Unilateral internal carotid artery dissection with syncope as the first symptom

Unilateral internal carotid artery dissection with syncope as the first symptom | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Research Article Unilateral internal carotid artery dissection with syncope as the first symptom Junyang Xia, Xin Jiang, Haojun Pan, Peipei Liu This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-1573490/v1 This work is licensed under a CC BY 4.0 License Status: Posted Version 1 posted You are reading this latest preprint version Abstract Internal carotid artery dissection(ICAD) is a series of pathological processes caused by intimal tear of the internal carotid artery. Syncope refers to a transient loss of consciousness caused by transient global brain hypoperfusion. ICAD with syncope is rare. Here we present a case of unilateral ICAD with syncope as the first symptom. We also review the literature and discuss the pathogenesis of syncope in ICAD patients. The main message we want to convey to readers is that unilateral ICAD can have syncope as the first symptom, which should not be ignored in the differential diagnosis of syncope. Furthermore, the pathogenesis of syncope in ICAD is more likely to be that subintimal blood flow can easily increase the mechanical stretch of adventitia, stimulate the baroreceptors and cause hyperactive carotid sinus reflex. Figures Figure 1 Figure 2 Figure 3 1. Patient A 35-year-old male suddenly lost consciousness and fell to the ground when he was on the phone. About 30 seconds later, his consciousness improved. However, he still suffered from vomiting, sweating, and weakness of right limbs. About 2 hours later his symptoms were completely relieved. 3 hours later, he was admitted to a local hospital. His brain MRI and MRA conducted 5 hours after onset reported no obvious abnormalities. Then he received conservative treatment including aspirin and atorvastatin. 10 days later, he developed a sudden and severe headache in the left temporal and occipital. After about an hour of interval, the pain eased slightly though can be occasionally aggravated by coughing. Then, he was transferred to our hospital for further medical intervention. In his admission, neurological examination revealed right lingual palsy, as well as incomplete left Horner syndrome including unequal bilateral pupil diameters (the right pupil diameter was 4.0mm, the left pupil diameter was 2.0mm), drooping left eyelid, slightly sunken left eye ball and slightly congested left eyelid conjunctiva. His past medical history was unremarkable and he denied any recent trauma or massage of his neck. 24-hour electrocardiogram monitoring revealed no abnormality. When we reviewed his brain MRI conducted in the local hospital, intermural hematoma of the left internal carotid artery was found(Fig. 1 ). MRI reconducted in our hospital showed acute cerebral infarction in the left paraventricular area and left basal ganglia(Fig. 2 ). TOF-MRA revealed double-lumen sign from the initial segment to the cavernous sinus segment of the left internal carotid artery (Fig. 3 ). Based on the evidence above, diagnosis of left ICAD was established. Then, our patient received anticoagulation therapy. During the 3-month follow-up, syncope did not occur again and the symptoms did not worsen with a MRS score of 0. 2. Discussion Syncope is rare in ICAD cases. After searching and screening on Pubmed with "syncope" and "carotid artery dissection" as keywords, only three ICAD cases with syncope were found. Two of them are bilateral ICAD cases with syncope as the first symptom[1, 2]. The third case is a right ICAD patient with slurred speech and left hemiplegia at the time of onset reported by Dulay et al[3]. This patient had a history of vasovagal syncope and developed syncope caused by sinus arrest after hospitalization. Our patient, diagnosed with unilateral ICAD with syncope as the first symptom, was different from the above all. The first pathophysiological mechanism theory of syncope in ICAD is that ICAD causes vascular stenosis, restricts carotid blood flow, and thus induces transient hypoperfusion of cerebral hemispheres[1, 2]. However, many clinical cases have proved that unilateral internal carotid artery stenosis can