BackgroundCan the application of local anesthetics (Neural Therapy, NT) alone durably improve pain symptoms in referred patients with chronic and refractory pain?If the application of local anesthetics does lead to an improvement that far exceeds the duration of action of local anesthetics, we will postulate that a vicious circle of pain in the reflex arcs has been disrupted (hypothesis).MethodsCase series design. We exclusively used procaine or lidocaine. The inclusion criteria were severe pain and chronic duration of more than three months, pain unresponsive to conventional medical measures, written referral from physicians or doctors of chiropractic explicitly to NT. Patients with improvement of pain who started on additional therapy during the study period for a reason other than pain were excluded in order to avoid a potential bias. Treatment success was measured after one year follow-up using the outcome measures of pain and analgesics intake.Results280 chronic pain patients were included; the most common reason for referral was back pain. The average number of consultations per patient was 9.2 in the first year (median 8.0). After one year, in 60 patients pain was unchanged, 52 patients reported a slight improvement, 126 were considerably better, and 41 pain-free. At the same time, 74.1 % of the patients who took analgesics before starting NT needed less or no more analgesics at all. No adverse effects or complications were observed.ConclusionsThe good long-term results of the targeted therapeutic local anesthesia (NT) in the most problematic group of chronic pain patients (unresponsive to all evidence based conventional treatment options) indicate that a vicious circle has been broken. The specific contribution of the intervention to these results cannot be determined. The low costs of local anesthetics, the small number of consultations needed, the reduced intake of analgesics, and the lack of adverse effects also suggest the practicality and cost-effectiveness of this kind of treatment. Controlled trials to evaluate the true effect of NT are needed.

Whereas the autonomic nervous system (ANS) and the immune system used to be assigned separate functions, it has now become clear that the ANS and the immune system (and thereby inflammatory cascades) work closely together. During an acute immune response (e. g., in viral infection like Covid-19) the ANS and the immune system establish a fast interaction resulting in "physiological" inflammation. Based on our knowledge of the modulation of inflammation by the ANS we propose that a reflectory malfunction of the ANS with hyperactivity of the sympathetic nervous system (SNS) may be involved in the generation of acute hyperinflammation. We believe that sympathetic hyperactivity triggers a hyperresponsiveness of the immune system ("cytokine storm") with consecutive tissue damage. These reflectory neuroimmunological and inflammatory cascades constitute a general reaction principle of the organism under the leadership of the ANS and does not only occur in viral infections, although Covid-19 is a typical current example therefore. Within the overreaction several interdependent pathological positive feedback loops can be detected in which the SNS plays an important part. Consequently, there is a chance to regulate the hyperinflammation by influencing the SNS. This can be achieved by a stellate ganglion block (SGB) with local anesthetics, temporarily disrupting the pathological positive feedback loops. Thereafter, the complex neuroimmune system has the chance to reorganize itself. Previous clinical and experimental data have confirmed a favorable outcome in hyperinflammation (including pneumonia) after SGB (measurable e. g. by a reduction in proinflammatory cytokines).

A total of 22 patients suffering from idiopathic Parkinson's disease and 20 age-matched volunteers were questioned about autonomic disturbances and all underwent four non-invasive tests examining cardiovascular reflexes. Significantly more autonomic disturbances were reported by the patients than by the controls. Resting blood pressure was significantly decreased in patients taking dopamine agonists, whereas it was normal in those patients who only received levodopa and anticholinergics. Resting heart rate and resting beat-to-beat variation were normal in the patients, as were the blood pressure response to standing and the postural heart rate response. No pathological response to the Valsalva manoeuvre could be detected. On the other hand, the heart rate variation evoked by deep breathing as well as the blood pressure response and the heart rate response to sustained isometric exercise were significantly diminished in the patients with idiopathic Parkinson's disease. These findings indicate a central disturbance of cardiovascular reflex control, whereas the corresponding peripheral pathways seem to be normal.

