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Magnetic resonance and dynamic angiography findings in patients with atypical patterns of rotational vertebral artery occlusion. A, In patient 13, MR angiography shows patent bilateral vertebral arteries (VAs; A-1). Dynamic angiography demonstrates simultaneous compression of the left VA at the C1-2 level (A-2) and the right VA at the C6 level (A-3) during rightward head rotation. B, In patient 15, cerebral angiography shows patent bilateral VAs (B-1 and B-2). Dynamic angiography discloses compression of the left VA during rightward head rotation (B-3) and compression of the right VA during leftward head rotation at the C1-2 level (B-4). C, In patient 16, MR angiography reveals a dominant left VA and a nondominant right VA terminating in posterior inferior cerebellar artery (C-1). Dynamic angiography exhibits compression of the nondominant right VA at the C1-2 level (C-2) and patent basilar artery flow through the left VA during leftward head rotation (C-3). D, In patient 19, cerebral angiography shows a patent left VA (D-1) and a complete occlusion of right VA at its origin from the subclavian artery (D-2). Dynamic angiography discloses compression of the left VA at the C4 level during rightward head rotation (D-3).
Source publication
Background and purpose:
To elucidate the mechanisms and prognosis of rotational vertebral artery occlusion (RVAO).
Methods:
We analyzed clinical and radiological characteristics, patterns of induced nystagmus, and outcome in 21 patients (13 men, aged 29-77 years) with RVAO documented by dynamic cerebral angiography during an 8-year period at 3 U...
Contexts in source publication
Context 1
... remaining 9 patients showed (1) patent bilateral VAs and simultaneous compression of the VAs during head rotation to 1 side at the C6 level in the ipsiversive VA and at the C1-2 level in the contraversive VA (n=2; patients 13 and 14; Figure 3A); (2) patent bilateral VAs and compres- sion of the either VA at the C1-2 level during contraversive head rotation (n=1; patient 15; Figure 3B); (3) compression of the nondominant VA terminating in PICA at the C1-2 level during contraversive head rotation (n=2; patients 16 and 17; Figure 3C) 19 ; (4) compression of the dominant VA at the sub- axial levels from the origin of VA to the C4 level during ipsi- (n=1; patient 18) or contraversive (n=2; patients 19 and 20) head rotation ( Figure 3D); or (5) compression of the domi- nant VA at the C1-2 level during ipsiversive head tilt (n=1; patient 21). 16 Of the 24 VAs with a documented compression during head rotation or tilt, 19 (79.2%) had compression at the C1-2 level during contraversive head rotation (n=18) or ipsiversive head tilt (n=1), whereas the remaining 5 (20.8%) exhibited com- pression at the subaxial levels from the VA origin to the C4 level during ipsi-(n=3) or contraversive (n=2) head rotation. ...
Context 2
... remaining 9 patients showed (1) patent bilateral VAs and simultaneous compression of the VAs during head rotation to 1 side at the C6 level in the ipsiversive VA and at the C1-2 level in the contraversive VA (n=2; patients 13 and 14; Figure 3A); (2) patent bilateral VAs and compres- sion of the either VA at the C1-2 level during contraversive head rotation (n=1; patient 15; Figure 3B); (3) compression of the nondominant VA terminating in PICA at the C1-2 level during contraversive head rotation (n=2; patients 16 and 17; Figure 3C) 19 ; (4) compression of the dominant VA at the sub- axial levels from the origin of VA to the C4 level during ipsi- (n=1; patient 18) or contraversive (n=2; patients 19 and 20) head rotation ( Figure 3D); or (5) compression of the domi- nant VA at the C1-2 level during ipsiversive head tilt (n=1; patient 21). 16 Of the 24 VAs with a documented compression during head rotation or tilt, 19 (79.2%) had compression at the C1-2 level during contraversive head rotation (n=18) or ipsiversive head tilt (n=1), whereas the remaining 5 (20.8%) exhibited com- pression at the subaxial levels from the VA origin to the C4 level during ipsi-(n=3) or contraversive (n=2) head rotation. ...