not cause syncope[4]. Therefore, this “carotid blood flow restriction” theory is only applicable for bilateral ICAD, rather unilateral ICAD like our case. The second pathophysiological mechanism theory of syncope in ICAD is that ICAD induces arrhythmia and the following syncope by causing insular cortex stroke. The insula, especially the right insula, is involved in the autonomous control of heart activity[5–7]. When ischemic stroke affects the insular cortex, it may cause autonomic dysfunction, bradyarrhythmia and syncope[8]. No cerebral infarction was revealed in two of the ICAD cases with syncope[1, 2]. In the third ICAD case with syncope, acute cerebral infarction was only presented in the right posterolateral frontal lobe[3]. In our case, acute cerebral infarction just involved the left basal ganglia and the left lateral ventricle. All of the four cases did not support this “insular cortex stroke” theory. The third pathophysiological mechanism theory of syncope in ICAD was proposed by Dulay et al when describing their patient[3]. They believed that thrombosis in internal carotid artery caused sinus arrest as well as syncope by activating the carotid sinus reflex. If the thrombus blocks the initial segment of the carotid artery, the pressure on the carotid sinus baroreceptors should decrease. Therefore, this pathogenesis was negated by Sarikaya et al. [4]. In addition, in the case provided by Dulay et al., the temporal relationship between the ICAD and vasovagal syncope is unclear. In other words, the "history of vasovagal syncope" may appear after the onset of ICAD and be one of the clinical symptoms of the latter. At the initiation of carotid, when entering the junction of adventitial and media membranes, myelinated nerve fibers lose myelin, end up with abundant branches. These branches distribute in the inner layer of the adventitial membrane, forming the carotid sinus baroreceptors. By detecting changes in the degree of stretch on the blood vessel wall, baroreceptors in adventitial inner layer indirectly sense changes in blood pressure. Their nerve signals are transmitted up through Hering nerve (sinus nerve) and glossopharyngeal nerve to nucleus of solitary tract. Then transmitted down through the hypothalamus, sympathetic and parasympathetic nerve, affecting the activity of the heart and blood vessels, regulating blood pressure and heart rate[9]. When the intrasinus pressure changes within the range of the normal mean arterial pressure, carotid sinus reflex is very sensitive. As the pressure increases, the reflected signal strengthens. After the blood pressure drops, the reflected signal weakens[10]. When the reflex makes brain blood perfusion lower than the minimum level for maintaining consciousness, transient loss of consciousness may occur, that is, syncope. In many carotid artery stenting operations, syncope caused by carotid sinus reflex can be observed[11]. Baroreceptors are more widely distributed in the inner layer of aortic arch adventitia than in carotid artery. Subadventitia pressure is more likely to stimulate aortic arch baroreceptors, cause abnormally increased aortic arch reflex and induce syncope[12]. Thus syncope is common in aortic arch dissection cases[12, 13]. From the above all we can make the following speculation, the deeper the dissection lesion breaks through the vascular wall, the greater the dilation force to the adventitia, the easier the stimulation to baroreceptors, and the stronger the reflected signal and effect. When global cerebral perfusion is reduced to the minimum level for maintaining consciousness by this effect, syncope occurs. In all of the previously reported ICAD cases with syncope, as well as our patient, the initial segments of the internal carotid arteries were involved. Our view can explain the mechanism of syncope in all the above ICAD patients. 