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1 Int Clinc Med Case Rep Jour (ICMCRJ) 2025 | Volume 4 | Issue 12 1 International Clinical and Medical Case Reports Journal Review Article (ISSN: 2832-5788) More than one Century: Intravenous Procaine Therapy - A Systematic Review More than one Century: Intravenous Procaine Therapy - A Systematic Review Ralf Oettmeier1, Hüseyin Nazlikul2,3,4*, Laura Bibiana Pinilla-Bonilla5, FatmaGülçin Ural Nazlikul6 and MUwe Rudolf Reuter7,8 1Alpstein Clinic, CH-9056 Gais/AR, Switzerland 2President of IFMANT (International Federation of Medical Associations of Neural Therapy), Schattenhalb, Switzerland 3Specialist in General Medicine, Pain Medicine, and Medical Biophysics. Private practice at the Natural Health Clinic, Istanbul, Turkey 4Faculty of Medicine, Department of Biophysics, Istanbul University of Health and Technology, Istanbul, Turkey 5Faculty of Medicine, Master's in Alternative Medicine, Neural Therapy Area, Universidad Nacional de Colombia. Bogotá, Colombia 6Department of Physical Medicine and Rehabilitation, Istanbul Health and Technology University, Istanbul, Turkey 7Professorship of Naturopathy, University of Applied Sciences, Anhalt, Germany 8Klinik im Leben, D-07973 Greiz, Germany Citation: Oettmeier, R., Nazlikul H, Pinilla Bonilla, L.B., Ural Nazlikul F.G, Reuter, U.M. More than one Century: Intravenous Procaine Therapy - a Systematic Review. Int Clinc Med Case Rep Jour. 2025;4(12):1-25. Received Date: 01 December 2025; Accepted Date: 09 December 2025; Published Date: 11 December 2025 *Corresponding author: Prof. Dr.Dr.Hüseyin NAZLIKUL, President of IFMANT (International Federation of Medical Associations of Neural Therapy), Schattenhalb, Switzerland; Faculty of Medicine, Department of Biophysics, Istanbul University of Health and Technology, Istanbul, Turkey; President of (BNR) Turkish Academic Society for Neuraltherapy-Regulation Therapy, Istanbul, Turkey; Specialist in General Medicine, Pain Medicine and Medical Biophysics. Private practice Istanbul, Turkey; President of the Society for Manual Medicine and Pain Therapy (MTAR), Istanbul, Turkey. Copyright: © Oettmeier, R., Nazlikul H, Open Access 2025. This article, published in Int Clinc Med Case Rep Jour (ICMCRJ) (Attribution 4.0 International), as described by http://creativecommons.org/licenses/by/4.0/ ABSTRACT/SUMMARY Procaine, traditionally introduced as a local anaesthetic, has revealed over more than a century a broad spectrum of systemic, pleiotropic pharmacological properties that far exceed its classical use. More than thirty distinct biological mechanisms have now been identified, including anti-inflammatory, vasodilatory, sympatholytic, membrane-stabilising, neuromodulatory, geroprotective, and epigenetically active effects. These actions provide the scientific foundation for its expanding clinical relevance in pain medicine, neuro-regulation, cardiovascular modulation, immune-related and degenerative disorders, and complementary oncology. Within Neural Therapy, Procaine occupies a central and irreplaceable role: its segmental, interference-field–oriented and autonomic-regulatory actions uniquely position it as the primary agent capable of restoring disturbed vegetative patterns, resolving chronic dysfunctions, and re-establishing physiological self-regulation. Beyond its local anaesthetic function, intravenous Procaine—especially in combination with bicarbonate—demonstrates profound regulatory effects on microcirculation, autonomic balance, inflammatory cascades, and mitochondrial and cellular resilience. The so-called “Procaine reset” reflects its capacity to transiently interrupt maladaptive neural patterns, modulate limbic activation, influence neurotransmitter systems, and restore homeostatic regulatory loops. The addition of bicarbonate prolongs Procaine’s plasma availability, enhances its intracellular penetration, and amplifies its eutrophic and anti-inflammatory properties. Although Procaine remains the primary therapeutic molecule in Neural Therapy, Lidocaine has also been utilised in selected clinical contexts. Lidocaine shares certain membrane-stabilising and anti-inflammatory features; however, its pharmacodynamics, autonomic influence, and regulatory depth are comparatively limited. Thus, Lidocaine may complement specific applications but cannot replace the superior vegetative-regulatory potential documented for Procaine. Procaine-Base infusion, when properly adapted to the patient's acid–base balance, represents a cornerstone therapy in regenerative medicine, improving pain thresholds, vascular perfusion, lymphatic drainage, and emotional equilibrium. Its safety profile—documented in hundreds of thousands of applications—is exceptionally favourable, with adverse effects being rare, transient, and mild. Given rising global burdens of chronic inflammatory, neurodegenerative, cardiovascular, metabolic, and oncologic disorders, Procaine emerges as a valuable multi-target regulatory agent capable of reducing symptom burden, complementing multimodal therapeutic strategies, and potentially lowering long-term health-care costs. Future highquality, large-scale studies are warranted to validate its systemic mechanisms, clarify dose–response relationships, and further integrate Procaine-based therapies into modern evidence-based frameworks. Keywords: Procaine Base infusion; Bicarbonate; Neural Therapy; Systemic regulation; Iidocaine
2 Int Clinc Med Case Rep Jour (ICMCRJ) 2025 | Volume 4 | Issue 12 2 International Clinical and Medical Case Reports Journal Review Article (ISSN: 2832-5788) More than one Century: Intravenous Procaine Therapy - A Systematic Review Introduction: The use of infusion with the local anaesthetic lidocaine is widespread in pain therapy, anaesthesia, and neurology. Established indications include the treatment of periand postoperative pain [1-6], cancer-induced pain [2], neuropathy [3] and postherpetic neuralgia [4], migraine [5.6.7], and trigeminal neuralgia [8]. Ferguson and Huber also have reported a positive effect in patients with arthritis [10]. The present review addresses the local anaesthetic Procaine, whose intravenous and, particularly, infusion administration has a history of over 100 years and is characterized by specific features within its therapeutic spectrum. The synthesis of the local anaesthetic Novocain (also known as Procaine) by Einhorn in 1905 provided us with a pleiotropic agent [10-14]. In 1906, Vishnevsky elucidated the anti-inflammatory properties of Novocain upon its application [15]. In subsequent years, several