Trigeminal neuralgia in United Kingdom: Symptoms, Causes & Treatment | aihealz
ICD variantTrigeminal neuralgia is a specific ICD-10 coded subtype of Trigeminal Neuralgia. The clinical content below covers Trigeminal Neuralgia in general.
NeurologysevereICD-10 · G50.0
Trigeminal neuralgia.Care & specialists in United Kingdom
In United Kingdom, trigeminal neuralgia is managed by neurologists. Trigeminal neuralgia is a facial pain disorder defined by brief paroxysms of electric-shock-like pain in the territory of the trigeminal nerve, usually triggered by light touch, chewing, brushing the teeth, or a breeze across the cheek. Incidence runs at roughly 12-27 new cases per 100,000 people each year, with women affected 1.7 times more often than men and peak onset between ages 50 and 70.
Trigeminal neuralgia (ICD-10: G50.0) is a paroxysmal facial neuropathic pain syndrome arising from dysfunction of the fifth cranial nerve. The International Classification of Headache Disorders, 3rd edition (ICHD-3) defines it as recurrent unilateral brief electric-shock-like pain abrupt in onset and termination, limited to the distribution of one or more divisions of the trigeminal nerve, and triggered by innocuous stimuli. ICHD-3 separates the condition into three forms: classical trigeminal neuralgia, caused by morphological changes in the trigeminal nerve root from neurovascular compression at the root entry zone (most often by the superior cerebellar artery); secondary trigeminal neuralgia, caused by an identifiable underlying disorder such as a multiple sclerosis plaque, vestibular schwannoma, epidermoid cyst, or arteriovenous malformation; and idiopathic trigeminal neuralgia, where no compression or lesion is found on high-resolution MRI. A subset of patients also experiences continuous background facial pain between paroxysms, formerly called atypical or type 2 trigeminal neuralgia and now described in ICHD-3 as trigeminal neuralgia with concomitant continuous pain.
key facts
Prevalence
Incidence 12-27 per 100,000 per year; lifetime prevalence approximately 0.16-0.3%
Demographics
Female-to-male ratio 1.7:1; right side affected slightly more often than left; bilateral involvement under 5% and raises suspicion of multiple sclerosis
Avg. age
Peak onset age 50-70; under-40 onset, especially bilateral, suggests secondary cause such as MS
Global cases
Roughly 2-3% of multiple sclerosis patients develop trigeminal neuralgia, often younger and bilaterally
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How you might notice it
The key symptoms of Trigeminal neuralgia are: Sudden, severe, unilateral facial pain described as electric-shock-like, stabbing, or lancinating, lasting from a fraction of a second up to two minutes per paroxysm., Pain limited to one or more divisions of the trigeminal nerve, most commonly the maxillary (V2) and mandibular (V3) branches; isolated ophthalmic (V1) involvement is seen in fewer than 5% of cases., Trigger-evoked attacks brought on by innocuous stimuli — light touch to the face, chewing, brushing the teeth, shaving, washing the face, talking, smiling, or a draft of cool air across the cheek., Discrete trigger zones, usually small areas around the nasolabial fold, upper lip, or chin, where minimal contact reliably provokes a paroxysm., A brief refractory period of seconds to minutes after a severe attack during which the same trigger fails to produce pain., Clusters of attacks lasting hours, separated by pain-free intervals of days, weeks, or months — the natural history is often relapsing and remitting in early disease., Preserved sensation and normal neurological examination between attacks in classical and idiopathic forms; persistent sensory loss raises suspicion of a secondary cause..
01Sudden, severe, unilateral facial pain described as electric-shock-like, stabbing, or lancinating, lasting from a fraction of a second up to two minutes per paroxysm.
02Pain limited to one or more divisions of the trigeminal nerve, most commonly the maxillary (V2) and mandibular (V3) branches; isolated ophthalmic (V1) involvement is seen in fewer than 5% of cases.
