The vital processes undoubtedly run their course according to certain laws, but the means available to us are incapable of recognizing these laws.

Much

The nerve cell consists essentially of a cytosome with its nucleus and of fibrous processes (one axon and several dendrites). In the past it was assumed that the cell was supplied only from without and that the nerve fibers merely had the function of electrical leads. Modern neurobiology has revised this picture. We now know that the nerve cell is a minute but very powerful computer, which not only transmits information but also coordinates all bodily functions. In doing so, it gathers intelligence in the form of experiences, which is then stored in its stimulus memory. The nerve cell is an active building block that can produce and transport materials and that, in an emergency, can even repair itself. From all the materials available it carefully selects only those that it needs for its own requirements. From these it continually produces in the body of the cell the material it needs for its own maintenance and function. This material has about three to four times the volume of the cell itself. From this it is possible to conclude that the process of excitation uses energy and is subjected to attrition losses that must be constantly replaced. A continuous stream of neural material moves the nerve-fiber membrane and the whole of the neuroplasma column with all the organelles it contains (mitochondriae, tubuli, filaments) at a speed of 1–3 mm per day from the cell itself out to the fiber-end zones. But apart from this there is also a much faster supply stream for particle-specific neuroplasma components, which moves at 40–70 mm per day, including transmitter substances and phospholipids.

These two supply systems moving at different speeds ensure that all the chemical building blocks arrive at their destinations at the right time. The same also applies to the transmitter substances (e. g., noradrenalin) that are given off during the excitation process into the cell’s environmental system or into the synaptic gap. The electrical excitation can be transmitted by one cell to another only by means of chemical processes. Thus, the nerve cell is not a stable structure, but rather subjected to constant change. Its metabolism can also be influenced from without. We know that the antibiotic Actidion can cause the slower of the two supply systems to stop, whilst the alkaloid colchicine halts the faster of the two. Amongst local anesthetics, procaine does not interfere with this important transport of building blocks in the axons, whilst lidocaine (Xylocaine, Xyloneural), like the hallucinogenic drug mescaline, acts as inhibitor to these supplies. This doubtless also has a negative effect on the functional activity at the synapses (G. W. Kreutzberg).

M. Zimmermann states that long-term disturbances of the neural and humoral regulation will also cause disturbances of the axoplasmatic transport. This will lead to relay changes in the synapses of the posterior horn and can become the origin of faulty motor and synaptic reflexes. Vasoactive substances, for example the polypeptide Substance P, are released from sensory nerve endings in the skin, internal organs, and the teeth. Some of the sensory nerve fibers transport the substance from the spinal ganglion to the periphery where it is secreted. At this point, it presumably regulates the microcirculation and the vasopermeability. An adaptive regulation through Substance P has to occur if a nerve lesion interrupts the substance transport. The axoplasmatic transport includes substances that the nerve fibers absorb from the outside, including toxins (tetanus), viruses (herpes), as well as medication.

The peripheral autonomic fibrils in the human organism are unimaginably fine, having a thickness of only 0.002–0.01 mm. What happens in these extremely fine conductors is still only vaguely known, but we do know that within they have a negative electrical charge and outside they are positively charged. In between lies a surface membrane that normally provides perfect insulation. It is thought probable that the limiting surfaces of the nerve fibers at rest are impermeable and that the sodium, potassium, and hydrogen ions are in equilibrium. When this is the case, the electrical potential of the cell membrane is very high. The concentration of potassium ions within the cell is about 20 to 40 times greater than in the extracellular space. This concentration differential is the reason for the high electrical potential of the membrane, amounting to about –40mV to –90mV in the case of nerve and muscle fibers.

Fig. 1.3 The potassium–sodium pump. Every stimulus depolarizes the cell and produces stimulus patterns. The membrane resting potential (MRP) is lowered by permanent irritation and oxygen metabolism is disturbed. Local anesthesia seals the cell membrane. The MRP is increased and this leads to more intensive metabolism. Potassium ions re-enter and sodium ions leave. Toxins and metabolic waste are carried off to the cell environment. The cell is stabilized and its function again becomes normal.

