formulation
Beta Blockers Advantages • Thoroughly studied and widely used • Timolol (Blocadren) and propranolol (Inderal) are FDA approved • Good choice for patients with HTN, CAD, tremor, or anxiety Disadvantages • Side effects = fatigue, dizziness, depression , exercise intolerance, may worsen aura • Avoid in patients with severe asthma, depression, bradycar dia, Raynaud's, overt CHF
Calcium Channel Blockers . Although the mechanism by which calcium channel antagonists affect migraine is not known, . vasoconstriction , prevention of platelet aggregation and alterations in release and reuptake of serotonin. . Several trials have indicated some benefit for verapamil and flunarizine In recurrent migraine. . Verapamil in doses of 80 to 160 mg 3 times a day reduces the incidence of migraine with aura, but it is not as useful in migraine without aura.
Tricyclic Antidepressants • Amitriptyline (Elavil) 10-200 mg nightly • Nortriptyline (Pamelor) 10-150 mg nightly • Desipramine (Norpramin) 25-200 mg nightly • Imipramine (Tofranil) 10-200 mg nightly • Doxepin (Sinequan) 10-200 mg nightly Lower end of dosage range is usually effective for migraine prevention
Tricyclic Antidepressants Advantages • Inexpensive • Once daily dosing • Good choice for patients with insomnia, neuropathy, m ood disorders, fibromyalgia Disadvantages • None are FDA-approved • Side effects = sedation, weight gain, dry mouth, urinary retention • Avoid in sz disorder, cardiac conduction abnormalities, BPH
Other Antidepressants • Efficacy not established in clinical trials – Best for fluoxetine (Prozac) 20 mg daily – Anectodal evidence for other SSRIs, trazodone, mirtazapine, bupropion, venalfaxine, and duloxetine • Migraines are more likely to be poorly controlled if mood disorders are untreated
NSAIDs • Long-acting agents taken on a scheduled basis have low risk of causing MOH • Consider for patients who: – Have other chronic pain conditions – Frequently use short-acting NSAID for acute treatment – Are at low risk for developing complications from daily NSAID • Caution patients about exceeding maximum daily dose • Limited evidence to support efficacy
NSAIDs • Diclofenac 75 mg PO BID • Naproxen 500 mg PO BID • Meloxicam 7.5-15 mg PO daily • Celecoxib 200 mg PO daily • Aspirin 81-325 mg PO daily – May be especially helpful for reducing aura
Antiepileptic Drugs (AEDs) • FDA approved for migraine prevention – Divalporex Sodium (Depakote) – Topiramate (Topamax) • Limited evidence for migraine prevention – – – – Gabapentin (Neurontin) Lamotrigine (Lamictal) Levetiracetam (Keppra) Zonisamide (Zonegran)
Divalproex Sodium (Depakote) • Increases GABA and stabilizes nerve membrane activation thresholds • Dose = 500 - 1500 mg daily divided BID or TID – ER formulation allows for once daily dosing • NNT = 2.8 to 4.2 (to ↓ migraine frequency 50%) • Therapeutic plasma concentration = 50-100 mg/L
Divalproex Side Effects Common/dose related • Tremor • Drowsiness • Nausea/vomiting • Easy bruising • Weight gain • Nystagmus Rare/idiosyncratic • Hepatotoxicity • Pancreatitis • Alopecia • Thrombocytopenia • Agranulocytosis • Rash (SJS) • Suicidal behavior
Topiramate (Topamax) - MOA • Not completely understood • Blocks NMDA receptors • Blocks voltage dependant sodium channels • Enhances GABA • Weakly inhibits carbonic anhydrase .
Topiramate Dosing • Dose titration in clinical trials: – Initial dose = 25 mg daily – Titrate by 25 mg every week – No consistent additional benefit seen in doses >100 mg • Dose titration in U of U Headache Clinic – – – – Initial dose = 12.5 mg at bedtime Titrate by 12.5 mg every week Goal of 50 mg BID May eventually increase up to 100 mg BID in certain patients
Topiramate Side Effects Common • Paresthesias • Cognitive problems • Fatigue • Weight loss • Dizziness • Nausea • Taste perversion Rare or Serious • Metabolic acidosis • Depression • Nephrolithiasis • Glaucoma • Oligohydrosis • Suicidal behavior
Gabapentin (Neurontin) • Mechanism of action – – – – Enhances GABA activity Binds to alpha-2-delta subunit of voltage gated calcium channels Inhibits high-voltage-activated calcium currents Result is decreased synaptic transmission • Limited evidence from clinical trials for migraine prevention – NNT = 3 (50% reduction in migraine frequency) – Only 2 RCT, did not use typical migraine outcomes Vikelis and Rapoport. CNS Drugs 2010.
Botulinum Toxin • Recently FDA approved for chronic migraine • Dose = 155-195 units injected into muscles of face, neck and head • Mecahnism of Action (purposed) – Blocks release of Substance P and CGRP Inhibits peripheral signals to CNS and blocks central sensitization Dodick DW. Headache 2010.
Botulinum Toxin • Efficacy – Botulinum Toxin superior to placebo in 2 large, double blind, randomized, controlled trials – Botulinum Toxin similar to topiramate and amitriptyline in small, shorter duration studies – Botulinum toxin = placebo for episodic migraine • Side effects = muscle weakness, injection site pain, and “spread of toxin effect”
2. Tension-type headache 2.1 2.2 2.3 2.4 Infrequent episodic tension-type headache Frequent episodic tension-type headache Chronic tension-type headache Probable tension-type headache ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
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
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**
3. Cluster headache and other trigeminal autonomic cephalalgias 3. Cluster headache and other trigeminal autonomic 3.1 Cluster headache cephalalgias 3.2 Paroxysmal hemicrania 3.3 Short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT) 3.4 Probable trigeminal autonomic cephalalgia ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
3.1 Cluster headache A. At least 5 attacks fulfilling criteria B-D B. Severe or very severe unilateral orbital, supraorbital and/or temporal pain lasting 15-180 min if untreated C. Headache is accompanied by 1 of the following: 1. ipsilateral conjunctival injection and/or lacrimation 2. ipsilateral nasal congestion and/or rhinorrhoea 3. ipsilateral eyelid oedema 4. ipsilateral forehead and facial sweating 5. ipsilateral miosis and/or ptosis 6. a sense of restlessness or agitation D. Attacks have a frequency from 1/2 d to 8/d E. Not attributed to another disorder ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
3.1 Cluster headache 3.1.1 Episodic cluster headache A. Attacks fulfilling criteria A-E for 3.1 Cluster headache B. At least two cluster periods lasting 7-365 d and separated by pain-free remission periods of 1 mo 3.1.2 Chronic cluster headache A. Attacks fulfilling criteria A-E for 3.1 Cluster headache B. Attacks recur over >1 y without remission periods or with remission periods lasting <1 mo
Cluster Headache Abortive Treatment • Inhalation of 100% oxygen up to 15 L/min • Sumatriptan (Imitrex) 4-6mg subQ or 20 mg nasally • Zolmitriptan (Zomig) 5-10 mg nasally or PO • Dihdroergotamine (Migranal) 1 mg nasally up to 3 mg in 24 hours • Prednisone 40-100 mg burst and taper Bajwa and Wootton. Up to Date 2007
Cluster Headache Prevention • Verapamil 120-360 mg PO daily • Lithium 300 mg PO BID to TID • Divalproex 500-1500 mg PO daily to BID • Topiramate 50-200 mg PO divided BID • Prednisone 40-100 mg burst and taper • Melatonin 3 mg PO QPM Bajwa and Wootton. Up to Date 2007
The Headache Diary • Pain score • Characteristics of the pain • Associated symptoms • Acute treatments used and response • Triggers
The Headache Diary • Makes the patient responsible for their disease • Aids in diagnosis and differentiating between headache types • Assesses efficacy of acute and preventive treatment • Identifies triggers • Minimizes recall bias
3.2 Paroxysmal hemicrania A. At least 20 attacks fulfilling criteria B-D B. Attacks of severe unilateral orbital, supraorbital or temporal pain lasting 2-30 min C. Headache is accompanied by 1 of the following: 1. ipsilateral conjunctival injection and/or lacrimation 2. ipsilateral nasal congestion and/or rhinorrhoea 3. ipsilateral eyelid oedema 4. ipsilateral forehead and facial sweating 5. ipsilateral miosis and/or ptosis D. Attacks have a frequency >5/d for > half of the time, although periods with lower frequency may occur E. Attacks are prevented completely by therapeutic doses of indomethacin F. Not attributed to another disorder ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
