The etiology of most cases of many common chronic pain conditions including low back pain and headaches is not understood.
Complex regional pain syndrome (CRPS) types I and II, previously called reflex sympathetic dystrophy (RSD) and causalgia, respectively.
CRPS is characterized by substantial pain in a distal limb, and approximately 90% of cases are triggered by physical limb trauma, such as an injury or operation.
CRPS associated vasomotor and sudomotor changes of thought to be related to neurogenic inflammation and abnormal regional autonomic activation.
Neurogenic inflammation, is an inflammatory response to tissue caused by antidromic release of neuropeptides, including substance, P and calcitonin gene related peptide, from sensory nerve endings, which caused swelling, warmth, redness, nail and hair growth, and hyperhidrosis.
Abnormal regional autonomic activation of regional autonomic nerves may contribute to temperature regulation, skin color changes, swelling, sweating, nail and hair growth.
CRPS is associated with specific microbiome signatures with the harboring of circulating auto reactive IgM and IgG antibodies.
CRPS typically commences immediately to less than one month after the inciting event.
CRPS is associated with two or more abnormalities in the affected region: tenderness, color change, or swelling.
It is classified as a chronic primary pain disorder along withchronic migraines, fibromyalgia syndrome, and other disorders.
Usually occurs after injury to the limb, such as fracture or surgery.
The difference between Types I and II is that in the latter there is evidence of a definable nerve lesion.
The incidence of CRPS is unclear as many cases are never diagnosed.
CRPS is identified by its association with substantial functional disability or psychological distress.
It is a nociplastic pain disorder, noting it is caused by dysfunction of the peripheral nervous system, CNS, or both.
CRPS Type I especially may go unrecognized because of the absence of an identifiable peripheral nerve injury.
Almost always follows some trauma to the affected body part, usually an extremity.
Type I CRPS is caused by an injury will prolonged immobilization from casting.
The trauma can range in severity from surgery to accidental injury to chronic overuse.Clinically the two types of indistinguishable with pain, allodynia, hyperalgesia of the limb that is out of proportion to the initial injury.
Approximately 50 000 new cases per year in the United States.
Among patients with fractures of the distal radius approximately 18% develop CRPS Type I (Pulchaski,P et al).
Among 162 soldiers wounded in the Iraqi war seen in pain clinics reported that 4.3% suffered CRPS Type II and 1.9% CRPS Type I (Cohen SP et al).
Many patients have no clinical signs of injury, the pain may be out of proportion to the nature of the original injury, and with prolonged discomfort the process is not recognized and may be misdiagnosed as malingering.
No correlation between the severity of the trauma and the development of the long-lasting and burning pain.
The original injury may be clinically insignificant, and no predictive factors have been discovered.
The sympathetic nervous system involved in symptoms of edema, blood flow, and sudomotor changes.
The etiology of CRPS is believed to be the result of a combination of peripheral and central factors.
Suspected peripheral mechanisms include: inflammation, peripheral sensitization, and changes in sodium channels that may result in central changes including an exaggerated response to peripheral input and a reduction of descending inhibitory pathways.
No consistent correlation exists between the presence of mental health disorders and the development of CRPS.
A clinical diagnosis of associated pain with allodynia and hyperalgesia.
Allodynia refers to pain caused by a stimulus which is not usually painful.
Allodynia is commonly the most dramatic presenting symptom of CRPS.
Hyperalgesia, refers to a normally painful stimulus that causes more discomfort than expected.
Both allodynia and hyperalgesia are considered with the term hyperesthesia―an increased sensitivity to stimulation.
In most cases sudomotor and vascular changes will occur, with edema and changes in blood flow resulting in skin temperature changes in the affected site.
Approximately 80% of cases are monophasic involving a single episode without relapse that improves substantially within an 18 months.
Lasting motor dysfunction, including reduce grip strength and other symptoms such as cold sensitivity may occur as a post CRP syndrome associated with functional impairment.
CRPS may spread to other limbs in 5% of cases where pain in additional areas of the body will develop in some patients.
Many patients develop dystrophic changes several months after the onset of the pain.
Patients are typically in their 40s to 60s.
CRPS is rare in children and adolescents.
A bone scan with increased pooling present in the early bone uptake phase is considered to be confirmatory of the diagnosis, but the absence of these changes does not rule out the diagnosis.
The earlier it is treated the greater the likelihood of the reduction in the pain.
Many different treatments have been tried, but few are beneficial.
Treatment focuses on functional restoration of the affected limb primarily through physical and occupational therapies.
Patients tend to protect and limit use of an affected limb due to pain or the fear of pain, leading to atrophy and increasing weakness that resulting in increased pain and decreased function.
Improvement is lacking unless the patient tries to remain as active and functional.
CRPS primarily a neuropathic form of pain, and medications efficacious for neuropathic pain are recommended for initial treatment.
Agents used are primarily the serotonin-norepinephrine reuptake inhibitor (SNRI) antidepressants including the tricyclics, duloxetine, and venlafaxine and anticonvulsants, most notably pregabalin and gabapentin.
Opioids also may be beneficial for pain.
The lidocaine 5% patch provides pain relief with a minimal risk of side effects, and may decrease environmental stimuli that may exacerbate the pain.
Heat application may acutely exacerbate CRPS pain because of the associated allodynia.
If swelling is present nonsteroidal anti-inflammatory drugs an corticosteroids may be beneficial.
Sympathectomy, sympathetic blocks and stellate ganglion blocks generally not beneficial and may increase pain.
Sympathetic blocks, if they can be administered within 6 to 8 weeks after the initial onset of the pain may be beneficial, but such timely diagnostic efforts are rare.
Limited value for regional anesthesia agents.
Psychotherapy is a therapeutic option with biofeedback, cognitive behavioral management and anti depressive treatment.
Because of the severe nature of the pain, the difficulty obtaining a diagnosis, failure of treatments, many patients do suffer from depression.
The course of CRPS varies from improvement, stability or worsening, and is not predictable.
Can spontaneously resolve, even after years.