1. Department of Medicine, University College Hospital, Ibadan. Nigeria

E-Mail Contact - OWOLABI Mayowa Ojo : mayowaowolabi@yahoo.com


Background and Purpose

Although in the past cervical vertigo was considered a myth by some, recent studies using dynamic imaging have established the association between vertigo and cervical spondylosis demonstrated by rotational vertebral artery occlusion (RVAO). However the subject of spondylotic RVAO still remains controversial. The purpose of this study is to review the literature on the vascular mechanisms for cervical vertigo.


A systematic review of the literature was conducted according to the Center for Reviews and Dissemination Guidelines using Pubmed and Google Scholar databases. 86 publications describing vascular mechanisms for cervical vertigo were included. Articles that were neither related to cervical vascular pathology nor written in English or German language were excluded. Data was extracted on vascular mechanisms of cervical vertigo and the interrelationship among the quartet of vertigo, head rotation, cervical spondylosis and vascular risk factors.


The occurrence of the tetrad has been described in literature even though no specific attempt has been made to associate them as a possible syndrome such that the occurrence of cervical vertigo would prompt investigations for spondylosis and vascular risk factors.

Discussion and Conclusions

RVAO resulting from cervical spondylosis in the presence of atherosclerosed collateral vessels is a cause of posterior circulation insufficiency manifesting as vertigo. Attention should be paid to the control of modifiable vascular risk factors. The proposed syndrome of cervical vertigo tetrad requires further study to fully highlight its pathophysiology and develop excellent diagnostic, therapeutic and prophylactic guidelines for its management.

Keywords: vertigo, cervical spondylosis, vertebrobasilar insufficiency, rotational vertebral artery occlusion, vascular risk factors


It is an established fact that vascular risk factors – e.g. age (42), hypertension, diabetes mellitus, cigarette smoking and hyperlipidemia- predispose to vertebrobasilar atherosclerosis and subsequent posterior circulation ischemia or infarction. However, in the past the phenomenon of cervical vertigo – e.g. vertebrobasilar ischemia (VBI) secondary to spondylophytic compression of the vertebral artery (VA) – was considered a myth by some. This was because of the coexistence of vertigo and cervical spondylosis particularly in the elderly and the absence of convincing causal relationship between the two. Nevertheless, recent studies using dynamic neurovascular imaging techniques have established the veracity of the association between vertigo and cervical spondylosis mediated by rotational vertebral artery occlusion (RVAO) (4,8,23,28,32,49-52,55,58, 67,70,73,76,79,88). RVAO occurs when cervical osteophytes impinge on the VA causing transitory or permanent mechanical occlusion during head turning to the same or opposite side. (4,8,23,28,32,49-51,55,58,67,70,73,76,88). When RVAO occurs in the absence of sufficient collateral blood flow, the common presentation with vertigo may be explained by the selective vulnerability of the vestibular labyrinth to ischemia.(7,13,26,47,50,51) This VBI can be devastating and may be antecedent to major posterior circulation infarction.(48).

Nevertheless the subject of spondylotic RVAO has remained controversial. Therefore the objectives of this study were to review the literature on vascular mechanisms for cervical vertigo including the interrelationship among the quartet of vascular risk factors, cervical spondylosis, head rotation and vertigo; and modes of investigation, management and prevention of RVAO.


A systematic review of the literature was carried out. A structured search strategy was conducted according to the Center for Reviews and Dissemination Guidelines using Pubmed and Google Scholar databases.(10) For the Google Scholar database the search item ‘cervical vertigo’ with the exact phrase ‘cervical vertigo’ yielded 687 results out of which only 121 contained the term ‘spondylosis’. The Pubmed search for ‘cervical vertigo’ returned 430 papers. Some of the publications retrieved from Pubmed were also present in Google Scholar. The retrieved publications were screened for possible inclusion. 86 publications describing vascular mechanisms for cervical vertigo were included. Articles that were neither related to cervical vascular pathology nor written in English or German language were excluded. The reference lists of key papers were screened to obtain more publications.

The retrieved papers were reviewed for vascular mechanisms of cervical vertigo including RVAO and the interrelationship among vertigo, head rotation, cervical spondylosis and vascular risk factors. Data was also extracted on anatomical and pathophysiological mechanisms, as well as diagnosis and management strategies for vascular cervical vertigo. Because of the heterogeneity of the publications, a meta-analysis was impossible. However data from the key papers were tabulated (Table 2).


Proposed Mechanisms for Cervical Vertigo.

