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Understanding, Diagnosing & Treating the World's Most Painful Condition

The Condition Salman Khan Called ‘The Disease with the Highest Rates of Suicide’

TL;DR — Key Takeaways at a Glance

Trigeminal Neuralgia (TN) is ranked by medical science as the worst pain known to humans. It is caused by irritation of the trigeminal nerve (the face’s main sensory nerve). A blood vessel pressing on the nerve is common but not the only cause. TN must be distinguished from cluster headaches, migraines, and other facial syndromes. Highly effective treatments exist  from medication to day-procedure nerve ablation to surgery  and you do not always need an operation.

  • TN is not a headache it is a neuropathic face pain
  • Affects V2 (cheek) and V3 (jaw) most commonly
  • Electric-shock attacks lasting seconds triggered by eating, speaking, touch
  • Over 34% of patients report suicidal ideation (Harvard, 2025)
  • Salman Khan has spoken publicly about his TN since 2007
  • A standard brain MRI is NOT sufficient trigeminal protocol (FIESTA/CISS) required
  • Carbamazepine: gold standard drug requires HLA-B*1502 screening in Indian patients
  • RFA: day procedure, ~85% success, ideal for elderly or medically unfit patients
  • MVD: gold standard surgery for young fit patients with confirmed vascular compression
  • Surgery is NOT always required most patients can be managed without it

34.6%

of TN patients reportsuicidal thoughts(Harvard Medical School, 2025)

85–90%

pain reliefachieved with Radiofrequency Ablation

70–80%

long-term cure ratewith MicrovascularDecompression (MVD)

When a Smile Becomes Agony — The 'Suicide Disease'

Imagine that the simple act of brushing your teeth sends a lightning bolt of searing electric pain across half your face. Or that a gentle breeze, a sip of cold water, or even the act of speaking triggers an excruciating jolt lasting a few agonising seconds then vanishes as suddenly as it came, leaving you terrified of when the next strike will arrive.

This is the daily reality for people living with Trigeminal Neuralgia (TN) — widely regarded by the medical community as the most severe pain condition known to humanity.

 

Salman Khan and Trigeminal Neuralgia — Breaking the Silence

Bollywood superstar Salman Khan first experienced TN symptoms whilst filming Partner in 2007. He underwent surgery in the United States in 2011. Speaking whilst promoting Sikandar in Dubai in 2025, he described TN plainly: ‘one disease that basically has the highest rates of suicides.’ He was not exaggerating. A 2025 Swedish study the most comprehensive population study to date  confirmed TN as a true suicide disease, associated with increased risk of suicide, depression, and cardiovascular events.

Yet despite this, TN remains widely misdiagnosed often confused with toothache, sinusitis, migraine, or dental problems  leaving patients without appropriate treatment for years. Patients are given antidepressants or dental treatments that do not work. Some have had healthy teeth extracted. This article aims to change that.

Why Is It Called the Suicide Disease?

A landmark 2025 study from Harvard Medical School (Fishbein et al., J Pain Research) recruited 229 adults with TN. Results: over 34.6% reported suicidal thoughts in the past two weeks; 57.7% reported thinking about their own death; over 28% had elevated depression. Crucially, this is not psychiatric illness — it is the direct consequence of extreme, relentless, untreatable-feeling pain. The name is not metaphor. It is clinical reality

Anatomy — The Three Postal Districts of the Face

Think of your face as a large country estate with three postal districts upper, middle, and lower. The trigeminal nerve (the fifth cranial nerve, CN V) is the national postal service responsible for carrying all sensation from the face to the brain.

It has three main branches (divisions), referred to by Roman numerals:

Branch
Name
Area Served
TN Involvement
V1
Ophthalmic
Forehead, eye, upper nose, scalp
Less common (~10%)
V2
Maxillary
Cheek, upper lip, upper teeth, side of nose
Very common (~35%)
V3
Mandibular
Lower jaw, lower teeth, chin, part of ear
Very common (~35%)
V2+V3
Mixed
Combined cheek + jaw distribution
Most common (~40%)

All three branches converge at the Gasserian (trigeminal) ganglion think of it as the main sorting office located deep inside the skull. In TN, this nerve misfires dramatically: instead of calmly relaying sensation, it erupts with extreme, uncontrolled electrical signals — like a faulty live wire sparking without warning.

