Postgraduate Medical Journal (December 1984) 60, 858-864

An approach to chronic pain of non-malignant origin

B. L. CRUE* J. J. PINSKYtM.D., F.A.C.S. M.D.

*Department of Neurological Surgery, University of Southern California School of Medicine, Los Angeles, andNew Hope Pain Center and tNew Hope Pain Research Foundation, Pasadena, California, U.S.A.

Introduction

There is no such thing as a pain stimulus in nature.Only tissue damage, or, in the intact integument,mechanical displacement or thermal change (Ken-ton, Crue and Carregal, 1975, 1976) is adequate toinitiate primary sensations. There is no place for painto be classified as a primary sensation (Crue andCarregal, 1975; Crue et al., 1976). Acute pain is betterconsidered as a perception; the related physiologicalmechanisms are largely within the central nervoussystem itself, and require a consciously functioningbrain for the subjective experience of pain. Theperipheral causative input mechanism necessary toinitiate the perception of pain has been labelled asnociception, and there is some specificity in thehuman peripheral nervous system, with high thresh-old thermal receptors and high threshold mechanore-ceptors (called nociceptors) both capable of initiatingperipheral nociceptive input. These nociceptors,along with chemoreceptors, seem to be activated inmost cases by acute injury and tissue damage totransmit the very slow C fibre and faster A deltainput system that constitute only a small part of anoverall patterning of input. There are both peripheraland central nervous system spatial overlap factors,convergence, temporal summation, and amplitudeintensity factors that then give rise to the centralperceptual event of pain. In the human, this pain'begins' in the region of the dorsal horn of the spinalcord (Crue and Carregal, 1975). We still do not knowenough about the patterning of input into the spinalcord dorsal horn region; but, apparently, pressure,temperature change, or tissue damage can, if thepattern is correct, lead to message transmissioncentrally, that comes to be perceived in consciousnessas pain (Fig. 1). However, it should be noted that thisgeneral mode of patterned inputs could also beinvolved in non-noxious stimulus transmission thatcan also be perceived in consciousness as pain (videinfra).A classification of pain (Agnew, Crue and Pinsky,

1979; Crue and Pinsky, 1984; Crue et al., 1979) based

on the length of time that pain has been present isshown in Table 1.

Acute pain

From a neurophysiological standpoint it wouldappear that acute pain in the human implies tissuedamage with subsequent sequential afferent nocicep-tive input. The acute pain generally responds well tothe natural healing process, often with treatment, byrepair, removal, or neutralization of the originalaetiological source. There is, however, no goodevidence for the presence of continuing active tissueinjury or disease in the chronic non-cancer painproblems on which we will focus our attention.

In normal use by many patients and physicians,the phrase 'acute pain' is often extended to includereference to an amplitude or intensity factor. It is as ifan acute pain is synonymous with a severe pain. Thiscommon usage creates problems because it implies orrelegates attributes to the pain that are the bases forthe formation of conceptual errors about the painexperience. Acute pain should only mean pain thathas not gone on for very long, and it can range frommild to severe in intensity and seriousness.

Chronic painTo discuss chronic pain, we must decide on the

temporal difference that divides chronic from acutepain. We indicate a period after which the pain is nolonger generally considered acute, or even subacute(days to weeks usually). Empirically, Stembach(1974) has suggested the cut-off time of 6 months.While this may be a valid statistical designation,bona fide chronic pain syndromes can be seen earlierthan 6 months, particularly following an acute event.One then wonders whether all chronic pain must

have arisen originally as acute pain, and only beencalled chronic after the passage of time. This wouldbe true if chronic pain were the same physiologicalentity as acute pain. It is at that point that we feelthere is a major obstacle in the understanding of

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Chronic pain of non-malignant origin 859

Afferent inputof

spinal dorsal root

) Cutaneous(a ) Touch - Discriminative - fast adapting and fast

conducting (Hair nets and Meisnercorpuscles) and some slowly adaptingbut fast conducting type II mechano-receptors. Up ipsilateral dorsalcolumn with some branches to dorsalhom + to ventral horn for motor reflex