4. Other primary headaches 4.1 Primary stabbing headache 4.2 Primary cough headache 4.3 Primary exertional headache 4.4 Primary headache associated with sexual activity 4.5 Hypnic headache 4.6 Primary thunderclap headache 4.7 Hemicrania continua 4.8 New daily-persistent headache (NDPH) ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
4.5 Hypnic headache New entrant to classification A. Dull headache fulfilling criteria B-D B. Develops only during sleep, and awakens patient C. At least two of the following characteristics: New entrant to classification 1. occurs >15 times/mo 2. lasts 15 min after waking 3. first occurs after age of 50 y D. No autonomic symptoms and no more than one of nausea, photophobia or phonophobia E. Not attributed to another disorder 4.5 Hypnic headache ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
4.6 Primary thunderclap headache A. Severe head pain fulfilling criteria B and C B. Both of the following characteristics: 1. sudden onset, reaching maximum intensity in <1 min 2. lasting from 1 h to 10 d C. Does not recur regularly over subsequent weeks or months D. Not attributed to another disorder ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
4.7 Hemicrania continua New entrant to classification A. Headache for >3 mo fulfilling criteria B-D B. All of the following characteristics: 1. unilateral pain without side-shift 2. daily and continuous, without pain-free periods 3. moderate intensity, with exacerbations of severe pain C. At least one of the following autonomic features occurs during exacerbations, ipsilateral to the pain: 1. conjunctival injection and/or lacrimation 2. nasal congestion and/or rhinorrhoea 3. ptosis and/or miosis D. Complete response to therapeutic doses of indomethacin E. Not attributed to another disorder ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
4.8 New daily-persistent headache New entrant to classification A. Headache for >3 mo fulfilling criteria B-D B. Headache is daily and unremitting from onset or from <3 d from onset C. At least two of the following pain characteristics: New entrant to classification 1. bilateral location 2. pressing/tightening (non-pulsating) quality 3. mild or moderate intensity 4. not aggravated by routine physical activity D. Both of the following: 1. not >1 of photophobia, phonophobia or mild nausea 2. neither moderate or severe nausea nor vomiting E. Not attributed to another disorder 4.8 New daily-persistent headache ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
Primary Chronic Daily Headache Disorders of Long-Duration (>4 h) Disorder Demographic Clinical Features Recommended Treatments Chronic migraine Headache ≥15 days per month for >3 mo, of which ≥8 days Female/male, 3 : 1 Prevalence Topiramate, divalproex sodium, meet ICHD-II criteria for 2% amitriptyline migraine without aura or relief with triptan or ergot Mild-moderate severity; no Chronic tension-type headache Equal sex ratio Prevalence 2% migrainous symptoms; bilateral, Amitriptyline nonthrobbing New daily persistent headache Female > male Bilateral, persistent, moderately severe; may be preceded by viral infection; may resemble Amitriptyline migraine or tension-type headache Hemicrania continua Rare; unilateral, constant, exacerbations of severe headache, cranial autonomic Indomethacin symptoms, and ice-pick pain; responsive to indomethacin by definition Female > male
Diagnostic criteria for secondary headaches A. Headache with one (or more) of the following [listed] characteristics and fulfilling criteria C and D B. Another disorder known to be able to cause headache has been demonstrated C. Headache occurs in close temporal relation to the other disorder and/or there is other evidence of a causal relationship D. Headache is greatly reduced or resolves within 3 mo (shorter for some disorders) after successful treatment or spontaneous remission of the causative disorder ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
6. Headache attributed to cranial or cervical vascular disorder 6.1 Headache attributed to ischaemic stroke or transient ischaemic attack 6.2 Headache attributed to non-traumatic intracranial haemorrhage 6.3 Headache attributed to unruptured vascular malformation 6.4 Headache attributed to arteritis 6.5 Carotid or vertebral artery pain 6.6 Headache attributed to cerebral venous thrombosis 6.7 Headache attributed to other intracranial vascular disorder ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
6.4.1 Headache attributed to giant cell arteritis A. Any new persisting headache fulfilling criteria C and D B. At least one of the following: 1. swollen tender scalp artery with elevated erythrocyte sedimentation rate (ESR) and/or C reactive protein (CRP) 2. temporal artery biopsy demonstrating giant cell arteritis C. Headache develops in close temporal relation to other symptoms and signs of giant cell arteritis D. Headache resolves or greatly improves within 3 d of high-dose steroid treatment ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
6.7.1 CADASIL A. Attacks of migraine with aura, with or without other neurological signs B. Typical white matter changes on MRI T2WI C. Diagnostic confirmation from skin biopsy evidence or genetic testing (Notch 3 mutations) ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
7.4.2 Headache attributed directly to neoplasm A. Headache with 1 of the following characteristics and fulfilling criteria C and D: 1. progressive 2. localised 3. worse in the morning 4. aggravated by coughing or bending forward B. Intracranial neoplasm shown by imaging C. Headache develops in temporal (and usually spatial) relation to the neoplasm D. Headache resolves within 7 d after surgical removal or volume-reduction of neoplasm or treatment with corticosteroids ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
9.1 Headache attributed to intracranial infection 9.1.1 Headache attributed to bacterial meningitis 9.1.2 Headache attributed to lymphocytic meningitis 9.1.3 Headache attributed to encephalitis 9.1.4 Headache attributed to brain abscess 9.1.5 Headache attributed to subdural empyema ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
9.1.1 Headache attributed to bacterial meningitis A. Headache with 1 of the following characteristics and fulfilling criteria C and D: 1. diffuse pain 2. intensity increasing to severe 3. associated with nausea, photophobia and/or phonophobia B. Evidence of bacterial meningitis from examination of CSF C. Headache develops during the meningitis D. One or other of the following: 1. headache resolves within 3 mo after relief from meningitis 2. headache persists but 3 mo have not yet passed since relief from meningitis 9.1.1 Headache attributed to bacterial meningitis ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
9.1.1 Headache attributed to bacterial meningitis Notes • Criterion D does not relate to evidence of causation • Causation is established by onset during diagnosed bacterial meningitis, whilst it is well recognised that this headache often persists • When this occurs, 9.4.1 Chronic post-bacterial meningitis headache is diagnosed • Criterion D2 allows a default diagnosis within 3 mo, before it is known whether headache will resolve or persist ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
9.2 Headache attributed to systemic infection A. Headache with 1 of the following characteristics and fulfilling criteria C and D: 1. diffuse pain 2. intensity increasing to moderate or severe 3. associated with fever, general malaise or other symptoms of systemic infection B. Evidence of systemic infection C. Headache develops during the systemic infection D. Headache resolves within 72 h after effective treatment of the infection ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
Headache ppt
Headache ppt
Headache ppt