3. Summary Unilateral ICAD can also have syncope as the first symptom, which cannot be ignored in the differential diagnosis of syncope. The most possible pathogenesis of syncope in ICAD is that the subintimal blood increases the mechanical stretch of the adventitia, stimulates the baroreceptors, thereby causing carotid sinus hyperreflexia. Declarations Grant support: This work did not have grant support. Data availability: Data sharing is not applicable to this article as no new data were created or analyzed in this study. Declarations: Ethics approval this study received ethical approval from the Ethics Committee of Huaihe Hospital of Henan University. Consent to participate: The patient’s guardians provided written informed consent for publication. Conflict of interest: The authors declare that they have no conflicts of interest. References 1. Gallerini S, Chiti A, Bartalucci M, Marsili L, Marconi R (2015) A case of isolated syncope due to bilateral carotid artery dissection: a lesson from ancient Greece. Neurol Sci 36:1299-1301 2. 常万生, 潘伟, 林峰, 张海奇, 吴川杰 (2017) 以晕厥起病的双侧颈内动脉夹层1例报告. 中国实用神经疾病杂志 20:127-128 3. Dulay D, Gould PA, Leung A, Krahn AD (2008) Images in cardiovascular medicine. A sensitive dissection: profound bradycardia complicating carotid dissection. Circulation 118:e152-153 4. Sarikaya H, Baumgartner RW, Arnold M (2009) Letter by Sarikaya et al. regarding the article, "A sensitive dissection: profound bradycardia complicating carotid dissection". Circulation 119:e545; author reply e546 5. Tokgözoglu SL, Batur MK, Topçuoglu MA, Saribas O, Kes S, Oto A (1999) Effects of stroke localization on cardiac autonomic balance and sudden death. Stroke 30:1307-1311 6. Cheung RT, Hachinski V (2000) The insula and cerebrogenic sudden death. Arch Neurol 57:1685-1688 7. Colivicchi F, Bassi A, Santini M, Caltagirone C (2005) Prognostic implications of right-sided insular damage, cardiac autonomic derangement, and arrhythmias after acute ischemic stroke. Stroke 36:1710-1715 8. Oppenheimer S (2006) Cerebrogenic cardiac arrhythmias: cortical lateralization and clinical significance. Clin Auton Res 16:6-11 9. Wallbach M, Koziolek MJ (2018) Baroreceptors in the carotid and hypertension-systematic review and meta-analysis of the effects of baroreflex activation therapy on blood pressure. Nephrol Dial Transplant 33:1485-1493 10. Kougias P, Weakley SM, Yao Q, Lin PH, Chen C (2010) Arterial baroreceptors in the management of systemic hypertension. Med Sci Monit 16:RA1-8 11. Harrop JS, Sharan AD, Benitez RP, Armonda R, Thomas J, Rosenwasser RH (2001) Prevention of carotid angioplasty-induced bradycardia and hypotension with temporary venous pacemakers. Neurosurgery 49:814-820; discussion 820-822 12. Nallamothu BK, Mehta RH, Saint S, et al. (2002) Syncope in acute aortic dissection: diagnostic, prognostic, and clinical implications. Am J Med 113:468-471 13. Hagan PG, Nienaber CA, Isselbacher EM, et al. (2000) The International Registry of Acute Aortic Dissection (IRAD): new insights into an old disease. JAMA 283:897-903 Cite Share Download PDF Status: Posted Version 1 posted You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. We do this by developing innovative software and high quality services for the global research community. Our growing team is made up of researchers and industry professionals working together to solve the most critical problems facing scientific publishing. Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-1573490","acceptedTermsAndConditions":true,"allowDirectSubmit":true,"archivedVersions":[],"articleType":"Research Article","associatedPublications":[],"authors":[{"id":101027827,"identity":"7d8d3573-e08f-4f90-91fd-b50394a583e8","order_by":0,"name":"Junyang Xia","email":"","orcid":"","institution":"Huaihe Hospital of Henan University","correspondingAuthor":false,"submittingAuthor":false,"prefix":"","firstName":"Junyang","middleName":"","lastName":"Xia","suffix":""},{"id":101027828,"identity":"5fd380fc-8529-4ff7-a162-c5cb901e91db","order_by":1,"name":"Xin Jiang","email":"","orcid":"","institution":"Huaihe Hospital of Henan University","correspondingAuthor":false,"submittingAuthor":false,"prefix":"","firstName":"Xin","middleName":"","lastName":"Jiang","suffix":""},{"id":101027829,"identity":"66aeaf59-572b-4a45-ba10-869e42d1f339","order_by":2,"name":"Haojun Pan","email":"","orcid":"","institution":"Huaihe Hospital of Henan University","correspondingAuthor":false,"submittingAuthor":false,"prefix":"","firstName":"Haojun","middleName":"","lastName":"Pan","suffix":""},{"id":101027830,"identity":"486f059a-3654-4b19-8a83-54082fdedae3","order_by":3,"name":"Peipei