7b) Pressure Both slow adapting butfast conducting type I

Temp (hot and cold) mechanoreceptors, andIC' fibres with free

Tissue damage 0endings, into dorsal(injury, horn complex, then upinflammation and contralateral anterior? ischemia) _ quadrant of spinal cord

if pattern correct.

|(2) Assorted visceral afferents-vessel, periosteum, viscera, )etc. (Some via autonomic chain)

| also largely into dorsal horn. (Slowly adapting+slow conducting). (Inflammation, ischemia, and ? injury) J

(3) Proprioception portion of gravity sense, largely 'non-adapting and fast conducting, up ipsilateral dorsalcolumn to higher CMS (including consciousness) withbranches to dorsal born + ventral born for gamma loopplus for motor reflex + spinocerebellar tracts forequilibrium (subconscious)

FIG. 1. The patterning of the input of the spinal cord dorsal horn region.

chronic pain. What all too commonly occurs is thatchronic pain is referred to and explained as though itwere a direct continuation of acute pain withcontinuing constant nociceptive input from an in-jured area. The quasi-explanations of continuingpathophysiology in the periphery include: 'it [thelesion] has failed to heal,' 'it [the injured area] wasnot fixed right' (usually by another surgeon). Whenthere have been numerous surgical attempts to quellthe pain, a frequent explanation that is given is that'the pain is from the scar remaining after the priorsurgery'. There is no evidence that most people withchronic pain have scarred in a different anatomicalpattern or with an altered physiological responsive-ness when compared to people without chronic painwho have had the same history of tissue damage andreparative efforts. Patients with chronic pain havenot been identified as having any unusual character-istics of tissue healing.

Chronic pain that continues as more or lessconstant pain should be regarded as a central pain,without any need to invoke the presence of intermit-tent events or continued peripheral nociceptive input.This may be regarded as a tautological classification,but the absence of a source of peripheral nociceptive

input is much more the rule than the exception whenthere is chronic pain of a more or less constantnature. If a pain problem is accompanied by clearevidence of a source of nociceptive input in theperiphery, we would not classify it as chronic pain(Crue et al., 1980). The best available evidencesuggests that there is no need for any classification ofchronic benign (non-neoplastic) pain with continuingnociceptive input. The classification of chronic painin Table 1 is based on the acceptance of theassumptions that the maintenance of chronic painchronically is due only to central factors (or genera-tors) in the absence of continued peripheral nocicep-tive input.When there is chronic pain as we have defined it,

the idea that there is continued nonciceptive stimula-tion from the periphery as its cause is not supportedby fact. Nonetheless, nociceptive input continues tobe used commonly as reason for the constant paineven when its somatic source(s) can rarely bedefinitively isolated. It is necessary that these rela-tionships be grasped so that treatment can be linkedto the syndrome's existing aetiological and perpetuat-ing factors, and not to undemonstrable hypothesizedpathophysiological mechanisms. At this juncture, we

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B. L. Crue and J. J. Pinsky

TABLE 1. Temporal classification of pain complaints

(l) AcuteUp to a few days' durationMild or severeCause known or unknownPresumed nociceptive inputThe 'fix me' medical model

(2) SubacuteA few days' to a few months' durationThough no longer an emergency, in most ways treat likeacute pain

(3) Recurrent acuteRecurrent or continued nociceptive input from underlyingchronic pathological processExamples: arthritis (rheumatoid or osteoarthritis)

(4) Ongoing acuteDue to uncontrolled malignant neoplastic diseaseContinued nociceptive input

(5) Chronic benignNon-neoplasticUsually >6 months durationNo known nociceptive peripheral inputPain often made more severe by any type of subsequentsensory inputBasically a 'central' painSeemingly adequate adaptation to functioning in the lifeprocess by the patient

(6) Chronic intractable benign pain syndrome (CIBPS)Chronic pain(s) with poor adaptation to the life processby the patient (i.e., pain becomes the central focus ofthe patient's existence)

can begin to see the necessity for acceptable workingdefinitions and classification, because they affect howwe form our concepts of the aetiology of acute andchronic pain from which people suffer, and thisstrongly affects the approach to treatment.

