The Derailment of Railway Spine: A Timely Lesson for Post-Traumatic Fibromyalgia Syndrome

[Pain Reviews 1996; 3: 181-202]
Staff Specialist in Rheumatology, St. Vincents' Hospital, Sydney, New South Wales. Associate Professor, University of NSW, Sydney, Australia.
Consultant Physician in Rheumatology and Pain Medcine, Perth, Western Australia.


"Railway Spine" was the pejorative term applied in the mid-nineteenth century to any of a number of presentations of spinal pain which followed in time railway accidents. The term included "obscure affections of the brain and spinal cord",1 and "real or imaginary affections of the spine".2

"Railway Spine" has been further labelled a "distressing episode in the history of back pain", as for the first time chronic spinal pain which followed relatively minor trauma became accepted as a cause of compensable disability.³

It has been claimed that the original connotation of "railway spine" as a purely physical (structural) spinal condition obscured the importance of psychosocial factors in the causation of disability and thus "introduced a bias which has continued to the present day".³

Going further, some contemporary historians see "Railway Spine" as an "apparently psychogenic paralysis" developed by those involved in railway accidents4 and even as a "novel and hitherto unfathomable ailment" which provided an important stimulus to the development of American psychotherapy.5

Others 6,7 concentrated on the cerebral sequelae of these accidents, the symptoms of which became known as "Railway Brain".8 Finally, "Railway Spine" was considered to have played a "significant role in the evolution of modern railroad operation" and was a phenomenon by which the "sometimes bestial callousness of the Industrial Revolution had been brought to heel".9

It will be shown in this paper that the construct of "Railway Spine", originally formulated as a painful somatic spinal disorder, was subsumed by the popular "Neurosis" construct of the latter part of the nineteenth century. In the twentieth century, "Neurosis" was redefined from being an organic disorder of the nervous system to being entirely psychogenic ("psychoneurosis"), an epistemological error which has had a profound effect on all subsequent clinical formulations of post-traumatic musculoskeletal pain syndromes, especially those which have been banded together under the construct of "Fibromyalgia Syndrome"10 as "Post-traumatic Fibromyalgia".11 These conceptual difficulties and the ensuing vigorous arguments over nosology, which persist to the present, have obscured the quest to explain the observed clinical phenomena in neuroscientific terms.Railway safety

The advent of the steam railways in the early nineteenth century not only revolutionised the freight haulage industry but also for the first time made it possible for large numbers of passengers to undertake quick journeys over long distances.12 As passenger rail travel became popular in the 1840s, its relative safety was emphasised:

"Travelling by railway at any of the common rates of speed is attended with less personal danger than stage-coaching, because the locomotives are perfectly under control. Any deaths or personal injuries which have occurred on railways are, with scarcely an exception, attributable to the carelessness of the engine drivers, and by the employment of a superior class of men to direct the motions of the trains, this fruitful cause of mischief is in the course of being obviated."13

However, following a series of disastrous railway accidents which occurred in England over the next 20 years, railway safety became an urgent medico-political issue described by Lord Rosebery in 1885 as "a public scandal".12 As observed by The Lancet , "railway travelling undoubtedly grows faster than the discovery or application of means of preventing accidents."14

Although initially opposed by the large landowners as well as by those who ran other forms of freight haulage, the commercially successful railway companies had many devoted investors and enjoyed immense popularity despite the numerous accidents.15 The increasing alarm amongst the populace moved Queen Victoria, on behalf of her subjects, to ask the railway companies to provide safe conditions for the journeys of their 250 million passengers each year.16 The Lancet, taking up the cause of railway safety in the 1860s ("The Railway Question"), complained that the recommendations of Government railway inspectors inquiring into accidents were largely ignored by railway companies. Even when pertinent questions were asked in the Houses of Lords and Commons, the great political influence of the railway companies seemed to have placed them beyond the reach of Government control, such that "the whole system of government inspection and of parliamentary committees in reference to railway accidents is a gigantic sham, as those in authority very well know".17

In contrast to Prussia where in 1838 the railway companies were compelled by law to compensate injured persons, employees and passengers,18 in Great Britain damages for personal injury arising from railway accidents were only recoverable under the common law system, with the amount to be paid determined by a jury. Although most claims were settled "out of court", their scale was linked to the amounts awarded in court. The lack of any limit placed upon the amount of compensation for damages awarded by courts was of great concern to the railway companies who, by the early 1860s, were paying out very large sums of money in compensation. But this was seen by the editor of The Lancet as "[T]he best security the public possesses for the diligent employment of precautions against catastrophes".14Role of medical profession in court

The medical issues arising out of railway travel in the first half of the nineteenth century concerned mainly the possible ill-effects that this form of travel might have upon the general health and well being of both railway employees and railway passengers.19,20 However it fell to the courts to determine the 'reality of some of the injuries to health, physical and mental, which those interested in recovering "substantial" damages assign to railway collisions’.14 The medical profession was required to assist the courts in this determination under the instruction to be careful "of importing any statements into the report of a case other than those of a strictly scientific character".21

Distinguishing between those with genuine complaints and those who feigned disease and were claiming compensation following railway accidents was a major problem for physicians.22,23 At this time simulation of neurological disease was an issue of similar difficulty confronting physicians engaged in military medicine.24 The importance of obtaining an assessment of the person’s "moral and physical habits and physical motives" was stressed by Hall,2 who also pointed out that the simulator of disease was apt to "overact his part, to give a detail of incompatible symptoms, and greatly to exaggerate unimportant lesions". Disappointed that juries could ignore the carefully reasoned evidence of experienced medical witnesses such as himself, Skey1 observed that in medical practice the imagination of the doctor "will on occasions conjure up resemblances and suggest reasonings fatal to a correct diagnosis".

Nonetheless the courts found great difficulty in determining the exact amount of pecuniary damages to be awarded to plaintiffs with alleged injuries sustained in railway accidents, as all too often there were no physical signs of injury to explain ongoing and apparently disabling symptoms.2 The strongly held but often divergent opinions of expert medical witnesses called by either side to give evidence in these cases became a source of embarrassment to the whole medical profession.25 When the courts found "expert" medical opinions irreconcilable, they preferred the "sensible view of them, rather than the highly scientific one ... which commends itself most to reason and justice".21

This represented the first testing in the Courts of the problem of chronic pain, with which the judicial systems of today are still grappling.26 How is it that now, a century and a half later, so little progress has been made? To address this question the construct of "Railway Spine" must first be dissected.EVOLUTION OF THE CONSTRUCT OF "RAILWAY SPINE"

Spinal cord injuryBy the middle of the nineteenth century, spinal cord injuries had been well defined clinically, even though their underlying pathology was still not fully understood. Since the time of Hippocrates27 it had been known that limb paralysis and loss of bladder function, often resulting in death, could follow concussion to the spine, without there being any macroscopic evidence of injury to the spinal cord or its coverings.28 Other ways in which the spinal cord could be injured included penetrating wounds, compression (usually due to vertebral fracture or subluxation) and by a process of inflammation "excited" by the injury. The clinical manifestations of this presumed spinal inflammation included a combination of progressively developing "positive" and "negative" motor and sensory phenomena involving the limbs and trunk. An early symptom, often mistaken for "rheumatism", was deep spinal pain which, although initially localised, could extend along the whole spine and be exacerbated by spinal movement. It was said that the progress of the "inflammatory process" could be determined by the (painful) response to light percussion over each spinous process. In fact this phenomenon, tenderness or more correctly in modern terminology allodynia, is a feature central to the neurobiology of pain. However the clinical picture attributed to "spinal inflammation" was usually dominated by the presence of motor paralyses and contractures, limb pain, and disturbances of bladder and bowel function.28The clinical picture following railway injuries

In 1861, Dr Waller Lewis, principal Medical Officer of Her Majesty’s Post-office, reported a consistent group of symptoms which had developed gradually in some travelling employees of railway post-offices who had been involved in accidents and collisions but in whom no injury had been apparent at the time of the accident.14 These symptoms included sleep disturbances, dreams of collisions, tinnitus, vasomotor instability and intolerance of railway travel. Headache, spinal pain and spinal tenderness were also reported in the absence of external signs of injury or of objective signs of neurological damage.2,29,30 However there were also reports of the slow and insidious development of neurological symptoms of more serious import following severe railway accidents: paraesthesiae involving the extremities; local paralysis; paraplegia; impairment of bladder function; and impairment of intellect.31

John Erichsen, Surgeon to University College Hospital, London, was well aware of these presentations characterised by delayed onset of symptoms following trauma, their persistence and progressive increase in severity.32 He noted a remarkable analogy between cases of railway passengers who had also received a shock to the spine and a case under his care of a previously fit man who had fallen 30 feet from a scaffold onto his back.33 Erichsen noted that the effects of railway injuries were no different from those following other injuries although railway accidents were usually more severe; furthermore he had observed similar sequelae when monetary compensation was not an issue. Disability of a severe nature could follow what appeared to be relatively minor trauma, as judged by the absence of external signs of tissue damage. Any emotional disturbances in these patients were thought by Erichsen to be the consequence of the steadily deteriorating health of the sufferer:

"It is, unfortunately, not uncommon for a railway passenger to receive a shock to the spine which leaves no mark of injury to the tissues and yet, by the patient's own account, disables him as this man [Erichsen's patient] is disabled. He can have no reason for exaggeration ... no claim for compensation ... his whole anxiety has been to get about again to his work ... because family driven to destitution ... were this man a plaintiff in an action against a railway company the fact of the bladder and sphincter functions being perfectly performed, and the entire absence of palsy of sensation, might tend to throw great doubt over the genuineness of the partial palsy of motion with which he is affected."33

Erichsen32 proposed that the clinical entity "concussion of the spine" could develop after apparently minor accidents in which the spine was subjected to a sudden shaking or jarring. The symptoms of this entity could be "of the most serious, progressive, and persistent character" (page 93). The various clinical presentations of "concussion of the spine" included:

  1. cerebral symptoms: headache, confusion of thought, loss of memory and a variety of disturbances of the organs of special sense;
  2. spinal symptoms: pain at one or more points of the spine, increased by pressure or movement of any kind*, resulting in extreme rigidity of the vertebral column;
  3. symptoms in the limbs: painful sensations along the course of the nerves, paraesthesiae, variable degrees of lower limb weakness and resultant disturbances of gait.

