Category: Studies & Research

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Feasibility of Olive Oil for Reducing Facial Pain of Trigeminal Neuralgia

STUDY Feasibility of Olive Oil for Reducing Facial Pain of trigeminal neuralgia.
Brief Summary:
This is a 16-week non-blinded, parallel, controlled trial to determine the feasibility and potential efficacy of an olive oil dietary intervention to alleviate facial pain caused by trigeminal neuralgia type 1 (TGN).
Detailed Description:

Trigeminal neuralgia (TGN) pain is debilitating and unpredictable. Alleviation of intensity or frequency to any degree will improve the quality of life of the individuals affected. Current medical treatments for TGN are often not effective. In some cases, the pain is a result of myelin degeneration. If diet can provide the basic building blocks for myelin regrowth, then the investigators may be able to reduce facial pain by supporting the myelin nerve sheath.

Animal studies have shown that a dietary intervention with olive oil favorably impacts myelin but no human study has been conducted to date. The investigators propose undertaking a feasibility study to determine if a comparable intervention may work in a similar way in humans. If olive oil impacts myelin repair, then pain will be decreased by this dietary intervention and quality of life will be improved. However, it is not known if individuals with TNG will be able to consume a diet relatively high in olive oil. Feasibility will include testing the logistics of distributing the olive oil intervention to the study subjects, incorporation of olive oil into the participants’ daily diets, and online/distance monitoring of compliance and reporting of pain intensity, pain frequency, and quality of life. This feasibility study will lay the groundwork for potential future studies examining the efficacy of olive oil on alleviating facial pain caused by TNG and may provide data for a power analysis for a future interventional trial.

https://clinicaltrials.gov/ct2/show/NCT05032573?id=NCT05032573+OR+NCT05217628&draw=2&rank=2&load=cart

Olive Oil Information 

Recognized for its’ abundant health benefits, olive oil is being chosen by many consumers as a preferred form of fat in diets and is being recommended by nutritionists and health professionals as one of the best alternative oils to traditional fats and oils. Olive oil has great diversity in how it can be used as an ingredient in recipes and as a food-enhancer.

Olive trees originated in Asia, but are more commonly know as an agricultural product in Mediterranean countries. Olive oil comes from the process of pitting, grinding, and pressing of the olive fruit.

In countries where olive is most highly consumed – Italy, Greece, and Spain, the incidences of cardiovascular disease is low and this is attributed the health benefits olive oil provides. One tablespoon of olive oil contains 120 calories and 14 grams of fat. However, the fat in olive oil is primarily monounsaturated which, when consumed can help reduce blood cholesterol levels leading to improved cardiovascular function.

Other Health Benefits of Olive Oil:

  • Olive oil is beneficial as an antioxidant since it contains high levels of vitamin E.
  • When consumed, olive oil promotes digestion, stimulates metabolism, and lubricates mucous membranes (olive oil contains vegetable mucilage that helps protect the gastrointestinal tract).
  • Olive oil can aid in relieving constipation. Consuming 1 teaspoon of olive oil with lemon juice (preferably on an empty stomach) can promote proper bowel movements.
  • Olive oil for skin therapy. Olive oil can be added to dry skin acting like a moisturizer and can also be applied to nails to increase nail strength and to promote healthy cuticles.

How to Choose Olive Oil:

  • Explore how you can replace butter, margarine, and low quality vegetable oils in your cooking especially in preparing salads, sautéed dishes, and sauces.
  • Purchase olive oil that is labeled as“extra virgin”, which insures that the oil has been cold pressed. Cold pressed olive oil has been produced with freshly harvested olives and has gone through less processing and has not been degraded with heating or chemicals.
  • A good quality olive oil will be golden yellow in color versus lower quality olive oils that are light green in color.
  • Note: olive oil will congeal (form as a solid) in the refrigerator, but remains a liquid at room temperature.

When used in moderation, olive oil is a nutritious fat that promotes a great deal of health benefits. Like wines, olive oils will have differences in flavor depending on the region and producer of the oils. Olive oils can also be infused with herbs, garlic, peppers and other flavorful ingredients to add extra excitement to your dishes.

 

 

 

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FPA – New Life for Cancer Drug

  • Published October 11, 2021

New life for cancer drug that reprograms pain pathway to fight chronic pain

Chronic pain associated with nerve injury and chronic bone pain from metastatic cancer are unmet medical needs. This sober sentence vastly understates the crushing and devastating impact of these forms of pain on victims’ lives, their families, and their social and professional lives.

“I just can not sleep any more because turning in bed hurts, my spine hurts lying down, and sitting up to sleep hurts even more. During daytime, I have constant brain fog, interrupted by pain that within minutes gets worse (10-out-of-10) against a background of constant burning pain which gets worse toward the afternoon and evening. I hurt more when I go to the bathroom. The pain medication makes my brain fog worse, I feel like a zombie, I am badly constipated and itch all over.” That is how a patient with bone cancer pain feels. Testimony from victims of chronic nerve injury pain, through peripheral nerve damage from diabetes or medications, or in the aftermath of shingles, indicates that their lives are equally turned upside down from the pain.

