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 (< 1 /month),

freq episodic (1-14/month), and chronic (> 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. 2002. 137(10): 840-849.

• Clinch CR. Evaluation of Acute Headaches in Adults. Am Fam Physician. 2001. 63(4): 685-693.

• Tepper SJ, Spears RC. Acute Treatment of Migraine. Neuro Clinics 2009. 27(2): 417-427