03Trigger-evoked attacks brought on by innocuous stimuli — light touch to the face, chewing, brushing the teeth, shaving, washing the face, talking, smiling, or a draft of cool air across the cheek.
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How it’s diagnosed
diagnosis
Trigeminal neuralgia is a clinical diagnosis built on the ICHD-3 criteria: recurrent unilateral brief paroxysms of electric-shock-like facial pain in trigeminal distribution, triggered by innocuous stimuli, with no clinically evident neurological deficit between attacks. A careful history that establishes the lancinating quality, paroxysmal time course, trigger sensitivity, refractory period, and exact branch distribution is more diagnostic than any test. Examination should look for sensory loss in V1, V2, or V3, jaw weakness, corneal reflex change, and other cranial nerve findings — any of which raises suspicion of a secondary cause. Dental and sinus pathology must be excluded clinically; a dental opinion is often part of the workup because patients frequently present after multiple unsuccessful dental procedures. High-resolution MRI of the brain with dedicated trigeminal nerve sequences is mandatory in all patients, both to identify neurovascular compression with morphological change (supporting a classical diagnosis and informing surgical planning) and to exclude multiple sclerosis plaques and cerebellopontine angle tumors. Constructive interference in steady state (CISS) and fast imaging employing steady-state acquisition (FIESTA) sequences depict the trigeminal nerve, surrounding cisternal vessels, and any compressing vascular loop with high spatial resolution. Time-of-flight MR angiography adds vascular detail. The AAN/EFNS 2008 guideline recommends routine MRI for every patient with trigeminal neuralgia regardless of clinical confidence in a classical diagnosis. Electrophysiological testing, including trigeminal reflex studies, can support diagnosis in atypical cases but is not required for routine practice.
Key tests
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Detailed clinical history and ICHD-3 criteriaEstablishes the diagnosis. Key features are unilateral pain limited to trigeminal distribution, attacks lasting seconds to two minutes, electric-shock or stabbing quality, trigger-evoked attacks from innocuous stimuli, refractory period after severe attacks, and absence of clinically evident neurological deficit.
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Treatment & cost
medical treatments
✓Carbamazepine (100 mg twice daily, titrated to 400-1200 mg per day in divided doses)
✓Oxcarbazepine (300 mg twice daily, titrated to 600-1800 mg per day)
✓Lamotrigine (25 mg daily, slow titration to 200-400 mg per day)
✓Baclofen (5 mg three times daily, titrated to 30-80 mg per day)
surgical options
Microvascular decompression (Jannetta procedure)Initial pain freedom in 80-90% of patients; durable pain freedom at 10 years in approximately 70% (Barker 1996 long-term series, Tatli and Sindou subsequent reports). Mortality under 0.3% and major complication rates under 5% in high-volume centers.
Percutaneous radiofrequency thermocoagulation of the Gasserian ganglionInitial pain relief in around 90% of patients; pain freedom at 5 years roughly 50%. Sensory loss in the treated division is expected and is part of the mechanism.
Percutaneous glycerol rhizotomyInitial pain relief in 80-90%; pain freedom at 5 years approximately 40-50%; recurrence rates higher than with thermocoagulation.
Percutaneous balloon compressionInitial pain freedom in 85-90%; 5-year pain freedom in roughly 50-60%.
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Causes & risk factors
known causes
Neurovascular compression at the trigeminal root entry zone
An artery (most often the superior cerebellar artery, less often the anterior inferior cerebellar artery or a vein) pulses against the nerve root where it leaves the pons. Over years this produces focal demyelination and ectopic spontaneous discharges in adjacent fibers, generating the paroxysmal pain. This is the dominant cause in classical trigeminal neuralgia.
Multiple sclerosis plaque in the central trigeminal pathway
A demyelinating lesion in the pontine root entry zone disrupts conduction in the trigeminal sensory tract. Trigeminal neuralgia develops in roughly 2-5% of MS patients, often years before classical neuralgia would otherwise begin, frequently bilaterally, and at a younger age.
