Joint instability as the cause of nerve pain – Treatment of neuralgia
Ross Hauser, M.D.
Joint instability and ligament injury are almost always the missing diagnoses to problems of chronic nerve pain from a musculoskeletal cause. Even in patients with nerve pain from such conditions as neuritis, neuroma, nerve entrapments, neuralgia, and unusual nerve syndromes. Nerves alert the brain of the presence of an injury or problem because they themselves are either being inflamed or undergoing neurogenic inflammation; entrapped or experiencing compression by nearby bone or myofascial tissue; or encountering excessive stretch.
When a person moves, they are generally not aware that all tissues of the body are stretching a little bit, including nerves, without sustaining any damage. Once a nerve is compressed or its ability to stretch compromised, it starts shooting off pain signals. These pain signals can occur from the small nerves within the ligaments or joint capsule themselves, nerves that innervate the ligaments and joints, or nerves being affected by the long-term manifestations
of unresolved joint instability.
As in other chronic painful conditions, patients seek all sorts of suppressive, ablative, or surgical therapies for relief of nerve irritations not realizing that these treatments are actually causing more harm than good. It is often not understood that ALL pain has a nerve component. As in other sensations, pain is carried by nerves to the central nervous system ultimately to be interpreted and experienced by the brain. To understand how treatments can resolve, correct, decompress, and cure, the various nerve pain disorders, it is necessary to provide an overview understanding that pain comes from four different sources. Once you understand this key concept, it is very simple to understand why the curative treatment of nerve pain must be in the realm of regenerative injection therapies as these treatments may resolve neurogenic inflammation, nerve entrapment, and the excessive stretching of nerves by tightening ligaments and restoring joint stability, whether directly or indirectly.
The four primary causes of almost all painful conditions are an excessive stretch of a primary ligament, the many harmful effects of joint instability, neurogenic inflammation, and nerve entrapment.
1. Ligament laxity
2. Manifestations of joint instability
3. Neurogenic inflammation
4. Nerve entrapment
Damaged ligaments are why we have pain
While ligaments are predominantly known as the stabilizing agents of the joints, they hold the bones in place as they attach bone to bone, they have an equally important role as a sensory organ for the joint. They contain many nerve endings (called Ruffini, Pacician, and Golgi free-nerve endings) that are very sensitive to stretch. The brain is notified if they (or the joint) are under too much tension. If the tension is too great, then they stimulate muscle contraction via the ligamento-muscular reflex. The muscles contract (spasm) to preserve joint stability. The sharp pain experienced during activity or trauma is from the ligament being stretched too much, but the low-level long-term pain is from chronic muscle spasms.
What are we seeing in this next image? “Receptors of the knee joint are able to produce a discriminating afferent inflow to the central nervous system (CNS), thereby contributing to the protection and function of the joint through the musculature.”
Location of the various ligament joint receptor types demonstrated for the knee joint and a schematic representation of the four types of ligament joint receptors. The Type I, Type II, and Type III receptors are mechanoreceptors. Type IV receptors are nociceptors. What does this mean? It means that the nerves in your knee talk to the muscles to make it function and the nerves in your knee talk to the brain, by way of causing pain, that your knee is hurt.
Let’s get an explanation from a 1991 paper (1) titled: “Neuroreceptors in the tissues of the knee joint.” It comes from the Department of Anatomy, Louisiana State University Medical Center.
- “Ruffini endings, Pacinian corpuscles, and free nerve endings are most prevalent in the fibrous joint capsule; (Note: The fibrous joint capsule describe all the soft-tissue in the knee that makes it work, the knee ligaments, the knee tendons, the bursa, the articular cartilage, the meniscus, and the fascia) the Golgi tendon organs are most common in the collateral and cruciate ligaments and the menisci. (Note: The Golgi tendon organs in your everyday life allow the muscles to stretch and then stretch further without the muscles’ protective spasm response being initiated. The Golgi tendon organs act as “stretch managers).
- In the anterior and posterior cruciate ligaments (ACL, PCL), receptors are concentrated at the tibial and femoral attachments of the ligaments. In the menisci, neural elements penetrate the horns and the outer and middle thirds of the body. Ruffini mechanoreceptors are believed to contribute mainly to the maintenance of muscle tone, Pacinian corpuscles, and Golgi tendon organs are stimulated during movement, and free nerve endings are nociceptors.
