Accepted Manuscript Successful treatment by microvascular decompression surgery of a patient with hemiparesis due to vertebral artery compression of the medulla oblongata: A case report and literature review Jibin Ren, Hongtao Sun, Yunfeng Diao, Xuegang Niu, Hang Wang, Zhengjun Wei, Fei Yuan PII: S1878-8750(17)31520-6 DOI: 10.1016/j.wneu.2017.09.016 Reference: WNEU 6460 To appear in: World Neurosurgery Received Date: 19 May 2017 Revised Date: 1 September 2017 Accepted Date: 2 September 2017 Please cite this article as: Ren J, Sun H, Diao Y, Niu X, Wang H, Wei Z, Yuan F, Successful treatment by microvascular decompression surgery of a patient with hemiparesis due to vertebral artery compression of the medulla oblongata: A case report and literature review, World Neurosurgery (2017), doi: 10.1016/j.wneu.2017.09.016. This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. ACCEPTED MANUSCRIPT Successful treatment by microvascular decompression surgery of a patient with hemiparesis due to vertebral artery compression of the medulla oblongata: A case report and literature review Wei1, Fei Yuan3* 1 The Sixth Department of Neurosurgery, Affiliated Hospital of Armed Police Forces Logistical College, Tianjin, 300162, China Postgraduate Training Base in Affiliated Hospital of Logistics University of People’s SC 2 RI PT Jibin Ren1,2#, Hongtao Sun1#*, Yunfeng Diao1, Xuegang Niu2, Hang Wang1, Zhengjun Armed Police Forces, Jinzhou Medical University, Jinzhou, 121000, China Department of Radiology, Affiliated Hospital of Armed Police Forces Logistical College, Tianjin, 300162, China # M AN U 3 These two authors contribute equally to this work. * Corresponding authors TE D Hongtao Sun, the Sixth Department of Neurosurgery, Affiliated Hospital of Armed Police Forces Logistical College, No. 220, Chenglin Road, Hedong district, Tianjin, 300162, China; Tel: 022-60577142; E-mail: sunhongtao_2015@163.com EP Fei Yuan, Department of Radiology, Affiliated Hospital of Armed Police Forces AC C Logistical College, No. 220, Chenglin Road, Hedong district, Tianjin, 300162, China Running title: hemiparesis due to vertebral artery compression ACCEPTED MANUSCRIPT Abstract Little literature is available on hemiparesis caused by vascular medullary compression, which may occur as a result of dolichoectasia of the vertebrobasilar RI PT arterial system. In this paper, we report a case of vertebral artery compression of the medulla oblongata in a 67-year old woman. The patient was hypertensive and SC developed hemiparesis and intermittent spasms for five years, which became worsened for one year. Cranial nerve MRI showed compression of the medulla M AN U oblongata by the left vertebral artery. Motor evoked potential (MEP) examination showed abnormal conduction of MEPs of bilateral toe abductors. The patient underwent microvascular decompression surgery under general anesthesia via the retrosigmoid keyhole approach, which led to relief of vascular compression and TE D symptomatic improvement. Our case suggests that detailed history, imaging studies and electrophysiological studies help lead to a correct and early diagnosis of EP hemiparesis due to vascular compression of the rostral ventrolateral medulla. MVD surgery improves patient symptoms and intraoperative electrophysiological AC C monitoring helps avoid injury to important adjacent nerves. Key words: hemiplegia; microvascular decompression; medulla oblongata; vascular compression; primary hypertension; literature review ACCEPTED MANUSCRIPT Introduction Cranial neuralgias are characterized by pain in the distribution of a cranialnerve. Pain arising from cranial neuralgias can be severe and often poses a significant health RI PT burden to the patient. Vascular compression against a cranial nerve has been widely accepted as a main cause of cranial neuralgias [1] and may be an underlying cause of SC trigeminal neuralgia, hemifacial spasm, gloss pharyngeal neuralgia, or other cranial neuralgias[2]. Vascular compression of the medulla oblongata may occur as a result M AN U ofdolichoectasia of the vertebrobasilar arterial system or rarely due to the tortuous course of an intracranial vessel, which may cause primary hypoglossal nerve palsy[3], hypertension[4], dysphagia, dysarthria, gait ataxia, quadriplegia and other symptoms[5-9]. Other documented contributory vascular anomalies include a TE D fusiform aneurysm[10] and a persisting