Caring Medical - Where the world comes for ProlotherapyLyftogt Perineural Injection Treatment™

Lyftogt Perineural Injection Treatment™ (also called Neurofascial Prolotherapy, as well as Neural Prolotherapy and Subcutaneous Prolotherapy) is a sometimes used side-by-side treatment with traditional dextrose based Prolotherapy. As these techniques work by different mechanisms they can diminish the pain of similar conditions, so they can be given together or separately. In Dextrose base Prolotherapy the ligament and tendon attachments are being treated, in Perineural Injection, the nerves are being treated.

Research into the healing effects of this type of Prolotherapy have primarily been done by a family physician from New Zealand named John Lyftogt, MD.1,2,3

On a physical examination, areas of chronic pain can be palpitated to find the “pain generator,” that is the the exact spot of weakness and instability in the joint that is causing the pain.

As most chronic pain is caused by joint instability from ligament laxity, this trigger point is found where the ligaments attach to the bone.

Sometimes tender points are found. This is a term used  to describe areas of pain located deep in the muscle or areas where small subcutaneous nerves are located.

In these latter situations, Perineural Injection Therapy on these tender points could be indicated.

An example of this is when a person has trauma to the medial or inner part of the knee. In such a situation, a sprain of the medial collateral ligament could have occurred and would be tender upon palpation.

In this situation, Prolotherapy would be used to stimulate repair of the medial collateral ligament (and also the medial meniscus if indicated). But just as likely would be a stretching, shearing or tearing of the saphenous nerve, also located on the medial side of the knee. In this latter situation, the person would be recommended to perineural treatment to decrease neurogenic inflammation.


Nerve Inflammation


In a series of medical lectures in the 1860’s, famed anatomist John Hilton noted in his studies that often the nerve that innervates a joint also tends to innervate the muscles that move the joint and the skin that covers the distal attachments of those muscles. For example, the musculocutaneous nerve supplies the elbow joint of humans with pain and position sensation. It also supplies the biceps brachii and brachialis muscles as well as the forearm skin close to the insertion of each of those muscles.

In his research, Dr. Lyftogt found that patients with chronic elbow pain often need Perineural Injections into the musculocutaneous nerve and other nerves around the elbow to resolve chronic elbow pain.

The nerve supply to the elbow when inflamed not only causes elbow pain, but can also contribute or be the sole cause of degeneration of the elbow and the structures that support (ligaments) and move the elbow (muscles and tendons). Thus to assist regeneration of these degenerated structures, treatment is given to decrease the neurogenic inflammation, so once again the musculocutaneous nerve (and other elbow nerves) can supply “normal” health maintenance and health renewal to the elbow joint and structures around the joint.

Dr. Lyftogt found that a 5% dextrose solution injected subcutaneously (versus at the fibro-osseous junction) could completely eliminate a person’s pain immediately; though the treatment often has to be repeated 5-8 times for complete pain resolution.


Treating sensory nerves


In research from 1997, Doctors at the University of Calgary found that the knee’s collateral ligaments possess a complex nerve supply. The presence of peptidergic nerves suggests that ligaments may be susceptible to neurogenic inflammation and heightened sense of pain.4

Peptidergic sensory nerves maintain the health of tissues such as ligaments and tendons because they respond to harmful stimulus. In one case these nerves may tell your knee to stop doing something because it is hurts and when something hurts it is prone to further damage. Or in another case, your knee hurts, something is wrong and you should seek help.


Inflammatory neuritis as cause of ligament and tendon damage


The concept of inflammation on the nerve causing pain and even degeneration of tissues has been documented in articles in the 1950s and 1960s from Dr. George Hackett, the person who coined the term Prolotherapy.5,6,7

He noted that “inflammation neuritis and other antidromic impulses (nerve impulses that are traveling in the wrong direction and cause confusion) are transmitted to blood vessels in nerves and surrounding tissues stimulating a release of excess neurohumoral mediator substance (the nerves are over-reacting as in panic) which cause a neurovascular vasdilation-edema-sterile inflammation neuritis (immune breakdown which contributes to radiating nerve pain).

This accounts for the pain and tenderness of inflamed nerves we find in the arm with neuritis originating at the cervical vertebra and in the thigh and leg with sciatic neuritis originating in the 5,6 lumbar vertebra and pelvis in sacroiliac-piriformis-sciatica.7 This neurogenic inflammation can also lead to ligament weakness and bone decalcification.”8,9


Why is a 5% dextrose solution used for Lyftoght Perineural Injection Treatment/Neurofascial Prolotherapy?


The concentration of dextrose or glucose in the blood is 0.5%.  Thus a 5% dextrose solution is ten times the concentration of what is contained in the blood. This is a high enough concentration of dextrose to decrease the pain from the peptidergic sensory nerves but not so much to actually cause an inflammatory reaction.

This concentration of dextrose blocks calcium influx into the nerves. This decreases neurogenic inflammation.

The 12.5% dextrose solution of Hackett-Hemwall Prolotherapy induces an inflammatory reaction (to stimulate ligament and tendon cell proliferation) but that can cause mild pain. The goal of Neurofascial Prolotherapy is to decrease neurogenic inflammation, so the solution must do that without causing its own inflammatory reaction.  In essence, dextrose restores the physiology of the nerve cell.

Why isn’t an anesthetic used with Lyftoght PIT/Neurofascial Prolotherapy?

A patient’s pain that is relieved using 5% dextrose injected in this manner diagnostically reveals that part or all of the person’s pain is coming from peptidergic sensory nerves. These are the only nerves that are turned off by 5% dextrose. Lidocaine or procaine, as well as other “caines” turn off all the nerves (if used in a high enough concentration). So using an anesthetic in the solution would not be helpful diagnostically. Local anesthetics also cannot change inflammation, only pain, whereas dextrose can affect both inflammation and pain. For a long-term treatment, dextrose has a lot of potential, anesthetics very little.


1 Lyftogt J. Subcutaneous prolotherapy for Achilles tendinopathy. Australia’s Musculoskeletal Medicine Journal. 2007; 12:107-109.
2 Lyftogt J. Prolotherapy for recalcitrant lumbago. Australia’s Musculoskeletal Medicine Journal. 2008; 13:18-20.
3 Lyftogt J. Subcutaneous prolotherapy treatment of refractory knee, shoulder and lateral elbow pain. Australia’s Musculoskeletal Medicine Journal. 2007;12:110-112.
4 McDougall JJ1, Bray RC, Sharkey KA. Morphological and immunohistochemical examination of nerves in normal and injured collateral ligaments of rat, rabbit, and human knee joints. Anat Rec. 1997 May;248(1):29-39.
5 Hackett GS. Ligament Uninhibited reversible antidromic vasdilation in brochiogenic pathophysiologic disease. Lancet. 1966;86:398-404.
6 Hackett  GS. Ligament relaxation and osteoarthritis, loose jointed versus close jointed. Rheumatism. 1959;15:28-33.
7 Hackett GS, Huang TC, Raftery A. Prolotherapy for Headache. Pain in the Head and Neck and Neuritis. Headache. 1962;3-11.
8 Hackett GS, Huang TC. Prolotherapy for sciatica from weak pelvic ligaments and bone dystrophy. Clinical Medicine. 1961; 8:2301-2316.
9 Hackett GS. Uninhibited reversible antidromic vasdilation in pathophysiologic diseases: arteriosclerosis, carcinogenesis, neuritis and osteoporosis. Angiology. 1966;17, 2-8.

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