Neurovascular Decompression of the Rostral Ventrolateral Medulla Decreases Blood Pressure and Sympathetic Nerve Activity in Patients With Refractory Hypertension

Sasaki, Susumu; Tanda, Shuji; Hatta, Tsuguru; Morimoto, Satoshi; Takeda, Kazuo; Kizu, Osamu; Tamaki, Shinji; Saito, Mitsuru; Tamura, Yoji; Kondo, Akinori

doi:10.1111/j.1751-7176.2011.00522.x

Cited by 21 publications

(17 citation statements)

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“…Több, hypertoniás betegek körében végzett vizsgálatban a plazma noradrenalinszintje igazolt NVC esetén magasabb volt a kontrollcsoporthoz képest [8,9]. Japán munkacsoport 4, NVC miatt műtött betegnél műtét után a vérnyomáscsökkenés mellett a n. tibialis szimpatikus aktivitásának csökkené-sét, a vizelet adrenalinszintjének csökkenését igazolta a műtét előtti értékhez képest [10].…”

Section: Esetismertetésunclassified

Neurovascular compression of the medulla oblongata, case report. The rare cause of secondary hypertension

et al. 2014

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A nyúltvelő bal ventrolateralis részének kompressziója a terápiarezisztens hypertonia okaként ritkán diagnosztizált eltérés. A neurovascularis kompresszió okozta hypertonia gyógyszerre nem reagáló eseteiben dekompressziós műtét végzése jön szóba. A 20 éves férfi betegnél a hypertonia hátterében meghúzódó okot a szekunder hypertonia egyéb lehetőségeinek kizárása, a MR-angiográfi ával igazolt neurovascularis kompresszió és a vérnyomáskiugrások alatt jelentkező fokozott szimpatikus aktivitás (sinus tachycardia) bizonyította. Ismételten jelentkező hypertoniás kríziseket követően műtétre került sor, amely során a bal arteria vertebralis és az agytörzs közé izomgraft behelyezése történt. A beteg a műtét után hat hónapig panaszmentes volt, a vérnyomáscsökkentő gyógyszereket jelentősen csökkenteni lehetett, a koponya MR-angiográfi a is a nyúltvelői kompresszió megszűnését mutatta. Hat hónap után a vérnyomás-kiugrások újra jelentkeztek, bár ritkábban és kisebb mértékben. A műtét után 22 hónappal készült koponya MR-angiográfi a lelete alapján a betegnek reoperációt javasoltak. Szakirodalmi adatok alapján dekompressziós műtét után hosszú távon fennmaradó kedvező hatás csak az esetek harmadában várható. A betegek nagyobbik hányadában a műtét a vérnyomás csökkenéséhez, a vérnyomáscsökkentő terápia kifejezettebb hatásához, a vérnyomáskiugrással járó rosszullétek ritkulásához és ezzel a betegek életminőségének javulásához vezethet. A beteg története ez utóbbi kór-lefolyást példázza. Orv. Hetil., 2014, 155(21), 838-842.Kulcsszavak: szekunder hypertonia, neurovascularis kompresszió, dekompressziós műtét Neurovascular compression of the medulla oblongata, case report The rare cause of secondary hypertensionCompression of the rostral ventrolateral medulla oblongata is one of the rarely identifi ed causes of refractory hypertension. In patients with severe, intractable hypertension caused by neurovascular compression, neurosurgical decompression should be considered. The authors present the history of a 20-year-old man with severe hypertension. After excluding other possible causes of secondary hypertension, the underlying cause of his high blood pressure was identifi ed by the demonstration of neurovascular compression shown by magnetic resonance angiography and an increased sympathetic activity (sinus tachycardia) during the high blood pressure episodes. Due to frequent episodes of hypertensive crises, surgical decompression was recommended, which was performed with the placement of an isograft between the brainstem and the left vertebral artery. In the fi rst six months after the operation, the patient's blood pressure could be kept in the normal range with signifi cantly reduced doses of antihypertensive medication. Repeat magnetic resonance angiography confi rmed the cessation of brainstem compression. After six months periodically increased blood pressure returned, but in smaller extent and less frequent. Based on the result of magnetic resonance angiography performed 22 months after surgery, re-operation was considerd. Accor...

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Section: Esetismertetésunclassified

Neurovascular compression of the medulla oblongata, case report. The rare cause of secondary hypertension

et al. 2014

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“…Ten of 12 patients experienced reduction in systolic blood pressure of more than 20 mm Hg. Sasaki et al 35 decompressed the RVLM in 4 patients with refractory hypertension. All 4 patients had decreased sympathetic nerve activity after the decompression and normalization of blood pressure without any antihypertensive medication.…”

Section: 43mentioning

confidence: 99%

“…Compression of this center might yield a heightened sympathetic tone, leading to AH. 2,7,12,25,29,35 Jannetta et al [17][18][19] demonstrated that microvascular decompression (MVD) of the RVLM could normalize or improve a raised blood pressure. Because the RVLM is close to the origin of the facial nerve, vessel loops originating from the vertebral/basilar arteries might be responsible for multiple neurovascular compressions (NCs), inducing both hemifacial spasms (HFSs) and AH.…”

Section: 14mentioning

confidence: 99%

Hypertension in patients with cranial nerve vascular compression syndromes and comparison with a population-based cohort

