Category: Autoimmune, Infectious & Structural

CIDP and length-dependent peripheral neuropathy differ in how they damage the nerve, in where they strike and in how they unfold. CIDP stands for chronic inflammatory demyelinating polyradiculoneuropathy. It is immune-driven inflammation of the nerve roots and the nerves of the limbs. Its symptoms must last at least 8 weeks for the diagnosis [1]. Length-dependent neuropathy follows the length of the nerve fiber instead. So the exam starts at the top of the big toe on both sides and moves upward [3].

That difference is not just for textbooks. It changes which pattern your clinician looks for, which tests are worth running, and in what order.

What is CIDP?

CIDP is immune-mediated. Inflammation hits both the nerve roots and the nerves of the limbs [1]. The damage is segmental demyelination and remyelination: the nerve’s coating is stripped and rebuilt in patches. Repeated rounds of that leave ring-shaped layers of Schwann cells known as onion bulbs [1].

Because nerve roots are involved, the weakness does not stay in the feet. The typical picture is weakness on both sides that keeps getting worse. It hits muscles near the trunk and far out in the limbs, with numbness at the far ends. It builds over at least eight weeks [2].

Course

CIDP can run a single course, relapse, or keep getting worse. About one-third of patients have a relapsing-remitting pattern, and others get steadily worse [1]. A course that flares and settles is one of the features that raises the question.

Which sensations are affected

CIDP hits position and vibration sense more than pain and temperature. That reflects mostly large-fiber damage [1]. Patients often describe unsteadiness and a sense that they cannot tell where their feet are, rather than burning.

What is length-dependent peripheral neuropathy?

Length-dependent neuropathy is the pattern where the longest nerve fibers are hit first. So symptoms begin in the toes and move upward. In diabetes, the American Diabetes Association says the exam follows the typical distal symmetric polyneuropathy pattern. It starts at the top of the big toe on both sides and moves up the leg [3].

Which sensations are affected

The most common early symptoms come from small-fiber damage. They include pain and dysesthesias (unpleasant burning feelings), described as burning, stabbing, tingling or shooting [3]. Large-fiber damage causes numbness, tingling without pain, and loss of protective feeling. That marks more advanced neuropathy and raises the risk of foot ulcers [3].

What that pattern means in practice, and how it is examined, is covered in peripheral neuropathy of the feet, symptoms and patterns.

How is CIDP different from peripheral neuropathy?

This is a guide to what to ask and what to test. It is not a self-diagnosis tool. Your clinician makes the diagnosis.

Distribution

Length-dependent neuropathy starts at the far ends and climbs [3]. CIDP involves nerve roots as well as limb nerves. It shows up with weakness near the trunk as well as far out in the limbs [1][2].

Sensory profile

CIDP hits position and vibration sense more than pain and temperature [1]. Length-dependent disease more often starts with small-fiber symptoms, meaning burning and other painful dysesthesias [3].

Timeline

CIDP must last at least eight weeks [1][2]. Length-dependent neuropathy builds more slowly. It tracks the cause behind it, whether metabolic, nutritional, toxic, autoimmune or structural.

How common each is

CIDP is rare. New cases are estimated at 0.15 to 1.6 per 100,000 person-years. Prevalence is estimated at 0.67 to 10.3 per 100,000. It usually starts between 40 and 60 years, and men get it about 2:1 over women [2]. Distal symmetric polyneuropathy in diabetes is far more common. It affects at least 20% of people with type 1 diabetes after 20 years. In type 2 diabetes it ranges from 10% to 15% of newly diagnosed patients to 50% after 10 years [3].

When should CIDP be suspected instead of typical neuropathy?

Certain features should raise the question, not settle it.

• Weakness that is not limited to the feet, including weakness near the trunk [1][2]
• Symptoms that have lasted and changed beyond eight weeks [1]
• Lost feeling that hits vibration and position sense more than pain and temperature [1]
• A course with relapses, not steady climbing from the feet [1]

If your symptoms are changing fast, if weakness is severe, or if breathing is affected, that is an emergency. Do not wait for a scheduled visit.

What tests separate CIDP from other neuropathy?

We do electrodiagnostic testing (EMG and nerve conduction studies) on site. We read it alongside where your symptoms are, the exam and the likely causes. CIDP is uncommon and length-dependent causes are not. So the order of the workup follows your pattern and timeline, not a fixed checklist.

