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EMERGENCY:New facial pain with progressive facial numbness or weakness, pain in a young patient (under 40) or bilateral pain, or pain not responding to carbamazepine at adequate doses —call040-46324365immediately — 24 hours, 7 days— 24/7

HEADACHE & PAIN SYNDROMES

Trigeminal Neuralgia in Hyderabad: The Electric-Shock Facial Pain That Has a Cure — MVD Surgery at KIMS

Expert ICHD-3 diagnosis, MRI posterior fossa protocol, carbamazepine and oxcarbazepine medical management with HLA-B*1502 screening, and Microvascular Decompression (MVD) surgery performed by the KIMS Neuroscience team, Secunderabad, Hyderabad — the most durable surgical treatment for TGN with >80% long-term success.

Trigeminal neuralgia is a primary facial pain disorder characterised by recurrent, brief, electric-shock-like, extremely severe unilateral pain in the distribution of one or more branches of the trigeminal nerve (cranial nerve V). Attacks last seconds to 2 minutes and are triggered by light touch to a specific trigger zone from innocuous stimuli — eating, talking, brushing teeth, or a puff of cold air. This light-touch triggering by innocuous stimuli is pathognomonic and distinguishes TGN from dental pain. The most common cause: pulsatile vascular compression of the trigeminal nerve root, most commonly by the superior cerebellar artery. MVD surgery — placing a Teflon cushion between the vessel and the nerve — offers >80% long-term pain freedom at 5 years at KIMS.

What it is: Electric-shock facial pain lasting seconds, triggered by light touch to the cheek, lip, or nasolabial fold. V2/V3 distribution most common. Between attacks: complete pain freedom (classical TGN).
Why teeth are extracted first: TGN in V2/V3 mimics toothache. But dental pain is not triggered by light skin touch — TGN is. If touching the skin of the cheek triggers the pain: stop all dental procedures and assess for TGN at KIMS.
HLA-B*1502 testing at KIMS: Present in 6–8% of South Asian patients. Predisposes to Stevens-Johnson syndrome from carbamazepine. KIMS tests all Indian patients before starting carbamazepine. If positive: oxcarbazepine or lamotrigine preferred.
Medical treatment: Carbamazepine 200–800mg/day (70–80% response) · Oxcarbazepine (better tolerability, no HLA-B*1502 risk) · Add-on: pregabalin, lamotrigine, baclofen for partial responders.
MVD at KIMS: Retrosigmoid craniotomy — Teflon sponge between SCA and nerve — no nerve destruction — no facial numbness — 90% initial relief — 80–85% at 5 years. KIMS team with intraoperative BAEP and facial nerve EMG monitoring.
Non-surgical options: Gamma Knife (non-invasive, delayed response 2–6 months, ~70–75% success) · Radiofrequency thermocoagulation · Glycerol rhizotomy · Balloon microcompression — all cause facial numbness.
Contact KIMS: 040-44885000 · ICHD-3 diagnosis · MRI posterior fossa · HLA-B*1502 screening · MVD surgical consultation

Fact	Details
Pain character	Sudden electric-shock or lightning bolt · Seconds to 2 minutes · Triggered by light skin touch · Complete pain freedom between attacks (classical TGN)
Distribution	V2 (cheek/upper lip/upper teeth) most common · V3 (lower lip/jaw/chin) frequent · V2+V3 together most common · Bilateral: suspect MS or tumour
Classical cause	Superior cerebellar artery compressing trigeminal root at posterior fossa · Demyelination · Abnormal electrical discharge · Identified on thin-cut FIESTA/CISS MRI
HLA-B*1502 (India)	6–8% South Asian patients · Fatal SJS risk from carbamazepine · Test before prescribing at KIMS · If positive: oxcarbazepine or lamotrigine
MVD outcomes	90% initial pain relief · 80–85% at 5 years · 70–75% at 10 years · No facial numbness · Hospital stay 3–5 days
When to consider surgery	Medication side effects unacceptable · Confirmed neurovascular contact on MRI · Patient prefers durable solution · >2 years medication management with incomplete relief
Non-MVD options	Gamma Knife (non-invasive, delayed) · RF thermocoagulation (immediate, facial numbness) · Glycerol rhizotomy · Balloon microcompression