- Thus, receptors of the knee joint are able to produce a discriminating afferent inflow to the central nervous system (CNS), thereby contributing to the protection and function of the joint through the musculature.”
A 2021 study published in the journal Arthroscopy, Sports Medicine, and Rehabilitation (2) cited this 1991 article in its own presentation of creating a neuro mapping of the knee including the isolation and understanding of the anterior (ACL) and posterior cruciate ligaments (PCL) messages to the muscles and brain among other structures.
The many painful effects of joint instability – your nerve endings are talking
A myriad of consequences from joint instability unfolds once a ligament becomes injured besides just the nerve endings within the ligament firing to produce pain. Once a joint begins excessively moving, the body will compensate in almost all of the structures involved in that particular joint, including the other ligaments, tendons, muscles, and other stabilizing structures such as menisci, discs, labrum, as well as the nerves that supply the joints. These compensatory changes initially produce beneficial effects to temporarily stabilize the joint and disperse the forces more evenly across the joint by tightening various muscles and swelling the joint. This process works fine for a few days, a week, possibly a few weeks, but it was never meant to be the long-term solution. If you think about it, at this point, the injured patient has three sources of pain: the original ligament injury, the muscle spasms, and the joint swelling.
Nerve injury to ligaments hurt and impedes ligament healing
What are we seeing in this image?
A 2002 paper is cited that came from the University of Calgary and was published in the Journal of orthopaedic research (3). What we are highlighting is that at six weeks after an injury, there were dramatic differences in the structural biomechanical properties and blood supply in the ligaments whose nerve supply was cut. Let’s let the researchers explain this in their own words.
“Little is known about the contribution of innervation to ligament healing after traumatic disruption, although there is good evidence of an important role for the peripheral nervous system in the healing of fractures and skin injuries. Tissues such as ligament, with a low resting (poor circulation) blood supply, are dependent on substantial increases in blood flow and vascular volume during the initial stages of repair. (To repair ligament blood and healing factors – the typical swelling surrounding a new injury – must be present).
(The researchers) hypothesized that this initial healing response would be strongly promoted by neurogenic inflammation. (The nerves themselves are initiating the inflammatory healing response).” The results of this study were achieved with rabbits. The main findings were that an “intact innervation (non-inured nerves) makes a critical contribution to the early healing responses of the MCL.”
What do rabbits have to do with you? A lot of you are an athlete with a ligament injury and “poor sleep, increased anxiety, and poorly regulated hormone and cytokine levels”
The rabbit study above was cited in a March 2020 study Knee Surgery, Sports Traumatology, Arthroscopy. (4) What the researchers of this study were seeking to demonstrate was ” the essential elements of cruciate ligament recuperation, micro-trauma repair, and remodeling.” Getting the athlete to heal. As in the 2002 rabbit study, a focus was on the ability to create inflammation as a healing response. Here is what the researchers suggested:
“Current sports training practice, lifestyle psycho behavior, and environmental factors combine to increase both primary non-contact knee injury risk and the nervous and immune system dysregulation that lead to poor sleep increased anxiety, and poorly regulated hormone and cytokine levels. These factors may create a worst-case scenario leading to poor ligament recuperation, micro-trauma repair, and remodeling. Early recognition and modification of these factors may decrease knee ligament injury rates and improve cruciate ligament repair or reconstruction outcomes.”
Nerves, ligaments, and pain – one step further
In the image below I make these points:
- When innervation or nerve supply to the ligaments is compromised ligament healing is also suboptimal and compromised. To make this a point further. The knee joint, for example, is supplied by branches of the femoral, sciatic, and obturator (the nerve supply from the thighs) nerves.
- Nerves within the ligaments are responsible for most of the pain of joint instability the nerve density within the ligaments of a joint or more concentrated in the most important stabilizing ligaments the nerve density with an individual ligament can also vary with the importance of which part of the ligament is most under strain the nerve density in the ligament is largest where it attaches to the Bone
At this point, the injured patient has three sources of pain: the original ligament injury, the muscle spasms, and the joint swelling.
