Normal blood flow response and vasomotion in the diabetic Charcot foot

Vasomotion, the spontaneous rhythmic contraction exhibited by small arteries and arterioles is dysregulated in patients with diabetic neuropathy. We examined the relationship between Charcot arthropathy and vasomotion at the dorsum of the foot. We studied nine diabetic patients with clinically diagnosed neuropathy and Charcot arthropathy in 13 feet (n = 13), twelve subjects with diabetic neuropathy and no Charcot deformity (n = 12), and 11 healthy controls (n = 11). Following neuropathy assessment, blood flow was measured by laser Doppler flowmetry with local skin warming. Fast Fourier transformation was performed to provide an index of vasomotion. Subjects with Charcot osteoarthropathy had more severe somatic neuropathy and higher circulating levels of serum calcium (9.8 ± 0.1 versus 9.3 ± 0.1 mg/dL). Raising local temperature increased skin blood flow and vasomotion in both control subjects and Charcot subjects, but not in diabetic patients with neuropathy alone (p < 0.05 for blood flow, p < 0.02 for vasomotion). Patterns of peripheral vasomotion and blood flow which are clearly disordered in diabetic neuropathy are intact in patients with a Charcot osteoarthropathy, despite a more severe sensory nerve impairment. These findings suggest that the loss of peripheral blood flow and vasomotion often seen in diabetic neuropathy may actually be protective against Charcot arthropathy by preventing bone resorption. It remains unclear then whether the Charcot arthropathy is a direct result of a failure to decrease blood flow to bone, or is the manifestation of some other pathology.