More Related Content

PPT
Approach to headache
byDr. Faisal Al Haddad
 
PPTX
Headache types & management
bySameh Abdel-ghany
 
PPTX
Headache
byNeurologyKota
 
PPTX
Headache
byHAMAD DHUHAYR
 
PPTX
Practical Approach to headache
byDr Surendra Khosya
 
PPTX
Approach to headache
byOmkar Singh
 
PPT
Headache and associated emergencies
byAhmad Shahir
 
PPTX
Headache
byHarunMohamed7
 
Approach to headache
byDr. Faisal Al Haddad
 
Headache types & management
bySameh Abdel-ghany
 
Headache
byNeurologyKota
 
Headache
byHAMAD DHUHAYR
 
Practical Approach to headache
byDr Surendra Khosya
 
Approach to headache
byOmkar Singh
 
Headache and associated emergencies
byAhmad Shahir
 
Headache
byHarunMohamed7
 

What's hot

PPTX
Vertigo
byNishitha Ashok
 
PPTX
Tremors
byNeurologyKota
 
PPTX
Vertigo
byNeurologyKota
 
PPTX
Ischemic stroke
bySyed Muhammad Ali Shah
 
PPTX
Tremor
bybausher willayat
 
PPTX
Benign Paroxysmal Positional Vertigo (BPPV)
bysunil kumar daha
 
PPTX
Lateral medullary syndrome {Wallenberg Syndrome}
byProf. Ahmed Mohamed Badheeb
 
PPTX
Wernicke’s encephalopathy
byShyala Chand
 
PPTX
Headache (tension type headache, migraine)
byautumnpianist
 
PPTX
Hepatomegaly
byDr. AKSHATA C
 
PPTX
Neurosyphilis
byEkta Patel
 
PPTX
Benign Paroxysmal Positional Vertigo (BPPV)
byEverydayHearing.com
 
PPT
Diabetic neuropathy
byDr. Tushar Patil
 
PPTX
Migraine
byAhmed Abouelela
 
PPTX
Coma
bysm171181
 
PPTX
Facial palsy
byDr. Vibhash Kumar Vaidya
 
PDF
Differences UMN lesion vs LMN lesion
byDr Nilesh Kate
 
PPTX
Splenomegaly
byRamzee Small
 
PPTX
Management of coma
byPS Deb
 
PPTX
Compressive Myelopathy
byStanley Medical College, Department of Medicine
 
Vertigo
byNishitha Ashok
 
Tremors
byNeurologyKota
 
Vertigo
byNeurologyKota
 
Ischemic stroke
bySyed Muhammad Ali Shah
 
Tremor
bybausher willayat
 
Benign Paroxysmal Positional Vertigo (BPPV)
bysunil kumar daha
 
Lateral medullary syndrome {Wallenberg Syndrome}
byProf. Ahmed Mohamed Badheeb
 
Wernicke’s encephalopathy
byShyala Chand
 
Headache (tension type headache, migraine)
byautumnpianist
 
Hepatomegaly
byDr. AKSHATA C
 
Neurosyphilis
byEkta Patel
 
Benign Paroxysmal Positional Vertigo (BPPV)
byEverydayHearing.com
 
Diabetic neuropathy
byDr. Tushar Patil
 
Migraine
byAhmed Abouelela
 
Coma
bysm171181
 
Facial palsy
byDr. Vibhash Kumar Vaidya
 
Differences UMN lesion vs LMN lesion
byDr Nilesh Kate
 
Splenomegaly
byRamzee Small
 
Management of coma
byPS Deb
 
Compressive Myelopathy
byStanley Medical College, Department of Medicine
 

Viewers also liked

PPT
Headache
byPraveen Nagula
 
PPTX
HEADACHE - CLASSIFICATION
byRajesh Kabilan
 
PPTX
Stroke
byzuni1412
 
PPT
Headaches Lecture
bytest
 
PPTX
Headache
byAbino David
 
PPT
Head trauma & Management
byUthamalingam Murali
 
PPT
Stroke
byCarlos Rene Espino de la Cueva
 
Headache
byPraveen Nagula
 
HEADACHE - CLASSIFICATION
byRajesh Kabilan
 
Stroke
byzuni1412
 
Headaches Lecture
bytest
 
Headache
byAbino David
 
Head trauma & Management
byUthamalingam Murali
 
Stroke
byCarlos Rene Espino de la Cueva
 

Similar to Headache ppt

PPTX
primary headche by smsmc.pptx jaipur rajasthan
bydineshdandia
 
PPT
HEADCHE : Migraine
byVaroon Vadodaria
 
PPTX
Migraine in children by Rafi
byMahammad Rafi
 
PPT
Neurological lectures...Migraine
byProfessor Yasser Metwally
 
PPTX
Primary headache and its types (Migraine)
byDikshya upreti
 
PPTX
Pathophysiology: Migraine & Headache
byBrian Piper
 
PPTX
diapos de la clasificacion internacional de cefalea ingles.pptx
byEvitaBame
 
PPTX
Neuropsychiatric aspects of headache
byJITHIN T JOSEPH
 
PPTX
Lecture on Pediatric headache.pptx
byMarthaBolanos
 
PPTX
328dc252-007e-4d7f-a3ac-f1f15731252b.pptx
bydoctorrezaeian
 
PPTX
Migraine - Diagnosis and Management.pptx
byfadglover
 
PPT
headache neurological sight of question.ppt
byborykbay
 
PPT
Headache in clinical practice
byKhaled Osama
 
PPTX
The best presentation on primary and secondary types ofheadache (fasik.pptx
byMisaleHaile
 
PPTX
APPROACH TO HEADACHE AND CRANIO FASCIAL PAIN.pptx
byneurologykotaseminar
 
PPTX
Seminar rare headache syndromes
bySucharita Ray
 
PPTX
Headache Biruk.pptx approach and management
byAddisuFekede
 
PPT
Bash Guidelines Slides
byMedicineAndHealthNeurolog
 
PPTX
Recent Migraine Headache Approach and Treatment.pptx
bySURENDRAKHOSYA2
 
PPT
headache1bbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbb.ppt
byssuser4c6a4b
 
primary headche by smsmc.pptx jaipur rajasthan
bydineshdandia
 
HEADCHE : Migraine
byVaroon Vadodaria
 
Migraine in children by Rafi
byMahammad Rafi
 
Neurological lectures...Migraine
byProfessor Yasser Metwally
 
Primary headache and its types (Migraine)
byDikshya upreti
 
Pathophysiology: Migraine & Headache
byBrian Piper
 
diapos de la clasificacion internacional de cefalea ingles.pptx
byEvitaBame
 
Neuropsychiatric aspects of headache
byJITHIN T JOSEPH
 
Lecture on Pediatric headache.pptx
byMarthaBolanos
 
328dc252-007e-4d7f-a3ac-f1f15731252b.pptx
bydoctorrezaeian
 
Migraine - Diagnosis and Management.pptx
byfadglover
 
headache neurological sight of question.ppt
byborykbay
 
Headache in clinical practice
byKhaled Osama
 
The best presentation on primary and secondary types ofheadache (fasik.pptx
byMisaleHaile
 