trigeminal artery[11]. Little literature is available on hemiparesis caused by vascular medullary EP compression. In 1985, Kim et al. described the first case of progressive left hemiparesis due to vascular compression of the medulla oblongata, which was AC C relieved by microvascular decompression (MVD)[12]. Since then, only anecdotal cases have been reported. In this paper, we report a case of vertebral artery compression of the medulla oblongata which caused hemiparesis and possibly primary hypertension. The patient was successfully managed by MVD, which helped relieve the symptoms. A literature review was also undertaken of 15 patients with vascular medullary compression that had resulted in hemiparesis or quadriparesis. ACCEPTED MANUSCRIPT Case Report A 67-year old female patient was admitted to our hospital in March 3, 2016because of worsening of right limb weakness and intermittent spasms for one RI PT year. In January, 2011, the patient began experiencing weakness of the right upper and lower extremities and intermittent spasms for no obvious reason. The onset of SC weakness of the upper extremity preceded that of the lower limb and limb weakness became gradually worsened over time. The patient did not seek treatment because of M AN U its insidious course. In February, 2015, limb weakness became noticeably exacerbated without any apparent causes and interfered with her daily activities. The patient had a 15-year history of hypertension, with the highest blood pressure at 180/110 mmHg. She took oral nifedipine sustained release tablets (30 mg, 2 times/day), and irbesartan TE D (0.15 g, once daily) and her blood pressure declined to 140/100 mmHg. A head MRI scan at a local hospital suggested white matter atrophy, and cervical MRI and head CT EP scan showed ossification of posterior longitudinal ligament, cervical spinal stenosis, and cervical spondylotic myelopathy. AC C The patient sought treatment at our hospital on March 3, 2016. The patient was alert. Physical examination revealed no deformity of the spine. Mild tenderness was noticed at the C4-C7 spinouts process. There was no irradiating pain in both the upper and lower extremities. The muscle power of the right upper and lower extremities was grade 4and that of the left upper and lower extremities was normal. Both lower limbs had no deformity and no muscle atrophy. The right limb muscle tone was slightly increased while the left limb muscle tone was normal. The biceps and triceps reflex ACCEPTED MANUSCRIPT were hyperactive, and right Hoffmann’s sign was positive (+). The knee tendon reflex and Achilles tendon reflex were hyperactive, and right Babinskis sign was positive (+). RI PT On admission, hypertension (160/100mmHg) was noted. Cranial nerve MRI showed compression of the medulla oblongata by the left vertebral artery (Figure 1). Brainstem auditory evoked potential (BAEP) examination revealed bilateral normal SC conduction from the auditory nerve to the brainstem. Somatosensory evoked potential M AN U (SEP) examination showed normal conduction of deep sensation from bilateral upper extremities to the cortex, but abnormal conduction from the lumbar spinal cord to the cortex [criteria for abnormal SEPs: N13–N20, >6.5 ms; P14–N20, >5.5 ms; interside latency (either N13–N20 or sCCT), >1.5 ms] while peripheral conduction was normal. TE D Motor evoked potential (MEP) examination showed abnormal conduction [criteria for abnormal MEPs: mCCT of >6.5 ms and mCCT interside latency of >1 ms (abductor pollicis brevis); mCCT of >15 ms and mCCT interside latency of >2.3 ms (tibialis EP anterior)] of MEPsof bilateral toe abductors, especially the right toe abductor. The AC C patient received an admission diagnosis of vascular medullary compression syndrome (right hemiparesis). The patient underwent MVD under general anesthesia via the retro sigmoid keyhole approach. At the same time, the use of electrophysiological monitoring, assures the safety of the operation. The cranial content was explored from the lateral cerebellum to the left vertebral artery under the microscope. The left vertebral artery was found to be ectatic(the diameter of the vertebral artery was greater than 4.5 mm) and tortuous, ACCEPTED MANUSCRIPT forming an angle and compressing the medulla oblongata with an obvious indentation. The intraoperative findings confirmed preoperative cranial nerve MRI findings (Figure 2). The left vertebral