New treatments against pain are needed. What is the desired profile ? “New drugs and other therapies against chronic pain need to be safe, i.e the fewer side effects the better, especially non-addictive and non-sedative, and effective. For example they should work against nerve injury pain and cancer pain, finally and practically, with minimal time to official drug approval. “Since chronic pain, like many chronic diseases, has an important root in genetic switches being reprogrammed in a ‘bad’ way, a disease-modifying treatment for chronic pain should reset the genetic switches, not just cover up the pain as with opioid and aspirin/tylenol-like painkillers,” says Dr. Wolfgang Liedtke, who practiced pain medicine for the last 17 years at Duke University Medical Center in Durham, NC, USA, and directed the former Liedtke-Lab to elucidate basic pain mechanisms. Dr. Liedkte moved to an executive position at Regeneron Pharmaceuticals in Tarrytown NY, in April 2021.

Liedtke’s Duke team, jointly with colleagues from University of California Irvine, tackled the problem by starting with a collection of “junkyard of cancer drugs”, 1,057 compounds originating from two Compound Libraries of the National Cancer Institute. Liedtke picked cancer drugs because a sizeable number of them influence epigenetic regulation of genes, which stops rapidly dividing cancer cells from dividing, but can reset maladaptive genetic switches in non-dividing nerve cells. In order to identify useful candidate anti-pain drugs from this starting pool, Liedtke’s team devised a screening method that relied on brain nerve cells from genetically-engineered mice that were “knockin” for a convenient reporter gene system so that compounds that enhance expression of an anti-pain target gene would generate a bio-luminescent signal which can be readily measured, allowing 1,057 compounds to be tested.

The selected anti-pain target gene was Kcc2 which encodes a chloride extruding transporter molecule, KCC2. KCC2 churns out chloride from nerve cells, low chloride means strong function of inhibitory neurotransmission, also in pain pathways, thus silencing the pain signal, or not allowing it to break through. In essentially all forms of chronic pain studied in experimental animals and also human spinal cord models, KCC2 disappears from the primary pain gate in the dorsal spinal cord. Liedtke’s team identified 137 first-round winners, i.e Kcc2 gene expression-enhancers, which then were retested iteratively, with a yield of four final co-winners. Kenpaullone was selected for work-up because the compound had a strong record of protecting nerve cells in human ALS models, also hearing and brain neurons from damage. In mice, Kenpaullone functioned effectively against pain caused by nerve constriction injury and by cancer cells seeding in the femur. Pain relief was profound, long lasting and with protracted onset, indicative of Kenpaullone impacting gene regulation.

Says Liedtke “At this stage, we knew we had met the basic requirement of our screen of shelved cancer drugs, namely identified Kcc2 gene expression-enhancers, and demonstrated that they are analgesics in valid preclinical pain models.” Thus encouraged, Liedtke’s team addressed whether Kenpaullone affected spinal cord processing of pain, with affirmative findings, then whether the pain-relaying nerve cells in the dorsal spinal cord can lower their elevated chloride, caused by nerve injury, by Kenpaullone treatment – again with resoundingly affirmative results. This was great news and prompted the investigators to query how exactly Kenpaullone works in nerve cells so that the Kcc2 gene is expressed stronger.

They discovered the underlying signaling mechanism, a key element of it completely new. Kenpaullone inhibits the kinase GSK3-beta which adds phosphate tags to other proteins which in turn switches their function powerfully. They found that the kinase target of GSK3beta is delta-catenin, delta-cat, which when phosphorylated is tagged for the cellular garbage bin. That means that chronic pain, via activation of GSK3-beta leads to loss of delta-cat in pain relaying neurons. What is the original function of delta-cat in relation to pain relay, and in relation to gene expression of Kcc2 ?  Liedtke’s team found that non-phosphorylated delta-cat transfers into the cell’s nucleus and binds to the Kcc2 gene’s DNA in its promoter region, where it switches back on the switched-off Kcc2 gene. To prove the relevance of this pathway for pain, they devised a gene-therapeutic approach so that phosphorylation-resistant delta-cat becomes the payload of an AAV9 gene-therapy viral vector, which infects spinal cord dorsal horn neurons. Injection of this gene therapy vector into the cerebrospinal fluid of mice was similarly analgesic as Kenpaullone.

These findings suggest that Kenpaullone and similarly-acting kinase-inhibitory compounds, also delta-cat gene therapy can become new tools in our toolbox against chronic “refractory” pain, also caused by nerve injury, also caused by cancer bone pain, likely against other forms of chronic pain where Kcc2 is not expressed well (trigeminal pain), and possibly other neurologic and psychiatric disorders where this mechanism appears to contribute to disease.

Amidst Duke co-authors, 1st author Dr. Michele Yeo successfully elucidated basic regulation of the Kcc2 gene together with Liedtke for more than a decade and ran the 1,057 compound screen, co-first author Dr. Yong Chen provided skillful animal experimentation, and co-senior author Dr. Ru-Rong Ji (Director of Translational Pain Research) and his team covered dedicated assessment of spinal cord relay mechanisms. Collaboration with Dr Jorge Busciglio’s laboratory at UC Irvine was key to validate human relevance of Kenpaullone.