APPROACH TO HEADACHE AND CRANIO FASCIAL PAIN.pptx
byneurologykotaseminar
 
Seminar rare headache syndromes
bySucharita Ray
 
Headache Biruk.pptx approach and management
byAddisuFekede
 
Bash Guidelines Slides
byMedicineAndHealthNeurolog
 
Recent Migraine Headache Approach and Treatment.pptx
bySURENDRAKHOSYA2
 
headache1bbbbbbbbbbbbbbbbbbbbbbbbbbbbbbbb.ppt
byssuser4c6a4b
 

More from Dr Surendra Khosya

PPTX
Final ppt epilepsy
byDr Surendra Khosya
 
PPTX
Recent Advances in The Treatment of Epilepsy
byDr Surendra Khosya
 
PPTX
Violence against doctors: A viral epidemic ?
byDr Surendra Khosya
 
PPTX
Novel coronavirus(2019 n cov)
byDr Surendra Khosya
 
PPTX
Approach to acute stroke BE FAST
byDr Surendra Khosya
 
PPTX
INTERACT-2 (SAMURAI-ICH)early blood pressure (BP) variability and clinical ou...
byDr Surendra Khosya
 
PPTX
Approach to temporal lobe anatomy,function,epilepsy MRI finding
byDr Surendra Khosya
 
PPT
Cerebellum and afferent ayaxia
byDr Surendra Khosya
 
PPTX
new gene and new target in alzheimer disease
byDr Surendra Khosya
 
PPTX
Approach to temporal lobe
byDr Surendra Khosya
 
PPTX
approach to Language dysfunction and speech disorder
byDr Surendra Khosya
 
PPTX
Marchiafava–Bignami disease (MBD)
byDr Surendra Khosya
 
PPTX
Marchiafava–Bignami disease (MBD)
byDr Surendra Khosya
 
PPTX
Epilepsia ppt
byDr Surendra Khosya
 
Final ppt epilepsy
byDr Surendra Khosya
 
Recent Advances in The Treatment of Epilepsy
byDr Surendra Khosya
 
Violence against doctors: A viral epidemic ?
byDr Surendra Khosya
 
Novel coronavirus(2019 n cov)
byDr Surendra Khosya
 
Approach to acute stroke BE FAST
byDr Surendra Khosya
 
INTERACT-2 (SAMURAI-ICH)early blood pressure (BP) variability and clinical ou...
byDr Surendra Khosya
 
Approach to temporal lobe anatomy,function,epilepsy MRI finding
byDr Surendra Khosya
 
Cerebellum and afferent ayaxia
byDr Surendra Khosya
 
new gene and new target in alzheimer disease
byDr Surendra Khosya
 
Approach to temporal lobe
byDr Surendra Khosya
 
approach to Language dysfunction and speech disorder
byDr Surendra Khosya
 
Marchiafava–Bignami disease (MBD)
byDr Surendra Khosya
 
Marchiafava–Bignami disease (MBD)
byDr Surendra Khosya
 
Epilepsia ppt
byDr Surendra Khosya
 

Recently uploaded

PPTX
COVID -19 or SARS-CoV-2(2019-nCoV) disease
byNandiniM72
 
PPTX
PLASMA ENZYMES IN CLINICAL DIAGNOSIS AND TREATMENT I.pptx
bybenedictao083
 
PPTX
Acid Base Balance (acids, bases, buffer system, Henderson Hasselbalch's equat...
byDr. Santhosh Kumar. N
 
PPTX
Back Pain Evaluation: Red Flags, Neurological Examination & Special Tests | S...
byDaradia: The Pain Clinic
 
PPTX
Mental Status Examination | B.Sc Nursing 5th Semester | Mental Health Nursing I
bydhananjaydongare5
 
PPTX
THE-SKELETAL-SYSTEM. and its importance,
byedralinkalix
 
PPTX
gram positive bacteria bacteriology medical.pptx
byjobmwitah
 
PPTX
Management_of_Maternity_Women in outpatient .pptx
byMudaSsarChaudhary2
 
PPTX
From Planning to Delivery: Precision Workflows That Reduce Errors, Toxicity, ...
bySubrata Roy
 
PPTX
Drug use evaluation and WHO drug use Indicators.pptx
byLok Raj Pant
 
PPTX
Sacroiliac Joint Pain: Clinical Diagnosis, Provocation Tests, and SI Joint Bl...
byDaradia: The Pain Clinic
 
PPTX
EBOLA VIRUS DISEASE ppt -Ayurveda Detailing
byNandiniM72
 
PPTX
Describe affinity in proper way on ppt.pptx
bymedhiuddipan045
 
PDF
overview of human urinary system anatomy
bynusratjahanpharmacy
 
PDF
Understanding Olaparib Therapy for Cancer Treatment
byLetsMeds
 
PPTX
Diabetic retinopathy- Investigation and Management
byDr. Sambandha Khati
 
PPTX
Acute Peritonitis and Acute Mesenteric Ischemia: Pathophysiology, Diagnosis, ...
byGuganesh Vasan G
 
PPTX
professionalism in nursing presentation slides
bynyongesadickson10
 
PPTX
CH01 Red Blood Cell and Platelet Preservation Historical Perspectives and Cur...
byJingchunLiu2
 
PPTX
Cardio-Respiratory-System-to-Physical-Education.pptx
byedralinkalix
 
COVID -19 or SARS-CoV-2(2019-nCoV) disease
byNandiniM72
 
PLASMA ENZYMES IN CLINICAL DIAGNOSIS AND TREATMENT I.pptx
bybenedictao083
 
Acid Base Balance (acids, bases, buffer system, Henderson Hasselbalch's equat...
byDr. Santhosh Kumar. N
 
Back Pain Evaluation: Red Flags, Neurological Examination & Special Tests | S...
byDaradia: The Pain Clinic
 
Mental Status Examination | B.Sc Nursing 5th Semester | Mental Health Nursing I
bydhananjaydongare5
 
THE-SKELETAL-SYSTEM. and its importance,
byedralinkalix
 
gram positive bacteria bacteriology medical.pptx
byjobmwitah
 
Management_of_Maternity_Women in outpatient .pptx
byMudaSsarChaudhary2
 
From Planning to Delivery: Precision Workflows That Reduce Errors, Toxicity, ...
bySubrata Roy
 
Drug use evaluation and WHO drug use Indicators.pptx
byLok Raj Pant
 
Sacroiliac Joint Pain: Clinical Diagnosis, Provocation Tests, and SI Joint Bl...
byDaradia: The Pain Clinic
 
EBOLA VIRUS DISEASE ppt -Ayurveda Detailing
byNandiniM72
 
Describe affinity in proper way on ppt.pptx
bymedhiuddipan045
 
overview of human urinary system anatomy
bynusratjahanpharmacy
 
Understanding Olaparib Therapy for Cancer Treatment
byLetsMeds
 
Diabetic retinopathy- Investigation and Management
byDr. Sambandha Khati
 
Acute Peritonitis and Acute Mesenteric Ischemia: Pathophysiology, Diagnosis, ...
byGuganesh Vasan G
 
professionalism in nursing presentation slides
bynyongesadickson10
 
CH01 Red Blood Cell and Platelet Preservation Historical Perspectives and Cur...
byJingchunLiu2
 