According to Fleckenstein and Hardt, procaine (Novocaine) acts as a true antagonist in these electrophysiological and biochemical processes in the local occurrence of pain in both tissues and sensory nerves. Local anesthetics consist of a water soluble (hydrophilic) amino group, an intermediate chain, and a fat soluble (lipophilic) aromatic rest. The hydrophilic part allows the local anesthetics to reach the nerve via tissue fluids. The lipophilic part enables it to penetrate the nerve. Due to this structure it is membrane-active. It can block the sodium channels by docking on the external side of the cell membrane. All persistent pain stimuli increase the permeability of the membranes and lead to a potassium loss in the cells and hence to depolarization. L. Eppinger states that, “the more we look into problems with permeability the more we get the confirmation that at the beginning of nearly every disease process we discover membrane damage or change in membrane permeability.”

Local anesthetics act precisely in the opposite sense, and do so in lower concentrations than those needed for local anesthesia, by protecting the surface membranes against long-term excitation patterns, since they seal the membrane and prevent depolarization of the nerve cell by low-power stimuli. Thus, they stabilize the membrane potential and protect it against any depolarizing noxious influences. Equally important is the fact that by the “nerve block” produced by the procaine, which acts like a chemical means of setting the cell in a state of rest, the cell is made capable of recharging itself under its own power with the electrical potential lost as a result of the pathological stimulus. With the disappearance of pain the reactive inflammation also disappears. In procaine’s ability to permit this repolarization by increasing the membrane resting potential and to protect the nerve cell against depolarization by low-power stimuli, together with the temporary transmission break, which it produces along the pain pathways, we obtain an intelligible and adequate explanation for the undeniable and wide-ranging therapeutic capabilities of local anesthetics.

Fleckenstein and Hardt reached the conclusion that pain-producing substances can also produce interruptions in the nerve circuits and that procaine is able to repair these interruptions. Fleckenstein concluded from these apparently contradictory results that procaine can act in either (or both) senses, depending on the initial autonomic state, and that it can thus compensate for any deficient performance:

Whilst normally modulating excitatory waves which mutually complement one another to a harmonious overall picture in accord with the outside world are transmitted to the central nervous system by the concerted action of all the peripheral receptors, we must assume that depolarization due to painful stimuli leads to unmodulated excitation streams that deviate from the normal type and form a discord in this harmony.

This is how Fleckenstein formulated what we, as neural therapists, know as the interference-field effect. He studied only the processes that occur in the causation and transmission of pain, but we believe that his conclusions can be extended to all “noxious stimuli” that run their course in the so-called nociceptive system. It is today assumed that these noxious stimuli are conducted primarily by the C fibers, but that the A-delta fibers also play their part.

Procaine first of all blocks the finest fibers. It acts on and progressively eliminates the dull pain, then the sharp pain and finally the sensitivity to pressure. Since the conduction velocity of the A-delta fibers is substantially greater than that of the C fibers, it is thought that the sharp superficial pain is transmitted by the A-delta fibers, and the deep, dull secondary pain by the C fibers. Local anesthetics are not narcotics, since brain function and pain perception remain fully intact. Local anesthetics prevent not only the pain from being generated but also the nervous impulse from being transmitted further, by inhibiting the fundamental process required to generate the nerve potential, namely the substantial temporary increase of membrane permeability to sodium ions. The threshold of electrical excitability is continually raised as the anesthetic effect in the nerve increases until its onward transmission is ultimately blocked completely. The precise mechanism by which the membrane is influenced by local anesthetics is still unknown.

Mechanical or chemical processes in the nerve or its surroundings, such as pressure, scars, inflammation, edema, or agents that are artificially introduced to the nerve are generally able to decrease and increase the passing nerve stimuli. We believe that some hyperesthesias, hyper-reflexias, and contractions originate this way. The analysis of such disease pictures has to be difficult if it is assumed that their origins lie in the center alone and the nerve is merely the “wick” that transports “all or nothing.”

The term “procaine block” has become so well established in medicine that we need to spend a moment in discussing it. It tends to suggest that the procaine injection sets up something like a barrier between synapse and terminal neuroreticulum, and that this barrier interrupts the neural reaction mechanism. By this means the centrally controlled stimuli from outside the organ that precede and sustain the pathological processes are switched off. The segment would thus be neurally isolated from the relay station and left subject only to its autonomous peripheral control. The reflex processes that no longer obey the normal rules and that secondarily govern local events are thereby guided back to normality and thus produce a new initial position.

