top of page
Neural therapy is a healing technique developed in Germany that involves the injection of local anesthetics such as procaine or xylocaine, sometimes in combination with homeopathic and isopathics remedies, into autonomic nerve ganglia, surgical and trauma scars, the thyroid gland, acupuncture points, and other tissues around peripheral nerves.
Neural therapy is in part based on the idea that trauma can produce long-standing disturbances in the electrochemical function of tissues. Among the types of tissues affected by trauma include scars, nerves or a cluster of nerves called ganglions.
When the autonomic nervous system is injured or not functioning correctly, various consequences result. The autonomic nervous system is that part of the nervous system responsible for the “automatic” functions of the body, including the immune system, circulation, hormone release, and the body’s healing ability. If there is a disturbance of the autonomic nervous system, the resulting dysfunction can last indefinitely unless repaired. A correctly administered neural therapy injection can often instantly and lastingly resolve chronic long-standing illness, chronic pain, as well as help resolve the psychoemotional effects associated with trauma. In short, neural therapy is designed to repair dysfunction of the autonomic nervous system.
Although several thousand European physicians are now using neural therapy, most physicians in the U.S. are unfamiliar with its extensive therapeutic usage.
One type of neural therapy more common in the U.S. is “trigger point injections”. These are generally used for pain management and based on the work of Janet Travell, M.D.1
A considerable body of scientific research supporting neural therapy’s basic principles has been published in German and Spanish, but most has never been translated into English.
The original local anesthetic used in the late 1800’s by the great scientists Ivan Pavlov and Sigmund Freud was cocaine. Dr. Freud shared his knowledge of cocaine therapy with his friend, ophthalmologist Carl Koller, who was the first physician to perform eye surgery using a cocaine solution.
Koller immediately recognized cocaine’s potential as a perioperative analgesic agent. Shortly after Koller‘s historic lecture in Heidelberg in 1884, the whole medical world knew about this new method for pain-free surgery. Local anesthesia for operations quickly found its way into medical routines worldwide. Though Sigmund Freud discovered the therapeutic effects of cocaine, most of the credit went to Carl Koller.2 However, because of the addictive nature of cocaine, a search for a safer local anesthetic ensued and resulted in the discovery of procaine (introduced under the trade name “Novocain”) in 1905 by Einhorn.3
In 1906, Karl Ludwig Schleich showed that certain rheumatic diseases and muscle pains could be controlled with the infiltration of cocaine. However, his reports were largely ignored.4 In 1906, Gustav Spiess pointed out that inflammation could be rapidly reduced with procaine injections.5 Both discovered that the healing lasted much longer than the duration of the actual anesthesia.
In the early 1920s, the French surgeon René Leriche, who treated many patients with nerve injuries, was one of the first to observe healing reactions produced by local procaine administered before an operation and praised procaine as the “surgeon’s bloodless knife”.6 Around that time, Oregon surgeon William Livingston also treated his patients with multiple procaine injections, sometimes as many as 8 over a period of 2 years or more. He found that serial injections of procaine often resulted in permanent remission of pain.7
Independent of these doctors, two German physicians, who were brothers practicing in the early 1900s, Ferdinand and Walter Huneke, began using procaine as a therapy for pain and various neurological diseases. Realizing they may have found an effective new therapy for pain, they dubbed it “Healing Anesthetics”.
Ferdinand and Walter first reported their research results on the healing properties of local anesthetics with the 1928 publication Unknown Distant Effects of the Local Anesthesia. The Huneke brothers reported that reaction to the injections could help organs at a distant site and described this phenomenon as a "reflex". From their extensive research and practice the Huneke's are considered the founders of Neural Therapy.8 The 1948 book Cybernetics by Norbert Wiener led to further clarification about neural therapy in that the body functions as a whole, and that every disease, every scar, and every treatment affects the whole-body system.9
Biochemical Mechanisms of Neural Therapy
Local anesthetics such as procaine and lidocaine have a multitude of effects on the nervous and circulatory systems. Besides the well-known action as a sodium channel blocker, they also provide neuroprotection to the central nervous system.10 Additionally, they protect against sympathetic sprouting in neuropathic pain11 and reduce intracranial hypertension.12 Procaine is a vasodilator, unlike cocaine, which is a vasoconstrictor. Procaine, an ester anesthetic, is metabolized in the plasma by the enzyme pseudocholinesterase through hydrolysis
into para-amino benzoic acid (PABA), an antioxidant that some classify as part of the vitamin B complex. This then acts to improve nerve membrane integrity.
