01Approach to the Critical Patient/attcp33

Immediate priorities

›Life-threatening presentations requiring immediate action

›Severe dehydration from inability to eat or drink

›IV fluid resuscitation with normal saline or lactated Ringer

›Electrolyte repletion as indicated

›NPO status to minimize trigger exposures

›New neurologic deficits suggesting secondary cause

›Acute focal weakness, diplopia, or ataxia

›If new deficits present, emergent neuroimaging required

›Neurology or neurosurgery consult trigger

›Status neuralgicus — prolonged cluster of attacks unresponsive to oral medication

›IV pharmacotherapy required in monitored setting

›Analgesia-resistant pain cycle requiring ED-level intervention

Key concepts

›TN is a clinical diagnosis based on ICHD-3 criteria

›Recurrent unilateral paroxysmal facial pain in trigeminal distribution

›Paroxysms lasting less than 2 minutes

›Electric shock quality triggered by innocuous stimuli

›Triggered paroxysmal pain reported in 91–99% of patients; may be pathognomonic

›Classification drives management decisions

›Classic TN: neurovascular compression with nerve morphological changes (~75%)

›Secondary TN: MS, tumor, AVM (~15%)

›Idiopathic TN: no identifiable cause (~10%)

›Opioids are ineffective and should be avoided

›Associated with need for additional medications in 72% of ED cases

›NSAIDs are also generally ineffective for neuralgic pain

PITFALLS

›Diagnostic pitfalls

02History/hx75

Pain characterization

›Quality and duration

›Electric shock, shooting, stabbing, or lancinating quality

›Paroxysms typically lasting a fraction of a second to 2 minutes

›Individual attacks usually last only seconds

›Severity

›Often rated 10/10 at peak

›Attacks may cluster hundreds of times per day

›Refractory period

›Brief period after a paroxysm during which pain cannot be retriggered

›Nearly pathognomonic when present

›Distribution

›Unilateral facial pain within trigeminal territory

›V2 (maxillary) or V3 (mandibular) most commonly affected

›Right side more commonly affected than left

›V1 (ophthalmic) involvement alone is atypical; consider alternative diagnoses

›Pain does not cross midline simultaneously

›Bilateral simultaneous pain requires alternative explanation

›Sequential bilateral pain possible but uncommon

Triggers and pattern

›Trigger factors

›Light touch to face, cheek, lips, or nose

›Trigger zones are small and discrete

›Discrete trigger zones are nearly pathognomonic

›Functional triggers

›Talking, chewing, swallowing

›Brushing teeth

›Shaving or touching the face

03Physical Exam/exam43

Neurologic examination

›Cranial nerve assessment

›Trigeminal nerve sensory testing

›Light touch in V1, V2, V3 distributions bilaterally

›Pinprick discrimination

›Sensory loss is NOT expected in classic TN

›Corneal reflex

›Afferent limb carried by ophthalmic branch (V1)

›Reduced or absent reflex raises concern for secondary TN

›Facial motor function

›Masseter and pterygoid muscle strength

›Motor branch travels with V3

›Trigger zone identification

›Light touch in discrete zones can reproduce paroxysm

›Do not probe trigger zones unnecessarily

›Extended cranial nerve exam

›Facial nerve (CN VII) function

›Facial weakness suggests mass lesion or MS plaque

›Hearing and vestibular function

›CN VIII involvement may indicate cerebellopontine angle lesion

›Extraocular movements

›Diplopia with CN VI palsy suggests elevated ICP or posterior fossa pathology

General and systemic exam

›General appearance

›Pain behavior during exam

›Wincing or guarding with facial touch

›Inability to speak during severe attacks

›Nutritional and hydration status

04Differential Diagnosis/ddx66

Life-threatening mimics

›Intracranial mass

›ICD-10 C71.9 (malignant neoplasm of brain, unspecified)