Chronic pain syndromes

Peripheralist and centralist conceptualizations

The peripheralist generally considers chronic painin the same neurophysiological and organic medicalmodels used for acute pain. A causal link is assumedbetween the chronic pain and continued nociceptiveinput that is presumed to be related to an activeperipheral abnormality that continues to be a sourceof nociceptive stimuli. It is regarded for hypotheticalreasons that the original causative injury or patholo-gical condition has not healed adequately, or newtrouble has started. This conceptual model is basedon presumed continuing active tissue or anatomicalabnormality, even when no abnormality is foundwith a thorough medical investigation. When non-

cancer related pain becomes the central feature of a

chronic syndrome, what is conveniently not con-

fronted by the peripheralist is the fact that manymore patients with similar past injuries and treat-

ments have had a decrease or disappearance of theirpain in spite of the omnipresent viscissitudes associ-ated with the normal healing process. If the peripher-alist conceptual model is pursued for a problem ofchronic pain, it then quite properly would follow thattherapy would be centered around attempts 'to fix'the presumed remaining peripheral problem or toblock the assumed continued nociceptive input,either by anaesthetic peripheral afferent nerve blocks(Kamdar, 1979) or by more central neurosurgicalsensory pathway blocking or ablative procedures(Felsoory and Crue, 1976).The centralist does not presume the presence of

continued peripheral nociceptive input as an expla-nation for chronic pain in most human chronicbenign pain syndromes. In our experience, theperipheralist approach to chronic pain has resulted intoo many surgical and pharmaceutical invasivetreatments for these medically based chronic painsyndromes.

There are some apparent exceptions, and there aresome chronic pain syndromes that seem to originateentirely within the central nervous system afterspecific organic lesions. Examples of this includesome infarcts of the thalamus (Dejerine-Roussy painsyndrome), and from pain after infarcts lower in thebrainstem (Wallenberg syndrome with pain). How-ever, even in these syndromes, it must be remem-bered that most people who have these types oflesions do not present for medical treatment sufferingwith chronic pain as part of their clinical picture(Agnew, 1984).

There is also general agreement that the centralnervous system is able to pervert non-noxious lighttouch, pressure, thermal, or auditory sensory input sothat these stimuli act as though they were noxiousand can trigger acute and severe paroxysms of painlocated by the patient in the periphery and usuallylabelled as 'neuralgia' or 'neuralgic jabs' (Crue andCarregal, 1974; Crue and Saltzberg, 1979; Crue,Todd and Carregal, 1968). Examples of this are seenin multiple sclerosis, or in primary idiopathic trigemi-nal neuralgia, in which a light touch almost any-where on the face can trigger paroxysms of severeneuralgic jabs of pain in distributions of the fifthcranial nerve. The important point to remember isthat these events represent a central perversion ofnon-noxious peripheral input. Also, there is thephenomenon of 'slop over' that is not fully under-stood. It appears to apply in conditions in whichthere is close neuroanatomical intertwining betweenan area injured and one without injury. An exampleof this is the ulnar distribution arm pain withmyocardial infarction related to a shared visceralafferent input to the T, cord level by the myocardiumand the ulnar nerve. None of these are examples ofspontaneous central pain states, and most neuralgic

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Chronic pain of non-malignant origin

pain is spontaneous. This implies a central generatormechanism that, on occasion, without peripheralinput as a trigger, can be the source of a painexperience that is perceived as being felt in, and'coming from', some specific peripheral anatomicarea, as part of the body image. Crue has longconsidered that such neuralgic pain can be consi-dered a form of 'central sensory epilepsy', and musthave an underlying neurophysiological centralmechanism (Carregal, Crue and Todd, 1963; Crue,Carregal and Todd, 1964; Crue et al., 1967; Crue etal., 1956; Crue and Sutin, 1959; Crue, Todd andCarregal, 1970).

