Urol Res (2008) 36:327–334

DOI 10.1007/s00240-008-0156-2

ORIGINAL PAPER

A neural model for chronic pain and pain relief by extracorporeal shock wave treatment

Othmar J. Wess

Received: 22 April 2008 / Accepted: 19 September 2008 / Published online: 7 October 2008© The Author(s) 2008. This article is published with open access at Springerlink.com

Abstract The paper develops a new theory of chronicpain and pain relief by extracorporeal shock wave treat-ment. Chronic pain without underlying anatomical disorderis looked at as a pathological control function of memory.Conditioned reXexes are considered to be engraved mem-ory traces linking sensory input of aVerent signals withmotor response of eVerent signals. This feature can bedescribed by associative memory functions of the nervoussystem. Some conditioned reXexes may cause inappropriateor pathological reactions. Consequently, a circulus vitiosusof pain sensation and muscle and/or vessel contraction isgenerated when pain becomes chronic (pain spiral). Thekey feature is a dedicated engram responsible for a patho-logical (painful) reaction. The pain memory may beexplained by the concept of a holographic memory modelpublished by several authors. According to this model it isshown how nervous systems may generate and recall mem-ory contents. The paper shows how extracorporeal shockwave treatment may reorganize pathologic memory traces,thus giving cause to real and permanent pain relief. In ageneralized manner, the idea of associative memory func-tions may help in the understanding of conditioning as alearning process and explain extracorporeal shock waveapplication as an eYcient treatment concept for chronicpain. This concept may open the door for new treatmentapproaches to chronic pain and several other disorders ofthe nervous system.

Keywords ESWT · Chronic pain · Pain memory · Shock wave treatment · Associative memory · Holographic brain model · CPPS

Introduction

Chronic pain distresses are among the most frequent dis-eases in the western world. Patients often suVer from severepain sensations such as frozen or calciWed shoulder, tenniselbow, lower back pain, heel spurs etc. Many patientsremain without any improvement in spite of injections ofcorticoids, massages and other treatment modalities. Inurology the chronic pelvic pain syndrome (CPPS) andremaining pain symptoms after successful stone clearancemay stand for chronic pain without clear anatomical disor-ders.

Since 1980 shock waves have been frequently used forfragmentation of body concrements. Extracorporeal shockwave lithotripsy (SWL) is the method of choice for frag-mentation of urinary stones and is also utilized for disinte-gration of several other types of body calculi. In the 1990s,the idea of fragmentation of calciWed deposits led to shockwave applications for indications such as tendinosis calc-area, tennis elbow and others. During recent years, extra-corporeal shock wave treatment (ESWT) of soft tissue painclose to bone has gained signiWcant interest in Europe andthe USA.

Surprisingly, most extracorporeal shock wave treatmentsin orthopedics resulted in signiWcant reduction of pain evenif the calcium deposit, primarily, could not be disintegrated.It turned out that shock wave treatment shows a stimulatingand healing eVect beyond fragmentation of body calculi.

Typically, shock wave treatment of chronic pain is per-formed by application of hundreds to a few thousands of

O. J. Wess (&)Storz Medical AG, Lohstampfestrasse 8, 8274 Tägerwilen, Switzerlande-mail: wess.othmar@storzmedical.com

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shock wave pulses with a repetition frequency of 1–4pulses per second to the area of highest pain sensation. Theshock wave energy is relatively low, approximately 1/10 ofthe energy levels used for stone fragmentation. Shockwaves are applied extracorporeally, by coupling the therapyhead of the device to the painful area. They may be focusedor not to reach the appropriate area of interest within thebody or at the surface. Shock waves may be guided by aidof ultrasonic or Xuoroscopic localization devices. Mostoften they are guided by the feedback of the patient himselfby responding to the level of pain sensation during thetreatment (biofeedback).

The application of shock waves is slightly painful andcauses an acceptable but usually not negligible discomfort.Local anesthesia has been used to reduce pain sensationduring ESWT; however, it turned out that it reduced thehealing eVect of shock waves simultaneously [1]. Usuallythe treatment is split into several sessions (1–6) with a timeinterval of a few days or weeks.