Causes — The Faulty Insulation Story

Neurovascular Conflict — The Most Common Cause (But NOT the Only One)

The most well-understood cause is neurovascular conflict: a blood vessel (most often the Superior Cerebellar Artery) pressing against the trigeminal nerve root where it enters the brainstem.

The Fraying Cable Analogy

Think of the nerve like an electrical cable covered in protective insulation (myelin). Over years, the rhythmic pulsing of an artery against the nerve gradually damages this insulation. Once exposed, the bare wire misfires — creating lightning-bolt pain attacks with no warning. This process is called segmental demyelination.

IMPORTANT: Neurovascular Conflict Is Not Always the Cause — and Surgery Is Not Always the Answer

Not everyone who has a blood vessel touching their trigeminal nerve on MRI will develop TN. Conversely, some patients with classic TN symptoms show no compression at all on imaging. A finding on a scan must always be interpreted in the full clinical context. Surgical decompression is not automatically indicated by an MRI finding alone.

Other Causes of TN

Cause
Clinical Note
Multiple Sclerosis (MS)
Demyelination plaques can affect the trigeminal pathway. TN in patients under 40 should always prompt MS screening.
Tumours
Meningiomas, acoustic neuromas, epidermoid cysts pressing on the nerve.
Post-herpetic neuralgia (Shingles)
TN following a shingles (Herpes Zoster) outbreak in the V1 region.
Idiopathic
No identifiable cause found despite thorough investigation.

Types of Trigeminal Neuralgia — Typical vs Atypical

Type 1 — Classical / Typical TN (TN1)

The textbook presentation. Responds best to all treatments.

  • Sudden, electric shock or stabbing pain ‘lightning in the face’
  • Duration: seconds to two minutes per episode
  • Unilateral one side only (bilateral TN is rare; <3% of cases)
  • Trigger-dependent  eating, speaking, smiling, cold air, light touch
  • Complete pain-free intervals between attacks
  • Neurological exam normal between episodes

Type 2 — Atypical TN (TN2) / Mixed

More treatment-resistant. Constant background pain with or without sharp attacks.

  • Constant aching or burning pain never fully pain-free
  • Sharp attacks may still occur superimposed on background ache
  • Less clearly defined trigger zones
  • Often greater psychological overlay due to unrelenting nature
  • May overlap with other neuropathic facial pain syndromes
  • Responds less predictably to surgery; medication + psychology often required

Differentiating TN from Other Facial Pain Syndromes

TN is one of the most misdiagnosed conditions in medicine — frequently confused with its closest mimics. The treatment for each condition is entirely different, making accurate diagnosis essential.

TN vs Cluster Headache (Trigeminal Autonomic Cephalalgias — TACs)

The Single Most Important Distinguishing Feature

In TN, patients sit very still during an attack moving the face worsens the pain. In cluster headache (and other TACs), patients cannot sit still they pace, rock, and are visibly agitated. This single observation often clinches the diagnosis at the bedside.

Feature
Trigeminal Neuralgia
Cluster Headache
Pain character
Electric shock, stabbing, lancinating
Deep, boring, excruciating orbital/eye pain
Duration per attack
Seconds to 2 minutes
15 minutes to 3 hours
Autonomic features (tearing, red eye, drooping, nasal congestion)
ABSENT
PRESENT — hallmark of TACs
Triggers
Touch, eating, talking, cold air
Alcohol, sleep disruption, seasonal patterns
Patient behaviour during attack
Sits very still (movement worsens it)
Cannot sit still — paces and rocks
Predominant sex/age
Women >50 years
Men 20–40 years
Response to carbamazepine
Excellent
None
Response to oxygen/triptans
None
Excellent
TN vs Migraine vs Dental Pain
Feature TN Migraine Dental Pain
Location Face — jaw, cheek, eye Hemicranial (one side of head) Tooth, jaw, localised
Duration Seconds–2 minutes 4–72 hours Continuous or aching
Light/noise sensitivity No Yes — prominent No
Nausea/vomiting No Common Occasional
Feather-light skin trigger Yes — hallmark No No
Complete pain-free intervals Yes Yes No
Response to dental treatment None None Partial

The Dental Misdiagnosis Trap

TN is one of the most commonly misdiagnosed conditions in dentistry. Patients may undergo unnecessary tooth extractions, root canal treatments, and even sinus operations before TN is recognised. Key distinguishing feature: dental pain does not resolve completely between episodes, and is not triggered by a feather-light touch to the skin whereas TN typically is. If tooth extraction has not relieved the pain, consider a pain specialist referral immediately.

