What causes complex regional pain syndrome (CRPS) in hemiplegia?

Updated: Feb 08, 2019
  • Author: Robert Gould, DO; Chief Editor: Stephen Kishner, MD, MHA  more...
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Answer

Answer

Complex regional pain syndrome (CRPS) is also known as shoulder-hand syndrome, RSD, causalgia, sympathetically maintained pain, Sudeck atrophy, and minor dystrophy. The International Association for the Study of Pain (IASP) has advocated using the terms CRPS type 1 (RSD) and CRPS type 2 (causalgia). The IASP categorization states that RSD develops secondary to noxious stimuli that are not limited to the distribution of a single peripheral nerve, while causalgia starts after a nerve injury.

The incidence of CRPS varies in the literature. Davis and coauthors reported that CRPS occurs in 12.5% of patients who have had a stroke, [27] while Chalsen and colleagues reported the incidence to be 61%. [28]

Onset of CRPS is within 3 months poststroke and rarely after 5 months poststroke. In a study, Davis and coworkers demonstrated that of those patients who developed CRPS, 65% had done so by 3 months poststroke, and 98% had done so by 5 months poststroke. [27]

CRPS is most commonly precipitated by bone or soft-tissue injuries, but in up to 30% of the cases, the patient does not remember experiencing an injury. Snider reported that about 5-8% of patients have an incomplete nerve injury. [29] Other precipitating factors may include the following:

  • Upper extremity immobilization

  • Myocardial infarction

  • Stroke

  • Rotator cuff tear

  • Shoulder spasticity

  • Glenohumeral joint subluxation

CRPS more commonly affects the upper extremity. Tepperman and colleagues reported metacarpophalangeal (MCP) joint tenderness to be the best diagnostic indicator, having a sensitivity and specificity of 85.7% and 100%, respectively. [30] Intuitively, however, it is questionable whether any one physical examination maneuver could have such high sensitivity and specificity for a syndrome as complex as RSD.

Using electromyography (EMG), Cheng and Hong found a significant correlation between the presence of spontaneous activity and the development of clinical RSD in 65% of subjects, whereas only 4% of those without spontaneous activity developed RSD. [31] However, this is not consistent with the definition of RSD set forth by the IASP, which dictates that patients with identifiable nerve lesions may have causalgia but not RSD.


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