›Progressive pain without remission

›Associated neurologic deficits

›MRI with contrast required

›Cerebellopontine angle tumor

›Acoustic neuroma or meningioma

›May compress trigeminal nerve at root

›Hearing loss and CN VII involvement possible

›Multiple sclerosis

›ICD-10 G35

›TN may be the presenting symptom of MS

›More common in younger patients

›MRI demyelinating plaques at trigeminal root entry zone

Vascular and headache syndromes

›Cluster headache

›ICD-10 G44.009

›Longer attacks 15–180 minutes versus TN seconds to 2 minutes

›Orbital or supraorbital location predominantly

›Prominent autonomic features: lacrimation, rhinorrhea, ptosis

›Restlessness during attack differentiates from TN

›SUNCT and SUNA

›Short-lasting unilateral neuralgiform headache

›Periocular location

›Prominent autonomic symptoms

›No refractory period unlike TN

›Can switch sides

05Laboratory Tests/lt42

Baseline metabolic labs

›Basic metabolic panel

›Sodium level

›Carbamazepine causes hyponatremia (SIADH mechanism)

›Baseline sodium before initiation

›Repeat at 1–2 weeks after starting or dose increase

›Renal function

›Dosing adjustment for oxcarbazepine

›Hydration status assessment in acute exacerbation

›Liver function tests

›Carbamazepine hepatotoxicity monitoring

›Baseline transaminases before initiation

›Complete blood count

›Baseline before carbamazepine initiation

›Rare but serious risk: aplastic anemia and agranulocytosis

›Repeat every 3–6 months on therapy

›Leukopenia monitoring on chronic therapy

›Mild leukopenia common and often not requiring discontinuation

›Severe leukopenia warrants drug cessation

Pharmacogenomic and safety testing

›HLA-B*15:02 screening

›Required before carbamazepine initiation

›Patients of Southeast Asian, South Asian, or other at-risk ancestry

›Risk of fatal Stevens-Johnson syndrome and toxic epidermal necrolysis

›Positive result contraindicates carbamazepine

›HLA-A*31:01 testing

›Associated with hypersensitivity in European, Korean, and Japanese populations

›Risk of drug reaction with eosinophilia and systemic symptoms (DRESS)

06Diagnostic Tests/dt72

Scoring Systems

›ICHD-3 diagnostic criteria for TN

›Criterion A: at least 3 attacks of unilateral facial pain

›Fulfilling criteria B and C

›Criterion B: occurring in one or more trigeminal nerve divisions

›With no radiation beyond trigeminal distribution

›Criterion C: pain with at least 3 of 4 characteristics

›Recurring in paroxysmal attacks lasting from a fraction of a second to 2 minutes

›Severe intensity

›Electric shock, shooting, stabbing, or sharp quality

›Precipitated by innocuous stimuli to the affected side of the face

›Criterion D: no better accounted for by another diagnosis

›TN classification grading (Cruccu et al., Neurology 2016)

›Clinically definite TN: fulfills ICHD-3 criteria

›Without additional tests

›TN with neurovascular compression on MRI

›Classic TN confirmed

›TN with causative lesion (MS, tumor)

›Secondary TN confirmed

›Numeric Pain Rating Scale (NRS)

›0–10 scale for attack severity

›Greater than or equal to 7 considered severe

›Tracks response to pharmacotherapy

›Guides admission decisions in status neuralgicus

MRI

›MRI brain with and without contrast

›Indication: all new TN diagnoses

›American Family Physician guideline recommendation

›EAN guideline recommendation

›Identifies secondary causes in approximately 15% of cases

›Protocol for TN evaluation

›3T MRI preferred over 1.5T for neurovascular detail

›FIESTA or CISS sequence (constructive interference steady state)

›High-resolution cisternography to visualize trigeminal nerve at REZ

›MPRAGE or T1 volumetric for anatomical correlation

›Diagnostic yield

›Sensitivity for neurovascular compression varies 52–100% depending on protocol

›Specificity improved with 3T and dedicated sequences

›Systematic review 2026 (Henssen et al.) confirms protocol dependence

›Key findings to report

›Vascular contact at root entry zone (REZ)

