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the recovery stage of stroke and were living relatively normal lives despite neurological impairment. Twenty-one of the 24 patients had experienced strokes between 4 and 10 AM. None were taking any other drugs. Throughout the period of our study, all patients were requested to maintain their routine daily schedules. We conducted our study using oral nitrendipine (Nantong Pharmaceutical Factory, Hebei, China) and tested its efficacy in relation to the circadian changes of blood pressure using different therapies. The trial was carried out in the following order: blood pressure (both systolic and diastolic) was measured from the right brachial artery at 2-hour intervals over a 24-hour period beginning at 8 AM. At the same time, all hypertensive patients were given 10 mg nitrendipine T.I.D. daily over 1 week, followed by another 24-hour period of blood pressure measurements. Finally, a new therapy was instituted as follows: 20 mg nitrendipine was administered once daily in the early morning over a 1-week period, followed by the same investigation of blood pressure described above. As reported by Millar-Craig et al, the circadian change of blood pressure was expected during the first stage of our trial without nitrendipine. During the second stage of the trial, the previous therapy could have reduced the blood pressure at any time in the twelve 2-hour intervals each day, but the daily rhythm of circadian change was only slightly different from that without nitrendipine. In the third stage, with the new regimen, there was a varied pattern of circadian change of blood pressure, which avoided the profound nocturnal fall and reduced the elevated blood pressure in the morning hours. This regimen not only decreased hypertension in the peak hours of blood pressure, but also helped stabilize blood pressure during the circadian period. We conclude that this new regimen may be superior to previous therapies in the prevention of ischemic stroke onset.

Pure lemniscal sensory deficit caused by pontine hemorrhage.