When the pattern points to a metabolic, nutritional, toxic or structural cause, testing and diagnosis drive the plan, not the other way around. That sequence is set out in the Regenerve Protocol for peripheral neuropathy.

How we use the diagnosis

We treat the cause behind the label, not the label. We do not promise nerve regeneration or reversal of established nerve damage. If the pattern suggests an immune process such as CIDP, that belongs with the clinicians who manage immune therapy. Our role is to help get the question asked.

Frequently asked questions

How long do symptoms have to last before CIDP is considered?

At least eight weeks. CIDP symptoms must last at least 8 weeks for the diagnosis [1]. The typical picture is weakness on both sides that keeps getting worse, near the trunk and far out in the limbs, with numbness at the far ends, building over that time [2]. Burning that comes and goes over days is a different question. See small fiber neuropathy symptoms and testing.

Does burning in my feet point toward CIDP?

Usually the opposite. CIDP hits position and vibration sense more than pain and temperature [1]. Burning and other painful dysesthesias are the early small-fiber symptoms of distal symmetric polyneuropathy [3]. What follows from that difference is covered in peripheral neuropathy treatments for the feet.

Is CIDP common?

No. New cases are estimated at 0.15 to 1.6 per 100,000 person-years. Prevalence is estimated at 0.67 to 10.3 per 100,000 people. It usually starts between ages 40 and 60, and men get it about twice as often as women [2]. Because it is so rare, the more common causes are usually worked through first. Our sequence is described in our neuropathy services.

Should I bring my medication list to the evaluation?

Yes, and bring the full list, including anything started or stopped in the last few years. Medicine history is one of the groups we review, along with metabolic, nutritional, toxic and autoimmune causes. Our discussion of the medicines patients ask about most is at statins, metformin and nerve health.

What are the first signs of CIDP?

The typical picture is weakness on both sides of the body that keeps getting worse. It hits the muscles near the trunk as well as the hands and feet, with numbness at the far ends of the limbs. It builds over at least eight weeks [2]. Many people notice unsteadiness and trouble sensing where their feet are before they notice pain. That is because position and vibration sense take the biggest hit [1].

Is CIDP a type of peripheral neuropathy?

Yes, but a rare one that works differently. CIDP is immune-driven inflammation of the nerve roots and the limb nerves. It strips and rebuilds the nerve’s insulating coating in repeated cycles [1]. The far more common length-dependent pattern follows the length of the nerve fiber instead. It starts in the toes, climbs, and tracks a metabolic, nutritional, toxic, autoimmune or structural cause [3].

What causes CIDP?

CIDP is immune-mediated. The body’s own inflammation targets the nerve roots and the limb nerves [1]. The damage is repeated loss and repair of the myelin coating. That leaves layered Schwann cells known as onion bulbs [1]. When your pattern points to an immune process like this, it belongs with the clinicians who manage immune therapy. Our job is to make sure the question gets asked.

Can CIDP symptoms come and go?

They can. CIDP can run a single course, relapse, or keep getting worse. About one-third of patients have a relapsing-remitting pattern [1]. A course that flares and then settles is one of the features that should raise the CIDP question. Steady worsening that starts in the toes and climbs fits the length-dependent pattern much better [3].

Start with the Nerve Damage Score

The Nerve Damage Score is a free five-question check. It helps find which cause is most likely behind your symptoms. That way your workup starts with a direction instead of a guess.