This treatment regime or a similar one is used forchronic pelvic pain as well as shoulder pain, heel spur andangina pectoris for example.

As a mechanism of pain relief by extracorporeal shockwave treatment several theories are discussed [2, 3].

1. Shock waves stimulate the nociceptors to Wre high-fre-quent nerve impulses (hyperstimulation). Propagationof nerve impulses is blocked according to the gate-con-trol theory [4].

2. Shock waves distort parts of or the total cell mem-brane. The nociceptors cannot build up a generatorpotential; thus pain sensation is avoided.

3. Shock waves change the chemical environment of thecell membranes by generating free radicals, which inturn result in pain-inhibiting chemicals in the vicinityof the cells.

Recent publications [5, 6] claim revascularization stimu-lated by shock waves to be the basic mechanism of painrelief and tissue healing.

Pain relief is not the only eVect associated with ESWT.Lohse-Busch et al. [7] reported reduction of muscular rigid-ity and spastic co-contractures after shock wave applicationin patients suVering from tetraspastic disorders due toinfantile cerebral palsy. Manganotti et al. [8] demonstrateda long-term eVect of shock wave therapy on patientsaVected by stroke. Russo et al. [9] saw a stimulation ofmicro-vascularization after shock wave treatment. CPPS[10], angina pectoris and wound healing [11] are promisingnew Welds of shock wave application. The underlyingmechanism, however, is still speculative.

This paper describes a potential neural mechanism forreorganization of pathological reXex patterns by extracor-poreal shock wave therapy for chronic pain relief.

Associative memory model for establishing reXex functions

Conditioned reXexes are considered engraved memory con-trol functions linking sensory input of aVerent nervous sys-tem with motor output of eVerent signals. Associativememory is a very eYcient and fast mechanism enabling liv-ing beings to react fast and appropriately to changing envi-ronmental conditions. An overwhelming majority of ourexperiences stored within the memory is well matched andoptimally responds to daily living conditions. Some condi-tioned reXexes, however, may cause inappropriate or patho-logical reactions. Chronic pain, for example, withoutunderlying anatomical disorders is considered a pathologi-cal control function. An interaction between aVerent sensorinput and eVerent motor output is postulated to form areXex-like response. Accordingly, a circulus vitiosus ofpain sensation and muscle and/or vessel contraction is gen-erated when pain becomes chronic.

Learning model of reXex functions on the concept of engrams

The term associative pain memory reXects the fact that paingenerates its own associative memory eVect, linking pain-speciWc sensory inputs to particular motor outputs assketched in Fig. 1.

If we consider, for example, pain sensation in the shoul-der, consequently, shoulder muscles contract for pain reliefby aid of protective posture. The modiWed muscle tonuscauses reduction of blood circulation and metabolism inthat particular area, which in turn may induce additionalpain. If this reXex bow lasts signiWcantly long or if it is veryintense, pain sensation and contracted muscles are linkedand engraved as an associative pair of items. Whenever apain sensation is present, the muscle tonus is aVected andvice versa. Thus, a feedback loop with positive reverbera-

Fig. 1 Basic concept of associative memory linking pain sensationand muscle and/or vessel tonus associatively

Reflex bow

Afferent signals,(pain sensation)

Efferent signals,(muscle and/or vessel tonus)

Associativelinkage

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tion is established. The linking memory eVect is locatedsomewhere on the nervous pathway in between sensorinput and motor output depending on the involved nervousstructure Fig. 2.

As known from learning experiments in general, it isassumed that memory eVects are based on modiWcations ofthe synaptic junctions between nervous cell ensembleswithin the CNS. Storing information in the long-term mem-ory, usually, requires strong and repeated stimulation of theinvolved neurons on diVerent hierarchic levels of the CNS.The result of such a successful learning procedure is con-sidered an engram.

This type of associative memory is a basic factor for theenormous eYciency of the human brain.

