Natural Nerve Pain Relief | Neuralgia Pain Relief

Nerve pain was previously referred to as "non-inflammatory pain".

It was believed to be the one type of pain unrelated to inflammation, and therefore most difficult to treat.

More recent investigation has shown that nerve pain also results from inflammation.

Though nerve pain remains difficult to treat, Banjo addresses the root cause of pain and inflammation - the root cause of nerve pain. Expect significant relief, most often starting after about 30 days of use.

Nerve Pain Notes

Nerve Pain is Common

More than 100 types of peripheral neuropathy (nerve pain) have been identified.

Globally, the most common cause of neuropathic pain is leprosy.

Various studies suggest that 1.5% of those in the U.S., and 7.5% of those in Europe, suffer with neuropathic pain.

Approximately 65% of diabetes patients are reported to have nerve pain.

Nearly half of all women continue to experience post-mastectomy nerve pain after three years. In about 25% of cases, nerve pain remained for 9 years or longer.

Up to 70% of post-amputation patients suffer with neuropathic pain.

By 2018 there will be an estimated 6 million people in the U.S. with chronic nerve pain.

Nerve pain is notoriously difficult to treat. Many people find that currently available prescription medications have little if any effect on their nerve pain.

Frequency of neuropathic pain in diabetes

Neuropathic pain is a current reality for up to 25% of the 20 million Americans with diabetes. However, of all those with diabetes, approximately half will eventually develop diabetic neuropathy.

Diabetic neuropathy is an extremely common complication of diabetes and results in pain and numbness that can affect the individual’s sleep, function, sense of well being and overall quality of life. The pain is often accompanied by unpleasant sensations such as tingling and burning. The pain may range from sharp stabbing pain to a consistent dull ache.

Neuropathic pain was previously called “non-inflammatory” pain, because it was thought to be the one (and only) type of pain not consistently associated with inflammation.

Neuropathic pain is no longer referred to as “non-inflammatory” because there is now overwhelming evidence that inflammation is either the cause of neuropathic pain or a significant contributor to neuropathic pain.

Granted, the inflammation of neuropathic pain is not fulminant  inflammation, as might be seen with an infection, but  results from a more ‘subtle’ (and chronic) form of inflammation. Still, it’s inflammation. So the key to its effective treatment may be the ability to eliminate inflammation at its very earliest stages. Indeed, getting to the root of inflammation might mean getting to the root of all pain, including neuropathic pain.

How can we explain nerve pain in fibromyalgia?

Neuropathic Pain in Fibromyalgia
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Quick Look

Why do those with fibromyalgia often experience nerve pain?

Science: Pro-inflammatory cytokines trigger NF-kappaB activation leading to enhanced pain transmission.

Conclusion: Pro-inflammatory cytokine excess may be responsible for the neuropathic pain of fibromyalgia.


Nerve pain represents a substantial component of total fibromyalgia pain.

It’s likely that pain in fibromyalgia syndrome is of several different types. Fibromyalgia patients not infrequently report burning, tingling or sometimes stabbing pain characteristic of neuropathic pain. This pain is unique from the diffuse pain (“aching”) that is also reported by most with fibromyalgia.

Neuropathic pain is commonly thought to result from nerve damage, but the actual cause of neuropathic pain remains unknown. Of interest, neuropathic pain was formerly referred to as ‘non-inflammatory’ pain, but recent evidence has shown that inflammation plays a critical role in the onset and progression of all pain, including neuropathic pain.

Neuropathic pain may result from NF-kappaB activation by cytokines, especially IL-8.

How might neuropathic pain arise in fibromyalgia syndrome? Perhaps in part as the result of excess cytokine production.

Nerve Pain in FibromyalgiaThe study briefly summarized below discusses pro-inflammatory cytokines. It was observed that pro-inflammatory cytokines in and around the spinal cord can turn on NF-kB. NF-kB is something like an inflammation ‘master switch’. As a result of NF-kB activation, cells ‘turn on’ inflammation and begin generating mediators of inflammation, including more cytokines. The net result, the authors conclude, is neuropathic pain. So at least some neuropathic pain might be attributed to cytokine activation of NF-kB in and around the spinal cord.