Summary Figure
Upper right “Junkyard of cancer” drugs were screened, akin to sieving through sand, looking for gold nuggets. Kenpaullone was identified as a “winner”, capable of switching on the Kcc2 gene, which previous research predicted to be beneficial for chronic pain.
Upper left Nerve injury pain and bone cancer pain are serious and pressing unmet medical needs. Preclinical models were used totest Kenpaullone which proved to be highly effective in both.
Middle panels, left-hand Nerve injury by constriction or cancer cells populating a bone activates GSK3ß, an enzyme that tags other proteins with phosphate. In nerve cells dedicated to pain relay in the spinal cord, GSK3ß tags d-catenin
(d-CAT), which routs d-CAT to the cellular garbage bin. Without d- CAT in the cells’ nucleus, the Kcc2 gene remains switched off. This in turn makes the pain relay neurons run full of chloride which makes them electrically more jittery, with chronic “refractory” pain a result.
Right-hand panel Treatment with Kenpaullone inhibits GSK3b’s phosphate-tagging capability, so that d-CAT becomes untagged, which clears the way to the nerve cells’ nucleus. There it binds to the DNA region of the Kcc2 gene critical for switch-on or switch-off, the promoter. By binding there, d- CAT reverts the switch-off to switch-on and the Kcc2 gene is running again, making KCC2 protein. KCC2 in turn pumps chloride ions out of the pain-relay nerve cells, making them electrically more stable. This leads to circuit repair and pain relief, based on resetting of the genetic switches. Instead of Kenpaullone, d-CAT can serve as payload of a gene therapy approach that directs expression of d-CAT and hence KCC2 to pain relay nerve cells in the spinal cord.

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Magnetic Therapy for Trigeminal Neuralgia

Magnetic Therapy – can it form part of a trigeminal neuralgia pain Treatment Plan?

This article is for information and education purposes – we do not recommend individual treatment – always consult your medical team to evaluate the best course of treatment for your circumstances.

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Pulsed Electromagnetic Field Energy

Pulsed Electromagnetic Field (PEMF) Therapy is non-static, unlike therapy with standard magnets, which are constant or static. To create a PEMF, an electrical current is introduced into a looped wire thereby creating a magnetic field. The electrical current is then activated and then deactivated in cycles between one time per second to thousands of times per second. The cycles and frequencies are dependent upon the unique design of any particular PEMF Device.

 In main stream western medical communities, Pulsed Electromagnetic Field Therapy is utilized in the two following ways:

  1. A specially engineered version of PEMF known as repetitive transcranial magnetic stimulation (rTMS) is designed specifically to treat the brain with low-frequency magnetic pulses. This special form of electromagnetic therapy is undergoing additional studies, and many of these studies indicate that rTMS might be beneficial for depression. It is also being studied for the treatment of Parkinson’s disease, epilepsy, schizophrenia, and obsessive-compulsive disorder.

  2. PEMF Therapy has been used to stimulate bone repair in non-union (the broken bone ends do not join together) and other fractures since the 1970’s. This is the specific use that has been approved by the FDA.

Studies using PEMF have shown great promise for other conditions, such as, healing soft-tissue wounds by suppressing inflammatory responses at the cell membrane level, alleviating pain, and increasing range of motion. Interestingly, vision, an area that is still undergoing study, has been shown to improve in some instances through PEMF.  At this time, PEMF is being investigated for its effect on osteoarthritis, stress, incontinence, migraines and a host of other conditions

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QMAGNETs – Neuromagnetics Australia Pty Ltd PO Box 5238 Cranbourne, VIC 3977 AUSTRALIA

Phone: From Australia only phone freecall – 1800 Qmagnets or 1800 762 463

Magnetic therapy is applying static magnets that produce a therapeutic magnetic field for pain relief and recovery for a variety of issues.

Today many people use magnet therapy for pain management. Health professionals such as physiotherapists, acupuncturists, massage therapists, chiropractors, neurologists, nutritionists, sports performance trainers, vets and rehabilitation centers might be surprised with the latest advancements in magnetic therapy.

Painaustralia estimated 3.24 million (~16%) Australians were living with chronic pain in 2018. In United States in 2016, an estimated 20.4% of adults had chronic pain. These studies also point to unhealthy treatment practices. Clinical trials have shown that magnetic therapy can benefit a number of painful conditions, therefore it should definitely be considered and is worthy of further research.

This article, covers the basics of magnetic therapy and will assist readers to understand what kind of magnetic therapy is the most effective. If you’re a home user, you’ll get a fair idea of how to assess magnetic therapy products and get a better understanding of magnetic therapy. Professionals will get an in-depth insight into how it works and what are the current advancements in magnetic field therapy.

What are the benefits of magnetic therapy? read the full article HERE

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Links to Magnetic therapy providers – we are not affiliated with any of these providers

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Medical Definition of Magnet therapy

Reviewed on 3/29/2021

Magnet therapy: Magnetic therapy, also called magnetic field therapy and bioenergy therapy, is an alternative therapy that uses magnets of varying sizes and strengths that are placed on the body to relieve pain and treat disease. Thin metal magnets are attached to the body alone or in groups. They can be worn as bracelets or necklaces, attached to adhesive patches to hold in place, placed in bands or belts to be wrapped around the wrist, elbow, knee, ankle, foot, waist, or lower back. Also available are magnetic insoles, blankets, and slumber pads. These magnets may be worn for just a few minutes or for weeks, depending on the condition being treated and the practitioner.