Cardio-Respiratory-System-to-Physical-Education.pptx
byedralinkalix
 

Headache ppt

  • 1.
    Origins of Painin the Head • Extra-cranial pain sensitive structures: – – – – – – – Sinuses Eyes/orbits Ears Teeth TMJ Blood vessels 5,7,9,10 cranial nerves carry pain from thes strucure • Intra-cranial pain sensitive structures: – Arteries of circle of willis and proximal dural arteries, – Dural Venous sinuses,veins – Meninges – Dura
  • 2.
    Classification of Headaches •PRIMARY - NO structural or metabolic abnormality: – Tension – Migraine – Cluster • SECONDARY – structural or metabolic abnormality: – Extracranial: sinusitis, otitis media, glaucoma, TMJ ds – Inracranial: SAH, vasculitis, dissection, ce ntral vein thrombosis, tumor, abscess, meningitis – Metabolic disorders: CO2 retention, CO poisoing
  • 3.
    RED Flags • • • • • • • • New onsetheadache in a patient >50 y.o. Sudden, worst headache of one’s life Morning headache associated with N/V Fever, weight loss Worsens with valsalva maneuvers Focal neurologic deficits, jaw claudication Altered LOC Hx of trauma, cancer or HIV
  • 4.
    Part 1: The primaryheadaches 1. Migraine 2. Tension-type headache 3. Cluster headache and other trigeminal autonomic cephalalgias 4. Other primary headaches ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
  • 5.
    Primary Headache Types Migraine Tension Pain Throbbing,mod Pressure, t Description erate to ightness, severe, worse waxes and w/exertion wanes Associated Photo/phonoSymptoms phobia, n/v, aura Bajwa and Wootton. Up to Date 2007 None Cluster Abrupt onset, deep, continuous, excruciating, explosive Tearing, congestion, rhinorrhea, pallor, sweating
  • 6.
    Primary Headache Types Migraine Location Duration Patient Appearance Tension Cluster 60-70% unilateral 4-72hr Bilateral Unilateral 0.5-3 hr, many per day Resting in Remains Remains quiet dark active or active, prefers room; young prefers to hot shower, female rest male, smoker Bajwa and Wootton. Up to Date 2007 Variable
  • 7.
    1. Migraine 1.1 Migrainewithout aura 1.2 Migraine with aura 1.3 Childhood periodic syndromes that are commonly precursors of migraine 1.4 Retinal migraine 1.5 Complications of migraine 1.6 Probable migraine ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
  • 8.
    Pathophysiology • Brainstem neuronalhyperexcitability • Cortical spreading depression w/aura • Abnormalities of 5-HT, CGRP, NE, DA, GABA, glutamate, NO, and endorphins • Trigeminal Activation Marcus, DA. Headache Simplified 2008.
  • 9.
    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 Cortex and Thalamus (Head pain) Marcus, DA. Headache Simplified 2008. Activation of cervical trigeminal system (Muscle spasm)
  • 10.
    1.1 Migraine withoutaura A. At least 5 attacks fulfilling criteria B-D B. Headache attacks lasting 4-72 h (untreated or unsuccessfully treated) C. Headache has 2 of the following characteristics: 1. unilateral location 2. pulsating quality 3. moderate or severe pain intensity 4. aggravation by or causing avoidance of routine physical activity (eg, walking, climbing stairs) D. During headache 1 of the following: 1. nausea and/or vomiting 2. photophobia and phonophobia E. Not attributed to another disorder ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
  • 11.
    1.1 Migraine withoutaura Notes • If <5 attacks but criteria B-E otherwise met, code as 1.6.1 Probable migraine without aura • When attacks occur on 15 d/mo for >3 mo, code as Notes 1.1 Migraine without aura + 1.5.1 Chronic migraine • Pulsating means varying with the heartbeat • In children: – attacks may last 1-72 h – occipital headache requires caution • In young children: – photophobia and/or phonophobia may be inferred from their behaviour 1.1 Migraine without aura ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
  • 12.
    ‘Not attributed toanother disorder’ Note For all primary headaches, this criterion means: • History and physical/neurological examinations do not suggest any of the disorders listed in groups 5-12, or history and/or physical/ neurological examinations do suggest such disorder but it is ruled out by appropriate investigations, or such disorder is present but headache does not occur for the first time in close temporal relation to the disorder ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
  • 13.
    1.2 Migraine withaura 1.2.1 1.2.2 1.2.3 1.2.4 1.2.5 1.2.6 Typical aura with migraine headache 1.2 aura with non-migraine headache TypicalMigraine with aura Typical aura without headache Familial hemiplegic migraine (FHM) Sporadic hemiplegic migraine Basilar-type migraine ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
  • 14.
    1.2 Migraine withaura A. At least 2 attacks fulfilling criterion B 1.2 Migraine with aura B. Migraine aura fulfilling criteria B and C for one of the subforms 1.2.1-1.2.6 C. Not attributed to another disorder ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
  • 15.
    1.2 Migraine withaura Subtypes new to classification 1.2.1 Typical aura with migraine headache • 1.2 Migraine with with headache aura most migraine auras are associated Subtypes new to classification fulfilling criteria for 1.1 Migraine without aura 1.2.2 Typical aura with non-migraine headache 1.2.3 Typical aura without headache • migraine aura is sometimes associated with a headache that does not fulfil these criteria • or occurs without headache ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
  • 16.
    1.2.1 Typical aura withmigraine headache A. At least 2 attacks fulfilling criteria B–D B. Aura consisting of 1 of the following, but no motor weakness: 1. fully reversible visual symptoms including positive and/or negative features 2. fully reversible sensory symptoms including positive and/or negative features 3. fully reversible dysphasic speech disturbance 1.2.1 Typical aura with migraine headache ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
  • 17.
    1.2.1 Typical aura withmigraine headache C. At least two of the following: 1. homonymous visual symptoms and/or unilateral sensory symptoms 2. at least one aura symptom develops gradually over 5 min and/or different aura symptoms occur in succession over 5 min 3. each symptom lasts 5 and 60 min D. Headache fulfilling criteria B-D for 1.1 Migraine without aura begins during the aura or follows aura within 60 min E. Not attributed to another disorder 1.2.1 Typical aura with migraine headache ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
  • 18.
    1.2.2 Typical aura withnon-migraine headache As 1.2.1 except: D. Headache that does not fulfil criteria B-D for 1.1 Migraine without aura begins during the aura or follows aura within 60 min ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
  • 19.
    1.2.3 Typical aura withoutheadache 1.2.3 Typical aura without headache As 1.2.1 except: D. Headache does not occur during aura nor follow aura within 60 min ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
  • 20.
    1.2.4 Familial hemiplegic migraine(FHM) A. At least 2 attacks fulfilling criteria B and C B. Aura consisting of fully reversible motor weakness and 1 of: 1. fully reversible visual symptoms including positive and/or negative features 2. fully reversible sensory symptoms including positive and/or negative features 3. fully reversible dysphasic speech disturbance ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