At this point, patients are at a crossroads and need to decide on a treatment path. For some, the treatment path they already took was the path of pain management and pain suppression. Typically these treatments surround eliminating joint swelling as the cause of pain. Once these treatments are received, such as anti-inflammatory medications, corticosteroid injections, and muscle relaxants, the joint is put in an unprotected, unstable state making it very vulnerable to worsening and further injury. This then leads down the path of joint destruction and often leads to various potentially harmful surgeries.
I am fond of using this example in the examination room:
If your house was on fire and the smoke detectors were sounding, would it be in your best interest to remove the batteries in the smoke detectors so the alarms stopped blaring, or should you actually put out the fire or call the fire department? When patients receive pain suppressing therapies, such as corticosteroid shots, anti-inflammatory, narcotic, or muscle relaxation medications or receive radiofrequency ablation or neurectomy and other pain sensation removing therapies, they are, in essence, not allowing the body to “sound the pain alarms.”
Pain protects the body from further harming itself. Anyone who receives pain suppression therapies runs the risk of increasing the joint damage to such a point that even surgery will not be able to work.
Nerve entrapment: Cause and effect
Any nerve in the body can become entrapped or compressed. The three main causes, from most to least prevalent, are joint instability, direct trauma, and degenerative arthritis. Far and away, the most common reason for nerve entrapment in the spine, whether the neck or the back, affecting the spinal nerve roots or autonomic nervous system is joint instability. It is common when patients come to our office to already have seen five or more doctors and been given diagnoses such as spinal stenosis, cervical radiculopathy, lumbar degenerative disc disease, sciatica, and been told that they need various surgeries such as decompressive laminectomy with or without spinal fusion to decompress the compressed nerve and/or spinal cord. Again we cannot emphasize this enough if the symptom is not present in a significant manner 24/7 and specific activities reduce the symptoms such as sitting or lying down, then dynamic joint instability is the correct diagnosis. If the degenerative process is well-advanced, and it is causing a significant narrowing of the nerve canal and it is strangling the nerve 24/7, then clearly no motion or position will relieve symptoms. This type of static compression does affect nerve transmission and significant symptoms are normally present. If the nerve transmission is not going to your skin, you get a true numbness, and the same goes for muscles, as weakness and atrophy are seen. When these are present, and an MRI shows narrowing of the appropriate spinal nerve root from excessive bone spurring and arthritis, then a surgical consultation is needed.
The long term manifestations of joint instability leading to nerve pain
The long-term manifestations of joint instability include the following: autonomic nervous system dysfunction, radiculopathies, tendinopathies, recurrent joint swelling, chronic muscle spasms, accelerated joint degeneration, myofascial restrictions, nerve entrapments, and neurogenic inflammation. As the scenario is likely to be repeated in the next adjacent joints, it is really easy to understand that unresolved joint instability can progress very quickly to severe chronic disabling pain and joint degeneration.
When thinking about all of the various pain treatments utilized, including botulism injections, medications or supplements, radiofrequency ablation, electrothermal coagulation, massage therapy, electrical stimulation treatments, exercise, and epidural injections, it makes sense that these have little hope of curing pain, on account that they treat the manifestations, not the cause of the pain, which is joint instability.
Unresolved long-term joint instability causes forces to be concentrated on the same side of the primary injury, accelerating articular cartilage, tendon, meniscus, labrum, or disc injury on that particular side of the joint. As the unresolved process lingers, muscles and tendons fatigue, no longer able to limit joint motion. A subtle change in bony anatomical alignment results, on the order of 1-2 mm. This small change causes microinstability of the joint which leads to myofascial restrictions, as well as irritation to the local milieu of nerves. This subtle micro instability can directly and/or indirectly cause inflammation, entrapment, and excessive stretching of the nerves. These nerves become hyperirritable, swollen, and inflamed, causing the symptoms of allodynia and hyperalgesia which are characteristic of neuropathic pain. Allodynia occurs when a nonpainful stimulus, like a very gentle touch of stretch, is extremely painful. Hyperalgesia involves an exaggerated pain response to something that is minimally painful.
This stretchability of the nervous system has normal and abnormal limits. Under normal conditions, nerve fibers are able to comply with low to moderate strain or compression associated with physiological (normal) joint movements. When nerves are healthy no pain signals are produced with normal motions or stretch.
