How do physicians recognise somatization?
The charge most commonly levied by patients and health workers against
doctors who diagnose somatization is that this diagnosis dismisses the patients'
complaint as somehow not 'real' or even as 'imagined'. Although caused by
ideas and emotional factors, the pain and symptoms of hysteria and somatization
are as real as any other and very few patients can differentiate the psychogenic
from the organic with any degree of confidence. In some instances the questioner
has a genuine desire to find out how a doctor might differentiate between
hysteria and other disorders as he or she is concerned about the possibility
of missing an organic disorder and is uncertain if emotional factors are
at the basis of the patient's symptoms.
The question, 'How do doctors know?' is sometimes facetious: a mocking,
thinly veiled insult aimed at the personal integrity and competence of the
diagnostician. Dr Nick Crofts, for example, demanded to know the answer
in relation to RSI in a provocative publication in the New Doctor:
I understand that there are psychiatrists in existence today who consider
that RSI is a form of 'hysterical conversion disorder'. I hope you have
noted the quotation marks, because I consider that such terms say a lot
more about the person who uses them and nothing about the person they are
used against.
Dr Crofts demonstrated a number of the attitudes and positions adopted
by those doctors who had become involved in the diagnosis and treatment
of RSI. Dr Crofts took the position that the word 'psychosomatic' meant
imaginary, 'all in the head', and that such a diagnosis was used 'against'
a patient. Dr Crofts admonished his patients to ask their doctors: 'How
do you know?'
It is fair enough for patients to demand justification of a diagnosis.
A doctor should be able to explain why he or she considers that a given
set of symptoms is psychogenic rather than evidence of disease.
Somatization is not a diagnosis to be made solely by exclusion; it can
also be a positive diagnosis requiring all the three following criteria.
1. The presence of symptoms in the absence of a disease diagnosis which
could account for them.
2. The presence of the subject's belief system about the body which underpins
the relevant somatic symptoms.
3. The presence of social stressors, needs and conflicts which might have
made that subject symptomatic and sometimes ill.
Somatization in the upper limbs in this epidemic
Differentiating cramp from disease
Diseases have specific criteria and their characteristics have been the
subject of many textbooks. Such complaints as constitute somatization in
upper limbs needed to be distinguished from the disease entities which they
suggested or mimicked. Cramp may mimic disease, may co-exist with disease
and may prolong symptoms from old lesions well past their expected recovery
time. The examination of a medical file of a cramp subject reveals how changing
symptoms attracted multiple diagnostic formulations over the period of the
affliction. As Hércule Poirot would say: 'There are too many clues'.
Differentiating cramp from diseases of nerves
Cramp symptoms move from site to site, suggesting simultaneous involvement
of the sensory and motor nervous systems. The well intentioned doctor recognises
conversion or somatization symptoms when they are of a classical glove and
stocking or long glove distribution. The diagnosis should be as evident
if the distribution is equally inexplicable but of a different pattern and
yet does not accord with the territory of a peripheral nerve.
Various neuropathies need to be excluded: peripheral neuritis involves
the feet long before the hands and there is generally an over-riding medical
reason for having it. A neurological examination of a cramp subject would
reveal that all the relevant muscles and peripheral nerves are intact and
there is no muscle wasting.
Cramp symptoms were commonly attributed to 'radicular irritation at the
cervical spine' but this is a neurologically unsound formulation as it rests
on signs that should relate specific muscle weakness to discrete sensory
deficits and these are not found. In contradistinction to neurological lesions,
specific muscle wasting does not occur in cramp subjects. The resemblance
ends if the motor deficits expected to occur with the suspected lesion can
not be found. Atrophy in splinted or over-rested limbs is common and affects
all muscles.
Differentiating cramp from tenosynovitis
The contention that 'keyboard work predisposes to tenosynovitis' is anecdotal,
not expert. Stenosing tenosynovitis is not a reported disorder of typists
yet writers' cramp, in a painful mode, has recurrently and erroneously been
attributed to tenosynovitis. Cramp is differentiated from tenosynovitis
and from other common conditions of traumatic origin primarily by its excessive
symptomatology in both motor and sensory modalities and, secondarily, by
its failure to recover with the usual treatments for inflammation or injury.