Central neurologicalfeaturesTable 2 reviews central factors that might be

operative in either initiating or maintaining such acentral generator mechanism underlying chronicpain (Crue, 1979). At times there can be organicabnormalities within the brain itself. However, theremay be no central pathophysiology as far as isknown, and yet central mechanisms can becomeoverwhelmed by abnormal patterns of altered per-ipheral input. This is assumed to be the mechanismunderlying many cases in which there is a partialinjury of a mixed motor and sensory peripheralnerve, or even a nerve root, that results in 'cross-talk';as a result of this, there may be the establishment of aphysiologically abnormal neuronal pool or networkcentrally. It is suspected that this situation leads tocontinuing uncontrolled neuronal discharge, bothcephalad to consciousness and peripherally to abnor-mal reflex output mechanisms. This is the situationthat is generally accepted to apply in causalgia andthe deafferentiation and reflex sympathetic dystro-phy syndromes. It appears that there is a combina-tion of both above mechanisms in the so-calledcentral deafferentiation states in which the painsyndrome seems to have been initiated by someperipherally-based pathophysiology. Trigeminalneuralgia is an example of this proposed mechanism.The question of the pathologically involved anatomi-cal level(s) within the central nervous system indeafferentiation or causalgic pain states remains notfully settled. There is no question that some centralpain syndromes may be considered to be based morestrongly on organic features than the more frequentchronic pain syndromes (Table 2, no. 3) in whichactive organic features have essentially ceased to playa role.There is no conclusive evidence about the presence

of inherited or acquired characteristics in the neuro-anatomical circuitry or the neurochemical generativesystems of the brain related to hypersensitive percep-tion of pain. Balances or imbalances of nervous

TABLE 2. Chronic pain-predisposing central factors

(1) Organic abnormality within the central nervous system(a) Pathological (such as post-stroke)(b) Physiological, from abnormal peripheral input(such as causalgia)(c) Mixture of pathological and physiological (suchas tic douloureux possibly)

(2) Possible genetic or acquired differences with respectto perception of pain

(3) Psychological factors with no known physiologicalabnormality(a) Past input into memory storage, particularly includingearly life events and developmental pattern(b) Life situational events that accompany acute pain,injury or illness that act as causative triggersand sustaining forces(c) Mixture of both of these (the CIBPS syndrome)

system activity, viscissitudes of excitation or inhibi-tion, or differences in any number of central nervoussystem transmitter substances have not as yet ex-plained pain hypersensitivity (Table 2, no. 2). How-ever, there is no doubt that the converse is true; and,there are families with congenital insensitivity topain. However, these people's characteristics arepresent without any known neuroanatomic or neuro-physiological basis. Most normal individual differ-ences in sensitivity to acute pain, when studied, turnout to be idiosyncratic with some more or lesscultural/learned patterns superimposed (Zborowski,1969).The dynamics of chronic pain syndromes in the

central nervous system include the possibility thatwithin the central nervous system there is some typeof underlying central generator. The latter can bepictured as an epileptiform focus (foci), or as aspecific and functionally interlacing neuronal net-work. The latter may be generally conceptualized asbeing within the limbic lobe system that feeds back toloci of the nociceptive input modulating mechanism,related to the endorphin and enkephalin systems.These neuromodulator systems may affect not onlyacutely occurring or continuing afferent nociceptiveinput ascending from below. There are no researchfindings to tell us with any certainty whether or notthis exists or how it might work. But the patient withchronic pain continues, after the nociceptive inputwanes, to perceive pain and suffer with it. We havelong suggested (Crue et al., 1964; Crue and Todd,1968; Crue et al., 1968) that the appropriate genericpain label for this group of patients is 'neuralgia'.Furthermore, we believe this type of mechanism canexplain all chronic pain syndromes in categories 5and 6 of the classification in Table 1. This type ofchronic pain syndrome has been described by us inthe past (Pinsky, 1978, 1983) as a chronic intractablebenign pain syndrome (CIBPS). Descriptors of thissyndrome are presented in Table 3.