Vertigo resulting from cervical pathologies has been attributed to many causes.(7,39). It was first described in 1858 by Claude Bernard.(7,39). Brandt in a review article proposed labyrinthine, vestibular, ocular, vascular and toxic mechanisms.(7) Proprioceptive and autonomic mechanisms have also been suggested.(68,72). However, the sympathicotonic mechanism proposed by Barre has been disputed.(7).

Of particular significance due to its commonness is unilateral or bilateral RVAO in cervical spondylosis.(8,9,11,16,23,32,47,49,52,55,57,58,61,67,70,72,75,77,79). Nwaorgu reported the presence of cervical spondylosis in up to 40% of all cervical spine roentgenographs.(47). The anatomy of the vertebral artery and the mechanisms of its occlusion are presented in Table 1.

A rotational contralateral VA occlusion was initially considered physiologic after Toole and Tucker found compromised blood flow in vertebral arteries due to head rotation in hemodynamic studies of cadavers.(7) Although this was not supported by initial studies with conventional vertebral angiography at the atlantoaxial joint, recent in vivo studies with better techniques have validated the phenomenon of RVAO across its entire length.(7,79). (Table 1)
Mitchel used Transcranial Doppler (TCD) sonography to measure intracranial vertebral artery (VA) blood flow in 30 young, healthy, female subjects, with the cervical spine in the neutral position and with sustained, end-of-range rotation. Statistically significant decreases in blood flow were demonstrated bilaterally with contralateral preponderance.(40). In another study of 240 VAs in 120 normal subjects, he showed significantly decreased blood flow in intracranial VAs following neck rotation. This was also more pronounced in the contralateral VA and supports the works of Sakaguchi, Weintraub, Rossitti et al, Refshauge, Rossitti and Volkmann, Licht et al, Li et al, and Haynes and Milne.(40,41,63,80-86). This decreased blood flow was interpreted to imply mechanical, extrinsic constriction of the vertebral artery.(41)
Neck rotation is considered an independent risk factor for VA obstruction and VBI.(79, 82,84) Usually, when one rotates the head, there is compression of the contralateral vertebral artery at the atlantoaxial level, which is compensated by the presence of a normal ipsilateral vertebral artery that provides blood flow to the basilar system. In patients with rotational VBI, one vertebral artery is usually hypoplastic or occluded by atheromatous plaques and there is no significant collateral blood flow from the anterior circulation to the basilar system through the posterior communicating arteries. This explains the typical symptoms of rotational VBI which are caused by a temporary hemodynamically significant compression or complete occlusion of the dominant extracranial vertebral artery during head rotation, with resultant diminished blood flow to the basilar system.(79).

Similarly, rotational VBI was observed in a case-control study by Peterson using TCD ultrasound especially in patients with bilateral VA lesions.(56). In another case-control study involving 52 patients with atherosclerosis and spondylotic changes Ozdemir documented significant RVAO (53) while Barton demonstrated rotational angiographic obstruction at C1/C2 level in 2 patients with VBI.(5).

Thus, it has been shown that the VA can be compressed or occluded at any point from its origin at the subclavian artery to the point of dural entrance into the posterior fossa. (Table1). (40,41,63, 80-86). By far the most common cause of RVAO is an osteophyte arising from the uncinate process and compressing the vertebral artery at some point along its course in the subaxial spine. (79). A fibrous ring adherent to the adventitia is often found at the site of the compression, constricting the artery, and seems to play an important role in the pathogenesis of this syndrome.(79). In relation to the direction of head rotation, the vertebral artery being compressed is usually the contralateral one in cases of compression at C1-C2 and the ipsilateral one when the compression is at the subaxial cervical spine. (79). Hypertrophied facet joint and prolapsed disc can also cause RVAO in patients with cervical spondylosis.(32).

