Neuropathic Pain
Burning, electric, stabbing pain from damaged or dysfunctional nerves — with treatments aimed at the nerve, not the symptom.
Neuropathic Pain is a symptom. The source is the answer.
Neuropathic pain arises from damage or dysfunction in the nervous system itself, rather than from injured tissue. Patients describe it as burning, electric, shooting, stabbing, or icy — and it often comes with numbness, tingling, or sensitivity so extreme that a bedsheet becomes intolerable.
Because the problem lives in the nerve, treatments aimed at muscles and joints accomplish little. And because neuropathic pain frequently coexists with central sensitization, it can persist long after any original injury has healed.
The strategy is to identify which nerve, where, and why — then treat that specific nerve with the most precise tool available, while addressing the nervous-system amplification that keeps the pain alive.
The distinction matters enormously for treatment. Anti-inflammatory medication addresses inflamed tissue; it does relatively little for a nerve that has begun firing on its own. Opioids, meanwhile, are both poorly effective for neuropathic pain and capable of making it worse over time through opioid-induced hyperalgesia — increasing pain sensitivity in a condition already defined by pathological pain signaling.
What does work is precision. Identify the specific nerve. Confirm it with a diagnostic block. Treat that nerve directly — with a targeted block, with ablation where appropriate, or by relieving whatever is compressing it. And address the central sensitization that has developed alongside it, because after months or years, the nerve is no longer the only problem.
Neuropathic pain is a signaling problem. Treating the tissue will never fix the signal.
What can cause neuropathic pain
Below are the conditions we most commonly identify and treat. Many patients have more than one contributing source at the same time — which is precisely why careful diagnosis matters.
Peripheral Neuropathies
Diabetic Peripheral Neuropathy
The most common cause. Chronically elevated blood sugar damages small nerve fibers, producing burning, numbness, and tingling that typically begins in the feet and progresses upward.
Postherpetic Neuralgia
Persistent burning pain in the distribution of a prior shingles outbreak, caused by nerve damage from the varicella-zoster virus. Early treatment substantially improves outcomes.
Nerve Entrapment Syndromes
Carpal tunnel, cubital tunnel, tarsal tunnel, meralgia paresthetica, and others — where a nerve is compressed along its course, producing pain in that nerve’s specific distribution.
Chemotherapy-Induced Peripheral Neuropathy
Certain chemotherapy agents damage peripheral nerves, leaving burning and numbness in the hands and feet that can persist long after treatment ends.
Nerve Root & Central Causes
Radiculopathy
Compression or irritation of a spinal nerve root — cervical or lumbar — producing radiating neuropathic pain in that root’s distribution, often with numbness or weakness.
Post-Surgical & Scar-Related Neuropathic Pain
Nerves injured or entrapped during surgery, or tethered in scar tissue afterward, can generate persistent burning pain around and beyond the surgical site.
Traumatic Nerve Injury & Neuroma
Direct nerve trauma, including amputation-related neuroma and phantom limb pain, produces neuropathic pain that can be severe and highly treatable when properly targeted.
Central Neuropathic Pain
Pain arising from damage within the central nervous system itself — after stroke, spinal cord injury, or in multiple sclerosis.
Face, Trunk & Amplifiers
Trigeminal Neuralgia
Sudden, severe, electric facial pain triggered by light touch, chewing, or wind. Distinct, dramatic, and specifically treatable.
Occipital Neuralgia
Sharp, shooting pain from the skull base over the back of the head, arising from irritation of the occipital nerves and routinely misdiagnosed as migraine.
Intercostal & Abdominal Wall Neuralgia
Nerve pain along the ribs or abdominal wall, often after surgery, trauma, or shingles — and frequently mistaken for internal organ pathology.
Central Sensitization
Long-standing neuropathic pain amplifies within the central nervous system. This is why some patients still burn after the nerve compression is relieved — and why the amplification itself must be treated.
Underlying Causes That Must Be Addressed
Diabetes & Metabolic Dysfunction
Blood sugar control directly influences the progression of diabetic neuropathy. Treating pain without addressing the metabolic driver is incomplete care — which is why our team includes a double board-certified internal and obesity medicine physician.
Vitamin B12 & Nutritional Deficiency
Correctable deficiencies can cause or worsen peripheral neuropathy. They are simple to identify and simple to treat — and routinely overlooked.
Autoimmune & Inflammatory Neuropathies
Certain neuropathies are driven by immune-mediated processes requiring specific systemic treatment rather than interventional pain procedures alone.
Ongoing Nerve Compression
A nerve that remains compressed will continue to generate pain no matter how it is medicated. Relieving the compression, where possible, is the treatment.
Living With Neuropathic Pain
Sleep Disruption
Neuropathic pain characteristically worsens at night, destroying sleep — and poor sleep amplifies central sensitization, worsening the pain. Both must be treated.
Balance, Falls & Deconditioning
Numbness and altered sensation impair balance and increase fall risk, particularly in peripheral neuropathy. Addressing this is a safety issue, not merely a comfort one.