The type of chronic pain we are interested in is consid-ered to be stored as an engram in the above-mentionedsense. Pain signals modify an ensemble of nerve cells of theperipheral nervous system (PNS) as well as in the centralnervous system (CNS), forming a pain memory for thisspeciWc pain sensation which, in turn, links a dedicatedmotor response to the eVecting organs such as muscles andvessels (Fig. 3).

The hypothesis of this paper can be described as follows:When acute pain develops into chronic pain, sensor

input and motor output are stored associatively in the PNSand/or CNS and act in a feedback type circle.

From that particular point of time on, the cause of that(chronic) pain has shifted from the organ itself to higherlevels of the PNS or CNS. Consequently, successful treat-ment regimes must aVect the pathological reXex bow anderase the particular memory instead of modifying the organitself.

Information storage by modiWcation of synapses

Nerve signals are transmitted by means of action potentialsalong axons and chemical substances within the synapticjunctions. If the signals are strong enough or if many adja-

cent synapses are releasing transmitter substances fromtheir vesicles simultaneously, the contacted nerve cell inturn will Wre subsequent electrical signals. They propagatevia the axons to succeeding nerve cells. This may result inthe appropriate reaction of the muscles in order to get rid ofthe primary pain. For example, a person may touch theXame of a burning candle and retract the Wnger to get out ofthis painful situation. This is considered as a “normal” reac-tion. In some cases, however, the painful situation maycontinue for quite a while so that the involved synapticjunctions may be activated in a repeat manner. It is wellknown that frequently activated synapses transmit signalswith a lower threshold so that after the “training or learningprocess” even very small inputs may activate the followingcells. The synaptic strength of particular synapses isincreased (long-term potentiation, LTP). Thus, a reXex bowof connecting sensor input (pain) with a speciWc motorresponse (muscle or vessel contraction) is established.Trained sequences of (aVerent) sensation and (eVerent)motor response are the basis of all trained skills. It becomesa problem only if it develops into a reverberating self-enhancing feedback loop as in chronic pain.

Associative memory and its impact on pain therapy

In cases of chronic pain without organic reasons the theoryof associative memory draws the attention away from thepainful organ to a higher hierarchic memory level. Theorgan itself is no longer the region of primary therapeuticinterest but the according pain memory located in the mod-iWed synaptic structure within the related reXex bow. Directmechanistic view is replaced by looking at higher controlfunctions of the nervous system and its memory potential.Obviously, this idea leads to a radical change of therapeuticapproaches of chronic pain distresses. Therapeutic treat-Fig. 2 Feedback circuit of sensor input and motor output

„Conditioned Reflex“

CNS

Brain Stem

Spinal Cord

Organ

SensorInput

MotorOutput

Memory

Fig. 3 Schematic view of input and output pathways from peripheralorgans to the CNS

Sensor Input Motor Output

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ment modalities are no more focused on speciWc organsunder pain but on pain memory. In other words: Pain treat-ment strategies are directed towards reorganization of thememory structure instead of direct (physical or chemical)modiWcation of the organ.

The existence of memory capabilities in general is obvi-ous in humans and highly developed living beings; how-ever, the knowledge about the underlying mechanism isfragmentary and requires further investigation.

Several brain models were developed to shine some lighton the subject and to enhance understanding of memoryfunctions.

Holographic memory model

Neuronal memory function of the CNS can be described bya variety of diVerent brain models. Some brain functionscan be simulated by neural nets taking into account somespeciWc features of the synaptic junctions such as adapta-tion, non-linear behavior and response thresholds [12].There are non-holographic models [13] as well as holo-graphic models. They make use of correlation functionswhich are assumed to be performed by neural systems [14].

A holographic model, in particular, matches associativememory functions of the brain quite well. There are strikinganalogies between a holographic system and the memoryfunctions of information processing by the CNS.

Neural and holographic analogies are listed below:

The idea of a holographic brain model was developed byseveral authors [16–20]. Associative memory chains basedon non-linear concepts and three-dimensional storage medi-ums were developed by Mager et al. [21], Wess et al. [22].

