(Stroke. 2000;31:1997.)
© 2000 American Heart Association, Inc.
Case Reports |
From the Departments of General Medicine (A.M.P., D.L.J.), Neurology (P.J.P.), Radiology (T.H.), and Cardiology (H.I.), Christchurch Hospital (New Zealand).
Correspondence to D.L. Jardine, Department of General Medicine, Christchurch Hospital, PO Box 4710, Christchurch, New Zealand.
Abstract
BackgroundParoxysmal neurogenic hypertension has been associated with a variety of diseases affecting the brain stem but has only rarely been reported after brain stem stroke. The mechanism is thought to involve increased sympathetic activity and baroreflex dysfunction. We undertook microneurographic recordings of muscle sympathetic nerve activity (MNSA) during beat-to-beat blood pressure (BP) monitoring to investigate this hypothesis.
Case DescriptionWe investigated a 75-year-old woman who developed paroxysmal hypertension (BP 220/110 mm Hg) after a large left-sided medullary infarct. The paroxysms were triggered by changes in posture and were accompanied by tachycardia, diaphoresis, and headache. 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 ms2, respectively; normal level, 0.14±0.02 ms2). MNSA was increased in frequency (61 bursts per minute; normal level, 34±18 bursts per minute), and the burst amplitude was not inversely related to diastolic BP. BP and MNSA responses to cold pressor and isometric handgrip stimuli were intact.
ConclusionsExtensive 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.
Key Words: baroreflex hypertension lateral medullary syndrome stroke
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