artery was determined to be the culprit vessel, and was RI PT separated from the medulla oblongata by inserting soft Teflon felt for full decompression. The operation was uneventful, with no active bleeding. Intermittent spasms of the right extremities disappeared postoperatively, and limb weakness was SC gradually eased. One month after the discharge from the hospital, cranial nerve MRI M AN U showed no compression of the medulla (Figure3).At the 6-month follow up visit, arterial pressure was 130/80 mmHg; irbesartan was discontinued and oral nifedipine was reduced to 30 mg, once daily. At the 12-month followed up visit, right limb weakness was noticeably relieved, and the muscle power was grade 5- and no spasms TE D recurred. Blood pressure was well controlled within the normal range. (The video episode for the surgery is available here). EP Discussion AC C In the current report, we have described a case of hemiparesis due to compression of the medulla oblongata by an ectatic and tortuous vertebral artery. The patient was also hypertensive, highlighting a role of the rostral ventrolateral medulla in medicating central pressor response. Hemiparesis and hypertension of the patient were markedly attenuated with successful MVD surgery. Vascular compression of the brainstem, even with severe distortion, is rarely associated with overt clinical manifestations though subtle subclinical dysfunctions ACCEPTED MANUSCRIPT may be frequently present. So far, fewer than twenty cases of vascular medulla compression syndrome have been reported that had overt hemiparesis or quadriparesis (Table 1). Vascular medullary compression is more common in the vicinity of the RI PT pyramidal decussation and is often unilateral. Among these anecdotal cases, ten cases including the current case (10/19, 52.6%) had an anomalous left vertebral artery including an ectatic and tortuous left vertebral artery or an elongated and curved left SC vertebral artery. In four cases (4/19, 21.1%), both left and right vertebral arteries were M AN U involved. The right vertebral artery was less frequently involved (5/19, 26.3%). Interestingly, thrombosis was demonstrated in the right vertebral artery in both cases. The culprit vessel(s) compresses against the corticospinal tract superior to the medulla oblongata, impairing neural conduction at the compression site, and at the same time TE D compromising hemodynamics, leading to regional medulla ischemia and contralateral hemiparesis. In the previous literature, unilateral paralysis, contralateral paralysis and even bilateral paralysis may have a certain relationship between the occurrence of EP paralysis and the site of vascular compression of the medulla oblongata. Pyramidal AC C decussation may be an important site of vascular compression, which is related to paralysis. It is speculated that vascular compression of the medulla oblongata may have caused local anatomical changes, such as reduction in blood flow or distortion and regurgitation in some perforators caused by pressure on perforating branches of the vertebral artery[13]. Our patient had a history of cervical spondylotic myelopathy, which may also cause hemiparesis. However, when severe compression of the spinal cord occurs, cervical ACCEPTED MANUSCRIPT spondylotic myelopathy can cause injury to the corticospinal tract and anterior horn neurons. Furthermore, sensory abnormalities below the level of lesions are present on top of paralysis or paraplegia. The current case had no sensory abnormalities below RI PT the level of lesions. The nerve fibers controlling the upper extremities are located laterally while those controlling the lower extremities are located medially in the corticospinal tract superior to the pyramidal decussation. The culprit vessel SC compresses the lateral surface of the medulla oblongata, involving the lateral nerve M AN U fibers in the corticospinal tract first, thus causing the appearance of symptoms in the upper limb to precede that of the lower limb. This is consistent with the disease pattern in our patient; therefore, the patient's hemiplegic symptoms were not likely caused by cervical spondylotic myelopathy, but rather due to vascular compression of TE D the rostral ventrolateral medulla. Furthermore, there was no parenchymal lesion of the medulla and the course of symptoms and signs in our patient was insidious; these together implicate direct