A normal nerve can stretch approximately 6% without any damage or resultant symptoms. Mechanotransduction is the process whereby the nerves tell the body what is going on with regard to a force. A normal pressure or motion is not painful; however when local inflammation occurs in a nerve, then normal physiological pressures and motions can cause significant pain. This is called pressure mechanosensitivity and can be documented by local tenderness over the nerve with palpation or various movements. This occurs due to neurogenic inflammation. Once these small nerves are inflamed, they can produce a pain signal with as little as only 3% stretch, which occurs with just normal motions.
When normal motions and pressures produce significant symptoms, the diagnosis is neuropathic pain.
When normal motions and pressures produce significant symptoms, the diagnosis is neuropathic pain. This can accompany ligament injury and joint instability or be present by itself. Perhaps the most underappreciated but most profound long-term manifestations of joint instability are nerve entrapments, radiculopathy (spinal stenosis), and autonomic nervous system dysfunction. The body will do whatever it takes to protect the spinal cord, spinal nerves, and peripheral nerves, even encasing them in bone (spinal vertebrae) or having them run close to the bone or in bony tunnels. The course through which all nerves run to get to their final destination contains only 1-2 mm of extra space.
Another way to look at this: at some point, a nerve is within 1-2 mm of a bone or bony prominence as it zig-zags from its origin through the myofascial plane between muscles, through bony tunnels to its endpoint. As a person with stable joints goes about their daily activities, including exercise and sports, adjacent bones normally move about 1-2 mm. This extremely small space is what prevents the bone from hitting the nerve. When the joint is unstable, however, the bones that make up the joint move excessively resulting in the nerve being hit or compressed producing zinging pain and/or numbness. The compression (inflammation) of the nerve can also be documented with ultrasound. The key characteristic finding is to determine that the nerve irritation is coming from joint instability. When a patient can eliminate or significantly reduce a symptom by placing himself in a particular position, such as lying down, or placing his arm or leg in a certain position, then almost assuredly the underlying cause of that symptom is joint instability. Even a patient who has been diagnosed with a pinched nerve in the neck or low back will normally report the ability to get into a comfortable position when lying down, where the arm or leg pain is significantly reduced. Generally, pinched nerves in the neck feel better when looking down (versus looking up at the sky); whereas pinched nerves in the lower back feel better when the patient sits down vs standing or walking. This improvement of neck pain and arm pain with the head facing down and the improvement of low back pain and leg pain vanishing when sitting down are clues that the symptoms are positional and should respond to certain injection treatments which I will explain below.
If we could view the nerve when the patient is in the asymptomatic position, we would see that the nerve is not being compressed or touched by any bone in that position. Likewise, the nerve space narrows when micro instability is present while taking on other positions or movements which produce symptoms. We call this process dynamic (with movement) nerve compression.
What are we seeing in this image? Normal and swollen ulnar nerve at the elbow.
Ultrasound can show nerve entrapments, such as this one in a patient with ulnar nerve entrapment of the elbow, or cubital tunnel syndrome.
Modified from: Soo-Jung Choi, et al. Ultrasonography for nerve compression syndromes of the upper extremity. Ultrasonography. 2015;34(4):275-291. Figures 8 & 9.
We must point out that dynamic nerve compression even applies when the patient has been given diagnoses of degenerative arthritis, osteophytes, or spinal stenosis. If symptoms are aggravated by a certain position or movement, then they have a dynamic quality and can be realistically projected as being successfully treated with dextrose or platelet injections which are explained below. If the symptom(s) is constant, which is called static compression, signifying symptoms 24/7 and in all positions and activities, then most likely joint instability is not the cause and a decompression surgery may be necessary.
The nerve entrapment and unusual pain syndromes (and their various names) are classified according to the anatomical part affected as facial, trigeminal, occipital, intercostal, and according to the cause as in diabetes. Thus, nerve pain in the location of the trigeminal nerve would be called trigeminal neuralgia. All trigeminal neuralgia means is nerve pain in the nerve distribution of the trigeminal nerve. It actually does not tell a person anything about what is causing the condition. When a physician and a patient believe that a nerve is getting compressed it is easy to see why surgery would be recommended. Unfortunately, when joint instability is the cause of neuralgia, the surgery may not help relieve the pain.