Making the Diagnosis — Clinical Assessment & Specialist MRI

Clinical Diagnosis — The History Is King

The diagnosis of TN is fundamentally clinical based on a thorough history and examination. There is no blood test for TN. The International Headache Society’s ICHD-3 criteria require:

  • Recurrent paroxysms of unilateral facial pain in the distribution of one or more trigeminal nerve branches
  • Pain is intense, electric-shock quality, and abrupt in both onset and offset
  • Precipitated by innocuous stimuli to trigger zones (light touch, eating, speaking)

A skilled pain specialist or neurologist should be able to diagnose classical TN1 from the history alone. Investigations serve to classify the subtype and guide treatment planning.

The Specialist MRI Trigeminal Protocol — Beyond a Standard Brain Scan

An ordinary MRI brain scan is insufficient for TN assessment. A dedicated trigeminal MRI protocol is required  specifically designed to visualise the fine anatomy of the nerve root entry zone.

MRI Sequence Purpose & What It Shows
FIESTA / CISS (3D) Gold standard for TN. Visualises the trigeminal nerve as a bright structure against dark CSF. Identifies vascular loops pressing against the nerve root — neurovascular conflict.
3D TOF MRA Maps blood vessels near the nerve to identify the specific culprit artery (usually Superior Cerebellar Artery).
T1 / T2 / FLAIR (standard) Excludes secondary causes: tumours, MS plaques, stroke, or other structural lesions.
DWI Excludes acute ischaemic events that may present as acute facial pain.

Important — A Negative MRI Does NOT Rule Out TN

A negative or inconclusive MRI must never lead a clinician to dismiss a patient’s symptoms. Many patients with classical TN have no vascular contact visible on imaging  yet their symptoms, treatment response, and clinical course are entirely consistent with TN. The diagnosis remains clinical. The MRI guides treatment choice, not the diagnosis itself.

Treatment — From Tablets to Theatre

The good news: TN is one of the most treatable chronic pain conditions in medicine. The pathway is progressive  starting with the simplest interventions and escalating as needed. Surgery is not always required.

TIER 1 — Medications: The First Line of Defence

Carbamazepine (Tegretol, Mazetol) is an anticonvulsant  originally designed to treat epilepsy. In TN, it stabilises sodium channels in nerve membranes, essentially turning down the volume on an overexcited nerve.

The Faulty Car Alarm Analogy

The trigeminal nerve in TN is like a faulty car alarm going off at the slightest disturbance. Carbamazepine is the mechanic who adjusts the sensitivity threshold so only a genuine emergency (actual injury or touch) triggers the alarm, not a gentle breeze or a sip of water.

Efficacy: 70–80% of patients experience significant initial pain relief. This is the only medication with Level A evidence for TN from the European Federation of Neurological Societies (EFNS).

MANDATORY BLOOD TESTS & MONITORING FOR INDIAN PATIENTS Carbamazepine Safety

Carbamazepine is not a drug to take without careful medical supervision. The following monitoring is essential before starting and during treatment:

Test Required Why It Matters
Full Blood Count (FBC) — before start, then 2-weekly x 3 months, then every 6 months Carbamazepine can rarely cause agranulocytosis (dangerous drop in white cells) or aplastic anaemia — a potentially fatal condition.
Liver Function Tests (LFTs) Monitors for hepatic effects and drug metabolism.
Serum Sodium (Na+) Carbamazepine commonly causes hyponatraemia (low sodium) — especially dangerous in elderly patients, causing confusion and falls.
HLA-B*1502 Genetic Test — CRITICAL IN INDIAN PATIENTS South and East Asian populations have a higher prevalence of this genetic variant, which dramatically increases risk of Stevens-Johnson Syndrome (SJS) / Toxic Epidermal Necrolysis — potentially fatal skin reactions. At IBAP Clinics, we routinely perform this test before initiation.
Other Medication Options
Drug Mechanism Role in TN
Oxcarbazepine (Trileptal) Sodium channel stabiliser (similar to carbamazepine, cleaner profile) Often preferred first-line in India — less blood monitoring required, better tolerated. Check sodium levels.
Gabapentin Calcium channel modulator Adjunct therapy or monotherapy when carbamazepine intolerable. Better for TN2 (constant burning component).
Pregabalin Calcium channel modulator Similar to gabapentin; TN2, MS-related TN, atypical facial pain.
Baclofen GABA-B receptor agonist Useful as add-on therapy. Evidence for TN1 as adjunct.
Lamotrigine Sodium/calcium channel modulator Adjunct to carbamazepine. Very slow titration required to avoid rash.
Amitriptyline Tricyclic antidepressant (TCA) More useful in TN2 with constant background aching — NOT effective for classical TN1 attacks.
IV Lidocaine infusions Sodium channel blockade Bridging therapy during acute severe episodes or medication transitions — hospital-based.