  • 21.
    1.2.6 Basilar-type migraine As1.2.1 except: B. Aura consisting of 2 of the following fully reversible symptoms, but no motor weakness: 1. dysarthria; 2. vertigo; 3. tinnitus; 4. hypacusia; 5. diplopia; 6. visual symptoms simultaneously in both temporal and nasal fields of both eyes; 7. ataxia; 8. decreased level of consciousness; 9. simultaneously bilateral paraesthesias C. At least one of the following: 1. at least one one aura symptom develops gradually over 5 min and/or different aura symptoms occur in succession over 5 min 2. each aura symptom lasts 5 and 60 min ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
  • 22.
    1.3 Childhood periodicsyndromes that are commonly precursors of migraine 1.3.1 Cyclical vomiting 1.3.2 Abdominal migraine 1.3.3 Benign paroxysmal vertigo of childhood ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
  • 23.
    1.3.2 Abdominal migraine A.At least 5 attacks fulfilling criteria B-D B. Attacks of abdominal pain lasting 1-72 h C. Abdominal pain has all of the following characteristics: 1. midline location, periumbilical or poorly localised 2. dull or “just sore” quality 3. moderate or severe intensity D. During abdominal pain 2 of the following: 1. anorexia; 2. nausea; 3. vomiting; 4. pallor E. Not attributed to another disorder ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
  • 24.
    Types of MigraineTreatment • Acute – Taken during an attack – Reduces pain, associated symptoms and disability and stops progression • Preventive – Taken daily for months to years – Reduces frequency, severity, and duration – Used in addition to acute treatments .
  • 25.
    Acute Treatment Principles •Treat attacks rapidly and consistently • Tailor treatment to the patient and the sx • Minimize adverse events and cost • Limit to 3 days per week or less
  • 26.
    Antiemetics • Prevent andtreat nausea • Improve GI motility • Enhance absorption of other anti-migraine medications • Limited RCT to support their use in migraine
  • 27.
    Phenothiazines • Promethazine (Phenergan) –Available PO, IM, PR – Dose = 25-50 mg Q6H PRN – Blocks dopamine and histamine receptors • Prochlorperazine (Compazine) – Available PO, IM, IV, PR – Dose = 5-10 mg Q6H PRN – Blocks dopamine receptors • SE = sedation, dizziness, dystonic rxn
  • 28.
  • 29.
    Acute Treatment -Triptans Fast onset/short duration • Sumatriptan • Rizatriptan • Zomitriptan • Almotriptan • Eletriptan • Treximet (Suma + Naproxen) Slow onset/long duration • Naratriptan • Frovatriptan
  • 30.
    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
  • 31.
    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 Johnston et al Drugs 2010 Loder NEJM 2010 Precautions • Ischemic heart dz or stroke • High risk for CAD • Pregnancy • Hemiplegic or basilar migraine • Ergots • Use w/ SSRIs?
  • 32.
    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
  • 33.
    Triptan Comparison Drug Tmax (h) T1/2(h) Metabolism Sumatriptan 50 &100 mg tablets 2.5 2 MAO-A Sumatriptan 20 mg nasal 1 2 Sumatriptan 6 mg subQ 0.16-0.2 2 Zolmitriptan 2.5 mg tab 2 3 Zolmitriptan 2.5 mg ODT 3.3 2.5-3 Zolmitriptan 5 mg nasal 4 2.82 Rizatriptan 10 mg tab 1.2 2 Rizatriptan 10 mg ODT 1.6-2.5 2 Naratriptan 2-3 5-6 P450, 50% unchanged Almotriptan 1.4-3.8 3.2-3.7 MAO-A, 3A4, and 2D6 Frovatriptan 2-4 26 Mostly unchanged Eletriptan 1-2 3.6-5.5 3A4 2D6 and MAO-A MAO-A
  • 34.
    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
  • 35.
    Ergot Side Effects •Nausea and vomiting (pre-treat with antiemetic) • Coronary artery spasm, angina, MI • Tingling, numbness, Dizziness • Increased BP and HR • “Ergotism”
  • 36.
    Choosing Acute Rx EarlyN/V Recurrence • Nasal triptans • Sumatriptan SubQ • ODT triptans? • Nara, Frova, Almotriptan • Ergots • Triptan + NSAID Sensitive to SE Rapid Onset • Naratriptan • Frovatriptan • Almotriptan • Sumatriptan SubQ • Nasal Triptans • DHE nasal or IM
  • 37.
    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
  • 38.
    Beta Blockers • FDAapproved for migraine prevention – Propranolol (Inderal) 60-240 mg PO once daily for ER or divided BID or TID for IR – Timolol (Blocadren) 10-30 mg PO daily in 2 divided doses • Limited evidence for migraine prevention – Nadolol (Corgard) 20-240 mg PO once daily – Atenolol (Tenormin) 50-150 mg PO daily or divided BID – Metoprolol (Lotensin, Toprol XL) 100-200 mg daily or divided BID for IR formulation
  • 39.
    Beta Blockers Advantages • Thoroughlystudied and widely used • Timolol (Blocadren) and propranolol (Inderal) are FDA approved • Good choice for patients with HTN, CAD, tremor, or anxiety Disadvantages • Side effects = fatigue, dizziness, depression , exercise intolerance, may worsen aura • Avoid in patients with severe asthma, depression, bradycar dia, Raynaud's, overt CHF
  • 40.
    Calcium Channel Blockers .Although the mechanism by which calcium channel antagonists affect migraine is not known, . vasoconstriction , prevention of platelet aggregation and alterations in release and reuptake of serotonin. . Several trials have indicated some benefit for verapamil and flunarizine In recurrent migraine. . Verapamil in doses of 80 to 160 mg 3 times a day reduces the incidence of migraine with aura, but it is not as useful in migraine without aura.
  • 41.
    Tricyclic Antidepressants • Amitriptyline(Elavil) 10-200 mg nightly • Nortriptyline (Pamelor) 10-150 mg nightly • Desipramine (Norpramin) 25-200 mg nightly • Imipramine (Tofranil) 10-200 mg nightly • Doxepin (Sinequan) 10-200 mg nightly Lower end of dosage range is usually effective for migraine prevention
  • 42.
    Tricyclic Antidepressants Advantages • Inexpensive •Once daily dosing • Good choice for patients with insomnia, neuropathy, m ood disorders, fibromyalgia Disadvantages • None are FDA-approved • Side effects = sedation, weight gain, dry mouth, urinary retention • Avoid in sz disorder, cardiac conduction abnormalities, BPH
  • 43.
    Other Antidepressants • Efficacynot established in clinical trials – Best for fluoxetine (Prozac) 20 mg daily – Anectodal evidence for other SSRIs, trazodone, mirtazapine, bupropion, venalfaxine, and duloxetine • Migraines are more likely to be poorly controlled if mood disorders are untreated
  • 44.
    NSAIDs • Long-acting agentstaken on a scheduled basis have low risk of causing MOH • Consider for patients who: – Have other chronic pain conditions – Frequently use short-acting NSAID for acute treatment – Are at low risk for developing complications from daily NSAID • Caution patients about exceeding maximum daily dose • Limited evidence to support efficacy
  • 45.
    NSAIDs • Diclofenac 75mg PO BID • Naproxen 500 mg PO BID • Meloxicam 7.5-15 mg PO daily • Celecoxib 200 mg PO daily • Aspirin 81-325 mg PO daily – May be especially helpful for reducing aura
  • 46.
    Antiepileptic Drugs (AEDs) •FDA approved for migraine prevention – Divalporex Sodium (Depakote) – Topiramate (Topamax) • Limited evidence for migraine prevention – – – – Gabapentin (Neurontin) Lamotrigine (Lamictal) Levetiracetam (Keppra) Zonisamide (Zonegran)
  • 47.
    Divalproex Sodium (Depakote) •Increases GABA and stabilizes nerve membrane activation thresholds • Dose = 500 - 1500 mg daily divided BID or TID – ER formulation allows for once daily dosing • NNT = 2.8 to 4.2 (to ↓ migraine frequency 50%) • Therapeutic plasma concentration = 50-100 mg/L
  • 48.
