The International Association for the Study of Pain defines1 pain as "an unpleasant sensory and emotional experience associated with actual and potential tissue damage, or described in terms of such damage", chronic pain as "pain, that persists beyond the normal time of healing..."
Chronic pain is a complex condition influenced by a variety of factors, including biological, physiological variables, behavioural, environmental, and social variables2.
The current psychological terminology is Chronic Pain Disorder Associated with Psychological Factors (Diagnostic and Statistical Manual of Mental Disorders, 4th Edition, DSM-IV).
A useful model3 for personal injury litigators identifies 4 components of chronic pain, nociception - pain - suffering - behaviour.
Nociception is the appreciation of injury that triggers the experience of pain. In Acute Pain there is a direct and readily understood linkage with suffering and Pain Behaviour.
By the time litigators are actively involved, the original physical injury is fully healed and the pain - suffering - behaviour elements have a life of their own.
In Chronic Benign Pain, the causal linkage between the appreciation of injury and the experience of pain is a temporary occurrence that can be established only by examination of contemporaneous documentation.
Thus the tissue damage that gave birth to the pain is gone, the umbilical cord of medical causation cut.
The experience of pain, suffering and pain behaviour now have a life of their own, and this autonomous phenomenon is determined3 by "toughness", cultural values and Secondary Gain (
MLN V2I7).In medicolegal terminology, a significant segment of society have the psychological thin skull that translates temporary injury into long-term disability.
Chronic benign pain is very common in all industrialised nations studied.
At any time, according to reports in the world research literature, between two and forty percent of various populations suffer from Chronic Pain4: 25-30% is a realistic estimate in industrialised countries5.
The annual cost to the US economy was 16 years ago estimated6 at a crippling 40 billion dollars.
A simple model of nerves as wires that transmitted electrical impulses held sway until 1952 when Dr Glen Player7 [] suggested that the signals could be "restrained".
The major neurotransmitter known as acetylcholine was soon understood to be only one of many chemical messengers that mediate communications through the nervous system.
In 1965 Melzack and Wall8 proposed that a "gate" could be closed to block onward relaying of electrical pain signals.
They used the analogy of throwing a track switch to give precedence to an express train over a slower pain train on converging rail-tracks.
With further investigation, it became clear that pain could be magnified as well as attenuated.
Neurophysiological research has revealed some of the immensely complex chemistry whereby this modulation of pain is effected by neurotransmitters in the dorsal horn of the spinal cord9.
Anatomists and physiologists have now demonstrated specialised nerve pathways from the brain to the dorsal root ganglion of the spinal cord that can not only dampen but also amplify pain signals.
There is, then, a readily understood and empirically-confirmed mechanism whereby emotions, attitudes and beliefs can modify the experience of acute and chronic pain.
Empirical confirmation and refinement of the Gate Theory has improved understanding and management10 [] of pain, for instance that arising from multiple nerves11 [] and chronic abdominal pain12 [].
It provides a model for the conundrum of pain where there is no evidence of tissue damage.
Pain modulation explains why sensations that most would experience as pleasant or neutral - light touch or pressure - are painful to a few (allodynia).
The changes that cause chronic pain are in the spinal cord, not in the injured tissue or the psyche.
In 1990 McQuay and Dickenson13 suggested that the spinal cord was not only highly sophisticated but also plastic.
Neuroplasticity means that spinal cord and brain can be physiologically and anatomically altered long-term or even permanently by a single pain event14.
Severe acute pain during Personal Injury can thereby trigger chronic changes in the functioning of the spinal cord that amplify or generate pain.
Empirical support for this revolutionary theory is increasing9: there are demonstrable changes in the structure and function of the dorsal horn of the spinal cord.
Even though general anesthesia makes a patient unconscious and therefore completely unaware of pain during major surgery, adding complete blocking of pain signals in the form of epidural analgesia materially reduces postoperative pain15 [].
Such pre-emptive analgesia is an important clinical application of neuroplasticity, for severity of postoperative pain is a major determinant of subsequent chronic pain16 [].
Physicians and lawyers alike had previously been looking for the mechanisms of chronic benign pain in the injured tissues, the local nerves or the psyche.
For the first time, validated measures of Alexithymia have confirmed17 that Chronic Pain patients are less able to identify and verbalise their emotions, and suggests that this disability contributes to their psychological vulnerability.
A review18 of the medical research literature on Chronic Pain and Depression concludes that there is some evidence for Depression-proneness before the onset of the pain, and that the psychological disability largely results from, rather than causes, the Chronic Pain.
Citing the difficulties in assessing Depression in sufferers from Chronic Pain, the authors caution against faulty conclusions that Depression antedates the pain.
Inhibiting the expression of angry feelings strongly predicted Pain Intensity and Pain Behaviour as reported by a group of chronic pain patients19.
Compensation is associated with greater pain and resistance to treatment.
A meta-analysis20 of 32 studies, nearly 4000 patients and a similar number of controls, showed a highly significant effect of litigation on pain severity and prognosis.