authors, including Leriche [15,16], Braun [15], and Spiess [11], documented numerous beneficial outcomes in the treatment of illnesses such as trigeminal neuralgia, migraine, throat cancer, fractures, post-operative pain, and a diverse array of dystrophic disorders. Its use has been much more developed in the field of Neural Therapy, created by the Huneke brothers, with observations of a broad spectrum of possible beneficial effects at the local, segmental, and systemic levels. A little dosage of Procaine, utilized to address neuromodulatory triggers[12] Alternatively, via intravenous injection, it might also elicit significant systemic changes. Summarizing systemic acting features of Procaine The Huneke brothers, in the first decades of the twentieth century, examined various effects of Procaine, discovering its potential utility in treating multiple disorders by subcutaneous, intradermal, intramuscular, and neural infiltrations. Consequently, they initially designated this therapy as "therapeutic anesthesia.” Subsequently, they discovered improvements in disease when applied segmentally, as well as immediate changes at a distance (referred to as “phenomenon in seconds or lightning reaction"). They subsequently endorsed this form of therapy, now known as neural therapy [15]. Numerous Russian authors have also described Procaine's medicinal effects. Speransky, a protégé of Pavlov, published "Basis for a New Theory of Medicine" in 1936, in which he developed a new understanding of the general pathological process (acute or chronic) as a dystrophy secondary to an irritative process in the nervous system. He also verified the therapeutic properties of Procaine, which act through the nervous system to reduce or eliminate inflammation and the dystrophic process in several acute and pathologic conditions, even infectious ones [17]. Vishnevsky corroborated his discoveries by confirming Procaine's mechanism of action as exerting a eutrophic effect on the organism, which is fundamentally rooted in Pavlov's Conditioned Reflexes Theory [16,13]. The term "trophism" in this context denotes a physiological and metabolic process that maintains the normal physicochemical state of an organism's interior environment, regulated by the collective function of all innervation systems [18]. In Romania, Aslan, a protégé of neurologist Marinescu, collaborated with Pharon to examine the effects of intravenous procaine injections, using Leriche's methodology, as well as intramuscular injections. Subsequently, she concentrated her treatment on several geriatric illnesses, applying Vishnevsky's principles regarding the eutrophic effects of Procaine. She presented statistical data demonstrating the extensive therapeutic effectivity of Procaine on neurological, cardiovascular, locomotor, dermatological, and gastrointestinal disorders in the elderly [16]. Prof. Aslan, the originator of the eponymous therapy, described it as possessing a vitamin-like function in addition to its anaesthetic properties [15]. Unlike all other anesthetic agents, it induces vasodilation of arteries and capillaries [15-19]. Consequently, this therapy enables the effective targeting and enhancement of inadequately perfused tissue, particularly in instances of inflammation and discomfort. Additional advantages of Procaine include its favourable tractability and minimal toxicity, attributed to its brief half-life and plasma breakdown [14,15], as well as its capillary impermeability effect and anti-inflammatory properties [16-21], anti-oxidative and fat-reducing action [17,18,19]. Krause demonstrated that the anti-inflammatory efficacy of Procaine in rheumatic diseases was particularly pronounced when combined with alkali [29]. In addition to the impact of inhibiting voltage-dependent sodium channels, resulting in transient anesthesia [20], the supplementary effects of Procaine on cell membranes and the extracellular matrix, together with its sympatholytic properties, were also emphasized [21-26]. The impact of Procaine on mitigating the adverse effects of radiation in oncology [22,23] or strategies to enhance the efficacy of Chemotherapy are documented (See Table 1) [24,25,26,27]. Furthermore, Procaine's wide-ranging epigenetic effects have been demonstrated. It was reported in 2003 that partial
3 Int Clinc Med Case Rep Jour (ICMCRJ) 2025 | Volume 4 | Issue 12 3 International Clinical and Medical Case Reports Journal Review Article (ISSN: 2832-5788) More than one Century: Intravenous Procaine Therapy - A Systematic Review inhibition of DNA methyltransferase in vitro resulted in a growth suppression during incubation with human cancer cells [28]. A study showed that Procaine could act as a tumour suppressor gene through reducing the effect of 5-methylcytosine on general genomic DNA and cell proliferation [29]. Tada et al. discovered in human hepatoma cells a decrease in DNA methylation [30]. In vitro studies have demonstrated that Procaine suppresses the proliferation and migration of colon cancer cells and exhibits an anti-tumour activity against human stomach and lung cancer [31,32,33]. Grandhi and Perona reviewed the efficacy of Procaine in preventing cancer recurrence post-surgery in a systematic analysis in 2020 [34]. In 2016, Sabit et al. demonstrated that Procaine and carboplatin together were the most effective treatment for lowering overall DNA methylation levels in colon cancer cells. [35]. Procaine is utilized to mitigate cytotoxicity and adverse effects associated with Chemotherapy [36-41] and radiotherapy [37] in oncology. Procaine is utilized in cardiac and coronary surgery as an addition in cardioplegic solutions to inhibit neuronal ion flow and to maintain and preserve the membrane [38-42]. Gradinaru et al classified Procaine as a geroprotector due to its ability to regulate the fundamental mechanisms of aging that are prevalent in several age-related disorders (see Figure 1), including responses to oxidative damage, inflammation, hypermethylation, cellular senescence, autophagy, and tumour protection [39]. Figure 1:New biological and pharmacological effects of Procaine—demonstrated within novel experimental approaches— which could acknowledge its consideration as a geroprotector candidate (Taken from Gradinaru et al 2021) Ultimately, Procaine affects the MAPK signaling pathway, among other factors. This subsequently modulates, among other factors, the expression of cytokines such as IL-6, as well as the replication of many RNA viruses, including influenza, hantavirus, respiratory syncytial virus (RSV), and SARS-CoV-2, which causes COVID-19. Procaine and the subsequently described ProcCluster® inhibit SARS-CoV-2 replication in vitro by over 90 percent (see figure 2)[40,41]. Comparable effects were observed with the Influenza A virus, the Aspergillus species, and Herpes simplex [42-44]. Figure 2: For SARS-CoV-2 infection in Calu-3 cells and IAV infection in A549 cells, in the absence or presence of Procaine, immunofluorescence microscopy was performed at 24 h p.i. In untreated, SARS-CoV-2-infected samples, accumulation of spike protein is visible (H2O), which is reduced in procaine-treated samples (Taken from Häring et al. 2022)