›Vessel identification: superior cerebellar artery most common

›Morphological nerve changes: displacement, atrophy, or T2 signal change

›Demyelinating plaques at pontine REZ

›Confirms secondary MS-related TN

›Mass lesion in posterior fossa or cerebellopontine angle

›Acoustic neuroma, meningioma, epidermoid

›AVM or vascular malformation

CT

›CT head without contrast

›Role in acute TN presentation

›Not diagnostic for TN itself

›First-line imaging to exclude hemorrhage, mass, or hydrocephalus

›Appropriate when neurologic deficits present acutely

›Limitations

›Cannot visualize neurovascular compression

›Inferior soft tissue resolution compared to MRI

›Does not replace MRI for TN workup

›CT angiography of the head

›Vascular mapping for surgical planning

›Identifies offending vessels before microvascular decompression

›Superior cerebellar artery anatomy for surgical approach

›Used as adjunct to MRI in surgical candidates

›Not a first-line ED investigation for TN

Ultrasound

›Ultrasound role in TN

›No established role in primary TN diagnosis

›Cannot visualize intracranial trigeminal nerve anatomy

›High-frequency ultrasound of superficial trigeminal branches

›Investigational use for guided nerve block procedures

›Infraorbital and mental nerve identification for injection

›Not standard of care but emerging as procedural guide

›Temporal artery ultrasound

›Indicated when giant cell arteritis is on differential

›Halo sign sensitivity 69%, specificity 82% for GCA

›Doppler signal loss in affected segment

07Disposition/dispo40

Admission criteria

›Indications for hospital admission

›Severe exacerbation with inability to eat or drink

›Significant dehydration risk

›Malnutrition in prolonged attacks

›IV hydration and monitoring required

›IV pharmacotherapy requirement

›IV fosphenytoin administration requires monitored setting

›IV lidocaine infusion requires cardiac monitoring

›Inadequate response to oral medications in ED

›Acute drug titration needs

›Refractory cases requiring rapid dose escalation

›Monitoring for drug toxicity during initiation

›New neurologic deficits

›Urgent neuroimaging and specialist workup required

›Cannot be safely managed as outpatient

Discharge criteria

›Criteria for safe discharge

›Pain adequately controlled with oral medications

›NRS score reduced to tolerable level

›Patient able to continue prescribed regimen

›Tolerating oral intake

›No ongoing dehydration risk

›Able to swallow medications

›Outpatient follow-up arranged

›Neurology referral for all new diagnoses

›MRI ordered or scheduled if not yet done

›Prescription provided with clear titration instructions

08Treatment/t115

Acute ED management

›Immediate pain management in ED

›IV fosphenytoin

›Achieved satisfactory relief in 64% of ED cases in retrospective series

›Requires monitored setting for cardiac rhythm

›Administer at rate not exceeding 150 mg/min (phenytoin equivalent)