Differentiating cramp from disease of muscles
The suggestion that cramp is a 'disease of muscles' is not corroborated
by any reliable relationship of seemingly involved tissues to occupational
tasks. Moreover, there is no known organic disorder where a group of muscles
becomes dysfunctional and painful for one intentional activity but not for
another, nor is any kind of pathology known where activity is followed,
at an irregular interval, by collapse, exhaustion and pain. The idea that
RSI is a 'musculo-tendinous injury' fails to account for multiple sensory
symptoms and for generalised weakness and fatigue in many subjects.
Differentiating cramp from myofacial dysfunctions
One can not assume that pseudo-neurological symptoms which are not attributable
to peripheral neuropathies are functional in origin. Tingling in fingers
might also be a referred symptom from strained or pulled forearm muscles
and it is experienced along the finger which the traumatised muscle supplies.
Myofascial dysfunctions, cramps, spasms and occupational myalgias are all
task-related and, like their counterparts in sport, they go on to a normal
predictable recovery with rest or treatment. Diagnosis of such lesions lies
in the ability to correlate the muscles affected to the muscles used.
Testing muscle in functional groups might identify the tasks and actions
that have made those muscles sore, especially at their insertions as with
epicondylitis. Soreness in forearm muscles supplying the flexors of the
middle, ring and little fingers is commonly caused by the carrying of plastic
shopping bags or a briefcase on those digits. This symptom can last for
months especially if it is aggravated, but such soreness is not a result
of an occupational task which had not involved those actions.
Arthritis in various locations is not a mobile symptom and there are
clinical and radiological signs of it.
Differentiating cramp from over use and misuse
Overuse syndromes are a matter for common knowledge, particularly in
limbs unaccustomed to activity. Physical injuries tend towards recovery
and start to recover when put to rest and have a known and predictable natural
history. Somatization endures beyond these time limits and has an entirely
different natural history.
The occupational myalgias
In some cases, return to the task perceived as culpable seems to excite
symptoms which develop before sufficient time has elapsed to attribute them
to fatigue. This symptom is called 'intention myalgia' and it has been reported
in the literature, as far as I can see, only during epidemics which coincide
with periods where there is a generalised belief that a task is intrinsically
dangerous. There is a substantial literature on the occupational myalgias
accommodating this phenomenon. Intention myalgia which persists can be conceptualised
as 'tension myalgia' and such muscle tension is reported particularly by
persons who are tense or angry or want to be somewhere other than at work
and are continuing to work in that state. Their tension, anger or conflicts
are not necessarily related to issues at work. Farmer construed tension
myalgia as a 'signal from the body' to which the patient might attend to
see if there were more pressing demands on her time. In those cases where
intention myalgia is extended to normal domestic chores, it seemed to be
closely associated with the subjects believing that such activities are
likely to harm them.
Disturbances of sensation
Reported sensations included neuralgic, stabbing, shooting, sharp or
dull pain, burning, numbness, pins and needles, hot and cold and cramping.
Pain moved around and affected several sites, crossed over into an unused
limb and spread in any direction from its perceived point of origin.
The commonest images presented accorded with long or short glove distribution
and these were seen in the most artless subjects. Other less regular distributions
accorded with the patient's idea of an injured hand, with whatever part
of the hand or arm the patient perceived as over used. The impression was
that a random sensation had been inaccurately remembered.
A subjective sensation of being swollen is a common complaint but swelling
is not visible to the dispassionate observer. Many persons were unaware
that the dominant hand was larger than the other and they presented this
as an abnormal finding. Symptoms occurred in each subject in various combinations
and the predominant sensations change frequently and are susceptible to
suggestion. Unusual sensations might be volunteered with the claimant seemingly
fascinated with their details.