Against this it may be possible to object that in such a case, once the local anesthetic has ceased to act, the defective overriding control from the center will again allow the peripheral events that depend on it to continue from the point at which they left off. In that case, everything would again return to the earlier state. But this is not so, for the therapeutic effect may persist for days, weeks and sometimes as a complete cure for a lifetime, provided always that the injection is given at the correct site, and regardless of the fact that this site is by no means limited to predetermined nerve pathways.

As we have seen, the regulation-therapeutic stimulus is produced by quantities well below those needed for local anesthesia. Nor is it limited to the use of an anesthetic. As we know, it can be produced by the use of bicarbonate of soda, formic acid, planosol, air, or simply by inserting a needle in the right place, although these alternatives produce stimuli of another order of quality. In our view, the neural-therapeutic effect is a non-specific irritation therapy in which, after unblocking the nerve circuits by means of autogenous healing powers that have again been set free, the stimulus threshold is raised in such a way that the stimuli that were earlier able to induce morbidity now remain below this threshold.

F. Huneke also fought against the idea that procaine merely produces a nerve block, since the healing effects of his therapy cannot be explained by this. Neural therapy in its wider sense includes acupuncture, selective massage, spinal manipulation, and other cognate forms of treatment, and he argued that these were all capable of producing healing phenomena similar to those of neural therapy with correctly sited procaine injections. He could not therefore believe that all such cures could be produced as a result of some temporary interruption of the nervous system, but was convinced that they could be nothing other than healing stimuli that unblocked and reactivated nerve function.

In his view, whenever the needle used for an injection or in acupuncture penetrates the skin, it passes through thousands of electrically charged autonomic fibrils and hence also through their protective covering. This produces short circuits in the electrical structure of the neurovegetative system. The injection of procaine intensifies this short circuit, because it is also capable of putting the insulating nerve covering temporarily out of action. Electrostatic energy can thus flow into the surrounding tissue and pathogenic differences in electrical potential are again brought into balance. The nerve is therefore temporarily without current and is thus biologically dead. This short circuit acts as if it were a stimulating force to the entire neurovegetative system, to which the system then responds as a whole. If this occurs at a point where the building blocks have been displaced and whose displacement has, as it were, caused the whole building to lean, then these displaced building blocks can be put back where they belong, and this at lightning speed. According to him, the correctly sited procaine injection blocks nothing; it influences the functional unity of the neurovegetative system in the sense of a functional correction far beyond the injection site. He therefore felt unable to accept the misleading term “nerve block.” In addition, the complicated methods used in the studies that led to the use of this term contained so many possible sources of error that any conclusion based on them could not be justified. Even if all the measurements obtained by research on dead building blocks could be assumed to be correct, they did not suffice for explaining and understanding the holistic healing processes that, in his view, occurred within the non-rational area of life. This neovitalist attitude shown by F. Huneke is one of the reasons that he encountered disapproval and rejection from the medical establishment with its materialistic outlook. However, one need not share Huneke’s philosophy in order to make successful use of his teachings.

Based on the latest neurophysiological research, the fact has now been established that a barrier is created in the nerve fibers at the site of a Novocaine injection, which blocks the passage of neural stimuli. The electrical potential of the nerve-fiber membrane is not in any way reduced by this but, on the contrary, it is increased. The studies at our institute, made for this specific purpose on isolated nerve fibers, have shown that Novocaine reduces the ion permeability of the membranes, i.e., that it has a stabilizing and not a relaxing effect on these fibers. Perforation of the nerve fibers by the needle produces purely local depolarization of the membranes in the immediate neighborhood of the puncture, but not more than 2 mm away from this point the electrical potential of the nerve-fiber membrane remained unchanged.

To this one may add that a short circuit within a radius of 2 mm from a 1 mm diameter needle will in fact involve many thousands of nerve fibers on each occasion, when we bear in mind that a fibril has a diameter of only 0.002–0.01 mm, and that Huneke’s assumptions about the injection site would therefore seem to have been confirmed.

Despite these important partial results we are still not in a position at the time of writing to state exactly all that does in fact happen in the non-isolated nerve with its normal, numerous interlaced connections in every direction, when first the needle (on being inserted) and then the procaine act upon it. We still know too little and must have the requisite humility to admit our ignorance.