Cerebellopontine angle tumor
Vestibular schwannoma, meningioma, or epidermoid cyst can stretch or distort the trigeminal root. These tumors account for roughly 2-5% of trigeminal neuralgia cases; the pain may be the first symptom before cranial nerve deficits appear.
Arteriovenous malformation or basilar dolichoectasia
Vascular anomalies that produce sustained mechanical pressure on the nerve. Basilar dolichoectasia — an elongated, tortuous basilar artery — is the most common vascular cause beyond simple loops of the superior cerebellar artery.
Post-traumatic or post-surgical injury
Injury to peripheral branches of the trigeminal nerve during dental procedures, maxillofacial surgery, or facial trauma can produce neuropathic pain that resembles trigeminal neuralgia. ICHD-3 classifies this as painful post-traumatic trigeminal neuropathy, a separate diagnosis, but presentations can overlap.
Genetic predisposition
Familial clustering is reported in roughly 1-2% of cases, with autosomal dominant inheritance described in a small number of pedigrees. Genome-wide studies have not identified a single dominant locus, but ion-channel variants are under active investigation.
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Living with it
01Trigeminal neuralgia cannot be primarily prevented because the underlying neurovascular or structural mechanisms cannot be predicted or modified before symptom onset
02Control blood pressure long-term to limit arterial elongation and tortuosity, which contribute to root compression
03Adhere to disease-modifying therapy in multiple sclerosis to reduce the formation of new pontine plaques that can cause secondary trigeminal neuralgia
04Once diagnosed, prevent attack escalation by adhering to medication, avoiding sudden drug discontinuation, and identifying personal triggers
05Continue dental care under the supervision of a dentist familiar with trigeminal neuralgia — local anesthetic blocks can be planned to avoid trigger zones
recommended foods
•Soft foods such as well-cooked vegetables, yogurt, oatmeal, eggs, fish, and tender meats that require minimal chewing
•Cool or room-temperature drinks taken through a straw to bypass trigger zones around the lips and cheek
•Smoothies and pureed soups during severe flares to maintain calorie and protein intake
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When to seek help
why see a neurology
A neurologist should be involved at diagnosis to confirm the ICHD-3 criteria, coordinate the MRI workup, and initiate or supervise carbamazepine or oxcarbazepine titration. Refer to neurosurgery when pain is uncontrolled on adequate medical therapy, when significant adverse effects prevent therapeutic doses, when MRI shows clear neurovascular compression in a patient who is a surgical candidate, or when MRI identifies a structural lesion requiring intervention.
Classical trigeminal neuralgiaCaused by demonstrable neurovascular compression with morphological change (atrophy or displacement) of the trigeminal nerve root at the brainstem entry zone, typically by an arterial loop of the superior cerebellar or anterior inferior cerebellar artery. Accounts for roughly 75% of cases.
Secondary trigeminal neuralgiaAttributed to an identifiable underlying disorder — multiple sclerosis plaque in the pontine trigeminal pathway, cerebellopontine angle tumor (vestibular schwannoma, meningioma, epidermoid cyst), arteriovenous malformation, or basilar dolichoectasia. Accounts for approximately 15% of cases.
Idiopathic trigeminal neuralgiaNo neurovascular compression with morphological change and no underlying disorder identified on high-quality MRI. Accounts for around 10% of cases.
Trigeminal neuralgia with concomitant continuous painParoxysmal attacks plus a background of continuous or near-continuous moderate facial pain between attacks. Responds less reliably to drug therapy and to surgery than purely paroxysmal disease.
Living with Trigeminal neuralgia
Timeline
Pharmacological response to carbamazepine or oxcarbazepine typically appears within 24-72 hours of reaching an adequate dose, with full effect over 1-2 weeks of stable dosing. Microvascular decompression patients leave hospital in 3-5 days, return to light activity in 2-4 weeks, and reach maximal recovery by 3 months; pain relief is usually immediate after surgery. Percutaneous procedures provide pain relief within 24-48 hours and recovery to normal activity within 1-2 weeks. Stereotactic radiosurgery is delayed in effect, with pain relief emerging 4-8 weeks after treatment and continuing to develop for up to 6 months.
