Central and cerebrovascular effects of leg crossing in humans with sympathetic failure

Leg crossing increases arterial pressure and combats symptomatic orthostatic hypotension in patients with sympathetic failure. This study compared the central and cerebrovascular effects of leg crossing in patients with sympathetic failure and healthy controls. We addressed the relationship between middle cerebral artery blood velocity (MCA V_mean, TCD), frontal lobe oxygenation (oxyhemoglobin (O₂Hb) and mean arterial pressure (MAP), cardiac output (CO) and total peripheral resistance (TPR) in 6 patients (aged 37 to 67 years; 3 women) and age- and gender-matched controls during leg crossing. In the patients, leg crossing increased MAP from 58 (42-79) to 72 (52-89) vs. 84 (70-95) to 90 (74-94) mmHg in the controls. MCA V_mean increased from 55 (38-77) to 63 (45-80) and from 56 (46-77) to 64 (46-80) cm.s^-1, respectively (p<0.05) with a larger rise in O₂Hb (1.12 (0.52-3.27)) in the patients vs. the controls (0.83 (-0.11-2.04) µmol.l^-1)). In the control subjects CO increased 11% (p<0.05) with no change in TPR. By contrast, in the patients CO increased 9% (p<0.05) but also TPR increased by 13% (p<0.05).
In conclusion, leg crossing improves cerebral perfusion and oxygenation both in patients with sympathetic failure and in healthy subjects. However, in healthy subjects cerebral perfusion and oxygenation improve by a rise in CO without significant changes in TPR or MAP, whereas in patients with sympathetic failure cerebral perfusion and oxygenation improve through a rise in MAP due to increments in both CO and TPR.

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Central and cerebrovascular effects of leg crossing in humans with sympathetic failure

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