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…
Basically, the immune system becomes activated during times of stress. ‘Stress’ can be an infection, an injury, or emotional/psychological stress. The activated immune system releases cytokines (pro-inflammatory cytokines) that communicate with your brain by stimulating nerves. Then your brain also begins releasing cytokines, with a resulting effect on sleep, mood and certain behaviors.
That makes sense, because if you have an injury, an infection, or you’re under a great deal of psychological stress, it’s probably good for you to sleep more. A general sense of fatigue is also beneficial. Your body wants you to stay home, not go out, not work – just lay low until you feel better.
Ultimately the infection clears, the injury heals, or the stressful time passes. Your body sounds the ‘all-clear’ and you’re good to go again.
Back and neck pain are the most common chronic pain conditions.
Back and neck pain can arise from any part of the back or neck, including joints, ligaments, muscles, bones and connective tissue. Not infrequently, a specific cause for the pain cannot be identified.
Common causes of back and neck pain include:
* Degenerative disk disease
* Nerve compression
* Nerve compression within the spine itself
* Back strain or sprain
* Pain that persists for more than 3 months is considered chronic.
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…
Approximately half of those with multiple sclerosis (48%) are reported to experience chronic pain in association with their condition. Severe, chronic fatigue is reported by 75% of those with multiple sclerosis.
Multiple sclerosis is characterized by areas of demyelination (lesions) in the central nervous system (CNS: the brain and spinal cord.) It is believed that lesions in the CNS result when auto-antibodies specific to myelin attack and destroy the protective covering that surrounds the nerve fibers in the CNS.
The presence of CNS lesions can account for many of the unique symptoms of multiple sclerosis, but in many instances cannot explain…
I started using Banjo because I have bad fibromyalgia and have had constant pain for over 15 years, starting in 1993, and my life since that time has been constantly limited by chronic, daily pain. It’s been a long time of suffering. Before starting Banjo I was also getting 2-4 migraines per month and had sciatica. I’ve been using Banjo for about 7 weeks. During that time I have not had a migraine…
I just wanted to say that after trying Banjo for the last month I have had an increase in stamina and energy that seemed impossible for the last 15 years when I was diagnosed with what the Rheumatologist called “old fashioned” Rheumatism. Which is now called Fibromyalgia. Also my osteoarthritis is greatly improved and my diabetic neuropathy pain is slowly getting better. I have not had the stabbing pain that I would frequently get with the neuropathy that actually prevented me from sleeping since I started Banjo. It’s great to finally be able to get though the day without…
I was called an “anomalous anomaly” by Mayo Clinic doctors in 1998. Since then, pain has been a constant part of my life. I have been diagnosed with fibromyalgia, Sjogren’s, degenerative discs, carpal tunnel, and an unknown autoimmune inflammation disease.
Then, about a month ago I reconnected with Steve Roberts (“Dr. Steve”) through Facebook…
Migraine is triggered by nerve signals that cause the release of inflammation causing substances. Odd as it might seem, nerve impulses release these inflammation causing substances all the time – in everyone – in moderation. Migraine means that something’s not quite right. It might be that too many nerve signals are being generated – or too much of the ‘substance’ is being released – or that there is an excessive reaction to that substance – or some other thing/combination that results in excess sensitivity.
The inflammation that’s caused by nerve activity is called neurogenic inflammation. In the case of migraine, it’s the blood vessels of the brain that become inflamed – and probably the nerve itself . We’ll look at that nerve in a moment. It’s a big one – the trigeminal – with a central portion located in the brainstem and numerous branches – some of which go to the face – others of which go to the blood vessels of the brain.
The pain of both TMJ and migraine is mediated through the trigeminal nerve.
NMDA receptors are believed to play a key role in the transmission of pain in the trigeminal.
IL-6 is an important pro-inflammatory cytokine that is under the control of NF-kB.
In the study briefly summarized below:
* Blocking IL-6 eliminated pain.
* Blocking NF-kB eliminated pain.
* Administering IL-6 in the absence of inflammation caused pain.
The implied mechanism of trigeminal pain is inflammation => NF-kB activation => IL-6 production => pain.
By inhibiting NF-kB, both migraine pain and TMJ pain can be effectively treated.
Spinal cord injury is often followed by increased pain perception. There is both immediate gross inflammation and chronic micro-inflammation.