Diagnostic Pearl

The Most Common TGN Misdiagnosis: Dental Pain and Unnecessary Tooth Extractions

Four unnecessary tooth extractions before the correct diagnosis. This is the most common TGN misdiagnosis pattern worldwide, and it is even more prevalent in India where tooth pain is culturally assumed as the most likely explanation for facial pain. Trigeminal neuralgia in the V2 (maxillary) or V3 (mandibular) division produces pain that appears to come from the teeth and gums; it is triggered by jaw movement, eating, and drinking — all of which are also associated with toothache. The critical distinguishing feature: TGN is also triggered by light touch to the skin of the cheek, lip, or nasolabial fold — and this is not a feature of dental pain. Every tooth in the distribution of a trigger should be considered potentially innocent until TGN is excluded.

About This Condition

Trigeminal Neuralgia at a Glance

The essential facts that shape how trigeminal neuralgia is recognised, classified, and treated at KIMS — from the electric-shock pain triggered by light touch through the vascular compression cause and on to Microvascular Decompression, the surgical cure performed at KIMS by the KIMS Neuroscience team.

What it is

A primary facial pain disorder characterised by recurrent, brief, electric-shock-like, extremely severe unilateral pain in the distribution of one or more branches of the trigeminal nerve (cranial nerve V). The pain is triggered by light touch to a specific trigger zone on the face — often the upper lip, nasolabial fold, or cheek — from innocuous stimuli such as eating, drinking, talking, brushing teeth, touching the face, a puff of wind, or cold air. Between attacks: either complete pain freedom (classical TGN) or a background ache (with concomitant continuous pain).

The most painful condition known

Trigeminal neuralgia is consistently ranked among the most severe pain conditions experienced by humans. Patients describe attacks as electric shocks, stabbing, burning, or lightning bolts through the face. Many patients lose significant weight because eating — a reliable trigger — becomes terrifying. Attacks during eating, talking, and dental hygiene can make normal life functionally impossible. The severity has historically earned it the name 'tics douloureux' (French for 'painful tic').

Cause

In the majority of cases (classical TGN): pulsatile compression of the trigeminal nerve root at the root entry zone in the posterior fossa, most commonly by the superior cerebellar artery. The repeated compression causes demyelination of the trigeminal nerve fibres, producing abnormal electrical discharge. In some cases: multiple sclerosis plaque at the trigeminal root entry zone; tumour compression (acoustic neuroma, meningioma, epidermoid cyst); or no identifiable cause (idiopathic).

Who it affects

Prevalence approximately 4–13 per 100,000. Slightly more common in women (female:male 3:2). Most common over 50, though can occur at any age. In younger patients (<40), the index of suspicion for secondary causes (MS, tumour) is higher. The diagnosis is fundamentally clinical — no test is required to diagnose TGN — but MRI is needed to identify vascular compression and exclude secondary causes.

The surgical cure

Microvascular Decompression (MVD) — surgery to separate the offending artery from the trigeminal nerve root — offers the most durable long-term pain relief of any TGN treatment, with >80% of patients achieving complete or near-complete pain relief at 5 years. MVD is performed at KIMS by the KIMS Neuroscience team, with full intraoperative neurophysiological monitoring (BAEPs, facial nerve EMG).

Emergency

040-46324365

Appointment

040-44885000

About This Condition

The Pain That Stopped Her Eating

A 62-year-old woman in Hyderabad has lost 8 kilograms in three months. Her family is concerned she has cancer. At KIMS, the story emerges: she has been having episodes of sudden, violent, electric-shock pain in her right cheek and upper lip for the past 4 months. Each episode lasts 2–3 seconds but is so severe that she gasps and cannot move. They are triggered without fail by eating — the movement of her jaw, the food touching the right side of her mouth. She has stopped eating solid food. Speaking on the phone triggers attacks. Brushing her teeth on the right side has become impossible.

