Clinical Headache

Trigeminal Autonomic Cephalalgias

Trigeminal Autonomic Cephalalgias

What You'll Learn

  • TACs: unilateral headache + ipsilateral cranial autonomic features mediated by the trigeminal-parasympathetic reflex
  • Cluster headache: male predominance (3–4:1), 15–180 min attacks, circadian/circannual periodicity; acute: 100% O2 12–15 L/min + sumatriptan 6 mg SC; preventive: verapamil (requires ECG monitoring)
  • Paroxysmal hemicrania: female predominance, shorter attacks (2–30 min), >5/day, absolute indomethacin response (diagnostic criterion)
  • SUNCT/SUNA: shortest attacks (1–600 sec), highest frequency (3–200/day), first-line treatment lamotrigine; must exclude pituitary adenoma
  • Hemicrania continua: continuous unilateral headache with exacerbations + autonomic features; absolute indomethacin response (diagnostic criterion)
  • Key differentiator: cluster = restlessness/pacing; migraine = lying still in dark
  • Indomethacin-responsive TACs: PH and HC (NOT cluster)
HighYield Pearls
  • TAC definition: ALL TACs = strictly unilateral pain + ipsilateral cranial autonomic features (conjunctival injection, lacrimation, rhinorrhea/congestion, ptosis/miosis, facial sweating/flushing, eyelid edema) ± restlessness; bilateral pain should prompt reconsideration
  • Cluster headache: unilateral orbital/temporal severe pain 15–180 min, 1–8 attacks/day, circadian + circannual periodicity (nocturnal “alarm-clock”), MALE predominance (3:1), restlessness/agitation (paces)
  • Cluster acute: HIGH-FLOW O2 12–15 L/min via NRB ×15 min + SC SUMATRIPTAN 6 mg; AVOID opioids
  • Cluster prevention: VERAPAMIL (high-dose, ECG monitoring for PR prolongation/AV block), galcanezumab (only CGRP mAb FDA-approved for episodic CH), brief steroid bridge, greater occipital nerve block
  • Paroxysmal hemicrania (PH): unilateral 2–30 min ×5–40+/day, FEMALE predominance, ABSOLUTE response to INDOMETHACIN (diagnostic); celecoxib/topiramate if intolerant
  • SUNCT vs. SUNA: ultra-short attacks 1–600 sec, 3–200/day; SUNCT = conjunctival injection AND tearing; SUNA = one or neither but with another autonomic feature; LAMOTRIGINE first-line; IV lidocaine for status
  • Hemicrania continua (HC): CONTINUOUS unilateral pain + episodic exacerbations with autonomic features ± migrainous features; ABSOLUTE response to INDOMETHACIN (diagnostic); side-locked
  • Indomethacin-responsive headaches: PH and HC (mnemonic: “PHat HC”) — absolute response is diagnostic; 25 mg TID titrated to 75 mg TID with GI prophylaxis
  • MRI brain + pituitary (microadenoma, posterior fossa neurovascular conflict) is mandatory in SUNCT/SUNA; in cluster headache, image when atypical features are present (refractory, abnormal neurologic exam, older onset, side-locked new headache, suspicion for secondary TAC) — not required for every typical cluster
  • Differential traps: trigeminal neuralgia (V2/V3 stabs, no autonomic features, refractory period present); cavernous sinus / pituitary macroadenoma / ICA dissection / posterior fossa lesion as secondary causes
🔍 Quick ReferenceClinical · Treatment / response pattern
Clinical phenotype
  • “Alarm-clock” nocturnal attacks + restlessness/pacing + maleCluster headache
  • “Worst headache, like an ice pick or hot poker behind the eye”Cluster headache
  • Alcohol triggers attacks only during a cluster bout + seasonal/circannual patternCluster headache
  • V1 distribution pain + partial Horner syndrome (ptosis/miosis) ipsilateralCluster headache (can persist between bouts)
  • Brief 2–30 min attacks, many per day, femaleParoxysmal hemicrania
  • Ultra-brief 1–600 sec stabs with conjunctival injection AND tearingSUNCT
  • Ultra-brief stabs with only one (or neither) of injection/tearing but another autonomic featureSUNA
  • Cutaneous triggers (light touch, chewing, brushing teeth, wind) with NO refractory periodSUNCT/SUNA (refractory period present = trigeminal neuralgia)
  • Continuous side-locked unilateral baseline pain + autonomic exacerbationsHemicrania continua
Treatment / response pattern
  • High-flow O2 12–15 L/min + SC sumatriptan 6 mg aborts attackCluster headache
  • Verapamil first-line preventive (ECG for PR prolongation)Cluster headache
  • Greater occipital nerve block as bridge to verapamilCluster headache
  • Galcanezumab / CGRP mAb FDA-approved for preventionEpisodic cluster headache
  • ABSOLUTE response to indomethacin (diagnostic)Paroxysmal hemicrania & Hemicrania continua (“PHat HC”)
  • Lamotrigine first-line (slow titration for SJS risk)SUNCT/SUNA
  • IV lidocaine for refractory statusSUNCT/SUNA
  • Mandatory pituitary MRI for SUNCT-like presentationSUNCT/SUNA (microadenoma mimic)
  • Opioids ineffective / avoid in ALL TACsAll TACs
TAC Overview & Pathophysiology

