The Trigeminal Atlas

The trigeminal system is a shared route, not a master diagnosis. The pattern of pain and the quality of evidence decide what the route means.

Start with time course, triggers, associated symptoms and sensory findings. Then review the nerve map. A shared anatomical pathway does not make migraine, cluster headache, trigeminal neuralgia (TN) and painful trigeminal neuropathy the same disease.

Randomized trial: estimates an intervention effect in a defined sample and time window. Guideline: combines evidence with clinical judgment and local priorities. Imaging association: shows a correlated signal, not necessarily a cause. Hypothesis: a model still being tested.

ICHD-3 criteria are classification rules. A stated duration or frequency is a practical diagnostic boundary, not a biological wall. People can have overlapping disorders, atypical presentations or secondary causes. [1]

Percentages in this atlas retain their denominator and outcome. Results from different endpoints or study designs should not be compared as if they were a single contest.

The organizing principle: identify the clinical phenotype first; interpret mechanism second; choose treatment by evidence, risk and context.

Cranial nerve V sensory + motor

Forehead, upper eyelid, cornea and parts of the nose. Sensory division; its corneal afferents are clinically important.

Midface, cheek, upper lip, palate and upper teeth. Sensory division.

Lower face, lower teeth, and general sensation from the anterior tongue. Also carries motor fibers to muscles of mastication.

V2 midface · upper jaw

V3 lower face · jaw motor

The trigeminal ganglion houses the primary sensory cell bodies for most facial sensation. A notable exception is proprioception: primary sensory neuron cell bodies for jaw-muscle proprioception lie in the mesencephalic trigeminal nucleus. V3’s mixed sensory-motor role is one reason facial and jaw complaints can involve sensation, chewing or both. [2,3] Territory is not etiology. Pain over a V2 region may come from tooth disease, sinus/eye disease, migraine, neuralgia, neuropathy or other causes. A face map guides examination; it cannot make the diagnosis by itself.

Pain transmission is not a wire from a sore spot to a single “pain center.” It is a set of relays, descending pathways and interacting networks.

Spinal trigeminal nucleus / caudalis

ascending projections are predominantly crossed parallel brainstem / autonomic modulation

Facial nociceptive afferents enter the pons. Many travel caudally in the spinal trigeminal tract and synapse in the spinal trigeminal complex, especially its caudal region. Second-order projections ascend—predominantly across— to thalamic relays and cortical networks. Parallel brainstem circuits shape autonomic responses, arousal and affect. This simplified drawing leaves out multiple nuclei and bilateral connections. [2,3]

Touch, temperature and nociceptive inputs interact in trigeminal brainstem circuits. Their convergence is relevant to tactile triggers and sensitization, but does not mean every condition uses the same cellular pathway.

Brainstem and higher networks can amplify or dampen sensory input. The same incoming signal can be experienced differently across contexts, attacks and individuals.

Headache science moved beyond the older idea that migraine is simply a dilated artery. Current models include peripheral trigeminal afferents, meninges, brainstem relays, hypothalamic and cortical systems, chemical mediators and sensitization. The diagrams below distinguish biological pathways from claims of causal sufficiency. H O W C O N F I D E N T LY C A N W E S AY I T ?

Established clinical pattern classification criteria

Therapeutically validated target changes outcomes

Observed association co-varies with attacks

Open mechanism causal ordering uncertain

These are different kinds of evidence, not a ranking of scientific value.

Meningeal afferents and ascending trigeminovascular pathways provide a supported route for nociceptive

Cutaneous allodynia and hypersensitivity can accompany migraine and other pain states. Peripheral

signaling. This explains how meningeal inputs can engage the trigeminal system; it does not settle what initiates every migraine attack. [8]

and central sensitization are distinct concepts; clinical markers are indirect and causal roles in chronification remain unsettled. [8]

Human provocation studies and effective CGRPtargeting therapies support a role for CGRP in migraine. They do not show that CGRP is necessary or sufficient for all spontaneous attacks. [9–11]

No single mechanism explains all phenotypes. A response to a medicine does not prove the disorder’s origin, and imaging activation is not proof that a region caused an attack.

Evidence discipline: “involved in,” “associated with,” “can provoke,” and “causes” are not interchangeable verbs.

