Headaches Alan Chan, MD. 12-16 % prevalence Tension most common Cluster HA men > women All other types women > men International Headache Society (IHS)

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Presentation transcript:

Headaches Alan Chan, MD

12-16 % prevalence Tension most common Cluster HA men > women All other types women > men International Headache Society (IHS) classification updated in 2004 HA, cranial neuralgia, facial pain syndromes.

HA Migraine – 2/3 unilat, 1/3 bilat or global; crescendo pattern, pulsating; 4-72 hr; +/- aura Tension – bilat, pressure/tightness variable; indeterminate length Cluster – unilat, quick and explosive; patient active; < 3 hr; ipsilat facial symptoms – tearing, nasal congestion, Horner’s, rarely focal neuro symptoms

Ddx – less common Paroxysmal hemicrania Idiopathic stabbing headache Cold-stimulus headache Benign cough headache Benign exertional headache Headache associated with sexual activity

Other HA Secondary HA – associated with trauma, vascular disorder, nonvascular intracranial disorder, substance use or withdrawal, infection, metabolic disorder, other facial or cranial structures

Get some hx Triggers –Diet, stress, hormones, sensory stimuli, change in habit or environment Important questions in history –frequency of severe headache (difficult to function) –frequency of milder HA –frequency of taking analgesics –change in HA

Image if… recent significant change in pattern, frequency, or severity worsening despite therapy focal neurological signs/symptoms HA with exertion, cough, or sexual activity Orbital bruit Onset after age 40

Migraine episodes of severe HA typically with nausea +/- photo/phonophobia

Pathophysiology - NOT vascular dilatation of blood vessels Primary neuro dysfunction leading to premonitory symptoms, aura, HA, and postdrome Central process either brainstem or cortical spreading depression –causes aura, activates trigeminal nerve afferent fibers, alter blood brain barrier (BBB) permeability

trigeminovascular system – activity leading to stimulation releases vasoactive neuropeptides of substance P, calcitonin gene-related protein (CGRP, which is a profound endogenous vasodilator), neurokinin A, activation of arachadonic acid cascade sensitization – neurons get progressive more sensitive to nociceptive and non-nociceptive stimulation

More… Genetics – approx 3x risk in patients with relatives who had migraines. Non-Mendelian pattern of inheritance Prodrome – 60% of people with migraine; can occur 1-2 days prior to HA onset. Includes depression, irritability, constipation, euphoria, food craving, increased yawning. Aura – 25%; typically visual like scotoma, but can be sensory, verbal, or motor Headache – typically unilateral and throb/pulse Postdrome – exhausted, sudden head mvt causes pain

Diagnosis – without aura Headache attacks last 4 to 72 hours Headache has at least two of the following characteristics: unilateral location; pulsating quality; moderate or severe intensity; aggravation by routine physical activity During headache at least one of the following occurs: nausea and/or vomiting; photophobia and phonophobia At least five attacks occur fulfilling the above criteria History, physical examination, and neurologic examination do not suggest any underlying organic disease

Aura At least one of the following characteristics without motor weakness: –Fully reversible visual symptoms including positive features (eg, flickering lights, spots, or lines) and/or negative features (eg, loss of vision) –Fully reversible sensory symptoms including positive features (eg, pins and needles) and/or negative features (eg, numbness) –Fully reversible dysphasic speech disturbance Aura has at least two of the following characteristics: –Homonymous visual symptoms and/or unilateral sensory symptoms –At least one aura symptom develops gradually over ≥5 minutes and/or different aura symptoms occur in succession over ≥5 minutes –Each symptom lasts ≥5 and ≤60 minutes

Complications Chronic (>15 days a month for > 3 months in absence of drug overuse) Status migrainosus - > 72 hr and debilitating Persistent aura without infarction – aura > 1 wk Migrainous infarction – deficit > 1 hr and positive imaging Migraine triggered seizure

Acute therapy NSAIDs, combo Tylenol/ASA/caffeine, triptans, ergots like dihydroergotamine (DHE), opioids (but weak evidence only for butorphanol nasal and worry about abuse and transformation into chronic daily HA), IV metoclopramide.

Preventive Tx – can take as long as 2-3 months to see benefit. Treat if >2 a month that last > 3 days of disability, contraindication to acute tx, > 2 times a week use of acute tx, presence of uncommon conditions Nonselective beta blockers – propranolol studied the most TCA (better for mixed migraine and tension HA) like amitriptylline as others not studies as much; limited evidence for fluoxetine Anticonvulsants - divalproex sodium and sodium valproate, limited evidence for gabapentin NSAIDs – only naproxen with modest effect, but overuse syndrome Serotonergic agent – ergot like DHE

Keep a headache diary of related activities and triggers!

Cluster Headache trigeminal autonomic cephalalgias, which are short, unilat, severe with autonomic symptoms (ptosis, miosis, lacrimation, conjunctival injection, rhinorrhea, nasal congestion)

Prevalence - <1 % Dx – very typical. < 3 hrs Tx – Acute – O2, triptans, octreotide, lidocaine (intranasal), ergot Preventive – CCB like verapamil, glucocorticoids, lithium (limited evidence), topiramate Others less used – pizotifen (anti serotonergic), valproic acid, capsaicin, ergot, melatonin, indomethacin, triptans

Tension type headache (TTH) Most common Types – infrequent episodic ( 15 days a month) PP – multifactorial. Normally innocuous stimuli are interpreted as pain in the dorsal horn neurons. Some genetic role. Women slightly more than men. Blacks less than whites.

Dx – usually non descript! TTH is characterized by having at least two of the following four features: The location of the pain is bilateral in either the head or neck The quality of the pain is steady (eg, pressing or tightening) and nonthrobbing The intensity of the pain is mild to moderate There is no aggravation of the headache by normal physical activity

In addition to these criteria, there must be at least 10 headache episodes fulfilling all other ICHD-2 criteria, which include the following: The duration of pain is between 30 minutes to 7 days The headache is not attributable to another disorder

Tx Acute – early tx, some may require a higher dose, avoid overuse, consider preventive. Tylenol, NSAIDs, ASA. Add some caffeine, but may get side effects. Butalbital and opioids generally not recommended. Preventive – TCAs, Serotonin-NE reuptake inhibitors like venlafaxine, behavioral like CBT, relaxation, biofeedback

References Uptodate.com Snow V, Weiss K, Wall EM, et al. Pharmacologic Management of Acute Attacks of Migraine and Prevention of Migraine Headache. Ann Int Med (10): Clinch CR. Evaluation of Acute Headaches in Adults. Am Fam Physician (4): Tepper SJ, Spears RC. Acute Treatment of Migraine. Neuro Clinics (2):