mechanical compression rather than ischemia as a possible EP cause of the clinical findings. AC C Detailed preoperative neurological examination including electrophysiological studies, high-resolution MRI scans, and angiographic studies are important for a prompt and correct diagnosis of vascular medullary compression syndrome, as illustrated in our current case. MEP allows examination of conduction from the cortex to the muscles, shedding light on the synchronicity and integrity of the corticospinal tract. We documented abnormal conduction of MEPs of bilateral toe abductors, especially the right toe abductor, lending further support to the diagnosis of vascular medulla ACCEPTED MANUSCRIPT compression syndrome. There has not been a consensus on the treatment of vascular medullary compression syndrome. It has been reported that microvascular compression can be RI PT relieved by MVD surgery, resulting in symptomatic improvements. Our patient showed moderate improvement following MVD surgery. Electrophysiological monitoring was undertaken intraoperatively, which has the advantage of ensuring the SC safety of adjacent cranial nerves, greatly increasing the feasibility and safety of MVD M AN U surgery. Vascular medullary compression syndrome patients are also managed conservatively such as with anti-platelet drugs and anticoagulants or analgesics. Currently, there is lack of clinical evidence on whether MVD leads to a superior outcome compared with conservative therapy. Different from our surgical approach, TE D Choudhri et al. [14] and Lin et al. [15]used a sling technique to tether the vertebrobasilar artery aneurysm with the help of clips to the cliva dura for macrovascular decompression. The technique achieved anteromedial transposition of EP the vertebrobasilar artery aneurysm from an inferolateral surgical approach with sling AC C fixation to the clival dura using aneurysm clips, which may be worthwhile for further exploring for use in macrovascular decompression. Given the role of the rostral ventrolateral medulla in medicating central pressor response, vascular compression of the rostral ventrolateral medulla has been reported to be associated with refractory hypertension[16]. Jannetta et al. hypothesized that vascular compression of the left root entry zone of the gloss pharyngeal and vagus nerves by looping arteries may play an important role in the pathogenesis of essential ACCEPTED MANUSCRIPT hypertension[2].The rostral ventrolateral medulla is a major centre of the sympathetic system and is implicated in regulating the cardiovascular system. Vascular ventrolateral medulla compression was also documented in hemifacial spasm[17-19] RI PT patients with arterial hypertension than without arterial hypertension. Our patient also had hypertension, which was partially relieved following MVD surgery. In conclusion, detailed history, imaging studies and electrophysiological studies SC help lead to a correct and early diagnosis of hemiparesis due to vascular compression M AN U of the rostral ventrolateral medulla. MVD surgery relieves vascular compression and improves patient symptoms and intraoperative electrophysiological monitoring helps Acknowledgement TE D avoid injury to important adjacent nerves. EP This study is supported by The Key Projects of the Seeding Fund of the Affiliated AC C Hospital of Armed Police Forces Logistical College (No.FYZ201604). ACCEPTED MANUSCRIPT References 1. RI PT 2. Moller AR: The cranial nerve vascular compression syndrome: II. A review of pathophysiology. Acta neurochirurgica 1991, 113(1-2):24-30. Jannetta PJ: Outcome after microvascular decompression for typical trigeminal neuralgia, hemifacial spasm, tinnitus, disabling positional vertigo, and glossopharyngeal neuralgia (honored guest lecture). Clinical neurosurgery 1997, 44:331-383. Kuroi Y, Tani S, Ohbuchi H, Kasuya H: Microvascular decompression for hypoglossal nerve palsy secondary to vertebral artery compression: A case report and review of the literature. Surgical neurology international 2017, 8:74. Hanggi D, Steiger HJ: Symptomatic vertebral artery conflicts to the medulla oblongata and microsurgical treatment options: review of the literature. Neurosurgical review 2009, 32(2):143-148; discussion 148-149. Hongo K, Nakagawa H, Morota N, Isobe M: Vascular compression of the medulla oblongata by the vertebral artery: report of two cases. Neurosurgery 1999, 