But in any event one thing seems clear enough: the term “Novocaine block” is a bad choice. For ultimately the neural-therapeutic effect is obtained not solely by any temporary interruption of the nerve pathways that the procaine may produce, but in my view only by the rehabilitation of the nerve fiber that has previously been damaged by stimuli. By restoring the electrical potential of about –40mV to –90mV, the regulatory disturbances in those parts of the neurovegetative system are eliminated where we, as neural therapists, see the “block.” Once order has been restored at every level of the neurovegetative system, all vasal, humoral, hormonal, and even psychological and other forms of secondary disturbances are restored to normality, i.e., health. The normalizing stimulus produced at disturbed and disturbing points is what really matters. Only the extent of this stimulus will vary, according to whether it is produced by acupuncture, selective massage, Kneipp’s hydrotherapy or other forms of skin stimulation, by irradiation, or by procaine. However, the healing stimulus produced by procaine has a dominant, outstanding place in this scheme of things, on account of its safety in use, and the speed and extent of its effect.

Fig. 1.4 Diagram of the gate-control system theory of pain perception according to Melzack and Wall. The fibers lead to the gelatinous substance and to the first T (transmitter) cells of the posterior horn. The inhibitory effect produced by the gelatinous substance on the afferent fiber ends is sustained by activity in the large fibers and the gate is thus closed. Activity in the small fibers attenuates the inhibitory action and the gate opens. The central feedback control mechanism, which receives its information from the posterior and lateral columns, is shown by a line from the large-fiber afferences to the central control system and thence back again to the gate-control system. The T cells are linked to the entrances to the action system.

L (A-beta): Large A-beta fibers

S (A-delta, C): Small A-delta and C fibers

SG: Subtantia gelatinosa

T: Transmitter cells

+ Excitation

− Inhibition

(Source: R. Melzack. The puzzle of pain. Harmondsworth: Penguin Books; 1973.)

As possible causes of positive feedback by efferent action of the sympathetic system, other mechanisms are also under discussion:

a. By reflex vasoconstriction, positive feedback may reduce the blood supply. In the affected area, this may progress to the point of ischemia, which can then activate the pain receptors to a greater extent.

b. One theory holds that there may be a direct transfer of the sympathetic system’s efferent activity to closely adjacent nociceptive afferent fibers, e. g., in the case of neuromas.

c. Wall assumes that neurotransmitters belonging to the sympathetic system, particularly noradrenalin, may intensify the nociceptive afferent stimuli and so produce positive feedback.

Therapeutic measures can interrupt the stimulation circuit. Local anesthetics can interrupt the vicious circle in the segment at nociceptors, pain-conducting nerves, and at the sympathetic chain. In the case of interference fields, it can be interrupted at its origin. Natural regulation (negative feedback) can be restored.

Transcutaneous electrical nerve stimulation (TENS) interrupts the stimulation circuit in a different way. Two electrodes are placed on the skin above a nerve or its surroundings. From there, the nerve is stimulated through the skin. This is done using a low electrical stimulus of 40 to 100 Hertz, which equals 40 to 100 stimuli per second. The intensity of the stimulus remains considerably below the pain threshold. The patient perceives it as a vibrating or prickling sensation. The muscles respond with mild tonic contractions. The paresthetic stimulations superimpose and suppress the pain because they only stimulate the bigger nerve fibers that conduct sensitivity to touch (not the pain!), which results in a narrowing of the gate (according to the gate-control system theory). The analgesic effect exceeds the application time by 30 minutes up to several hours. TENS can be used with patients who are taking anti-coagulants, not with patients who are using a pacemaker or other metallic implants, in the case of thalamus pain or areas with sensitivity disorders.

My personal working hypothesis

Hypotheses are actually essential for the progress of science. Their revision requires the development of new technology and the use of new skills. It is ultimately of no importance whether the hypothesis was right or wrong. Its purpose is to initiate progress (A Carrel).

The current idea of how the procaine “block” acts is approximately as follows: while the neural pathways are temporarily interrupted, all pathological reflexes that are normally transmitted along them are also stopped. By eliminating the sensory part of the nerve I can block pain, paresthesia, itching, and other sensory phenomena and so prevent abnormal reflex mechanisms from being produced secondarily via the efferent branch. If I interrupt the somatic motor nerve, I can relieve spasm in the skeletal musculature. If I interrupt autonomic channels, especially the sympathetic system, I eliminate a pathological autonomic activity, which can originate either from a pathological state within the segment or from a focus.