4 Int Clinc Med Case Rep Jour (ICMCRJ) 2025 | Volume 4 | Issue 12 4 International Clinical and Medical Case Reports Journal Review Article (ISSN: 2832-5788) More than one Century: Intravenous Procaine Therapy - A Systematic Review The intravenous administration and Infusion of Procaine The injection of Procaine into a vein to produce local anaesthesia of a limb was described by Bier in 1909. A tourniquet was advised to prevent the entry of the drug into the general circulation and to prolong the anaesthesia [43]. Also, the Huneke brothers administered Procaine intravenously [1]. It has been used empirically in a wide variety of disorders, including bronchospasm, allergic conditions, myositis, diverse pain states, tinnitus, acute arrhythmias, status epilepticus, migraine, and even senility [44]. In these clinical conditions, dosages of Procaine have ranged from 20 to 50 mg given slowly intravenously, up to 4mg/kg given in 20 minutes as a so-called “Procaine unit” [45,46]. The Procaine unit, representing dosages in the range of 0.2 mg/kg in a 70 kg adult, was derived from the rat hydrolysis of Procaine hydrochloride in rabbit plasma, although it is known that hydrolysis of the drug in the human plasma is more rapid [47,48]. The only well-defined syndrome for which Procaine is currently accepted as having established therapeutic value in academic medicine is that of acute cardiac arrhythmias. Here, Procaine is given as an intravenous bolus of 300 to 500 mg, representing dosages in the range of 4 to 8 mg/kg for a 70 kg adult [49]. A brief mention of intravenous Procaine appeared in the textbook on anesthesia by Lundy [50], who noted the effectiveness in relieving the pruritus of jaundice. Gordon reported on intravenous Procaine analgesia for the dressing of burns in war casualties. He commented on the absence of respiratory depression often seen when large doses of Morphine are used for this purpose. It became evident that comparatively large amounts of Procaine injected intravenously could be tolerated by humans if the injection was made slowly [51]. Ameuille, a French researcher, has described one of the most promising applications of Procaine: the improvement of dyspnoea caused by several types of pulmonary and cardiac conditions. [52]. Additionally, several authors have described significant effects of intravenous Procaine in relieving sympathetic and somatic pain. Mushin and RendellBaker summarized the following selection: postoperative pain, pain of dressing burns, angina pectoris, thrombophlebitis, intermittent claudication of vascular disease, and arthritis [53]. Increasingly, the high antiinflammatory potency of Procaine was recognized. Bennee reported about a complete healing from a South-African farmer aged 55 years suffering from an advanced Scleroderma. He treated the person for over three years with approximately 600 injections of Procaine 2 % intravenously, with only slight occasional reactions [54]. The action of intravenously administered Table 1. An overview according to the main systemic effects induced by Procaine: Pharmacological effect of Procaine Medical field of Use / Indication Local anaesthesia Pain treatment Vasodilatation All kinds of vascular diseases anti-inflammatory Acute and autoimmune diseases Sympatholytic Chronic pain, stress relief Broncho-spasmolytic Lung diseases, asthma Increase in coronary perfusion Heart diseases, heart protection Negative inotrope and antiarrhythmic Tachycardia, heart protection Anti-rheumatic and joint-protective Rheumatic diseases Anti-cancerous Cancer prevention and treatment Reduction of side effects from radioand Chemotherapy Oncology Virustatic, inhibition of multiplication Different kinds of viral diseases Antifungal Mold diseases Anti-oxidative Against oxidative stress Anti-depressive, anxiety loss, emotional balancing Dysthymia, depression, brightened mood membrane stabilization Transplant preservation Influencing multiple age-related diseases Geroprotection Source: own elaboration
5 Int Clinc Med Case Rep Jour (ICMCRJ) 2025 | Volume 4 | Issue 12 5 International Clinical and Medical Case Reports Journal Review Article (ISSN: 2832-5788) More than one Century: Intravenous Procaine Therapy - A Systematic Review bolus doses of Procaine on 24 subjects of psychiatric patients (7 with affective disorders, 17 with borderline personality disorder) as a probe of limbic system activity was described by Kellner in 1986 [55]. Topographic EEG analysis indicated selective increases in activity over the temporal lobes. Procaine was associated with increased secretion of Cortisol, ACTH, and Prolactin. Other uses of Procaine infusion were first described by Seifen et al. [56,57] specifically as a continuous treatment in cases of acute pancreatitis [58-60]. Also, it has been reported for use in epidural anaesthesia in infants, children, and high-risk patients, highlighting the substance's minimal toxicity [59-66]. O'Donnell et al. documented the use of procaine infusion to block cardiac nerves. [60]. For example, Layer et al. reported the results of a randomized clinical trial evaluating the effects of continuous systemic administration of 2 g of Procaine per day or placebo in 56 consecutive patients with acute pancreatitis. They were able to show that Procaine treatment was associated with a more substantial decrease in pain, and the proportion of patients hospitalized after 2 weeks was reduced to 80 % [61]. Already in 1957, Farrington reported on the importance of Procaine infusion in the management of manifestations of collagen diseases. The initial dose consisted of 500 cc. of 0.1% Procaine in normal saline or 5% glucose solution. If there were no untoward reactions to this amount, the patient was usually given 1.000 cc once per day for the succeeding 6 days at a rate of 45 drops per Minute. Of 71 cases of all types of scleroderma, about half were acrosclerotic or generalized. All patients have shown improvement in several symptoms, including difficulty with