She was told by her dentist that her upper right molar needed extraction. The tooth was removed. The pain continued. A second tooth was removed. The pain continued. She has now had four teeth extracted on the right side and the pain is unchanged. Her neurologist referred her to KIMS.

At KIMS, the diagnosis is established immediately from the history. ICHD-3 criteria for trigeminal neuralgia: unilateral, severe, electric-shock quality, lasting 2–3 seconds, in the distribution of V2 (maxillary division) of the trigeminal nerve, triggered by eating and talking, with complete pain freedom between attacks. MRI brain with thin-cut posterior fossa sequences shows the superior cerebellar artery in contact with the right trigeminal nerve root at the root entry zone.

This is classical trigeminal neuralgia from vascular compression. It is eminently treatable. Carbamazepine is started at 200mg twice daily and titrated upward. Her attacks reduce significantly within a week. The surgical option — Microvascular Decompression (MVD) — is discussed. Given the confirmed vascular compression on MRI, her age and fitness for surgery, and her preference for a durable solution, she elects for MVD. the KIMS Neuroscience team performs the retrosigmoid approach at KIMS, identifying the superior cerebellar artery looped against the trigeminal nerve root and placing a Teflon sponge between them. She is pain-free from the following morning and remains so at her 12-month review.

Book a Consultation

Speak directly with our trigeminal neuralgia specialist team — neurology, MRI posterior fossa imaging, carbamazepine and HLA-B*1502 screening, and Microvascular Decompression (MVD) surgery by the KIMS Neuroscience team coordinated under one roof. No referral required. Monday to Saturday.

040-44885000Emergency line: 040-46324365

Recognising Trigeminal Neuralgia

Clinical Features of Trigeminal Neuralgia

The clinical profile of trigeminal neuralgia is unmistakable when each feature is considered: the electric-shock pain, the trigeminal branch distribution, light-touch trigger zones, the brief refractory period that distinguishes it from SUNCT/SUNA, the characteristic eating-induced weight loss, and the bilateral pattern that signals secondary causes.

The pain — electric shock, stabbing, lightning bolt

Each attack is sudden, violent, electric-shock quality — patients consistently use the same metaphors: 'electric shock,' 'lightning bolt,' 'stabbing,' 'burning bolt.' Severity is maximum from the first fraction of a second. Duration is seconds to 2 minutes (typically under 30 seconds). Pain-free intervals between attacks are complete (in classical TGN) or nearly complete. Multiple attacks per day occur in severe episodes — from a few to hundreds, sometimes in salvos (clusters of rapid-fire attacks). The pain is so severe that patients freeze, wince, or cry out involuntarily — hence the historical name 'tic douloureux' (the painful tic or wince).

The distribution — trigeminal nerve branches

V1 (ophthalmic division — forehead, eye, nose): affected alone in approximately 5% of classical TGN. V2 (maxillary division — cheek, upper lip, upper teeth, hard palate): most commonly affected, alone or with V3. V3 (mandibular division — lower lip, lower jaw, lower teeth, chin): frequently affected, alone or with V2. V2 and V3 together is the most common pattern. Bilateral TGN occurs in approximately 3–5% of cases — when bilateral, MS or a compressive lesion is more likely and must be investigated.

Trigger zones and trigger stimuli — the defining diagnostic feature

A specific area of the face — the trigger zone — from which attacks are reliably provoked by light touch. Common trigger zones: the nasolabial fold, the upper lip, the corner of the mouth, the cheek, the gum. Common triggers: chewing, speaking, drinking cold or hot liquids, touching the face with a hand or towel, a puff of cold air, or a breeze. The trigger is innocuous — a light touch that would not be noticed by an unaffected person. This light-touch triggering is pathognomonic of TGN and distinguishes it from dental pain (which is not triggered by light skin touch).