An Important Clinical Reality — Medication Efficacy Fades Over Time

Many patients initially respond well to medication, but drug efficacy tends to diminish as the disease progresses. Side effects also accumulate with higher doses. This is the typical juncture at which interventional options become appropriate — and should not be delayed unnecessarily.

TIER 2 — Interventional Procedures: Minimally Invasive Options

All percutaneous (needle-based) procedures target the Gasserian ganglion the central sorting office of the trigeminal nerve  via a needle passed through a small natural opening in the skull called the foramen ovale, under X-ray fluoroscopy guidance.

A. Radiofrequency Ablation (RFA) — The Day Procedure

A fine, insulated needle is advanced through the foramen ovale to the Gasserian ganglion. Electrical stimulation confirms correct position  the patient feels tingling in exactly the distribution of their pain. Heat is then applied (60–80°C for 60–90 seconds), selectively damaging the pain fibres whilst attempting to spare the touch fibres.

The Selective Wire-Burning Analogy

Imagine a bundle of wires causing a short circuit. RFA is the electrician who selectively burns only the faulty wires, leaving the rest of the cable functional. The pain fibres are damaged, whilst larger touch fibres are largely preserved.

Benefits of RFA

  • Day procedure  home same day
  • Local anaesthesia + light sedation (no general anaesthetic needed)
  • ~85–90% immediate pain relief
  • Ideal for elderly and medically unfit patients
  • Excellent for V2 and V3 distributions
  • Repeatable if pain recurs
  • Most widely available in India at specialist pain centres

Risks to Discuss

  • Facial numbness (expected  most patients accept this trade-off)
  • Corneal numbness (V1 RFA)  requires eye care and monitoring
  • Anaesthesia dolorosa (rare, ~2–5%)  numb but paradoxically painful face
  • Masticatory weakness (V3)  temporary jaw weakness
  • Recurrence 20–30% at 5 years  procedure can be repeated
  • Not nerve-preserving (destructive approach)
B. Percutaneous Balloon Compression (PBC)

A catheter with a small balloon at its tip is advanced through the foramen ovale. The balloon is inflated inside Meckel’s cave (a small pocket around the Gasserian ganglion), applying mechanical pressure to the nerve. This damages pain fibres whilst tending to preserve corneal touch fibres better than RFA.

The Pause Button Analogy

If RFA is the electrician burning wires selectively, balloon compression is a gentle squeeze that disrupts the signal pathway physically like pressing the pause button rather than cutting wires. Because it spares corneal fibres, it is particularly preferred for V1 (eye/forehead) TN.

Procedure: Performed under brief general anaesthesia (typically under 30 minutes). Excellent for V1 TN and multi-branch involvement. Key side effect: temporary facial numbness and chewing difficulty. Bradycardia during balloon inflation is monitored by the anaesthetic team.

C. Microvascular Decompression (MVD) — The Gold Standard Surgery

A neurosurgical procedure under general anaesthesia. A small opening (craniotomy) is made behind the ear. The trigeminal nerve is visualised under a microscope, and the offending blood vessel is carefully separated from the nerve using a small Teflon sponge or padding.

The Maintenance Engineer Analogy

MVD is like the maintenance engineer who discovers an electrical cable has been chafed by a pipe for years. Rather than cutting the cable (ablation), the engineer inserts padding between the pipe and cable  removing the source of irritation and allowing the cable to heal naturally. MVD is the only procedure that corrects the underlying cause rather than disrupting the pain pathway.

