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THE DERAILMENT OF RAILWAY SPINE: A TIMELY LESSON FOR
POST-TRAUMATIC FIBROMYALGIA SYNDROME
[Pain Reviews 1996; 3:
181-202] Milton L Cohen MB
BS MD FRACP FAFRM
FFPMANZCA Staff Specialist in Rheumatology, St. Vincents'
Hospital, Sydney, New South Wales. Associate Professor,
University of NSW, Sydney, Australia. John L Quintner MB BS
MRCP FFPMANZCA Consultant Physician in Rheumatology and Pain
Medcine, Perth, Western
Australia.Introduction
"Railway spine" "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.
Rheumatism
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).
Fibrositis
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.
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