A compact differential starts with the shape of an attack. Duration alone is never enough, but it is a powerful first clue. Pattern

4–72 h untreated in adults [4]

Nausea and/or photophobia + phonophobia; activity aggravation; aura in a subset

Same-side tearing/red eye/nasal symptoms and/or agitation

Frequent unilateral autonomic attacks; absolute indomethacin response in criteria

Very brief unilateral neuralgiform attacks with cranial autonomic signs

Fraction of a second–2 min

Shock-like paroxysms triggered by innocuous stimulation

Burning/tingling pain; sensory dysfunction or nerve lesion may be present

These are ICHD-3 descriptors, not a biological stopwatch. A series of TN paroxysms can feel like a prolonged bout; a person can have more than one headache disorder; and TN can include continuous interictal pain. Classify individual attack form and the overall clinical course separately. [1,4–7,17–19,23,24] Ask in order: When did it begin? How long is each burst? What provokes it? What occurs on the same side? Is sensation normal between attacks? Is the pattern new or changing?

For migraine without aura, ICHD-3 requires at least five attacks lasting 4–72 hours untreated or unsuccessfully treated. At least two of these pain features are present: unilateral location, pulsating quality, moderate/severe intensity, or aggravation by routine activity. The attack also includes nausea/vomiting or both photophobia and phonophobia. Unilateral pain is common but not mandatory. [4]

Associated symptoms nausea or light + sound sensitivity

Attack burden is not captured by severity alone. Record headache days, migraine-feature days, duration, acute medicines, function and recovery. A diary can make frequency and medication use visible across weeks.

Headache on ≥15 days/month for >3 months, with migraine features on ≥8 days/month, meets the ICHD-3 chronic migraine framework. Medicationoveruse headache can coexist and is separately considered. [5]

Aura is not “any visual symptom” Typical aura consists of fully reversible visual, sensory and/or speech-language symptoms with characteristic development. NICE describes gradual development over at least 5 minutes and duration of 5–60 minutes. A new or atypical focal neurologic symptom should not automatically be assumed to be migraine aura. [6,30] Clinical classification is not an imaging result. There is no routine scan that “shows migraine.” Imaging decisions depend on the presentation, examination, stability and red flags; see the diagnostic pathway on page 19.

Cortical event?

Hypothesized relation; not a fixed sequence in every attack.

Aura-associated cortical propagation: about 3–3.5 mm/min in human observations.

Cortical spreading depolarization (CSD)—a slowly propagating wave of altered cortical activity—is strongly associated with migraine aura. It is biologically plausible that such a cortical event can influence trigeminal nociceptive pathways; animal models support interactions. But CSD is not established as the initiator of all headache, nor as a universal explanation for migraine without aura. [7] A 2025 intracranial EEG report recorded aura-associated propagating activity at about 3 mm/min in one patient monitored for epilepsy surgery. It offers rare direct human evidence, but a single case cannot establish how often this occurs or whether it causes the headache phase. [7] M E C H A N I S M S TAT U S

Well supported: CSD and aura association. Open question: whether/how CSD triggers headache in different migraine phenotypes. Not supported: treating one case or rate as a universal attack blueprint.

Peptide signaling CGRP among mediators

Sensory networks pain + symptoms

The trigeminovascular framework links nociceptive fibers around intracranial meninges and vessels to trigeminal ganglion and central pain pathways. CGRP can be released from trigeminal sensory neurons and participates in signaling. Human provocation studies show that CGRP infusion can trigger migraine-like attacks in susceptible participants; this supports biological relevance, but does not prove CGRP is necessary or sufficient for every spontaneous attack. [8,9] Therapeutic success with CGRP monoclonal antibodies and gepants validates the target. It does not mean migraine is simply “too much CGRP,” a vascular disorder, or a single-pathway disease. The initiating event, central/peripheral ordering, and how peptide signaling interacts with cortical and autonomic networks remain active questions. [10,11]

Heightened responsiveness of peripheral nociceptive terminals is one candidate contributor to throbbing pain and mechanical sensitivity.

Amplified responsiveness within central circuits may help explain cutaneous allodynia and sensory gain. Human signs do not reveal every underlying cell mechanism.

