Medicine & Science in Sports & Exercise:
E-22 Free Communication/Poster - Blood Flow: JUNE 3, 2011 7:30 AM - 12:30 PM: ROOM: Hall B
1University of Texas at Austin, Austin, TX. 2Brain & Spine Recovery Center, Austin, TX.
(No relationships reported)
Individuals with spinal cord injury (SCI) demonstrate reduced limb blood flow and muscle spasticity. It is plausible that the accumulation of metabolites, resulting from reduced perfusion, could exacerbate spasticity via activation of fusimotor neurons by Group III and IV afferents.
PURPOSE: To determine the association between peripheral blood flow and muscle spasticity in persons with SCI.
METHODS: A total of 14 individuals with SCI were classified into high (N=5), low (N=4), and no (N=5) spasticity according to their spasticity levels indicated by the modified Ashworth scale scores. Blood flow was measured in femoral and brachial arteries using duplex Doppler ultrasound and was normalized to limb lean mass obtained with dual energy X-ray absorptiometry.
RESULTS: There were no significant group differences in age (31.8±4.8, 37.2±5.7, 32.6±4.9 years), time post SCI (10±4.8, 16±6.5, 6.8±1.7 years), American SCI Association motor scores (41±8.9, 56±15.5, 53.4±1.1), or sensory scores (102±25.9, 140±17, 130.4±13.8). Femoral artery blood flow, adjusted for limb lean mass, was significantly different (p=0.009) across the three leg spasticity groups (high 78.2±7.5, low 93.8±19.9, no 142.5±10.9 ml/min/kg). Total leg muscle spasticity scores were significantly and negatively correlated with femoral artery blood flow (r=-0.59, p=0.026). There was no significant difference in brachial artery blood flow between the three groups, indicating that the reduction in blood flow was confined to injured limbs and not due to systemic cardiovascular disorder.
CONCLUSION: Among SCI patients, whole-leg blood flow is progressively lower in individuals with greater spasticity scores. These results suggest that a reduction in lower limb perfusion, among other factors, plays a significant role in the pathogenesis leading to muscle spasticity after SCI.