Fig. 1.5 The difference in the effects of anesthesia and of neural therapy using local anesthetics. The healthy nerve and muscle cell requires a stimulus to reach a certain level before it begins to become depolarized from the membrane resting potential (MRP) and emits excitation patterns. Following the administration of a local anesthetic the cell becomes hyperpolarized and is desensitized. When the anesthetic effect has worn off, the cell recovers its original MRP. Everything is as before. The diseased nerve and muscle cell has a lower initial MRP. A weaker stimulus will suffice to depolarize such cells. This cell will tend to a much greater degree to produce long-term excitation patterns. When the anesthetic is administered, hyperpolarization is produced, which again desensitizes the cell. But something substantially new happens as a result: in this phase, cell metabolism is intensified to such an extent that the cell attempts to dispose of all metabolic waste products and toxins into the adjacent environment. If it succeeds in this, the MRP no longer reverts to its low initial value; instead, the cell becomes stabilized at a normal level.

In neural therapy according to Huneke, “therapeutic anesthesia,” “therapeutic local anesthesia,” and the “nerve block” are not prime considerations. What happens here is something that goes far beyond local anesthesia and occurs only when the anesthetic strikes the diseased, pathologically altered tissue. This is precisely where we use the local anesthetic to supply a substantial amount of energy to the tissues, in order to help the cell to rebuild its electrical potential. In addition, the tissue-cell membrane is also stabilized by it. We are thus re-establishing normal bioelectrical conditions and the normal physiological conditions that depend on them. An essential part of this process is to reconnect the cell to the normal information exchange on which, as part of the whole, it depends. The change that occurs in the local energy situation has its effects on the whole organism via the cybernetic network.

The initial level of the membrane resting potential (MRP) of individual cells is not identical. If the cell is diseased, this can sink considerably without necessarily causing the cell to die. So, for example, a normal lung cell has a mean MRP of –15 mV (with a standard deviation of ±20%). Lung cells in non-malignant disorders (such as pneumonia, bronchitis, tuberculosis) have an MRP of –14 mV ±20%. Lung cells that have undergone malignant change may have an MRP as low as –9.8 mV ±3 mV. Healthy human cervical cells have an MRP of –33 mV, tumor cells about –22 mV. Some measurements obtained from tumor cells even produce positive values (Steinhaeusler).

When the cell damage and the consequences it has produced have been repaired, the previously damaged excitatory process and the autonomic (neural, humoral, hormonal, and cellular) regulating function is restored as far as possible to all functional circuits. In other words, procaine therapy produces an electro-biological rehabilitation. Initially, it acts only locally, and after modifying the cell-environment system (Pischinger) it also acts on the whole of the organism. From the beginning, Huneke referred to a “change in the energy structure of the autonomic system.” I would go further and call it the restoration of the normal structure of the autonomic system to the extent that this is still possible. Today, this includes a focus on positive changes in the basic system (the matrix).

The correct site for the injection is decisive, because this neural-therapeutic normalizing effect upon the neurovegetative system can be produced only if the injection strikes previously damaged tissues that can no longer recover by their own efforts. Procaine used as a local anesthetic forms a block; used in neural therapy it eliminates a nerve block that was previously present. This fundamental difference is the reason for the plea that the outdated term “procaine block” be used, if at all, only for the state produced in local anesthesia. If it is not, it is likely to continue to block the way to understanding the processes that occur in neural therapy. The fact that we need to repeat our injections whenever their positive effect begins to wear off suggests that the cell can at first retain the electrical potential supplied to it for only a limited time. But with every repetition it seems to learn more effectively to build up and maintain the required potential by its own efforts.

Thus, in disturbed segmental tissue and especially in the “interference field” we have zones of strong stimuli or the summation of stimuli over longer periods, which the body is unable for the time being to compensate, i.e., the organism finds them to be irreversible. In this state the cell becomes refractory, it no longer responds to external stimuli and withdraws from the continual information transfer and to some extent also from the higher-order cortical overall information system. Despite this, however, these zones do not remain mute. They fire off streams of irregular irritative impulses (Thompson, Kimball), which, in my view, have the characteristic ability to set up a disturbance. In doing so they inundate the stimulus-inhibiting and selective functional elements of the synapses and the “ubiquitous synapses” of the basic autonomic system. This roughly corresponds with Melzack and Wall’s gate-control system theory.

Nerve fibers turn into synapses, into other nerve fibers, or they end at the motor end plates of muscle fibers. Synapses are switch-points where electrical signals are transformed into chemical signals. The information is carried across the synapses via transmitter substances, for example, acetylcholine. When the acetylcholine has completed its task it is split by the enzyme acetyl cholinesterase (cholinesterase). Procaine blocks cholinesterase, the excitability of the peripheral choline receptors, and inhibits the acetylcholine formation.