Lifestyle
01Eat soft, room-temperature foods during active disease, cut food into small pieces, and use a straw if oral movement provokes attacks
02Adopt a daily oral hygiene routine using a soft-bristled brush and lukewarm water; consider a water flosser if mechanical brushing triggers pain
03Shield the face from cold wind and air-conditioning drafts with a scarf or shawl during flare periods
04Keep a pain diary recording timing, triggers, and medication doses — patterns guide titration and surgical timing decisions
05Schedule activities and meals during periods of best pain control, typically after the day's first medication doses take effect
06Address depression, anxiety, and sleep disturbance with a clinician early; these magnify pain experience and disability
07Avoid alcohol during initial carbamazepine titration because of additive sedative effects
Complementary approaches
Acupuncture and transcutaneous electrical nerve stimulation (TENS)Small randomized studies suggest modest short-term reduction in attack frequency. Adjunctive only; should never replace evidence-based pharmacotherapy for an active disorder of this severity.
Cognitive behavioural therapy and pain-coping psychologyReduces the impact of pain on mood, sleep, and function. Particularly important given the elevated rates of depression and suicidality in untreated trigeminal neuralgia.
Choosing a doctor
Look for board certification in neurology with subspecialty interest in headache or facial pain. For surgical management, choose a neurosurgical center with a documented annual volume of at least 20 microvascular decompressions or stereotactic radiosurgery cases, published outcomes data, and access to high-resolution MRI with CISS/FIESTA imaging. Continuity of care matters — diagnosis is clinical and follow-up is multi-year.
Patient support resources
Facial Pain Association →US-based patient association with educational materials, peer support, and clinician finder for trigeminal neuralgia and related disorders.
Patients describe trigeminal neuralgia as sudden electric-shock-like or stabbing pain on one side of the face, lasting seconds to two minutes per attack. The pain is usually in the cheek, upper or lower jaw, and is triggered by light touch, chewing, brushing the teeth, talking, or a breeze. Many people describe it as the most severe pain they have experienced.
What triggers a trigeminal neuralgia attack?▾▴
Common triggers are light touch to the face, chewing, brushing the teeth, shaving, washing the face, talking, smiling, and a cool draft of air across the cheek. Triggers are typically innocuous stimuli that would not be painful in a healthy person, and trigger zones are usually small areas around the nasolabial fold, upper lip, or chin.
How is trigeminal neuralgia diagnosed?▾▴
Trigeminal neuralgia is diagnosed clinically using the International Classification of Headache Disorders criteria — recurrent unilateral brief electric-shock-like facial pain in trigeminal distribution triggered by innocuous stimuli. High-resolution MRI of the brain with dedicated trigeminal nerve sequences is required in every patient to identify neurovascular compression and to exclude multiple sclerosis or a tumor.
Why do I need an MRI for trigeminal neuralgia?▾▴
MRI identifies neurovascular compression at the trigeminal root, which supports a classical diagnosis and guides surgical planning. It also detects multiple sclerosis plaques and cerebellopontine angle tumors that cause secondary trigeminal neuralgia. The AAN/EFNS 2008 guideline recommends MRI for every patient regardless of how typical the clinical picture appears.
What is the first-line medication for trigeminal neuralgia?▾▴
Carbamazepine is the first-line medication and the only drug with Level A evidence in international guidelines. Treatment is usually started at 100 mg twice daily and increased every 3-7 days to clinical effect, with most patients responding between 400 and 1200 mg per day in divided doses. Reported numbers needed to treat are 1.7-2.6.
