Brain Stem Stroke Causing Baroreflex Failure and Paroxysmal Hypertension

Abstract

Background-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. 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 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 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, Ͻ3.8 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, 0.14Ϯ0.02 ms 2 ). MNSA was increased in frequency (61 bursts per minute; normal level, 34Ϯ18 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. Key Words: baroreflex Ⅲ hypertension Ⅲ lateral medullary syndrome Ⅲ stroke N eurogenic hypertension has been demonstrated in animal models and is well known to occur in humans after subarachnoid hemorrhage, hydrocephalus, and stroke. 1 Blood pressure (BP) is increased after stroke, particularly after lacunar infarction or hemorrhage and in patients with preceding hypertension. 2,3 It is usually maximal on day 1 and may fall more during the first week in those with higher initial values. 4 The mechanism may involve a transient increase in sympathetic activity or baroreflex dysfunction, although current evidence for this is unsatisfactory. Spectral analysis techniques, measuring heart rate (HR) and BP variability, suggest that baroreflex sensitivity is decreased after a cortical stroke. 5 Serum catecholamine levels are raised in some patients during the first week. 6 In addition to being increased, BP may also become more variable after stroke. 7 Paroxysmal neurogenic hypertension has been associated with a variety of pathologies affecting the brain stem but has only rarely been attributed to stroke. 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. Conclusions-Extensive Case ReportA 75-year-old woman presented with sudden onset of slurred speech, double vision, and left-sided incoordination. She was on long-term treatment for essential hypertension consisting of cyclopenthiazide 0.5 mg daily and nadolol 40 mg BID. Examination findings were consistent with a left-sided lateral medullary syndrome and included the following: rotatory nystagmus on left gaze; left-sided Horner's syndrome, facial hemiane...

Components of arterial systolic pressure and RR-interval oscillation spectra in a case of baroreflex failure, a human open-loop model of vascular control

“…[16][17][18][19][20][21][22] Moreover, rare reports describe this syndrome as due to degenerative neurological disorders or genetic diseases. [23][24][25][26][27] In our patient, the impairment in baroreceptor reflex was due to a posterior fossa tumour, as already described. 7 Animal studies reported that arterial baroreceptor denervation induces selective changes in the spectrum of RR and SAP variability, suggesting that the baroreceptor reflex exerts its major buffering effect on the very low-frequency (VLF) fluctuations.…”

Stroke‐induced chronic systolic dysfunction driven by sympathetic overactivity

“…Several clinical and animal studies have observed associations between IS and cardiac diseases,8, 11 such as cardiac arrhythmias,33 stress‐induced cardiomyopathy (Takotsubo syndrome),34 myocardial infarction,35 paroxysmal arterial hypertension,36 or autonomic dysfunction 9. Thereby, autonomic dysfunction is underlying the impaired physiologic regulation of heart rate and blood pressure as well as the increased secretion of catecholamines and cortisol 6, 37, 38, 39.…”

Arterial baroreflex function and cardiovascular variability: interactions and implications

“…Brain death is characterized by attenuated variability and baroreceptor sensitivity. Extensive unilateral infarction of the brain stem in the region of the nucleus of the solitary tract may result in baroreflex dysfunction, increased sympathetic activity, and paroxysmal neurogenic hypertension (93). Among the supramedullary structures, the insular cortex (the dorsal section of the rhinal sulcus) seems to be importantly involved in cardiovascular regulation (for review, see Ref.…”