mastication, stiffness, soreness, swelling of various peripheral joints and fingers, and Raynaud's phenomenon. Similar effects they reached in three cases of dermatomyositis [62]. Currently, it is stated that prolonged calming, antidepressant, and anxiolytic effects are frequently found following intravenous injections or shortterm infusions of Procaine. [63,64]. Some research has shown that intravenous administration of Procaine in humans enhances blood flow to the anterior paralimbic regions and the amygdala.65], as well as improving the hemodynamic effects on the heart. [66]. Following procaine treatment in animal models, other limbic system regions have been investigated, revealing activation of several muscarinic cholinergic receptors in the hippocampus. Numerous publications have documented Procaine's effects on various biochemical systems, including dopamine, norepinephrine, serotonin, and glutamate. Consequently, Procaine is regarded as beneficial for the investigation of the limbic system and emotions [67,68]. Recent findings indicate that procaine injection into the ventral tegmental region can inhibit the fear-conditioned avoidance response in rats and also influences hippocampal theta rhythms associated with alertness and attention [69]. The extra pharmacologic effects of Procaine are due to its metabolites. By increasing endocannabinoid levels, DEAE inhibits fatty acid amide hydrolase, which in turn has anti-inflammatory effects [70,71]. Because of its ester bond with ceramide, the second metabolite, PABA, has multiple functions, including antihistamine, capillary sealant, and membrane stabilizer [72-74]. The effective combination of Procaine and bicarbonate for infusion The initial mention of the combination of Procaine with alkaline salts was recorded in 1930 [24]. To amalgamate the renowned pure alkaline infusion [73] The pluripotent characteristics of Procaine were originally documented in the 1997 study known as "neural infusion therapy" [74]. Following the demonstration of significant favorable outcomes in patients with chronic pain [75], the concept rapidly acquired popularity in German-speaking nations and was integrated into textbooks on pain and brain therapy [76,77]. Glusa et al. confirmed the vasodilatory impact of Procaine-Base mixture utilizing an animal model [78]. An elevation of intracellular Procaine levels resulting from the incorporation of sodium bicarbonate [79]An expedited initial effect was also noted in animal experiments. [80,81]. The sustained administration of Procaine-Base through a medical pump exhibited remarkable outcomes in numerous severe instances of pain and inflammation [82-84]. A comprehensive analysis of over 20 years of experience with Procaine-based infusion was recently published [83]. In the osteoarthritic rat model, the anti-rheumatic and joint-protective effects of Procaine-Base following intra-articular injection were significantly superior to those of Dexamethasone [84]. The main goal of incorporating the natural buffer sodium bicarbonate was to influence the plasmatic breakdown of Procaine, as mediated by serum esterase activity. All local anesthetics exhibit comparable properties of general distribution and ionization. The significance of these attributes lies in their impact on voltage-
6 Int Clinc Med Case Rep Jour (ICMCRJ) 2025 | Volume 4 | Issue 12 6 International Clinical and Medical Case Reports Journal Review Article (ISSN: 2832-5788) More than one Century: Intravenous Procaine Therapy - A Systematic Review Table. 2: The main differences between Procaine and Procainium-hydrogen-carbonicum (ProcCluster®) dependent sodium channels. The uncharged Procaine molecule acts as the transport structure that enables permeation. The ionized form, Procaine-H+, attaches to the sodium channel receptor, consequently blocking impulse propagation. The pH value of the solution and the terrain can affect the ionized and non-ionized forms of Procaine [85]. Source: own elaboration Table 2 shows that a shift in pH can significantly affect solubility and membrane permeability. Consequently, the incorporation of an alkaline addition alters the correlation between the mode of transport and the mode of action. At a low pH value (<6), just 0.1% of Procaine was detected in the lipid-soluble form [40]. Moreover, varying amounts of sodium bicarbonate can affect intracellular pH [86]. It was hypothesized that, under alkaline conditions, the conversion of Procaine to para-aminobenzoic acid (PABA) and diethylaminoethanol (DEAE) would be significantly diminished. Contrary to this idea, it is posited that, following intravenous injection of Procaine-Base, it is diluted in the blood of prominent capillaries, resulting in a rapid decrease in pH, ultimately returning to normal physiological values. Furthermore, the pulmonary circulation will induce a respiratory compensation for alkalosis. The slowing of Procaine degradation can be explained as follows: The aforementioned pH-dependent dissociation change will lead to elevated levels of the more effectively penetrating transport forms. This is characteristic of all local anesthetics, with 3-40% of the released base present, depending on the anesthetic agent's pKa. In addition to the steady-state distribution, the distribution rate is also significant. The distribution speed is the limiting factor, indicating that membrane diffusion is the rate-determining step[87]. The distribution is directly dependent on the drug's lipophilicity. Altering the pH modifies the lipophilic characteristics. An increased concentration of free base correlates with enhanced penetration, which is readily accessible to adjacent tissue and is not readily degraded by serum esterase [40]. Procaine Base Infusion Methodology A test application of one drop of 1% Procaine into the conjunctiva is recommended if prior information regarding Procaine tolerance is unavailable before the infusion. The patient may experience a transient, mild burning sensation (attributable to HCl) and mild acute erythema (resulting from increased blood flow). Additionally, numbness is expected. Please refrain from administering parenteral infusions if the burning sensation persists for an extended period. It is imperative to emphasize that only Procaine-HCl with pharmacological authorization for intravenous administration and devoid of preservatives (e.g., parabens) should be used. It is advisable to initiate treatment with a carrier solution of 250 to 500 ml, a dosage of 50-100 mg Procaine-HCl, and 20 ml of diluted sodium hydrogen carbonate (8.4%). Simultaneously, a comparable electrolyte solution may be used to prevent hypernatremia instead of the isotonic sodium chloride solution, which has been used for many years. The infusion lasts approximately 45 to 60 minutes. The Procaine-Base infusion should be titrated at a rate of 50 mg Procaine-HCl and 10 ml sodium bicarbonate
