Complex regional pain syndrome (CRPS) is a peripherally limited pain syndrome. It is characterized by intense pain, inflammation, altered autonomic function, abnormal motor function and trophic changes. Although most individuals recover rapidly from mild to moderate injury to the distal limbs, a small proportion will develop CRPS, and in some it may occur spontaneously. The disorder was first described by Mitchell following battlefield injuries. Numerous terms have been used to describe the condition, from causalgia to reflex sympathetic dystrophy and algodystrophy. Currently, CRPS is the accepted terminology, and is divided into two subtypes: CRPS type I occurs without nerve injury and CRPS II in which significant nerve injury can be demonstrated. Although the majority of individuals recover within 12 months, CRPS may result in severe long-term pain, and sufferers report a very low quality of life.
MECHANISMS
Explanatory models of CRPS must account for abnormal inflammation, nociceptive sensitization, autonomic dysfunction and maladaptive neuroplasticity.
It has been debated as to whether CRPS I can be defined as a neuropathic pain syndrome, on the basis of the most recent diagnostic criteria for neuropathic pain. Symptoms and signs suggestive of neuropathic pain are present in CRPS I. Some studies have demonstrated a mild loss of small nerve fibres, providing support for a neuropathic mechanism.
Inflammation
There is evidence for abnormal immune activation in CRPS, but most proinflammatory cytokine markers found in blood and blister fluid return to normal levels after 6 months.
Nociceptors release peptide neurotransmitters including substance P and calcitonin gene-related peptide (CGRP), which may activate immune cells in peripheral tissues. Levels of substance P and its receptor neurokinin-1 are elevated following fracture in a rat model of CRPS, and mast cell degranulation may consequently be triggered via a substance P pathway. Numerous substances are released from mast cells, including tryptase, histamine and cytokines.
Binding of histamine, substance P and CGRP to receptors on small blood vessels results in oedema, vasodilation and pain – characteristic of both early CRPS and neurogenic inflammation.
Mechanism of reflex sympathetic dystrophy syndrome (RSD), a chronic pain syndrome where high amounts of nerve signals are sent to one area of the body, causing a sympathetic response of pain and swelling.
Original injury initiates a pain impulse carried by sensory nerves to the central nervous system. The pain impulse in turn triggers an impulse in the sympathetic nervous system which returns to the original site of injury. The sympathetic impulse triggers the inflammatory response causing changes in the soft tissue including blood vessels. Eventually, leading to swelling, temperature changes, color changes and increased pain. The pain appears to become entrained in the patient’s nervous system, establishing a cycle of pain, swelling, color changes and inability to move the affected limb. Resulting in burning, stinging pain. Swelling eventually gives way to atrophy of soft tissue.
DIAGNOSING RSD
Common Methods used to diagnose the condition, include:
- Bone scan. A radioactive substance is injected into you in order to view your bones with a special camera.
- X-Rays. Can show loss of minerals in the bones, as well as progression/severity of condition.
- Sympathetic nerve tests. Tests such as thermography measure skin temperature and blood flow at RSD site.
- Sweat testing
As RSD attorneys, we have frequently seen our clients receiving delayed or incorrect diagnoses. Many of our clients go to more than one medical specialist, before obtaining an RSD or CRPS diagnosis. Many doctors do not have an objective diagnostic test for RSD. We have also had clients with a RSD or CRPS diagnosis, where X-rays, MRIs or bone scans have failed to detect RSD condition.
According to Dr. Hooshmand, a neurologist in Vero Beach, Florida, there is up to 80% reversal rate of RSDS, if diagnosed and properly treated, in the first three to six months following initial symptom onset. The younger the patient, the better the odds of reversal.
