Brain stem stroke causing baroreflex failure and paroxysmal hypertension

Background-Paroxysmal neurogenic hypertension has been associated with a va riety of diseases affecting the brain stem but has only rarely been reporte d after brain stem stroke. The mechanism is thought to involve increased sy mpathetic activity and baroreflex dysfunction. We undertook microneurograph ic recordings of muscle sympathetic nerve activity (MNSA) during beat-to-be at blood pressure (BP) monitoring to investigate this hypothesis. Case Description-We investigated a 75-year-old woman who developed paroxysm al hypertension (BP 220/110 mm Hg) after a large left-sided medullary infar ct. The paroxysms were triggered by changes in posture and were accompanied by tachycardia, diaphoresis, and headache. Serum catecholamines were subst antially increased (norepinephrine level, 23.9 nmol/L 9 days after stroke; normal level, <3.8 nmol/L), and heart rate variability, measured by spectra l analysis, was decreased in both low- and high-frequency domains (0.04 and 0.06 ms(2), respectively; normal level, 0.14+/-0.02 ms(2)). MNSA was incre ased in frequency (61 bursts per minute; normal level, 34+/-18 bursts per m inute), and the burst amplitude was not inversely related to diastolic BP. BP and MNSA responses to cold presser and isometric handgrip stimuli were i ntact. Conclusions-Extensive unilateral infarction of the brain stem in the region of the nucleus tractus solitarius may result in partial baroreflex dysfunc tion, increased sympathetic activity, and neurogenic paroxysmal hypertensio n.