28/04/2026
Inferno on the face
°°°°°°°°°°°°°°°°°°°°°°°°°°
While operating on the Patient with extreme pain of trigeminal neuralgia, I turned the beam of neuromicroscope deep into the depth of the lower part of brain— on the very important structure of the brain called the pons. Under the cold, brilliant light, the trigeminal nerve came into view. The fifth cranial nerve. The great "sensory highway" of the face, carrying sensations of touch and temperature and pain from the right cheek, the right eye, the right jaw, directly into the core of the brainstem and then to the part of brain that perceives physical pain and it's emotional components.
Her trigeminal nerve was not the smooth, pearl-white cord it was supposed to be. It had been crushed flat. A blood vessel — large, unyielding, pulsing — had buried itself into the nerve's most vulnerable segment: the root entry zone, that narrow stretch where the protective myelin sheath is thinnest and the nerve most exposed. The vessel had not merely rested against the nerve.....but over the years, it had bored into it, and the nerve had frayed apart in response — its fibers separating like threads pulled from a torn cloth.
Seventy-five to eighty times a minute, the artery pulsed. With its each beat, a blow of hammer on the nerve. For years. Day after day, month after month, year after year.
The nerve looked like a crushed ribbon.
⸻
This sight, I must be honest, is not unfamiliar to us. At the Trigeminal Neuralgia Centre, we have seen it many times. And yet it never becomes routine for me. Each time I look through that microscope at a nerve ground down by the pinch and hammer blows, I feel the same deep frustration — not at the pathology, which is predictable and correctable, but at what surrounds it.
This degree of damage need not have happened !!!
If surgery had been performed earlier — even a few years earlier — this patient would not have suffered so long. She would not have spent years consuming medications that blunt the entire nervous system just to manage a problem rooted in a single, identifiable point of compression. The delay, in case after case, has the same cause:
"the patient simply did not know. The family did not know. Often enough, even the trating doctors did not know."
Trigeminal neuralgia has spent too long entangled in a web of misunderstanding. For the last 20 years, we have worked to change that. With focus. With persistence.
Progress has been made. But the road remaining is still long. It is with this in mind that I write in some detail today.
⸻
Nivedita Bhatnagar: An Architect Without Words
Embedded in that surgical scene is the story of the patient on the table and her severe suffering.
Nivedita Bhatnagar (name changed) an architect from Delhi. Deeply capable. Perceptive. And, it would turn out, extraordinarily eloquent about her own suffering.
When she first came to our centre, she could only gesture. She could not speak. Even the small act of opening her mouth to form words triggered a bolt of electricity through the right side of her face — through her gum, her cheek, her eye. The simple daily architecture of language had become a minefield.
A year after her MVD surgery — a year of complete freedom from pain — she returned to Pune from Delhi to describe what her illness had been. Her account was one of the most searching I have heard. She was, by nature, a person who observed things carefully and thought about them carefully. And she had thought carefully about everything: the specific quality of the pain, the slow way it had reshaped her personality over years, the medications and their long consequences, and the bewildering journey through treatments that addressed her symptoms while the underlying cause quietly worsened.
There was something else in her account, too. A regret, steady and lucid. She had not known, for many years, that this disease could be cured. She had not known that the root cause could be identified and corrected. She had not known that a specialised centre existed in India — in Pune — devoted entirely to this problem. The information had simply not reached her. Years of suffering and research, most of it conducted while in pain, before she found her way to us.
Here is her story, in her own words:
"Doctor, it truly began in January 2004. A sudden, sharp pain would start in the upper right gum and radiate into the right cheek. Within a month or two it spread further — into the right eye and the right temple. The pain was like an electric shock. Instant. Without warning. Brushing my teeth, if the brush touched the right gum — or while chewing on that side — these were enough to trigger it. Then later, even washing my face, touching my right cheek with a towel, or driving with the window open and feeling wind on the right side of my face — any of these could set it off. An unbearable, shattering jolt."
She went first to a dentist, as almost every patient with this condition does. The upper right molar received a root canal. The pain not only persisted — it grew. Another doctor recognized a nerve problem and began medications. The drug was carbamazepine.
"The medicine helped while it worked. But it made me drowsy. I began forgetting things. As the dose increased, I started losing my balance when I walked."
She did what an intelligent, trained person does: she researched. She found that carbamazepine works by suppressing neural excitability throughout the nervous system — not in one nerve, not in one region, but everywhere. The entire central and peripheral nervous system is blanketed by its effect.
"I thought about this. If one nerve in one small location is the problem, why am I numbing every nerve in my body? It felt like the old remedy for a severe toothache — drink enough to stop feeling anything. That is not treatment. That is suppression. Our bodies contain billions of nerve fibers. All of them are affected by this medication. How can there not be consequences?"