Refractory period

After a trigger provokes an attack, there is typically a brief refractory period of several seconds to minutes during which the trigger zone is temporarily unresponsive. This refractory period distinguishes TGN from SUNCT/SUNA (another TAC with no refractory period) and is diagnostically useful.

The eating problem — the weight loss signal

Chewing is among the most reliable triggers for TGN affecting V2/V3. Patients stop eating solid food, develop dietary habits centred on foods requiring minimal jaw movement (liquids, soft foods, food placed on the unaffected side), and lose significant weight. Weight loss of 5–15kg over 1–3 months before diagnosis is common in severe TGN. The weight loss should not be attributed to a systemic cause before TGN is excluded in any patient with facial pain.

Understanding the Disease

Classification of Trigeminal Neuralgia

Trigeminal neuralgia is classified into classical, idiopathic, and secondary forms based on the underlying cause, with a distinct atypical pattern (Type 2) where paroxysmal attacks are accompanied by continuous background pain. The classification directly determines the management approach and MVD candidacy.

Classical TGN — Vascular Compression

Most common · MVD candidate · >80% long-term success

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Cause: Vascular compression of the trigeminal nerve root by an aberrant artery or vein — superior cerebellar artery in ~80% of cases.

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MVD candidacy: Yes — MVD is the most effective treatment with >80% long-term success in classical TGN.

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Repeated pulsatile compression causes demyelination of the trigeminal nerve fibres, producing abnormal electrical discharge and the electric-shock pain.

Idiopathic TGN — No MRI Compression

Typical clinical features without demonstrable cause on MRI

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Cause: No demonstrable cause on MRI despite typical clinical features.

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MVD candidacy: MVD if no compression found on MRI but clinical picture is compelling; GKRS as alternative.

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Diagnosis remains clinical, supported by ICHD-3 criteria — TGN is fundamentally a clinical diagnosis.

Secondary TGN — Tumour or MS

Acoustic neuroma, meningioma, epidermoid cyst, or MS plaque

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Cause: Tumour (acoustic neuroma, meningioma, epidermoid cyst) or demyelination (multiple sclerosis) compressing the nerve.

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MVD candidacy: Treatment of the underlying cause first; MVD if residual TGN after tumour management.

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Bilateral TGN, young patients (<40), or facial numbness should prompt urgent imaging for secondary causes.

Diagnosis at KIMS

Diagnosis at KIMS — Clinical Criteria, MRI, and HLA-B*1502 Screening

The diagnosis of TGN is fundamentally clinical — no test is required to diagnose TGN. The KIMS pathway combines ICHD-3 clinical criteria, MRI posterior fossa protocol with thin-cut FIESTA/CISS sequences to identify neurovascular contact and exclude secondary causes, trigeminal nerve electrophysiology, and HLA-B*1502 pre-treatment screening to prevent Stevens-Johnson syndrome from carbamazepine in Indian patients.

Clinical diagnosis using ICHD-3 criteria

The diagnosis of TGN is clinical. At least 3 attacks of unilateral facial pain meeting all of: in the distribution of one or more branches of the trigeminal nerve; pain quality is sudden, intense, short-lived, electric-shock, stabbing, or sharp; pain provoked by innocuous stimuli to the trigger zone; no neurological deficit (numbness, weakness). Neurological deficit in the face — particularly numbness — suggests secondary TGN from tumour or MS and requires urgent imaging.

MRI brain with posterior fossa protocol

Thin-cut 3D FIESTA/CISS sequences through the posterior fossa at KIMS, specifically to: (1) identify neurovascular contact at the trigeminal root entry zone (the artery or vein responsible for compression in classical TGN); (2) exclude secondary causes — acoustic neuromas, meningiomas, epidermoid cysts (visible as T2 bright masses in the cerebellopontine angle), and MS plaques at the trigeminal root. Neurovascular contact on MRI predicts surgical success and is an important part of MVD planning.