Context 3
... remaining 9 patients showed (1) patent bilateral VAs and simultaneous compression of the VAs during head rotation to 1 side at the C6 level in the ipsiversive VA and at the C1-2 level in the contraversive VA (n=2; patients 13 and 14; Figure 3A); (2) patent bilateral VAs and compres- sion of the either VA at the C1-2 level during contraversive head rotation (n=1; patient 15; Figure 3B); (3) compression of the nondominant VA terminating in PICA at the C1-2 level during contraversive head rotation (n=2; patients 16 and 17; Figure 3C) 19 ; (4) compression of the dominant VA at the sub- axial levels from the origin of VA to the C4 level during ipsi- (n=1; patient 18) or contraversive (n=2; patients 19 and 20) head rotation ( Figure 3D); or (5) compression of the domi- nant VA at the C1-2 level during ipsiversive head tilt (n=1; patient 21). 16 Of the 24 VAs with a documented compression during head rotation or tilt, 19 (79.2%) had compression at the C1-2 level during contraversive head rotation (n=18) or ipsiversive head tilt (n=1), whereas the remaining 5 (20.8%) exhibited com- pression at the subaxial levels from the VA origin to the C4 level during ipsi-(n=3) or contraversive (n=2) head rotation. ...
Context 4
... remaining 9 patients showed (1) patent bilateral VAs and simultaneous compression of the VAs during head rotation to 1 side at the C6 level in the ipsiversive VA and at the C1-2 level in the contraversive VA (n=2; patients 13 and 14; Figure 3A); (2) patent bilateral VAs and compres- sion of the either VA at the C1-2 level during contraversive head rotation (n=1; patient 15; Figure 3B); (3) compression of the nondominant VA terminating in PICA at the C1-2 level during contraversive head rotation (n=2; patients 16 and 17; Figure 3C) 19 ; (4) compression of the dominant VA at the sub- axial levels from the origin of VA to the C4 level during ipsi- (n=1; patient 18) or contraversive (n=2; patients 19 and 20) head rotation ( Figure 3D); or (5) compression of the domi- nant VA at the C1-2 level during ipsiversive head tilt (n=1; patient 21). 16 Of the 24 VAs with a documented compression during head rotation or tilt, 19 (79.2%) had compression at the C1-2 level during contraversive head rotation (n=18) or ipsiversive head tilt (n=1), whereas the remaining 5 (20.8%) exhibited com- pression at the subaxial levels from the VA origin to the C4 level during ipsi-(n=3) or contraversive (n=2) head rotation. ...
Citations
... In the first hit, one of the vertebral arteries is severely hypoplastic or stenotic due to congenital or acquired cause. In the second hit, there is affection of the contralateral vertebral artery by a structural variation or anomaly like bony spurs, fibrous bands or disc herniation [3]. The most common cause of BHS has been found to be cervical vertebral osteophytes [4]. ...
... Of these dynamic digital subtraction angiography plays the most important role in diagnosis. The procedure while being performed the patient can be instructed head rotation which confirms the diagnosis and makes it the gold standard imaging technique for BHS [3]. ...
... The treatment of BHS is decided according to the etiology. Surgical options include cervical fusion, cervical decompression and endovascular stents within the unaffected vertebral artery to maintain adequate posterior circulation [3]. Conservative management includes long term anticoagulation and hard cervical collars with prevention of head rotation [8]. ...
Background
Bow Hunter syndrome (BHS) is a rare, but important cause of posterior circulation stroke. It is also known as Rotational vertebral artery syndrome and is caused by transient dynamic vertebro-basilar insufficiency on movement of the neck in the presence of certain soft tissue or bone anomalies in the cranio-vertebral region.