45(4):907-910. Nakahara Y, Kawashima M, Matsushima T, Kouguchi M, Takase Y, Nanri Y, Yakusiji Y: Microvascular decompression surgery for vertebral artery compression of the medulla oblongata: 3 cases with respiratory failure and/or dysphagia. World neurosurgery 2014, 82(3-4):535 e511-536. Ozcan TA, Meral H, Ulukok MD, Serce AG, Yucel G: A case of vocal cord paralysis secondary to vertebral artery dolichoectesia: a rare presentation. Turkish neurosurgery 2013, 23(5):688-689. Schobel HP, Frank H, Naraghi R, Geiger H, Titz E, Heusser K: Hypertension in patients with neurovascular compression is associated with increased central sympathetic outflow. Journal of the American Society of Nephrology : JASN 2002, 13(1):35-41. Ubogu EE, Chase CM, Verrees MA, Metzger AK, Zaidat OO: Cervicomedullary junction compression caused by vertebral artery dolichoectasia and requiring surgical treatment. Case report. Journal of neurosurgery 2002, 96(1):140-143. Shiraishi S, Takahashi M, Watanabe M, Tsuchida M: Surgical repair of aortico-left ventricular tunnel: report of two cases. Asian cardiovascular & thoracic annals 2013, 21(1):67-70. Okanishi T, Saito Y, Miki S, Nagaishi J, Hanaki K, Tomita Y, Fukuda C, Fujii S, Fujiwara K, Kawamoto K et al: Lower brainstem dysfunction in an infant with persistent primitive trigeminal artery. Brain & development 2007, 29(3):189-192. Kim P, Ishijima B, Takahashi H, Shimizu H, Yokochi M: Hemiparesis caused by vertebral artery compression of the medulla oblongata. Case report. Journal of neurosurgery 1985, 62(3):425-429. Hongo K, Kobayashi S, Hokama M, Sugita K: Vertebral artery section for treating arterial compression of the medulla oblongata. Case report. Journal of neurosurgery 1993, 79(1):116-118. Choudhri O, Connolly ID, Lawton MT: Macrovascular Decompression of the 3. SC 4. M AN U 5. 6. 8. 9. AC C 10. EP TE D 7. 11. 12. 13. 14. ACCEPTED MANUSCRIPT 19. 20. 21. 22. 23. RI PT AC C 24. SC 18. M AN U 17. TE D 16. EP 15. Brainstem and Cranial Nerves: Evolution of an Anteromedial Vertebrobasilar Artery Transposition Technique. Neurosurgery 2017, 81(2):367-376. Lin CF, Chen HH, Hernesniemi J, Lee CC, Liao CH, Chen SC, Chen MH, Shih YH, Hsu SP: An easy adjustable method of ectatic vertebrobasilar artery transposition for microvascular decompression. Clinical neurology and neurosurgery 2012, 114(7):951-956. Ishikawa T, Nagayama M, Iida M, Shinohara Y: [Bulbovascular compression by megadolichobasilar artery manifested as neurogenic and refractory hypertension]. Rinsho shinkeigaku = Clinical neurology 2004, 44(6):359-364. Chan LL, Lee E, Fook-Chong S, Tan EK: Case control MR-CISS and 3D TOF MRA imaging study of medullary compression and hypertension in hemifacial spasm. Movement disorders : official journal of the Movement Disorder Society 2008, 23(13):1820-1824. Morimoto S, Sasaki S, Miki S, Kawa T, Itoh H, Nakata T, Takeda K, Nakagawa M, Kizu O, Furuya S et al: Neurovascular compression of the rostral ventrolateral medulla related to essential hypertension. Hypertension 1997, 30(1 Pt 1):77-82. Rudzinska M, Wojcik-Pedziwiatr M, Malec-Litwinowicz M, Grabska N, Hartel M, Flak M, Szczudlik A: Is hypertension a risk factor of hemifacial spasm? Neurologia i neurochirurgia polska 2016, 50(2):69-74. Dembo T, Tanahashi N: Opalski syndrome caused by vertebral artery compression of the lateral surface of the medulla oblongata. Internal medicine 2013, 52(10):1115-1120. Kobayashi T, Ogawa A, Kameyama M, Uenohara H, Yoshimoto T: Chiari malformation with compression of the medulla oblongata by the vertebral arteries. Case report. Journal of neurosurgery 1992, 77(2):307-309. Takano S, Saitoh M, Miyasaka Y, Fujii K, Takagi H: [A case report of hemiparesis due to compression of the medulla oblongata by an elongated vertebral artery]. No shinkei geka Neurological surgery 2001, 29(3):247-251. Tomasello F, Alafaci C, Salpietro FM, Longo M: Bulbar compression by an ectatic vertebral artery: a novel neurovascular construct relieved by microsurgical decompression. Neurosurgery 2005, 56(1 Suppl):117-124; discussion 117-124. Sadashiva N, Shukla D, Bhat DI, Devi BI: Vertebral artery dolicoectasia with brainstem compression: role of microvascular decompression in relieving pyramidal weakness. Acta neurochirurgica 2016, 158(4):797-801. Salvi F, Mascalchi M, Bortolotti C, Meletti S, Plasmati R, Rubboli G, Stecchi S, Villari N, Calbucci F, Tassinari CA: Hypertension, hyperekplexia, and pyramidal paresis due to vascular compression of the medulla. Neurology 2000, 55(9):1381-1384. Koyama S, Maeda T, Komine A: [Medulla and upper cervical cord compression by bilateral vertebral artery presented with myelopathy and drop attack: case report]. No to shinkei = Brain and nerve 2002, 54(5):435-439. Maruyama K, Tanaka M, Ikeda S, Tada T, Yanagisawa N: [A case report of quadriparesis due to compression of the medulla oblongata by the elongated left vertebral artery]. Rinsho shinkeigaku = Clinical neurology 1989, 29(1):108-111. Murata H, Waga S, Kojima T, Shimizu T, Shimizu S: [Medulla oblongata compression 25. 