Rotational vertebral artery occlusion and vertebrobasilar ischemia

RVAO is important in those who have vascular risk factors that may compromise the integrity of the Circle of Willis thereby jeopardizing compensatory collateral blood flow. (7,34,47,50,51). The common presentation with vertigo may be due to age-dependent microvascular damage to the vestibular organs, and the fact that the vascular supply to the vestibulocochlear organ, being an end artery, may be more susceptible to vertebrobasilar ischemia (VBI).(31,37,42,47,50). Neurons, axons, and hair cells are known to respond to ischemia by depolarizing, causing transient hyperexcitability with ectopic discharges, manifesting in this scenario as vertigo.(7,69). Vertigo in the absence of other brainstem symptoms and signs is considered to be peripheral in such instances.(7,13,37).
Other features of VBI include cerebellar, pontine, medullary, mesencephalic and occipital lobe syndromes manifesting as ataxia, diplopia, dysarthria, visual disturbances, syncope or near syncope, drop attacks, sensory symptoms, motor symptoms, and Wallenberg syndrome.(18,32). Broadly speaking, VBI can result from intraluminal, mural or extrinsic occlusion or stenosis, or retrograde flow in the posterior circulation (subclavian steal syndrome) that is not sufficiently compensated for by collateral circulation. Dissection of the VA is a spontaneous or traumatic cause of VBI.(54,60,62). (Tables1, 2) Acquired mural and intraluminal stenosis and occlusion usually results from vascular risk factors which lead to atherosclerosis, thrombosis and artery-to-artery embolism. (18,20). Hypertension, diabetes mellitus, hyperlipidaemia and cigarette smoking are the strongest modifiable vascular risk factors.(9,18,20). (Tables 1, 2)
In summary, extrinsic rotational vertebral artery occlusion resulting from cervical spondylosis in the presence of stenosis of collateral vessels – induced by vascular risk factors – is an important cause of posterior circulation insufficiency manifesting as vertigo.(4,9,23,28,32,49-53,55,58,67,70,73,76,79, 88). A summary of the key publications illustrating the tetrad is presented in Table 2. However, many of the studies did not assess for vascular risk factors other than the documentation of the age of the patient.


The Tetrad in Literature

Kuether, Strek, Ogino and Olzewski published many cases with the tetrad. Although age was the only reported risk factor for vasculopathy,(32,49,50,51,72,) other vascular risk factors might have been present but were neither sought for nor reported. Conversely, Neuheuser reported 1003 cases with vertigo and vascular risk factors. Cervical spondylosis was not investigated for and it was not stated if the vertigo was related to head rotation.(46). However the complete tetrad was present in cases reported by Citow, Nwaorgu, Owolabi, Vilela, Vates, Chen, Ozdemir, Jagiello and Bulsara.(8, 11,14, 29, 47, 52, 53, 77,79). Further studies with particular attention to the identification of vascular risk factors and their effects on the posterior circulation in cases of vertigo in patients with spondylophytic RVAO are warranted.

Differential diagnoses

The cervical vertigo tetrad needs to be distinguished from other causes of vertigo such as benign positional vertigo, Ménière disease, basilar migraine, vestibular neuritis, toxic damage to labyrinths, perilymph fistula, multiple sclerosis, cerebellopontine angle tumors, vestibular epilepsy, and phobic postural vertigo. The distinction is usually possible after a detailed history and clinical examination, but some special bedside tests – eg Dix-Hallpike’s test and other dizziness simulation battery- are often required. The differential diagnosis of vertigo is discussed in greater details elsewhere.(43,74).

Investigation of the tetrad

Plain radiographs of the cervical spine may show flat lordosis, discopathy, osteophytes, and subchondrial sclerosis. The occurrence of both discopathy and osteophytes has an odds ratio of 28.14 for RVAO.(50,90). However, cervical spine radiograph alone may be insufficient to confirm RVAO.(1).
Dynamic extracranial and transcranial Doppler and duplex ultrasound of the vertebral, basilar and posterior cerebral arteries (PCA) is a non-invasive time-saving way of visualising RVAO while it has the added advantage of detecting functional flow abnormalities in the posterior circulation resulting from RVAO and vascular risk factors.(47,50). The value of TCD ultrasound in the evaluation and diagnosis of rotational VBI has been shown by many studies.(79). It is very useful as an initial diagnostic tool because of its low costs, reproducibility, ease of use, and the possibility of performing a real-time correlation between the PCA velocities and the symptoms.(63,79 ).

Typically, there is a significant decrease in the PCA velocities of at least 50% but more commonly to a mean of 20% of baseline when patients rotate their head. This is followed by a reactive hyperemic response of at least 10% above baseline velocities when the patient resumes the neutral position, which correlates with the disappearance of symptoms.(79). This reactive hyperemia is a normal response to ischemia and reflects a vasodilatory phenomenon that occurs at the level of arterioles and capillary bed. (79).

Power Doppler is also useful in demonstrating RVAO. However it may not be sensitive enough in advanced spondylosis with masking osteophytes.(29). Carotid Doppler ultrasound may also be used for the detection of steal syndromes resulting from carotid insufficiency.(29,39). However, ultrasound studies are operator-dependent and may be influenced by shadowing and vascular tortuosity.(63).