Case presentation
We present a case of Bow hunter syndrome in an 18-year-old adult male who presented with vomiting, occipital headache and loss of balance, with findings of posterior circulation stroke on imaging. Medical causes of young stroke, including vasculitis and clotting disorders were ruled out, following which a diagnostic conventional angiography and CT angiography was performed. The cause of vascular compromise in our case was the presence of vertebral anomalies, in particular, the presence of a partial ponticulus posticus with formation of an incomplete arcuate foramen. He was treated with cervical spine immobilisation and C1–C2 fixation. In addition, our patient had a single posterior inferior cerebellar artery (PICA) on the side of the dynamic insufficiency, which lead to bilateral cerebellar infarcts. Our case is unique because it demonstrates a combination of osseous and vascular developmental anomalies resulting in posterior circulation stroke.
Conclusions
Though uncommon, BHS should be considered in the list of differentials in otherwise unexplained cases of posterior circulation stroke. Conventional angiography with dynamic manoeuvres is the modality of choice for documenting the rotational vertebral artery occlusion.
... Conservative treatment includes education and avoidance of prolonged head rotation, use of cervical orthosis and preventative antiplatelet or anticoagulant therapy [1,6]. Choi, et al., pushed a series of 21 patients with RVAO and 19 of them were managed conservatively with good outcome [15]. In contrast, our review shows that the majority of cases where the thyroid cartilage is involved have recurrence with conservative treatment. ...
Thyroid cartilage compression of the Vertebral Artery (VA) has been implicated as a rare cause of Rotational Vertebral Artery Occlusion (RVAO). 10 cases have been reported in the literature. This has a higher tendency to affect males and younger patients than other forms of stroke. Patients present with multiple episodes prior to diagnosis. Radiologic studies prove crucial for confirming this condition. An aberrant VA course appears to be a necessary factor. All cases suffer from right side VA compression by the superior thyroid cornu. Conservative therapy with antiplatelet treatment is employed commonly. Most patients have definitive treatment with surgical resection of the right superior thyroid cornu. Theories proposed for these characteristics include VA dominance, structural variability in the thyroid cartilage between genders and also variable thyroid cartilage ossification. Given these findings, we propose the term “thyro-vertebral artery syndrome” for this condition.
... Moreover, there is a recognized convergence of connective tissue disorders and "complex Chiari," characterized by basilar invagination, kyphotic clival axial angle (CXA), and craniocervical instability [6][7][8][9][10]. This association has prompted increased consideration of dynamic imaging to better characterize the pathology and determine whether occipito-cervical fusion (OCF) may be indicated [11][12][13][14][15][16][17][18]. Emblematic of the HDCT are the 13 types of Ehlers-Danlos syndrome (EDS), characterized by weakness of connective tissue and many comorbid conditions, including neurological findings and dysautonomia attributed in part to chronic craniocervical and spinal instability [2,19]. ...
... A growing body of literature suggests that chronic CCI manifests as a broad array of deleterious biomechanical effects upon the neural axis, in addition to causing altered cerebrospinal fluid and vascular flow [4,8,9,12,[15][16][17]20]. Headaches, long tract findings, motor delay and quadriparesis, dyspraxia, gait instability, and altered autonomic function are recognized as consequences of chronic biomechanical deformation of structures at the craniocervical junction in many hereditary connective tissue disorders [8,13,16,19,[21][22][23][24][25]. ...