Trigeminal nerve conduction studies

Blink reflex and trigeminal evoked potential studies at KIMS provide objective electrophysiological evidence of trigeminal nerve dysfunction. Abnormal findings in a patient with clinical TGN support the diagnosis and can identify which nerve division is predominantly affected. Normal trigeminal nerve conduction does not exclude TGN but reduces the likelihood of MS as the cause.

Treatment

Treatment at KIMS — Medical, MVD Surgery, Percutaneous Procedures, and Gamma Knife

Microvascular Decompression (MVD)

Surgical Treatment — Microvascular Decompression (MVD) at KIMS

MVD is the most effective and most durable treatment for classical TGN with confirmed neurovascular contact on MRI. It is the treatment of choice for patients who are fit for surgery and who want the best long-term outcome.

The procedure: A small (2–3cm) retrosigmoid craniotomy behind the ear, in the posterior fossa. Using the operative microscope, the trigeminal nerve is identified at its root entry zone. The offending blood vessel (most commonly the superior cerebellar artery) is identified compressing or deforming the nerve. A small Teflon (PTFE) sponge is placed between the vessel and the nerve, permanently separating them. The vessel continues to supply the brain normally — it is not cut or occluded.

Outcomes: Complete initial pain relief in approximately 90% of patients. At 5 years: approximately 80–85% maintain significant relief. At 10 years: approximately 70–75%. MVD provides the highest long-term pain-free rate of any TGN treatment. Unlike percutaneous procedures, MVD does not cause facial numbness.

At KIMS: The KIMS Neuroscience team performs MVD with full intraoperative neurophysiological monitoring including Brainstem Auditory Evoked Potentials (BAEPs) to protect hearing, facial nerve EMG to protect the facial nerve, and somatosensory evoked potentials. The KIMS neurosurgical team has performed this procedure with consistently excellent outcomes. Typical hospital stay: 3–5 days. Recovery: 2–4 weeks.

Medical Treatment — First-Line

Carbamazepine, Oxcarbazepine, and Add-On Agents

• Carbamazepine 200–800mg/day in divided doses: the most effective medical treatment for TGN and the only one specifically approved for this indication. Acts by blocking voltage-gated sodium channels in the trigeminal nerve, reducing ectopic neuronal firing. Response rate approximately 70–80%. Starting dose 100–200mg twice daily, increasing slowly to effect. Full blood count and liver function monitored (rare risk of aplastic anaemia, hepatotoxicity). Hyponatraemia (low sodium) is common, especially in older patients — sodium monitored at KIMS.

• Oxcarbazepine 600–1,800mg/day: a closely related drug with a more favourable side effect profile than carbamazepine (less sedation, no HLA-B*1502 risk). Effective in approximately 70–80% of patients. Hyponatraemia risk is higher than with carbamazepine. Used as first-line alternative at KIMS, particularly in younger patients and those concerned about carbamazepine side effects.

• Add-on medications for partial responders: Gabapentin 900–3,600mg/day; pregabalin 150–600mg/day; lamotrigine 200–400mg/day (titrated slowly to avoid Stevens-Johnson syndrome); baclofen 30–80mg/day. These are added to carbamazepine when the response is partial or the dose cannot be increased further due to side effects.

HLA-B*1502 Testing — India-Specific

HLA-B*1502 Testing Before Carbamazepine in Indian Patients

The HLA-B*1502 allele, which predisposes to Stevens-Johnson syndrome and toxic epidermal necrolysis from carbamazepine, is present in approximately 6–8% of South Asian (Indian) patients compared to less than 1% in Europeans.

KIMS recommends HLA-B*1502 testing before starting carbamazepine in Indian patients. If the allele is present, oxcarbazepine or lamotrigine is preferred (lower SJS risk with these agents in B*1502 carriers).

This simple blood test prevents a potentially fatal complication.