Proponents state the magnetic fields produced from the negative pole of the magnet have healing powers. Negative magnetic fields are thought to stimulate metabolism, increase the amount of oxygen available to cells, and create a less acidic environment within the body. Conditions diagnosed or treated include arthritis, cancer, circulatory disorders, diabetic neuropathy (nerve disease), fibromyalgia, HIV/AIDS, immune dysfunction, infection, inflammation, insomnia, multiple sclerosis, muscle pain, neuropathy, pain, rheumatoid arthritis, sciatica, stress and to increase energy and prolong life.

Although there are anecdotal reports of healing with magnetic therapy, available scientific evidence does not support these claims. The U.S. Food and Drug Administration (FDA) considers magnets harmless and of no use for medical purposes.

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Below are various studies referencing Magnetic Therapy for Trigeminal Neuralgia

 

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MLS Treatment Therapy

So what is MLS Treatment Therapy, and how can it help sufferers of trigeminal neuralgia?

What is a Multi Wave Locked System?

The Multiwave Locked System (MLS®) is a new patented LLLT system that combines 905nm pulsed emissions with 808nm continuous emissions.I

It was developed by ASA Laser to help overcome some of the limitations on previous LLLT systems. The aim is to produce simultaneous actions on pain, inflammation and oedema. With the MLS® system it is possible to achieve strong anti-inflammatory, anti-oedema and analgesic effects simultaneously and in a short period of time.

The unique synchronised laser beam delivers a balance of the two wavelengths and powers providing safe and effective delivery. The optical design of the delivery system transfers energy up to 3 – 4 cm deep to effect tissue at a cellular level. The synchronised wave results in a synergistic effect where both the analgesic and anti-oedema effects are greater than if two single lasers had been used.

Research suggests for lasting effects from MLS Laser you will likely require 5-6 treatments depending on how your condition responds. Often you will experience a noticeable improvement after just 2 treatments.

For further information about the technology please See Here

This technology has been utilised for a number of years and research has been undertaken  Successful treatment for neuropathic pain with MLS®: a case study.

Some clinics use different terminology, however the MLS is used to deliver the treatment.

How does it work?

MLS Laser Therapy is a medical breakthrough therapeutic device with unparalleled applications and treatment outcomes. The laser works by converting light into biochemical energy, resulting in normal cell function, which causes symptoms (PAIN) to reduce significantly.

The primary biological action of PBM (MLS) Therapy results from stimulation of cellular transport mechanisms in the mitochondria, cell membranes and epithelial tissues. This action causes the release of vasodilating chemicals, the stimulation of DNA and RNA (building blocks) synthesis, an increase in enzyme production, normalisation of tissue Ph and increased ATP production (healing of the cells from the inside).

 

10 BENEFITS OF MLS LASER THERAPY

  1. Anti-inflammatory: MLS Laser Therapy has anti-oedema effect as it causes vasodilation, but also because it activates the lymphatic drainage system which drains swollen areas. As a result, there is reduction in swelling caused by bruising or inflammation.
  2. Analgesic: MLS Laser Therapy has a beneficial effect on nerve cells, it blocks pain transmitted by these cells to the brain which decreases nerve sensitivity.  Also, due to the decreased inflammation, there is less oedema and less pain.  Another pain blocking mechanism involves the production of high levels of pain killing chemicals such as endorphins and enkephalin from the brain and adrenal gland.
  3. Accelerated Tissue Repair and Cell Growth: Photons of light from the laser penetrate deeply into tissue and accelerate cellular reproduction and growth.  The laser light increases the energy available to the cell so the cell can take on nutrients faster and get rid of waste products.  As a result of exposure to laser light, cells are repaired faster.
  4. Improved Vascular Activity: Laser light will significantly increase the formation on new capillaries in damages tissue which speeds up the healing process, closes wounds quickly and reduces scar tissue.  Additional benefits include acceleration of angiogenesis, which causes temporary vasodilation and increase in the diameter of blood vessels.
  5. Increases Metabolic Activity: MSL Laser Therapy creates higher outputs of specific enzymes, greater oxygen and food particles loads for blood cells.
  6. Trigger Points and Acupuncture Points: MLS Laser Therapy stimulates muscle trigger points and acupuncture points on a non-invasive basis providing musculoskeletal pain relief.
  7. Reduced Fibrous Tissue Formation: MLS Laser Therapy reduces the formation of scar tissue following tissue damage from cuts, scratches, burns or surgery.
  8. Improved Nerve Function: Slow recovery of nerve functions in damaged tissue can result in numbness and impaired limbs.  Laser light speeds the process of nerve cell reconnection and increase the amplitude of action potentials to optimise muscle healing.
  9. Immuno-regulation:Laser Light has a direct effect on immunity status by stimulating immunoglobulins and lymphocytes.  Laser emissions are absorbed by chromophores (molecule enzymes) that react to laser light.  Upon exposure to the laser, the enzyme flavomononucleotide is activated and starts the production of ATP (adenosine-triphosphate), which is the major carrier of cell energy and the energy source for all chemicals reactions in the cells.
  10. Faster Wound Healing: Laser light stimulates fibroblast development in damaged tissue. Fibroblasts are the building blocks of collagen, which is the essential protein required to replace old tissue or to repair tissue injuries.  As a result, Laser Therapy is effective post surgically and in the treatment of open wounds and burns.

