A small but important disclaimer to start: I am not a physician. This post is not medical advice and does not attempt to offer diagnoses. It was written as a result of my own reflections, reading, and thinking about a chapter from *The Challenge of Pain* by Ronald Melzack and Patrick Wall — one of the key works I've encountered that describes how pain functions within the nervous system.
Like most posts here, this is an attempt to organize knowledge and experience, and to name mechanisms that are often overlooked or oversimplified in everyday conversations about pain.
I'm writing from the perspective of someone living with chronic pain who is trying to understand what happens when pain doesn't go away — even though "everything should be fine by now."
So let's begin.
More than just "irritation"
Long-lasting pain after nerve injury is not a simple consequence of tissue "irritation." In many cases, it is the result of a deep reorganization of nervous system function that involves both the peripheral nerve and central structures — the brainstem, thalamus, and cerebral cortex.
Importantly, these mechanisms are common across different types of injury — mechanical, chemical, inflammatory, or ischemic.
The trigeminal nerve — why it's special
The trigeminal nerve:
- Is the main sensory nerve of the face
- Has a highly precise somatotopic map in the central nervous system (a somatotopic map is an organized "plan" in the brain, thanks to which signals from specific body parts always arrive at the same location — this allows the brain to accurately identify where pain originates, for example from the forehead or the jaw)
- Contains a large number of pain fibers (especially unmyelinated C fibers)
- Strongly participates in modulating the excitability of sensory centers
This means that even minor damage can lead to disproportionately intense and long-lasting pain.
What happens at the moment of nerve injury
Damage to the trigeminal nerve — for example during:
- Tooth extraction
- Implant placement
- Sinus procedures
- Anesthetic injections
- Aesthetic medicine procedures
- Or during inflammation or infection
...triggers two parallel signals:
A fast electrical signal — sudden, atypical bursts of nerve impulses.
A slow chemical signal — a change in the composition of substances transported along the axon to the nerve cell body and onward to central structures.
It is this second mechanism that is responsible for long-term changes.
Why pain can persist despite tissue healing
After trigeminal nerve damage, a phenomenon occurs that can be called a homeostatic overreaction of the nervous system.
1. Loss of normal stimulation
A sensory neuron that:
- Stops receiving typical signals from the periphery
- Loses normal chemical signaling
- Does not "quiet down" — quite the opposite
2. Increased excitability of central neurons
Cells in the sensory nuclei of the trigeminal nerve:
- Lower their excitation threshold
- Begin responding to weaker stimuli
- May exhibit spontaneous activity
This means that pain:
- Can appear without a stimulus
- Can be burning, searing, stabbing
- Is often difficult to describe — or, as in my case, manifests as a piercing sensation resembling a rusty nail being driven in and moved side to side
3. Loss of inhibition
Under normal conditions, the spinal cord and brainstem employ strong inhibitory mechanisms (including those involving GABA — a neurotransmitter I'll dedicate more attention to another time).
After nerve damage:
- Presynaptic and postsynaptic inhibition weakens
- Pain signals are no longer effectively "filtered"
- An excess of sensory information reaches the brain
Expanding receptive fields — the key to chronic pain
One of the most important mechanisms is the expansion of neuronal receptive fields.
In practice, this means that:
- A neuron that normally "served" one area of the face
- Begins responding to stimuli from neighboring areas as well
Clinical effect:
- Radiating pain
- Difficulty pinpointing the exact location of pain
- Hypersensitivity to touch, cold, heat, or movement
Importantly:
New nerve connections do not form — previously "silent," inhibited synapses become activated.
What about inflammation? Does it fit this model?
Yes — absolutely.
Nerve damage does not have to mean the nerve was severed.
Inflammation:
- Periapical
- Sinus-related
- In soft tissues
- Viral infections (e.g., herpes zoster)
- Chronic inflammation
- Diabetes
...can cause:
- Damage to nerve sheaths
- Disruption of axonal transport
- Prolonged exposure to inflammatory mediators
From the perspective of neuronal function:
The end result is very similar: altered chemistry, loss of inhibition, increased excitability.
That is why neuropathic pain can appear:
- Without a visible "injury"
- After inflammation has resolved
- With a delay
Why this pain is so difficult to treat
Because the source of pain:
- Is no longer the peripheral tissue
- But rather altered function of the central nervous system
This explains why:
- Conventional painkillers don't work
- Pain can be resistant to local treatment
- Methods that affect neuronal excitability may be effective (neuromodulatory pharmacotherapy, neuromodulation, multimodal therapy)
What this means for you
If you experience long-lasting pain after a procedure, inflammation, or infection in the facial area, there is one thing worth knowing: what you feel has a real and well-documented physiological basis.
The persistence of pain does not mean that "something didn't heal" or that the problem is purely in your head.
In these situations, pain becomes the effect of altered nervous system function — not a simple signal from damaged tissue. That is precisely why it can be difficult to describe, variable over time, and resistant to standard pain treatment.
Understanding this mechanism is often the first step toward regaining control: it allows you to view your symptoms differently, seek appropriate help, and stop doubting your own experience. Because this pain is real — and it deserves real, targeted treatment.
Reference:
*The Challenge of Pain* — Ronald Melzack and Patrick Wall
Natalia — since 2014 I've been living with trigeminal nerve pain. I write in plain language, based on reliable sources and personal experience. Read my story →
Frequently Asked Questions
What is trigeminal neuralgia?
Trigeminal neuralgia is a chronic facial pain condition. It manifests as sudden, severe, usually one-sided pain attacks — often described as an electric shock. A single attack typically lasts from a few seconds to about two minutes.
What is the difference between neuralgia and neuropathy?
In simple terms: neuralgia primarily involves paroxysmal pain along a nerve, usually without loss of sensation. Neuropathy involves nerve damage that more often causes constant pain along with numbness and sensory loss.
Do regular painkillers help with neuropathic pain?
Usually not. Neuropathic pain responds poorly to paracetamol or anti-inflammatory drugs. Instead, medications that act on nerves are used, such as anticonvulsants like carbamazepine.
What is postherpetic neuralgia?
This is chronic nerve pain following shingles (herpes zoster), resulting from nerve damage caused by the virus. It is a distinct condition and can be challenging to treat.
Does alpha-lipoic acid (ALA) help with neuropathy?
Some people use ALA as a supportive supplement, but evidence is limited and comes mainly from studies on diabetic neuropathy. It is considered a supplement, not a proven therapy. Always consult your doctor.
Related Articles
Chronic Pain and Mental Health: The Conversation We Need to Have
Today I want to address a topic that sits in all of our minds but is rarely spoken about aloud. Trigeminal neuralgia — in all its forms — also carries a se…
Chronic Pain and Cognitive Decline: How Trigeminal Neuralgia Affects the Brain
Memory is one of the most important functions of our brain. It's what allows us to learn new things, recognize people and places, and build a sense of cont…
Why the Brain Defaults to Fear — And What It Means for Chronic Pain
The human brain was not designed for us to feel calm and happy. Its primary mission is to protect us from threat. That is why, in situations of uncertainty…
Track your attacks, triggers, and medications — and show your doctor a clear picture of your condition.