Prerequisite: Confirmed vascular contact on MRI trigeminal protocol is strongly recommended before MVD is offered. MVD where no vascular conflict is found intraoperatively has a lower success rate. Long-term pain-free rates of 70–80% at 5 years are the best of any procedure for classical TN1 with confirmed neurovascular conflict.

D. Gamma Knife Radiosurgery (Stereotactic Radiosurgery)

A completely non-invasive option for patients unfit for any needle or open procedure. Over 200 highly focused beams of radiation are precisely directed at the trigeminal nerve root entry zone. No incision, no needle, no general anaesthesia.

The 200 Torchbeams Analogy

Imagine 200 weak torch beams, each harmless on its own, all focused to converge at a single point. At that convergence, the energy is sufficient to damage the nerve selectively without touching anything else in the path. Pain relief typically takes 4–8 weeks to develop, unlike the immediate relief from RFA or MVD.

Ideal for: Elderly, very frail patients; those on anticoagulants (blood thinners); those who have failed other interventions; patients who refuse any invasive procedure. Available at select major centres in Hyderabad including Apollo Hospitals.

Outcomes: Approximately 60–70% pain-free at 2 years. Slightly inferior long-term outcomes compared to MVD, but the lowest procedural risk of any invasive option.

RFA vs MICROVASCULAR DECOMPRESSION — Head-to-Head Comparison
Parameter Radiofrequency Ablation (RFA) Microvascular Decompression (MVD)
Mechanism Nerve ablation — destroys pain fibres (destructive) Nerve-preserving — removes vascular pressure (non-destructive)
Anaesthesia Local + light IV sedation General anaesthesia + craniotomy
Hospital stay Day procedure / 1 night maximum 3–5 days inpatient
Immediate pain relief ~85–90% ~90–95%
Pain-free at 5 years 50–60% 70–80%
Recurrence risk 20–30% at 5 years 10–20% at 5 years
Facial numbness Expected — common side effect Minimal to none
Serious complication risk Low — anaesthesia dolorosa ~2–5% Higher — stroke, hearing loss, CSF leak (rare but real)
MRI NVC required No — effective even without NVC Yes — strongly preferred prerequisite
Nerve preserved? No Yes
Repeatability Yes — can be repeated Generally a one-time procedure
Ideal patient profile Elderly, frail, medically unfit, MS-related TN, no NVC Young, fit, confirmed NVC on MRI, willing to accept surgical risk
Availability in India Widely available at specialist pain centres Major neurosurgical centres only

The Clinical Bottom Line

For a fit 45-year-old with MRI-confirmed vascular compression, MVD is the gold standard best long-term cure rates and nerve preservation. For an 80-year-old with significant medical comorbidities and the same diagnosis, RFA is the wiser, safer choice. Neither is universally superior. The right answer is always patient-specific determined by age, fitness, MRI findings, patient preference, and the surgeon’s or interventionalist’s experience.

The Psychological Dimension — It Is Not in Your Head, But It Affects Your Head

TN is not a psychiatric condition but it profoundly affects mental health. Research shows a significantly higher risk of newly diagnosed depression, anxiety disorders, and sleep disturbances following TN diagnosis largely due to its devastating impact on psychological, behavioural, and social functioning.

Suicidality is an urgent yet under-addressed concern. It is associated not with psychiatric illness per se, but with high levels of anxiety, depression, and pain intensity. Patients are often reluctant to discuss the psychological impact of their pain particularly in India, where mental health discussions carry stigma.

At IBAP Clinics, our pain management approach is holistic: we treat the pain and address the psychological burden, working collaboratively with psychiatry and psychology as needed.

Crisis Support — If You Are Struggling

If you or a loved one are experiencing suicidal thoughts due to chronic pain, please reach out. iCall (India): 9152987821. Vandrevala Foundation: 1860-2662-345. You are not alone, and effective treatment exists.

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Some quick information

Trigeminal neuralgia (TN) is a chronic pain condition of the fifth cranial nerve causing sudden, intense electric-shock pain in the face, jaw, or eye. It is called the suicide disease because studies show over one-third of TN patients report suicidal thoughts  not from psychiatric illness, but because the pain is so extreme and often unrecognised. Bollywood star Salman Khan has publicly described his battle with TN.

TN causes brief (seconds), electric-shock facial pain triggered by touch or eating, with no autonomic symptoms. Cluster headaches cause longer (15 min–3 hrs) boring orbital pain with tearing, red eye, and nasal congestion and patients cannot sit still. Migraines cause throbbing head pain lasting hours, often with nausea and light sensitivity. Treatment for all three is completely different.