That might explain neuropathic pain in fibromyalgia, because cytokines, especially IL-8, are consistently elevated in those with fibromyalgia. At least six studies document elevated IL-8 in those with fibromyalgia (one study found normal levels.) Further, at least three studies have shown a direct correlation between the level of IL-8 and pain severity.

While IL-8 is not specifically mentioned in the abstract, IL-8 is a pro-inflammatory cytokine that is known to activate NF-kB. And it is NF-kB activation that the authors suggest is responsible for generating neuropathic pain.

In summary:

1. Pro-inflammatory cytokine levels (especially IL-8) are elevated in fibromyalgia.

2. Pro-inflammatory cytokines (including IL-8) turn on NF-kappaB.

3. NF-kappaB activation in and around the spinal cord appears to play a significant role in generating neuropathic pain.

Therefore it’s likely that pro-inflammatory cytokine excess is largely responsible for the neuropathic pain of fibromyalgia.

What’s the solution?

Inhibition of NF-kB should lead to an immediate reduction in neuropathic pain. And, because it was excess activation of NF-kappaB that led to pro-inflammatory cytokine excess in the first place (can you see the vicious cycle?) – inhibiting NF-kB should provide a long-term benefit by lowering pro-inflammatory cytokine levels.

We get twice the pain killing power by going after NF-kB. That’s good. We need all the pain killing power we can get.

The publication:

October, 2005

Involvement of spinal cord nuclear factor kappaB activation in rat models of pro-inflammatory cytokine-mediated pain facilitation.

Summary of the abstract

Pro-inflammatory cytokines, such as IL-1 and TNF are released by activated cells in the spinal cord and play a major role in pain.

Those cytokines exert their actions, at least partially, through the activation of the transcription factor, nuclear factor kappaB (NF-kappaB). In turn, NF-kappaB regulates the transcription of many inflammatory mediators, including more cytokines.

This study investigated whether NF-kappaB is involved in neuropathic pain induced by sciatic nerve inflammation.

The results of the study demonstrated that spinal cord NF-kappaB activation plays a role in exaggerated pain states.

Neurogenic inflammation in fibromyalgia skin

Skin Rash in Fibromyalgia

Neurogenic inflammation found on skin biopsy in about 30% of fibromyalgia patients

Some fibromyalgia patients are reported to respond relatively well to non-steroidal anti-inflammatory drugs (NSAIDs.)

Some fibromyalgia patients (about 30% in the study below) have evidence of neurogenic inflammation on skin biopsy. This might explain, at least in part, why some patients respond better than others to NSAIDs. Presumably, those with neurogenic inflammation evidenced on skin biopsy might respond more favorably to treatment with NSAIDs.

The role of inflammation in fibromyalgia remains unclear, and controversial. But inflammation clearly plays some role, and may play a significant role, at least for a percentage of fibromyalgia patients.

The publication:

January, 2003

Detection of interleukin 1beta (IL-1beta), IL-6, and tumor necrosis factor-alpha in skin of patients with fibromyalgia.

Summary of the abstract

OBJECTIVE: To determine if abnormal collagen metabolism is correlated with neurogenic inflammation, a potential activator of collagen metabolism, in patients with fibromyalgia (FM).

RESULTS: Positive results were detected in skin tissues of FM patients for IL-1, IL-6, and  TNF. None of the cytokines could be detected in healthy control skin.

CONCLUSION: The detection of cytokines in FM skin indicates the presence of inflammatory foci (neurogenic inflammation) in the skin of certain patients (about 30% of FM patients), suggesting an inflammatory component in the induction of pain. This may explain the response to nonsteroidal antiinflammatory therapy in a subset of FM patients.

NF-kappaB in neuropathic pain

Neuropathic pain has sometimes been referred to as non-inflammatory pain. But there is now overwhelming evidence that inflammation is a crucial, probably essential, contributor to neuropathic pain – and NF-kB is the Master Switch controlling that inflammation.

NF-kappaB in neuropathic pain model

Blocking NF-kB in this model of neuropathic pain eliminated the pain stimulus.