26. 27. 28. ACCEPTED MANUSCRIPT AC C EP TE D M AN U SC RI PT 29. by tortuous vertebral artery: case report]. No shinkei geka Neurological surgery 1995, 23(4):349-353. Kamada T, Tateishi T, Yamashita T, Nagata S, Ohyagi Y, Kira J: [A case of medulla oblongata compression by tortuous vertebral arteries presenting with spastic quadriplegia]. Rinsho shinkeigaku = Clinical neurology 2013, 53(5):356-361. ACCEPTED MANUSCRIPT RI PT Table 1 Clinical characteristics of reported cases of quadriparesis or hemiparesis due to vascular compression against the medulla oblongata Patient No. Age, years /gender Kim et al.[12] 1 53/M Progressive hemiparesis,CN XII left the left vertebral artery Dembo et al.[20] 2 55/M vertigo, nystagmus, and gait ataxia followed by left hemiparesis (Opalski syndrome); hypertension (164/104 mmHg) The left vertebral artery Kobayashi 3 39/F Hemiparesis 4 61/M consciousness disturbances, left hemiplegia, and Imaging studies Metrizamide computerized tomography cisternography reveals that the left vertebral artery compresses and distorts the left lateral surface of the medulla T2W MRI and diffusion tensor imaging; Magnetic resonance angiography (MRA) and 3-dimensional computed tomography angiography reveal a tortuous and dolichoectatic left vertebral artery MRI reveals Chiari malformation and compression of the medulla oblongata by both vertebral arteries CT, MRI and digital subtraction angiogram show partial M AN U TE D EP AC C et al.[21] Shiraishi et al.[10] Culprit vessel SC Authors bilateral vertebral arteries fusiform right vertebral artery aneurysm with Treatment Outcome MVD Improved Conservative treatment Recovered MVD following posterior fossa decompression Improved Intra-aneurysmal embolization Improved ACCEPTED MANUSCRIPT partial thrombosis severe occipital-nuchal headache and nausea with vomiting, left facial hyperalgesia, right hemihypesthesia and mild right hemiparesis, hoarseness, hypertension (180/100 mmHg) Dysphagia, weakness of left arm and both lower limbs Elongated and curved V4 portion of the left vertebral artery with normal diameter Left ectatic VA 5 53/F Tomasell o et al.[23] 6 58/M 7 55/F Dysphagia, weakness of the right limbs Right ectatic VA 8 67/M Weakness of bothupper and lower limbs Right ectatic VA 9 73/M 10 36/M Weakness of both upper and lower limbs left hemiparesis Improved N/A MVD Improved coronal T2-weighted MRI scan demonstrating a right ectatic VA with compression of the medulla oblon-gata axial T2-weighted MRI scan demonstrating a right ectatic VA with compression of the medulla oblon-gata N/A MVD Improved MVD Improved MVD Improved T2-weighted images showing compression of anterolateral medulla by ectatic vertebral artery MVD Cured M AN U TE D EP AC C Sadashiva et al.[24] with Guglielmi detachable coils MVD SC Takanoet al.[22] thrombosis and bulbar compression Coronal T2W MRI and metrizamide CT scan RI PT subsequent respiratory arrest Left ectatic VA, hypoplasia right VA Right ectatic VA ACCEPTED MANUSCRIPT 30/M Right hemiparesis, gait ataxia The left vertebral artery Hongo et al.[5] 12 36/M Right Hemiparesis The right vertebral artery Salvi et al. [25] 13 54/F Hypertension, hemiparesis The left vertebral artery Koyama et al.[26] 14 51/M Quadriparesis and unconsciousness, hyper-reflexia of his left lower extremity and moderate decrease of sense of pain, temperature, and tactile sensation in his left extremities and trunk bilateral vertebral artery Maruyam a et al.