›Limited controlled evidence but supported by clinical experience

›IV lidocaine

›Effective per clinical experience; requires cardiac monitoring

›Dose: 1.5–5 mg/kg IV over 30–60 minutes

›Requires monitoring for QT prolongation and CNS toxicity

›Reserved for refractory acute exacerbation

›Trigger zone lidocaine injection

›Provides short-term relief for refractory acute pain

›Infraorbital nerve block: 1–2 mL 1–2% lidocaine without epinephrine

›Mental nerve block for V3 distribution

›IV fluid resuscitation

›Normal saline or lactated Ringer for dehydrated patients

›Correct electrolyte abnormalities including hyponatremia

›Agents to avoid in acute setting

›Opioids

›Ineffective in safe doses for TN

›Associated with need for additional medications in 72% of cases

›NSAIDs

›Generally ineffective for neuralgic pain

›Not recommended in TN management guidelines

First-line pharmacotherapy

›Carbamazepine — drug of choice

›Initiation and titration

›Starting dose: 200 mg twice daily

›Titrate by 200 mg per day every few days to effect

›Target dose: 400–800 mg per day in most patients

›Maximum dose: 1,200 mg per day

›Efficacy

›NNT approximately 2 for meaningful pain relief

›Initial response rate approximately 75%

›Efficacy may wane in 50% of patients over 5–10 years

›ACEP Level A equivalent recommendation; Class I evidence

›Monitoring requirements

›CBC and LFTs at baseline and 3–6 months

›Sodium level at baseline and 1–2 weeks after initiation

›Carbamazepine level if toxicity suspected

›Key drug interactions

›CYP3A4 inducer — affects oral contraceptives, warfarin, many medications

›Counsel patients about contraceptive failure risk

›Dose self-adjustment counseling

›Patients may self-adjust within prescribed range based on pain severity

›Reduce dose during remission periods

›Lancet Neurology guideline recommendation

›Oxcarbazepine — alternative first-line

›Dosing

›Starting dose: 150–300 mg twice daily

›Titrate to 300–1,800 mg per day in divided doses

›Advantages over carbamazepine

›Potentially fewer CNS side effects

›Less hepatic enzyme induction

›Fewer drug-drug interactions

›Cautions

›High cross-reactivity if carbamazepine allergy present (25–30%)

›Hyponatremia risk similar to carbamazepine

›Monitor sodium levels

Second-line and adjunctive pharmacotherapy

›Lamotrigine

›Adjunctive therapy when first-line insufficient

›Starting dose: 25 mg daily, titrate slowly over 6–8 weeks

›Target dose: 200–400 mg per day

›Risk of SJS/TEN with rapid titration; slow escalation mandatory

›EAN guideline supported

›Gabapentin

›Add-on therapy for partial responders

›Starting dose: 300 mg three times daily

›Titrate to 900–3,600 mg per day in divided doses

›Side effects: sedation, dizziness, weight gain

›Pregabalin

›Alternative to gabapentin

›Starting dose: 75 mg twice daily

›Target dose: 150–600 mg per day in divided doses

›More predictable pharmacokinetics than gabapentin

›Baclofen

›Adjunctive agent

›Starting dose: 5 mg three times daily

›Titrate to 10–25 mg three times daily

›Particularly useful in MS-related TN

›Botulinum toxin type A

›For medically refractory TN or intolerance to oral medications

›Injection into trigger zones subcutaneously or submucosal

›Dose: 25–75 units total per session

›Effect onset within days to weeks; duration 3–4 months

›EAN guideline Level B recommendation

Surgical treatment

›Microvascular decompression (MVD)

›Indication

›First-line surgical option for classic TN with neurovascular compression on MRI

›Medically refractory TN after 2 or more adequate medication trials

›Outcomes

›62–89% pain-free at 3–11 year follow-up

›5-year prospective study: 59% MVD patients pain-free without medication vs 19% medical management alone