Some studies have shown additional molecular mechanisms in neural therapy. Local anesthetics induce Gq–protein-complex mediated intracellular anti-inflammatory mechanisms13 and deactivate overactive granulocytes by inhibition of the signaling of human N-methyl-D-aspartate receptors (NMDA).14
The NMDA receptor is a glutamate receptor and ion channel protein found in nerve cells that is very important for controlling synaptic plasticity and memory function. These local anesthetics also have an effect on the synthesis and release of inflammatory mediators as eicosanoids, histamines, prostaglandins, and cytokines.15 Homeostasis is thought to be re-established by extinguishing peripheral irritation and stimulating regulatory processes.
There are several theories on how and why neural therapy works. One basic idea is that neural therapy restores the “nerve membrane potential”. Cells of multicellular organisms such as animals and plants exhibit an electrical potential difference across the cell plasma membrane. That is to say that there is an electrical potential difference between the inside of the cell and the surrounding bathing medium of the cell. This potential difference is referred to as the membrane potential. The numerical value of the membrane potential is generally negative, meaning that the inside of the cell is negative with respect to the outside solution, which is taken as the reference or zero value. Normal resting nerve cells have a resting membrane potential of approximately -70 mV. This means that the inside of the neuron is 70 mV less than the outside. At rest, there are relatively more sodium ions outside the neuron and more potassium ions inside the neuron. The resting potential is mostly determined by the concentrations of the ions in the fluids on both sides of the cell membrane and the ion transport proteins that are in the cell membrane.
An action potential is a very rapid change in membrane potential that occurs when a nerve cell membrane is stimulated. Specifically, the membrane potential goes from the resting potential (typically -70 mV) to some positive value (typically about +30 mV) in a very short period (just a few milliseconds). When it changes to a positive value or “drops” there is an “action potential” generated and the nerve fires an impulse. In a nerve cell damaged by trauma, infection or surgery, the resting membrane potential becomes chronically more positive, thus it loses its negative voltage. This means the nerve will fire off a nerve impulse with much less of a stimulus - thereby creating chronic pain.
While different theories exist as to the mechanism of action for local anesthetics such as procaine, it is well known that they raise the resting membrane potential, making the nerve less likely to fire a nerve impulse even with more stimuli.16, 17 In addition, studies with procaine have shown its ability to increase the refractory period or the time interval between nerve firing.18 It is believed that by repeatedly infiltrating the local anesthetic around the nerve, the sodium potassium ion pumps progressively resume normal activity and eventually the autonomic nervous system starts functioning properly again.
Conditions Treated with Neural Therapy
Neural therapy is potentially useful for numerous musculoskeletal and neurological conditions involving inflammation and pain. Additionally, it is helpful for painful, sensitive surgical scars, as well as keloid scars. Chronic pelvic pain is frequently responsive to neural therapy, as are dysmenorrhea and menstrual irregularities. What are often considered “regional pain syndromes” are frequently secondary to autonomic dysfunction and amenable to neural therapy. Headaches and trigeminal neuralgia can be effectively treated with neural therapy.
Treatment is always more effective when complemented with dietary changes, food supplementation and other forms of bioregulatory medicine treatment.