Many nerve syndromes have joint instability (and thus ligament injury) as their underlying etiology. The easiest of these to understand is when a nerve is entrapped in a tunnel such as the median nerve in the carpal tunnel. These bony tunnels are designed to protect key structures such as arteries and nerves, but again the space is pretty crowded. Nerves often traverse through tunnels or narrow bony canals. At their limiting (smallest) height, depth, or width the most common nerve tunnels including the cubital, carpal, and tarsal tunnels are less than 10mm. This amount of space is decreased by certain positions and movements. When the space in the tunnel becomes reduced, the nerve is compressed, the pressure inside the nerve rises which compromises its microvascular blood supply and leads to focal ischemia of the nerve. This in turn leads to demyelination (disruption of the outer coating of the nerve), which disrupts nerve signal transmission; prolonged compression can lead to more permanent damage to the neurons themselves, including degeneration distal to the point of compression. The neurogenic inflammation and ischemia also lead to fibrosis (scarring), which can further tether the nerve and lead to more traction (stretch) injury during motion.
Carpal tunnel syndrome. One cause of median nerve compression is subluxation of the carpal bones from ligament laxity.
The ability of peripheral nerves (and also ligaments) to stretch and slide is of paramount importance to maintain ideal neural function. Like ligaments, nerves can stretch to a certain degree. When a nerve becomes sensitized, meaning injured and neurogenic inflammation sets in, the nerve is no longer stretchable and will produce severe stinging pain when stretched even a little. In the office, when a patient asks on the first visit, “Please don’t move my leg, or touch these specific spots because they are so sensitive,” we know that a neurogenic inflammation in some of the nerves is present. Healthy nerves do not elicit pain with normal movement. When a nerve is irritated with normal movements or pressure, you know that the nerve is experiencing neurogenic inflammation.
There are many nerve syndromes, such as carpal tunnel syndrome, that clearly involve entrapment of a certain nerve. The median nerve which supplies many of the muscles and sensations in the hand resides in the carpal tunnel of the wrist. The carpal tunnel walls are lined by bone on the sides and bottom and a tough fibrous tissue on the top called the transverse carpal ligament. The bones that comprise the walls of the carpal tunnel (as in other bony tunnels) are connected to other bones which make up the wrist. When a person sustains a wrist ligament injury, the adjacent bones can move too much, thus narrowing the carpal tunnel. A key clue that a nerve entrapment syndrome such as carpal tunnel syndrome stems from joint instability is associated with cracking, popping, or clicking in the joints near the bony tunnel. On physical examination, other clues include excessive motion or soft joint end feel compared to the non-symptomatic side, as well as tenderness when the ligaments of the nearest joint are palpated and stressed. When these signs or symptoms are not present, the cause of the nerve entrapment is most likely not joint instability, thus a different type of injection therapy should be utilized: Nerve Release Injection Therapy (NRIT).
The nervous system of the body is akin to an electrical grid. At any point in the grid, a blockage or short can occur. Everything we do, including our very thoughts, is related to the nervous system. Nerves connect your brain and spinal cord to everything in the body, including muscles, ligaments, skin, and organs, providing movement and feeling. Nerves are primarily responsible for the transmission of communication between cells and even between organs or joints and the brain. The function of the nerve is to deliver a message from one cell to another cell. In that sense, cells can function independently, as well as cooperatively. Rest assured, however, the local environment of the cell takes priority compared to the organism as a whole. What does that mean? Let’s take knee joint instability as an example. The nerves in and around the knee will be sensitized to this instability. They know something is wrong locally and will notify the brain by sending out pain signals. These sensitized nerves in the area of an injury, including joint instability, are said to have neurogenic inflammation, whereby the compressed nerves themselves release inflammatory substances such as substance P, histamine, interleukins, and cytokines that can cause significant local pain. Nerve homeostasis, fortunately, can be restored with injection therapy such as Lyftogt Perineural Injection Therapy. If the injury is due to nerve compression, an interruption in the transformation of information occurs to the soft tissue end organs such as local muscles, ligaments, and skin. This can produce far-reaching effects on organs and even physiological changes in the central nervous system (brain and spinal cord) including the autonomic nervous system, which controls everything that happens in the body automatically such as breathing, heart rate, and blood flow. As you can see, these types of injuries need to be taken very seriously and treated as soon as possible.