7 Int Clinc Med Case Rep Jour (ICMCRJ) 2025 | Volume 4 | Issue 12 7 International Clinical and Medical Case Reports Journal Review Article (ISSN: 2832-5788) More than one Century: Intravenous Procaine Therapy - A Systematic Review (8.4%) until the desired therapeutic effect is achieved. The maximum permissible dosage of Procaine-HCl for an individual of normal weight is 300 mg (refer to dosing table 3). It is recommended that, for individuals with cardiovascular risk factors, a monitoring technique (e.g., single-canal electrocardiogram/oximetry) be used when the concentration of Procaine-HCl exceeds 300 mg. It is suggested that a 30-minute observation period be maintained after the treatment. After infusion, the patient should refrain from operating a motor vehicle for approximately 1 hour. To prevent the degradation of unstable Procaine, the Procaine-base mixture should be used within 2 hours. In the absence of prior acid-base diagnostics, the Procaine-Base infusion should not be delivered more than 3 times weekly, with at least 1 day of rest between treatment sessions. A series of 6 to 10 infusions has been authorized based on the medical situation. Table 3a: Dosage table for Procaine 1% (modified acc. to Oettmeier et al 2019) Procaine dosage 1 % Sodium-hydrogencarbonate dosage 8.4 % Sodium chloride 0.9 % Total volume 100 mg = 10 ml 20 ml 500 ml 530 ml 200 mg = 20 ml 40 ml 500 ml 560 ml 300 mg = 30 ml 60 ml 500 ml 590 ml 400 mg = 40 ml 80 ml 500 ml 620 ml 500 mg = 50 ml 100 ml 500 ml 650 ml The standard haematological indicators of inflammation, including the erythrocyte sedimentation rate and C-reactive protein (CRP), are expected to increase following a series of Procaine-Base infusions. Patients often report a significantly enhanced mood and improved overall condition after 6 to 10 treatments. In cases of a favorable response to treatment (termed "responders," occurring in approximately 80% of patients), it is recommended, particularly for chronic conditions, to continue long-term therapy with an adequate dosage at extended intervals, such as once or twice monthly [34,35,36]. General experiences with Procaine-Base-Infusion The alleged hypersensitivity to Procaine, referred to as “para-group allergy” in older texts, has not yet been substantiated [88,89]. A meta-analysis of critical data during Procaine-Base infusions in 5,698 patients, which included comprehensive documentation of vital parameters during and after the injection, did not reveal any statistically significant differences between the primary groups [90]. The readings remained exceptionally stable, even at elevated Procaine concentrations. Most recorded treatment protocols consisted of medium concentrations of Procaine (100Table 3b:Dosage table for Procaine 2% (modified acc. to Oettmeier et al 2019) Procaine dosage 2 % Sodium-hydrogencarbonate dosage 8.4 % Sodium chloride 0.9 % Total volume 100 mg = 5 ml 20 ml 500 ml 525 ml 200 mg = 10 ml 40 ml 500 ml 550 ml 300 mg = 15 ml 60 ml 500 ml 575 ml 400 mg = 20 ml 80 ml 500 ml 600 ml 500 mg = 25 ml 100 ml 500 ml 625 ml
8 Int Clinc Med Case Rep Jour (ICMCRJ) 2025 | Volume 4 | Issue 12 8 International Clinical and Medical Case Reports Journal Review Article (ISSN: 2832-5788) More than one Century: Intravenous Procaine Therapy - A Systematic Review 300 mg) and sodium hydrogen carbonate (8.4%, 20-60 ml), which are considered standard everyday practice. High concentrations of Procaine (exceeding 500 mg) and sodium bicarbonate (8.4%, exceeding 100 ml) resulted in a marginal increase in average blood pressure. Moreover, it is essential to note that the blood pressure recorded did not exhibit any significant variation at 15 or 30 minutes after the infusion. Despite administering Procaine treatment infusions in nearly 2 million cases in accordance with the established protocol, we have not documented a single case of chronic or severe adverse effects in our clinics and outpatient facilities. The absence of any reports of severe allergic emergencies further substantiated Becke's conclusions regarding the substantial therapeutic safety of Procaine. We have not documented a single instance of long-term or severe adverse effects in our clinics and outpatient facilities, despite administering Procaine treatment infusions in nearly one million cases in accordance with the established protocol. Becke's The absence of any reports of severe allergic emergencies further supported Becke's conclusions regarding the substantial therapeutic safety of Procaine. [58]. Heart palpitations (6%) and excessive perspiration (5%) are occasionally reported by individuals. Patients taking calcium antagonists, nitro compounds, and betablockers appear to be more susceptible to these adverse effects, according to our observations. In such cases, the negative isotropic and negative rhythmotropic properties of Procaine are overshadowed by the reflecting and over-segmental disinhibitory effects of anesthesia. As anticipated, approximately 6% of patients may experience a transient decrease in blood pressure and vasovagal syncope during the procedure. These symptoms subside within a few minutes, particularly when the infusion rate is reduced [34,63]. A subset of patients (5%) experiences sleep disturbances and a general sensation of hyperactivity that persists for up to 1 day post-infusion, without a reduction in physical labor capacity. Mild dizziness and transient migraines were reported by approximately 4.5% of the treated individuals. In accordance with the holistic principles of brain therapy, such reactions may manifest as the "first reaction" (Hering's effect), particularly during the initial infusions [1] and homeopathy [91]. The main Indications of Procaine-Base-Infusions The wide range of therapeutic actions of Procaine, when combined with an alkaline addition, accounts for the extensive range of medical indications (Table 4). Table 4: Main indications of Procaine-Base-Therapy Infection (acute and chronic) flu-like symptoms, Influenza A, Herpes simplex, Aspergillusniger, post COVID-19 and post vaccination COVID-19 syndrome, Lyme disease, Herpes zoster Pain Management (acute and chronic) migraine, headache, activated osteoarthrosis, postoperative pain, Radicular syndrome, pseudo-radicular syndrome, Sudeck’s syndrome, Sudeck’s syndrome, early stage of algodystrophy, multiple arthralgia, Fibromyalgia autoimmune Diseases Scleroderma, Lupus erythematosus, rheumatoid arthritis, psoriatic arthritis, Hashimoto's and Crohn's disease, neurodermatitis, multiple sclerosis, algodystrophy, all kinds of neuralgia, ulcerative colitis, polymyalgia rheumatica, Complementary Oncology as an essential part of complementary oncology and immunotherapy,pain management of cancerous diseases, to reduce side effects of tumor-destructive treatments (Chemotherapy, radiation), and prevention of recurring as an essential part of complementary oncology and immunotherapy, Oncology Internal Medicine periphery circulatory disorders, constipation, dysmenorrhea, Clinical and para-clinical hints for tissue acidosis, osteoporosis, Source: own elaboration