Craniocervical instability (CCI) is increasingly recognized in hereditary disorders of connective tissue and in some patients following suboccipital decompression for Chiari malformation (CMI) or low-lying cerebellar tonsils (LLCT). CCI is characterized by severe headache and neck pain, cervical medullary syndrome, lower cranial nerve deficits, myelopathy, and radiological metrics, for which occipital cervical fusion (OCF) has been advocated. We conducted a retrospective analysis of patients with CCI and Ehlers-Danlos syndrome (EDS) to determine whether the surgical outcomes supported the criteria by which patients were selected for OCF. Fifty-three consecutive subjects diagnosed with EDS, who presented with severe head and neck pain, lower cranial nerve deficits, cervical medullary syndrome, myelopathy, and radiologic findings of CCI, underwent open reduction, stabilization, and OCF. Thirty-two of these patients underwent suboccipital decompression for obstruction of cerebral spinal fluid flow. Questionnaire data and clinical findings were abstracted by a research nurse. Follow-up questionnaires were administered at 5–28 months (mean 15.1). The study group demonstrated significant improvement in headache and neck pain (p < 0.001), decreased use of pain medication (p < 0.0001), and improved Karnofsky Performance Status score (p < 0.001). Statistically significant improvement was also demonstrated for nausea, syncope (p < 0.001), speech difficulties, concentration, vertigo, dizziness, numbness, arm weakness, and fatigue (p = 0.001). The mental fatigue score and orthostatic grading score were improved (p < 0.01). There was no difference in pain improvement between patients with CMI/LLCT and those without. This outcomes analysis of patients with disabling CCI in the setting of EDS demonstrated significant benefits of OCF. The results support the reasonableness of the selection criteria for OCF. We advocate for a multi-center, prospective clinical trial of OCF in this population.
... Синдром компрессии ПА подтверждается, когда вестибулярное головокружение возникает во время поворота или наклона головы с одновременной компрессией по данным ангиографии доминантной ПА [55] или в случае индуцированного вращением головы снижения кровотока в ВББ (нулевая диастолическая скорость кровотока), выявленного при помощи транскраниальной допплерографии [56]. Головокружение при синдроме компрессии ПА возникает вследствие преходящей ишемии центральных вестибулярных структур, т. е. при совпадении двух обстоятельств: значительного снижения кровотока по компримируемой ПА и неспособности коллатералей компенсировать это снижение. ...
Among the various causes of acute vestibular vertigo, vascular factors are of particular importance. Numerous studies show that the diagnosis of vascular vertigo remains inadequate, often leading to overdiagnosis of stroke and transient ischemic attacks in patients with peripheral vestibular disorders and vestibular migraine, on the one hand, and underestimation of the importance of cerebrovascular pathology, especially in patients with the first attack of persistent vestibular vertigo, on the other.
The International Barany Society has developed and published diagnostic criteria for vascular vertigo. These criteria are intended to facilitate the identification of vascular causes of acute vestibular syndrome. Particular emphasis is placed on clinical signs because imaging techniques often do not allow detection of foci small in volume and area, especially in cases when stroke is manifested by an isolated vestibular syndrome. Key clinical signs to analyze when a vascular etiology of acute vestibular syndrome is suspected include nystagmus, corrective saccades on the Halmagyi test, smooth visual pursuit, visual saccades, severity of trunk ataxia, and hearing loss.
... Cai et al10 reported a case with a right hypoplastic vertebral artery (VA) and a dynamically compressible left VA, managed surgically. Similarly, Choi et al11 found that ischemia can be triggered by rotational head movements or tilting, leading to vertigo and syncope. As a result, excessive tilting of the head in the semirecumbent position during dynamic pilates performance in PHA may have caused syncope, similar to exacerbation of ischemia. ...
Persistent hypoglossal artery is a rare primitive anastomose which mainly supplies the posterior cerebral circulation by itself in the case of the absent vertebral arteries. This artery is an embryological remnant and is commonly found incidentally. It originates from the upper cervical vertebra (C1-C2 level) of the internal carotid artery. Here we present a unique case suffering from syncope related to persistent hypoglossal artery which supplies the posterior cerebral blood flow in the absence of the vertebral arteries with the classical findings on magnetic resonance imaging and our clinical approach.
... 10 Cai et al 10 reported a case with a right hypoplastic vertebral artery (VA) and a dynamically compressible left VA, managed surgically. Similarly, Choi et al 11 found that ischemia can be triggered by rotational head movements or tilting, leading to vertigo and syncope. As a result, excessive tilting of the head in the semirecumbent position during dynamic pilates performance in PHA may have caused syncope, similar to exacerbation of ischemia. ...