Sandell

Holmen

Eide

2013

JNS

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Object. Although essential arterial hypertension (AH) represents a major health issue, its underlying causes remain unknown. An intriguing hypothesis is that AH in some cases may be caused by vascular compression of the rostral ventrolateral medulla (RVLM). Because hemifacial spasms (HFSs) are caused by vascular compression of the seventh cranial nerve in close proximity to the RVLM, one would, if this hypothesis is correct, expect to find a positive association between the occurrence of AH and chronic HFSs. Such a positive association would not be expected in patients with trigeminal neuralgia (TN), since TN is caused by vascular compression of the fifth cranial nerve, which is not close to the RVLM.Methods. In view of this background, the authors conducted a retrospective population-based study to investigate how the occurrence of AH in patients with either HFSs or TN compares with the prevalence of AH in the general population, when adjusted for sex and age. The general population was represented by participants of the NordTrøndelag Health Study 3 (HUNT3).Results. The prevalence of AH in the authors' patients with HFSs was significantly higher than in a sex-and age-adjusted sample from the general population; this was not true for the patients with TN.Conclusions. The authors suggest that the data provide supporting evidence to the theory that compression of the RVLM may be one cause of AH. (http://thejns.org/doi/abs/10.3171/2013.7.JNS13231) Key WordS • arterial hypertension • essential hypertension • hemifacial spasm • trigeminal neuralgiaAbbreviations used in this paper: AH = arterial hypertension; CI = confidence interval; HFS = hemifacial spasm; HUNT3 = Nord-Trøndelag Health Study 3; MRA = MR angiography; MVD = microvascular decompression; NC = neurovascular compression; OR = odds ratio; RVLM = rostral ventrolateral medulla; TN = trigeminal neuralgia.

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“…This concept has been confirmed by autopsy, MRI, intraoperative observation, and animal studies. 5 MRI, computed tomography, and angiography have been used to assess neurovascular compression of the RVLM. To date, MRI is the most effective method for studying details of the brainstem and the surrounding vessels involved in neurovascular compression because of its noninvasiveness and sensitiveness.…”

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confidence: 99%

One Cause of Secondary Hypertension

et al. 2016

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A 37-year-old woman was referred to us with a 20-year history of hypertension. She was examined by cardiologists for secondary hypertension. Results from blood tests including renin-angiotensin-aldosterone system and catecholamine were normal, and computed tomography of the abdomen was also normal. Her blood pressure (BP) was 190/120 mm Hg despite combination therapy with amlodipine 10 mg, olmesartan 40 mg, doxazosin 4 mg, diltiazem 100 mg, spironolactone 25 mg, indapamide 2 mg, bisoprolol 5 mg, and guanabenz 4 mg. MRI of the brain showed that the left vertebral artery (VA) was obviously compressing the left medulla oblongata ( Figure C), and a presumptive diagnosis of refractory neurogenic hypertension was made. To ensure our diagnosis, an angiographic examination was performed for preoperative evaluation under direct measurement of arterial pressure. Angiography showed marked contortion of the left VA to the medial side ( Figure A). Straightening the left VA with a guidewire to relieve the compression of the medulla decreased her BP ( Figure B). The effect of BP lowering continued for 24 hours, but her BP gradually increased again. Taking the successful angiographic evaluation into consideration, neurovascular decompression through a left lateral suboccipital approach was performed. The medulla oblongata was obviously compressed by the left VA, and the left VA was lifted up to separate it from the medulla by using Teflon tape. The patient's BP was significantly decreased immediately after surgery. Postoperative MRI showed that the left VA was apart from the medulla ( Figure D). Her BP decreased to a normal range without any medications. The patient was monitored for 1 year, and her BP still remained within a normal range.Hypertension is a major risk factor for heart disease, stroke, congestive heart failure, and kidney disease. Approximately 90% patients are classified as having essential hypertension when no obvious underlying medical cause is identified. Physicians believe that 5% to 30% of the overall hypertensive population have refractory hypertension.1 Previous research suggests that ≈20% of patients with essential hypertension have an underlying neurogenic etiology resulting in refractory hypertension.2 Vascular compression of the brainstem at the level of the rostral ventrolateral medulla (RVLM) has been suggested as 1 cause of secondary hypertension. 3 RVLM is a major cardiovascular center that regulates systemic control of blood pressure. RVLM contains neurons that are the major tonic source of supraspinal sympathoexcitatory outflow to the heart, kidneys, and vessels. Arterial pulsatile of the RVLM seems to enhance sympathetic nerve activities, which could contribute to refractory hypertension. Jannetta et al 4 introduced the concept of neurogenic hypertension caused by neurovascular compression of the left RVLM. They reported that vascular decompression of the RVLM could normalize high BP. This concept has been confirmed by autopsy, MRI, intraoperative observation, and animal studies.5 MRI, comput...

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Neurovascular Decompression of the Rostral Ventrolateral Medulla Decreases Blood Pressure and Sympathetic Nerve Activity in Patients With Refractory Hypertension

Cited by 21 publications

References 8 publications

Neurovascular compression of the medulla oblongata, case report. The rare cause of secondary hypertension

Neurovascular compression of the medulla oblongata, case report. The rare cause of secondary hypertension

Hypertension in patients with cranial nerve vascular compression syndromes and comparison with a population-based cohort

One Cause of Secondary Hypertension

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