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Sources

1. Gogia B, Rocha Cabrero F, Khan Suheb MZ, Lui F, Rai PK. “Chronic Inflammatory Demyelinating Polyradiculoneuropathy.” In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing. Last updated 4 March 2024. https://www.ncbi.nlm.nih.gov/books/NBK563249/ — cited for the requirement that symptoms persist at least 8 weeks to establish the diagnosis; inflammation of nerve roots and peripheral nerve; segmental demyelination and remyelination producing onion bulbs; the monophasic, relapsing and progressive courses with about one-third relapsing-remitting; and involvement of position and vibration sense more than pain and temperature.
2. “Diagnosis of Chronic Inflammatory Demyelinating Polyneuropathy.” Practical Neurology, April 2024 issue. https://practicalneurology.com/diseases-diagnoses/neuromuscular/diagnosis-of-chronic-inflammatory-demyelinating-polyneuropathy/32112/ — cited for the typical presentation of symmetric progressive proximal and distal muscle weakness with distal numbness evolving over at least 8 weeks; the progressive, monophasic and relapsing-remitting courses; incidence of 0.15 to 1.6 cases per 100,000 person-years; prevalence of 0.67 to 10.3 per 100,000; onset around 40 to 60 years; and the approximately 2:1 male-to-female ratio.
3. Pop-Busui R, Boulton AJM, Feldman EL, Bril V, Freeman R, Malik RA, Sosenko JM, Ziegler D. “Diabetic Neuropathy: A Position Statement by the American Diabetes Association.” Diabetes Care, 2017;40(1):136–154. DOI: 10.2337/dc16-2042. https://pmc.ncbi.nlm.nih.gov/articles/PMC6977405/ — cited for assessment following the typical distal symmetric polyneuropathy pattern starting distally at the dorsal aspect of the great toe on both sides and moving proximally; small-fiber symptoms of pain and burning dysesthesias described as burning, lancinating, tingling or shooting; large-fiber symptoms of numbness, tingling without pain and loss of protective sensation; and prevalence of at least 20% in people with type 1 diabetes after 20 years and 10–15% of newly diagnosed type 2 patients rising to 50% after 10 years.

Lupus and rheumatoid arthritis damage nerves two ways. Vasculitis inflames the tiny vessels that feed a nerve and starves it of oxygen. Autoantibodies attack the myelin sheath and nerve fibers directly. A patchy, lopsided pattern points to this autoimmune cause, such as a wrist drop on one side and a foot drop on the other.

When the immune system goes haywire, nerves are rarely the target. But they are often the casualties. Autoimmune diseases such as lupus, rheumatoid arthritis, and Sjögren’s syndrome can cause peripheral neuropathy as collateral damage from body-wide inflammation. This article covers the two main ways autoimmunity hurts nerves. It explains why the damage can take several forms. And it shows why treatment must handle both the whole-body disease and the nerve.

Can lupus and rheumatoid arthritis cause neuropathy?

In an autoimmune disease, the immune system can no longer tell friend from foe. It starts attacking the body’s own tissue. In lupus (systemic lupus erythematosus) and rheumatoid arthritis, the main targets are joints, skin, kidneys, and other organs. But the same inflammation can reach the nerves in the arms and legs. Here the nerve damage is a downstream result of a whole-body process. That is why treating the nerve alone is not enough.

How does vasculitis damage nerves?

Nerves depend on a web of tiny blood vessels, the vasa nervorum, for oxygen and nutrients. In autoimmune disease, these vessels can become inflamed. That is called vasculitis. Inflammation thickens and plugs the vessel walls. Blood flow stops, and stretches of nerve are starved of oxygen (ischemia). The nerve tissue past the blockage is injured or dies.

Vasculitis nerve damage often makes a telltale pattern called mononeuritis multiplex. Several single nerves get damaged in a patchy, lopsided way. For example, you may get a wrist drop on one side and a foot drop on the other. Diabetic neuropathy is different: it shows up evenly, in a stocking-glove pattern. This lopsided pattern is a key clue that points to a vasculitic, autoimmune cause. Vasculitic neuropathy can get worse fast, so it calls for a prompt workup.

Can autoimmune antibodies attack nerves directly?

The second route is more direct. Autoimmune disease makes autoantibodies and immune complexes. These can latch onto parts of the nerve and attack them, including the myelin sheath and the nerve fibers. Sjögren’s syndrome is closely tied to sensory neuropathies. One form is a sensory ganglionopathy, where the sensory nerve cell bodies themselves are hit. It can cause numbness, poor balance, and painful burning. Each autoimmune disease favors its own antibody targets. That is part of why autoimmune neuropathy is not one disease but a family of patterns.

How do you know if neuropathy is autoimmune?

Several signs suggest a neuropathy is autoimmune. One is a lopsided or patchy pattern (mononeuritis multiplex). Another is a fairly fast onset. Others are whole-body symptoms (joint pain, rash, dry eyes and mouth, fatigue) and a known or suspected autoimmune diagnosis. When these show up, the workup grows. It adds autoimmune blood tests and, in some cases, nerve conduction studies or a nerve biopsy to pin down the process.

How is autoimmune neuropathy treated?

