Neurovascular compression of medulla oblongata – Association for gestation-induced hypertension Levent Tanrikulu a,b,⇑ , Ramin Naraghi a,c , Veronika Ernst a,d,f , Franziska Voigt f,g , Peter Hastreiter a , Arnd Doerfler e , Michael Buchfelder a , Matthias Beckmann f , Tamme W. Goecke f,g a Department of Neurosurgery, Friedrich-Alexander-University of Erlangen-Nuremberg, Schwabachanlage 6, 91054 Erlangen, Germany b Department of Neurosurgery, University of Aachen Medical Center, Pauwelsstrasse 30, 52074 Aachen, Germany c Department of Neurosurgery, Military Hospital Ulm, Oberer Eselsberg 40, 89081 Ulm, Germany d Department of Obstetrics, Hospital Nuremberg South, Breslauer Strasse 201, 90471 Nuremberg, Germany e Department of Neuroradiology, Friedrich-Alexander-University of Erlangen-Nuremberg, Schwabachanlage 6, 91054 Erlangen, Germany f Department of Gynecology and Obstetrics, Friedrich-Alexander-University Erlangen-Nuremberg, Universitätsstrasse 21-23, 91054 Erlangen, Germany g Department of Obstetrics and Gynecology, University of Aachen Medical Center, Pauwelsstrasse 30, 52074 Aachen, Germany article info Article history: Received 22 December 2014 Accepted 28 March 2015 abstract Patients with essential hypertension may show neurovascular compression (NVC) at the rostral ventro- lateral medulla oblongata (RVLM). Ectatic loops of the vertebral artery (VA) or the inferior posterior cere- bellar artery (PICA) cause NVC. This study aims to show the existence and morphology of NVC in patients with gestation-induced hypertension. 17 females were prospectively examined between 19 + 0 and 35 + 6 weeks of gestation. 3 patients with chronic hypertension (group A), 10 patients with preeclampsia (group B), 3 patients with superimposed preeclampsia (chronic hypertension with preeclampsia; group C) and one normotensive patient were included. Groups B and C represented patients with gestation-in- duced hypertension. All 17 patients underwent imaging by high resolution magnetic resonance imaging (MR-CISS, constructive interference in the steady state). Image processing was done with segmentation and three-dimensional (3D)-visualization was implemented with direct volume rendering of the individ- ual neurovascular details of each patient. 9 of 17 patients (53%) showed NVC of the RVLM. Right-sided NVC was seen in 7 patients (41%). Left-sided NVC was seen in 6 patients (35%). Bilateral NVC was seen in 4 patients (24%). NVC was missing in 8 of the examined 17 patients (47%). The existence of NVC with high-resolution MRI was analyzed in gestation-induced hypertensive pregnant females for the first time. Neurovascular conflicts were seen in hypertensive pregnants. It is possible that NVC is potentially associ- ated in patients with gestation-induced hypertension. Ó 2015 Elsevier Ltd. All rights reserved. Introduction NVC at the RVLM caused by atherosclerotic and elongated loops of the VA and PICA may result in hypertension [1–4]. Pulsatile stimulation of the root entry/exit zones (REZ) of cranial nerves (CN) IX and X, which are localized within the RVLM, can induce an increase of sympathotonic output [5–7]. A normalization of blood pressure (BP) levels can be achieved with microvascular decompression of the affected neurovascular conflict [8,9]. Former works showed a correlation of sympathetic activity and an increase of BP in patients with preeclampsia [7]. The rate of sympathetic activity in preeclampsia is three-times higher than in normotensive pregnants and is four-times higher compared to non-pregnant hypertensive females [10]. Preeclampsia is a risk fac- tor for hypertension, coronary heart disease and stroke [11–16]. The patient with preeclampsia can also develop hypertension after delivery based on the association with NVC [17–20]. The blood volume is raised about 20–30% during the 2nd trimester and the cerebral perfusion pressure is elevated within the anterior cerebral artery and the posterior cerebral artery in hypertensive pregnant females [21–25]. The boosted filling of vessels and the increased intravascular pressure may lead to an elongation of the vessel walls and promote the development of NVC at the medulla oblongata [9,12,26]. The decline of hypertension in the postpartal period can be explained by a regression of blood volume of the intracranial vessels and NVC diminishes 6–8 weeks after delivery [10,27]. Currently, the most popular theory explaining the pathogenesis of pre-eclampsia http://dx.doi.org/10.1016/j.mehy.2015.03.024 0306-9877/Ó 2015 Elsevier Ltd. All rights reserved. ⇑ Corresponding author at: Department of Neurosurgery, Pauwelsstrasse 30, 52074 Aachen, Germany. Tel.: +49 241 80 88486; fax: +49 241 80 82410. E-mail address: ltanrikulu@ukaachen.de (L. Tanrikulu). Medical Hypotheses 84 (2015) 605–610 Contents lists available at ScienceDirect Medical Hypotheses journal homepage: www.elsevier.com/locate/mehy