Erichsen thus attempted to explain a number of different syndromes involving the spine and/or the central nervous system by postulating a common neural pathology, specifically a post-traumatic inflammatory process involving meninges and neuraxis. He also considered the prognosis to be gloomy in many cases. However these ideas were received with scepticism by others working in the field, not only because of the apparent lack of clinico-pathological correlation1,2 but also arising out of a number of perplexing clinical features of these syndromes which included their often delayed onset, the persistence of symptoms beyond reasonable "healing" time, their progressive increase in severity and the disproportion between their severity and the extent of discernable injury.Debate concerning diagnosis

Erichsen recognised that some of the symptoms which he attributed to "spinal concussion" could also occur in the better-described cerebral concussion associated with head injury.35 The main differential diagnoses were other forms of cerebrospinal disease (probably tuberculous or luetic), "rheumatism" and "hysteria". The absence of articular inflammation and the presence of neurological symptoms, including those related to the brain, were said to distinguish "spinal concussion" from "rheumatism", itself a poorly defined concept. To Erichsen "rheumatism" had apparently denoted only articular pathology, although the term was then being used in a wider sense to denote affections of fibrous, tendinous and muscular tissues.36 In his later work, Erichsen37 acknowleged the real difficulty at times in separating the symptoms of "spinal concussion" from those due to injury of the "motor apparatus" of the spine. Both presumed pathologies could result in persistent and intractable spinal pain and rigidity. The clinical spectrum of "hysteria" itself included spinal pain and tenderness. However Erichsen maintained that not only was the course of "hysteria" unpredictable and thus at variance with that of "spinal concussion" but also that it tended to occur in excitable, imaginative and emotionally unstable young women, whereas "spinal concussion" syndromes were often seen in stable, middle-aged working men of sober habits (page 126). Thus differential diagnosis was a "choice" between three poorly defined entities which shared many clinical features.

Not infrequently there was discordance between the extent and duration of disability and the injury reported by patients. Erichsen attributed this to the "inherent vulnerability of the spine", which in fact was a self-fulfilling argument.32 If this were so, it would be difficult to understand why all those who incurred spinal fractures did not develop symptoms of "spinal concussion".38 In response to this important question, all Erichsen could offer was a principle imparted to him by a watchmaker: if one dropped a watch and its glass were broken, the movement would rarely be damaged; however if the glass were unbroken, the movement was likely to stop.

Another proposed explanation was the reputed tendency for persons who have received minor injuries to greatly exaggerate their symptoms if compensation were involved. In support of this opinion were some reports of the rapid recovery of the health of accident victims which followed favourable jury verdicts and payment of damages.2,21 It was argued that true disease of the spine of serious import invariably manifested itself by objective signs, whereas in "imaginary" spinal disease subjective symptoms alone were present and did not denote "real affections of the nerve centres".2 There was also a danger that "hysteria" (then held to be a functional disturbance of the nervous system) was not unknown in males and might be mistaken for organic disease of the nervous system.1,2 Debate concerning pathophysiology

In the nineteenth century a debate began concerning the pathophysiology of diffuse spinal pain and tenderness following spinal trauma. As shown in Figures 1-3, this debate was between those who espoused somatic models, with damage either to spinal neural tissues or to the surrounding musculoskeletal tissues, and those who viewed the clinical phenomena either as manifestations of psychologically-induced central nervous system dysfunction ("neurosis") or a "purely" emotional disturbance. This unresolved debate led to insurmountable semantic and epistemological difficulties for the construct of "Railway Spine".Somatic hypotheses (Fig. 2)

Erichsen's model

The nature of the primary change in the spinal cord produced by a concussion was unknown. Erichsen suggested that "the nervous force is to a certain extent shaken out of a man, and that he has in some way lost nervous power" (page 95).32 The particular analogy suggested by him was the loss of magnetism which one could induce by striking a magnet a heavy blow with a hammer. This formulation was consistent with the basic concept of "nervous energy" as promulgated in 1769 by Cullen in his "System of Nosology".39

More important than the presumed primary changes in the nervous system were the subsequent "secondary effects" of the injury. Arising out of the dearth of post-mortem studies conducted on these patients, Erichsen made a bold intuitive guess as to their pathological basis. Influenced by the work of earlier investigators such as Abercrombie (1828) and Ollivier (1837), he argued that the pathology underlying the secondary and progressive symptoms of "concussion of the spine" was chronic inflammation of the spinal membranes and cord. The cerebral symptoms were the result of direct extension of this inflammatory process from the spinal to the cerebral meninges. Abercrombie and Ollivier were the accepted authorities on diseases of the spinal cord, their clinicopathological descriptions of cases of spinal meningitis and myelitis following trauma having pre-dated the era of railway accidents (and the resultant medico-legal battles fought out between expert medical witnesses).

Another English surgeon, Hilton,40 had noted that "concussion of the spinal marrow" was being seen more frequently as a result of railway accidents. To explain widespread pain, stiffness and hyperaesthesia following spinal trauma, he postulated the presence of minor structural disturbances within the spinal cord and its nerve roots. The cord could be injured by its impingement against the vertebral arches, whilst the nerve roots, fixed within the intervertebral foramina, could be hurt by tension created "if the spinal marrow be dragged from them". Hilton warned that premature and too vigorous exertion before healing had taken place could "increase the exhaustion of the spinal marrow" and render likely the prospect of paraplegia.

The theory that subtle disturbances of spinal cord function could result from spinal trauma in humans received some support from the animal experimental studies of Schmaus (1890) (reviewed by Knapp41) and those of Watson.42 However these authors disagreed as to whether the lesions so produced in animals could result in the slowly developing and progressive symptoms of "spinal concussion" as described by Erichsen.32

Spinal irritation

There were obvious similarities between the constructs of "spinal concussion" and "spinal irritation", the latter having been formulated in the 1820s to denote an idiopathic painful spinal disorder mainly affecting young females.43 Early writers on "spinal irritation" considered the pain to be the result of "irritation" or "subacute inflammation" of spinal nerve roots or of the spinal cord itself.44 The cardinal and often only clinical features of "spinal irritation" were diffuse spinal pain and tenderness. Whereas the reality of "spinal irritation" as an entity was denied by some, others attributed the same clinical presentation to (extra-spinal) "rheumatism", "with which inflammation of the spinal cord, in its acute or chronic form, may, by a possibility, be confounded".45

Having rejected the "nervous irritation" theory of spinal pain and tenderness in females, and finding the diagnosis of "hysteria" to be illogical, Inman46 postulated a musculo-tendinous origin for these clinical phenomena. Any factor which caused general debility, such as overwork, menorrhagia or poor diet, could lead to muscle fatigue, with overstrained muscle origins, of which pain was a manifestation.

"Spinal irritation" gradually fell from popularity as a diagnosis in Europe, being replaced by the "rival wave of hysteria, and the surge of neurasthenia".44 However in the United States of America it remained in use to denote a functional disturbance of the spinal cord and its membranes, resulting either from an injury to the spine or from a "lowered condition of the general health from various causes".47

Traumatic spinal neuralgia

Pain, usually associated with deep seated tenderness, was not only common but also frequently the predominant symptom following all forms of spinal trauma, according to Gowers.48 Remarkably prescient of current concepts, he theorised that persistent pain reflected a state of sensitisation of the nerves supplying either spinal joints and ligaments or those supplying the spinal meninges ("traumatic spinal neuralgia"). He attributed the cerebral symptoms of Erichsen’s "spinal concussion" to a disturbance of brain function caused partly by physical concussion but mainly attributable to the "mental shock which an accident necessarily causes". Contrary to the assertion made by those physicians employed by railway companies, it was Gowers' experience that pain tended not to subside, even with the "sovereign balm" of substantial compensation.