Generally, neural therapy helps to regulate the autonomic nervous system and helps with cellular functioning, so it can have a positive benefit on many conditions, which may include:
Back and neck pain
Chronic pain from whiplash and head injuries
Jaw and head pain
Joint pain, muscular pain, and athletic injuries
Post-surgical pain (including dental)
Sinusitis of all types
Types of Neural Therapy
There are three basic types of neural therapy treatment:19, 20, 21
1. Segmental therapy - This form of neural therapy aims to exploit segmental reflexes and referred pain mechanisms. Segment therapy comprises an intracutaneous injection (stimulating spot) and deeper injections into the muscles, tendons, ligaments and bones, which can be painful. This field of neural therapy shows some short-term efficacy on pain. There has so far not been any evidence of long-term effects. As part of neural therapy, local anesthetics are also injected peridurally, at the nerve roots, at the sympathic ganglia and at peripheral nerves. There are charts of the location of these cutaneous branches for many body organs so that the practitioner knows where to locate sites of injections.
2. Injection of scars - Scars are often sites of dysfunctional nerve tissue. Direct injection of scars with local anesthetic, such as procaine, is thought not only to help restore function of damaged nerve cells, but has a secondary benefit of reducing the disturbance of the scar on other normal tissue. For example, a
C-section scar on a patient’s lower abdomen may cause pelvic pain or lower back pain. Injections into the scar release neuromuscular tension and reduce the pain.
3. Treating interference fields - An interference field may be defined as local tissue irritation with the potential to cause destabilization of the autonomic nervous system (ANS) either locally or systemically. Interference fields are areas of altered nerve-cell resting membrane potential where nerve cells are not functioning normally. An interference field exists in an area of the body that has become depolarized (weakened) due to previous trauma - such as an old scar, concussion or injury, surgical trauma, or from dead necrotic tissue - such as a root canal treated tooth or dental cavitation, and thus, becomes more susceptible to toxin accumulation. Even though a trauma may be very old and is no longer painful, it can still act like a powerful short-circuit of the body’s natural energy flow, reflexing to a specific organ or gland, thus creating many problems.
Interference fields can occur almost anywhere in the body and are often distant from the part of the body that is experiencing symptoms. Hence, they are sometimes termed “focal interference fields”. Scars of all types (trauma, surgical), deep autonomic ganglia (grouping of nerves), internal organs, teeth (non-vital root-canal treated), tonsils, and paranasal sinuses are regarded as susceptible to the formation of interference fields. The theoretical basis used is the Pischinger "cell milieu system", which cites the significance of the unity of cell, interstitium with capillaries and nerve endings. The interference field is then switched off by the injection of local anesthesia into the affected structure. Interference fields usually occur on the same side of the body as the symptoms, however the symptoms or signs may be bilateral or contra-lateral. Interference fields are often unresolvable with pharmaceuticals.
Neural therapy is performed with local anesthetics. Procaine is the preferred local anesthetic due to its short duration of action and its positive effect on tissue perfusion. Some practitioners may use lidocaine or a combination of the two. Occasionally, carbocaine is used if allergy problems are encountered. These anesthetics should never contain epinephrine. A small amount of sodium bicarbonate may be added to buffer the pH and decrease the pain of the injection, although the sodium bicarbonate is optional. Some Swiss and German physicians may also incorporate various homeopathic and isopathic remedies into the injection.
Autonomic nervous system dysfunction is common and can lead to chronic pain. Neural therapy is a powerful treatment that can be quite effective in resolving autonomic nervous system dysfunction and pain, especially in the complex pain patient. Neural therapy requires training and practice by the pain practitioner to be most effective. However, even with application of only basic principles such as injection of scars, the patient may greatly benefit.
Where to learn Neural Therapy
Klinghardt Academy - Dietrich Klinghardt MD PHD. 14500 Juanita Dr. NE, Kenmore WA - Dr. Klinghardt is Founder of the Klinghardt Academy, the American Academy of Neural Therapy, Medical Director of the Institute of Neurobiology, and lead clinician at the Sophia Health Institute, located in Woodinville, Washington. He is also Founder and Chairman of the Institute for Neurobiology (Germany) and (Switzerland). Klinghardt Academy (USA) provides teachings to the English-speaking world on biological interventions and Autonomic Response Testing assessment techniques.