Dynamic conventional or 2D/3D CT angiograms with progressive head rotation and multiple views are invaluable as part of the workup for those patients who have a confirmed decrease in the PCA velocities on TCD. It demonstrates precisely the nature, cause and location of the vertebral artery compression and shows the vascular anatomy of the anterior and posterior circulation.(8). It is important to visualize the entire course of both vertebral arteries from their origin all the way to the posterior fossa and interpret the results carefully so as to prevent misdiagnosis particularly when surgery is intended.(32,79).

Whereas routine MRI provides information on brain ischemia/infarction it may not reveal the specific cause of dizziness.(15). Such cryptogenic VBI requires dynamic neurovascular imaging to demonstrate the entire vasculature and exclude intermittent or permanent, extrinsic, mural or intraluminal occlusive factors. Dynamic MRA may be useful in this regard.(80,84,85). In evaluating the tetrad, it is paramount to investigate for vascular risk factors such as hypertension, diabetes mellitus, and dyslipidemia among others.


Treatment is multidisciplinary involving the otorhinolaryngologist, orthopaedic surgeon, physiotherapist, neurologists, psychiatrist, and neurosurgeons.(6,47). Conservative approach consists of control of vascular risk factors and neck immobilization either by instructing the patient to refrain from excessive head turning or by the use of cervical collar.(16,32). While immobilization of the neck reduces friction between the VA and the osteophyte, anti-inflammatory drugs may facilitate healing by reducing inflammation and fibrotic constriction of the VA.
Surgical treatment, where indicated, must be tailored to the identified cause of the obstruction.(79). Surgery is indicated when symptoms are incapacitating and recurrent and diagnostic tests clearly demonstrate a hemodynamically significant compression of the VA as being responsible for the symptoms.(44,79). Options include fascial decompression, vertebral artery decompression (anterior and posterior approach). (8). osteophytectomy, C1-C2 fusion, decompressive foraminotomy, decompressive transverse foramenectomy and discectomy. (8,32,79). Intraoperative and postoperative dynamic angiography and dynamic TCD ultrasound may be useful in the evaluation of the outcome of the surgery.(8,32,78). Overall success rate for surgery was put at 85% by Kuether. (32).

Cases of cervical vertigo have been reported in literature with resolution effected by conservative (16) or surgical therapy such as facetectomy or transverse foraminotomy with removal of the osteophyte. (4,8,14,32,44,49).


RVAO with VBI in addition to vertebral artery dissection may have implications for manipulative procedures undertaken by physiotherapists and chiropractors in the management of cervical spondylosis and neck trauma.(12,41). Care should be taken to avoid RVAO in patients at risk during cervical manipulation and perhaps during tracheal intubation.(82). Those at risk can be identified by clinical or Doppler ultrasound screening for RVAO.(12,89). Proper management of RVAO can prevent stroke.(79).


Based on this systematic review, a syndrome comprising the tetrad of vascular risk factors, cervical spondylosis, head rotation and vertigo is being proposed. Patients presenting with this syndrome should be evaluated for modifiable cardiovascular risk factors. Management could be conservative or surgical.

Table 1: mechanisms of vertebrobasilar insufficiency

Mechanisms Risk Factors
Intraluminal occlusion Thrombosis, embolism (87)
Mural factors Atherosclerosis resulting from vascular risk factors, hypoplasia (13). arterial dissection (35, 36,54,60,62,87,89).
Extrinsic factors (V0 to V4) (32, 87). Osteophytes (9) – With the head rotated to side with osteophyte: ipsilateral VA compressed against osteophyte, contralateral VA compressed at the foramina.(32). Chiropractic manipulation, surgical positioning, rheumatoid subluxation. Beauty parlor stroke.(19,21,83,86)
V0 (32) Compressions at the scalenovertebral angle by ligaments of scalenus anterior (Power’s syndrome) (49, 58). scalenus medius musle, longus colli muscle(17), deep fascia.
V1 Factors compressing V0 , Thoracic outlet syndrome (66)
V2 C2 to C6: osteophytes compressing the VA anteriorly from the uncinate process or posteriorly from the facet complex. (9). Prolapsed disc.(77).

C1 to C2: obliquus capitis inferior muscle, intertransversarius muscle, vertebral subluxation. kinking and stretching of the contralateral vertebral artery with 30 degrees head rotation.(32). Looped VA (64)
V3 Hyper-rotation of the atlantoaxial joint- Bow hunter’s syndrome. (27, 49, 63,71). C1 to foramen magnum: muscles (32), atlanto-occipital membrane hypertrophy (32), Vertebral subluxation, Atlantoaxial joint dislocation with stretched loop sign;(33,65) craniovertebral junction anomalies, (2,59) hypoplacia, (59) narrowing at point of dural penetration, (3). Rotational kinking and stretching of the contralateral VA . (32) os odontoideum (24) C1 root schwannoma (30)
V4 (32) Vascular anomalies eg termination of VA in posterior inferior cerebellar artery (37), stenosis, aneurysms, arteriovenous malformations
Hemodynamic Subclavian steal syndrome, Absent posterior communicating artery.