In the early nineteenth century, "chronic rheumatism" was held to be a condition apt to affect joints surrounded by many muscles, particularly those whose the muscles "are employed in the most constant and vigorous exertions".49 It was believed that the muscles rather than the joints were the site of pathology and that "violent strains and spasms occurring on sudden and somewhat violent exertions, bring on rheumatic affections, which at first partake of the acute, but very soon change into the nature of the chronic, rheumatism". A case in point was "lumbago" (rheumatism affecting "the vertebrae of the loins").49 By the end of the nineteenth century the focus of attention had shifted from the spinal cord to the various extraspinal structures in the search for the source of severe and persistent spinal pain following trauma.42,50

A back injury was claimed in more than 60% of cases of "Railway Spine" personally seen by Page,51 who for 17 years had been Surgeon to the London and North-Western Railway Company. He found that injuries to the spinal cord were rare. Most back injuries were categorised by Page as "simple back sprains", the signs of which were stiffness, tenderness and pain, present at any level of the spinal column, although sometimes the involvement could be diffuse, a state referred to by Page as widely distributed "lumbago". The pathological lesions held responsible for these symptoms were muscular and ligamentous "strains" of various degrees of severity. Although "rheumatic" pains could often be persistent, or even recur with extra exertion, Page advocated exercise rather than rest and for patients to be reassured of their ultimate full recovery:

"In no wise would I undervalue the real importance of these vertebral sprains. They may be exceedingly distressing to the patient; the pains may last a very long time; there may even be occasional reminders of pain for months or years under suitable conditions; but it is right that we should attach no more import to them than they deserve, and their existence should not entail a needless dread of serious injury to the structures within the spinal canal" (page 9).


The term "fibrositis" was first used by Gowers52 to denote a form of presumed sterile inflammation of the fibrous tissue of muscles responsible for "lumbago in particular and muscular rheumatism in general". This speculative pathology involving the fibrous membranes or tissues was already the subject of debate during the nineteenth century.53 The pathological basis of many chronic musculoskeletal pain syndromes was believed to be an inflammatory process involving "different muscles of the body, their fascia, or tendons, in addition to the joints, or independent of them".54 Constitutional factors, through their interaction with unknown environmental agents, were thought to be important in the development of particular diseases. The so-called "rheumatic diathesis" consisted of a sensitivity to changes in atmospheric conditions, a proneness to perspiration (often with a disagreeable odour) and the presence of a urinary sediment. It should be noted, however, that in the mid-nineteenth century, chronic rheumatism was thought to share a common aetiology with the acute form of rheumatism (rheumatic fever).54

Gowers52 did recognise a post-traumatic form of fibrositis ("pain felt after strain"), to which the lumbar spinal muscles and ligaments were held to be especially prone. This diagnosis embraced the chronic spinal pain syndromes which could follow spinal injuries incurred in railway and other accidents. Lacking definitive histological studies, Gowers was hesitant to attribute this state of "hypersensitiveness after strain" as solely due to inflammatory changes in these tissues, pointing out that although the original symptoms reflected organic tissue damage, the "enduring sensitiveness after injury" probably reflected residual changes within the peripheral nervous system rather than a persistent inflammatory process. Psychogenic hypotheses

The nineteenth century concept of "nervous diseases" comprised all organic diseases of the nervous system, the major psychiatric disorders and lesser psychiatric disorders which would today be regarded as "psychoneuroses".55 These lesser psychiatric disorders (which included hysteria, hypochondria and mild depression) were regarded by many physicians as "functional" in the sense that, although there was no demonstrable organic disorder of the nervous system, a disturbance of brain function was nonetheless responsible and hence allowed them to be categorised as "neuroses".

Two major themes of the pathogenesis of "neurosis" permeate nineteenth century literature: firstly the concept of predisposition to develop nervous disorders ("neuropathic prediposition"); and secondly that of "commotion" of the predisposed nervous system, due to environmental or psychic factors. With respect to the latter, there was increasing interest in the effects of psychic and other non-physical environmental traumata upon the functioning of the central nervous system.56 This was encompassed in the concept of "ideodynamism", namely that symptoms could be caused by ideas in constitutionally predisposed individuals.57 In these cases the connection between the event and the symptoms was thought to be ideas and emotions (morbid ideation):

"some of the most serious disorders of the nervous system, such as paralysis, spasm, pain, and otherwise altered sensations, may depend upon a morbid condition of emotion, of idea and emotion, or of idea alone .... [T]he man becomes really ill, but the region of illness is idea".23

Erichsen had acknowledged that it was rare for spinal pain to be the only complication of railway accidents. The "nervous" or cerebral symptoms previously attributed to organic disturbances of the nervous system were reconceptualised by Page51 as "general nervous shock", defined as "some functional or dynamic disturbance of the nervous equilibrium or tone, rather than structural damage to any organ of the body". He believed that the "fright and mental shock" incidental to railway accidents was a common and potent cause of long-term disability, even in those who had received no bodily injury whatsoever. However this state of nervous exhaustion and depression of many bodily functions which could develop following railway collisions was in fact characteristic of the then popular diagnosis of "neurasthenia".

Neurasthenia and traumatic neurasthenia

Neurasthenia, meaning "lack of nerve strength", was formulated as a diagnostic entity in the late 1860s by Beard,58 an American physician. The unequivocally somatic model which he put forward for neurasthenia invoked the concepts of "nerve force" and "reflex action" to explain the nexus between bodily dysfunction and mental processes. The concept of "nerve force" was central to the neurasthenia construct, as it had been to that of "spinal concussion". Beard postulated a primary disturbance of cell nutrition of the nervous system in neurasthenia, which resulted in a "feebleness and instability of nerve action", a functional disturbance which could have profound effects upon many other parts of the body. The pathophysiology was said to be a "deficiency in quantity or impairment in quality of the nerve tissues; hence the exhaustion, the positive pain, the unsteadiness, the fluctuating character of the morbid sensations and phenomena to which the term neurasthenia is applied" (page 150). According to Beard, those predisposed to develop "neurasthenia and allied troubles" possessed the "nervous diathesis", the chief signs of which were "fine, soft skin, fine hair, delicately-cut features, and tapering extremities" (page 128).

Beard58 saw the normal bodily state as "a bundle of reflex actions" and the neurasthenic state as characterized by exaggerated reflex irritability (due to loss of inhibitory or controlling power of the central nervous system) primarily centred in three main bodily regions, the brain, the gastrointestinal tract and the reproductive organs:

"when any one of these reflex centres is irritated by over-use or direct abuse, the injury is likely to radiate or reverberate in any or in all directions; we cannot tell just where, any more than we can tell where lightning will strike ... in this way disease may be excited in parts quite distant from the seat of irritation ... immense number and variety of symptoms and abnormal sensations from which the nervously exhausted suffer ... hence difficult to tell from the symptoms, or the locality of the symptoms, just where the disease or source really is" (page 126).58

Neurasthenia, the fashionable neurosis of the late nineteenth century, appeared in "a thousand remarkable forms".59 Compared with the symptoms of organic disease which were usually "fixed and stable", those of neurasthenia were "fleeting, transient, metastatic, and recurrent" (page 123).58 Cerebral and spinal irritation were each seen as special local examples of the general neurasthenic state. Tenderness of the scalp signified cerebral irritation, tenderness of the bones of the spinal column indicated spinal irritation. Spinal pain, with or without spinal tenderness, could be a prominent symptom of neurasthenia, said to be distinguishable from the pain of "muscular rheumatism" by its variability, both in intensity and anatomical distribution.

Common causes of neurasthenia included chronic debilitating diseases, overwork or overstrain, anxiety, sleep deprivation and all varieties of mental shock, including that following trauma.60 Railway accidents were recognised as being capable of producing severe shocks to the nervous system which could render persons "neurasthenic". Dana,61 who was the first to use the term "traumatic neurasthenia", considered that: "[This] condition is a real pathological one, and the sufferers are unquestionably sometimes as much injured as if they had had a broken arm or leg, or an actual injury to the cord". Pain then became a manifestation of the exaggerated reflex irritability which was generally present in functional diseases.

Hysteria and traumatic hysteria

Throughout history "hysteria" was regarded as a disease characterised by fits or faints and "hysteric symptoms" (such as the globus hystericus, clavus hystericus) which could alternate with them.49 Used in its traditional sense, hysteria was a diagnosis peculiar to women at the commencement of menstruation but also prone to affect barren women and "healthy widows in whom matrimonial habits have been suddenly suspended and prostitutes on their first entering penitentiaries".62 Minor forms of hysteria in men had been seen to follow periods of enforced sexual abstinence during a protracted courtship, as well as the recourse to frequent masturbation.62

During the nineteenth century, hysteria came to be regarded as a functional disease of the nervous system ("neurosis") characterised by "nerve instability", the fundamental cause of which was still "wrapt in obscurity".63 However it had long been seen as "a fertile field of nosological controversy".64 Although the clinical phenomena of hysteria were intensively studied in France and Germany in the latter years of the nineteenth century, the disease still proved refractory to definition. On theoretical grounds it was variously seen as a disease of the emotions, a disease of dissociation of ideas, a restriction of the sphere of consciousness and as a mental (personality) disorder characterised by increased suggestibility.65

Although Erichsen32 had maintained that it was an easy matter to distinguish "spinal concussion" from hysteria, the obvious similarities between the two constructs could not be ignored when the teaching of the time held that one of the clinical presentations of hysteria was spinal pain and tenderness.54 Beard58 claimed to be able to distinguish neurasthenia from hysteria: he saw the former condition as "the door which opens into quite a large number of diseases of the nervous system", which included, as he grudgingly admitted, hysteria.