She was, of course, exactly right. This is one of the central frustrations of treating trigeminal neuralgia with medication alone. The drugs do not address the cause. They address the signal. And as the underlying compression worsens — as the artery, over months and years, drives deeper into the nerve — the signal grows louder, and the dose must rise to keep pace. The side effects multiply. The person diminishes.
"In 2009, I traveled for work to Paris and then to London. In the cold, the pain became much worse. The doctors there increased my dose. And naturally, the side effects grew worse as well."
⸻
The Architecture of Fear
**************************
There is another dimension to trigeminal neuralgia that deserves its own attention. It is not the pain alone that destroys a life — it is the anticipation of pain.
Between attacks, the person lives in a state of suspended dread. Will it happen now? This question follows every meal, every conversation, every walk in the wind. The face — that most human of surfaces, the site of every expression, every greeting, every shared glance — becomes a danger zone. People stop speaking in full sentences. They stop eating certain foods, stop going outside in cold weather, stop socializing. The whole architecture of daily life is quietly dismantled, piece by piece, around a single nerve.
Nivedita described it with precision: "My entire life began to revolve around the pain in my face. I was always afraid. Always waiting. Everything else became secondary."
This is not weakness. It is the rational response of an intelligent person to an unpredictable and extreme stimulus. The neuroscience of chronic pain is clear on this point: sustained pain remaps the brain. It alters threat perception, attention, sleep, and mood. A person with long-standing trigeminal neuralgia has not only a damaged nerve — they have a nervous system that has been reorganized by years of crisis.
⸻
What Is Trigeminal Neuralgia — The Science
****************************
The trigeminal nerve is the fifth and largest of the twelve cranial nerves. Its name comes from its three main branches: the ophthalmic, the maxillary, and the mandibular — covering, respectively, the forehead and eye, the cheek and upper jaw, and the lower jaw and chin. All sensation from the face — light touch, temperature, the feel of a breeze, the pressure of a cup against the lips — travels through one of these three branches before arriving, via the trigeminal root, at the brainstem.
In trigeminal neuralgia, something goes wrong at precisely this entry point. The nerve, where it enters the pons — the brainstem structure that sits at the crossroads of breathing and consciousness — is subjected to constant mechanical pressure from an adjacent blood vessel. Most often the superior cerebellar artery. Sometimes the anterior inferior cerebellar artery, or a vein.
At birth, or in early life, the geometry of this region is typically fine. Vessel and nerve coexist without conflict. But as we age, arteries lengthen and grow more tortuous. A vessel that once ran parallel to the nerve begins to loop, over years, toward it. It makes contact. It presses. It pulses — seventy, eighty, a hundred times a minute. Over years, this pulsatile trauma erodes the myelin sheath protecting the nerve's root entry zone. When the myelin is gone, bare axons are exposed. In this demyelinated state, the trigeminal nerve begins to misfire — generating action potentials in response to the lightest, most innocent stimuli. A brushstroke. A breath of cool air. A sip of water.
This is why the triggers are so innocuous and the pain so extreme. The nerve has been stripped of its insulation. It is live, exposed wiring.
The pain itself is extraordinary. Patients have described it as: an electric shock through the face; a white-hot needle driven through the eye; as though burning red chili were thrown into the cheek and eye socket; a fire that erupts without warning; a thousand needles, all at once, in the same square inch of face. Many neurologists consider it among the most severe pains the human nervous system can generate. Some have called it the su***de disease — not as metaphor, but because untreated cases, prolonged cases, cases where hope has been exhausted, carry a real risk of pushing patients toward self-harm. The pain is that severe and that relentless.
The disease predominantly affects people over forty five, and women more often than men. But it can strike younger — as it struck Nivedita at the height of her career.
⸻
The Inadequacy of Burning the Nerve
****************
When the diagnosis is made, what treatment is offered?
For most of the last century, and still in many settings today, treatments have been aimed at the nerve itself — not the offending vessel. Alcohol injections to numb the nerve. Radiofrequency ablation to burn the nerve's root. Glycerol injections into the trigeminal cistern. More recently, stereotactic radiosurgery, which delivers a focused beam of radiation to destroy the trigeminal root.
From the earliest centuries of medicine, physicians have rubbed the painful part of the face with red chili — the capsaicin burning the nerve endings into temporary silence. The logic, if crude, was the same: quiet the nerve.
But this logic misses the point entirely. The nerve is not malfunctioning because it is inherently defective. It is malfunctioning because it is being compressed. Burning or ablating the nerve addresses the symptom — the misfiring — while leaving the cause, the vessel, entirely in place. As the vessel continues to press, the disease continues to advance. The temporary silence created by ablation eventually breaks. Pain returns. The procedure must be repeated. Each repetition carries its own risks — including the risk of permanent facial numbness, or the development of an even more miserable condition: anesthesia dolorosa, in which the face is numb but burning simultaneously. It is a condition more difficult to treat than the original.