Table 2: review of articles on cervical vertigo

Authors and years No of cases Reported vascular risk factors Extrinsic compression of the VA Presence of rotational vertigo/dizziness
Sullivan HG, (73) 1975 1 Not reported Embolic occlusion of PCA triggered by spondylotic VA compression Not stated
Rock EH (61) 1989 Microatheromatous stenosis Vertigo only
Fujimoto S (22) 1989 2 out of 14 cases Rotational obstruction and spondylosis Vertigo, dysarthria, syncope
Kuether T (32) 1997 (Reviewed articles not duplicated in this paper.) 3 illustrative cases, plus a review of 19 articles with 131 cases from 1965 to 1985. Only age reported, other vascular risk factors not mentioned. 3 presented cases and 119 reviewed cases showed angiographic evidence of compression of V0 , V1, V2 or V3 Rotational vertigo present in the 3 presented cases and some of the reviewed cases
Matsuyama,(38) 1997 1 Left VA rotational occlusion at C1,C2 Wallenberg’s syndrome
Strek P, (72) 1998 130 Age (blood flow abnormality in the VA by Duplex sonography worsened with age) Cervical spondylosis (discopathy and or steophytes in all cases Vertigo, tinnitus
Galm R (25) 1998 67 Not reported Cervical spine dysfunction in 31 cases vertigo
Jagiello T (29) 1998 428 patients with VBI and spondylosis age Power doppler showed significant RVAO in 17% Symptoms of VBI including vertigo during head rotation in 66%
Citow JS, (14) 1999 1 Age, angina, ICA stenosis Compression of the VA at C5 by osteophyte Vertigo triggered by neck extension, change from supine to upright position or vice versa
Nan-Fu Chen, (11) 2000 1 Hypertension, age cerebral infarction, carotid atherosclerosis Osteophytic compression of the right VA with neck turning to the right and luminal reduction to less than half its original size on CTA Vertigo on turning head 60 degree to right
Vates GE (77) 2002 1 Age Rotational occlusion of the left VA at C4/C5 by herniated intervertebral disc Vertigo on turning the head to the left > 45o
Ogino M (49) 2002 1 Age, 66yr Compression of the right VA by osteophyte from C4 uncinate process and hypertrophied C3 transverse process. Resolved by resection Severe vertigo with head turned to the right
Nwaorgu et al, (47) 2003 43 Age (mean age 49.2 years), hypertension in 7 %, Cervical spondylosis in 74% of cases Vertigo in all cases. Not mentioned if rotational.
Neuheuser HK, (46) 2005 n = 1,003, response rate 87% Age (univariate analysis) Hypertension and dyslipidemia independent effect No radiological assessment was done Vestibular vertigo
Cagnie B, (9) 2005 111 transverse foramina Not reported About half of the osteophytes of the uncinate and of the superior articular process partially covered the transverse foramina obstructing the V2
Netuka D (45) 2005 1 Rotational compression of left VA at C1, C2 vertigo
Vilela MD (79) 2005 10 Age, hypertension, smoking, cholesterol RVAO demonstrated by Transcranial Doppler, MRI, CTA MRA Rotational Vertigo, syncope , tinnitus
Ozdemir H (53) 2005 52 patients with VBI and cervical spondylosis RVAO by doppler VBI symptoms
Olszewski J (50) 2006 80 Age .Basilar artery flow abnormality worsened with age Flow abnormalities in BA worsened with grade of radiological severity of cervical spondylosis 40 patients had vertigo. Flow abnormality worsened by neck rotation
Bulsara KR, (8) 2006 1 Age, Hypertension, diabetes mellitus, Obstruction of the right VA with head turning to the right by osteophyte at C5-C6 foramen transversarium Dizziness with head rotation
Owolabi MO (52) 2007 2 Hypertension, hyperlipidemia, age Cervical spondylosis, Rotational Vertigo relieved by neck collar
Tsutsumi S (75) 2008 1 Age Cervical spondylosis Rotational VBI symptoms, presyncope
Petridis AK, (57) 2008 1 Cervical spondylosis Rotational VBI symptoms, drop attacks


