In New Zealand, trigeminal Neuralgia is managed by pain medicine & palliative cares. 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.
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..
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.
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.
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.
Find specialists →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.
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.
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.
Medically reviewed by AIHealz Medical Editorial Board · May 12, 2026
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