Pain from a sensitized nerve may be treated with four different types of regenerative injections: Prolotherapy, Lyftogt Perineural Injection Therapy (LPIT), and Nerve Release Injection Therapy (NRIT). When joint instability is the primary etiology of the neuropathic pain (nerve being sensitized) then either Prolotherapy with PRP is given. When the nerve is located superficially or is larger and easy to identify then LPIT is given. When the nerve involved is deep and/or entrapped, then an ultrasound-guided nerve release injection technique (NRIT) is used.
To better understand why certain nerve injection techniques are used it is important to understand how a nerve travels from the lower back to the tips of the toes, or the neck to the tips of the fingers without normally becoming compressed. As nerves traverse from deep within the body to their final destinations, they travel between the muscles in fascial tissues along with the arteries and veins. This is how a person can lift heavy weights and contract muscles and not compress the nerves. Nerves, however, can get compressed in the fascial layers by various constrictions in the fascia, especially where bony prominences or places where the nerve has to change direction. These places are said to cause a chronic constriction injury to the nerves causing them to swell and become painful.
We often treat nerves along with the ligaments when a person has joint instability, with the hopes of speeding healing. Often repetitive motions or repetitive strains pinch the peptidergic nerves as they exit the fascia. LPIT is done at the sites of nerve restriction and inflammation, relieving the constriction and restoring homeostasis to the nerve. LPIT was discovered by a family physician from New Zealand, John Lyftogt, MD, who published several papers on it, demonstrating its efficacy. One interesting fact is the term inflammation neuritis was used in several papers by Dr. George Hackett, the inventor of Prolotherapy. He felt that neurogenic inflammation also could lead to a myriad of medical conditions including ligament weakness and bone decalcification. As it turns out, he was shown to be correct.
NRIT involves the injection of substances to mechanically release the nerve (also called hydrodissection) but also to nourish and restore homeostasis. NRIT is done under ultrasound guidance to direct the solutions to the exact nerve entrapment location. Because the nerve entrapment is resolved and the health of the nerve is immediately restored, the symptom-relieving effects are often felt instantly.
How many treatments of LPIT or NRIT are required? Sometimes just one, but often, approximately three to six visits are needed for permanent resolution of the nerve irritation and entrapment.
What are we seeing in this image?
Ultrasound showing Nerve Release Injection Therapy (NRIT). You can clearly see the entrapped nerve in the before image. The median nerve is released in the after image.
All pain has a nerve component. Nerves alert the brain to the presence of an injury or problem because the nerves are inflamed, entrapped, or encountering excessive stretch. The hallmark sign of nerve irritation is neurogenic pain which produces significant symptoms including sharp pains when an extremity is moved or touched in a normal non-painful way. This symptom is called allodynia.
The most common cause of all nerve pains is ligament injury leading to joint instability. Ligaments are the sensory organs of the joints. When a ligament is injured, the nerves within it experience excessive stretch and start firing. If the ligament injury is not addressed with Prolotherapy, joint instability develops which results in the development of many long term manifestations including tendinopathies, recurrent joint swelling, chronic muscle spasms, accelerated joint degeneration, myofascial restrictions, nerve entrapments, neurogenic inflammation, autonomic nervous system dysfunction, radiculopathy, and spinal stenosis, which may lead to the same processes occurring in adjacent joints as well!
When a symptom is improved or worsened by motion or activity, the symptom is said to be dynamic. Dynamic symptoms arise from joint instability. Many nerve entrapment conditions and syndromes including carpal tunnel syndrome, occipital neuralgia, thoracic outlet syndrome, piriformis syndrome, cervical and lumbar radiculopathy, and even spinal stenosis occur as a result of joint instabilities. Because the extra space for nerves, including vertebral foramina or tunnels, is only 1 to 2 mm, the microinstability of joints, can cause bones to move enough to compress nerves. When this happens, positions or movements where the tunnel or foramina is open may occur, thus temporarily eliminating the nerve compression, so symptoms abate. Other positions or movements may cause the nerve space to narrow and symptoms to increase. This dynamic (changing) component of the symptomatology is a sign that joint instability is the cause and Prolotherapy is the cure.