  1. ADAMS KRH, YUNG MW, LYE M, WHITEHOUSE GH. Are cervical spine radiographs of value in elderly patients with vertebrobasilar insufficiency? Age and Ageing. 1986; 15 (1): 57-9.
  2. AGRAWAL D, GOWDA NK, BAL CS, KALE SS, MAHAPATRA AK. Have cranio-vertebral junction anomalies been overlooked as a cause of vertebro-basilar insufficiency? Spine 2006; 31(7): 846-50.
  3. AKAR Z, KAFADAR AM, NECMETTIN T, DASHTI RS, ISLAK C, KOCER N, KUDAY C. Rotational compression of the vertebral artery at the point of dural penetration : Case report. J Neurosurg. 2000; 93 (2): 300-3.
  4. BAKAY L, LESLIE EV. Surgical treatment of vertebral artery insufficiency caused by cervical spondylosis. J Neurosurg 1965; 23(6): 596-602.
  5. BARTON J, MARGOLIS MT. Rotational obstruction of the vertebral artery at the atlantoaxial joint. Neuroradiology 1975; 9(3): 117-20.
  6. BRACHER ES, ALMEIDA CI, ALMEIDA RR, DUPRAT AC, BRACHER CB. A combined approach for the treatment of cervical vertigo. J Manipulative Physiol Ther. 2000; 23 (2): 96-100.
  7. BRANDT T, BALOH RW. Rotational vertebral artery occlusion: A clinical entity or various syndromes? Neurology. 2005; 65 (8): 1156-7.
  8. BULSARA KR, VELEZ DA, VILLAVICENCIO A. Rotational vertebral artery insufficiency resulting from cervical spondylosis: case report and review of the literature. Surg Neurol. 2006; 65(6): 625-627.
  9. CAGNIE B, BARBAIX E, VINCK E, D’HERDE K, CAMBIER D. Extrinsic risk factors for compromised blood flow in the vertebral artery: anatomical observations of the transverse foramina from C3 to C7. Surg Radiol Anat. 2005; 27 (4): 312-6.
  10. Center for Reviews and Dissemination. Undertaking systematic reviews of research on effectiveness: CRD’s guidance for those carrying out or commissioning reviews. http://www.york.ac.uk/inst/crd/report4.htm
  11. CHEN NF, SHEN CC, WANG YC. Vertebral Artery Stenosis Caused by Cervical Spondylosis: A Case Report. Acta Neurol Taiwan 2000; 9: 151-155.
  12. CHILDS JD, FLYNN TW, FRITZ JM, PIVA SR, WHITMAN JM, WAINNER RS, GREENMAN PE. Screening for Vertebrobasilar Insufficiency in Patients With Neck Pain: Manual Therapy Decision-Making in the Presence of Uncertainty. J Orthop Sports Phys Ther. 2005; 35(5): 300-6.
  13. CHOI KD, SHIN HY, KIM JS, KIM SH, KWON OK, KOO JW, PARK SH, YOON BW, ROH JK. Rotational vertebral artery syndrome: oculographic analysis of nystagmus. Neurology. 2005; 65(8): 1287-90.
  14. CITOW JS, MACDONALD R. Posterior Decompression of the Vertebral Artery Narrowed by Cervical Osteophyte: Case Report. Surg Neurol 1999; 51(5): 495-9.
  15. COLLEDGE N, LEWIS S, MEAD G, SELLAR R, WARDLAW J, WILSON J. Magnetic Resonance Imaging in people with dizziness: a comparison with non-dizzy people. J Neurol Neurosurg Psychiatry. 2002; 72: 587-9.
  16. DABUS G, GERSTLE RJ, PARSONS M, CROSS III DT, MORAN CJ, THOMPSON R, DERDEYN CP. Rotational Vertebrobasilar Insufficiency Due to Dynamic Compression of the Dominant Vertebral Artery by the Thyroid Cartilage and Occlusion of the Contralateral Vertebral Artery at C1-2 Level. J Neuroimaging. 2007; xx :1-4.
  17. DADSETAN MR, SKERHUT HE. Rotational vertebrobasilar insufficiency secondary to vertebral artery occlusion from fibrous band of the longus coli muscle. Neuroradiology. 1990; 32: 514-5.
  18. DOSS A, PHATOUROS CC. Vertebrobasilar insufficiency. Curr Treat Options Cardiovasc Med. 2006; 8 (2): 111-9.
  19. ENDO K, ICHIMARU K, SHIMURA H, IMAKIIRE A. Cervical vertigo after hair shampoo treatment at a hairdressing salon: a case report. Spine. 2000;25(5): 632-4.