Liu","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAAAyUlEQVRIiWNgGAWjYLCCBAYLHgb2xsaHH0jQIsHDwHO42ViCBHuAaiXS2wR4iFFrzt5++cWDCgkZg5sP24A67eR0Gwhosew5U2aRcEaCx+B2YtuDAoZkY7MDBLQY3MhJM0hsA2tpN5BgOJC4jaCW+2+AWv4Btdw8CNRIlJYb7IcfJDYAtdxgJFKLZU8OG0PCMQkeyTOJwEA2IMIv5uzHH3/8UWNjz3f8+MOHHyrs5Ah7n4HHTAKZSxgYMLA/Jj6ZjIJRMApGwcgEAGMJQ88SKRolAAAAAElFTkSuQmCC","orcid":"https://orcid.org/0000-0002-9097-3425","institution":"Huaihe Hospital of Henan University","correspondingAuthor":true,"submittingAuthor":false,"prefix":"","firstName":"Peipei","middleName":"","lastName":"Liu","suffix":""}],"badges":[],"createdAt":"2022-04-19 16:13:38","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-1573490/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-1573490/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":20925080,"identity":"62420d5b-bbcf-4701-94fd-72185d155d73","added_by":"auto","created_at":"2022-04-29 15:40:23","extension":"jpg","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":42801,"visible":true,"origin":"","legend":"\u003cp\u003eFlair sequence of Brain MRI\u003c/p\u003e\u003cp\u003eA crescent high signal lesion was revealed in the wall of left internal carotid artery(arrow), which was considered to be acute hematoma in left internal carotid artery dissection.\u003c/p\u003e","description":"","filename":"figure1.jpg","url":"https://assets-eu.researchsquare.com/files/rs-1573490/v1/f0457a9bbad4ea769b758fd9.jpg"},{"id":20925081,"identity":"5617e9dd-8f2d-49c8-bc29-1dbda4b04408","added_by":"auto","created_at":"2022-04-29 15:40:23","extension":"jpg","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":58938,"visible":true,"origin":"","legend":"\u003cp\u003eDWI sequence of Brain MRI\u003c/p\u003e\u003cp\u003eMultiple dots and patches of hyper intensity were revealed in the left basal ganglia and left paraventricular area.\u003c/p\u003e","description":"","filename":"figure2.jpg","url":"https://assets-eu.researchsquare.com/files/rs-1573490/v1/cf2fddb256b6263c021848ea.jpg"},{"id":20925082,"identity":"e916425d-e1af-4625-aa09-8dbe629ae99a","added_by":"auto","created_at":"2022-04-29 15:40:23","extension":"jpg","order_by":3,"title":"Figure 3","display":"","copyAsset":false,"role":"figure","size":89876,"visible":true,"origin":"","legend":"\u003cp\u003eHead and neck MRA\u003c/p\u003e\u003cp\u003eA: The original axial view of TOF MRA showed the double-lumen sign of left internal carotid artery(arrow). \u003c/p\u003e\u003cp\u003eB: TOF MRA 3D image showed that the initial segment of left internal carotid artery and its distal lumen were poorly filled (arrow), and the contralateral internal carotid artery was normal.\u003c/p\u003e\u003cp\u003eC: TOF MRA 3D image showed the poorly filled extracranial segment of left internal carotid artery (arrow), and the C7 segment of left internal carotid artery and left middle cerebral artery were normal.\u003c/p\u003e","description":"","filename":"figure3.jpg","url":"https://assets-eu.researchsquare.com/files/rs-1573490/v1/f4ee13e75a2d7d041b42d10f.jpg"},{"id":20925084,"identity":"e9c0279f-06c4-457a-a6b6-c3b0f5be6a7e","added_by":"auto","created_at":"2022-04-29 15:40:26","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":269765,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-1573490/v1/c0a910a6-efb9-48b6-bc25-7b3f3ef9f06d.pdf"}],"financialInterests":"","formattedTitle":"Unilateral internal carotid artery dissection with syncope as the first symptom","fulltext":[{"header":"1. Patient","content":" \u003cp\u003eA 35-year-old male suddenly lost consciousness and fell to the ground when he was on the phone. About 30 seconds later, his consciousness improved. However, he still suffered from vomiting, sweating, and weakness of right limbs. About 2 hours later his symptoms were completely relieved. 3 hours later, he was admitted to a local hospital. His brain MRI and MRA conducted 5 hours after onset reported no obvious abnormalities. Then he received conservative treatment including aspirin and atorvastatin.