Percutaneous Procedures

Percutaneous Procedures — When MVD is Not Suitable

For patients who are medically unfit for general anaesthesia and posterior fossa surgery (typically older patients with significant comorbidities), or who decline open surgery, percutaneous procedures deliver targeted injury to the trigeminal ganglion or rhizotomy through a needle passed through the cheek.

• Radiofrequency thermocoagulation: A needle is advanced through the foramen ovale under fluoroscopic guidance. Radiofrequency current selectively destroys the pain fibres. Immediate pain relief in >90% but with facial numbness as the trade-off. Recurrence rate approximately 20–25% at 2 years.

• Glycerol rhizotomy: Glycerol injected into the Meckel's cave damages the trigeminal ganglion. Effective in approximately 70–80%. Less predictable than RF thermocoagulation.

• Balloon microcompression: A balloon catheter is inflated in Meckel's cave to compress the ganglion. Effective but causes temporary masseter weakness (chewing difficulty) in many patients.

Stereotactic Radiosurgery

Stereotactic Radiosurgery (Gamma Knife) — Non-Invasive but Delayed

Focused radiation (Gamma Knife or CyberKnife) delivers a high dose to the trigeminal root entry zone, causing controlled nerve damage.

Advantages: non-invasive, no anaesthesia.

Disadvantages: response is delayed (typically 2–6 months), full response rate lower than MVD (~70–75%), recurrence at 3–5 years, and facial numbness in 10–20%.

At KIMS, Gamma Knife is considered for patients who are not MVD candidates and prefer non-invasive treatment.

Related Conditions

Trigeminal Neuralgia belongs to the family of facial pain and headache & pain syndromes evaluated and managed at KIMS Neuroscience:

Post-Herpetic Neuralgia Cluster Headache Central Pain Syndrome

FAQs

Frequently Asked Questions

Yes — and this is the most common TGN misdiagnosis story we hear at KIMS. Trigeminal neuralgia in the V2 (maxillary) or V3 (mandibular) division produces pain that appears to come from the teeth and gums. It is triggered by jaw movement, eating, and drinking — all of which are also associated with toothache. The critical distinguishing feature: TGN is also triggered by light touch to the skin of the cheek, lip, or nasolabial fold. This is not a feature of dental pain. If your pain is triggered by the gentlest touch to the skin of your face, by talking, by a cold breeze, or occurs as sudden brief electric shocks rather than a sustained ache — it is almost certainly TGN, not dental. Please stop further dental procedures and call KIMS on 040-44885000 immediately.

Yes — carbamazepine side effects (drowsiness, dizziness, unsteadiness, cognitive slowing, low sodium) are among the most common reasons patients reduce doses below the therapeutic level and consequently have inadequate pain control. Oxcarbazepine is the most direct alternative: it has a similar mechanism and similar efficacy but a better tolerability profile in most patients, with less sedation and no HLA-B*1502 risk. For patients who cannot tolerate either, add-on agents (pregabalin, lamotrigine, baclofen) alongside a lower carbamazepine dose may provide better control with fewer side effects. The most important consideration at this point is whether surgical treatment — MVD — should be discussed, as 2 years of medication management that is causing significant side effects is a reasonable trigger for surgical evaluation. Please call 040-44885000.

MVD is the only TGN surgery that addresses the underlying cause — the blood vessel compressing the nerve — without destroying nerve tissue. The surgeon uses a microscope through a small opening behind the ear, identifies the offending artery (usually the superior cerebellar artery), and places a tiny Teflon cushion between the vessel and the nerve. The nerve is preserved, blood flow continues normally, and pain relief is immediate. Because no nerve tissue is destroyed, facial numbness does not occur with MVD — unlike percutaneous procedures (radiofrequency, glycerol, balloon) which all cause some degree of facial numbness as part of their mechanism. MVD provides the longest-lasting pain relief (>80% at 5 years, ~75% at 10 years) of any TGN treatment. At KIMS, The KIMS Neuroscience team performs MVD with intraoperative hearing and facial nerve monitoring. Call 040-44885000 to arrange an MVD consultation.

