Reflex Sympathetic Dystrophy and Stroke Location
Current evidence does not establish a clear relationship between reflex sympathetic dystrophy (RSD) and specific stroke locations in the brain. The pathophysiology of post-stroke RSD appears to be related to peripheral nerve injury mechanisms and sympathetic dysfunction rather than specific central nervous system lesion locations.
Evidence for Lack of Location-Specific Association
RSD following stroke is primarily initiated by peripheral mechanisms rather than specific brain lesion locations. The syndrome develops from trauma to nerves, neural plexuses, or soft tissue, with pathophysiology involving sympathetic dysfunction and supersensitivity to catecholamines induced by autonomic denervation 1
The incidence of RSD after stroke is actually quite low (1.56%) when patients receive early comprehensive rehabilitation, which is substantially lower than historically reported rates of 12.5% 2. This suggests that RSD development is more related to management factors (positioning, early mobilization) than stroke location 2
RSD is recognized as a complication of stroke and cerebral injury in general, but the literature does not identify specific anatomical stroke locations as risk factors 3
Pathophysiological Mechanisms
The sympathetic dysfunction in RSD consists of supersensitivity to catecholamines rather than increased efferent sympathetic nerve impulses 1. This peripheral mechanism would not be expected to vary based on stroke location
Neurogenic inflammation at the peripheral level plays a key role, where excitation of sensory nerve fibers causes release of neuropeptides that induce vasodilation, increase vascular permeability, and excite surrounding sensory fibers 1
Central sensitization occurs at the spinal cord level due to increased input from peripheral nociceptors, altering central processing mechanisms 1, 4. This represents a secondary phenomenon rather than a primary stroke location effect
Clinical Implications
Focus prevention efforts on proper upper extremity positioning and early mobilization with sensory stimulation rather than attempting to predict risk based on stroke location 2
Diagnose RSD based on clinical criteria: regional pain and sensory changes following stroke, associated with skin color changes, temperature changes, abnormal sweating, edema, and motor abnormalities 1
Confirm diagnosis with triple-phase bone scan when three of five criteria are present (shoulder pain, decreased passive range of motion, wrist/hand pain, edema, skin changes) 2
Treatment should target sympathetic nervous system activity through sympathetic nerve blocks (surgical or chemical) or adrenoceptor blockers, combined with physical therapy 1, 5. Electroacupuncture may provide additional benefit for pain relief and functional improvement 3