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Central psychological features

Ramzy and Wallerstein (1958) have provided apsychoanalytic schematization of pain in man. Thegeneral sense of the points made by Ramzy andWallerstein are cogent and in concordance with avast clinical experience. Aside from the thorny issueof general psychoanalytic theory, their concepts arevery useful in understanding how chronic painreadily can be regarded as 'real' pain in the absenceof current nociceptive input. Their category of'bodily pain' includes the presence and absence ofcurrent nociceptive input with a painful body localeidentified. Their category of 'mental pain' includesdysphoric affect states of all types, usually without abody site located as painful. They have clearlydivided pain into that that is readily consciouslyidentified (with body locale) and pain that is largelysubsumed in 'painful affects'. Also, they have a sub-category of 'neurotic bodily pain' that includes allbodily pain without discernible 'stimulus', and thiscategory implies that memory mechanisms play a keyrole in this process. This is similar, if not identical, toour concept of pain without current nociceptiveinput. In their categorization, all the patients who fitin this category are characterized by them as having

TABLE 3. Chronic intractable benign pain syndrome

General characteristics(1) Cannot be shown to be causally related to the here-and-now

with any active pathophysiological or pathoanatomicalprocess

(2) Has an antecedent history of generally ineffective medicaland surgical intervention in the pain problem

(3) Has come to be accompanied by disturbed psychosocialfunction that includes the pain complaint and theepiphenomena that accompany it:

Epiphenomena(1) Drug addiction of varying severity with

attendant CNS side effects(2) Multiple surgical procedures or pharmacological treatments

with their own morbid side effects separate from thoserelated to above

(3) Escalated decrease in physical functioning related toaccompanying pain and/or fear that this pain is a signalof increased bodily harm and damage

(4) Escalated hopelessness and helplessness as persistent orincreased dysphoria does not give way in the face ofmounting numbers of 'newer' or different treatmentinterventions

(5) Emotional conflicts with medical care delivery personnel(doctors, nurses, therapists, technicians) that resultin therapeutic goal interference

(6) Interpersonal emotional confficts with significant others(7) Escalated withdrawal and loss of gratifications from

psychosocial activity(8) Decrease in feelings of self-esteem, self-worth and self-

confidence(9) Lasting, unpleasant mood and affect changes

(10) Decreased ability to obtain pleasure from the life process,reflected in the presence of profound demoralization and,at times, significant depression

pain based on mainly hypochondriacal or hystericalmechanisms. We have described the chronic intrac-table benign pain syndrome in earlier publica-tions (Pinsky, 1975, 1978, 1983; Pinsky and Crue,1984) and include Table 3 here in order to provideclinical descriptors for this syndrome in this discus-sion.To pursue further the concepts of Ramzy and

Wallerstein and the realities of the dynamic unity ofmind and body (hence, psychosomatic), Pinsky(1983) has used their general formulations in theareas of 'affects' and 'ideas' and emphasized thestrong input of cognitive factors. The dynamicinteraction of many of these factors along with thenon-nociceptive somatic input play the major role inchronic pain syndromes. The concept that non-nociceptive somatic stimuli may be 'perverted' in thecentral nervous system and be perceived as pain hasbeen discussed above.While there is no evidence to suspect any inherited

or acquired defect in the central nervous system itselfthat leads to a chronic pain experience, there is thedevelopment of psychological forces (Table 2, no. 3)that have no known underlying neuroanatomicalcircuitry problems that play crucial roles in theappearance and maintenance of chronic pain syn-dromes. Psychological patterns of thought and be-haviour, memory and fantasy can have significantroles in the development and the modulation of apain experience. General conditioning, operant con-ditioning, and social modelling can play significantroles in the shaping of some specific behaviours.However, the full syndrome generally seems toinvolve complex and multiple types of input to thelearning process. There is a body of information thatindicates that memories and attitudes about one's selfformed in early life development have large affectivecolorations and play a very large role in characterformation and subsequent abilities to acquire copingstrategies that determine the types and levels ofadaptation to the life process (Engel, 1959; Mersky,1980; Meyer, 1980; Rado, 1980). These chronic painsyndromes seem to result from unconscious attemptsto avoid, modify, or eliminate major problem lifesituations and patterns as well as affective states thatcan be of a highly complex nature.When people develop these chronic intractable

pain syndromes, we are confronted not only withpain behaviour (Fordyce, 1976) and abnormal illnessbehaviour (Mechanic, 1968; Pilowsky, 1969), butwith a more generalized maladaptive syndrome thathas multifaceted levels of disorder that are reflectedin poor adaptation (Pinsky, 1983). In addition, ourpsychological clinical experience with over 600 pa-tients with these types of chronic pain syndromesindicates that a large percentage have life historiesthat include early childhood abuse (sexual and