This is the main clinical message. A whole-body autoimmune process drives this neuropathy, so controlling that process is essential. That is usually the job of a rheumatologist, who uses immune-calming treatment to quiet the disease. But calming the inflammation does not by itself repair nerves already injured. The nerve also needs support. That means pain control, protecting the function that is left, and care for the same terrain factors any injured nerve needs to recover: circulation, nutrients, and mitochondrial energy.

A terrain-focused clinic works alongside a patient’s rheumatologist, not in place of them. The rheumatologist fights the fire. The nerve-focused care supports the tissue caught in it. Neither one is enough alone.

The overlap with other drivers

Autoimmune disease also raises the stakes on other neuropathy causes. Whole-body inflammation, some immune-calming drugs, and less activity can all add to nutrition and metabolic problems. So a full workup still checks every cause, rather than stopping at the autoimmune label.

Frequently asked questions

Key takeaways

• Lupus, RA, and Sjögren’s can damage nerves as collateral damage from whole-body autoimmunity.
• Vasculitis starves nerves of blood. It often causes lopsided mononeuritis multiplex.
• Direct antibody attack hits myelin and nerve fibers. Sjögren’s favors sensory neuropathies.
• A lopsided pattern, fast onset, and whole-body symptoms are clues to an autoimmune cause.
• Treatment must control the whole-body disease and support the injured nerve.

This article is educational and is not a substitute for evaluation, diagnosis, or treatment by a physician. Individual results vary. Do not start, stop, or change any medication without consulting your physician. Take the free Nerve Damage Score or call (314) 886-5739 or text (314) 886-5902.

References

1. Collins MP, Hadden RD. The nonsystemic vasculitic neuropathies. Nat Rev Neurol. 2017;13:302–316.
2. Mori K, et al. The wide spectrum of clinical manifestations in Sjögren’s syndrome–associated neuropathy. Brain. 2005;128:2518–2534.
3. Oomatia A, et al. Peripheral neuropathies in systemic lupus erythematosus. Arthritis Rheumatol. 2014.
4. Gwathmey KG, et al. Vasculitic neuropathies. Lancet Neurol. 2014;13:67–82.

Shingles pain that outlasts the rash is postherpetic neuralgia (PHN). The chickenpox virus wakes up and injures the nerve. The nerve then keeps misfiring as burning, stabbing or electric pain where the rash was. The 8% capsaicin patch, lidocaine patches and oral nerve-pain drugs treat it.

For most people, shingles is a miserable few weeks, and then it’s over. But for a sizable minority, the rash heals and the pain doesn’t. It settles into lasting, often severe nerve pain that can go on for months or years. This is postherpetic neuralgia (PHN), one of the most common and most distressing kinds of nerve pain. This article explains how a childhood chickenpox virus can come back decades later to injure nerves. It covers what makes the pain last, how it is treated, and how it can be prevented.

Why does the chickenpox virus come back as shingles?

Shingles is caused by the varicella-zoster virus (VZV), the same virus that causes chickenpox. After a childhood bout of chickenpox, the virus does not leave the body. It hides in the dorsal root ganglia. These are clusters of sensory nerve cell bodies that sit next to the spinal cord. The virus lies dormant there, sometimes for decades. The immune system holds it in check.

When immunity fades, the virus can wake up again. That can happen with age, illness, stress, or conditions and treatments that weaken the immune system. The virus travels back down the sensory nerve to the skin. There it causes the painful, blistering rash of shingles in a band along that nerve’s path. But the damage isn’t only skin-deep. As the virus wakes, it inflames and injures the nerve and its ganglion along the way.

Why does shingles pain last after the rash heals?

In postherpetic neuralgia, the nerve injury from shingles leaves the sensory pathway damaged and out of balance. The injured nerves become overexcitable and misfire. The pain-processing system itself can also become sensitized. Then even light touch on the healed skin triggers severe pain. This is called allodynia. The result is lasting burning, stabbing, or electric pain where the rash was. It often comes with extreme tenderness.

Several factors raise the risk of PHN. The biggest is older age, and the risk climbs a lot with each decade. A more severe first bout of shingles also raises it. This is why prevention and early treatment matter so much.

How is postherpetic neuralgia treated?

PHN is hard to treat, but there are real tools. They work best when combined and fitted to the person.