An interesting  in depth article covering every thing you need to know about MLS laser treatment in America, the history, the believers, the skeptics, the medical profession, the politicians and the people who use it

 Does it really work – blog

Pain clinics around Australia are now using this technology see below for examples – please note we do not recommend providers and suggest you discuss any new treatment options with your medical practitioners.

Introducing MLS Laser Therapy The first of its kind on the Central Coast

 

MLS Laser Therapy

Latest Technology

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Emergency Department – Break-through Trigeminal Neuralgia Pain

This week the Association launched our Emergency Department plastic wallet cards – to assist sufferers with communicating when attending a hospital emergency department with break-through trigeminal neuralgia pain

The following study highlights why this is such an important issue – and very relevant to all of our sufferers

Treatment of acute exacerbations of trigeminal neuralgia in the emergency department: A retrospective case series

Affiliations

  • 1Department of Neurology, Centro Hospitalar Universitário de São João, Porto, Portugal.
  • 2Department of Clinical Neurosciences and Mental Health, Faculty of Medicine, University of Porto, Porto, Portugal.

Abstract

Objective: To evaluate the response to treatment of acute trigeminal neuralgia (TN) exacerbations in the emergency department (ED).

Background: TN is characterized by recurrent and intense pain paroxysms. Some patients experience severe acute exacerbations requiring ED presentation. The optimal management of these episodes is not well established.

Methods: We present a case series of TN exacerbations in adults who presented to the ED of a tertiary centre from January 2008 to December 2020. We analysed demographic and clinical data, including pharmacological management in the ED. The primary outcome was pain relief, classified into “no relief,” “partial relief,” and “satisfactory relief” based on the qualitative description in the ED’s records.

Results: Ultimately 197 crisis episodes corresponding to 140 patients were included. Most were women (61%, 121/197) with a median age of 63 years (interquartile range: 52-73). Acute TN exacerbations were treated with opioids in 78% (108/139) of crisis episodes, nonsteroidal anti-inflammatory drugs in 42% (58/139), corticosteroids in 21% (29/139), intravenous phenytoin in 18% (25/139), and intravenous lidocaine in 6% (8/139). Of the 108 cases treated with opioids, 78 (72%) required additional drugs for pain management. Intravenous phenytoin allowed satisfactory pain relief in 64% of cases.

Conclusion: In our sample, opioids were the most used therapeutic approach in acute TN exacerbations despite their low efficacy and subsequent need for further drug treatment in most cases. Most crisis episodes managed with intravenous phenytoin reached total pain relief. Prospective studies are needed to guide the treatment of acute exacerbations of TN.

Keywords: emergency department; exacerbation; lidocaine; opioids; phenytoin; trigeminal neuralgia.

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References

REFERENCES

    1. Melek LN, Devine M, Renton T. The psychosocial impact of orofacial pain in trigeminal neuralgia patients: a systematic review. Int J Oral Maxillofac Surg. 2018;47(7):869-878.
    1. van Hecke O, Austin SK, Khan RA, Smith BH, Torrance N. Neuropathic pain in the general population: a systematic review of epidemiological studies. Pain. 2014;155(4):654-662.
    1. Zakrzewska JM, Wu J, Mon-Williams M, Phillips N, Pavitt SH. Evaluating the impact of trigeminal neuralgia. Pain. 2017;158(6):1166-1174.
    1. Headache Classification Committee of the International Headache Society (IHS). The International Classification of Headache Disorders, 3rd edition. 2018;38(1):1-211.
    1. Lambru G, Zakrzewska J, Matharu M. Trigeminal neuralgia: a practical guide. Pract Neurol. 2021;21(5):392-402.
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How Intractable Pain Causes Brain Tissue Loss

By Dr. Forest Tennant, PNN Columnist -August 09 2

The brain not only controls pain but the endocrine, cardiovascular, metabolic, respiratory and gastrointestinal systems. Any or all of these biologic systems may malfunction if there is brain tissue loss.

Beginning in 2004, brain scan studies began to document that brain tissue loss can be caused by intractable pain. Today, almost 20 years later, this important fact appears to be either unknown or a mystery to both the public and medical professionals.

Basic science researchers have unravelled the complex process of how and why this pathological phenomenon may occur. A good understanding of how this pathology develops is critical to properly care for and treat persons who develop intractable pain whether due to a disease or an injury.

What Causes Tissue Loss?

Tissue loss anywhere in the body is caused by inflammation, autoimmunity, or loss of blood supply due to trauma or disease. The brain scan studies done since 2004 that documented brain tissue loss were not done in persons who had a stroke or head trauma, but in pain patients experiencing inflammation and autoimmunity (i.e., collagen deterioration). It turns out that both biologic mechanisms may operate to cause brain tissue loss in intractable pain patients.

In the pursuit of understanding brain tissue loss and its accompanying malfunctions, it has been discovered that the brain and spinal cord (central nervous system or CNS) contain cells called microglia. They are closely akin to the immune protective cells in the blood stream which are called a “lymphocytes.”