Meanwhile the French neurologist Charcot66 considered the "obstinate nervous states" following railway accidents as simply manifestations of hysteria resulting from "psycho-nervous commotion", whether occurring in males or females. He hoped that a better understanding of hysteria in males by those working in the medicolegal field would overcome the deeply rooted prejudice still attached to the word "hysteria". Others agreed with him that hysteria in the male coming on after an injury was by no means uncommon.67 The main clinical features were paralyses, contractures, sensory alterations, disorders of the special senses, altered mental states, and epileptiform seizures provoked by pressure on certain regions.

According to Charcot66 "traumatic hysteria" could be caused by any of the abnormal sensations provoked by an injury. In this context "nervous shock" replaced the mechanisms of hypnotism and auto-suggestion which were central to Charcot’s model of hysteria.68 The patient's beliefs and ideas about injury were held to be potent factors not only in the genesis of the condition but also in retarding recovery. These usually revolved around compensation issues, projection of blame, frequent medical examinations and certifications, constant repetition of sufferings, accounts of the accident in the press and worry over legal proceedings.68,69

Traumatic neurosis

Challenging the primacy of auto-suggestion in these cases, Oppenheim,70 a German neurologist, introduced the term "traumatic neuroses". In his opinion both the psychical and physical concomitants of bodily injury induced "molecular alterations" within the cerebrum. Just as "shock of the affected part of the body" was transmitted centrally via the peripheral nerves, so peripheral bodily trauma could alter cerebral functions. The clinical picture of traumatic neurosis generally consisted of a combination of "hysteric and neurasthenic phenomena ", although it could also consist solely of either neurosis. Spinal pain and restriction of movement were generally the earliest complaints in the "neuroses following upon railroad accidents".69,70 The presence of cerebral symptoms was indicative either of cranial injury or that the accident had been combined with a severe "mental emotion". Other symptoms which developed were said to be recognisable as "the sign-posts of neurasthenia and hysteria" (vide supra). Under the heading of "disturbances of sensibility and of the special senses", Oppenheim listed pain, paraesthesias, hyperaesthesia, and hypoesthesia.

Commenting on the conflicts amongst his contemporary neurologists in Germany and France on the nature and origin of the traumatic neuroses, Strümpell69 felt that their differences of opinion were largely of semantic origin:

"For neurasthenia and hysteria are notions of so changeable a character that we are unable to set up definite and generally accepted criteria for the precise recognition of each case of disease. Further, also, I believe that we cannot put all cases of traumatic neurosis on the same level, and that we must employ varying considerations in judging of the individual cases"

Semantic and epistemological confusionThus both the somatic and the psychogenic models which sought to provide a heuristic for "railway spine" shared a number of features. Stemming from the absence of a defined pathology or pathophysiology, resort was taken to the dominant conceptual framework of the time, either "inflammation" or "neurosis" (in its initial connotation of a disorder of brain function). The conflation of physical and emotional clinical features admitted into the syndromic definition of "railway spine" carried the implication of a common pathogenesis, setting the stage for argument between different schools of thought. The exercise made a mockery of differential diagnosis, when the elastic "diagnostic criteria" for one entity shared most if not all of the criteria for another. Thus spinal pain and tenderness were clinical features of "hysteria", whilst "hysterical" features were part of the presentation of spinal pain. In essence, this was the error of tautology, where entities were defined so broadly as to include all possibilities, thus making it difficult to identify their essential components. "Railway spine" came to be attached to any situation of (post-traumatic) spinal pain; traumatic "hysteria" or "neurasthenia", with their multitudinous list of precipitating and aggravating factors, could be similarly appended. Both somatic and psychogenic features relied on a " constitutional predisposition", upon which the impact of trauma exerted a "commotion" of nerve function or of ideas.

By the end of the century the constructs of "traumatic neurosis", "traumatic hysteria" and "traumatic neurasthenia" as disturbances of the brain were collapsing, as it had become obvious that the nature of the particular clinical investigation and the pre-existing beliefs of the investigator could greatly influence symptoms of presumed psychic origin.65 Spinal pain and tenderness, so central to the diagnosis of "spinal concussion" in the 1860s, then became but two of many symptoms present in patients with so-called "functional" nervous disturbances following trauma.61,71 These symptoms were being now mainly discussed in the context of the differentiation between "real" disease and disease simulation or malingering in those claiming damages for personal injury,8,70,72 instead of their underlying pathophysiology.

The failure of the medical scientific community to recognise the tautologous nature of these constructs is the fundamental error in epistemology which emerges from this analysis. As a consequence, their inadequate explanatory power tended to persist, unchallenged, obscuring any quest towards an integrated understanding of the clinical problem. In the next section we will show that as a result of this error, there was widespread rejection that spinal pain and tenderness following trauma constituted a legitimate clinical entity.

The derailment of "railway spine"

The transmutation of "Neurosis" to "Psychoneurosis"When the construct of "spinal concussion" was formulated by Erichsen, the only pathophysiological explanations available to him were inflammation and alterations in "nervous energy". In the latter half of the nineteenth century, putative dysfunction of the nervous system became the dominant discourse in clinical conditions where somatic pathology was not obvious. During this period the concept of hysteria evolved from being a somatic disturbance of that portion of the brain responsible for receiving affective sensations to a state of "dissociation of consciousness", wherein certain neurophysiological processes become entirely split off from the mainstream functioning of the nervous system, thus permitting ideas to operate independently of the conscious state.73

According to Prince,74 the persistent pains which played so dominant a part in the clinical picture of "traumatic neuroses" were of a psychical nature, being "manifestations of the concentration of the mind upon the injured part". To support his opinion he drew upon the analogy of similar pain found in non-traumatic cases, the absence of all objective signs of injury in the area of pain and his purported ability to relieve the pain by means of suggestion.

In the early 1890s Breuer and Freud75 seized upon "traumatic neurosis" as exemplifying their paradigm of (conversion) hysteria. Ideas sufficiently powerful to cause psychic trauma ("commotion") were seen by them to act upon a nervous system which was abnormally excitable ("predisposition"). The "hysterical disposition" consisted of a higher than normal degree of suggestibility which would more easily favour the conversion of "affective excitation" into a dysfunctional state of the nervous system, leading to a variety of somatic symptoms. "Hysterical" pains were conceptualised as "hallucinations of pain" resulting from the action of often very vivid ideas upon abnormally excitable pain pathways. They preferred to leave unanswered the question whether or not the hyperexcitable state was itself of psychic origin.

With the rise to prominence of the Freudian school of psychoanalysis from 1895 to 1910, hysteria was reclassified as a psychoneurosis.76 Motor disturbances (for example, cramps, spasms and contractures without organic explanation) and sensory disturbances (for example, variable and intermittent anaesthesia, hyperaesthesia and chronic pain) were said to be prominent features of (now called) "conversion hysteria".77

For the first decades of the twentieth century, chronic post-traumatic spinal pain syndromes analogous to the prototypic "railway spine" were still being categorised as "traumatic neuroses" and subsumed under the diagnoses of either neurasthenia or hysteria.78 However these diagnoses had now acquired a different connotation, reflecting the "psychologization of the neurosis concept"79: "trauma" became "psychic trauma" and "neurosis" became "psychoneurosis" (Figure 4).

As this major change in medical thinking took place, the already somewhat loose anchoring of "neurosis" (a construct lacking a firm pathological foundation) to a preceding traumatic event could no longer be maintained. The combination of the post hoc ergo propter hoc fallacy with the failure to provide a mechanism for the clinical features resulted in the diagnosis of "traumatic neurosis" falling into disrepute, being used then to denote a particular psychological reaction seen only in those who wished to obtain some advantage, such as escape from the front-line in times of war, or an "unearned increment in cash in peace" 80 (Figure 5). This same fate befell other parallel constructs which sought to explain (unsuccessfully) the persistence of somatic symptoms, particularly pain and tenderness, which occurred in the context of other traumatic events, as for example those syndromes which were designated "Occupation Neuroses".81

The fall of neurasthenia

At the commencement of the Great War (1914-1918), the diagnosis of "spinal concussion" could be used in one of two senses: referring either to a neurological disorder caused by localized spinal pathology such as focal haemorrhage or softening resulting from true concussion or to a functional disorder of the spine induced solely by emotional factors ("the realm of ideas").82 As the war progressed and pensionable neuroses comprised up to 40% of the casualties evacuated home, the initial attribution of these conditions to physical causes could not be sustained.83

At this time, a condition known as "trench spine" was diagnosed in some who, having survived blast injuries, presented with spinal pain and transient dysfunction of the lower portion of the spinal cord. "Trench spine" was said to be "akin to railway spine" and therefore "traumatic neurasthenia". However Campbell,84 an Australian surgeon stationed at Cairo, doubted whether this condition should be included amongst the neuroses (as neurasthenia), commenting that the subjects whom he had treated were not "inherently neurotic" and that the clinical phenomena were not suggestive of a simple "functional" disorder.