\u003c/p\u003e\n \u003cp\u003e10 days later, he developed a sudden and severe headache in the left temporal and occipital. After about an hour of interval, the pain eased slightly though can be occasionally aggravated by coughing. Then, he was transferred to our hospital for further medical intervention. In his admission, neurological examination revealed right lingual palsy, as well as incomplete left Horner syndrome including unequal bilateral pupil diameters (the right pupil diameter was 4.0mm, the left pupil diameter was 2.0mm), drooping left eyelid, slightly sunken left eye ball and slightly congested left eyelid conjunctiva. His past medical history was unremarkable and he denied any recent trauma or massage of his neck. 24-hour electrocardiogram monitoring revealed no abnormality.\u003c/p\u003e\n \u003cp\u003eWhen we reviewed his brain MRI conducted in the local hospital, intermural hematoma of the left internal carotid artery was found(Fig. \u003cspan class=\"InternalRef\"\u003e1\u003c/span\u003e). MRI reconducted in our hospital showed acute cerebral infarction in the left paraventricular area and left basal ganglia(Fig. \u003cspan class=\"InternalRef\"\u003e2\u003c/span\u003e). TOF-MRA revealed double-lumen sign from the initial segment to the cavernous sinus segment of the left internal carotid artery (Fig. \u003cspan class=\"InternalRef\"\u003e3\u003c/span\u003e). Based on the evidence above, diagnosis of left ICAD was established. Then, our patient received anticoagulation therapy. During the 3-month follow-up, syncope did not occur again and the symptoms did not worsen with a MRS score of 0.\u003c/p\u003e"},{"header":"2. Discussion","content":"\u003cp\u003eSyncope is rare in ICAD cases. After searching and screening on Pubmed with \u0026quot;syncope\u0026quot; and \u0026quot;carotid artery dissection\u0026quot; as keywords, only three ICAD cases with syncope were found. Two of them are bilateral ICAD cases with syncope as the first symptom[1, 2]. The third case is a right ICAD patient with slurred speech and left hemiplegia at the time of onset reported by Dulay et al[3]. This patient had a history of vasovagal syncope and developed syncope caused by sinus arrest after hospitalization. Our patient, diagnosed with unilateral ICAD with syncope as the first symptom, was different from the above all.\u003c/p\u003e\n \u003cp\u003eThe first pathophysiological mechanism theory of syncope in ICAD is that ICAD causes vascular stenosis, restricts carotid blood flow, and thus induces transient hypoperfusion of cerebral hemispheres[1, 2]. However, many clinical cases have proved that unilateral internal carotid artery stenosis can not cause syncope[4]. Therefore, this \u0026ldquo;carotid blood flow restriction\u0026rdquo; theory is only applicable for bilateral ICAD, rather unilateral ICAD like our case.\u003c/p\u003e\n \u003cp\u003eThe second pathophysiological mechanism theory of syncope in ICAD is that ICAD induces arrhythmia and the following syncope by causing insular cortex stroke. The insula, especially the right insula, is involved in the autonomous control of heart activity[5\u0026ndash;7]. When ischemic stroke affects the insular cortex, it may cause autonomic dysfunction, bradyarrhythmia and syncope[8]. No cerebral infarction was revealed in two of the ICAD cases with syncope[1, 2]. In the third ICAD case with syncope, acute cerebral infarction was only presented in the right posterolateral frontal lobe[3]. In our case, acute cerebral infarction just involved the left basal ganglia and the left lateral ventricle. All of the four cases did not support this \u0026ldquo;insular cortex stroke\u0026rdquo; theory.\u003c/p\u003e\n \u003cp\u003eThe third pathophysiological mechanism theory of syncope in ICAD was proposed by Dulay et al when describing their patient[3]. They believed that thrombosis in internal carotid artery caused sinus arrest as well as syncope by activating the carotid sinus reflex. If the thrombus blocks the initial segment of the carotid artery, the pressure on the carotid sinus baroreceptors should decrease. Therefore, this pathogenesis was negated by Sarikaya et al. [4]. In addition, in the case provided by Dulay et al., the temporal relationship between the ICAD and vasovagal syncope is unclear. In other words, the \u0026quot;history of vasovagal syncope\u0026quot; may appear after the onset of ICAD and be one of the clinical symptoms of the latter.