[27] 15 30/M gait disturbance and numbness of both arms and legs, mild MRI reveals a tortuous vertebral artery compressing the medulla oblongata MRI indicating a tortuous right vertebral artery that was causing severe indentation at the medulla RI PT 11 SC Hongo et al. [13] M AN U TE D EP AC C MRI showed impingement of the vertebral artery on the left lateral medulla MRI reveals a flow-void area in the craniocervical junction and marked narrowing of the medulla oblongata and upper cervical cord by compression of the vertebral arteries. CT myelography shows the compression and narrowing of the spinal cord. Vertebral angiography demonstrates symmetrical running course of the arteries, which curve medially at the level of craniocervical junction. CT and MRI scan show that the left vertebral artery extends from the left vertebral artery MVD Improved MVD Improved MVD Improved MVD Improved MVD Progressed after initial ACCEPTED MANUSCRIPT 58/F Kamada et al.[29] 17 58/M SC 16 progressive tetraparesis and bilateral vertebral arteries sensory disturbance, sensory disturbance in all modalities below the level of C2, onion-skin pattern sensory disturbance of the face, and motor weakness of the sternocleidomastoid muscles weakness of both legs and gait bilateral vertebral arteries disturbance, lower-limb-dominant spasticity in all four extremities, lower-limb weakness, hyperreflexia in all extremities with positive Wartenberg's, Babinski's and Chaddock's signs, mild hypesthesia and hypopallesthesia in both lower AC C EP TE D M AN U Murata et al.[28] the left side of the medulla oblongata to the midline and distorts it by compression. Vertebral angiography reveals that the elongated left vertebral artery crosses the ventral aspect of the medulla oblongata MRI and vertebral angiography demonstrate ventrolateral compression of the medulla oblongata by bilateral tortuous vertebral arteries. slight improvement RI PT right facial hemiatrophy, bilateral pyramidal tract signs, muscular weakness of all extremities predominant of the right side, spastic gait and sensory disturbance Brain MRI and magnetic resonance angiography demonstrated bilateral tortuous vertebral arteries compressing the medulla oblongata Suboccipital craniectomy, C1.4 laminectomy, and decompression of the medulla oblongata Neurovascular decompression of the right vertebral artery Improved Improved ACCEPTED MANUSCRIPT the left vertebral artery Cranial nerve MRI reveals a tortuous and dolichoectatic left vertebral artery compressing the medulla oblongata RI PT 67/F SC 19 an ectatic left vertebral artery M AN U The current report the left vertebral artery TE D 70/M EP 18 AC C Ubogu et al.[9] limbs, and spastic gait partial bilateral abduction paralysis progressing to quadriparesis, ataxia, and areflexia right hemiparesis and intermittent spasms; hypertension emergency posterior fossa neurovascular decompression MVD Mild improvement Improved ACCEPTED MANUSCRIPT Figure legends Figure 1 (A) MRA obtained on admission shows the tortuous left vertebral artery (Red arrow) and (B) transverse T1-weighted MR image demonstrates intimate RI PT relation between the medulla oblongata and the vertebral artery (Red arrow). VA: the vertebral artery. SC Figure 2 (A) and (C) Intraoperative view shows the vertebral artery and the medulla. M AN U (B) and (D) The corresponding schematic representation of (A) and (C). MO: the medulla oblongata; T: Teflon felt; VA: the vertebral artery. Figure 3 (A) Preoperative transverse T2-weighted MR image clearly shows compression of the medulla oblongata (MO) (Yellow arrow) by the vertebral artery TE D (VA) (Red arrow). (B) Postoperative transverse T2-weighted MR image reveals decompression of the medulla oblongata by the Teflon pad cotton (Blue arrow) AC C EP between the vertebral artery and the medulla oblongata. AC C EP TE D M AN U SC RI PT ACCEPTED MANUSCRIPT AC C EP TE D M AN U SC RI PT ACCEPTED MANUSCRIPT AC C EP TE D M AN U SC RI PT ACCEPTED MANUSCRIPT ACCEPTED MANUSCRIPT AC C EP TE D M AN U SC RI PT Highlights 1. Little literature is available on hemiparesis caused by vascular medullary compression. 2. In this paper, we report a case of vertebral artery compression of the medulla oblongata which caused hemiparesisand possibly primary hypertension. 3. The patient was successfully managed by MVD, which helped relieve the symptoms. ACCEPTED MANUSCRIPT Abbreviations Magnetic Resonance Imaging (MRI); Motor evoked potential (MEP); microvascular decompression (MVD); Brainstem auditory evoked potential (BAEP); Somatosensory AC C EP TE D M AN U SC RI PT evoked potential (SEP) ACCEPTED MANUSCRIPT Conflict of interest AC C EP TE D M AN U SC RI PT All the authors declare that they have no conflict of interest.