In parallel with the dualistic interpretations of "spinal concussion", two schools of thought still existed regarding the pathology of "traumatic neurasthenia". There were those who believed that any injury at any site may produce "a physical condition of the nervous system but without any morbid anatomy", oblivious that this argument was tautological.85 Others viewed the signs and symptoms as those of an anxiety neurosis, aetiologically dependent on a number of psychological factors such as fear, questions of responsibility for injury, trivial remarks by doctors and possibly to "hereditary nervous instability". Physicians were advised to "bring the anxieties and fears and misunderstandings to the surface, expose their fallacies, and disperse the germs of revenge and greed".85 As the psychoneuroses became more clearly defined, neurasthenia lost much of its significance and gradually fell from favour as a somatic diagnosis.77

The demise of traumatic hysteria

Along with neurasthenia, hysteria was also recognised as a symptom complex of the emotional traumata experienced by soldiers in the zone of battle, known as "shell shock", originally attributed to organic dysfunction of the brain ("commotio cerebri"), or, as it evolved, "emotio cerebri".86-88 The many and varied clinical presentations of hysteria in this context were seen as unconscious means of escaping from an intolerable situation ("conversion hysterias") and were explained by using the newly developed theories of "dissociation" and "repression" of mental processes.87,89 "Shell-shock" became a euphemism for "hysteria", a diagnosis which was naturally unacceptable to soldiers as it carried the stigma of being an "essentially feminine failing".90

In civilian life, spinal pain and tenderness could also be interpreted as "hysterical".91-93 Hysteria was being used in this context as a rather pejorative diagnosis for those "men and women of the middle class, also those of good society, [who] pretend to be the victims of serious injuries after even mild railway accidents! There is a nervous condition left after the shock which partly explains this".92 By the 1940s there were those of the view that a "traumatic neurosis" was seen in civilian practice only as a sequel to accidents "in respect of which legislation has made compensation payable".94

Collie,95 an experienced medical examiner of compensation claimants in England, saw "railway spine" as:

"... merely a psychical condition, which is particularly intractable to treatment. There can be no doubt that in former days railway companies were mulcted in large sums, and that introspection and gross exaggeration brought heavy damages in their train. Modern methods of psycho-therapeutics would have led to different results".

In his historical review of psychology in relation to medicine, Culpin96 completed the derailment of railway spine (and its related constructs). He was extremely critical both of Erichsen for his somatic formulation of "spinal concussion" and of Charcot for his insistence that hysteria was a disorder of function of the nervous system. In Culpin’s opinion, Erichsen’s "mechanistic blinkers" had led him to describe a best-forgotten "mythopathology" wherein he had "described at length symptoms that I have only seen in a wardful of untreated and titubating shell-shockers". The failure of the "Railway Spine" debate to address the clinical problems

Various contemporary writers have claimed that "railway spine" was, in retrospect, an example of post-concussion syndrome,7 post-traumatic stress disorder,97 conversion reaction,98 or malingering and simulation for secondary gain.99 With the exception of Keller,9 who suggested that at least in some cases there may have been progressive spinal cord compromise as a result of undiagnosed spinal instability, it was not generally accepted that the painful spine was an intrinsically spinal problem but rather needed to be explained by invoking altered mental (that is, cerebral and intra-psychic) factors.

Detailed analyses of the history of development and subsequent progression of the "railway spine" construct have been undertaken by Trimble6 and Caplan.5 However neither author has appreciated that the most prominent clinical features of "spinal concussion" following railway accidents, as diagnosed by Erichsen,32,37 were diffuse spinal pain and tenderness, usually associated with loss of range of spinal movement. Consequently, when tracing the evolution of this construct, they failed to recognize the fundamental epistemological error which occurred whereby these important spinal symptoms were subsumed into theoretical models of primary psychogenesis, all of which were untestable. This previously undetected error has enabled some writers to use "railway spine" to bolster their argument that many other unexplained somatic symptoms must be psychogenic.

In their historical monograph on low back pain and disability, orthopaedic surgeons Allan and Waddell3 stated (incorrectly) that the idea of injury being a cause of chronic back pain originated in the latter half of the nineteenth century. They saw "railway spine" as a key event in this history which laid the foundations for our contemporary approach to back pain. To them it signified the merging of two nineteenth century ideas: that the spine could be the source of back pain and that trauma could be a cause. Central to their thesis was the claim that Erichsen, as did others, wholeheartedly embraced the concept of "spinal irritation" and therefore "accepted as physical a host of psychosomatic symptoms". The proof offered by Allan and Waddell is that by the end of the century the terms "railway spine" and "concussion of the spine" had been discredited as denoting "purely physical diseases" (due to contradictory attempts to explain their pathology) and were "generally felt to be hysterical".

Shorter,4 in his recent book "From Paralysis to Fatigue", defines psychosomatic illness as "any illness in which physical symptoms, produced by the unconscious mind, are defined by the individual as evidence of organic disease and for which medical help is sought" (page x). He uses "railway spine" as an example of a culturally determined psychosomatic illness in the nineteenth century: an hysterical paralysis, which could be unleashed by physical trauma (Page 114). The clinical presentations of spinal pain and tenderness in the early and mid-nineteenth century are discussed elsewhere in his book, only under the the diagnosis of "spinal irritation", a condition which he deems a "pseudodisease" affecting young women almost exclusively (Page 24). According to Shorter's analysis of this condition, "[P]atients certainly found it more comforting to think their spines were irritated than that their problems were psychological".

Thus the derailment of "Railway Spine" occurred when the debate over nosology took precedence over the phenomena that clinicians were purporting to describe [Figure 4]. Initially, Erichsen did try to process the clinical presentations through the only available and seemingly relevant pathology/pathophysiology at the time. He received support from others, including Gowers, Hilton, and Oppenheim, but was criticised for his inability to satisfactorily account for discordance between injury and disability. Coincident with development of the concept that ideas could cause intrapsychic commotion and thus generate symptoms, two major epistemological errors occurred which remain relevant today: the failure to recognise the tautological nature of the proposed heuristic contructs and the untestable nature of the primary psychogenic hypotheses. Hysteria came to be defined by the presence of spinal pain and tenderness rather than being identified as an emotional consequence of chronic spinal pain. This potential for error had been identified by Gowers:48

"... it is necessary to avoid the danger of over-estimating the effect of mental influence, and regarding as entirely due to this, symptoms which are real, and are merely intensified by attention. The danger is especially great in cases of railway injuries, concerning which an unbiased judgement is not easy to secure, and in which, when objective symptoms are absent, it is easy to minimise suffering, and attribute too much to the mental condition".

This historical review has shown that the series of mutually exclusive, competing constructs, each based on linear determinism, have provided neither useful clinical frameworks nor advances in knowledge. What has remained unaddressed by this debate are the nature and explanations for the cardinal clinical features of many post-traumatic spinal disorders, namely the complex biopsychosocial phenomenon of chronic pain and the difficult psychophysical phenomenon of tenderness or, more correctly, allodynia. Contemporary relevance of debate - the transmutation of fibrositis to fibromyalgia

As "neurasthenia" declined in popularity as a diagnosis, that of "fibrositis" as proposed by Gowers52 increased, largely on the basis of the reported inflammatory changes in tender subcutaneous fibrous tissues excised from "fibrositis" sufferers.100 Bodily trauma, either direct or indirect, continued to be regarded as a potent and sufficient cause of "fibrositis",101-103 although the vexed question of predisposition continued to be debated.102 The "rheumatic diathesis" still denoted persons who readily reacted to atmospheric and other environmental influences which left others unaffected but had expanded to include persons who were unfit physically, complaining of lassitude, mental irritability and depression,104 echoing the tautological problem of its cousin constructs.

Those sceptical of Gowers' construct saw psychological factors as being primary in many or most cases of "fibrositis". Halliday,105 a medical examiner for the Department of Health for Scotland, cautioned physicians against "discovering" non-existent structural abnormalities. With regard to fibrositis, he noted that "some practitioners find it frequently, whereas others in the same locality only discover its presence on rare occasions". In his opinion, symptoms commonly attributed to "rheumatism (or fibrositis, neuritis, sciatica, lumbago, myodynia, and so on)..." were best understood and treated as "incidental manifestations of a chronic psychoneurotic state". According to Halliday,106 "[T]he theory of fibrositis in its full-blown form clearly corresponds to a mode of obsessional thinking which goes on operating without reference to reality". He suggested that the term "fibrositis" be abandoned and in its place be substituted the problem of incapacitating pain, stiffness and soreness (P.S.S.).106 A self-limiting form of P.S.S. followed exposure to cold air, water, or sudden movements ("the crick"). The more persistent forms of P.S.S. were usually either psychosomatic (occurring in the course of chronic anxiety states and depression) or "hysterical".

