Definitions
• Primary HA: Includes migraine, tension, and cluster HAs
• Secondary HA: 2/2 underlying medical condition
• Etiologies include infxn, substance use or w/d from substance (often analgesic
overuse: >3–5 doses/wk), trauma, SAH/ICH, d/o of head and neck (e.g., tooth abscess, sinusitis, AOM, cranial pain), ↑ ICP or pseudotumor, vascular d/o, vasculitis, vasospasm, venous sinus thrombosis, PRES, psychiatric d/o, facial pain, refractive vision error, HTN
Diagnostic Studies (Pediatr Rev 2007;28:43; Neurology 2002;59:490; Pediatr Rev 1999;20:39; Neurology 2004;63:427)
• HPI: time patterns of HA, freq, duration, pre-HA sx, location, quality of pain, assoc sx, alleviating/exacerbating factors, degree debility 2/2 HA, sx btw Has, FamHx, SocHx
• PE: Assess vital signs, particularly BP
• Examine fundi for papilledema (may indicate incr ICP)
• Measure head circum (rapid growth may be sign of obstructive hydrocephalus)
• Assess for focal neuro signs/sx & signs of infxn (fever, rash, pain w/ neck flexion)
• Listen for cranial bruits 2/2 AVM (although absent in 50% of cases)
• Neuroimaging: Not recommended for recurrent HAs and normal neuro exam
• Consider if abnl neuro exam (e.g., focal exam, signs of ↑ ICP, ΔMS, concurrent
seizures), hx of acute onset of severe HA, if Δ in HA type
• Urgent neuroimaging required if ↑ ICP suspected (papilledema, pain worse w/ lying flat, HA awakening pt from sleep, pain worse w/ maneuvers that ↑ venous pressure → Valsalva, cough)
• Labs: No specific recs for routine lab workup. Consider Chem7 & UA if ↑ BP or CBC & blood cx if suspect infectious etiology
• EEG: Not recommended
• LP: Not recommended unless suspicion of CNS infxn, SAH, or pseudotumor cerebri. Obtain neuroimaging 1st if suspect ↑ ICP
Migraine
Subtypes of Migraine (Pediatr Rev 2007;28:43; Neurology 2004;63:427)
• Migraine w/o aura: Often unilateral in frontal/temporal region, pulsating, mod or severe pain intensity, aggravated by physical activity. +/− N/V, photophobia, & phonophobia
• Migraine w/ aura: HA similar to migraine w/o aura. Auras most commonly involve visual disturbances (scotoma, distortion, hallucination, obscuration, visual field defects). Less common auras include sensory sx (e.g., numbness/tingling), dysphasic speech disturbances, hemiparesis, CN palsies (most common oculomotor → ptosis)
• Basilar type migraine: Usually preceded by dizziness, vertigo, visual disturbances, ataxia, diplopia, ↓ consciousness, ↓ hearing, bilateral paresthesias, tinnitus, dysarthria, or other bulbar symptoms
Epidemiology (Pediatr Review 2007;28:43)
• +FHx in ∼80%; prev 1.2–3.2% in 3–7 yo; 4–11% in 7–11 yo, 8–23% in 15 yo
• Sex ratio: Prepuberty afflicts boys > girls, postpuberty afflicts girls > boys
• Migraine w/o aura is most common subtype (frequency 60–85%)
• May see in relation to cyclic vomiting syndrome or abdominal migraine
Pathophysiology (Pediatr Rev 2007;28:43; Pediatr Rev 1999;20:39)
• Exact mechanism unknown but evidence implicating calcium channels & 5HT changes
• Altered neuronal calcium channels → “cortical spreading depression” whereby neurons undergo hyperpolarization followed by depolarization
• Altered serotoninergic function → ? effect on vasculature or central pain pathways
• Triggers for migraine include sleep deprivation, stress/tension, lack of exercise, excessive caffeine, dehydration, dietary (e.g., cheese, chocolate, citrus fruits), analgesic overuse (>5×/wk), & hormonal factors (menarche, OCPs, premenstrual, pregnancy, premenopause)
Treatment (Pediatr Rev 2007;28:43; Neurology 2004;63:2215)
• Acute treatment: Tylenol and ibuprofen have proven efficacy and safety in
children and adolescents. Nasal sumatriptan also proven efficacy in adolescents but is
expensive, so oral sumatriptan more widely used in clinical practice. Limited data for
other triptans, such as zolmitriptan and rizatriptan
• Prophylaxis: Consider if ≥3 HA per mo and/or functional disability from HA. However, no migraine-specific meds FDA approved for use in children
• Rx w/ antihistamine (cyproheptadine), AEDs (topiramate, valproic acid, gabapentin), TCAs (amitriptyline, nortriptyline), NSAIDs (naproxen sodium), CCBs (verapamil), BBs (propranolol)
• Behavior modification: Adequate sleep, stress mgmt, avoid known triggers, stop analgesic overuse, ↑ exercise and hydration
Tension Headache (Pediatr Rev 1999;20:39; Pediatr Neurol 2005;33:303)
• Definition: Diffuse, bilateral, tightening/pressing quality in “band-like” distribution, duration ranging from min to days, typically no N/V. Generally aches but is
non-pulsatile & non-throbbing (Pediatr Neurol 2005;33:303)
• Epidemiology: More common in 
; age of onset ∼5 yo; prevalence ranges 11–72.8%
• Etiology: Often associated with psychological stress and/or analgesic overuse
• Treatment: Aimed at stress reduction through relaxation techniques, massage, etc. Avoid reliance on analgesic meds
Cluster Headaches (Pediatr Neurol 2005;33:303)
• Definition: Clustered intense periorbital or temporal pain, often unilateral, with autonomic sx (ipsilat rhinorrhea, tearing, congestion, eyelid edema, miosis, ptosis). Occurs in periods of wks to mos w/ long pain-free periods (up to 2 yr)
• Epidemiology: Affects <0.1% of children. Very rare in children <10 yo. Mostly in males
• Treatment: In adults, acute rx w/ O2 lidocaine aqueous drops intranasally, olanzapine, dihydroergotamine, sumatriptan. Most common preventative rx is steroids