The microglia in the CNS lay dormant until a harmful infection, toxin or bioelectric magnetic signal enters its domain, at which time it activates to capture and encapsulate the danger or produce inflammation to destroy the offender.

If the microglia are overwhelmed by some danger, such as a painful disease that isn’t cured, it produces excess inflammation that destroys some brain tissue which can be seen on special brain scans. Some viruses such as Epstein Barr may hibernate in microglia cells and create an autoimmune response, which magnifies inflammation and brain tissue loss.

Intractable pain diseases such as adhesive arachnoiditis (AA), reflex sympathetic dystrophy (CRPS/RSD), and genetic connective tissue diseases such as Ehlers-Danlos syndrome may incessantly produce toxic tissue particles and/or bioelectromagnetic signals that perpetuate microglial inflammation, tissue loss and CNS malfunctions.

This is the reason why proper pain management must have two targets: the pain generator and CNS inflammation.

How To Know You Have Lost Brain Tissue

If your pain is constant and never totally goes away, it means you have lost some brain tissue and neurotransmitters that normally shut off pain. If you have episodes of sweating, heat or anxiety, you probably have inflammation that is flaring. Naturally, if you feel you have lost some reading, calculating or memory capacity, it possibly means you have lost some brain tissue. MRI’s may also show some fibrous scars.

Fortunately, studies show that if a painful disease or injury is cured or reduced, brain tissue can regenerate. While we can’t guarantee that brain tissue will be restored, we offer here our simple, immediate and first step recommendations using non-prescription measures.

First, do you know the name and characteristics of the disease or injury that is causing your pain? Are you engaging in specific treatments to reduce or even cure your disease, or are you simply taking symptomatic pain relief medications?

Start at least two herbal-botanical agents that have some clinical indications that they reduce inflammation in the brain and spinal cord: serrapeptase – palmitoylethanolamide (PEA) and astragalus-curcumin-luteolin-nanokinase. You can take different agents on different days.

Increase the amount of protein (meat, fish, poultry, eggs) in your diet. Consider a collagen supplement. Limit starches and sugars.

Start taking these vitamins and minerals:

  • Vitamin C – 2,000mg in the AM & PM

  • Vitamin B-12, Vitamin D

  • Minerals: Magnesium and selenium

We recommend vitamins daily and minerals 3 to 5 days a week.

The above will help you stop additional tissue loss and hopefully regenerate brain tissue.

Forest Tennant, MD, DrPH, is retired from clinical practice but continues his research on the treatment of intractable pain and arachnoiditis. This column is adapted from bulletins recently issued by the Arachnoiditis Research and Education Project and the Intractable Pain Syndrome Research and Education Project.

The Tennant Foundation gives financial support to Pain News Network and sponsors PNN’s Patient Resources section.

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Vitamin D Deficiency Linked to Chronic Inflammation

We are always interested in research which can show what conditions may cause chronic inflammation

Australian Center for Precision Health, University of South Australia Cancer Research Institute,
Adelaide, Australia, 2
South Australian Health and Medical Research Institute, Adelaide, Australia and 3
Population, Policy and Practice, UCL Institute of Child Health, London, UK
*Corresponding author. Australian Center for Precision Health, University of South Australia Cancer Research Institute,
GPO Box 2471, Adelaide, SA 5001, Australia. E-mail: Elina.Hypponen@unisa.edu.au
Received 14 December 2021; Editorial decision 29 March 2022; Accepted 8 April 2022

 

Abstract
Background: Low vitamin D status is often associated with systemic low-grade inflam-
mation as reflected by elevated C-reactive protein (CRP) levels. We investigated the cau-
sality and direction of the association between vitamin D status and CRP using linear and non-linear Mendelian randomization (MR) analyses.

Methods: MR analyses were conducted using data from 294 970 unrelated participants
of White-British ancestry from the UK Biobank. Serum 25-hydroxyvitamin D [25(OH)D] and CRP concentrations were instrumented using 35 and 46 genome-wide significant variants, respectively.

Results: In non-linear MR analysis, genetically predicted serum 25(OH)D had an L-shaped
association with serum CRP, where CRP levels decreased sharply with increasing
25(OH)D concentration for participants within the deficiency range (<25 nmol/L) and lev-
elled off at – 50 nmol/L of 25(OH)D (Pnon-linear ¼ 1.49E-4).

Analyses using several pleiotropy-robust methods provided consistent results in stratified MR analyses, con-
firming the inverse association between 25(OH)D and CRP in the deficiency range
(P ¼ 1.10E-05) but not with higher concentrations. Neither linear or non-linear MR analysis supported a causal effect of serum CRP level on 25(OH)D concentration (Plinear ¼ 0.32 and Pnon-linear ¼ 0.76).
Conclusion: The observed association between 25(OH)D and CRP is likely to be caused by vitamin D deficiency.

Correction of low vitamin D status may reduce chronic inflammation.
Key words: Non-linear Mendelian randomization, vitamin D, serum 25-hydroxyvitamin D concentration, C-reactive
protein, chronic inflammation

 

The full study can be read below

Vitamin D deficiency and C-reactive protein: a bidirectional Mendelian randomization study
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Factors that may affect recurrence of trigeminal neuralgia after percutaneous balloon compression

Most sufferers with trigeminal neuralgia have heard of the surgical treatment, Microvascular Decompression (MVD for short), but fewer know about percutaneous balloon compression.