9 Int Clinc Med Case Rep Jour (ICMCRJ) 2025 | Volume 4 | Issue 12 9 International Clinical and Medical Case Reports Journal Review Article (ISSN: 2832-5788) More than one Century: Intravenous Procaine Therapy - A Systematic Review Absolute contraindications to the infusion are exceedingly rare, provided that both the therapist and their personnel are adequately trained in the methodology and have experience administering parenteral Procaine. It is suggested that the procaine base infusion be avoided or that only minimal doses be administered in cases of neurosis, psychosis, or hypersensitivity to Procaine with ambiguous compliance. Additionally, it is essential to check the manufacturer's product information for sodium bicarbonate and Procaine. Status: Procaine-Base-Infusion adapted to the acidbase-balance The author Saha reported that three of 13 patients experienced clinical manifestations of metabolic alkalosis as the eighth most common side effect after 7 Procaine-Base infusions with progressively escalating concentrations, culminating at 300 mg Procaine-HCl and 120 ml of 8.4% sodium bicarbonate.[92]. Base excess (BE) measured by arterial blood gas was always more than plus two before and after these infusions, confirming metabolic alkalosis. The Procaine-Base infusion approach prevents the need for daily sodium bicarbonate treatment at such high doses. Only patients with proper acid-base equilibrium can use this daily medicine. The body's buffer system must not overflow. Increasing numbers of people have metabolic alkalosis and impaired compensatory capacity for acid-base balance. This occurs in cases of advanced malignancy, hepatic insufficiency, and colon putrefactive dysbiosis. Antacids, alkaline powders, loop diuretics, and high salt intake worsen acid-base imbalance to alkalosis[93,94]. For the assessment of acid-base equilibrium, it is recommended that the traditional blood gas analysis EPOC[95]. The test provides precise information regarding base excess and specifies the exact quantity of base required. Metabolic alkalosis may also arise in the context of hyponatremia, hypokalaemia, and elevated ammonia concentrations in EDTA plasma. Metabolic acidosis is most observed in instances of inflammation, cardiac and renal failure, rheumatic conditions, and pain-related disorders[96]. These individuals require an elevated buffer base and should be administered sodium bicarbonate between 60 and 120 ml (8.4% solution) alongside Procaine. Unlike metabolic alkalosis, as seen in Figure three below, there is minimal or no need for supplementary base treatment. In this instance, we provide only ProcaineHCl infusions, with a carrier solution. Furthermore, we recommend administering 3-5 ampules of L(+)-lactic acid. Alternatively, the newly formulated Procainiumhydrogen-carbonicum compound, available as a readyto-use rapid infusion (0.1-0.3%), is advised[97]. Figure 3: Findings of metabolic alkalosis. Source: own elaboration based on the system EPOC, Siemens HealthCare AG. Based on the BE results of the acid-base test, we recommend the following adjustment of bicarbonate quantity for the infusion (Table 5):
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19 Int Clinc Med Case Rep Jour (ICMCRJ) 2025 | Volume 4 | Issue 12 19 International Clinical and Medical Case Reports Journal Review Article (ISSN: 2832-5788) More than one Century: Intravenous Procaine Therapy - A Systematic Review 67. BLEESE N, DÖRING V, KALMAR P, POKAR H, POLONIUS MJ, STEINER D: Intraoperative myocardial protection by cardioplegia in hypothermia. The Journal of thoracic and cardiovascular surgery. ;75(3):405–13 (1978). 68. ISSELHARD W, SCHORN B, HÜGEL W, UEKERMANN U: Comparison of three methods of myocardial protection.Thorac Cardiovasc Surg.;28(5):329–36 (1980). 69. EPTING WS, HOFFMEISTER HE, STUNKAT R: Aortic valve replacement utilizing induced ischemic arrest with magnesium-aspartate-procaine.J Cardiovasc Surg (Torino). ;18(4):421–6 (1977). 70. KALMÁR P, BLEESE N, DÖRING V, GERCKEN G, KIRSCH U, LIERSE W, POKAR H, POLONIUS MJ, RODEWALD G: Induced ischemic cardiac arrest. Clinical and experimental results with magnesiumaspartate-procaine solution (Cardioplegin).J Cardiovasc Surg (Torino). 16(5):470–5 (1975). 71. GRADINARU D, UNGURIANU A et al: Procaine – The controversial Geroprotector Candidate: New insights regarding its molecular and cellular effects. Oxidative Medicine and Cellular Longevity, 1–18 (2021) 72. HÄRING, C, SCHROEDER, J., LÖFFLER, B., ENGERT, B., Ehrhardt, Ch: The local anesthetic Procaine prodrugs ProcCluster® and Procainehydrochloride impair SARS-CoV-2 replication in vitro. Doi: https://doi.org/10.1101/2021.06.07.447335. (2022) 73. HÄRING C, JUNGWIRTH J, SCHROEDER J, LÖFFLER B, ENGERT B, EHRHARDT C: The Local Anaesthetic Procaine Prodrugs ProcCluster® and Procaine-Hydrochloride Impair SARS-CoV-2 Replication and Egress in Vitro. Int J Mol Sci 24(19), 14584 pp, 2024 74. HÄRING, C, SCHRÖDER J, JUNGWIRTH J, LÖFFLER B, HENKE A, ENGET B, EHRHARDT C: ProcCluster® and procaine hydrochloride inhibit the replication of influenza A virus in vitro. Frontiers in Microbiol. 1-17 (2024), DOI 10.3389/ fmicb.2024.1422651 75. König S, Schroeder J, Heinekamp T, Brakhage AA, Löffler B, Engert B, Ehrhardt C. ProcCluster® and procaine hydrochloride inhibit the growth of Aspergillus species and exert antimicrobial properties during coinfection with influenza A viruses and A. fumigatus in vitro. Front Cell Infect Microbiol. 2024 Oct 15;14:1445428. Doi: 10.3389/ fcimb. 2024.1445428. PMID: 39473925; PMCID: PMC11518849. 