This study, mainly of chronic low back pain, echoes the greater abnormality and disability seen in Mild Traumatic Brain Injury with financial incentive (Medical Litigation News Volume 2, Issue 1).
98% of patients referred for treatment of chronic pain were given a diagnosis of organic origin after multidisciplinary clinical assessment and exhaustive investigation21.
They were seen by between two and 9 (average 3-4) specialists, and routinely underwent such investigations as Electromyography (EMG), Magnetic Resonance Imaging (MRI), Computed Tomography (CT), diagnostic nerve blocks and measurements of regional blood flow in different positions.
The most frequent new diagnoses were Nerve Entrapment, Temporomandibular Joint (TMJ) pain, Thoracic Outlet Syndrome and Spinal Stenosis.
Whereas US osteopaths22 saw Traumatic Brain Injury as underdiagnosed in Chronic Pain patients, Canadian psychiatrists23 took a contrary view that cognitive symptoms of Post-Concussive Syndrome are nonspecific and occur in a majority of Chronic Pain patients with no history of head injury.
Expert opinion about such causal connection can be meaningful only if pre-injury clinical records are included in the analysis.
If nonpsychiatric specialists are proposing or implying significant psychological factors in pain lasting more than 6 months, psychometric testing can exclude or confirm significant pre-existing psychopathology or dysfunctional personality traits24.
Using the medical literature on chronic pain behaviour, the authors have developed a semistructured psychiatric interview for medicolegal reporting purposes.
Internists25 and medical students26 reading vignettes increased their estimates of patients’ pain and disability if it was medically explicable or if the reported pain intensity was low.
Both groups decreased their evaluations if there was inadequate medical explanation or the reported pain intensity was high.
Internists judged greater pain and disability if the reported patient-doctor relationship was negative.
Another paper27 from the United States documents both a surge in fraudulent claims for chronic pain and a capriciously wide range of jury awards for comparable pain and suffering with no objective findings.
Neuroplasticity is central to litigation of chronic pain after soft tissue Personal Injury.
Because the soft tissue damage is long healed, expert testimony by the traditional "tissue injury" specialists is largely irrelevant.
Once physical healing is complete, typically within 3 months of a soft tissue injury, physical medicine subspecialists have completed their contributions.
In their stead, chronic pain specialists (anesthetists and psychiatrists) should be asked explicitly to explain to the Court this current understanding of pain modulation and neuroplasticity.
Because narcotics are commonly misused and abused28,29 in Chronic Pain, the search continues for better pharmacological approaches.
The classic Antidepressant Amitryptiline has been shown30 to be an equally effective Chronic Pain-killer in high or low dosage.
Recent review31 of research confirmed efficacy of Prozac-type (SSRI) Antidepressants in some types of Chronic Pain.
Epidural Spinal Cord (Dorsal Column) Stimulation by implanted electrodes is effective in a wide range of localised Chronic Pain conditions, even though it has largely been used for Failed Back pain hitherto32.
More than half a series of 200 implanted patients needed analgesic medication occasionally at most to supplement the Stimulation.
The anatomically-restricted extent of the pain relief is being addressed by technical advances33.
Typically, orthopedic surgeons and rheumatologists no longer have a diagnostic, therapeutic or medicolegal role.
The principal physician is the physiatrist or anesthetist head of a multidisciplinary team of educators, physiotherapists, occupational therapists, psychologists and psychiatrists.
A new study34, of mainly nonsurgical low back pain, and another35 analysing past studies, of all types of chronic pain confirm the effectiveness of multidisciplinary nonsurgical treatment programmes in returning patients to stable employment and minimal drug usage.
Note that abolition or even reduction of pain experience is not a therapeutic goal36.
Thus, therapists are continually challenging the client’s faulty belief that Chronic Pain is protective against further injury.
Are psychological treatments of chronic pain and insomnia effective? A multidisciplinary medical panel weighed the evidence37.
There was strong empirical support for various relaxation techniques in many types of chronic pain, and for hypnosis in cancer pain, but only moderate evidence for cognitive-behavioural and biofeedback treatment.
Relaxation and biofeedback techniques improved some aspects of sleep, but effects on sleep onset and total sleep time were of doubtful clinical benefit.
3 distinct GROUPS of chronic pain patients can be distinguished38 by 4 characteristics: Interference with Activity, Emotional Distress, Pain Intensity and perceived Social Support.
The authors postulate that Adaptive Copers might have a good outcome irrespective of treatment, Dyfunctional patients might require medical interventions, whereas the Interpersonally Distressed could usefully be directed towards cognitive-behavioural therapy.
Beliefs that emotions affect pain, that others should be solicitous when one experiences pain, and (for subjects reporting low and medium pain severity) that one is disabled by pain were associated with psychosocial dysfunction39.
Beliefs that one is disabled and that activity should be avoided because pain signifies damage were associated with physical disability.
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