Is oxcarbazepine better than carbamazepine?▾▴
Oxcarbazepine has comparable efficacy to carbamazepine and is often better tolerated, with fewer drug interactions and less sedation. The trade-off is a higher rate of hyponatremia, which needs sodium monitoring. Many specialists now use oxcarbazepine as first-line for new patients, particularly older adults on multiple other medications.
What is microvascular decompression?▾▴
Microvascular decompression is a neurosurgical procedure that places a small Teflon felt pad between the trigeminal nerve and the blood vessel pressing on it. The operation addresses the cause rather than the symptom. Initial pain relief is achieved in 80-90% of patients with classical disease, and roughly 70% remain pain free 10 years later.
How does Gamma Knife treat trigeminal neuralgia?▾▴
Gamma Knife stereotactic radiosurgery delivers a single high-dose focused radiation beam to the trigeminal nerve root just proximal to the ganglion. The procedure is non-invasive and takes a few hours. Pain relief is delayed, emerging over 4-8 weeks. Roughly 70% of patients are pain free at one year and 50% at five years; it is preferred for older or medically frail patients.
Can trigeminal neuralgia be cured?▾▴
Microvascular decompression cures the underlying cause in classical trigeminal neuralgia with documented neurovascular compression, with around 70% of patients remaining pain free at 10 years without medication. Drug therapy and percutaneous and radiosurgical procedures control pain but do not address the cause, and recurrence is more common.
Does multiple sclerosis cause trigeminal neuralgia?▾▴
Yes. A demyelinating plaque in the pontine trigeminal pathway can produce trigeminal neuralgia. Around 2-5% of multiple sclerosis patients develop the condition during their illness, often at younger ages and more frequently bilaterally than classical neurovascular-compression disease.
Is trigeminal neuralgia the same as a migraine?▾▴
No. Migraine attacks last 4-72 hours with throbbing pain, nausea, light and sound sensitivity, and sometimes aura. Trigeminal neuralgia attacks last seconds to two minutes, are electric-shock-like, are triggered by innocuous facial stimuli, and have no nausea or aura. The two are distinct conditions managed differently.
Why is trigeminal neuralgia mistaken for a dental problem?▾▴
The pain often radiates into the upper or lower jaw and teeth, and patients commonly present first to a dentist. Repeated dental procedures, including root canals and extractions, fail to relieve the pain because the source is the trigeminal nerve, not the teeth. Persistent facial pain after adequate dental treatment should prompt a neurology referral.
Can young people get trigeminal neuralgia?▾▴
Peak onset is between ages 50 and 70, and the condition is uncommon under 40. When trigeminal neuralgia appears in a younger person, especially bilaterally, multiple sclerosis or another structural cause should be sought with MRI. Pediatric presentations are exceptional and almost always have an underlying lesion.
How long do attacks last?▾▴
Individual paroxysms last from a fraction of a second up to two minutes. Attacks can occur in clusters lasting hours, separated by pain-free intervals of minutes to weeks. The brief electric-shock quality and rapid termination distinguish trigeminal neuralgia from migraine, cluster headache, and dental pain.
What is the difference between classical and secondary trigeminal neuralgia?▾▴
Classical trigeminal neuralgia is caused by neurovascular compression at the trigeminal root with visible morphological change on MRI. Secondary trigeminal neuralgia is caused by an identifiable underlying disorder such as multiple sclerosis, a cerebellopontine angle tumor, or a vascular malformation. The two differ in age of onset, response to treatment, and surgical options.
Can I have trigeminal neuralgia on both sides of the face?▾▴
Bilateral trigeminal neuralgia is rare overall (under 5%) and raises suspicion of a secondary cause, particularly multiple sclerosis. Even when both sides are affected, attacks usually do not occur simultaneously. Bilateral disease should prompt detailed MRI assessment.
Discrete trigger zones, usually small areas around the nasolabial fold, upper lip, or chin, where minimal contact reliably provokes a paroxysm.
05A brief refractory period of seconds to minutes after a severe attack during which the same trigger fails to produce pain.