Foot Care & Injury Prevention
When a foot cannot feel, injuries go unnoticed. In diabetic neuropathy especially, meticulous foot care prevents ulceration and its consequences.
Mood, Isolation & the Toll of Invisible Pain
Neuropathic pain is invisible and frequently doubted. The resulting isolation and distress are consequences of the pain, not its cause — and whole-person support is part of proper treatment.
When neuropathic pain is an emergency
Seek immediate care — call 911 or go to an emergency room — for: sudden, rapidly progressive weakness or numbness; loss of bowel or bladder control; numbness in the groin or inner thighs; sudden facial droop, slurred speech, or vision loss; or a hot, painful, swollen limb with fever. This page is educational and is not a substitute for evaluation.
Diagnosis is a procedure, not a guess
Imaging alone rarely provides the answer. Findings of degeneration are extraordinarily common in people with no pain whatsoever — so an abnormal image doesn’t prove we’ve found the culprit. Conversely, some of the most treatable causes may not appear on imaging at all.
So we build the diagnosis from several converging sources:
01 — A genuinely thorough history and physical examination
The quality of the pain, its distribution, and a careful sensory and motor examination localize the involved nerve. Most of the diagnosis is made here — which is why our visits are longer than the industry norm.
02 — Identifying and treating the underlying cause
Neuropathic pain is a symptom. Diabetes, nutritional deficiency, thyroid disease, autoimmune conditions, and compression all require different management. Treating pain without addressing cause is incomplete care.
03 — Correlated imaging and nerve testing
MRI, nerve conduction studies, and EMG are used to characterize where and how a nerve is affected — interpreted against your symptoms, never in isolation.
04 — Diagnostic nerve blocks
Anesthetizing a specific nerve and observing whether your pain resolves confirms which nerve is generating it — the most direct answer available, and often the beginning of treatment.
This is the difference between treating a picture and treating a patient. We confirm the source before committing you to a therapeutic procedure.
Precise, non-opioid, physician-performed care
Once we know the source, treatment can be targeted. Every procedure is performed personally by Dr. Joshi, using low-dose imaging, non-opioid sedation when appropriate, and hand-selected medications and products. We do not delegate procedures, and we do not use opioids as a treatment strategy.
Targeted Peripheral Nerve Blocks
Precise, image-guided blocks of the specific nerve generating your pain — diagnostic and therapeutic. Occipital, intercostal, ilioinguinal, genicular, and others, chosen to match the anatomy of your pain.
Sympathetic Blocks
Stellate ganglion and lumbar sympathetic blocks interrupt sympathetic contributions to neuropathic pain, particularly valuable in CRPS and certain post-traumatic neuropathies.
Dr. Joshi is a published co-architect of the landmark unifying theory connecting the stellate ganglion block across sympathetically-mediated conditions — CRPS, hot flashes, and PTSD.
Epidural Steroid Injections
For radicular neuropathic pain from a compressed nerve root, targeted epidural injections reduce inflammation around the nerve.
Dr. Joshi pioneered the blunt-needle technique for lumbar transforaminal epidural injections, reducing the risk of catastrophic intravascular and intraneural injury. We do not perform transforaminal epidurals in the cervical or thoracic spine, where we consider the risk unacceptable.
Radiofrequency Ablation & Neuromodulatory Techniques
Where appropriate and confirmed diagnostically, ablation can interrupt pain transmission along a specific nerve. We use smaller-gauge needles and lower-temperature, tissue-sparing lesions.
Ketamine Infusion Therapy
Ketamine acts on the NMDA receptor, directly targeting the central sensitization that sustains chronic neuropathic pain. We built America’s first surgery-center-based outpatient ketamine program and have delivered thousands of infusions.
Regenerative & Adjunctive Options
For appropriate candidates, orthobiologic approaches may address contributing structural pathology. We are candid about what evidence supports and what remains emerging.
Rehabilitation, Desensitization & Whole-Person Care
Desensitization, graded exposure, movement, sleep, and metabolic health all modulate nerve pain. Our multi-disciplinary team addresses them together, not in sequence.
Why We Don't Use Opioids
Opioids are poorly effective for neuropathic pain and can increase pain sensitivity over time through opioid-induced hyperalgesia. Our approach targets the nerve and the amplification — not the signal.
Treating the Underlying Cause
Blood sugar optimization, nutritional correction, and management of contributing systemic disease — coordinated by our multi-disciplinary team, because pain control without cause control is temporary.
Sympathetic Blocks for Post-Herpetic Neuralgia
Early intervention in shingles-related nerve pain can meaningfully reduce the likelihood and severity of persistent postherpetic neuralgia. Timing matters.
Non-Opioid Medication Strategy
Certain agents act specifically on neuropathic pain signaling and have a legitimate role. We use them as part of a plan, alongside interventional treatment and rehabilitation — never as the whole of it.
Desensitization & Graded Exposure
Systematic retraining of a hypersensitive nervous system, integrated with interventional care rather than offered as a consolation prize when procedures aren’t attempted.