Age alone is not a contraindication to MVD, and outcomes in older patients in good general health are comparable to those in younger patients. The relevant question is not age but overall fitness for general anaesthesia and posterior fossa surgery: cardiac function, pulmonary reserve, and comorbidities. Many patients in their 70s and even 80s undergo MVD at experienced centres without significant additional risk. If you have significant comorbidities that make general anaesthesia and surgery genuinely high-risk, the percutaneous procedures (radiofrequency thermocoagulation, glycerol rhizotomy) are performed under brief sedation or local anaesthesia and are appropriate alternatives with good initial pain relief — accepting the trade-off of facial numbness and somewhat higher recurrence rates. At KIMS, The KIMS team will assess your individual surgical risk and discuss all options honestly. Please call 040-44885000.

This is the most important decision point in TGN management: when to move from medication to surgery. At KIMS, surgery is discussed when any of these apply: (1) the medication dose required for pain control causes unacceptable side effects (drowsiness, dizziness, cognitive effects); (2) the medication is working but you are taking it at maximum dose with incomplete relief; (3) you have had one or more periods of pain breakthrough requiring dose escalation; (4) you have confirmed neurovascular contact on MRI and prefer a durable cure over indefinite medication. MVD provides pain freedom without medication in approximately 80–85% of patients at 5 years. Many patients who are well-controlled on carbamazepine choose to continue if tolerated — the decision to operate is always the patient's to make, with full information. Call 040-44885000 for a surgical consultation.

What you describe is TGN with concomitant continuous pain — previously sometimes called TGN Type 2 or 'atypical TGN.' In some patients, TGN evolves from purely paroxysmal (episodic attacks only) to include a constant background ache or burning sensation between episodes. This pattern is associated with longer disease duration and may reflect progressive nerve damage from prolonged vascular compression. It is still TGN and responds to the same treatments, though the continuous pain component may require additional agents beyond carbamazepine (pregabalin, amitriptyline). Importantly, the presence of continuous pain makes MVD slightly less likely to achieve complete relief of all pain (as the paroxysmal component responds better than the constant component), though most patients still achieve significant improvement. Call 040-44885000.

This is the most important decision in TGN management and depends on your individual situation. MVD: highest long-term success (80%+ at 5 years), no facial numbness, requires general anaesthesia and 3–5 days in hospital. Best for patients <70 in good health with confirmed neurovascular contact on MRI who want the most durable solution. Gamma Knife: non-invasive, no anaesthesia, delayed response (2–6 months), lower success rate, some facial numbness. Best for patients who cannot have surgery or who prefer non-invasive treatment. Percutaneous procedures (RF thermocoagulation, glycerol, balloon): quick, done under sedation, immediate relief, causes facial numbness, higher recurrence rates. Best for very elderly patients with significant comorbidities where general anaesthesia is genuinely risky. the KIMS Neuroscience team will discuss each option specifically in the context of your age, health, MRI findings, and treatment goals. Call 040-44885000.

Teeth extracted one by one for a pain that came from a nerve, not a tooth. Years of medication that helped partially but cost cognition and steadiness. The cause was always identifiable — a blood vessel pressing on a nerve — and the solution was always available. MVD surgery at KIMS gives more than 80% of patients complete, durable, medication-free pain relief.

At KIMS Neuroscience, Secunderabad, Hyderabad, trigeminal neuralgia is diagnosed using ICHD-3 criteria and MRI posterior fossa protocol, distinguishing classical TGN (vascular compression), secondary TGN (MS or tumour), and idiopathic TGN. Medical management with carbamazepine or oxcarbazepine with HLA-B*1502 screening before prescribing in Indian patients. Microvascular Decompression surgery performed by the KIMS Neuroscience team with intraoperative BAEP and facial nerve monitoring — the most durable surgical treatment for TGN available in Hyderabad.

040-44885000

International enquiries: info@kimsneurosciences.com