Treatment with an NF-kB ‘decoy’ effectively blocks (inhibits) NF-kB activation, and was shown to improve outcome after spinal cord injury. Inflammation and pain were reduced, and an increase in GABA neurotransmitter was evidenced.
Brainstem dysfunction is favored in consideration of the diverse symptoms associated with the pain of migraine. Specifically, symptoms such as extreme sensitivity to lights and sounds most are most likely to originate in the brainstem.
The publication briefly summarized below suggests spreading inflammation of the trigeminal ganglion and associated structures as one possible means by which to account for both the pain and associated symptoms of migraine.
Neuropathic pain represents an often substantial component of the overall pain in fibromyalgia, and may result from NF-kappaB activation by cytokines, especially IL-8.
It is likely that pain in fibromyalgia syndrome is of several different types. Fibromyalgia patients not infrequently report burning, tingling or sometimes stabbing pain that is unique from the diffuse pain (“aching”) of fibromyalgia. Those unpleasant sensations are most often identified as neuropathic pain. Neuropathic pain is commonly thought to result from nerve damage, but the actual cause of neuropathic pain remains unknown.
How might neuropathic pain arise in fibromyalgia syndrome?
Inflammation is a key component of migraine, and can be observed in the trigeminal nerve and associated vasculature.
As the theory of what causes migraine has evolved, it is easy to neglect the fact that inflammation has always been seen as a key component of migraine pathology, regardless of whether the emphasis was on the blood vessels or the nerves.
The theory on the mechanism of action by which triptans work has also changed over the years. At first they were believed to work (and were in fact designed to work) primarily by constricting the vessels – as vessel dialtion was believed to be the source of pain in migraine.
More recently the triptans have been deemed to work by inhibiting the release of CGRP, and a new generation of CGRP inhibitors have been under development for some time. CGRP is a pro-inflammatory neuropeptide. To that extent, understanding of migraine pathology has again returned to inflammation.
In any case, ‘leaky’ blood vessels (plasma protein extravasation) are associated with migraine. Both the ergots and the triptans reduce extravasation.
While the publication briefly summarized below is somewhat dated, it nonetheless suggests inflammation, affecting the vessels, mediated through the trigeminal nerve – all of which is consistent with present day understanding of migraine, despite any change in ‘emphasis’ – past or present.
Migraine always has been and always will be a disease closely associated with inflammation.
Estrogen plus inflammation acts via trigeminal nerve to increase pain in TMJ and perhaps migraine.
The highest incidence of TMJ is observed in women between 20 and 40.
The authors note that TMJ is associated with estrogen. Their investigation concerned the possible mechanism by which estrogen might act as a risk factor in the development of TMJ.
They found that inflammation plus estrogen increased pain perception via the trigeminal nerve through a MAPK pathway.
The MAPK pathway does interact with NF-kB, but the primary point of interest here is the overlap with migraine. Migraine is also predominant in women (approximately two to three times as many women suffer with migraine as men.) Migraine is also most prevalent between ages 20 and 40. The trigeminal nerve is also central in migraine pain.
It may be that migraine and TMJ share, at least to some extent, the same underlying pathology.
Estrogen is generally anti-inflammatory and is considered ‘protective’ against certain conditions associated with inflammation (e.g. atherosclerosis.) Nonetheless, many of the conditions most closely associated with inflammation (e.g. autoimmune conditions) are far more common in women.
If the reason for this apparent paradox could be determined, it might be of great assistance in developing effective treatments for conditions associated with inflammation.
Unilateral head pain focused on frontal, orbital or parietal regions is a leading symptom of migraine attacks. Rarely, head pain in migraine can extend involving the maxillary or mandibular region of the face, sometimes isolated facial pain is the only and atypical presentation of migraine.
Inflammation initiated by nerve endings (neurogenic inflammation) can be observed on skin biopsy of those with fibromyalgia. It is now apparent that the role of peripheral nerve endings in fibromyalgia is much greater than previously thought.
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.
Blocking NF-kB in this model of neuropathic pain eliminated the pain stimulus.
In this study, mirtazapine (an anti-depressant) is found to inhibit NF-kB activation in the brain, thereby reducing inflammation and the mediators of inflammation in the brain.
