Related Experiment Videos
Diminished nocturnal blood pressure decline and lesion site in cerebrovascular disease
Y Yamamoto1, I Akiguchi, K Oiwa
1Department of Neurology, Kyoto Second Red Cross Hospital, Japan.
Insights
Reduced nocturnal blood pressure decline in cerebrovascular disease is linked to specific brain injuries, not just the extent of vascular disease. This finding helps understand stroke mechanisms and potential early indicators.
Area of Science:
- Neurology
- Cardiovascular Medicine
- Hypertension Research
Background:
- Diminished nocturnal blood pressure decline is linked to hypertensive vascular disease extent.
- Previous research indicated cerebrovascular lesion location also influences this decline.
- The mechanism in cerebrovascular disease requires further elucidation.
Purpose of the Study:
- To investigate the mechanism of reduced nocturnal blood pressure decline in cerebrovascular disease.
- To determine if reduced nocturnal blood pressure decline precedes cerebrovascular disease development.
- To examine patients with recurring stroke episodes.
Main Methods:
- Ambulatory blood pressure monitoring was performed on control subjects, hypertensive subjects, and patients with various cerebrovascular diseases.
- Patients included those with lacunar infarctions, putaminal/thalamic hemorrhages, pontine lesions, and cortical infarctions.
- Percentage of nocturnal blood pressure decline and correlations with systolic blood pressure and heart rate were analyzed.
Main Results:
- Significantly smaller nocturnal blood pressure decline was observed in patients with multiple lacunar infarction, thalamic hemorrhage, pontine tegmentum infarction, and pontine hemorrhage.
- No significant correlation between systolic blood pressure and heart rate was found in most groups with diminished decline.
- These findings suggest specific lesion locations are critical.
Conclusions:
- Diminished nocturnal blood pressure decline in cerebrovascular disease is associated with specific central autonomic nervous system injuries.
- Affected areas include the striatum, diencephalon, midbrain, and pontine tegmentum.
- These injuries and their connecting fibers likely disrupt normal blood pressure regulation during sleep.
Background And Purpose:
Many studies have suggested that diminished nocturnal blood pressure decline in hypertensive cardiovascular disease is associated with the extent of hypertensive vascular disease. In our previous observation of cerebrovascular disease, however, we found reduced nocturnal blood pressure decline to be associated not only with the extent of hypertensive vascular disease but also with the specific location of cerebrovascular lesions. The purpose of this study was to elucidate the mechanism of nocturnal blood pressure decline in cerebrovascular disease. Moreover, to clarify whether reduced nocturnal blood pressure decline occurs before cerebrovascular disease, we examined patients with recurring episodes.
Methods:
Ambulatory blood pressure monitoring was carried out every 30 minutes in 14 control subjects, 15 hypertensive subjects, 90 patients with cerebrovascular disease (16 single lacunar infarctions, 15 multiple lacunar infarctions, 10 putaminal hemorrhages, 14 thalamic hemorrhages, 11 pontine base infarctions, 15 pontine tegmentum infarctions, 8 pontine hemorrhages, 13 wide cortical infarctions), and 7 patients with recurring stroke episodes. The percentage of nocturnal blood pressure decline and the correlations for systolic blood pressure and heart rate were calculated.
Results:
The percentage of nocturnal blood pressure decline was significantly smaller in the groups with multiple lacunar infarction (systolic, P < .001; diastolic, P < .01), thalamic hemorrhage (P < .01, P < .05), pontine tegmentum infarction (P < .01, P < .05), and pontine hemorrhage (both P < .05). The correlation between systolic blood pressure and heart rate was not significant for almost all the groups with diminished blood pressure decline.
Conclusions:
Diminished nocturnal blood pressure decline in cerebrovascular disease is thought to be caused by specific injury to the central autonomic nervous system such as the striatum, diencephalon, midbrain, and pontine tegmentum and their connecting fibers.