Early antiviral treatment of the shingles bout can help. It should start promptly, within the first days of the rash. It can cut how bad the outbreak gets and how long it lasts. It may also lower the risk of lasting pain. That is one reason to get care quickly when shingles appears.

For established PHN, there are topical therapies you put on the skin. One is the high-concentration 8% capsaicin patch. It is FDA-approved for postherpetic neuralgia. It works by quieting the overactive pain fibers in the affected skin, as the capsaicin article explains in detail. Lidocaine patches are another. There are also oral neuropathic-pain medications, such as gabapentinoids and certain antidepressants. PHN often stays in one area. So skin treatments, which do not act on the whole body, are especially useful. They help you avoid whole-body side effects.

Beyond symptom control, a repair-and-support approach addresses the injured nerve terrain itself. The video notes measures aimed at supporting recovery. These include cannabinoid-based therapies and glutathione. To be accurate, here is where they stand. Cannabinoids have a growing but still-evolving evidence base for nerve pain. Glutathione support for nerve recovery makes biological sense, but it is not a proven cure. Both are add-ons (adjuncts) used within a personal plan guided by a physician. They are not established standalone treatments.

Can postherpetic neuralgia be prevented?

The single most effective way to deal with postherpetic neuralgia is to prevent the shingles bout that causes it. The recombinant shingles vaccine (Shingrix) is highly effective at preventing shingles, and so at preventing PHN. It is recommended for older adults and certain people with weak immune systems (immunocompromised). Are you in an at-risk group and not yet vaccinated? Then this is a talk worth having with a physician. Preventing the outbreak is far easier than treating the pain it can leave behind.

Where this fits

Postherpetic neuralgia is one of the infection-related drivers of nerve pain. The neuropathies of metabolic disease are spread out and start at the longest nerves first. PHN is different. It usually stays in the nerve area the shingles outbreak hit. That distinct pattern helps identify it. It also shapes the local, terrain-supportive approach to treatment.

Frequently asked questions

Key takeaways

• Shingles comes from varicella-zoster virus waking up in the dorsal root ganglia and injuring the nerve.
• Postherpetic neuralgia is the lasting nerve pain that can follow, driven by nerve damage and sensitization.
• Risk rises sharply with age and with a severe initial outbreak.
• Treatment combines skin treatments (including the FDA-approved 8% capsaicin patch), oral drugs, and terrain support. Cannabinoids and glutathione are adjuncts, not proven cures.
• The shingles vaccine is the most effective way to prevent PHN.

This article is educational and is not a substitute for evaluation, diagnosis, or treatment by a physician. Individual results vary. Do not start, stop, or change any medication without consulting your physician. Take the free Nerve Damage Score or call (314) 886-5739 or text (314) 886-5902.

References

1. Johnson RW, Rice ASC. Postherpetic neuralgia. N Engl J Med. 2014;371:1526–1533.
2. Gershon AA, et al. Varicella zoster virus infection. Nat Rev Dis Primers. 2015.
3. Backonja M, et al. NGX-4010 (capsaicin 8% patch) for postherpetic neuralgia: randomized studies. Lancet Neurol. 2008.
4. Dooling KL, et al. Recommendations of the ACIP for use of recombinant zoster vaccine (Shingrix). MMWR. 2018.

Not every case of numb hands or burning feet is a body-wide, metabolic neuropathy. Sometimes the nerve is simply being squeezed. It may be pinched at the wrist in carpal tunnel syndrome, pressed at the spine in sciatica, or caught at two points at once in double crush syndrome.

A physically squeezed nerve is a common and often very treatable cause of nerve symptoms. Telling it apart from a widespread neuropathy changes everything about the treatment. This article explains how pressure injures nerves and how to spot the pattern. It also explains why pressure and metabolic disease so often team up, in something called double crush syndrome.

How does a pinched nerve cause numbness and tingling?

A nerve under steady pressure suffers in two main ways. First, the pressure restricts blood flow to the nerve (ischemia). That starves it of oxygen and nutrients. Second, steady pressure damages the nerve’s insulating myelin at the pressure point (focal demyelination). That garbles the fast, clean flow of signals. If the pressure goes on, the nerve fibers themselves can be injured. The result is numbness, tingling, pain, and sometimes weakness. But there is a key difference from metabolic neuropathy. The problem is localized to the compressed nerve. It is not spread evenly across all the longest nerves.

What are the most common nerve compression syndromes?