Subcutaneous (s.c.) administration of Arg-vasopressin (AVP) prolongs retention of a learned behaviour and elevates arterial blood pressure. Intracerebroventricular (i.c.v.) injection of a thousandfold lower dose of AVP than needed with s.c. injection produces the same behavioural effect, suggesting that AVP acts on the brain to control behaviour. However, as i.c.v. injection of AVP also elevates arterial blood pressure, it was suggested that AVP, and perhaps other peptides as well, influences behaviour indirectly by eliciting a peripheral response, for example blood pressure changes, rather than by acting directly on the brain. The suprachiasmatic nuclei (SCN) of the hypothalamus, a source of vasopressin production, inhibit sexual receptivity in oestradiol-17 beta-treated ovariectomized rats during the light phase of the daily lighting cycle, leading to speculation that vasopressin might inhibit sexual behaviour. Here we report that i.c.v. injections of AVP (1, 4 or 10 ng) inhibit sexual behaviour in receptive rats. This behavioural response is prevented by i.c.v. injection of an antiserum to AVP 30 min before AVP injection. Subcutaneous injection of a high dose of AVP (1 microgram) has no behavioural effect but elevates arterial blood pressure within 30 min of administration. Intracerebroventricular injection of a behaviourally effective dose of AVP (1 ng) has no effect on blood pressure. The results provide direct evidence that AVP can alter behaviour by an action on the brain and independently of its effect on blood pressure.

We describe a patient with a three-year history of severe progressive left-sided glossopharyngeal neuralgia (GPN) that failed to adequately respond to various drug therapies. The application of lidocaine spray to the posterior pharyngeal wall provided no more than short-term relief. Apart from a large hypertrophic tonsillectomy scar on the left side all clinical and radiologic findings were normal. In terms of therapeutic local anaesthesia, the hypertrophic tonsillectomy scar tissue was completely infiltrated with the local anaesthetic (LA) procaine 1%. The patient has been almost completely pain-free ever since, and the lidocaine spray is no longer needed. Six weeks after the first treatment a repeat infiltration of the tonsillectomy scar led to the complete resolution of all symptoms. The patient has become totally symptom-free without the need to take any medication now for two and a half years. This is the first report of a successful therapeutic infiltration of a tonsillectomy scar using an LA in a patient with GPN that has been refractory to medical treatment for several years. A possible explanation may be that the positive feedback loop maintaining neurogenic inflammation is disrupted and “sympathetically maintained pain” resolved by LA infiltration.

Background: In neural therapy, local anesthetics are injected for diagnostic and therapeutic purposes. Up until now, a distinction has been made between “local/segmental neural therapy” and “interference field therapy”. This division dating back to the middle of the last century was based on the assumption that anatomical and clinical segments were identical. However, this is only true for the projection symptoms, which are limited to metamerism. All pathophysiological processes beyond this segment were called “interference field events” (“outside of any segmental order” and “not explainable by neuroanatomical circuitry”). Summary: However, modern neurophysiology no longer recognizes segmental boundaries, taking into account the occurrence of cross-segmental sensitization processes, neuroplastic changes, immune processes, and neurogenic inflammation. In addition, new insights into neuroanatomical circuitry have also contributed to segmental expansion. Thus, the former definition of the interference field effect (considered to be outside any segmental order) is considered obsolete. Nowadays, interference fields are called “neuromodulatory triggers”. They can act anywhere, both locally and fairly distant, and even systemically. Key Message: Thus, it is no longer tenable to classify interference field therapy as “unscientific” and “not recognized” while local and segmental neural therapy is being scientifically recognized.

Two groups of patients suffering from Parkinson's disease were studied. The first group consisted of 23 patients with an onset age before 40 years; in the second group of 21 patients the onset was after age 50. The clinical findings and the course of the disease were very similar in each group. In spite of a longer disease duration in the patients with early onset of the disease there was no difference in motor impairment; the younger patients did better in mental testing and they were taking less dopaminergic medication. These differences are thought to be due to the age difference rather than to the existence of different disease entities. In the early onset group more familial cases (mostly affecting siblings) were found than in the older ones. The points in favour of there being a hereditary subgroup of early onset Parkinson's disease or of environmental factors causing the disease are reviewed.

We describe a patient with a 35-year history of a severe chronic pelvic pain syndrome (CPPS) that failed to adequately respond to various drug therapies and other treatments by different specialists. In addition to the ongoing chronic pain, he suffered from week-long episodes of increased pain with no discernible trigger. At the first consultation with us the patient was in a particularly severe pain phase. He was taking four different analgesically effective drugs. In terms of therapeutic local anesthesia (neural therapy), we performed suprapubic injection of procaine 1% with infiltration of the vesicoprostatic plexus. Just a few minutes later, the pain decreased significantly. To maintain and further increase the effect, we performed the injection six more times. The patient gradually reduced and stopped all drugs and remained free of pain and discomfort ever since. This is the first report of a successful therapeutic infiltration of the vesicoprostatic plexus using a local anesthetic (LA) in a patient with CPPS that has been refractory to different treatments for many years. A possible explanation may be that the positive feedback loops maintaining pain and neurogenic inflammation are disrupted by LA infiltration. This can lead to a new organisation (self-organisation) of the pain-processing systems.