Stage I

Pain/sensory abnormalities, vasomotor and sudomotor dysfunction, and
prominent edema.

Stage II (Dystrophic Stage)
Occurs 3-6 months after onset. More marked pain/sensory dysfunction, vasomotor dysfunction, and development of significant motor/trophic changes.

Stage III (Atrophic Stage)
Decreased pain/sensory disturbance, vasomotor disturbance, and markedly increased motor/trophic changes.

CRPS may take two forms in sequential order. Acute CRPS consists of vasodilation and sudomotor dysfunction (hot, red, occasionally dry); in contrast, patients with chronic CRPS demonstrate signs of vasoconstriction and hyperhydrosis (cold, blue, sweaty). The sequential stages may reflect CRPS subtypes, symptoms tend to remain stable or improve, rather than progressively deteriorate, and sympathetic signs and symptoms are highly variable between and within patients over time.

CRPS remains one of the most complex and difficult pain conditions to treat. CRPS does not have a definitive pathophysiology; however, it is likely to be the result of multiple interacting mechanisms with varying contributions across different patients. Fractures and sprains appear to be the most common events triggering CRPS and it is more common in the upper extremities, in females, and most likely to occur in the 50-70 year age range.

CRPS patients experience sensory impairment including autonomic disturbances, allodynia, and hyperalgesia which can extend beyond the area affected by pain. Additionally, up to 50% of patients may experience hypoesthesia and hypoalgesia in a quadrantic or hemibody distribution ipsilateral to the pain. Sensory abnormalities are more likely to occur with greater CRPS chronicity indicating centralization of the pathology over time.

Evidence supports centralization in chronic CRPS. Nociception from trauma and/or neurogenic inflammation can cause rapid changes in the central nervous system (brain and spinal cord), a process commonly referred to as central sensitization.

Despite autonomic dysfunction being implicated as directly involved with CRPS pathology, the role of the sympathetic nervous system is unknown, but evidence points to an inhibition rather than an enhancement of sympathetic vasoconstrictor activity.

Patients often experience pain flare ups during cold weather and/or in response to psychological stress, when catecholamine secretion would be expected to increase such as in the Fight or Flight response. Vasoconstriction increases significantly on the affected side versus the unaffected side during pain changes.

This is older terminology and not used very often with modern treatment modalities.

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