When its presumed histopathological basis was dispelled,107 "fibrositis" was no longer regarded as a distinct medical condition but as a syndrome of deep diffuse or radiating pain characterised by a well-defined tender spot, which may or may not be the site of palpable induration.101 In England it was eventually acknowledged that "fibrositis" was an unsatisfactory name for what was more accurately described as "pain of unknown origin",108 and it was relegated to a "banal complaint"108 and the "diagnostic scapheap".109 Elsewhere "fibrositis" continued to be promoted as a somatic pain syndrome110 and defended (unsuccessfully as it turned out) against those who favoured a psychogenic aetiology for chronic regional pain.111,112

There persisted nonetheless a somatic focus on nosology in relation to post-traumatic spinal and other diffuse pain syndromes. The North American construct of "fibromyalgia" is currently presenting far-reaching societal including medicolegal consequences.113 As proposed in the American College of Rheumatology (ACR) criteria,10 this construct is the end result of a process initiated in the 1970s by Smythe and Moldofsky.111,114,115 They were not resurrecting Gowers' earlier construct; rather Smythe111 recognised the clinical problem of diffuse musculoskeletal pain with tender areas and tried to quarantine these patients away from implications of psychogenic aetiology:

"... [it is] important to emphasise those findings which indicate a disorder of pain modulation as the underlying mechanism, rather than the symbolic pain characteristic of classical psychoneurosis or pain consequent on anxiety-induced prolonged muscle tension .... The tender points are largely unknown to the patient and often not even central to their areas of pain".

Smythe believed that a "tender point count" could substitute for the "joint count" of conventional rheumatology in reaching a diagnosis. However those tender points did not necessarily bear any relationship to the pain and indeed were stated to be present in normal people (that is, those not complaining of pain). Thus those with the "new fibrositis" were recognised by being more tender than they should be and thus separable from those with psychogenic regional pain syndromes.112 Therefore Smythe simultaneously asserted that the tender points are central to the diagnosis but epiphenomenal to the pain, two mutually incompatible tenets. Nevertheless that quarantined concept evolved over the subsequent decade into "fibromyalgia", apparently defined by certain criteria but also able to coexist with other painful disorders.10

According to the ACR criteria, patients with "fibromyalgia" and controls (those with other painful disorders) are best differentiated by the presence of "widespread pain" together with 11 of 18 points of "mild or greater" tenderness. Those criteria and their predecessors115,116 remain unlinked to pathophysiology, other than the vague concept of "pain modulation".117-119 It has been argued that this jump from phenomenology to nosology held open the gate to tautology and the potential for clinical misuse of the construct of fibromyalgia.120

When the "new" primary fibrositis syndrome was being defined, a history of previous bodily trauma was initially considered to be an exclusion factor for this diagnosis,116 although it was suggested that a special category of "localised fibrositis" be created to embrace localised (regional) pain syndromes which had occurred in the context of trauma.121 Many rheumatologists continued to depreciate the possible aetiological role of physical trauma in favour of a multifactorial aetiology, including undefined "constitutional" factors.112,122-124 Others, denying a pathogenetic role to nociception, argued that the "fibrositis/fibromyalgia syndrome" is a purely psychosomatic disorder in which the "deep pain system" is activated by such factors as beliefs, emotions, culture, stress, sleep disturbance and personality, more readily when compensation or litigation are issues.125-127

Nevertheless, trauma was identified as the initiating factor by 10% of 205 patients with chronic diffuse musculoskeletal pain lacking identifiable disease or structural pathology, all of whom had been referred to a specialized centre for the investigation of persistent pain and sleep difficulties.113 When the criteria used were "light unrefreshing sleep", chronic fatigue, diffuse pain and 12 or more of 14 areas of tenderness in specific anatomical regions found in fibromyalgia syndrome, it was hardly surprising that all patients "had" fibromyalgia, .

In a retrospective study of 127 patients given the diagnosis of fibromyalgia by the one clinician, 29 (24%) reported a possible precipitating event, which was traumatic in 14 (10%).128 The criteria used by this examiner for the diagnosis of fibromyalgia were the presence of "diffuse aches and pains with prominent stiffness in 3 or more anatomic sites for at least 3 months and at least 7 tender points", aswell as the absence of co-existing rheumatic disease. The members of the group in whom a precipitating event was identified, designated "reactive" fibromyalgia, were assessed as being more disabled by their pain, with consequent adverse effects on their physical fitness, employability and financial status, when compared with others in the study who were designated as having primary fibromyalgia syndrome. This study reflects the biased beliefs and diagnostic habits of one clinician and illustrates the fallacy of assuming the truth of the conclusion which it purports to establish, that is, that fibromyalgia is a distinct condition. This fallacy having been ignored, post-traumatic fibromyalgia becomes a self-fulfilling prophecy, with important implications for the various systems of personal injury compensation.

Waylonis and Perkins11 then attempted to determine the long-term outcome for a group of patients who over the previous 10 years had been given (by Waylonis) a diagnostic label of "post-traumatic fibromyalgia" and whether that condition was the same as "primary (spontaneous) fibromyalgia". That 85% of their patients had long-term pain and disability was in accordance with the findings of other studies of patients after trauma.129 However their attempt to compare the symptom profiles of their patients with "post-traumatic fibromyalgia" (of whom only 85% fulfilled the ACR criteria for fibromyalgia syndrome) with those of 554 subjects with a self-reported diagnosis of fibromyalgia syndrome130 is bogus in the absence of a gold standard for diagnosis. For example the sole criterion used for the diagnosis of fibromyalgia syndrome was that subjects could name the physician who gave them this diagnosis. Implications of the fate of "railway spine" for "post-traumatic fibromyalgia"

It is now instructive to compare the constructs of "railway spine" and "fibromyalgia" as they have been applied in the context of chronic pain following injury (Figure 6). Both constructs have been used to denote discrete conditions or syndromes, when in fact they are symptom complexes. Due to the combination of clinical features discordant with outward signs of injury and insufficient explanatory power of the various somatic models of chronic spinal pain, "railway spine" became "railway brain" by default. The construct of "fibromyalgia" at present is unlinked to discernible pathology. It too has insufficient explanatory power and is therefore in danger of becoming regarded as psychogenic by default,131 even in the absence of obvious psychopathology.132

The true intent of those who invoked "disturbance of the deep pain system" is, in fact, to imply psychogenesis.126 When taken together with the post hoc ergo propter hoc fallacy of the term "post-traumatic", the stage is now set for the final condemnation of not only the construct of "fibromyalgia" but also, very importantly, the clinical syndrome which it purports to describe. That is, the rejection of a fallacious construct withdraws recognition from the still unexplained clinical problem.Rational salvage of the clinical problem

"Railway spine" has been and "fibromyalgia" is about to be discredited as valid clinical constructs invoked to describe pain and allodynia following nociceptive insult. The danger is that the clinical presentations themselves will be seen as illegitimate. However there must exist somatically-based explanations for the major clinical features of these syndromes. It has been argued elsewhere120,133 that the pathophysiological basis of these syndromes is secondary hyperalgesia, which itself has now been attributed with reasonable confidence to sensitisation of nociceptive pathways.134 These syndromes are in no way different from other chronic pain syndromes in that their presentation is coloured by cognitive, affective, and behavioural factors. To postulate an initial pertubation of nociception which sets in train both physiological and psychological processes provides a unifying model which avoids the fallacies of dualistic thinking.Conclusion

When "railway spine" became discredited "railway brain", the proponents of psychogenic hypotheses emerged dominant over those who sought neurophysiological explanations. That the arguments of the "victors" were tautological as well as untestable appears to have been unrecognised. But post-nociceptive chronic pain syndromes remain, their pathophysiology elusive. The introduction of the fibromyalgia construct has focussed attention on nosological issues rather than upon pain and hyperalgesia. Whilst fibromyalgia remains yet another tautological proposition with little explanatory power, its linking by some to "trauma" introduces a fallacy which invites perjorative dismissal which in turn threatens to withdraw clinical legitimacy from those who suffer. The fate of "Railway Spine", which was vulnerable to the assertion that altered nociception is due to emotional and other psychosocial factors, should be a warning. If, with the benefit of a century of hindsight, insight and new knowledge, "post-traumatic fibromyalgia" is overthrown without a legacy of increased understanding of the nature of chronic pain and of allodynia/hyperalgesia, history will not only have repeated itself but an opportunity to understand the plight of those suffering spinal pain and tenderness will have been lost.


1. Skey FC. Compensation for railway injuries [letter]. Lancet 1865; ii: 161-163.

2. Hall JC. Medical evidence in railway accidents. Brit Med J 1868; i: 216-217, 272-274, 325-327.

3. Allan DB, Waddell G. An historical perspective on low back pain and disability. Acta Orthop Scand 1989; 60 (suppl 234): 9-14.