Neuro-holographic memory model

Holographic brain models correlate well with associativememory functions of the brain. The crucial question iswhether we can Wnd biological structures capable of per-forming analog memory functions based on physiologicalfeatures of the CNS. If so, we may look for appropriatetherapeutic measures for chronic pain management.

Holographic storage and reconstruction of information isbased on interference of coherent waves (as generated bylasers) to generate a time-invariant interference patterns, aso-called hologram. The neural counterpart of coherence isa synchrony of neural oscillatory actions as described byGray et al. [23], Engel and Singer [24]. The underlyingmechanism of both systems (holographic as well as neural)is the ability to perform correlation functions on spatial pat-terns.

The concept of holographic associative pain memory(Fig. 4) may lead the way to develop optimized therapeuticstrategies.

Networked layers of nerve cells provide a basis for a sys-tems-theoretical approach.

Excitation of sensory nerve cells leads to action poten-tials generated in higher layers of nerve cells. The excita-tion pattern is laterally widened (spread) by passingfollowing layers of neurons up to the sensory cortex. Motorresponse, on the other hand, may be concentrated on aspeciWc group of muscles, activated by converging signals

CNS/PNS Hologram

Parallel information processing Parallel processing of two- or three-dimensional information

Divergence of aVerent signals Divergent waves (virtual images)

Convergence of eVerent signals Convergent waves (real images)

Memory contents not precisely localized [15]

Spatial distribution of storedinformation

Same group of neurons stores diVerent information

Separate storage of multiple holograms on the same storage medium

Pattern recognition independent from translation, magnitude and direction

Parallel translation invariant information processing

Content of long term memory 1010–1014 bit

Storage capacity 1011–1013 bit

Recall of pairs of connected events, associative learning

Associative storage and reconstruction

Sequential recall of linked memory chains

ConWguration of associative time chains

Plasticity of memory Dynamics of memory response Fig. 4 Neuro hologram formation (schematic)

sensor input(pain)

Organ

Neuro hologram

motor output(tone)

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controlled by an extended area of the motor cortex. Theprinciple of divergence and convergence is known fromphysiology text books and is well mimicked by holographicstorage and retrieval.

Analogous to the holographic model, interference ofdiVerent input/output signals may take place on all involvedlayers of neurons as schematically depicted in Fig. 5.

Since neurons are activated only if a certain threshold ofexcitation is surpassed, only those neurons may respondby generating action potentials, which were activated bytwo or more simultaneously arriving signals. A spatialinterference pattern is generated and transmitted through asequence of neuronal layers localized anywhere in betweensensor input and motor output. Figure 6 depicts this situa-tion schematically. Only if the action potentials (gray andblack dots) of two activated cells of the Wrst layer simulta-neously arrive at the cells of the subsequent layer, thethresholds of these cells are exceeded and the followingcells (black) are activated. Single asynchronously arrivingsignals stay below the cell’s thresholds and do not generatesucceeding action potentials. By aid of the threshold behav-ior of neurons, spatial neural interference patterns may beestablished analogous to interference of coherent waves inholography.

Frequently used synapses are modiWed as mentionedpreviously and, thus, provide a mechanism to memorize(store) spatial interference patterns such as repeated asso-ciative sensor input/motor output patterns. In cases ofchronic pain diseases pain sensation and muscle contrac-tion may be permanently stored as a synaptic thresholdmodiWcation pattern on various hierarchic levels of theCNS.

The concept of synaptic memory is based on the follow-ing Wndings and assumptions:

• Metabolism of intensely stimulated synapses is enhanced(long-term potentiation, LTP)

• Repeatedly stimulated synapses facilitate transmission ofsignals

• Neural interference patterns are permanently stored asexcitability (threshold) pattern of large numbers of cellsand synapses.

Hypothetic mechanism of shock wave therapy

Does the concept of associative holographic pain memoryprovide any idea how to cure chronic pain distresses in gen-eral and/or a consistent theory of ESWT? Which mecha-nism explains the selective erasure of an isolatedpathological reXex pattern between pain sensation and mus-cle/vessel contraction? The problem seems to be too com-plex for a simple answer since the location of the pathologyis considered not in the painful organ itself anymore but isdiVusely spread over extended areas as well as over severallevels of the PNS/CNS. How are isolated reXex patternsselectively erased without sacriWcing the total memory con-tent? The neuro-holographic model may provide a solutionto the problem.