Synapses can have an exciting or an inhibiting effect. They can filter off individual subliminal stimuli and prevent their passage. Their function as pressure-relief valves causes some preselection amongst the irritative impulses and nerve signals that travel only in one direction. The loss of this synaptic function leads to the inundation of the system by stimuli. The interference impulses from disturbed tissues or interference fields probably also transmit false information in the segment or to higher centers, depending on how far they reach. Regulatory disturbances result, and finally there is a disturbance in the total environment of the organism. If weaker disturbances limited in range to the largely autonomous control circuits with neurovegetative functions act only within the segment, once certain limits of tolerance are exceeded a segmental illness results that we have to treat by accurately placed procaine injections into the relevant part of the segment.

In addition to using hyperpolarization during anesthesia to break out of the vicious circle of positive feedbacks, I therefore regard the following as the major points in the pathological processes and in the therapeutic effects of procaine to counter them:

a. Stimulus-related processes affecting the cell membrane potential, i.e., the lowering of the membrane resting potential by excessive stimuli on the one hand, and in therapy its restoration by means of procaine on the other. If a cell membrane is damaged experimentally, the cell’s ion exchange can no longer be controlled by the surrounding environment. The neighboring cells immediately break off their (membrane conduction) contact with this “sick” cell. It is as if they were isolating themselves in order to protect themselves against being contaminated by its harmful influence. Being a surface-active substance, procaine can settle on these surfaces and make them impermeable. As a result, contact with the cell is re-established.

b. The production of stimuli triggered thereby and the channeling of these stimuli via the neurovegetative system, and the resultant negative or positive effects on the regulating mechanisms of this system. Life is bound to bioelectrical processes. The sympathetic and parasympathetic systems ultimately resolve in a common basic plexus and terminate in the mesenchymal interstitial tissue. The electrical impulses are then transmitted by means of special chemical transmitter substances (norepinephrine, acetylcholine etc.) to special receptors that, however, are doubtless also subject to some higher-order control and regulation.

c. The stimulus-related loss of the selective gate effect of the synapses and the resulting inundation by stimuli, leading ultimately to exhaustion as far as the reticular formation, and in reverse when synaptic function is restored and pathological ephapses are eliminated by means of procaine. This product supplies energy to the power stations of the synapses and enables them to resume their lost functions in supplying energy. According to the gate-control system theory the information-control gate is opened by activity in the small fibers. The C fibers respond especially rapidly to procaine and anesthesia then shuts the gate again. The equilibrium of activity in the large and small fibers is restored and the inundation of the reticular formation by stimuli inhibited. This also limits pain perception. If reflex vasoconstriction has led to ischemia, which then itself excites new pain receptors in affected tissue, procaine can dilate these vessels and so break through the vicious circle. The cybernetic interaction of physical and chemical reactions in the synapses and in what Pischinger has called the cell-environment system represents a refined arrangement of the organism in providing a fail-safe system for protecting the peripheral regulating functions, to maintain the bioelectrical potential at its correct level. We are able to intervene actively in these vital processes.

What Wedell found to apply to the injured nerve is likely to be true also for the interference field, with cells damaged by stimuli. By recording streams of neural impulses proximal to the injury he showed these to possess particularly penetrating and diffusing properties. Of special interest to us is the fact that in the region where there are injured nerves, pathological synapses can come into existence, so-called ephapses. These have all the characteristic features that we regard as prerequisites for interference-field activity, since they can lead to the pathological transmission of stimuli between otherwise well-insulated nerve fibers. In other words, in addition to the normal synapses there is short-circuiting of nerve channels and a transmission of information and unmodulated stimulus impulses on the wrong channels. Something like this happens if the insulation in the system is defective and we can hear another conversation when we use the telephone. Such short-circuiting across ephapses at points of injury has been proved experimentally for unmedullated fibers (Arvanitaki, Jasper, Katz, and others) and from medullated to unmedullated fibers (Granit). The discharges resulting from injuries have a pronounced tendency to diffuse. They are apparently forced away at the ephapsis from the more sensitive A and B fibers toward the C fibers, and it is precisely these last that are especially sensitive to procaine. They then trigger off a state of excitation in the posterior-horn complex of the spinal cord by causing a primitive rhythmic excitatory activity (Harrer). This is where inhibition, channeling and summation occur, and where ever more functional systems can become involved in the pathological state of excitation. This provides a plausible explanation for the diffusion of stimuli that we find time and again to occur in disorders due to interference fields that have persisted for some time. Erbsloeh has written that:

Practical experience has proved to us that we can eliminate such pathogenic short-circuit synapses (ephapses) via the Huneke phenomenon, and that together with such false information and excitatory states we also get rid of the remote disturbances in the entire basic autonomic system for which they have been responsible.

d. The initiation of pathogenic processes due to the liability to disturbance on the one hand, and the increase in resistance and the reactivation of cells, tissues, organs, and their interdependent functions on the other.

This theory of the genesis of a large number of disorders builds on the successes achieved in practice and can be extended to new fields surprisingly often. So, for example, I see the action of neurotropic toxins as a pure interference-field effect. The interference impulses originating from the primary entry point are conducted via the nerves, inundate all the synapses (or according to Melzack and Wall’s theory of the gate-control in the gelatinous substance of the spinal cord) and produce excessively strong stimuli in the cerebral centers. To me, “toxic effect” is primarily a result of an excessive response to a stimulus. The successful treatment of → snakebite and → tetanus by prompt treatment of the entry site with procaine seems to prove this.

Siegen has shown that it is reliably possible to prevent allergic necrosis in the Shwartzmann–Sanarelli phenomenon, that the antigen–antibody reaction is also controlled via neural channels and that any interference impulses related to it can be eliminated by administering procaine to the neural interference field. The problem of organ transplants has been solved by surgical techniques, but involving as they do the cellular, humero-hormonal and neurovegetative defense mechanism against the foreign body of the transplant, the high expectations of success still prove elusive. Immunotherapy is still one-eyed in its humero-seral views and has been unable to control the anaphylactic processes. To Siegen the transplanted organ is a classic interference field with a negative influence on the immunological processes that obviously also have a neural component that may to some extent even be dominant. This neural component can be influenced decisively by correctly localized procaine injections. According to Siegen, immunological assimilation of donor and recipient organism can be achieved only by observing the laws we have learned from the Huneke phenomenon and this assimilation is essential for permanently functional transplants.

The fact that a procaine injection suppurates only extremely rarely proves to me that tissues protected and returned to normality by procaine simply do not allow infection and → inflammation to occur. I am equally convinced that the development of tissue autarky known to occur in carcinogenesis (→ cancer) will be found to be made possible only if it is favored by an interference field.

This working hypothesis also provides a plausible explanation for the very wide range of indications for procaine therapy. We can use it wherever neurovegetative dysregulations lead to disorders. This is a very extensive field with a large number of diagnostic and therapeutic opportunities, but it naturally also has its limits. These theories are the result of experience and of experiments that require us to rethink some of what we have been taught. F. Huneke gave his first book the title Disease and Cure: Another View (Krankheit und Heilung anders gesehen). He meant this to indicate that in looking at illness from the point of view of neural therapy new ways of treatment have been opened to us.

My theory can be seen to receive support from an observation made by Descomps, who anesthetized the upper cervical ganglion and the retrostyloid region in 830 patients suffering from allergies. The treatment proved remarkably successful and the reactions were checked by EEG. He found that in two-thirds of the patients with allergic reactions, at rest and with their eyes closed, there was no sign of any alpha waves, i.e., that they were in a state of heightened excitation and fully awake. After anesthesia of the upper cervical ganglion of the sympathetic chain, alpha waves reappeared immediately, a fact that must be interpreted as a sign of central relaxation and reduced cortical activity. This permits the conclusion that following the anesthetic to this sympathetic → (T) ganglion the reticular formation and the cerebral cortex were no longer receiving the excessive number of autonomic and sensory stimuli that had previously irritated and overloaded them. It is well known that the reticular formation has the function of noting and classifying all stimuli and information received from the periphery and then coordinating the regulating mechanisms in such a way that the organism can at all times continually adapt itself to the internal and external environmental situation. If this control center becomes overloaded as a result of an excess of unfiltered incoming information, the mutual adjustment and balance of the various neurovegetative controls can be disturbed. Instead of acting as an attenuator or damper, it can then become an amplifier. Descomps could prove by striking hormonal, humoral, and neural reactions that correctly localized anesthesia quickly helps to correct these deviations and to guide them again into their regular channels.