4. Shorter E. From paralysis to fatigue. New York: The Free Press. A Division of Macmillan, Inc., 1992: 95-128.

5. Caplan EM. Trains, brains, and sprains: railway spine and the origins of psychoneuroses. Bull Hist Med 1995; 69: 387-419.

6. Trimble MR. Post-traumatic neurosis. From railway spine to the whiplash. Chichester: John Wiley & Sons, 1981.

7. Evans RW. The postconcussion syndrome: 130 years of controversy. Semin Neurol 1994; 14: 32-39.

8. Walton GL. Contribution to the study of the traumatic neuro-psychoses. The Journal of Nervous and Mental Disease 1890; 17: 432-449.

9. Keller T. Railway spine revisited: traumatic neurosis or neurotrauma. J Hist Med Allied Sci 1995; 50: 507-524.

10. Wolfe F, Smythe HA, Yunus MB, et al. The American College of Rheumatology 1990 criteria for the classification of fibromyalgia: report of the multicentre criteria committee. Arthritis Rheum 1990; 20: 160-172.

11. Waylonis GW, Perkins RH. Post-traumatic fibromyalgia. Am J Phys Med Rehabil 1994; 73: 403-412.

12. Simmons J. The railway in Britain 1825-1947. In: Simmons J, ed. Rail 150. London: Eyre Methuen, 1975: 47-118.

13. Chambers W, Chambers R, editors. Chamber's information for the people. Vol 1. Edinburgh: William and Robert Chambers, 1842: 433-448.

14. Railway injuries: a medico-legal subject. Lancet 1861; ii: 255-256.

15. Langer WL. Political and social upheaval 1832-1852. New York: Harper and Row, 1969: 25-53.

16. The railway question [medical annotations]. Lancet 1865; i: 183-184.

17. The recent railway accidents [medical annotations]. Lancet 1865; i: 679.

18. Sigerist HE. From Bismarck to Beveridge: development and trends in social security legislation. In: Roemer MI, ed. Henry E. Sigerist on the sociology of medicine. New York: MD Publications, 1960: 118-138.

19. Report of Commission. The influence of railway travelling on public health. Lancet 1862; i: 15-19, 48-53, 79-84,107-110, 130-132, 155-158, 231-235, 258-261.

20. Richardson BW. Diseases of modern life, third edition. London: Macmillan and Co., 1876: 184-192.

21. "Railway spine" [editorial]. Lancet 1869; ii: 244-245.

22. Syme J. On compensation for railway injuries [letter]. Lancet 1867; i: 2-3.

23. Reynolds JR. Paralysis, and other disorders of motion and sensation, dependent on idea. Brit Med J 1869; ii: 483-485.

24. Keen WW, Mitchell SW, Morehouse GR. On malingering, especially in regard to simulation of diseases of the nervous system. American Journal of the Medical Sciences 1864; 43: 367-394.

25. Medical evidence [ editorial]. Brit Med J 1865; i: 354-355.

26. Mendelson G. Compensation and chronic pain [editorial]. Pain 1992; 48: 121-123.

27. Hippocrates. On the articulations. Hutchins RM, ed. Great Books of the Western World. Vol 10. Chicago: Encyclopaedia Brittanica, Inc, 1952: 91-121.

28. Phillips B. Lectures on the principles and practice of surgery. The London Medical Gazette 1840; 26: 881-892.

29. Medical evidence on railway accidents [editorial]. Brit Med J 1865; i: 300-301.

30. Watson PH. Compensation for railway injuries [letter]. Lancet 1867; i: 159-160.

31. Report of Commission. The influence of railway travelling on public health. VI. Lancet 1862; i: 155-158.

32. Erichsen JE. On railway and other injuries of the nervous system. London: Walton and Maberly, 1866.

33. Concussion (?) of the spine from a fall from a scaffold [editorial]. Lancet 1865; ii: 288-289.

34. International Association for the Study of Pain subcommittee on Taxonomy. Pain terms: a current list with definitions and noted on usage. Pain 1986; Suppl 3: S216-221.

35. Hooper R. Lexicon Medicum, fourth edition. London: Longman, Hurst, Rees, Orme, and Co., 1820: 246-247.

36. Hooper R. Lexicon Medicum, seventh edition. London: Longman, Hurst, Rees, Orme, and Co., 1839: 1126-1130.

37. Erichsen JE. The science and art of surgery. Vol 1. London: Longmans, Green, and Co., 1884: 764-779.

38. Railway injuries [editorial]. The British and Foreign Medico-Chirurgical Review 1876; 52: 1-20.

39. Knoff WF. A history of the concept of neurosis, with a memoir of William Cullen. Amer J Psychiat 1970; 127: 120124.

40. Hilton J. Rest and pain, fifth edition. London: G. Bell & Sons, 1892: 44-90.

41. Knapp PC. Spinal concussion - traumatic spinal sclerosis. Boston Medical and Surgical Journal 1894; 131: 5-7 & 30-32.

42. Watson BA. The diagnosis of traumatic lesions in the cerebro-spinal axis, and the detection of malingering referred to this centre. Medical News

1891; 58: 634-640.

43. Gee SJ. Irritable spine, and spinal myalgia in particular. The Practitioner 1884; 33: 401-408.

44. Schiller F. Spinal irritation and osteopathy. Bull Hist Med 1971; 45: 250-266.

45. Hooper R. Lexicon Medicum, seventh edition. London: Longman, Hurst, Rees, Orme, and Co., 1839: 1209-1210.

46. Inman T. On so-called hysterical pain. Brit Med J 1858; 24-25.

47. Eskridge JT. Spinal irritation and some points in the diagnosis of affections that may be mistaken for it. The Alienist and Neurologist 1889; 10: 416-436.

48. Gowers WR. A manual of diseases of the nervous system. Vol 1. London: J. & A. Churchill, 1886: 446-454.

49. Duncan A. Medicine. In: Maclaren C, ed. Encyclopaedia Britannica, sixth edition. Vol 13. Edinburgh: Archibald Constable & Co., 1823: 187-486.

50. Moullin CWM. Sprains. Their consequences and treatment, second edition. London: H K Lewis, 1894: 131-150.

51. Page HW. Railway injuries: with special reference to those of the back and nervous system, in their medico-legal and clinical aspects. London: Charles Griffen and Company, 1891: 1-24.

52. Gowers WR. Lumbago: its lessons and analogues. Br Med J 1904;i:117-121.

53. Reynolds MD. The development of the concept of fibrositis. J Hist Med Allied Sci 1983; 38: 5-35.

54. Aitken W. The science and practice of medicine, fourth edition. Vol 2. London: Charles Griffin and Company, 1866: 6-37.

55. Drinka GF. The birth of neurosis. Myth, malady, and the Victorians. New York: Simon and Schuster, 1984: 29-59.

56. Parkin A. Neurosis and schizophrenia: I. historical review. Psychiatr Q 1966; 42: 3-216.

57. Hodgkiss A. Pain disorders. Clinical section. In: Berrios GE, Porter R, eds. A history of clinical psychiatry. London: Athlone, 1995: 193-202.

58. Beard GM. A practical treatise on nervous exhaustion (neurasthenia), fifth edition. New York: E B Treat & Company, 1905.

59. Erb W. Handbook of electrotherapeutics. London: Sampson Low, Marston, Searle, and Rivington, 1883: 289-297.

60. Gould GM, Pyle WL, editors . Neurasthenia. In: A cyclopedia of practical medicine and surgery. Philadelphia: P Blakiston's Sons & Co, 1900: (alphabetically arranged).

61. Dana CL. Concussion of the spine and its relation to neurasthenia and hysteria. The Medical Record 1884; 26: 617-621.

62. Tilt EJ. A handbook of uterine therapeutics and of diseases of women, fourth edition. New York: William Wood & Company, 1881: 81-108.

63. Oliver J. A few notes on hysteria. Brain 1887; 9: 218-223.

64. Gregory G. Elements of the theory and practice of medicine, fifth edition London: Henry Renshaw, 1839: 345-352.

65. Clarke JM. Hysteria and neurasthenia [critical digest]. Brain 1894; 17:119-178 & 263-321.

66. Charcot JM. Clinical lectures on diseases of the nervous system. London: The New Sydenham Society, 1889: 220-259.

67. Dreschfeld J. On hysteria in the male coming on after an injury. The Medical Chronicle 1886-7; 5: 169-182.

68. Thorburn W. On traumatic hysteria, especially in relation to railway accidents. The Medical Chronicle 1888-9; 9: 198-216 & 265-285.

69. Strümpell A. Traumatic neuroses. In: Clinical lectures on Medicine and Surgery by various German authors. London: The New Sydenham Society, 1894: 304-325.

70. Oppenheim H. Diseases of the nervous system. (1st American from 2nd German edition). London: JB Lippincott Company, 1901: 661-839.

71. Bramwell B. Concussion of the spine, more especially in its relationship with railway accidents and injuries. Brit Med J 1893; ii: 1089-1097.