We don't rush to implant
A spinal cord stimulator is a legitimate tool for the right patient at the right time. But it’s an implant, and we treat it as a genuine last resort — not an early default reached for after a couple of quick attempts. First we find the root cause, address it, and rehabilitate it. Only when the better options are truly exhausted do we consider going there.
The same procedure is not the same procedure
Two practices can list the same procedure on a website and deliver profoundly different experiences, risks, and outcomes. Here is what changes when the details are done right.
Performed personally by Dr. Joshi
Never delegated to a technician, resident, or rotating staff. You’re treated by the physician who developed and teaches the technique — and in image-guided procedures, the difference between physicians is measured in millimeters.
Dramatically less radiation
Pulsed, low-dose imaging and a few precisely targeted spot images instead of continuous live X-ray. Based on our own procedural dose data, this reduces radiation exposure by at least 50% — and often far more — versus conventional continuous fluoroscopy, with no compromise in accuracy. For conditions treated repeatedly over years, that difference compounds.
Non-opioid sedation
When sedation is used, we use ketamine-based sedation, not fentanyl. Opioid sedation exposes you to unnecessary opioids, can complicate workplace drug testing, and can actually increase pain sensitivity. Ketamine can do the opposite.
Smaller needles, tissue-sparing lesions
Precision means we don’t need to be destructive to be effective — smaller-gauge needles and lower-temperature, longer-duration ablation that spares the healthy tissue around the target.
We actually numb you first
Thorough local anesthesia of skin and underlying tissue before the procedure begins. It takes an extra minute. We take it.
Independent, and obsessive about quality
Nearly four out of five U.S. physicians now answer to a corporate owner. We’re physician-owned, so our only incentive is your outcome. What a practice refuses to do tells you as much as what it offers.
Neuropathic Pain, answered
Ordinary pain signals tissue damage. Neuropathic pain arises from the nerve itself being damaged or dysfunctional — so the pain persists without tissue injury and feels distinctly different: burning, electric, or stabbing, often with numbness or extreme sensitivity to light touch.
Because most analgesics act on tissue inflammation, not on nerve signaling. Opioids are particularly poor choices — they are relatively ineffective for neuropathic pain and can increase pain sensitivity over time.
Sometimes. Relieving compression, correcting metabolic causes such as blood sugar, and treating inflammation early can allow nerve recovery. Even when a nerve cannot fully heal, its pain signaling can often be interrupted or substantially reduced.
We anesthetize a specific nerve and observe what happens to your pain. If it resolves, we’ve identified the generator with a precision no scan can match — and we know exactly where to direct treatment.
Chronic neuropathic pain is sustained by central sensitization — amplified signaling in the nervous system. Ketamine acts on the NMDA receptor central to that amplification. It is one of the most valuable tools available for pain that has outlasted its original cause.
Very likely not, at least not initially. Implants are legitimate for carefully selected patients, but we treat them as a genuine last resort rather than an early default. First we identify the nerve, treat it precisely, address central sensitization, and rehabilitate.
Because the problem is in the nerve that supplies the foot, not the foot itself. Damaged nerves generate pain signals spontaneously. The brain interprets those signals as coming from the foot, because that is where that nerve normally reports from.
Progression can often be slowed substantially with blood sugar control, and pain can be treated effectively. This is a case where treating the underlying cause and the pain simultaneously matters — and it’s why our team includes an internal and obesity medicine specialist.
Not necessarily, and early treatment improves outcomes considerably. Targeted nerve blocks, sympathetic blocks, and other interventional approaches can meaningfully reduce both the intensity and the duration of the pain.
It is a paradoxical increase in pain sensitivity caused by opioid use. In neuropathic pain — a condition already characterized by amplified pain signaling — this is a particularly damaging outcome, and it is one of many reasons we do not use opioids as a treatment strategy.
Several factors converge: fewer distractions, changes in position and circulation, and the natural fluctuation of the nervous system’s activity. Nighttime worsening is characteristic of neuropathic pain and is a useful diagnostic clue rather than an inevitability to endure.
Sometimes the underlying cause can be corrected — a compression relieved, a deficiency replaced, blood sugar controlled — and the nerve recovers. When it cannot, pain signaling can very often be interrupted or substantially reduced with targeted treatment. “Incurable” and “untreatable” are not the same word.
A neuroma is a disorganized bundle of nerve fibers that forms after a nerve is cut or injured, generating pain signals spontaneously. Targeted injections, ablation, and other interventional approaches can be highly effective when the neuroma is correctly identified.
Find out what's actually causing your pain.
A precise diagnosis is the beginning of a real solution. Let’s find your pain generator — and treat it.
This page is provided for general educational purposes and does not constitute medical advice, diagnosis, or treatment, nor does it create a physician-patient relationship. Individual results vary, and no specific outcome is promised or guaranteed. Radiation-reduction figures reflect National Pain Centers’ own procedural dose data compared with conventional continuous-fluoroscopy technique. Certain regenerative therapies are considered emerging or investigational and are not FDA-approved for all uses. Always consult a qualified physician regarding your medical condition. If you are experiencing a medical emergency, call 911.