    Divalproex Side Effects Common/doserelated • Tremor • Drowsiness • Nausea/vomiting • Easy bruising • Weight gain • Nystagmus Rare/idiosyncratic • Hepatotoxicity • Pancreatitis • Alopecia • Thrombocytopenia • Agranulocytosis • Rash (SJS) • Suicidal behavior
  • 49.
    Topiramate (Topamax) -MOA • Not completely understood • Blocks NMDA receptors • Blocks voltage dependant sodium channels • Enhances GABA • Weakly inhibits carbonic anhydrase .
  • 50.
    Topiramate Dosing • Dosetitration in clinical trials: – Initial dose = 25 mg daily – Titrate by 25 mg every week – No consistent additional benefit seen in doses >100 mg • Dose titration in U of U Headache Clinic – – – – Initial dose = 12.5 mg at bedtime Titrate by 12.5 mg every week Goal of 50 mg BID May eventually increase up to 100 mg BID in certain patients
  • 51.
    Topiramate Side Effects Common •Paresthesias • Cognitive problems • Fatigue • Weight loss • Dizziness • Nausea • Taste perversion Rare or Serious • Metabolic acidosis • Depression • Nephrolithiasis • Glaucoma • Oligohydrosis • Suicidal behavior
  • 52.
    Gabapentin (Neurontin) • Mechanismof action – – – – Enhances GABA activity Binds to alpha-2-delta subunit of voltage gated calcium channels Inhibits high-voltage-activated calcium currents Result is decreased synaptic transmission • Limited evidence from clinical trials for migraine prevention – NNT = 3 (50% reduction in migraine frequency) – Only 2 RCT, did not use typical migraine outcomes Vikelis and Rapoport. CNS Drugs 2010.
  • 53.
    Botulinum Toxin • RecentlyFDA approved for chronic migraine • Dose = 155-195 units injected into muscles of face, neck and head • Mecahnism of Action (purposed) – Blocks release of Substance P and CGRP Inhibits peripheral signals to CNS and blocks central sensitization Dodick DW. Headache 2010.
  • 54.
    Botulinum Toxin • Efficacy –Botulinum Toxin superior to placebo in 2 large, double blind, randomized, controlled trials – Botulinum Toxin similar to topiramate and amitriptyline in small, shorter duration studies – Botulinum toxin = placebo for episodic migraine • Side effects = muscle weakness, injection site pain, and “spread of toxin effect”
  • 55.
    2. Tension-type headache 2.1 2.2 2.3 2.4 Infrequentepisodic tension-type headache Frequent episodic tension-type headache Chronic tension-type headache Probable tension-type headache ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
  • 56.
    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
  • 57.
    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
  • 58.
    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**
  • 59.
    3. Cluster headache andother trigeminal autonomic cephalalgias 3. Cluster headache and other trigeminal autonomic 3.1 Cluster headache cephalalgias 3.2 Paroxysmal hemicrania 3.3 Short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT) 3.4 Probable trigeminal autonomic cephalalgia ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
  • 60.
    3.1 Cluster headache A.At least 5 attacks fulfilling criteria B-D B. Severe or very severe unilateral orbital, supraorbital and/or temporal pain lasting 15-180 min if untreated C. Headache is accompanied by 1 of the following: 1. ipsilateral conjunctival injection and/or lacrimation 2. ipsilateral nasal congestion and/or rhinorrhoea 3. ipsilateral eyelid oedema 4. ipsilateral forehead and facial sweating 5. ipsilateral miosis and/or ptosis 6. a sense of restlessness or agitation D. Attacks have a frequency from 1/2 d to 8/d E. Not attributed to another disorder ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
  • 61.
    3.1 Cluster headache 3.1.1Episodic cluster headache A. Attacks fulfilling criteria A-E for 3.1 Cluster headache B. At least two cluster periods lasting 7-365 d and separated by pain-free remission periods of 1 mo 3.1.2 Chronic cluster headache A. Attacks fulfilling criteria A-E for 3.1 Cluster headache B. Attacks recur over >1 y without remission periods or with remission periods lasting <1 mo
  • 62.
    Cluster Headache AbortiveTreatment • Inhalation of 100% oxygen up to 15 L/min • Sumatriptan (Imitrex) 4-6mg subQ or 20 mg nasally • Zolmitriptan (Zomig) 5-10 mg nasally or PO • Dihdroergotamine (Migranal) 1 mg nasally up to 3 mg in 24 hours • Prednisone 40-100 mg burst and taper Bajwa and Wootton. Up to Date 2007
  • 63.
    Cluster Headache Prevention •Verapamil 120-360 mg PO daily • Lithium 300 mg PO BID to TID • Divalproex 500-1500 mg PO daily to BID • Topiramate 50-200 mg PO divided BID • Prednisone 40-100 mg burst and taper • Melatonin 3 mg PO QPM Bajwa and Wootton. Up to Date 2007
  • 64.
    The Headache Diary •Pain score • Characteristics of the pain • Associated symptoms • Acute treatments used and response • Triggers
  • 65.
    The Headache Diary •Makes the patient responsible for their disease • Aids in diagnosis and differentiating between headache types • Assesses efficacy of acute and preventive treatment • Identifies triggers • Minimizes recall bias
  • 66.
    3.2 Paroxysmal hemicrania A.At least 20 attacks fulfilling criteria B-D B. Attacks of severe unilateral orbital, supraorbital or temporal pain lasting 2-30 min C. Headache is accompanied by 1 of the following: 1. ipsilateral conjunctival injection and/or lacrimation 2. ipsilateral nasal congestion and/or rhinorrhoea 3. ipsilateral eyelid oedema 4. ipsilateral forehead and facial sweating 5. ipsilateral miosis and/or ptosis D. Attacks have a frequency >5/d for > half of the time, although periods with lower frequency may occur E. Attacks are prevented completely by therapeutic doses of indomethacin F. Not attributed to another disorder ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
  • 67.
    4. Other primaryheadaches 4.1 Primary stabbing headache 4.2 Primary cough headache 4.3 Primary exertional headache 4.4 Primary headache associated with sexual activity 4.5 Hypnic headache 4.6 Primary thunderclap headache 4.7 Hemicrania continua 4.8 New daily-persistent headache (NDPH) ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
  • 68.
    4.5 Hypnic headache Newentrant to classification A. Dull headache fulfilling criteria B-D B. Develops only during sleep, and awakens patient C. At least two of the following characteristics: New entrant to classification 1. occurs >15 times/mo 2. lasts 15 min after waking 3. first occurs after age of 50 y D. No autonomic symptoms and no more than one of nausea, photophobia or phonophobia E. Not attributed to another disorder 4.5 Hypnic headache ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
  • 69.
    4.6 Primary thunderclap headache A.Severe head pain fulfilling criteria B and C B. Both of the following characteristics: 1. sudden onset, reaching maximum intensity in <1 min 2. lasting from 1 h to 10 d C. Does not recur regularly over subsequent weeks or months D. Not attributed to another disorder ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
  • 70.
    4.7 Hemicrania continua Newentrant to classification A. Headache for >3 mo fulfilling criteria B-D B. All of the following characteristics: 1. unilateral pain without side-shift 2. daily and continuous, without pain-free periods 3. moderate intensity, with exacerbations of severe pain C. At least one of the following autonomic features occurs during exacerbations, ipsilateral to the pain: 1. conjunctival injection and/or lacrimation 2. nasal congestion and/or rhinorrhoea 3. ptosis and/or miosis D. Complete response to therapeutic doses of indomethacin E. Not attributed to another disorder ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