Carpal tunnel syndrome is the classic example. The median nerve gets squeezed as it passes through a tight tunnel at the wrist. It usually causes numbness and tingling in the thumb, index, middle, and part of the ring finger. It is often worse at night, and sometimes the grip gets weaker. It is one of the most common nerve disorders and is often very treatable.

Radiculopathy (including sciatica) happens when a nerve root is squeezed as it leaves the spine. A herniated disc or arthritic narrowing can do this. Sciatica is the well-known form: pain, numbness, or weakness running from the low back down the leg along the path of the affected nerve root. Because the pressure is at the spine, the symptoms follow one nerve’s territory, not a stocking-glove pattern.

Other trapped nerves (such as the ulnar nerve at the elbow) follow the same logic. One nerve, squeezed at one spot, causes symptoms in that nerve’s own area.

How do you tell a pinched nerve from neuropathy?

The pattern is the giveaway. Metabolic neuropathies (like diabetic neuropathy) are usually symmetric and length-dependent. Both feet go first, then it moves upward. Pinched-nerve problems are usually focal and asymmetric: one nerve, one area, often on one side. They are sometimes set off by certain positions or activities, like typing, a night with the wrist bent, or long sitting. Nerve conduction studies and electromyography can show where along a nerve the problem is. That helps confirm the pinch and pinpoint its spot. Getting this right matters. A squeezed nerve may be relieved by taking the pressure off, with or without surgery. A metabolic neuropathy needs a metabolic approach.

What is double crush syndrome?

Here is one of the most important and overlooked ideas in nerve medicine. In 1973, Upton and McComas, writing in The Lancet, proposed double crush syndrome. The idea is that a nerve squeezed at one point becomes more vulnerable to injury at a second point along its length. One mild pinch that might cause no symptoms on its own can start causing them when a second insult is added.

The idea goes beyond two physical pinches. A nerve under metabolic stress from diabetes, a nutrient shortage, or toxins is already weakened. That makes it far more likely to show symptoms from even modest pressure. This is why so many patients have both. A metabolic neuropathy has lowered the nerve’s reserve. Then a pinch (like carpal tunnel) pushes it over the line into symptoms. Treating only one of the two often leaves the patient frustrated.

How is double crush syndrome treated?

The double-crush idea points straight to treatment: address both the mechanical and the metabolic causes. Relieving the pressure removes the physical insult. That can be done through changes to how you work, splinting, injections, physical therapy, or, when fitting, decompression procedures. At the same time, supporting the nerve’s metabolic terrain raises its resilience so it can handle normal life and heal. That terrain includes blood sugar, nutrients, mitochondrial energy and inflammation. Neither alone fully solves a double-crush case; together they can. That is exactly why a thorough workup checks for a pinch even in someone with known metabolic disease. And it checks for metabolic causes even in someone with an obvious trapped nerve.

Where this fits

Nerve compression is the mechanical group in the three-domain framework of neuropathy causes. Double crush syndrome is the bridge that explains why the groups so often overlap. A full workup looks across all of them on purpose. The most common real-world case is not one cause but a mix, each making the others worse.

Frequently asked questions

Key takeaways

• Not all nerve pain is metabolic. A pinched nerve is common and often treatable.
• Carpal tunnel and sciatica squeeze one specific nerve, causing symptoms in one area, often on one side.
• Pressure injures nerves through ischemia and focal demyelination. The pattern sets it apart from widespread neuropathy.
• Double crush syndrome (Upton & McComas, 1973) explains why nerves under metabolic stress are more vulnerable to pressure.
• The best results come from treating both the mechanical and metabolic causes together.

This article is educational and is not a substitute for evaluation, diagnosis, or treatment by a physician. Individual results vary. Take the free Nerve Damage Score or call (314) 886-5739 or text (314) 886-5902.

References

1. Upton ARM, McComas AJ. The double crush in nerve-entrapment syndromes. Lancet. 1973;2(7825):359–362.
2. Padua L, et al. Carpal tunnel syndrome: clinical features, diagnosis, and management. Lancet Neurol. 2016;15:1273–1284.
3. Wilbourn AJ, Gilliatt RW. Double-crush syndrome: a critical analysis. Neurology. 1997;49:21–29.
4. Rempel D, et al. Pathophysiology of nerve compression syndromes. J Bone Joint Surg Am. 1999.