Don’t overread the vessel. The presence of vessels near nerve fibers is anatomy. It does not establish that dilation is the sufficient cause of migraine pain.

Acute therapies aim to reduce pain and associated symptoms, restore function and limit recurrence. Choice depends on attack features, previous response, contraindications, pregnancy status and medication-overuse risk. The 2025 American College of Physicians guideline recommends adding a triptan to an NSAID after inadequate response for moderate-to-severe acute episodic migraine in nonpregnant adults (strong recommendation); triptan plus acetaminophen is a conditional recommendation based on low-certainty evidence. [12]

Separate panels, separate disorders and endpoints. ACHIEVE II: single-attack, 2-hour pain freedom. Cluster oxygen trial: attack-level pain-free or adequate relief at 15 minutes. Do not compare across panels. [13,20]

In ACHIEVE II, a phase 3 single-attack study, ubrogepant 50 mg produced 2-hour pain freedom in 21.8% (101/464) versus 14.3% (65/456) with placebo: an absolute difference of 7.5 percentage points (95% CI 2.6– 12.5). Absence of the most bothersome symptom was 38.9% versus 27.4%. These results apply to that trial population, dose, attack and timepoint; they do not predict an individual’s response. [13] Outcome literacy: “pain-free at two hours,” “adequate relief at 15 minutes,” and “days reduced per month” answer different questions. Relative and absolute differences, denominators, duration and comparator all matter. For attacks with mild-to-moderate pain, an NSAID or acetaminophen may be considered when medically appropriate. For moderate-to-severe attacks, triptans remain an established acute option; antiemetics may be added when nausea is prominent, and non-oral routes can matter when vomiting or rapid escalation prevents reliable oral treatment. Gepants are acute options for some patients; triptan suitability, vascular history, drug interactions and pregnancy considerations need individual review. Opioids are generally avoided for routine migraine attack care because of limited role and potential harms. [12,30] Medication-overuse headache is considered when headache occurs on at least 15 days/month with regular overuse for more than three months; thresholds differ by acute drug class. A diary that captures headache days and medication days supports more accurate assessment. [5,30]

Preventive treatment is considered when attack burden, disability, acute-medication use or patient priorities justify it. Traditional options include oral medicines selected by comorbidity and safety; onabotulinumtoxinA is used for chronic migraine in appropriate settings; CGRP-targeting monoclonal antibodies and gepants add mechanismdirected options. Local approvals, access rules and contraindications vary.

ADVANCE, 12-week phase 3 trial. Group-level placebo-adjusted mean differences, not predicted individual responses. [14]

In ADVANCE, mean monthly migraine days fell 2.5 with placebo and 3.7, 3.9 and 4.2 with atogepant 10, 30 and 60 mg, respectively; placebo-adjusted differences were −1.2, −1.4 and −1.7 days (all P<.001). The trial establishes efficacy over its period; it does not establish superiority to every preventive or long-term comparative safety. [14]

The American Headache Society (2024) considers CGRP monoclonal antibodies and preventive gepants first-line prevention options without requiring failure of other classes. “First-line option” does not mean every patient should start there, or that head-to-head superiority is proven. [10]

NICE recommendations for rimegepant prevention use UK eligibility criteria, including prior preventive failures and reassessment. These are healthsystem access rules—not a global definition of efficacy. [15]

Established preventive classes include selected beta-blockers, topiramate, candesartan and amitriptyline, among others; their fit depends on comorbidities, adverse-effect profiles and reproductive considerations. OnabotulinumtoxinA is an evidence-based option for chronic migraine, studied in the PREEMPT program. Choice is not simply “old versus new”: tolerability, patient priorities, access and a measurable review plan matter. [16] Follow-up matters. Agree on what outcome counts—fewer migraine days, shorter attacks, less disability or reduced rescue-medication use—and reassess benefit and harms after an appropriate trial period.

Effect is not guaranteed. Trial averages describe groups. Individual benefit, adverse effects, time to response and practical access differ. Treatment changes belong with a clinician.