This epidemic of sensory and motor arm symptoms was characterised by
the presentation of material which was available in the form of pamphlets,
symptom lists and guides to diagnosis. These listed both motor and sensory
symptoms and described, without acknowledging it, the syndrome known as
writer's cramp. These were put out by employers, unions, lawyers, government
departments, employee groups, self help groups , and by health professionals
, and they generally purported to be literature focussed on the early diagnosis
and prevention of RSI.
Disturbances of function leading to disability in somatization
Abnormalities of function as well as sensation were essential for the
diagnosis of somatization.
All personal needs could still be attended with the affected limb which
was able to perform all normal movements while, at the same time, the person
was unable to perform a specific task. Sometimes a cramp subject could play
the piano but she could not type. She might sew but be unable to press on
an electronic keyboard without experiencing either pain or palsy.
While purporting to demonstrate that a hand or finger could not be moved
or an object could not be held, a cramp subject made use of both flexors
and extensors to maintain posture. The cramp subject displayed a denser
level of disability than the organically impaired who seemed happy to make
compensatory adjustments. The cramp subject might claim inability to cook
and clean. The person with a broken arm uses the healthy one and gets on
with it.
Signs in somatization are of the kind that can be turned on at will;
jerks and spasms can be imitated.
Disabilities
The culturally determined, paradigm-based presentation of symptoms was
a significant clue to somatization. By the time they were referred to my
practice, cramp subjects were able to recite the disabilities which had
been suggested to them. In my view, this created the impression that they
were familiar with the RSI guides or had been educated by having repeated
examinations or had attended support groups where some exchange of symptoms
and histories had been inevitable. The same disabilities were promoted:
the pain involved in holding a telephone in the course of non-typing duties,
of using hair rollers, a drier, a kitchen knife or peeling vegetables. Sometimes
the source of a subject's advice, the specific RSI guide to prevention,
could be identified from the claimant's selectively reported disabilities.
Such symptoms as had attracted the sympathetic attention of an 'expert in
RSI' were emphasised to the next medical examiner together with learnt attribution
theories.
Response of cramp subjects to treatment
Cramp subjects seemed to be willing to undergo any prescribed pharmacological,
medical surgical or physical or alternative therapies. Cramp subjects continued
to praise the doctors who had treated them with so little success. Results
were generally reported as unsuccessful and cramp subjects quite often admitted
to knowing that the same treatment had not been effective for their friends.
It was common to hear a placebo response reported in the medical examiner's
office as It helped at the time but the symptoms came back, [hours, days
or weeks] later. In the RSI epidemic, negative results for treatment were
reported for the use of acupuncture, cervical traction and cortisone, exercises,
electrical stimulation, hot wax, iodine, copper, local hydro-cortisone rest,
non-steroidal anti inflammatory drugs (NSAIDS), manipulation, physiotherapy,
plaster, slings, splints, supports, surgery, ultrasonic therapy, vitamin
B12. Co-proxamol and some potent centrally acting analgesics did give temporary
relief of a duration of hours but no more than was to be expected of mood
elevating drugs and they did not provide a 'cure'. Functional symptoms did
not respond to immobilisation, rather, their response to treatment tended
to be paradoxical and many cramp subjects reported that their symptoms started
to get worse after they had been prescribed a week's rest at home. Very
often symptoms crossed into a formerly unaffected arm during the first weeks
of the disability. After she had been sent home to rest, the subject reported
that this crossover of symptoms was due to over use of the non affected
arm because she was protecting the affected one.
Response to rest and to physical therapies was unpredictable and often
paradoxical. Nonetheless, some doctors were easily deceived by the occasional
remissions which occurred and they persisted in their administration of
physical remedies to cramp subjects., The amount or type of work done before
development of symptoms was not constant and varied between years and days
and the duration of the affectation ranged from moments to years. Disregard
for circumstantial evidence, including the situation in which the symptom
arose left a clinical phenomenon for which an organic mechanism could not
be postulated.
 Back
to top
|