Orthogonal-biplane imaging (X-plane) is relatively a new tooL and provides comprehensive information about mitral valve and left atrial appendage evaluation. On the other hand, X-plane method is a promising method in the diagnosis of semilunar valve pathologies. Below, we report 2 cases, in which X-plane method was used, in order to clarify diagnosis. Case 1: Case 1 was a 63-year-old male patient who was admitted to our clinic with dyspnea. Right ventricular dilatation and hypertrophy were assessed. In order to determine the exact reason for right ventricular pressure overload, the pulmonary valve was evaluated by X-plane, and a bicuspid pulmonary valve was represented. This patient underwent pulmonary valve percutaneous valvuloplasty. Case 2: Case 2 was a 48-year-old male patient who was admitted to our hospital with a history of cerebrovascular event. His initial transthoracic and transesophageal echocardiography showed a hyperechoic mobile mass on the non-coronary cusp. However, after X-plane was used to detect the aortic valve, it was the prolapsed part of the non-coronary cusp adjacent to the commissure. These 2 case reports demonstrated the efficacy of the X-plane method in the diagnosis of semilunar valve pathologies in daily practice.
... Causes of vertebral artery stenosis due to compression can be categorized as either primary or acquired causes [5]. Primary causes include muscular hypertrophy of the neck, large osteophytes, fibrous bands, idiopathic skeletal hyperostosis, cervical spondylosis, spondylolisthesis, herniated discs, atlantoaxial hypermobility, hyperflexion, hyperextension, distraction-flexion cervical injuries, and tumors [5,[30][31][32][33][34][35]. Acquired causes include spinal surgery, head trauma, and neck trauma [5]. ...
... Stenosis or occlusion of the vertebral artery unilaterally or bilaterally causes decreased artery perfusion and can result in several symptoms of a posterior circulation transient ischemic attack, such as vertigo, ataxia, diplopia, disturbance of speech, and bilateral hemianopia [37,38]. Vertebral artery stenosis can also result in recurring syncope, headaches, recurrent stroke, palsy of cranial nerves, change in consciousness, altered function of the sensory and pyramidal tracts, cerebellar infarcts, and tinnitus [8,24,27,34]. Vertebral artery stenosis can also result in decreased perfusion to the basilar artery and cause several symptoms, including vertigo, dizziness, diplopia, ataxia, dysarthria, nausea, nystagmus, drop attacks, loss of consciousness, motor symptoms, sensory symptoms such as numbness, and an increased risk of experiencing strokes or transient ischemic attacks [6,16,30,32,39]. These symptoms are typically observed when there is stenosis or occlusion of both vertebral arteries [16]. ...
Vertebral artery stenosis (VAS) is the cause of approximately 20% of ischemic strokes in the posterior circulation. There are several causes of vertebral artery stenosis, including atherosclerosis, calcification, dissections, fibromuscular dysplasia, giant cell arteritis, neurofibromatosis type 1, and bony compressions. The most common cause of VAS is atherosclerosis which is derived from the macrophage-induced oxidation of low-density lipoproteins (LDLs), alongside the accumulation of cholesterol. Calcification of the vertebral artery occurs when there is excess calcium and phosphate deposition in the vessel. Dissection of the vertebral artery can lead to the formation of a hematoma causing stenosis of the vertebral artery. Fibromuscular dysplasia can result in stenosis due to the deposition of collagen fibers in the tunica media, intima, or adventitia. Giant cell arteritis, an autoimmune disorder, causes inflammation of the internal elastic membrane resulting in eventual stenosis of the artery. Neurofibromatosis type 1, an autosomal dominant disorder, results in the stenosis of the vertebral artery due to the altered function of neurofibromin. Mechanical compression of the vertebral artery by bone can also cause stenosis of the vertebral artery. Digital subtraction angiography (DSA) is considered the current gold standard in diagnosing vertebral artery stenosis; however, its associated morbidity and mortality have led to increased use of non-invasive techniques such as duplex ultrasonography (DUS), computed tomography angiography (CTA), and magnetic resonance angiography (MRA). Currently, asymptomatic and symptomatic vertebral artery stenoses are treated by risk factor modification and medical treatment. However, it is recommended that surgical (endarterectomy, reconstruction, and decompression) and endovascular (balloon coronary, bare-metal, and drug-eluting stents) treatments are also used for symptomatic vertebral artery stenosis.