  20. ERRO ME, GALLEGO J, HERRERA M, BERMEJO B. Isolated pontine infarcts: etiopathogenic mechanisms.Eur J Neurol. 2005; 12 (12): 984-8.
  21. FOYE PM, NAJAR MP, CAMME AA, STITIK TP, DEPRINCE ML, NADLER SF, CHEN B. Pain, dizziness, and central nervous system blood flow in cervical extension: vascular correlations to beauty parlor stroke syndrome and salon sink radiculopathy. Am J Phys Med Rehabil. 2002; 81(6): 395-9.
  22. FUJIMOTO S, TERAI Y, ITOH T, KAWAUCHI M. [Extracranial surgery of vertebrobasilar insufficiency. Reconstruction of the vertebral artery in the distal first portion]. Neurol Med Chir (Tokyo). 1989; 29(4): 292-6.
  23. FUJITA N, UEDA T, YAMANAKA T, INUI H, MINAMI Y, MIYAHARA H, MATSUNAGA T. Clinical application of ultrasonic blood rheography in vertebral artery for vertigo. Acta Otolaryngol Suppl. 1995; 519: 178-83.
  24. GALLI J, TARTAGLIONE T, CALO L, OTTAVIANI F. Os Odontoideum in a Patient with Cervical Vertigo: A Case Report. Am J Otolaryngol. 2001; 22: 371-3.
  25. GALM R, RITTMEISTER M, SCHMITT E. Vertigo in patients with cervical spine dysfunction . Eur Spine J. 1998; 7: 55-8.
  26. GRAD A, BALOW RW. Vertigo of vascular origin. Clinical and electronystagmographic features in 84 cases. Arch Neurol. 1989; 46: 281-4.
  27. HOROWITZ M, JOVIN T, BALZAR J, WELCH W, KASSAM A. Bow Hunter’s Syndrome in the Setting of Contralateral Vertebral Artery Stenosis: Evaluation and Treatment Options. Spine. 2002;27: E495-8.
  28. HUSNI EA, BELL HS, STORER J. Mechanical occlusion of the vertebral artery. JAMA. 1966; 196: 475-8.
  29. JARGIELLO T, PIETURA R, RAKOWSKI P, SZCZERBO-TROJANOWSKA M, SZAJNER M, JANCZAREK M. Power Doppler imaging in the evaluation of extracranial vertebral artery compression in patients with vertebrobasilar insufficiency. Eur J Ultrasound. 1998; 8 (3): 149-56.
  30. KALAVAKONDA C, SEKHAR LN, JONES RV, REHAMAN AB. Intermittent vertebral artery compression caused by C1-root schwannoma: case report. Neurol Res. 2000; 22 (7): 679-84.
  31. KIMURA K, BERREBY M. Temporal bone histopathology associated with occlusion of vertebrobasilar artery. Ann Otol Rhinol Laryngol. 1983; 92: 33-8.
  32. KUETHER T, NESBIT GM, CLARKE WM, BARNWELL SL. Rotational Vertebral Artery Occlusion: A Mechanism of Vertebrobasilar Insufficiency. Neurosurgery. 1997; 41(2): 427-33.
  33. MAEKAWA T, SASAI K, IADA H, YAMASHITA K, SAKAIDA M. Atlantoaxial Arthrodesis for Vertebrobasilar Insufficiency Due to Rheumatoid Arthritis: A Case Report. The Journal of Bone and Joint Surgery. 2007; 85 (4): 711.
  34. MAJAK J, OLSZEWSKI J, MILONSKI J, KUSMIERCZYK K. [Influence of positional blood flow disorders in the vertebral and basilar arteries on the prevalence of vertigo in patients with cervical spondylosis]. Pol Merkuriusz Lek. 2005; 19: 398-9.
  35. MAROON JC, GARDNER P, ABLA AA, EL-KADI H, BOST J. “Golfer’s stroke”: golf-induced stroke from vertebral artery dissection. Surg Neurol. 2007; 67 (111): 163-8.
  36. MARSHMAN LA, BALL L, JADUN CK. Spontaneous bilateral carotid and vertebral artery dissections associated with multiple disparate intracranial aneurysms, subarachnoid hemorrhage and spontaneous resolution. Case report and literature review. Clin Neurol Neurosurg. 2007; 109 (9): 816-20.
  37. MARTI S, HEGEMANN S, VON BUDINGEN HC, BAUMGARTNER RW, STRAUMANN D. Rotational vertebral artery syndrome:3D kinematics of nystagmus suggest bilateral labyrinthine dysfunction. J Neurol. 2008. DOI: 10.1007/s00415-008-0773-2