Healing by selective erasing of pathologic reXex patterns

Holography is based on storage of interference patterns andreconstruction by interaction of an input signal with thestored pattern. The strength of the associatively retrievedoutput pattern depends on the quality of the interferencepattern, speciWcally on the depth of modulation, as shownin Fig. 7.

A characteristic feature of a hologram is, as listed above,that several interference patterns may be stored within thesame storage medium by simply storing one pattern abovethe other. Reconstruction of diVerent patterns is done by

Fig. 5 Divergence and convergence of nerve signals by transmissionthrough several layers of neurons

CNS

afferent,sensorinput

efferent,motoroutput

sensorcortex

motorcortex

Fig. 6 Formation of neural interference pattern

holographic storage

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simply selecting one speciWc input, which will basicallyretrieve only the according (associatively linked) output.Holographic storage dissipates information across wideareas of the storage medium. Consequently identical areasto store diVerent information are utilized.

The strength of a retrieved signal depends on the modu-lation depth of the stored interference pattern. Weak or nomodulation does prevent a signal from being retrieved byan input signal. As shown in Fig. 7, both signals (input andoutput) to be stored associatively require similar signalstrength (amplitude) in order to form an interference patternwith strong modulation. If the signals are of diVerentstrength, modulation is weak as shown in Fig. 8, and noassociative linkage will take place.

Hyper-stimulation by shock waves may be considered asstoring the speciWc strong sensor input (pain) with the weakmotor output interference pattern once again with weakmodulation. This weak (new) pattern overwrites the (old)

strong pattern and is stored instead of the old one. Perma-nent storage is facilitated by stimulating over a time periodof some 15–20 min and by periodically repeated treatmentsessions as frequently done in ESWT.

Shock wave treatment is a painful procedure. Seen tech-nically, the dynamic range of the neural memory may beexceeded. Figure 9 shows this eVect schematically. If thesignal strength reaches the saturated part of the responsecurve, the systems answer (output signal) is small. In otherwords: the former circulus vitiosus is broken since painsensation does not any more retrieve muscle/vessel tonus,at least not as strong as before.

The Wnal outcome of the procedure is characterized by aselective “erasure” of the pathological response or reXexpattern. New and normal reXex patterns may developinstead of the previously stored pair of pain and muscle/vessel tonus. Obviously, associative pain memory consid-ered as the real cause of chronic pain can be selectivelyreorganized by appropriate shock wave treatment.

Fig. 7 Signals of equal amplitudes (wave A and wave B) generate aninterference pattern with strong or deep modulation

Waves of Equal Amplitudes

Wave A

Wave B

StrongModulation Fig. 8 Small signals (wave A) interfere with strong signals (wave B)

and generate weak interference patterns with low modulation depth

Waves of Different Amplitudes

Wave A

Wave B

WeakModulation

Fig. 9 The dynamic range of any storage medium is limited and excessive utilization which may be performed by hyper-stimulation results in deforma-tion and degradation of the retrieved signal

0

Input

StrongMemoryOutput

Line

arReg

ion

Input Amplitude

Out

put A

mpl

it ude

Strong Modulation

Input

WeakMemoryOutput

0

Saturated Region

Out

put A

mpl

itude

Input Amplitude

Weak Modulation

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The eVect of selective erasing (forgetting) of memorycontents matches well the Wndings of Sandkuehler [25].According to Sandkuehler slightly painful counter-stimula-tion is best explained by a long-term depression (LTD) ofsynaptic strength in nerve Wbers.

Discussion

Associative pain memory linking a speciWc chronic paininput to particular muscle or vessel tone output may belooked at under two diVerent aspects: Wrst, as a general the-ory of chronic pain, oVering a new insight of pain mecha-nism and possible new therapeutic regimes and second, as aspeciWc explanation of the therapeutic eVect of ESWT andsimilar treatment modalities.