›Perioperative mortality: 0.3%

›Mechanism

›Insertion of Teflon sponge between offending vessel and trigeminal nerve

›Restores nerve integrity at root entry zone

›Percutaneous procedures

›Radiofrequency thermocoagulation

›Selectively ablates pain-transmitting fibers

›Preferred when MRI shows no neurovascular contact

›High initial success but higher recurrence than MVD

›Balloon compression

›Mechanical compression of Gasserian ganglion

›Performed under general anesthesia

›Preferred for ophthalmic division involvement

›Glycerol injection

›Chemical ablation of Gasserian ganglion

›Can be performed under local anesthesia

›Gamma knife radiosurgery

›Non-invasive stereotactic radiosurgery

›Pain-free in 30–66% at 4–11 years

›Delayed onset of effect: weeks to months

›Preferred in poor surgical candidates

›Destructive mechanism: demyelination of trigeminal root

09Special Populations/sp73

Pregnancy

›TN in pregnancy

›Pharmacotherapy safety considerations

›Carbamazepine: FDA category D; neural tube defect risk

›2–3 fold increased risk of neural tube defects

›Folate supplementation 4 mg per day recommended if used

›Discuss risk-benefit with multidisciplinary team

›Oxcarbazepine: FDA category C; fetal risk data limited

›Similar mechanism to carbamazepine; teratogenicity possible

›Avoid unless benefit clearly outweighs risk

›Lamotrigine: FDA category C; safer profile than carbamazepine

›Preferred anticonvulsant if pharmacotherapy necessary in pregnancy

›Pharmacokinetics change significantly in pregnancy; dose adjustment required

›Gabapentin and pregabalin: limited human safety data

›Insufficient evidence to recommend routine use in pregnancy

›Non-pharmacologic options

›Trigger avoidance as first-line strategy

›Nerve blocks with local anesthetics may be used

›Multidisciplinary pain team involvement recommended

›Surgical referral

›MVD can be performed in pregnancy in severe refractory cases

›Gamma knife: deferred if possible due to radiation

›Neurosurgery consultation for medically refractory cases

Geriatric

›Age-related considerations

›Pharmacokinetics in older adults

›Carbamazepine clearance reduced: risk of toxicity at standard doses

›Start at lower dose: 100 mg twice daily and titrate slowly

›Increased fall risk from dizziness and ataxia

›Increased hyponatremia risk: monitor sodium closely

›Oxcarbazepine and geriatric patients

›Also associated with hyponatremia; may be more problematic in elderly

›Polypharmacy interactions particularly common

›Cognitive effects

›Carbamazepine causes sedation and cognitive slowing

›May exacerbate baseline cognitive impairment

›Beers Criteria: use with caution in older adults

›Falls risk

›Gait disturbance and dizziness with anticonvulsants increase fall risk

›Assess baseline fall risk before initiation

›Recommend mobility aids if needed

›Surgical candidacy in older adults

›MVD carries higher anesthetic risk in elderly with comorbidities

›Percutaneous procedures preferred in poor surgical candidates

›Gamma knife suitable for frail elderly

›Comorbidity and nutrition

›TN in elderly may accelerate weight loss and nutritional decline

›Nutritional assessment at each visit

›Consider dietitian referral for severe cases

Pediatrics

›Pediatric TN

›Epidemiology in children

›TN is rare under age 20

›When present, secondary causes must be aggressively excluded

›MS and structural lesions are disproportionately common in pediatric TN

›Diagnostic approach

›MRI with and without contrast is mandatory in all pediatric cases

›Exclude structural mass, MS plaque, or vascular malformation

›Dedicated posterior fossa imaging protocol

›Neurology referral required for all pediatric cases

›Pharmacotherapy in children

›Carbamazepine

›Approved for pediatric use (epilepsy dosing used as reference)

›Weight-based dosing: 10–20 mg/kg/day in divided doses

›Titrate slowly with monitoring of CBC and LFTs

›Oxcarbazepine

›Approved for children greater than 4 years

›Weight-based dosing: 8–10 mg/kg/day titrated to 30–46 mg/kg/day

›Gabapentin

›Used as adjunctive therapy in pediatric neuropathic pain

›Dosing: 5 mg/kg/day increasing to 25–35 mg/kg/day

›Surgical options in children

›MVD performed in children with neurovascular compression

›Good outcomes reported in adolescents

›Pediatric neurosurgery referral required

›Percutaneous procedures used when MVD not feasible

10Background/b82

Epidemiology

›Incidence and prevalence

›Annual incidence approximately 4–13 per 100,000 population

›Increases with age; highest in those greater than 70 years

›Average age of onset 50–60 years

›Prevalence approximately 0.03–0.3% of the general population

›Female predominance; female-to-male ratio approximately 2:1

›Right side more commonly affected than left (60% vs 40%)