Trigeminal-Parasympathetic Reflex

  • Afferent: V1 (ophthalmic) trigeminal afferents → trigeminal nucleus caudalis
  • Central relay: trigeminal nucleus → superior salivatory nucleus (pons)
  • Efferent: VII nerve parasympathetic outflow → pterygopalatine ganglion → cranial autonomic symptoms
  • This reflex arc is the shared mechanism for autonomic features across all TACs

Hypothalamic Role

  • Posterior hypothalamus = "pacemaker" — activated in cluster headache (PET, fMRI studies)
  • Explains circadian (same time daily) and circannual (seasonal) periodicity
  • Basis for deep brain stimulation (DBS) of posterior hypothalamus in refractory cluster
  • Hypothalamic activation also seen in PH, SUNCT — suggests shared central generator

Cranial Autonomic Features

FeatureMechanismNotes
LacrimationParasympathetic (VII → lacrimal gland)Most common autonomic feature
Conjunctival injectionParasympathetic vasodilationKey feature in SUNCT
Nasal congestion / rhinorrheaParasympathetic (VII → nasal mucosa)Often misdiagnosed as "sinus headache"
Ptosis / miosisSympathetic dysfunction (partial Horner)Can become persistent between attacks
Eyelid edemaParasympathetic vasodilation + venous congestionIpsilateral only
Forehead / facial sweatingSympathetic dysfunctionIpsilateral to pain
💎 Board Pearl
  • All TACs are strictly unilateral — bilateral pain should prompt reconsideration of the diagnosis
  • Partial Horner syndrome (ptosis + miosis without anhidrosis) can persist between cluster periods — do NOT mistake for a new Horner requiring workup
Cluster Headache

ICHD-3 Diagnostic Criteria

  • Pain: severe to very severe, unilateral, orbital/supraorbital/temporal
  • Duration: 15–180 minutes (untreated)
  • Frequency: 1 every other day to 8 per day
  • ≥1 ipsilateral autonomic feature OR sense of restlessness/agitation
  • ≥5 attacks fulfilling criteria

Subtypes

SubtypeDefinition
Episodic cluster≥2 cluster periods lasting 7 days–1 year, separated by remission ≥3 months
Chronic clusterNo remission period ≥3 months for ≥1 year (or remissions <3 months)

Epidemiology & Clinical Features

  • Male:female = 3–4:1 (most male-predominant primary headache)
  • Onset typically age 20–40 years
  • Strong association with smoking (up to 65% of patients)
  • Circadian periodicity: attacks at same time daily, often nocturnal (1–2 AM) — "alarm clock headache"
  • Circannual periodicity: cluster bouts in spring and fall
  • Restlessness/agitation: pacing, rocking, head banging — key distinction from migraine (where patients lie still in dark)
  • Alcohol triggers attacks only during a cluster period (not during remission)

Acute Treatment

TreatmentDose / RouteDetails
100% O212–15 L/min via non-rebreatherFirst-line; 78% response within 15 min; no side effects; few contraindications (caution in severe COPD/CO2 retention; fire hazard with smoking — high-risk in cluster population)
Sumatriptan SC6 mg subcutaneousFirst-line pharmacologic; fastest triptan onset (5–15 min); can repeat ×1 in 24 h
Zolmitriptan intranasal5 mg nasal sprayAlternative to SC sumatriptan; effective within 15–30 min
Lidocaine intranasal4–10% ipsilateral nostrilAdjunctive; targets sphenopalatine ganglion

Transitional (Bridge) Therapy

  • Prednisone burst: 60–100 mg/day ×5 days, then taper over 2–3 weeks
  • Greater occipital nerve (GON) block: suboccipital injection of local anesthetic ± corticosteroid
  • Purpose: rapid suppression while waiting for preventive agents to reach therapeutic effect

Preventive Treatment

AgentDetailsMonitoring
VerapamilFirst-line preventive; doses often 240–960 mg/day; slow titrationECG before initiation and with every dose increase (PR prolongation, AV block)
LithiumMore effective for chronic cluster; 600–1200 mg/dayLithium levels, renal function, thyroid
GalcanezumabFDA-approved for episodic cluster (300 mg SC monthly, administered as 3 consecutive 100-mg SC injections; continue monthly while bout is active); only CGRP mAb with this indicationInjection site reactions
TopiramateThird-line; 100–200 mg/dayCognitive effects, kidney stones, weight loss
Melatonin10 mg at bedtime; adjunctive; reflects hypothalamic mechanismMinimal side effects
💎 Board Pearl
  • Verapamil requires ECG monitoring with each dose increase — risk of PR prolongation and heart block; doses in cluster often exceed standard cardiology doses
  • Cluster headache + restlessness/agitation = key distinguishing feature from migraine (patients pace, rock, or bang head)
  • Galcanezumab is the only FDA-approved CGRP mAb for episodic cluster headache
Clinical Pearl
  • Oral triptans are generally too slow for cluster attacks (15–180 min duration) — always use SC sumatriptan or intranasal zolmitriptan
  • Cluster patients frequently present to the ER — high-flow O2 should be tried before opioids (which are ineffective)
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