TACs typically combine unilateral trigeminal pain with ipsilateral cranial autonomic features, but are a family of distinct syndromes. The time bands below visualize ICHD-3 attack durations; frequency, autonomic signs, restlessness and indomethacin response also distinguish them. [17,18] Logarithmic attack-duration axis · ICHD-3 duration ranges 1 sec

SUNCT / SUNA 1–600 seconds

Hemicrania continua: continuous unilateral headache for more than 3 months; not a finite attack-duration interval and therefore not placed on this seconds-to-hours axis.

Severe/very severe orbital, supraorbital or temporal attacks lasting 15–180 minutes untreated; one every other day up to eight daily; ipsilateral autonomic signs and/or agitation. Episodic and chronic forms differ by remission pattern. [17]

Paroxysmal hemicrania and hemicrania continua require an absolute response to therapeutic-dose indomethacin in ICHD-3. This is a cliniciansupervised classification feature, not a self-test or proof of mechanism. [18]

SUNCT includes both conjunctival injection and tearing; SUNA has only one or neither of those specific features. Very short attack duration does not imply mild disease: frequency and pain intensity can be substantial. [18] New side-locked autonomic pain deserves careful assessment. A TAC-like phenotype may be primary or secondary; symptoms do not identify the cause on their own.

A plausible circuit model for same-side tearing, eye redness and nasal symptoms.

The trigeminal–autonomic reflex provides a plausible, supported circuit explanation for ipsilateral tearing, conjunctival injection and nasal symptoms: trigeminal input can engage parasympathetic output via the superior salivatory nucleus, facial nerve and sphenopalatine ganglion. [21] Hypothalamic-region activation in PET/fMRI studies, circadian/circannual regularity and melatonin observations support involvement of timing and distributed network systems—especially in cluster headache. Small samples and localization uncertainty mean these findings do not prove a single hypothalamic “attack generator.” Mechanistic evidence is concentrated in cluster and should not be generalized without qualification to every TAC subtype. [21] Three evidence labels: reflex circuitry—physiologically plausible; hypothalamic activation—imaging association; “the hypothalamus causes every attack”—not established.

Cluster treatment is organized around speed: stop an attack, bridge a bout while preventive therapy takes effect, and reduce attacks across the bout. The European Academy of Neurology guideline (2023; evidence search through July 2022) strongly recommends 100% oxygen at ≥12 L/min for 15 minutes and 6 mg subcutaneous sumatriptan for acute attacks. [19]

Acute minutes oxygen / triptan

Bridge days selected steroid / GON block

Prevent weeks verapamil / selected options

Right panel: randomized crossover cluster trial. At 15 minutes, 100% oxygen at 12 L/min yielded pain-free or adequate relief in 78% of 150 treated attacks versus 20% of 148 attacks with high-flow air; 76 participants analyzed. Attack-level outcome, not participant-level success. [20]

Verapamil is a standard preventive option; ECG monitoring is clinically important because conduction effects can occur. Corticosteroids and greater occipital nerve block are transitional approaches in selected cases. [19]

Galcanezumab reduced attacks in episodic cluster in a trial that ended recruitment early; the evidence is not a basis to generalize to chronic cluster or other TACs. Noninvasive vagus nerve stimulation evidence differs between episodic and chronic cluster. [19,22]

Acute oxygen is a treatment decision, not household oxygen advice. Delivery device, flow, safety, contraindications and access require clinical planning.

ICHD-3 describes recurrent unilateral pain in one or more trigeminal divisions: severe, electric-shock, shooting, stabbing or sharp paroxysms, typically triggered by innocuous stimuli, lasting a fraction of a second to two minutes. Some patients have concomitant continuous pain. [23] Washing, brushing teeth, talking, chewing or a light touch may provoke a burst. There can be a refractory period after an attack. V2 and V3 are frequently involved; this distribution is descriptive, not a rule-out test for V1 or a diagnostic test by itself. [27]

Paroxysm + trigger + territory A brief neuralgiform attack in a trigeminal distribution is more informative than a generic report of “facial pain.” Continuous pain does not automatically rule out TN.