Michael I. Gurevich, M.D.; Ralf Oettmeier, MD; David Vinyes, MD – 997 Glen Cove Avenue, Glen Head, NY 11545; Tel. 516-674-9489; Fax: 516-759-5946; email GurevichMD@gmail.com - https://www.holisticmd.org/treatments/neural-therapy/
Travell, J. G., & Simons, D. G. (1983). Myofascial pain and dysfunction: the trigger point manual (Vol. 2). Lippincott Williams & Wilkins.
Berggren L. Lakartidningen 2000;97(15):1846–7.
Goodman and Gilman’s The Pharmacological Basis of Therapeutics. The MacMillan Company. New York. 1965. p 372.
Wawersik J. History of anesthesia in Germany. J Clin Anesth. 1991 May-Jun;3(3):235-44.
Spiess, Gustav. Die Bedeutung der Anästhesie in der Entzündungstherapie. JF Lehmann, 1906.
Leriche, Rene, and Archibald Young. The surgery of pain. The American Journal of the Medical Sciences 198, no. 5 (1939): 720.
Rey R. The History of Pain. Wallace LE, Cadden JA, Cadden SW, trans. Cambridge, Mass: Harvard University Press; 1993.
Huneke J. Neural Therapy by Huneke presentation at Autonomic Nervous System Dysfunction Seminar. May 13-15, 1999. Sponsored by Caring Medical & Rehabilitation Services.
Wiener, N. (1948). Cybernetics.
Yamada A, et al. Protective actions of various local anesthetics against the membrane dysfunction produced by in vitro ischemia in rat hippocampal CA1 neurons. Neuroscience Research 2004;50(3):291–8.
Takatori M, Kuroda Y, Hirose M. Local anesthetics suppress nerve growth factor mediated neurite outgrowth by inhibition of tyrosine kinase activity of TrkA. Anesthesia and Analgesia 2006;102(2):462–7.
Brucia JJ, Owen DC, Rudy EB. The effects of lidocaine on intracranial hypertension. Journal of Neuroscience Nursing 1992;24(4):205–14.
Hollmann MW, et al. Receptors, G, and proteins, and their interactions. Anesthesiology 2005;103(5):1066–78.
Hahnenkamp K, et al. Local anaesthetics inhibit signalling of human NMDA receptors recombinantly expressed in Xenopus laevis oocytes: role of protein kinase C. British Journal of Anaesthesia 2006;96(1):77–87.
Cassuto J, Sinclair R, Bonderovic M. Anti-inflammatory properties of local anesthetics and their present and potential clinical implications. Acta Anaesthesiologica Scandinavica 2006;50(3):265–82.
Blaustein, Mordecai P., and David E. Goldman. Competitive action of calcium and procaine on lobster axon: a study of the mechanism of action of certain local anesthetics. The Journal of general physiology 49, no. 5 (1966): 1043-1063.
Kordaš, M. The effect of procaine on neuromuscular transmission. The Journal of physiology 209, no. 3 (1970): 689-699.
Katz, Bernhard. Depolarization of sensory terminals and the initiation of impulses in the muscle spindle. The Journal of physiology 111, no. 3-4 (1950): 261-282.
Huenke J. Neural Therapy by Huneke presentation at Autonomic Nervous System Dysfunction Seminar, May 13-15, 1999, sponsored by Caring Medical & Rehabilitation, Sanibel 6 Island, Florida.
Harris, Gerald R. Effective treatment of chronic pain by the integration of neural therapy and prolotherapy. Journal of Prolotherapy 2, no. 2 (2010): 377-386.
Kidd, Robert F. Neural Therapy: Applied Neurophysiology and Other Topics. GeneralStore PublishingHouse, 2005.
MICHAEL I GUREVICH, M.D. Presentations
Neural Therapy injection of Scar Tissue, Vancouver
¿Qué es la Terapia Neural? / What is Neural Therapy?
bottom of page