\u003c/p\u003e\n \u003cp\u003eAt the initiation of carotid, when entering the junction of adventitial and media membranes, myelinated nerve fibers lose myelin, end up with abundant branches. These branches distribute in the inner layer of the adventitial membrane, forming the carotid sinus baroreceptors. By detecting changes in the degree of stretch on the blood vessel wall, baroreceptors in adventitial inner layer indirectly sense changes in blood pressure. Their nerve signals are transmitted up through Hering nerve (sinus nerve) and glossopharyngeal nerve to nucleus of solitary tract. Then transmitted down through the hypothalamus, sympathetic and parasympathetic nerve, affecting the activity of the heart and blood vessels, regulating blood pressure and heart rate[9]. When the intrasinus pressure changes within the range of the normal mean arterial pressure, carotid sinus reflex is very sensitive. As the pressure increases, the reflected signal strengthens. After the blood pressure drops, the reflected signal weakens[10]. When the reflex makes brain blood perfusion lower than the minimum level for maintaining consciousness, transient loss of consciousness may occur, that is, syncope. In many carotid artery stenting operations, syncope caused by carotid sinus reflex can be observed[11]. Baroreceptors are more widely distributed in the inner layer of aortic arch adventitia than in carotid artery. Subadventitia pressure is more likely to stimulate aortic arch baroreceptors, cause abnormally increased aortic arch reflex and induce syncope[12]. Thus syncope is common in aortic arch dissection cases[12, 13]. From the above all we can make the following speculation, the deeper the dissection lesion breaks through the vascular wall, the greater the dilation force to the adventitia, the easier the stimulation to baroreceptors, and the stronger the reflected signal and effect. When global cerebral perfusion is reduced to the minimum level for maintaining consciousness by this effect, syncope occurs. In all of the previously reported ICAD cases with syncope, as well as our patient, the initial segments of the internal carotid arteries were involved. Our view can explain the mechanism of syncope in all the above ICAD patients.\u003c/p\u003e"},{"header":"3. Summary","content":"\u003cdiv class=\"Section2\" id=\"Sec4\"\u003e\n \u003cp\u003eUnilateral ICAD can also have syncope as the first symptom, which cannot be ignored in the differential diagnosis of syncope. The most possible pathogenesis of syncope in ICAD is that the subintimal blood increases the mechanical stretch of the adventitia, stimulates the baroreceptors, thereby causing carotid sinus hyperreflexia.\u003c/p\u003e\n\u003c/div\u003e"},{"header":"Declarations","content":"\u003cp\u003eGrant support: This work did not have grant support.\u003c/p\u003e\n\u003cp\u003eData availability: Data sharing is not applicable to this article as no new data were created or analyzed in this study.\u003c/p\u003e\n\u003cp\u003eDeclarations: Ethics approval this study received ethical approval from the Ethics Committee of Huaihe Hospital of Henan University.\u003c/p\u003e\n\u003cp\u003eConsent to participate: The patient\u0026rsquo;s guardians provided written informed consent for publication.\u003c/p\u003e\n\u003cp\u003eConflict of interest: The authors declare that they have no conflicts of interest.\u003c/p\u003e"},{"header":"References","content":"\u003cp\u003e1. \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;Gallerini S, Chiti A, Bartalucci M, Marsili L, Marconi R (2015) A case of isolated syncope due to bilateral carotid artery dissection: a lesson from ancient Greece. Neurol Sci 36:1299-1301\u003c/p\u003e\n\u003cp\u003e2. \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;常万生, 潘伟, 林峰, 张海奇, 吴川杰 (2017) 以晕厥起病的双侧颈内动脉夹层1例报告. 