V2 cheek / upper jaw V3 lower jaw Illustrative territories only

MRI is recommended during TN work-up because clinical features cannot reliably exclude secondary causes. The examination also helps assess neurovascular relationships for subtype classification and surgical planning. [25] Contact is not classical compression. A vessel touching the nerve on a scan can be incidental. Classical TN requires neurovascular compression with morphological nerve-root change, such as displacement or atrophy. [23,25]

Root compression

Leading explanatory model for some classical TN; not a complete proven account of every case. Channel abnormalities, central sensitization and other contributors remain under study.

Focal demyelination near the root-entry zone, ectopic firing and ephaptic cross-excitation are a leading model for classical TN: a hyperexcitable fiber might allow tactile input to recruit a neighboring pain signal. Sodium-channel abnormalities and central sensitization are also discussed. These are explanatory models, not settled universal causes. [26,27]

NICE recommends carbamazepine initially. EAN recommends carbamazepine or oxcarbazepine as first-choice long-term medicines. Evidence for alternatives/add-ons—including lamotrigine, gabapentin, baclofen, pregabalin or botulinum toxin A—is less robust and context-dependent. [25,28]

Carbamazepine has controlled-trial support, but the evidence base is largely small and short-term. It can cause rare serious skin reactions and blood dyscrasias; ancestry-related HLA screening and other monitoring depend on current product labeling and clinical setting. [28]

When control is inadequate or medicines are poorly tolerated: seek specialist review. Surgery is not a last-minute improvisation; it is a shared decision based on phenotype, MRI, health status and patient priorities. [25]

EAN recommends offering surgery when pain is inadequately controlled or medicines are poorly tolerated. For classical TN with morphological neurovascular compression, microvascular decompression (MVD) is the first-line surgical option in the guideline. If MRI shows no neurovascular contact, a neuroablative procedure may be considered. For idiopathic TN, evidence has not established a single best procedure. [25]

Open procedure intended to separate/compressing vessel from nerve while preserving the nerve. Requires suitable clinical/imaging context; entails operative risks and recovery.

Procedures such as radiofrequency, balloon compression or glycerol intentionally injure/alter nerve transmission. Facial numbness and recurrence trade-offs matter.

Non-incisional focused treatment; pain relief may be delayed, and sensory effects or recurrence are part of counseling.

2024 meta-analysis of repeat procedures only. Observational, heterogeneous studies; not randomized head-to-head comparisons or first-procedure results. [29]

Do not read this as a league table. Patient selection, prior procedures, pain definitions, follow-up and study design differ. These repeat-surgery estimates do not predict an individual’s result or describe initial surgery.

TRIGEMINAL NEURALGIA

Brief, severe, electric or stabbing bursts; innocuous trigger; trigeminal territory. Continuous concomitant pain can coexist.

Burning, pins-and-needles or squeezing pain, often with sensory deficit, mechanical allodynia or cold hyperalgesia and an identifiable lesion/disease. [24]

V1–V3: trigeminal territories V3 / oral territory: dental + jaw differentials Throat / tonsil / ear: glossopharyngeal neuralgia Back of scalp: occipital neuralgia / cervical referral

Brief unilateral pain in the ear, base of tongue, tonsillar region or beneath the jaw; swallowing, coughing, talking or yawning may trigger attacks. Rare vagal features include cough, hoarseness, syncope or bradycardia. [35]

Paroxysmal pain in occipital nerve territories with local dysesthesia/allodynia, tenderness or trigger points; cervical joints and muscles can refer pain to the back of the head. [36]

Post-traumatic trigeminal neuropathy may follow dental, facial or other nerve injury. Sensory abnormalities are common in reported clinical series, but prevalence estimates vary by definitions and study design. The treatment evidence is not interchangeable with classic TN trials. [37]

New / recurrent head or facial pain

Thunderclap / deficit / fever / change?

urgent assessment based on context

Imaging / tests guided by suspected cause

Typical migraine: often no routine imaging

e.g., sudden severe headache pathway

TN: MRI work-up recommended to assess causes

A schematic aid, not a clinical decision rule.

