Abstract

Aims: In this study, we attempted to identify clinical parameters predicting the absence or presence of Neurovascular Compression (NVC) at the Ventrolateral Medulla (VLM) in arterial hypertension (HTN) in MRI findings. Background: Cardiovascular and pulmonary afferences are transmitted through the left vagus and glossopharyngeal nerve to the brain stem and vasoactive centers. Evidence supports the association between HTN and NVC at the left VLM. Several independent studies indicate a reduction of HTN after Microvascular Decompression (MVD) of the left. Several independent studies indicate a reduction of HTN after Microvascular Decompression (MVD) of the left VLM. Image processing of MRI provides comprehensible detection of NVC. HTN affects hemodynamic parameters and organs. Objective: This study analyzes and correlates clinical data and MRI findings in patients with and without NVC at the VLM in treatment resistant HTN to obtain possible selection criteria for neurogenic hypertension. Methods: In 44 patients with treatment resistant HTN, we compared MRI findings of neurovascular imaging to demographic, clinical and lifestyle data, office and 24-hour ambulatory Blood Pressure (BP), and cardiovascular imaging and parameters. Results: Twenty-nine (66%) patients had evidence of NVC at the VLM in MRI. Sixteen patients (36%) had unilateral NVC on the left side, 7 (16%) unilateral right and 6 (14%) bilateral NVC. Fifteen (34%) had no evidence of NVC at the VLM. Patients with left sided NVC were significantly younger, than those without NVC (p=0.034). They showed a statistically significant variance in daytime (p=0.020) and nighttime diastolic BP (p<0.001) as the mean arterial pressure (p=0.020). Other measured parameters did not show significant differences between the two groups. Conclusion: We suggest to examine young adults with treatment resistant HTN for the presence of NVC at VLM, before signs of permanent organ damage appear. Clinical and hemodynamic parameters did not emerge as selection criteria to predict NVC. MVD as a surgical treatment of NVC in HTN is not routine yet as a surgical treatment of NVC in HTN is not routine yet. Detection of NVC by imaging and image processing remains the only criteria to suggest MVD, which should be indicated on an individual decision.

Highlights

  • Neurovascular Compression (NVC) describes a pathological contact between the Root Entry/Exit Zone (REZ) of a cranial nerve and a vessel at the brain stem, resulting in a hyperactive dysfunction

  • Clinical and hemodynamic parameters did not emerge as selection criteria to predict NVC

  • Detection of NVC by imaging and image processing remains the only criteria to suggest Microvascular Decompression (MVD), which should be indicated on an individual decision

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Summary

Introduction

NVC describes a pathological contact between the Root Entry/Exit Zone (REZ) of a cranial nerve and a vessel at the brain stem, resulting in a hyperactive dysfunction. A significant reduction of arterial HTN was observed after microvascular decompression (MVD) [1 - 3]. Animal models have defined the role of the sympathoexcitatory neurons of the rostral VLM and the inhibitory neurons of the caudal VLM in blood pressure regulation [4] It seems that NVC at the VLM leads to a permanent irritation and activation of the C1 neurons located at the VLM. Elevated sympathetic nerve activity was observed in hypertensive patients with NVC at VLM in magnetic resonance imaging (MRI) [18, 19]. Evidence supports the association between HTN and NVC at the left VLM. Several independent studies indicate a reduction of HTN after Microvascular Decompression (MVD) of the left. Several independent studies indicate a reduction of HTN after Microvascular Decompression (MVD) of the left VLM.

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