76. JUNGWIRTH J, SIEGERT L, GAUTHIER L, HENKE A, , KRÄMER OH, ENGERT B. and EHRHARDT CH. The Procaine-Based ProcCluster. Impedes the SecondEnvelopment Process of Herpes Simplex Virus Type 1. Int. J. Mol. Sci., 26, 7185 (2025) 77. BIER A. Münch Med Wsxhr, 1: 589 (1909) 78. LIVINGSTON KE, PERRIN RG: Central physiological effects of experimental intravenous Procaine hydrochloride. J Neurosurg 37: 188 (1972) 79. GRAUBARD DJ, RITTER HH: Intravenous Procaine in the treatment of trauma: preliminary study. Amer J Surg 74: 765 (1947) 80. MOOR F B: A resume of intravenous Procaine therapy. Med arts and Sciences: A scientific Journal of the college of Medical Evangelists: Vol 2, No 4, 129–134 (1948) 81. GOODMAN LS, GILMAN A: Cocaine, Procaine and other synthetic local anesthetics, in Goodman LS and Gilman A (eds): The Pharmacological Basis of Therapeutics. New York, Macmillan, ed 2, pp. 354 – 388 (1955) 82. KALOW W: Hydrolysis of local anesthetics by human serum cholinesterase. J Pharmacol Exp Ther 104: 122 (1952) 83. EDDLEMAN EE, RESNIK WH, HARRISON TR: Disorders of rate, rhythm, and conduction, in Harrison TR (ed): Principles of Internal Medicine. Toronto, McGraw-Hill (1966) 84. LUNDY JS: Clinical Anesthesia. Philadelphia (1942) 85. GORDON RA: Canad Med Ass J. 133: 849 (1943) 86. AMOILLE MP. Medical research in France during the war. Paris: 269 (1948) 87. MUSHIN WW and RANDELL-BAKER L: Intravenous Procaine. The Lancet 4: 619–670 (1949) 88. BENNEE J. Scleroderma treated with 2% Procaine intravenously. Canad M A J. 70: 71 (1954) 89. KELLNER C H, POST R M et al: Intravenous Procaine as a probe of limbic system activity in psychiatric patients and standard controls. Biol Psychiatry 22: 1107-1126 (1986) 90. SEIFEN AB, FERRARI AA, SEIFEN EE, THOMPSON DS, CHAPMAN: J Pharmacokinetics
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21 Int Clinc Med Case Rep Jour (ICMCRJ) 2025 | Volume 4 | Issue 12 21 International Clinical and Medical Case Reports Journal Review Article (ISSN: 2832-5788) More than one Century: Intravenous Procaine Therapy - A Systematic Review 111. BUTTERWORTH, J.F.T. AND L.R. COLE, Low concentrations of Procaine and diethylaminoethanol reduce the excitability but not the action potential amplitude of hippocampal pyramidal cells. Anesth Analg.;71(4): 404–10 (1990). 112. MATULEWICZ P, ORZEŁ-GRYGLEWSKA J, BRASZKA Ł, ZAWISTOWSKI P, JURKOWLANIEC E: Hippocampal theta rhythm after local administration of Procaine or amphetamine into the ventral tegmental area in fear conditioned rats. Neurosci Lett.; 589: 132–7 (2015). 113. LITTLE JW, FORD A, SYMONS-LIGUORI AM, CHEN Z, JANES K, DOYLE T, XIE J, LUONGO L, TOSH DK, MAIONE S, BANNISTER K, DICKENSON AH, VANDERAH TW, PORRECA F, JACOBSON KA, SALVEMINI D: Endogenous adenosine A3 receptor activation selectively alleviates persistent pain states. Brain.;138(Pt 1): 28-35 (2015) 114. VANDEVOORDE S, LAMBERT DM, SMART D, JONSSON KO, FOWLER CJ.: N-Morpholinoand N-diethyl-analogues of palmitoylethanolamide increase the sensitivity of transfected human vanilloid receptors to activation by anandamide without affecting fatty acid amidohydrolase activity. Bioorg Med Chem. ;11(6): 817–25 (2003). 115. ABOUNASSIF MA, EL-OBEID HA, GADKARIEM EA: Stability studies on some benzocycloheptane antihistaminic agents. J Pharm Biomed Anal.;36(5): 1011-8 (2005). 116. UCHIYAMA M, OGURI M, MOJUMDAR EH, GOORIS GS, BOUWSTRA JA: Free fatty acids chain length distribution affects the permeability of skin lipid model membranes. BiochimBiophys Acta.; 858(9):2050-9 (2016). 117. PALONCÝOVÁ M, DEVANE RH, MURCH BP, BERKA K, OTYEPKA M: Rationalization of reduced penetration of drugs through ceramide gel phase membrane. Langmuir. ;30(46): 13942–8 (2014). 118. WORLITSCHEK K: Practice of acid-base household. German. p. 117 ff. Haug Publisher, 6th Edition (2012). 119. REUTER U, OETTMEIER R: Regulation and pain treatment with infusion neural therapy. German. NaturaMed, 12: 20–25 (1997). 120. REUTER U, OETTMEIER R: The high-dose Procaine-Base-Infusion. German. Ärztezeitschrift f. Naturheilverfahren 11: 776-783 (1999). 121. BERG Fvd.(Eds.): Applied Physiology, Volume 4. Understanding and influencing pain. German. Thieme Publisher Stuttgart, (2004). 122. WEINSCHENK S (Eds.): Handbook of Neural Therapy – Diagnostics and Treatment with local Anesthetics. German. 2nd Ed., Urban and Fischer. ISBN 978-3-13-220491-1. (2020). 123. GLUSA E: Spasmolytic action of Procaine-Base on the aorta of rats. German. ID-Pharma, Research material. (1999). 124. IBUSUKI S; KASUKI H; TAKASAKI M: The effects of extracellular pH with and without bicarbonate on intracellular Procaine concentrations of anesthetic effects in crayfish giant cells. Anesthesiology, V 88/6: 1549–1557 (1998). 125. YUNG E, LAHOTI T, JAFARI S, WEINBERG JD, SCHIANODICOLA JJ, YARMUSH JM, RAY SD: Bicarbonate plus epinephrine shortens the onset and prolongs the duration of sciatic block using chloro-Procaine followed by bupivacaine in SpragueDawley rats. Reg Anesth Pain Med.;34(3): 196-200 (2009). 126. STEVENS RA, CHESTER WL, GRUETER JA, SCHUBERT A, BRANDON D, CLAYTON B, SPITZER L: The effect of pH adjustment of 0.5% bupivacaine on the latency of epidural anesthesia. Reg Anesth.;14(5): 236–9 (1989). 127. OETTMEIER R, REUTER U: The continuous Procaine-Basen infusion/-perfusion: New ways for systemic influencing regulation, inflammation and pain. German. Erfahrungsheilkunde; 2:, 75-84 (2000). 128. IUDENKOV NF: Intra-arterial infusion of penicillin and Procaine in the treatment of suppurative inflammations and open trauma. Russian. Voen Med Zh.;86(1):77-9 (1959) 129. FUZAYLOV G, KELLY TL, BLINE C, DUNAEV A, DYLEWSKI ML, DRISCOLL DN: Post-operative pain control for burn reconstructive surgery in a resource-restricted country with subcutaneous infusion of local anesthetics through a soaker catheter to the surgical site: Preliminary results. Burns. ;41(8):1811-5 (2015). 130. OETTMEIER, R, REUTER, U, PINILLA BONILLA, L.B.: The Procaine-Base-Infusion: 20Years of Experience of an Alternative Use with Several Therapeutic Effects. J Altern Complement Integr Med, 5: 061 (2019)