Neuropathic pain from neurogenic inflammation caused by nerve entrapment or excessive nerve stretch occurs because of joint instability and requires Prolotherapy to resolve the symptoms long-term. One of the common causes of neurogenic inflammation is chronic constriction injury in the fascia where nerves become entrapped. When joint instability is not present, other natural injection therapies may be provided directly to the nerve: Lyftogt Perineural Injection Therapy (LPIT) and Nerve Release Injection Therapy (NRIT). Both of these treatments involve the injection of natural solutions, including 5% dextrose, to release nerve entrapments and restore health and homeostasis to the inflamed nerves. These small peptidergic nerves are involved in the health maintenance and renewal of tissues such as ligaments, thus LPIT and NRIT are often given in conjunction with Prolotherapy. NRIT requires ultrasound guidance to direct the injection of fluid to release (hydrodissect) the nerve from entrapment, which often occurs in the nerve highways, which are the myofascial layers between muscles. It also occurs in various tunnels, like the carpal tunnel. As the entrapped nerve is released immediately, symptoms may often improve or resolve instantaneously. Sometimes several sessions may be required to produce a long-lasting resolution of the nerve pain and symptoms.
Perhaps the least appreciated nerve irritation is that which involves the autonomic nervous system (ANS). Because both the sympathetic and parasympathetic components of the ANS reside just anterior to the cervical spine, cervical instability may produce a wide array of symptoms including blurred vision, tinnitus, dizziness, swallowing difficulties, ear and eyeball pain, tachycardia (fast heart rate), lacrimation (tearing), memory loss, paresthesia, suboccipital headache, sweating, trembling, migraines, and neck pain. When these symptoms are associated with neck popping, cracking, or grinding with or without a history of chiropractic or self-manipulation, cervical instability can be assumed and the treatment of Prolotherapy may be recommended
Continued reading on treatment for the different types of nerve pain related disorders
Carpal tunnel syndrome: Non-surgical injections and nerve release treatments: A series of new studies affecting patients with Carpal Tunnel Syndrome are questioning the success and validity of Carpal Tunnel Syndrome surgery and how accurate recommendations to patients following surgery are as to when they can return to work. This is a question that is inspired by new research. This article will present various treatment options.
Pudendal Nerve Entrapment Syndrome: Underdiagnosed and inappropriately treated: Many times a patient will contact us via email or phone call and describe their long medical history of dealing with problems of pelvic area numbness and burning; they have sensations of pain or tenderness in the genitalia that would even make wearing underwear painful. Some people will describe that they have a feeling of a lump in the pelvic or groin area where there is actually no lump, just the sensation that one is there. This article describes diagnosis and treatment.
Non-surgical treatment for Trigeminal Neuralgia: We have seen many people with chronic pain of the head, neck, jaw, and face diagnosed with Trigeminal neuralgia. Trigeminal neuralgia means that there is nerve pain in the nerve distribution of the trigeminal nerve. It actually does not tell a person what is causing the condition. This article describes diagnosis and treatment.
1 Zimny ML, Wink CS. Neuroreceptors in the tissues of the knee joint. Journal of Electromyography and Kinesiology. 1991 Sep 1;1(3):148-57. [Google Scholar]
2 Seitz AM, Murrmann M, Ignatius A, Dürselen L, Friemert B, von Lübken F. Neuromapping of the Capsuloligamentous Knee Joint Structures. Arthroscopy, sports medicine, and rehabilitation. 2021 Apr 1;3(2):e555-63. [Google Scholar]
3 Ivie TJ, Bray RC, Salo PT. Denervation impairs healing of the rabbit medial collateral ligament. Journal of orthopaedic research. 2002 Sep;20(5):990-5. [Google Scholar]
4 Nyland J, Huffstutler A, Faridi J, Sachdeva S, Nyland M, Caborn D. Cruciate ligament healing and injury prevention in the age of regenerative medicine and technostress: homeostasis revisited. Knee Surgery, Sports Traumatology, Arthroscopy. 2020 Mar;28(3):777-89. [Google Scholar]