NICE lists thunderclap onset (peak within five minutes), fever with worsening headache, new neurologic/cognitive/personality/consciousness change, recent trauma, cough/Valsalva/exertional or orthostatic headache, suspected giant-cell arteritis or acute narrow-angle glaucoma, and a substantial pattern change among features that can prompt investigation or referral. Context matters; these are not diagnoses. [30]

Routine imaging is not universal

Noncontrast CT is commonly the initial imaging pathway. In a prospective cohort of neurologically intact adults scanned within six hours for acute headache peaking within an hour, CT detected all 121 SAHs (sensitivity 100%; 95% CI 97.0–100.0). Overall CT sensitivity was 92.9%; after six hours it was 85.7%. This conditional cohort result is not a universal guarantee. [32]

Stable typical migraine with normal examination and no red flags often does not need routine imaging. New/atypical TAC-like headache and suspected TN raise different imaging questions; EAN recommends MRI in all TN work-ups because symptoms cannot exclude secondary causes. [25,31,34]

SNNOOP10 is a structured prompt, not a validated rule-out score; the absence of listed features does not exclude every secondary cause. [33]

MIGRAINE

How do cortical events, meningeal afferents, CGRP, brainstem and hypothalamic systems interact—and which order applies to which phenotype?

Imaging and circadian patterns implicate networks, especially in cluster. They do not establish a single anatomical switch or explain all TAC subtypes.

Why do some contacts hurt? Morphological root change matters diagnostically, but the exact causes of pain, nerve hyperexcitability and treatment variation remain incomplete.

Mechanisms that need careful labels CGRP as target CGRP as sole cause CSD–aura link CSD causes all migraine pain Bars are qualitative evidence labels for this article—not measured percentages or a formal certainty scale.

Clinical response can validate that a pathway is useful to target, but response alone rarely proves an upstream cause. Human provocation studies, imaging, sensory tests, animal models and randomized treatment trials answer different questions. Progress depends on linking phenotype, biology and outcome without collapsing those evidence types into one story. What a global reference should do: make mechanisms intelligible, make uncertainty visible, and make treatment claims traceable to a dated source and defined population.

1 Where exactly?

5 Normal sensation between attacks?

2 How long per attack?

6 New or changing pattern?

Seconds + innocuous trigger Raises a neuralgiform phenotype such as TN; evaluate trigeminal distribution, sensory findings and secondary causes.

Hours + sensory accompaniments Consider migraine criteria; count days and associated symptoms, not just side or pain quality.

Unilateral pain + same-side autonomic signs Consider TAC subtypes; duration, frequency, agitation and specific diagnostic features matter.

Continuous pain + sensory change / injury Consider painful neuropathy and its cause; do not automatically transfer TN evidence.

Urgency overrides pattern matching. Sudden maximal headache, new neurologic deficit, fever with worsening headache, altered consciousness, recent trauma or major pattern change calls for prompt clinical evaluation.

The trigeminal nerve is a powerful map of facial sensation and pain circuitry. It is not a shortcut around diagnosis. Recognize the pattern, locate the pathway, inspect the evidence, and keep uncertainty in view.

[1] International Headache Society. ICHD-3 classification. ichd-3.org [2] Terrier L-M et al. The trigeminal pathways. J Neurol. 2022. doi:10.1007/s00415-022-11002-4 [3] Kim HK et al. The Trigeminal Sensory System and Orofacial Pain. 2024. PMC11508441 [4] ICHD-3. Migraine without aura. Criteria [5] ICHD-3. Chronic migraine. Criteria [6] ICHD-3. Migraine with aura. Criteria

[11] Sacco S et al. European Headache Federation guideline on CGRP monoclonal antibodies. 2022. PMC9188162 [12] Qaseem A et al. ACP guideline: acute episodic migraine in outpatient settings. 2025. Ann Intern Med [13] Lipton RB et al. Ubrogepant for the treatment of migraine. ACHIEVE II. 2019. PMID 31742631 [14] Ailani J et al. Atogepant for the preventive treatment of migraine. ADVANCE. 2021. NEJM [15] NICE. Rimegepant for preventing migraine, TA906. NICE

[7] McLeod GA et al. Mapping the migraine: intracranial recording of CSD in migraine with aura. Headache. 2025. doi:10.1111/head.14907

[16] Dodick DW et al. OnabotulinumtoxinA for chronic migraine: PREEMPT. 2010. PMID 20487038

[8] Burstein R et al. Migraine: multiple processes, complex pathophysiology. J Neurosci. 2015. PMC4498450