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23 Int Clinc Med Case Rep Jour (ICMCRJ) 2025 | Volume 4 | Issue 12 23 International Clinical and Medical Case Reports Journal Review Article (ISSN: 2832-5788) More than one Century: Intravenous Procaine Therapy - A Systematic Review 155. NAZLIKUL H, BILGIN MD: What is Neural Therapy? The Effect of Neural Therapy on Chronic Inflammatory Diseases (Chronic Inflammatory Bowel Diseases) - Nöralterapinedir? Kronikinflamatuarhastalıklarda (kronikinflamatuarbağırsakhastalıkları) nöralterapietkinliği. Babacan CA, editör. Ozon veNöralterapi. 1. Baskı. Ankara: Türkiye Klinikleri; p.3644. (2022). 156. VINYES D, SELLART MM, FISCHER L: Therapeutic Use of Low-Dose Local Anesthetics in Pain, Inflammation, and Other Clinical Conditions: A Systematic Scoping Review J. Clin. Med. , 12(23), 7221; https://doi.org/10.3390/jcm12237221 (2023). 157. NAZLIKUL H, URAL NAZLIKU, FG: Fibromyalgia Syndrome (FMS): Neural Therapy as a Key to Pain Reduction and Quality of Life. Int Clinc Med Case Rep Jour.;4(2):1-25.(2025) 158. EGLI S, PFISTER M, LUDIN SM, PUENTE DE LA VEGA K, BUSATO A, FISCHER L: Long-term results of therapeutic local anesthesia (neural therapy) in 280 referred refractory chronic pain patients. BMC Complement Altern Med 2015; 15: 200. (2015). 159. NAZLIKUL H: Die segmentale vertebrale Dysfunktion ist ein multikausales Geschehen. Manuelle Medizin. 2014; 52(5): 432–6. (2014). 160. NAZLIKUL H, BILGIN MD: What is Neural Therapy? The Effect of Neural Therapy on Chronic Inflammatory Diseases (Chronic Inflammatory Bowel Diseases) - Nöralterapinedir? Kronikinflamatuarhastalıklarda (kronikinflamatuarbağırsakhastalıkları) nöralterapietkinliği. Babacan CA, editör. Ozon veNöralterapi. 1. Baskı. Ankara: Türkiye Klinikleri; p.3644. (2022). 161. VINYES D, SELLART MM, FISCHER L: Therapeutic Use of Low-Dose Local Anesthetics in Pain, Inflammation, and Other Clinical Conditions: A Systematic Scoping Review J. Clin. Med. , 12(23), 7221; https://doi.org/10.3390/jcm12237221 (2023). 162. NAZLIKUL H, URAL NAZLIKU, FG: Fibromyalgia Syndrome (FMS): Neural Therapy as a Key to Pain Reduction and Quality of Life. Int Clinc Med Case Rep Jour.;4(2):1-25.(2025) 163. EGLI S, PFISTER M, LUDIN SM, PUENTE DE LA VEGA K, BUSATO A, FISCHER L: Long-term results of therapeutic local anesthesia (neural therapy) in 280 referred refractory chronic pain patients. BMC Complement Altern Med 2015; 15: 200. (2015). 164. NAZLIKUL H: Die segmentale vertebrale Dysfunktion ist ein multikausales Geschehen. Manuelle Medizin. 2014; 52(5): 432–6. (2014). 165. NAZLIKUL H, BILGIN MD: What is Neural Therapy? The Effect of Neural Therapy on Chronic Inflammatory Diseases (Chronic Inflammatory Bowel Diseases) - Nöralterapinedir? Kronikinflamatuarhastalıklarda (kronikinflamatuarbağırsakhastalıkları) nöralterapietkinliği. Babacan CA, editör. Ozon veNöralterapi. 1. Baskı. Ankara: Türkiye Klinikleri; p.3644. (2022). 166. VINYES D, SELLART MM, FISCHER L: Therapeutic Use of Low-Dose Local Anesthetics in Pain, Inflammation, and Other Clinical Conditions: A Systematic Scoping Review J. Clin. Med. , 12(23), 7221; https://doi.org/10.3390/jcm12237221 (2023). 167. NAZLIKUL H, URAL NAZLIKU, FG: Fibromyalgia Syndrome (FMS): Neural Therapy as a Key to Pain Reduction and Quality of Life. Int Clinc Med Case Rep Jour.;4(2):1-25.(2025) 168. EGLI S, PFISTER M, LUDIN SM, PUENTE DE LA VEGA K, BUSATO A, FISCHER L: Long-term results of therapeutic local anesthesia (neural therapy) in 280 referred refractory chronic pain patients. BMC Complement Altern Med 2015; 15: 200. (2015). 169. NAZLIKUL H: Die segmentale vertebrale Dysfunktion ist ein multikausales Geschehen. Manuelle Medizin. 2014; 52(5): 432–6. (2014). 170. NAZLIKUL H, BILGIN MD: What is Neural Therapy? The Effect of Neural Therapy on Chronic Inflammatory Diseases (Chronic Inflammatory Bowel Diseases) - Nöralterapinedir? Kronikinflamatuarhastalıklarda (kronikinflamatuarbağırsakhastalıkları) nöralterapietkinliği. Babacan CA, editör. Ozon veNöralterapi. 1. Baskı. Ankara: Türkiye Klinikleri; p.3644. (2022). 171. VINYES D, SELLART MM, FISCHER L: Therapeutic Use of Low-Dose Local Anesthetics in Pain, Inflammation, and Other Clinical Conditions: A Systematic Scoping Review J. Clin. Med. , 12(23), 7221; https://doi.org/10.3390/jcm12237221 (2023). 172. de CLIVE-LOWE SG, DESMOND J, NORTH J.: Intravenous lidocaine anesthesia. Anesthesia (1958)
24 Int Clinc Med Case Rep Jour (ICMCRJ) 2025 | Volume 4 | Issue 12 24 International Clinical and Medical Case Reports Journal Review Article (ISSN: 2832-5788) More than one Century: Intravenous Procaine Therapy - A Systematic Review 173. CASSUTO J, WALLIN G, HÖGSTRÖM S, FAXÉN A, RIMBÄCK G.: Inhibition of postoperative pain by continuous low-dose intravenous infusion of lidocaine. Anesth Analg, (1985) 174. KASTRUP J, PETERSEN P, DEJGÅRD A, ANGELO HR, HILSTED J. Intravenous lidocaine infusion – a new treatment of chronic painful diabetic neuropathy? Pain, (1987) 175. IMURA, A., et al.: Effects of intravenous lidocaine infusion in patients with herpes zoster and postherpetic neuralgia: A case series. Pain Physician, 27(2), 131–138 (2024) 176. QIAN, H., et al.: Intravenous lidocaine infusion for refractory herpes zoster-related neuropathic pain in transplant recipients: A case series. Frontiers in Pharmacology, 15, 1422778 (2024) 177. HUI, Y., et al.: Short-term analgesic effect of intravenous lidocaine in patients with postherpetic neuralgia: A randomized, double-masked, placebocontrolled study. Pain Medicine, 19(1), 56-64, (2018) 178. WEISS WA.: Intravenous use of lidocaine for ventricular arrhythmias. Anesth Analg, (1960) 179. PITT A, LIPP H, ANDERSON ST. Lidocaine is given prophylactically to patients with acute myocardial infarction.Lancet, (1971) 180. Tamam, Y., Özdemir, H. H., Gedik, A., Tamam, C., & Nazlıkul, H. (2017). Efficacy of peripheral lidocaine application (neural therapy) in the treatment of neurogenic detrusor overactivity in multiple sclerosis patients. Neurourology and Urodynamics, 36(7), 1832-1838. 181. Nazlikul, H., Ural Nazlikul, F. G., & Tamam, Y. (2025). The Significance of Thoracic Blockages for the Autonomic Nervous System–Neural Therapy and Its Clinical Relevance. Recent Adv Clin Trials. 2025; 5 (1); 1-17. DOI: 10.33425/2771-9057.1054. Volume, 5, 2. 182. Ural Nazlikul, F. G., & Nazlikul, H. (2025). Diaphragmatic Dysfunctions and Their Treatment: Neural Therapy and Manual Medicine as Effective Approaches. Int Clinc Med Case Rep Jour. 2025; 4 (1): 1, 8. 183. URAL NAZLIKUL, F. G., NAZLIKUL, H., ÖZKAN, N., ACARKAN, T., TAMAM, Y., ORAK, M., & BILGIN, M. Long-Term Effects of Neural Therapy in Fibromyalgia–A Retrospective Multicenter Analysis. Effectiveness of Neural Therapy in Patients with Fibromyalgia. IntClinc Med Case Rep Jour. 184. Jılta, O., Açanal, M. H., Velayi, M., Jilta, G. Y., & Nazlıkul, H. (2025). Effects of neural therapy in posttraumatic paraplegia: A case study of significant and permanent improvement in a cat. Journal of Istanbul Veterinary Sciences, 9(1), 15-22. 185. Nazlikul, H., & Ural, F. (2025). The diaphragm: recognizing functional disorders and treating them effectively with neural therapy and manual medicine Das Zwerchfell: Funktionsstörungenerkennen und wirksambehandelnmitNeuraltherapie und manuellerMedizin. Manuelle Medizin.