  • 71.
    4.8 New daily-persistentheadache New entrant to classification A. Headache for >3 mo fulfilling criteria B-D B. Headache is daily and unremitting from onset or from <3 d from onset C. At least two of the following pain characteristics: New entrant to classification 1. bilateral location 2. pressing/tightening (non-pulsating) quality 3. mild or moderate intensity 4. not aggravated by routine physical activity D. Both of the following: 1. not >1 of photophobia, phonophobia or mild nausea 2. neither moderate or severe nausea nor vomiting E. Not attributed to another disorder 4.8 New daily-persistent headache ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
  • 72.
    Primary Chronic DailyHeadache Disorders of Long-Duration (>4 h) Disorder Demographic Clinical Features Recommended Treatments Chronic migraine Headache ≥15 days per month for >3 mo, of which ≥8 days Female/male, 3 : 1 Prevalence Topiramate, divalproex sodium, meet ICHD-II criteria for 2% amitriptyline migraine without aura or relief with triptan or ergot Mild-moderate severity; no Chronic tension-type headache Equal sex ratio Prevalence 2% migrainous symptoms; bilateral, Amitriptyline nonthrobbing New daily persistent headache Female > male Bilateral, persistent, moderately severe; may be preceded by viral infection; may resemble Amitriptyline migraine or tension-type headache Hemicrania continua Rare; unilateral, constant, exacerbations of severe headache, cranial autonomic Indomethacin symptoms, and ice-pick pain; responsive to indomethacin by definition Female > male
  • 73.
    Diagnostic criteria for secondaryheadaches A. Headache with one (or more) of the following [listed] characteristics and fulfilling criteria C and D B. Another disorder known to be able to cause headache has been demonstrated C. Headache occurs in close temporal relation to the other disorder and/or there is other evidence of a causal relationship D. Headache is greatly reduced or resolves within 3 mo (shorter for some disorders) after successful treatment or spontaneous remission of the causative disorder ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
  • 74.
    6. Headache attributedto cranial or cervical vascular disorder 6.1 Headache attributed to ischaemic stroke or transient ischaemic attack 6.2 Headache attributed to non-traumatic intracranial haemorrhage 6.3 Headache attributed to unruptured vascular malformation 6.4 Headache attributed to arteritis 6.5 Carotid or vertebral artery pain 6.6 Headache attributed to cerebral venous thrombosis 6.7 Headache attributed to other intracranial vascular disorder ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
  • 75.
    6.4.1 Headache attributedto giant cell arteritis A. Any new persisting headache fulfilling criteria C and D B. At least one of the following: 1. swollen tender scalp artery with elevated erythrocyte sedimentation rate (ESR) and/or C reactive protein (CRP) 2. temporal artery biopsy demonstrating giant cell arteritis C. Headache develops in close temporal relation to other symptoms and signs of giant cell arteritis D. Headache resolves or greatly improves within 3 d of high-dose steroid treatment ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
  • 76.
    6.7.1 CADASIL A. Attacksof migraine with aura, with or without other neurological signs B. Typical white matter changes on MRI T2WI C. Diagnostic confirmation from skin biopsy evidence or genetic testing (Notch 3 mutations) ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
  • 77.
    7.4.2 Headache attributed directlyto neoplasm A. Headache with 1 of the following characteristics and fulfilling criteria C and D: 1. progressive 2. localised 3. worse in the morning 4. aggravated by coughing or bending forward B. Intracranial neoplasm shown by imaging C. Headache develops in temporal (and usually spatial) relation to the neoplasm D. Headache resolves within 7 d after surgical removal or volume-reduction of neoplasm or treatment with corticosteroids ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
  • 78.
    9.1 Headache attributedto intracranial infection 9.1.1 Headache attributed to bacterial meningitis 9.1.2 Headache attributed to lymphocytic meningitis 9.1.3 Headache attributed to encephalitis 9.1.4 Headache attributed to brain abscess 9.1.5 Headache attributed to subdural empyema ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
  • 79.
    9.1.1 Headache attributedto bacterial meningitis A. Headache with 1 of the following characteristics and fulfilling criteria C and D: 1. diffuse pain 2. intensity increasing to severe 3. associated with nausea, photophobia and/or phonophobia B. Evidence of bacterial meningitis from examination of CSF C. Headache develops during the meningitis D. One or other of the following: 1. headache resolves within 3 mo after relief from meningitis 2. headache persists but 3 mo have not yet passed since relief from meningitis 9.1.1 Headache attributed to bacterial meningitis ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
  • 80.
    9.1.1 Headache attributedto bacterial meningitis Notes • Criterion D does not relate to evidence of causation • Causation is established by onset during diagnosed bacterial meningitis, whilst it is well recognised that this headache often persists • When this occurs, 9.4.1 Chronic post-bacterial meningitis headache is diagnosed • Criterion D2 allows a default diagnosis within 3 mo, before it is known whether headache will resolve or persist ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4
  • 81.
    9.2 Headache attributedto systemic infection A. Headache with 1 of the following characteristics and fulfilling criteria C and D: 1. diffuse pain 2. intensity increasing to moderate or severe 3. associated with fever, general malaise or other symptoms of systemic infection B. Evidence of systemic infection C. Headache develops during the systemic infection D. Headache resolves within 72 h after effective treatment of the infection ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4

Editor's Notes

  • #37 NOT in Handout!!Similar choice for pt with rapid onset of migraine and with early n/v – need something non-oral or that works fastRecurrence = migraine initially gone, but comes back within 24 hours, something longer acting may outlast the migraine and keep it from coming back or addition of NSAID that lasts longer than triptanNara, Frova and Almo have lower rates of SE vs. other triptans and may be tolerated when other triptans were notNasal formulation available for sumatriptan, zolmitriptan, and DHEODT formulations available for rizatriptan and zolmitriptan
  • #48 NNT not in handout
  • #49 SJS = Steven’s Johnson SyndromeSuicidal behavior and AEDs – FDA pooled data of all RDBPCT trials of AEDs showed 0.43% of pt on AEDs vs. 0.24% of pt on placebo reported suicidal behavior, regardless of indication. Translates to 1 additional case of suicidal behavior/ideation per 530 pt. treated with AED. http://www.fda.gov/Drugs/DrugSafety/PostmarketDrugSafetyInformationforPatientsandProviders/ucm100192.htm
  • #53 NNT not in handout
  • #54 Additional info not in handout
  • #55 Not in handout