06Clusters of attacks lasting hours, separated by pain-free intervals of days, weeks, or months — the natural history is often relapsing and remitting in early disease.
07Preserved sensation and normal neurological examination between attacks in classical and idiopathic forms; persistent sensory loss raises suspicion of a secondary cause.
08Weight loss, dehydration, and avoidance of eating, drinking, talking, or oral hygiene because of fear that these activities will provoke an attack.
09Depression, anxiety, and suicidal ideation related to severe, unpredictable pain — the disorder has historically been called the suicide disease for this reason.
10Continuous low-grade aching or burning background pain between paroxysms in patients with the concomitant-continuous-pain subtype.
early warning signs
•Brief, fleeting jabs of facial pain triggered by light touch, often initially mistaken for a dental problem
•Pain that comes and goes in clusters with pain-free remissions of weeks or months — a relapsing pattern early in the disease
•Increasing avoidance of cold wind, shaving, or specific foods on one side of the face
•Repeated dental procedures (root canals, extractions) that fail to relieve facial pain — a frequent prelude to diagnosis
•Unexplained weight loss combined with new unilateral facial pain in an adult over 50
● emergency signs
•Bilateral trigeminal pain, especially in a patient under 50 — urgent MRI is needed to exclude multiple sclerosis or a structural lesion
•Persistent sensory loss, jaw weakness, hearing change, or other cranial nerve findings — suggests a secondary cause such as a cerebellopontine angle tumor
•Suicidal thoughts or active plans related to uncontrolled pain — requires urgent psychiatric and pain-management input
•Fever, neck stiffness, or rash in a patient with new facial pain — exclude herpes zoster ophthalmicus or other infectious cause
•Severe drug reaction within the first 8 weeks of carbamazepine or oxcarbazepine — rash, mucosal involvement, eosinophilia, hyponatremia under 125 mmol/L — requires immediate discontinuation and assessment
Neurological examinationIdentifies cranial nerve deficits that suggest a secondary cause. Specific attention to facial sensation in all three trigeminal divisions, corneal reflex, jaw strength and symmetry, and adjacent cranial nerves (VII, VIII).
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MRI brain with dedicated trigeminal nerve sequences (CISS/FIESTA)Mandatory in every patient. Identifies neurovascular compression with morphological change of the trigeminal root, multiple sclerosis plaques, cerebellopontine angle tumors, and vascular malformations. The AAN/EFNS 2008 guideline (Cruccu et al) recommends MRI as the only routine investigation in newly diagnosed disease.
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Time-of-flight MR angiographyDemonstrates the vascular anatomy around the trigeminal root entry zone in detail. Useful when planning microvascular decompression to identify the offending vessel and any accessory loops.
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Trigeminal reflex testing (blink reflex, masseter inhibitory reflex)Optional electrophysiological investigation. Used in research and in atypical cases to confirm dysfunction of the trigeminal sensory pathway and to support a diagnosis of symptomatic trigeminal neuralgia when imaging is unclear.
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Dental and oral-facial evaluationExcludes dental, periodontal, sinus, and temporomandibular joint pathology that mimics trigeminal neuralgia. Particularly valuable when the pain is restricted to V2 or V3 and the patient has had recent dental work.
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Blood tests before starting carbamazepine or oxcarbazepineBaseline complete blood count, liver function, sodium, and renal function. HLA-B*1502 screening is recommended in Han Chinese, Thai, and other Southeast Asian populations before carbamazepine because of a strong association with Stevens-Johnson syndrome.