In the case of ESWT, until now no direct relation of anyphysical shock wave parameter could be related to the ther-apeutic eVect of ESWT. A consensus group [26] selected alist of physical parameters of a shock wave Weld such aspeak pressure, diVerent focal volumes and related energycontents, energy Xux density values for positive and nega-tive pressure contents etc. in order to correlate clinicalresults with one or the other parameter. Since therapeuticeVects could be seen with low energies as well as with highenergies, a direct shock wave eVect is unlikely. All of theconventional shock wave mechanisms mentioned abovewould require a more or less linear relation of shock wavedose and treatment eVects. On the other hand, two or threerepeated treatments at an interval of several days or weeksare often performed in order to enhance the shock waveeVects. This behavior leads to the idea of looking for indi-rect eVects such as memory and learning. Obviously, mem-ory eVects of the nervous system are not only inXuenced bythe strength of the stimulus but also on predisposition, sen-sitivity, concentration and attention. Metabolism on thelevel of synaptic junctions may also be involved.

The theory of associative memory draws the attentionfrom direct interaction of the aVected organ to its relatedmemory traces on higher levels of nervous interactions.

In view of this theory, the therapeutic results of ESWTin diVerent heterogeneous indications such as pain diseases,non-unions, induratio penis plastica [27], and ESWT treat-ment of muscular malfunctions [6] may be considered asreorganization of pathologic reXex patterns. Muscle and/orvessel tone are considered to be aVected by intense stimula-tion of ESWT. Breaking up the pathological reXex bowdoes not only erase the pathological memory but gives riseto increased circulation and metabolism due to relaxation ofvessel tonus. This in turn is taken as a basis for real and per-manent healing.

It seems tempting to consider ESWT as a therapeutictool for the small, but nevertheless clinically extremely

demanding group of patients with chronic pain conditionsin the urological Weld. We are, for instance, well aware ofthe considerable problems that are associated with persis-tent pain after one or several stone episodes in patients inwhom no residuals or no obvious explanation for the paincan be found.

The latter patients might possibly be one group forwhom ESWT can be eVective.

Conclusion

The concept of associative pain memory provides a mecha-nism for chronic pain diseases and explains how ESWTmay act on a variety of heterogeneous indications such asclose to bone soft tissue pain CPPS, pseudarthrosis, muscu-lar malfunctions and others.

The hypothesis behind is a “malfunction” of the nervouscontrol system due to “pathologic reXexes” which may beconditioned by single overuse or long-term misuse of par-ticular organs or functions. Pathological adaptation tounnatural muscular and vascular tone conditions is assumedto take place within the nervous system on the synapticlevel by modiWcation of the synaptic strength of largeensembles of neurons. Adaptation of synaptic thresholdpatterns is deemed to be the basis of memory functions ingeneral. ESWT with strong and repeated stimulation ofsynaptic junctions may delete the pathologic memory reXexpattern selectively with respect to the treated pain area. Thehypothesis of selective deletion of dedicated pathologicalreXexes is the charming concept of ESWT. If so, futureresearch needs to show how ESWT interacts with brainfunctions. It is well known that application of a painfulstimulus activates distinctive areas within the brain asproven by modern imaging modalities such as functionalmagnetic resonance imaging (fMRI) or positron emissiontomography (PET). A similar eVect should be generated byESWT and proven accordingly.

Another aspect of future research may be focused on theeVect of speciWc drugs aVecting the metabolism of synapticactivity. The healing eVect of ESWT should be diVerentlyinXuenced by drugs either facilitating or depressing synap-tic thresholds during shock wave application.

The author believes that if the hypothesis presentedabove can be supported by further research, a new view ofchronic pain and related mechanisms may shine a clearinglight on several diseases of presently unknown etiology. Itmay be worth checking the theory on diseases such as Alz-heimer, Parkinson, multiple sclerosis (MS) and a widespectrum of rheumatic diseases.

Open Access This article is distributed under the terms of the Crea-tive Commons Attribution Noncommercial License which permits any

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noncommercial use, distribution, and reproduction in any medium,provided the original author(s) and source are credited.

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