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Chronic pain of non-malignant origin 863

physical), biological family alcoholism, and brokenand multiple family existences. Serious questionsabout the relationships between depression as adisorder of mood and chronic pain syndromesremain unanswered (Pinsky, 1983; Sunde, 1983).Situational problems that are normally considered ascontributing to psychological secondary gain are alsocommonly present. There is the as yet unansweredquestion about the extent to which premorbid psy-chological disorders play a role in the genesis ofconflict situations that encompass the secondarygains that develop. From the aspect of classification,we believe that when there is any continued nocicep-tive input from underlying chronic pathophysiologi-cal conditions, the patients should be classified ashaving recurrent acute pain with psychological po-tentiation. Over time, if a patient's problem with painbecomes chronic (Table 1, nos. 5, 6) and there is nolonger any evidence to invoke current nociceptiveinput, the classification of chronic pain is appropriateat that time. One can have recurrent acute pain towhich psychological factors contribute greatly. Thesame can apply when a person suffers with painrelated to cancer with ongoing nociceptive inputfrom advancing pathology.

Treatment and treatment outcome

Placebo response in the treatment of patients withchronic centrally generated pain is one of the mainreasons that we believe that results of treatment mustadhere to five general steps (Table 4) in order tocompare patient populations and their treatmentoutcome. The results of treatment of patients withchronic pain must attend mainly to long-term resultsbefore it can be determined if there were anybeneficial effects oftreatment (Crue, 1983). These aredifficult to perform long-term follow-up studies, andwe have reported on our work (Pinsky, 1983; Pinskyet aL, 1979).

It must be pointed out again that all patients withchronic pain do not fulfill sufficient criteria for adiagnosis of a chronic intractable benign pain syn-drome (CIBPS). As shown in Table 1, there are anumber of patients under category 5 that continue tofunction reasonably well with chronic pain. There isno reliable epidemiological evidence that allows us todistinguish these two patient populations from oneanother (Crook, Rideout and Browne, 1984) exceptthrough observable behaviour and careful psycholo-gical evaluation that includes psychodynamic assess-ment. There are individuals whose coping abilitieshave not allowed for other adaptive responses tointrapsychic and interpersonal life events and may beprone to develop a chronic intractable benign painsyndrome. We belief that when these general under-lying mechanisms are operative, they allow for

classification (Table 2 as a combination of 3a and 3b,3c), as the so-called CIBPS syndrome (Pinsky, 1975,1978, 1983; Pinsky and Crue, 1984; Pinsky et al.,1979).

Conclusions

Chronic pain is central 'neuralgic' pain which ispsychosomatic in nature. The treatment for it shouldinclude considerations ofthe mechanisms involved inits development. Patients should not be subjected touseless and repetitious nerve block, or irreversibleorthopaedic and neurosurgical procedures that canlead to procedure dependency, increased dysphoria,neurological deficits and increased suffering. Treat-ment should not include peripherally or centrallyacting analgesic agents on a regular basis. Whenthere is a depressive disorder of the type andmagnitude that would be expected to respond topsychopharmacological or somatic treatment, thisshould be treated in the normal way.Treatment for CIBPS should basically be psycho-

therapy, to enable somatic, intrapsychic, and lifesituational events to be interpreted and responded toby patients in ways that are less maladaptive.Because of the complex interplay of forces, thetreatment programme needs to be sufficiently inten-sive and extensive. This can best be provided by a fullinpatient or full-day treatment 4-5 days per week in adaycare treatment setting for 4-10 weeks. Thetreatment programme should be undertaken bytreators trained in different disciplines working as ateam in a medically-based setting (Crue, 1979). A fullorientation to the patient is provided that simultane-ously (not sequentially) attends to the medical(somatic) and psychological (intrapsychic, interper-sonal, cognitive and behavioural) determinants of thepain.

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