Understanding RSD




It is not uncommon to injure a body part – we may accidentally stub one of our toes, bang our knee on something, or sprain one of our ankles – but we often get up to keep going, not really considering the extent of injury. Although the initial sensation of pain may be absolutely excruciating, it usually tends to subside after waiting a moment, or “walking it off”. While this may work at time to reduce and ultimately relieve pain, in the case of some, this may not always be the outcome. The sensation of pain not only remains, it worsens over time, often to the point that it can become excruciating. This can severely affect the overall quality of life of the injured individual. These abnormal pain responses from common injuries characterized by chronic pain are a direct result of a pain syndrome called reflex sympathetic dystrophy, or RSD.

Reflex Sympathetic Dystrophy Syndrome, often called RSD for short, was initially identified by a Philadelphia based physician, Dr. S. Weir Mitchell. He outlined his description of the pain syndrome in “Injuries of Nerves and Their Consequences,” a research paper that he published for the medical community in 1872. Dr. Mitchell, a well-regarded doctor of the time, was most well-known for the research he produced in his lifetime of studying the human nervous system. He was employed as a surgeon and treated many wounded Civil War soldiers that fought for the Union Army. In treating the troops, he would often come across a recurring medical condition amongst the soldiers who had experienced some trauma but whose war wounds had essentially healed. These soldiers reported to Dr. Mitchell that they continued to experience ongoing pain from their injuries that seemed to make its way from the injured areas to other parts of the body. The most commonly reported symptoms included a dull, burning pain; extreme sensitivity to light touch at the site of the injury; and noticeable surface temperature fluctuations in the parts of the body that were affected by the pain.

A physician in Boston by the name of James Evans, in 1946, introduced the medical community to the term “reflex sympathetic dystrophy“. He used this name of the pain syndrome previously identified by Dr. Mitchell in his description of a similar pain disorder he had observed in some of his patients that had no identifiable damage to nerve tissue. Later in 1994, the International Association for the Study of Pain officially renamed what had been called reflex sympathetic dystrophy, also providing the medical community with further medical definition. It was redefined as “complex regional pain syndrome,” or CRPS for short, and was further classified by two types: CRPS Type 1 and CRPS Type 2. CRPS Type 1 is the form of pain syndrome that occurs when a patient has no known or identifiable nerve injury while CRPS Type 2 involves an identifiable injury or trauma to a nerve in the sympathetic nervous system. The World Institute of Pain, in a 2002 report, rightfully declared that intense “excruciating pain is the hallmark of the disease.”

As recently as the 1980s, some scientists wrongfully held on to the belief that the body’s pain impulses and responses all behaved in similar fashion. Research over the last three decades has now demonstrated that the human nervous system tends to exhibit a much more dynamic neural response to the various kinds of pain the body feels. The human nervous system has millions of neurons, or nerve endings. Under normal circumstances, each individual neuron joins with others to form connections called synapses. These neural connections result in the creation of multiple pathways that exists between the body’s spinal cord, the central part of the human nervous system, and a person’s brain. The path that an individual impulse may travel dictates the kind of pain the body feels, such as throbbing pain, dull, aching pain or ongoing burning sensations. That said, if for some reason a nerve does sustain some type of injury, there can be changes in how that nerve and surrounding nerves process pain signals from the body. This neurological change is a disease. Unfortunately for sufferers, pain is not only the symptom but the disease. After being injured, nerves can start to release some natural proteins that can cause edema, or temperature fluctuations, redness, and swelling in the tissue surrounding the site of an injury. It is this pathology that makes identifying RSD so difficult. That said, there are a number of advancements that have been made, in particular those that now allow doctors to provide an RSD diagnosis. Over time, as more research is done into the pathology of the disease, we are hopeful that a more clear set of causal conditions can be identified.


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