中国实用神经疾病杂志 20:127-128\u003c/p\u003e\n\u003cp\u003e3. \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;Dulay D, Gould PA, Leung A, Krahn AD (2008) Images in cardiovascular medicine. A sensitive dissection: profound bradycardia complicating carotid dissection. Circulation 118:e152-153\u003c/p\u003e\n\u003cp\u003e4. \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;Sarikaya H, Baumgartner RW, Arnold M (2009) Letter by Sarikaya et al. regarding the article, \u0026quot;A sensitive dissection: profound bradycardia complicating carotid dissection\u0026quot;. Circulation 119:e545; author reply e546\u003c/p\u003e\n\u003cp\u003e5. \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;Tokg\u0026ouml;zoglu SL, Batur MK, Top\u0026ccedil;uoglu MA, Saribas O, Kes S, Oto A (1999) Effects of stroke localization on cardiac autonomic balance and sudden death. Stroke 30:1307-1311\u003c/p\u003e\n\u003cp\u003e6. \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;Cheung RT, Hachinski V (2000) The insula and cerebrogenic sudden death. Arch Neurol 57:1685-1688\u003c/p\u003e\n\u003cp\u003e7. \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;Colivicchi F, Bassi A, Santini M, Caltagirone C (2005) Prognostic implications of right-sided insular damage, cardiac autonomic derangement, and arrhythmias after acute ischemic stroke. Stroke 36:1710-1715\u003c/p\u003e\n\u003cp\u003e8. \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;Oppenheimer S (2006) Cerebrogenic cardiac arrhythmias: cortical lateralization and clinical significance. Clin Auton Res 16:6-11\u003c/p\u003e\n\u003cp\u003e9. \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;Wallbach M, Koziolek MJ (2018) Baroreceptors in the carotid and hypertension-systematic review and meta-analysis of the effects of baroreflex activation therapy on blood pressure. Nephrol Dial Transplant 33:1485-1493\u003c/p\u003e\n\u003cp\u003e10. \u0026nbsp; \u0026nbsp; \u0026nbsp;Kougias P, Weakley SM, Yao Q, Lin PH, Chen C (2010) Arterial baroreceptors in the management of systemic hypertension. Med Sci Monit 16:RA1-8\u003c/p\u003e\n\u003cp\u003e11. \u0026nbsp; \u0026nbsp; \u0026nbsp; Harrop JS, Sharan AD, Benitez RP, Armonda R, Thomas J, Rosenwasser RH (2001) Prevention of carotid angioplasty-induced bradycardia and hypotension with temporary venous pacemakers. Neurosurgery 49:814-820; discussion 820-822\u003c/p\u003e\n\u003cp\u003e12. \u0026nbsp; \u0026nbsp; \u0026nbsp;Nallamothu BK, Mehta RH, Saint S, et al. (2002) Syncope in acute aortic dissection: diagnostic, prognostic, and clinical implications. Am J Med 113:468-471\u003c/p\u003e\n\u003cp\u003e13. \u0026nbsp; \u0026nbsp; \u0026nbsp;Hagan PG, Nienaber CA, Isselbacher EM, et al. (2000) The International Registry of Acute Aortic Dissection (IRAD): new insights into an old disease. JAMA 283:897-903\u003c/p\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":true,"hideJournal":true,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true},"keywords":"","lastPublishedDoi":"10.21203/rs.3.rs-1573490/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-1573490/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"Internal carotid artery dissection(ICAD) is a series of pathological processes caused by intimal tear of the internal carotid artery. Syncope refers to a transient loss of consciousness caused by transient global brain hypoperfusion. ICAD with syncope is rare. Here we present a case of unilateral ICAD with syncope as the first symptom. We also review the literature and discuss the pathogenesis of syncope in ICAD patients. The main message we want to convey to readers is that unilateral ICAD can have syncope as the first symptom, which should not be ignored in the differential diagnosis of syncope. Furthermore, the pathogenesis of syncope in ICAD is more likely to be that subintimal blood flow can easily increase the mechanical stretch of adventitia, stimulate the baroreceptors and cause hyperactive carotid sinus reflex.","manuscriptTitle":"Unilateral internal carotid artery dissection with syncope as the first symptom","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2022-04-29 15:40:21","doi":"10.21203/rs.3.rs-1573490/v1","editorialEvents":[{"type":"communityComments","content":0}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"d4df3d07-77b1-4bc3-a3d5-318488302168","owner":[],"postedDate":"April 29th, 2022","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"posted","subjectAreas":[],"tags":[],"updatedAt":"2022-04-29T15:40:21+00:00","versionOfRecord":[],"versionCreatedAt":"2022-04-29 15:40:21","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-1573490","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-1573490","identity":"rs-1573490","version":["v1"]},"buildId":"WrCJVZZCHTDjtuVLN7oU0","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}