... Nystagmus was not observed in the body-left position in the positional body test, but the presence of right upbeat torsional nystagmus in the body-right position. It has been shown that rotation and hyperextension of the neck compress the vertebral artery in the opposite direction of the rotated side in postmortem studies [7]. In a study, transient occlusion in the left vertebral artery was shown in the angiography of a case with vertigo and horizontal nystagmus that appeared when head to right position [8]. ...
Abstract
Aim: Sudden hearing loss can occur due to viral and vascular causes. Vertebrobasilar insufficiency, which is one of the vascular reasons, commonly cause vestibular problems in middle-aged and older patients, with or without hearing impairment. However, little is known about the association between sudden hearing loss and vertebrobasilar insufficiency.
Methods: A 51 years old male who had sudden onset hearing loss in his left ear and vertigo is presented. Initially, he was diagnosed of left-sided sudden idiopathic sensorineural hearing loss. Suspicion of vertebrobasilar insufficiency raised following completion of vestibular evaluations and diagnosed with imaging studies.
Results: It should be kept in mind that vertebrobasilar insufficiency can be an etiologic factor in cases presenting with sudden hearing loss.
Keywords: Dizziness; sudden hearing loss; Vertigo; Vertebrobasiler insufficiency; Vestibular diseases; Rehabilitation
... Acquired etiologies are also possible, such as complications from cervical spine surgery and neck trauma. 3 Patients with the bow hunter's syndrome also commonly have vascular risk factors, including hypertension, hyperlipidemia, diabetes, smoking, and coronary artery disease. 4 Furthermore, some occupations that require extreme neck rotation, such as auto mechanic or construction worker, can exacerbate symptoms. ...
... 9 However, outcomes vary widely by report with another series of 19 conservatively managed patients showing none developed posterior circulation stroke and four had resolution of symptoms over a median of 37.5 months. 3 Clinical presentation should prompt a thorough imaging workup. Importantly, standard noninvasive studies do not always exclude the diagnosis, and often dynamic imaging is necessary. ...
... Позиционный провоцирующий фактор определяет необходимые диагностические тесты -пробу Дикса-Холлпайка при ДППГ заднего и переднего полукружных каналов, пробу Макклюра-Пагнини при ДППГ горизонтального полукружного канала и ортостатическую пробу при ортостатической гипотензии. Спровоцированный ЭВС с позиционным головокружением центрального генеза может возникнуть также при опухоли, инфаркте или кровоизлиянии в задней черепной ямке, наиболее часто в области червя или узелка мозжечка, дна IV желудочка и в продолговатом мозге [12,13], а также крайне редко -при ротационном синдроме позвоночной артерии [9,14]. ...
The review deals with approaches to the differential diagnosis of the causes of vertigo in emergency neurology. The main causes of episodic and acute vestibular syndrome are discussed. Clinical diagnostic methods for acute vestibular syndrome (evaluation of nystagmus, test of skew, head-impulse test and neurological status) are considered. Clinical signs of “benign” acute vestibular syndrome and symptoms indicating a stroke in the vertebrobasilar system are presented. Differential diagnostic criteria for peripheral and central vestibular disorders are presented. Transient ischemic attacks, features of the otoneurologic status in vestibular neuronitis and different localizations of cerebral infarction focus are considered. Errors in the diagnosis of the vertigo causes are discussed.