Nivedita had understood this through her own research before she reached us. She had grasped that no one was addressing the origin of the problem. She had simply not yet found anyone who could.
⸻
Peter Jannetta and the Surgery That Changes Everything
In the 1960s, an American neurosurgeon named Peter Jannetta changed the course of this disease permanently. Building on earlier anatomical observations — by Walter Dandy, who had noted vascular contact with the trigeminal nerve decades before — Jannetta developed the surgical approach now called microvascular decompression, or MVD. His premise was, in retrospect, elegant in its simplicity: if the problem is a blood vessel compressing a nerve, the solution is to separate them.
The surgery is delicate but definitive. The patient is positioned carefully. A small opening is made in the skull behind the ear — a retromastoid craniotomy, roughly the size of a large coin. The cerebellum is gently retracted. The neuromicroscope is brought to bear, its illumination flooding the dark, crowded space of the posterior fossa. The surgical team navigates through the cranial nerve complex, past the facial nerve and the auditory nerve, until the trigeminal root and its offending vessel come into view.
Then, with instruments no wider than a matchstick, the vessel is carefully lifted away from the nerve. A small pad of Teflon felt — chosen for its softness, its inertness, and its ability to hold position — is placed between the vessel and the nerve. The vessel is secured. The nerve, freed from pressure, is left entirely intact.
The recovery of patients after MVD is, from a scientific standpoint, remarkable. In large published series, immediate and complete pain relief is achieved in seventy to ninety percent of well-selected patients. Not reduced pain. Absent pain. Patients who have been unable to speak, eat, or feel wind on their face for years awaken from surgery able to do all of these things. The nerve, once decompressed, can recover over time — remyelinate, resume normal conduction, return to silence.
This was the operation we performed on Nivedita.
"After surgery, the pain was gone. Completely gone. The fear was gone. The medications were stopped. I had forgotten what it was like to simply eat a meal, or speak freely, or feel wind on my face."
She paused. Then she said something I have not forgotten.
"And I was sad. Not for myself — I was cured. I was sad because I had not found this sooner. Seven years. Seven years of suffering that did not have to happen."
⸻
The Gap That Must Be Closed
***************
Seven years. For want of information.
Trigeminal neuralgia is not a rare disease. It affects roughly one in ten thousand people — which means, in a country of over a billion, tens of thousands of people are living with it at any given moment. Diagnosis, once a clinician considers it, is not technically difficult. The history alone — lightning-bolt pain triggered by touch, on one side of the face, in a person of middle age or older — is in most cases sufficient to raise strong suspicion. MRI with specific sequences can in many cases visualize the vascular compression. The surgery, in experienced hands, offers durable relief.
What is missing is not the knowledge. The knowledge exists. What is missing is the bridge between the knowledge and the patient.
For twenty years, our centre in Pune has been building that bridge. Inspired by Peter Jannetta's work, and driven by the conviction that this surgery should be available to patients in India who would otherwise never find it, we have operated, we have taught, and we have written. To my knowledge, dedicated centres of this kind, focused on trigeminal neuralgia as a sole and serious mission, exist in only a handful of places worldwide: certain institutions in the United States, some in Japan, and ours.
Patients continue to arrive — many of them, like Nivedita, years into their illness. Damaged by prolonged compression. Burdened by the side effects of escalating medications. Diminished by years of anticipatory fear. We continue to operate. And we continue to write, and speak, and explain — because awareness remains the most powerful instrument available to us.
The general practitioner who recognizes the lightning-bolt description and refers promptly. The neurologist who knows that MVD exists and spares the nerve. The family member who searches and finds the right centre. Each of these links in the chain saves years of suffering.
⸻
A Note on This Writing — Gudi Padwa
I first wrote about this on Gudi Padwa — the Marathi New Year, a day of beginnings and renewed resolve. The gudi is a decorated staff erected each year as a banner of victory, a symbol of rising above adversity.
Peter Jannetta raised such a banner in the operating rooms of Pittsburgh in the 1960s. He offered freedom from one of the cruelest pains the human nervous system can generate. That banner is still flying. The work of carrying it forward — to patients who need it, to doctors who can diagnose and refer, to families who can recognize the signs — is the work of every year, not only of one day.
If someone you know lives with lightning pain in one side of the face — pain triggered by the lightest touch, by food, by cold air, by the simple act of speaking — know this:
There is a cause. The cause can be found. And in most cases, it can be corrected.
The face need not remain a burning inferno.
Dr Jaydev Panchawagh
Neurosurgeon.
Pune, India.
⸻