Outlook
The natural course of trigeminal neuralgia is relapsing and remitting, with progressively shorter pain-free intervals over years. With adequate carbamazepine or oxcarbazepine, around 70-80% of patients achieve initial pain control, but long-term tolerability falls to roughly 50% over time as nerve injury advances and drug doses required to maintain response approach the tolerability ceiling. Microvascular decompression offers the best chance of long-term cure in classical neurovascular-compression disease, with approximately 80-90% pain free at one year and 70% at 10 years. Percutaneous procedures and stereotactic radiosurgery offer high initial relief with recurrence rates that rise after 3-5 years and the possibility of repeat treatment. Secondary trigeminal neuralgia from multiple sclerosis is more refractory, with higher relapse rates after every modality. Untreated, the disorder carries substantial morbidity from malnutrition, weight loss, depression, social isolation, and elevated suicide risk; mortality from the disease itself is low, but quality-of-life impairment is among the worst measured in any chronic pain condition.
risk factors
Age over 50non-modifiable
Incidence rises sharply after age 50, peaking between 60 and 70, as the vertebrobasilar arterial tree becomes more tortuous and more likely to compress the trigeminal root.
Female sexnon-modifiable
Women are affected 1.7 times more often than men; the reasons are not fully explained but may relate to differences in cerebellopontine angle anatomy and longer life expectancy.
Multiple sclerosisnon-modifiable
MS patients have a 20-fold increased risk of trigeminal neuralgia compared with the general population; roughly 2-5% of MS patients develop it during their illness.
Hypertensionmodifiable
Long-standing hypertension contributes to arterial elongation and tortuosity, increasing the likelihood of neurovascular contact with the trigeminal root. The association is most consistent in older women.
Family history of trigeminal neuralgiagenetic
A first-degree relative with the condition raises personal risk modestly. Familial cases tend to present earlier and more often bilaterally.
Prior facial or dental traumamodifiable
Significant facial trauma, dental implant placement, or third-molar extraction can precipitate trigeminal neuropathic pain, sometimes mimicking trigeminal neuralgia.
Cerebellopontine angle pathologynon-modifiable
Schwannomas, meningiomas, epidermoid cysts, and arteriovenous malformations all elevate risk by deforming the trigeminal root.
•Adequate hydration with water at neutral temperature, monitoring sodium status if on carbamazepine or oxcarbazepine
•Small frequent meals rather than large meals that require prolonged chewing
foods to avoid
•Very hot or very cold foods and drinks if temperature is a personal trigger
•Hard, crunchy, or sticky foods such as raw apples, crusty bread, nuts, and chewy candies during flares
•Excessive caffeine in the evening, which can disrupt the sleep needed for pain recovery
•Alcohol while titrating sodium-channel blockers because of additive central nervous system depression
•Foods that consistently trigger personal attacks, identified through diary tracking
Surgical complications of microvascular decompression — cerebrospinal fluid leak, hearing loss, facial weakness, cerebellar injury — in roughly 1-5% of cases
07Persistent facial sensory loss, anesthesia dolorosa, or corneal anesthesia after ablative procedures or radiosurgery
TMJ disorder produces dull, aching pain over the joint or chewing muscles, worsened by jaw movement, often with clicking, locking, or restricted opening. Pain is mechanical and continuous rather than paroxysmal, and is not triggered by light touch to the face.
01Take carbamazepine or oxcarbazepine at the same times each day, with food, to maintain steady plasma levels
02Monitor for warning signs of severe drug reaction in the first 8 weeks — new rash, mouth ulcers, fever, swollen lymph nodes — and seek urgent review if these occur
03Recheck sodium and full blood count at 2 weeks, 1 month, and every 3-6 months while on chronic carbamazepine or oxcarbazepine
04Carry a brief written summary of diagnosis, MRI findings, current medications, and emergency contacts in case of unexpected severe flare
05Plan a rescue strategy for breakthrough pain in discussion with the prescriber — short-acting baclofen, additional carbamazepine dose, or scheduled botulinum toxin top-up
Exercise
Low-impact aerobic exercise such as stationary cycling, walking, and swimming is safe and recommended during periods of pain control. Avoid activities that provoke trigger zones — wind on the face during outdoor cycling, cold-water swimming, or contact sports with facial impact. Resume normal exertion as pain allows; physical activity reduces depression and improves general pain tolerance.