Sympathetic hyperactivity, perceived pain, and anxiety in post-amputee pain

Neurophysiologic adaptations after amputation predispose amputees to sympathetic hyperactivity. Anxiety is linked to increased catecholamine levels, which may exacerbate sympathetic activation of nociceptors. Sustained sympathetic discharge can further reduce efferent sympathetic action potential thresholds. This cyclic facilitation would expectedly result in increased signs of sympathetic hyperactivity over time, including hypoesthesia, epidermis color change, epidermis temperature change, edema, skin breakdown, allodynia, hyperalgesia, and contracture. Our study seeks to elucidate relationships between sympathetic hyperactivity, pain, anxiety and time since amputation. Thirty-four amputees recruited from an urban rehabilitation hospital underwent a physical exam, in which signs of sympathetic hyperactivity were recorded. Current pain levels were measured using the Visual Analog Scale (VAS) and the McGill Pain Questionnaire Short Form (MPQ), which included Affective and Sensory sub-scores. The Pain and Anxiety Symptoms Scale-20 (PASS) was used to measure pain anxiety, which included Cognitive, Fear, Escape/Avoidance, and Physiological sub-scores. Relationships between sympathetic hyperactivity, pain, anxiety and time since amputation were analyzed. Total number of sympathetic hyperactivity signs correlated with VAS Now, MPQ Total, MPQ Sensory, and MPQ Affective scores. Total number of sympathetic hyperactivity signs did not correlate with any PASS scores. Time since amputation did not correlate with epidermis color change, edema, tactile epidermis temperature, skin breakdown, hypoesthesia, allodynia, hyperalgesia, contracture, or total number of sympathetic hyperactivity signs. Correlations between pain levels and signs of sympathetic hyperactivity suggest that post-amputee pain is linked to sympathetic hyperactivity. Our results contrast prior findings, suggesting that anxiety in anticipation of pain does not increase sympathetic overdrive. This pilot work suggests several explanations, including that sympathetic hyperactivity in amputees stems from neurophysiologic adaptations, rather than psychological contributions. Finally sympathetic sensitization in post-amputee pain subjects does not appear to be present. This may be due to central nervous system reorganization after amputation, which could affect expected synaptic pathways.