72. Schuster P. Traumatic neuroses. In: Church A, ed. Diseases of the nervous system. London: Sydney Appleton, 1908: 1098-1127.

73. Hart B. Psychopathology. Cambridge: Cambridge University Press, 1927: 30-93.

74. Prince M. The pathology, genesis and development of some of the more important symptoms in traumatic hysteria and neurasthenia. Boston Medical and Surgical Journal 1898;138: 511-514, 536-540, & 560-562.

75. Freud S, Breuer J (1893). The Pelican Freud library, volume 3. Studies on hysteria. Middlesex: Penguin Books, 1974: 259-333.

76. Crichton-Miller H. Psychoneuroses. In: Hutchinson R, Sherren J, eds. An index of treatment by various writers, ninth edition. Bristol: John Wright and Sons, 1925: 705-711.

77. Glover E. Psycho-analysis. 2nd ed. London: Staples Press, 1949: 139-169.

78. Osler W. The principles and practice of medicine, tenth edition. London: D. Appleton and Company, 1925: 1141-1144.

79. Micale MS. On the "disappearance" of hysteria. A study in the clinical deconstruction of a diagnosis. Isis 1993; 84: 496-526.

80. Ross TA. The common neuroses, second edition. London: Edward Arnold & Co., 1937: 217-218.

81. Quintner JL, Cohen ML. Occupation neuroses and the psychogenic connotation of 'Repetition Strain Injury': the misconstruction of neurosis. Integrative Psychiatry 1994; 10: 3-14.

82. Buzzard EF. Warfare on the brain. Lancet 1916; ii: 1095-1099.

83. Wittkower E, Spillane JP. A survey of the literature of neuroses in war. In: Miller E, ed. The neuroses in war. London: Macmillan and Co, 1940: 1-32.

84. Campbell AW. Remarks on some neuroses and psychoses in war. Med J Aust 1916; i: 319-323.

85. Buzzard EF. An address on traumatic neurasthenia. Lancet 1923; ii: 1285-1288.

86. Bury JS. Remarks on the pathology of war neuroses. Lancet 1918; i: 97-99.

87. Mott FW. War neuroses. Introduction to the discussion. Brit Med J 1919; i: 439-442.

88. Myers CS. Shell shock in France 1914-18. London: Cambridge University Press, 1940: 24-48.

89. Rivers WHR. An address on the repression of war experience. Lancet 1918; i: 173-177.

90. Butler AG. The Australian army medical services in the war of 1914-18. Vol 3. Canberra: Australian War Memorial, 1943: 56-147.

91. Turner WA, Stewart TG. A textbook of nervous diseases. London: J & A Churchill, 1910: 522-546.

92. Oliver T. Diseases of occupation, third edition. London: Methuen & Co. Ltd, 1916: 1-53.

93. Ramsay J. Nervous disorder after injury. Brit Med J 1939; ii: 385-390.

94. Walshe FMR. Diseases of the nervous system. 4th ed. Edinburgh: E & S Livingstone Ltd., 1945: 321-345.

95. Collie J. Fraud in medico-legal practice. London: Edward Arnold & Co., 1932: 219-230.

96. Culpin M. Psychology in medicine. Lancet 1945; ii: 517-520.

97. Trimble MR. Post-traumatic stress disorder: history of a concept. In: Figley CR, ed. Trauma and its wake. The study and treatment of post-traumatic stress disorder. New York: Brunner/Mazel, 1985: 5-14.

98. Nemiah JC. Hysterical neurosis, conversion type. In: Freedman A, Kaplan H, Sadock B, ed. Comprehensive textbook of psychiatry-II, second edition. Vol 2. Baltimore: The Williams & Wilkins Company, 1975: 1208-1220.

99. Ellard J. Being sick and getting better. Med J Aust 1974; 1: 867-872.

100. Stockman R. The causes, pathology, and treatment of chronic rheumatism. Edin Med J 1904; 15: 107-116 & 223-235.

101. Kelly M. Fibrositis and the common pains of daily practice. Med J Aust 1946; ii: 480-485.

102. Fletcher E. Medical disorders of the locomotor system including the rheumatic diseases. Edinburgh: E & S Livingstone, 1947: 362-380.

103. Cyriax J. Fibrositis. Brit Med J 1948; ii: 251-255.

104. Bach F. The rheumatic diseases: their recognition and treatment. London: Cassell and Company, 1935: 256-293.

105. Halliday JL. Psychological factors in rheumatism. Brit Med J 1937; i: 213-217 & 264-269.

106. Halliday JL. "The obsession with fibrositis" [letter]. Brit Med J 1942; i: 164.

107. Collins DH. Fibrositis and infection. Ann Rheum Dis 1940; 2: 114-126.

108. Copeman WSC, Mason RM. Rheumatism. Fibrositis, arthritis, lumbago, sciatica, "slipped disc," gout, spondylitis. London: Gerald Duckworth & Co, 1954: 15-37.

109. Anderson JAD. Rheumatism in industry: a review. Br J indust Med 1971; 28: 103-121.

110. Kraft GH, Johnson EW, LaBan MM. The fibrositis syndrome. Arch Phys Med Rehabil 1968; 49: 55-162.

111. Smythe HA. 'Fibrositis' as a disorder of pain modulation. Clin Rheum Dis 1979; 5: 823-832.

112. Smythe HA. Nonarticular rheumatism and psychogenic musculoskeletal syndromes. In: McCarty DJ, ed. Arthritis and allied conditions, tenth edition. Philadelphia: Lea & Febiger, 1985: 1083-1094.

113. Moldofsky H, Wong MTH, Lue FA. Litigation, sleep, symptoms and disabilities in postaccident pain (Fibromyalgia). J Rheumatol 1993; 20: 1935-1940.

114. Smythe HA. Non-articular rheumatism and the fibrositis syndrome. In: Hollander JL, McCarty DJ, ed. Arthritis and allied conditions, eighth edition. Philadelphia: Lea and Febiger, 1972: 874-884.

115. Smythe HA, Moldofsky H. Two contributions to the understanding of the "fibrositis" syndrome. Bull Rheum Dis 1977; 28: 928-931.

116. Yunus M, Masi AT, Calabro JJ, Miller KA, Feigenbaum SL. Primary fibromyalgia (fibrositis): clinical study of 50 patients with matched normal controls. Semin Arthritis 1981; 11: 151-171.

117. Henriksson KG, Mense S. Pain and nociception in fibromyalgia: clinical and neurobiological considerations on aetiology and pathogenesis. Pain Reviews 1994; 1: 245-260.

118. Gerdle B, Ellert J. Disability and impairment in fibromyalgia syndrome: possible pathogenesis and etiology. Critical reviews in physical and rehabilitation medicine 1995; 7: 189-232.

119. Carette S. Fibromyalgia 20 years later: what have we really accomplished? J Rheumatol 1995; 22: 590-594.

120. Cohen ML, Quintner JL. Fibromyalgia syndrome, a problem of tautology. Lancet 1993; 342: 906-909.

121. Yunus MB. Fibromyalgia syndrome: a need for a uniform classification [editorial]. J Rheumatol 1983;10: 841-844.

122. Wolfe F. The clinical syndrome of fibrositis. Am J Med 1986; 81 (suppl 3A): 7-13.

123. Müller W. The fibrositis syndrome: diagnosis, differential diagnosis and pathogenesis. Scand J Rheumatol 1987; (Suppl. 65): 40-53.

124. Yunus MB. Fibromyalgia syndrome: new research on an old malady. Brit Med J 1989; 298: 474-475.

125. Littlejohn GO. Fibrositis/fibromyalgia syndrome in the workplace. Rheum Dis Clin North Am 1989; 51: 45-60.

126. Reilly PA, Littlejohn GO. Fibrositis/fibromyalgia syndrome: the key to the puzzle of chronic pain [editorial]. Med J Aust 1990; 152: 226-228.

127. Goldenberg DL. Fibromyalgia: why such controversy? Ann Rheum Dis 1995; 54: 3-5.

128. Greenfield S, Fitzcharles M-A, Esdaile JM. Reactive fibromyalgia syndrome. Arthritis Rheum 1992; 35: 678-681.

129. Mendelson G. Chronic pain, compensation and clinical knowledge. Theor Med 1991; 12: 227-246.

130. Waylonis GW, Heck W. Fibromyalgia: new associations. Am J Phys Med Rehabil 1992; 71: 343-348.

131. Bohr T. Problems with myofascial pain syndrome and fibromyalgia syndrome. Neurology 1996; 46: 593-597.

132. Dunne FJ, Dunne CA. Fibromyalgia syndrome and psychiatric disorder. Brit J Hosp Med 1995; 54: 194-197.

133. Quintner JL, Cohen ML. Referred pain of peripheral nerve origin: an alternative to the "myofascial pain" construct. Clin J Pain 1994; 10: 243-251.

134. Coderre TJ, Katz J, Vaccarino AL, Melzack R. Contributions of central neuroplasticity to pathological pain: a review of clinical and experimental evidence. Pain 1993; 52: 259-285.

Patient's Pain Communication Tool