[Ischemic white matter lesions may be caused by the baroreceptor reflex are dysfunction].

Muscle sympathetic nerve activity (MSNA, bursts/min) was recorded microneurographically from the tibial nerve in the control group (8 males and 8 females) and the cerebral infarction group (12 males and 12 females) with ischemic white matter lesions (WMLs) diagnosed on T2-weighted MR imaging. Subjects in the latter group were more hypertensive. A significant positive correlation between age and the MSNA at rest was detected in the control group, but not in the cerebral infarction group. The MSNA at rest was significantly low exclusively in infarcted females. Although the blood pressure did not decrease in either group during a 30 degrees head-up tilt, the MSNA was enhanced in the control group alone. On the cold pressor test, the control group demonstrated a significant pressor response, but not an increase in MSNA. In contrast, the cerebral infarction group showed a significant increase in MSNA, and, within the group, only infarcted females lacked a clear pressor response. These results indicated the existence of an insensitivity in the baroreceptor reflex arc on the part of infarcted males, as already indicated in hypertensive patients. On the other hand, on infarcted females, there were both a hypofunction of the baroreceptor reflex arc and a decline of the vascular reactivity, possibly due to an inadequate development of the sympathetic nervous system and a low level of estrogen. Interestingly mean WMLs%, which was calculated as total WMLs areas x 100/total subdural areas on four horizontal T2-weighted MR images, 10, 20, 30, 40 mm above the bicommisural plane, was significantly larger in infarcted females (8.7 +/- 0.7%, mean +/- S.E.) than males (5.1 +/- 0.7%). This discrepancy may be caused by the above-mentioned difference on the results between them. WMLs are mostly distributed in the watershed zone supplied by the long penetrating arteries. Therefore, the lesions may be produced by wide fluctuations in blood pressure as the result of a dysfunction of the baroreceptor reflex arc and a decrease of the vascular reactivity.