1 We describe a case of paroxysmal hypertension after left lateral medullary infarction and demonstrate, using microneurographic recordings of sympathetic activity, that the likely mechanism was partial baroreflex failure.Ī 75-year-old woman presented with sudden onset of slurred speech, double vision, and left-sided incoordination. 7 Paroxysmal neurogenic hypertension has been associated with a variety of pathologies affecting the brain stem but has only rarely been attributed to stroke. In addition to being increased, BP may also become more variable after stroke. 5 Serum catecholamine levels are raised in some patients during the first week. Spectral analysis techniques, measuring heart rate (HR) and BP variability, suggest that baroreflex sensitivity is decreased after a cortical stroke. 4 The mechanism may involve a transient increase in sympathetic activity or baroreflex dysfunction, although current evidence for this is unsatisfactory.
2 3 It is usually maximal on day 1 and may fall more during the first week in those with higher initial values. 1 Blood pressure (BP) is increased after stroke, particularly after lacunar infarction or hemorrhage and in patients with preceding hypertension. Neurogenic hypertension has been demonstrated in animal models and is well known to occur in humans after subarachnoid hemorrhage, hydrocephalus, and stroke. BP and MNSA responses to cold pressor and isometric handgrip stimuli were intact.Ĭonclusions-Extensive unilateral infarction of the brain stem in the region of the nucleus tractus solitarius may result in partial baroreflex dysfunction, increased sympathetic activity, and neurogenic paroxysmal hypertension. MNSA was increased in frequency (61 bursts per minute normal level, 34☑8 bursts per minute), and the burst amplitude was not inversely related to diastolic BP. Serum catecholamines were substantially increased (norepinephrine level, 23.9 nmol/L 9 days after stroke normal level, <3.8 nmol/L), and heart rate variability, measured by spectral analysis, was decreased in both low- and high-frequency domains (0.04 and 0.06 ms 2, respectively normal level, 0.14☐.02 ms 2). The paroxysms were triggered by changes in posture and were accompanied by tachycardia, diaphoresis, and headache. We undertook microneurographic recordings of muscle sympathetic nerve activity (MNSA) during beat-to-beat blood pressure (BP) monitoring to investigate this hypothesis.Ĭase Description-We investigated a 75-year-old woman who developed paroxysmal hypertension (BP 220/110 mm Hg) after a large left-sided medullary infarct. The mechanism is thought to involve increased sympathetic activity and baroreflex dysfunction. Customer Service and Ordering Informationīackground-Paroxysmal neurogenic hypertension has been associated with a variety of diseases affecting the brain stem but has only rarely been reported after brain stem stroke.Stroke: Vascular and Interventional Neurology.Journal of the American Heart Association (JAHA).Circ: Cardiovascular Quality & Outcomes.Arteriosclerosis, Thrombosis, and Vascular Biology (ATVB).
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