No. Most patients are initially managed successfully with medications (carbamazepine or oxcarbazepine). When drugs fail, minimally invasive day procedures such as radiofrequency ablation (RFA) achieve excellent relief without open surgery. Microvascular decompression (MVD) surgery is reserved for suitable younger, fitter patients with confirmed vascular compression on MRI.

A standard MRI brain scan cannot resolve the fine anatomy of the trigeminal nerve root. A dedicated trigeminal protocol uses FIESTA or CISS sequences — showing the nerve and adjacent blood vessels in high definition to identify neurovascular conflict. This finding directly guides treatment decisions, particularly regarding microvascular decompression surgery.

Carbamazepine requires careful monitoring. Key concerns in Indian patients: (1) regular blood counts to detect rare blood cell reduction; (2) liver function and sodium checks; and (3) HLA-B*1502 genetic testing — this variant is more prevalent in South and East Asian populations and significantly increases risk of Stevens–Johnson Syndrome, a potentially fatal skin reaction. At IBAP Clinics, we screen for this routinely before starting treatment

RFA involves passing a fine needle to the trigeminal ganglion and applying controlled heat to selectively damage pain-carrying nerve fibres. It is performed as a day procedure under local anaesthesia with light sedation no general anaesthesia required. This makes it ideal for elderly or medically unfit patients. Success rates are approximately 85–90%, with some expected facial numbness.

At IBAP Clinics (Banjara Hills and Hafeezpet, Hyderabad), Dr Vijay Bhaskar Bandikatla offers a complete, individualised TN pathway including specialist MRI review, evidence-based medication with appropriate safety monitoring including HLA-B*1502 screening, and the full range of interventional procedures. Appropriate neurosurgical referral pathways are in place for MVD and Gamma Knife when indicated.

Dr. Vijay Bhaskar Bandikatla

Founder IBAP Clinics, Pain Physician

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References & Evidence Base

  • Fishbein NS, Bakhshaie J, Greenberg J. Suicidal Ideation and Self-Injury in Trigeminal Neuralgia. J Pain Res. 2025;18:2003–2010. PMID: 40220323.
  • Maarbjerg S, Di Stefano G, Bendtsen L, Cruccu G. Trigeminal neuralgia — diagnosis and treatment. Cephalalgia. 2017;37(7):648–657. PMID: 28076964.
  • Zakrzewska JM, Linskey ME. Trigeminal neuralgia. BMJ. 2014;348:g474. PMID: 24451236.
  • Cruccu G, Di Stefano G, Truini A. Trigeminal Neuralgia. N Engl J Med. 2020;383(8):754–762. PMID: 32813951.
  • Lambru G, Zakrzewska J, Matharu M. Trigeminal neuralgia: a practical guide. Pract Neurol. 2021;21(5):392–402. PMID: 34234005.
  • Revuelta-Gutiérrez R, et al. TN secondary to epidermoid cyst and neurovascular conflict. Surg Neurol Int. 2024;15:36. PMID: 38468624.
  • Tuleasca C, et al. Microvascular decompression and radiofrequency for TN: a meta-analysis. Pain Physician. 2019;22(4):E327–E340. PMC6605044.
  • Altamirano et al. Comparison of MVD, radiofrequency rhizotomy, and stereotactic radiosurgery in TN. Pain Practice. 2024. doi:10.1111/papr.13327.
  • Headache Classification Committee of the IHS. ICHD-3rd edition. Cephalalgia. 2018;38(1):1–211.
  • TN associated with cardiovascular disease and suicide — nationwide Swedish study. J Headache Pain. 2026. doi:10.1186/s10194-026-02368-1.
Founder IBAP Clinics, Pain Physician

MBBS, DA, FRCA (UK), FFPMRCA (Pain Medicine, RCOA, UK)
CCT (Anesthesiology And Pain Management)
Neuromodulation & Advanced Pain Research Fellowship (London), MBA (HM)

Founder IBAP Clinics, Pain Physician
MBBS, DA, FRCA (UK), FFPMRCA (Pain Medicine, RCOA, UK)
CCT (Anesthesiology And Pain Management)
Neuromodulation & Advanced Pain Research Fellowship (London), MBA (HM)
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