I can speak from first-hand experience of both procedures, and of the success with the latter. That is, I remain pain and medication free after five and a half years since a simple and fast balloon compression procedure crushed my trigeminal nerve.  But I have always wondered and worried that the pain may return. To date I am extremely happy with the situation as are others I know who have undertaken this procedure.

The article ‘Factors that may affect recurrence of trigeminal neuralgia after percutaneous balloon compression’, was researched and written by Wenming Lv,  Wenjing Hu, Lingyi Chi, and Liangwen Zhang and published in Journal of Clinical Neuroscience Volume 99, May 2022, Pages 248-252, can be read here

If you are considering asking for a Balloon Compression procedure, be aware there are risks and side-effects and that your research should be thorough. You need to trust that your neurosurgeon has considerable experience with this procedure, and has informed you of all aspects.

One of the possible side-effects about which I was warned, was that I might have some or a lot of facial numbness on the affected side of my face.  I did have numbness on half an eyelid, half my nose and half the top of my upper lip. In the above article the finding was that numbness, on average, disappeared around three years.  That is about right for me, although on rare occasions in the past couple of years I have a sense of it in my upper lip and nose.  I am delighted to report that the numbness never caused my face to slump or change and has never been visible, it has always been mild, and it has never inconvenienced me.  Having said this, each person is different and the results for another could be dramatically different – so please gather all information from a knowledgeable professional if considering this.  For me, losing the pain and reliance on medication was worth some numbness. I was fortunate to be able to reclaim my life.

Helen Tyzack

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Trigeminal Neuralgia Research – The Facial pain Research Foundation

YouTube Trigeminal Neuralgia: The Facial Pain Research Foundation – Kim Birchiel MD

Research is happening around the world to better understand Trigeminal Neuralgia and this foundation has nine research programs ongoing

The Facial Pain Research Foundation – it’s time to find a cure! (facingfacialpain.org)

In Search of a Cure: Finding the Genes that Predispose to Trigeminal Neuralgia

A compressed trigeminal nerve is sometimes the reason why a patient suffers. However, it’s a fact that many people, if imaged, would present a similar compression, but experience no pain. Why? That question inspired our scientists to hypothesize there is a genetic predisposition to TN. Their plan is to find these defective genes in TN sufferers, which could then provide targets for designing customized drugs or gene therapy. For their analysis, they collected DNA samples from nearly 1,000 patients at seven US locations, one in Canada, and one in the UK. Their findings from this analysis may unlock the mystery of why some people suffer, and so many others do not.

Investigators:
Scott Diehl, Ph.D.
Kim Burchiel, M.D.
Ze’ev Seltzer, BMS, DMD

Towards Gene Therapy for Trigeminal Neuralgia

The primary goal of this project, led by Dr. Todd Golde at the University of Florida, is to identify a novel gene therapy approach to treat and cure TN and related neuropathic pain. Gene therapies rely on a modified viral vector to enable delivery of the genetic “payload” to cells. In this case, the viral vector is, in essence, the “shuttle” that enables the payload to be delivered to the nerve. There are many potential genetic “payloads” that might be used to dampen or block pain signaling in the nerve. Our team’s research involves systematically evaluating various viral vector shuttles, and various delivery methods. In addition, they will generate payloads that suppress pain signaling by either knocking out (CRISPR mediated gene silencing), or reducing the level (miRNA based antisense approaches) of factors important in pain signaling.

Investigators:
Todd Golde, M.D., Ph.D.
Robert Caudle, Ph.D.
Yona Levites, Ph.D.
John Neubert, DDS, Ph.D.

Identifying Sensory Genes That Are Critical to Neuropathic Pain, Including Trigeminal Neuralgia

We believe we still don’t know all of the elements responsible for the initiation of Trigeminal Neuralgia pain. The question is which genes are critical and can these be selectively regulated to manage TN, but, to date, the focus of the field has been on a relatively small number of genes.  Dr. Allan Basbaum is examining a relatively large number, and wider variety of, genes using the “one gene at a time” approach. This study was prompted to a great extent by his team’s comprehensive analysis of a dorsal root ganglion (DRG) from intact and nerve-injured mice. This analysis identified almost 1200 genes that affected pain after the injury. To prioritize genes for future study as causing TN, they chose some that have been reported repeatedly in the scientific literature, genes that showed the greatest change in expression after injury, and the so-called dark genes which until recently have largely been ignored. The plan is to identify the genes that impact TN, and then create or find the therapies needed to “manage or fix” them to end the pain.

Investigator
Dr. Allan Basbaum, Ph.D.

Mapping Towards a Cure: Finding the Brain Signature Centers that Cause Trigeminal Neuralgia

Led by Dr. John Neubert at the University of Florida, our team of researchers hypothesized that specific neural centers in the brain and spinal cord are active prior to, and during, a TN attack, essentially “lighting up” with activity. These neural centers hold the key to providing pain relief, as they give us a specific area to target for curative treatments- if we can block these centers, we can prevent the pain. Using highly advanced magnetic resonance imaging, our team has scanned over 60 TN patients, and located what we believe are the “pain centers” of TN patients.

