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.
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'.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.