›Disease associations

›Multiple sclerosis

›TN prevalence 2–5% in MS patients

›OR 8.9 compared to general population

›Demyelinating plaque at trigeminal REZ in MS-related TN

›Hypertension

›Associated with increased TN incidence (population data)

›Possible mechanism: arterial tortuosity causing neurovascular compression

›SLE

›OR 2.84 in propensity-matched analysis

›Diabetes and hyperlipidemia

›Associated at population level in National Inpatient Sample data

›Morbidity and quality of life

›Depression in 40–80% of TN patients

›Anxiety common; suicidal ideation in severe cases

›Social isolation from inability to talk, eat, or go outside

›Significant occupational impairment

›Inability to work during severe exacerbations

›Economic burden substantial

Pathophysiology

›Neurovascular compression mechanism (classic TN)

›Vascular loop contacts trigeminal nerve at root entry zone (REZ)

›Superior cerebellar artery most commonly implicated

›Anterior inferior cerebellar artery less common

›Arterial pulsation causes progressive demyelination of REZ

›Focal demyelination consequences

›Loss of myelin sheath insulation at REZ

›Ectopic impulse generation in hypersensitized axons

›Ephaptic transmission: cross-talk between non-nociceptive and nociceptive fibers

›Explains why light touch triggers severe pain

›Central sensitization

›Chronic demyelination leads to central sensitization

›Windup phenomenon in trigeminal nucleus caudalis

›Wind-up lowers threshold for pain perception

›May explain progressive shortening of remission periods

›Secondary TN mechanisms

›MS-related TN

›Demyelinating plaque at pontine trigeminal root entry zone

›Mechanism similar to neurovascular compression but immune-mediated

›Tumor-related TN

›Mass compression of nerve at any point along course

›Invasion or infiltration of nerve by malignancy

›Ion channel hypothesis

›Voltage-gated sodium channel Nav1.7 and Nav1.8 dysregulation

›Familial TN linked to VGSC mutations

›Carbamazepine and oxcarbazepine block sodium channels

›Explains selective efficacy of sodium channel blockers

Therapeutic Considerations

›Evidence base for pharmacotherapy

›Carbamazepine has highest quality evidence

›NNT approximately 2; supported by multiple randomized controlled trials

›AAN Practice Parameter Level A recommendation (Gronseth et al., Neurology 2008)

›Efficacy may wane over time due to pharmacologic tolerance

›Oxcarbazepine evidence level

›AAN Level B recommendation (Gronseth et al., Neurology 2008)

›Fewer drug interactions; preferred in polypharmacy patients

›EAN 2019 guideline recommendations

›Carbamazepine and oxcarbazepine as first-line

›Lamotrigine, botulinum toxin, and baclofen as second-line

›Surgical decision-making framework

›Medical management failure defined as inadequate response to 2 or more first-line agents

›Or intolerable side effects at therapeutic doses

›MVD preferred for classic TN with neurovascular compression on MRI

›Best long-term outcomes (59% pain-free without medication at 5 years)

›Lancet Neurology 2020 review recommendation

›Percutaneous procedures for patients without clear neurovascular compression

›Or those with high surgical risk from anesthesia

›Gamma knife appropriate for frail patients or patient preference for non-invasive approach

›Natural history considerations

›Spontaneous remission periods occur

›Taper medications during prolonged remissions

›Restart at onset of new cluster

›Remissions become shorter with disease duration

›Early aggressive treatment may not alter natural history

›Long-term medication use risks

›Carbamazepine: osteoporosis with chronic use (CYP3A4 induction reduces vitamin D)

›Monitor bone density in long-term users

11Patient Discharge Instructions/pdi43

copy discharge instructions

›Diagnosis: Trigeminal Neuralgia

›You have been diagnosed with trigeminal neuralgia, a condition causing sudden severe electric-shock-like pain in the face

›It is caused by a nerve in the face being irritated, most often by a blood vessel pressing on it