[17] ICHD-3. Cluster headache. Criteria

[9] Lassen LH et al. CGRP may play a causative role in migraine. Cephalalgia. 2002. PMID 11993614 [10] Charles AC et al. CGRP-targeting therapies are a first-line option for prevention of migraine: AHS position statement update. 2024. PMID 38466028

[18] ICHD-3. PH, SUNCT/SUNA, hemicrania continua. TAC chapter [19] May A et al. EAN guideline on treatment of cluster headache. 2023. PMID 37515405 [20] Cohen AS et al. High-flow oxygen for treatment of cluster headache: randomized crossover study. 2009. PMID 19996400

[21] May A et al. Trigeminal autonomic cephalalgias: mechanisms and treatment review. 2018. PMC5909131

[30] NICE. Headaches in over 12s: diagnosis and management, CG150; updated 2025. NICE

[22] Goadsby PJ et al. Galcanezumab in episodic cluster headache. 2019. PMID 31291515

[31] American College of Radiology. Headache imaging appropriateness criteria. ACR

[23] ICHD-3. Classical trigeminal neuralgia. Criteria

[32] Perry JJ et al. CT within six hours of headache onset to rule out subarachnoid hemorrhage. BMJ. 2011. doi:10.1136/bmj.d4277

[24] ICHD-3. Painful trigeminal neuropathy. Criteria [25] Bendtsen L et al. EAN guideline on trigeminal neuralgia. 2019. doi:10.1111/ene.13950 [26] Bendtsen L et al. Advances in diagnosis, classification, pathophysiology and management of TN. Lancet Neurol. 2020. doi:10.1016/S14744422(20)30233-7 [27] Lambru G et al. Trigeminal neuralgia: a practical guide. 2021. PMC8461413 [28] Wiffen PJ et al. Carbamazepine for chronic neuropathic pain and fibromyalgia in adults. Cochrane. 2019. PMC6491112

[33] Do TP et al. Red and orange flags for secondary headaches: SNNOOP10. 2019. PMC6340385 [34] Evans RW et al. Neuroimaging for migraine: AHS systematic review and guideline. 2020. doi:10.1111/head.13720 [35] ICHD-3. Glossopharyngeal neuralgia. Criteria [36] ICHD-3. Occipital neuralgia. Criteria [37] Post-traumatic trigeminal neuropathy review. PMC11428572 [38] Lambru G et al. Medical treatment for SUNCT and SUNA: prospective open-label study. PMC7892380

[29] Repeat surgery for TN: systematic review and meta-analysis. 2024. World Neurosurg

Scope: This is a public-facing educational atlas. Diagnostic criteria do not replace assessment. Medicine options, contraindications, monitoring, approvals and coverage differ across people and jurisdictions. Recheck current labels and guidelines before clinical use.

Every claim in this atlas points to a dated source. If something is wrong, out of date or unclear, tell us and it will be corrected in the next version.

Dr Mohamed Najm (Mohamed Najm Aldeen Alameen), neurologist in neurocritical care and neurological emergencies · FEBN.

The Tract Clinical Guides No. 7 · version 1.0 · November 2026.

Read online and download free at thetract.org/guides/trigeminal-atlas

How to cite Najm M. The Trigeminal Atlas: headache, facial pain and neuralgia — expanded edition. The Tract Clinical Guides No. 7, version 1.0. 2026. https://thetract.org/guides/trigeminal-atlas/

The ideas and direction are the author’s. AI tools were used for literature search, drafting support and language editing. The author is responsible for the content. Our AI

CC BY-NC-ND 4.0: share it unchanged, with credit, for non-commercial teaching.

policy. Illustrations are artistic renderings for orientation, not anatomical reference images.

Corrections and comments: contact@thetract.org Version 1.0 for The Tract completes references 7 and 29 and resets two clipped labels on page 19.

A teaching reference, not individual advice. Diagnostic criteria support assessment; they do not replace it. Doses, approvals, monitoring and access differ between people and countries — check current labels and local guidance before acting on anything here.

The Tract · Independent Neurology Press A free neurology library — no ads, no subscriptions, no sign-up. More clinical guides at thetract.org/guides