Investigators:
John Neubert, DDS, Ph.D.
Marcello Febo, Ph.D.
Mingzhou Ding, Ph.D.
Robert Caudle, Ph.D.

Evaluation of a Cellular Therapeutic for the Treatment of Trigeminal Pain

Neurona Therapeutics is a pre-clinical stage biotechnology company that was founded by four leading-edge neuroscientists and stem cell pioneers at The University of California, San Francisco. Led by Dr. Cory Nicholas, Ph.D., Neurona has formed a strategic research collaboration with the Facial Pain Research Foundation, to develop a human inhibitory interneuron therapeutic (neuro-stem cells) for the treatment of neuropathic pain conditions like TN.  As an example of the unique collaboration we foster between our scientists, our researchers at The University of Florida are providing the animal subjects to test whether Neurona’s neural stem-cells can stop neuropathic facial pain in animals. If successful, we will then move to human trials.

Investigators:
Dr. Cory Nicholas, Ph.D.
Dr. John Neubert, Ph.D.
Dr. Allan Basbaum, Ph.D. 

Determining Efficacy of CODA ‘Switch’ Receptors in a Model of Neuropathic Pain

CODA Biotherapeutics, Inc., is a preclinical-stage biopharmaceutical company developing a gene therapy to stop TN. Led by Dr. Orion Keifer, CODA has formed a strategic research collaboration with the Facial Pain Research Foundation, with the goal of utilizing CODA’s chemogenetic gene therapy platform to identify and develop potential new therapies and cures for Trigeminal Neuralgia, and related neuropathic pain. Under the collaboration, CODA is working with the FPRF to establish a research continuum that is dedicated to identifying the mechanisms underlying neuropathic facial pain and to developing groundbreaking therapeutic strategies that aim to permanently stop the pain.

Investigators:
Orion P. Keifer, Jr., M.D., Ph.D.

Cholesterol Homeostasis in Peripheral Nerve Myelin with a Focus on Statins

The aim of this research, led by Dr. Lucia Notterpek, Ph.D., was to prove that unhealthy and/or damaged myelin- the protective coating of nerves- is the reason why some patients have TN pain. We have confirmed this in animal subjects, and treatments to stop their pain by repairing this damaged myelin have been successful. We hope to achieve this in humans organically, through dietary supplements, rather than with medications, and believe this will be an effective therapy for those who’ve developed TN as a result of myelin-related causes.

Investigators:
Dr. Lucia Notterpek, Ph.D.
Dr. Susan Percival, Ph.D.
Dr. Wendy Dahl, Ph.D.

Exploring Neuropeptide Guided Botulinum Light Chain for Use in Blocking Pain Transmission

The overall long-term goal of this project is to begin a search for new, novel, pain control therapies to supplant highly addictive opioids.  Dr. Rob Caudle at the University of Florida has chosen botulinum toxins as his therapeutic agent, which have already proven very successful in treating migraine headaches.  However, he has modified these toxins with a unique research approach. The newly created substances are directed to the appropriate sensory neurons, which Dr. Caudle and his team have identified, where they are internalized, and disrupt neurotransmission- the result of which, is the inhibition of pain.

Investigators:
Robert Caudle, Ph.D.

The Role of TMD in the Diagnosis of Trigeminal Neuralgia

There is considerable confusion regarding the diagnosis of TMD (Temporomandibular Disorder), and because of the lack of good diagnostic tools, many TMD patients end up being referred to neurologists and neurosurgeons as TN patients. Since there is significant symptom overlap between the two conditions, some of these TMD patients end up being mistakenly treated for TN.

The study will quantify how often TMD patients are mistakenly referred as TN patients. It will determine how many patients fit the diagnostic tools for both TN and TDM, and will define new diagnostic tools that will correctly predict a TMD patient. The result being a new protocol to screen oral facial pain patients for TMD suspects. The benefit of this work will be that TMD patients will be less likely to be treated for TN, and TN patients less likely to be treated for TMD because of an overlap in symptoms and the lack of good diagnostic tools.

Investigator
Kim Burchiel, M.D

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A research on quality of life score (QOLS) of patients with trigeminal neuralgia

A research on quality of life score (QOLS) of patients with trigeminal neuralgia

When I visit my medical professionals they always ask questions in order to be sure of the diagnosis, and to be sure the treatment they recommend is appropriate to me personally.

I have discovered the following article which may interest you.

While it contains scientific language and in parts may be difficult to work through, you can read at the end before the list of references, a list of questions with the words for a five point rating system. There are some questions on that list that I am going to remember so when I visit my GP or Neurologist or Neurosurgeon I need to provide the answers, even if not asked – because I believe it may make a difference and help them help me.  Perhaps you might feel this way.

The article, ‘A research on quality of life score (QOLS) of patients with trigeminal neuralgia (TN)’ written by Yejiao Luo, Mingjie He, Chenjun Li, and Hongya Yang and published in the

Journal of infection and Public Health Vol. 12 Issue 5  September–October 2019, Pages 690-694,

Quality of life research

Article by Helen Tyzack