›This is a neurological condition, not a dental problem

›Your medications

›Carbamazepine (Tegretol) — take exactly as prescribed

›Start at the dose given to you; your doctor will adjust it

›You may feel dizzy or unsteady, especially when starting; avoid driving until stable

›Take with food to reduce stomach upset

›Do not stop your medication suddenly without speaking to your doctor

›Stopping abruptly can cause more pain or seizures

›If you are prescribed a second medication (oxcarbazepine, lamotrigine, or gabapentin), follow the same instructions

›Blood test monitoring

›You will need blood tests to check your sodium level, blood count, and liver function

›First blood test within 1–2 weeks of starting carbamazepine

›Your doctor will tell you the schedule after that

›Trigger avoidance

›Identify and avoid your personal triggers

›Common triggers: gentle face touch, eating, talking, tooth brushing, cold wind

›Eat soft foods at room temperature to reduce attack triggering

›Use a straw for beverages if swallowing triggers attacks

›Adjusting your dose

›Your doctor may allow you to adjust your dose based on pain level and side effects

›Increase during pain flares (within prescribed range only)

›Decrease or stop during pain-free periods after discussion with your doctor

›Return to emergency department immediately for

›Skin rash of any kind — STOP carbamazepine immediately and go to the ER

12References/r37

Guidelines and key sources

›Cruccu G, Di Stefano G, Truini A. Trigeminal Neuralgia. N Engl J Med. 2020.

›NEJM review: classification, pathophysiology, management

›https://www.nejm.org/doi/full/10.1056/NEJMra1914484

›Amaechi O. Trigeminal Neuralgia: Rapid Evidence Review. Am Fam Physician. 2025.

›Current evidence-based clinical practice review

›https://www.aafp.org/pubs/afp/issues/2025/0500/trigeminal-neuralgia.html

›Bendtsen L, Zakrzewska JM, Heinskou TB, et al. Advances in Diagnosis, Classification, Pathophysiology, and Management of Trigeminal Neuralgia. Lancet Neurol. 2020.

›Lancet review: classification, ED management, surgical outcomes

›https://pubmed.ncbi.nlm.nih.gov/32822636

›Gronseth G, Cruccu G, Alksne J, et al. Practice Parameter: Diagnostic Evaluation and Treatment of Trigeminal Neuralgia. Neurology. 2008.

›AAN/EFNS evidence-based practice parameter

›https://doi.org/10.1212/01.wnl.0000326598.83183.04

›Bendtsen L, Zakrzewska JM, Abbott J, et al. European Academy of Neurology Guideline on Trigeminal Neuralgia. Eur J Neurol. 2019.

›EAN guideline: pharmacotherapy and surgical recommendations

›https://doi.org/10.1111/ene.13950

›Pinto MJ, Gomes A, Pinto M, Abreu P, Costa A. Treatment of Acute Exacerbations of Trigeminal Neuralgia in the Emergency Department. Headache. 2022.

›Retrospective case series: IV fosphenytoin 64% efficacy in ED

›https://pubmed.ncbi.nlm.nih.gov/36005285

›Cruccu G, Finnerup NB, Jensen TS, et al. Trigeminal Neuralgia: New Classification and Diagnostic Grading. Neurology. 2016.

›ICHD-3 classification grading framework

›https://pubmed.ncbi.nlm.nih.gov/27306631

›Henssen D, van Grinsven M, Vissers K, van Goethem J. MRI in the Diagnosis of Trigeminal Neuralgia: A Systematic Review. Eur Radiol. 2026.

›Protocol dependence and diagnostic accuracy of MRI for TN

›https://pubmed.ncbi.nlm.nih.gov/41307659

›Worm J, Heinskou TB, Rochat P, et al. Five-Year Prospective Outcomes of Medical Management and MVD in Trigeminal Neuralgia. J Neurol. 2025.

›59% MVD pain-free vs 19% medical management at 5 years

›https://pubmed.ncbi.nlm.nih.gov/41102594

Evidence & Review