  38. MATSUYAMA T, MORIMOTO T, SAKAKI T. Bow Hunter’s stroke caused by a nondominant vertebral artery occlusion: case report. Neurosurgery. 1997; 41(5): 1393-5.
  39. Michigan Ear Institute. http://www.michiganear.com/index_real.html
  40. MITCHELL J, KEENE D, DYSON C, HARVEY L, PRUVEY C, PHILLIPS R. Is cervical spine rotation, as used in the standard vertebrobasilar insufficiency test, associated with a measureable change in intracranial vertebral artery blood flow? Manual Therapy. 2004; 9(4): 220-7.
  41. MITCHELL JA. Changes in vertebral artery blood flow following normal rotation of the cervical spine. J Manipulative Physiol Ther. 2003; 26(6): 347-51.
  42. MORALES C, DE MARINIS A, LABATUT G, VASQUEZ I, ARAVENA F. [Clinical significance of cervical arthropathy in patients with vertigo]. Rev Med Chil. 1990; 118(6): 657-61.
  43. MUKHERJEE A, CHATTERJEE SK, CHAKRAVARTY A. Vertigo and dizziness–a clinical approach. J Assoc Physicians India. 2003; 51: 1095-101.
  44. NAGASHIMA C. Surgical treatment of vertebral artery insufficiency caused by cervical spondylosis. J Neurosurg. 1970; 32: 512-21.
  45. NETUKA D, BENES V, MIKULIK R, KUBA R. Symptomatic rotational occlusion of the vertebral artery -case report and review of the literature. Zentralbl Neurochir. 2005; 66(4): 217-22.
  46. NEUHAUSER HK, VON BREVERN M, RADTKE A, LEZIUS F, FELDMANN M, ZIESE T, LEMPERT T. Epidemiology of vestibular vertigo: a neurotologic survey of the general population. Neurology. 2005; 65 (6): 898-904.
  47. NWAORGU OG, ONAKOYA PA, USMAN MA. Cervical vertigo and cervical spondylosis – a need for adequate evaluation. Niger J Med. 2003; 12(3): 140-4.
  48. NYBERG-HANSEN R, LØKEN AC, TENSTAD O. Brainstem lesion with coma for five years following manipulation of the cervical spine. Journal of Neurology. 1978; 218 (2): 97-105.
  49. OGINO M, KAWAMOTO T, ASAKUNO K, MAEDA Y, KIM P. Proper management of the rotational vertebral artery occlusion secondary to spondylosis. Clin Neurol Neurosurg. 2001; 103(4): 250-3.
  50. OLSZEWSKI J, MAJAK J, PIETKIEWICZ P, LUSZCZ C, REPETOWSKI M. The association between positional vertebral and basilar artery flow lesion and prevalence of vertigo in patients with cervical spondylosis. Otolaryngol Head Neck Surg. 2006;134 (4): 680-4.
  51. OLSZEWSKI J, MAJAK J, PIETKIEWICZ P, REPETOWSKI M. [Analysis of select diagnostic examination results and their connection with cervical vertigo diagnosis]. Pol Merkuriusz Lek. 2005; 19(111): 393-5.
  52. OWOLABI MO, OGAH OS, OGUNNIYI A. Episodic vertigo resulting from vascular risk factors, cervical spondylosis and head rotation: Two case reports. Neuropsychiatric Disease and Treatment. 2007; 3 (5): 675-8.
  53. OZDEMIR H, CIHANGIROGLU M, BERILGEN S, BULUT S. Effects of Cervical Rotation on Hemodynamics in Vertebral Arteries. Journal of Diagnostic Medical Sonography. 2005; 21(5): 384-1.
  54. PACIARONI M, GEORGIADIS D, ARNOLD M, GANDJOUR J, KESERU B, FAHRNI G, CASO V BAUMGARTNER RW. Seasonal variability in spontaneous cervical artery dissection. J Neurol Neurosurg Psychiatry. 2006; 77 (5): 677-9.
  55. PASZTOR E. Decompression of vertebral artery in cases of cervical spondylosis. Surg Neurol. 1978; 9: 371-377.
  56. PETERSON B, VON MARAVIC M, ZELLER JA, WALKER ML, KOMPF D, KESSLER C. Basilar artery blood flow during head rotation in vertebrobasilar ischemia. Acta Neurologica Scandinavica. 1996;94(4):294-301.
  57. PETRIDIS AK, BARTH H, BUHL R, MEHDORN HM. Vertebral artery decompression in a patient with rotational occlusion. Acta Neurochir (Wien ). 2008.
  58. POWERS SR, DRISLANE TM, NEVINS S. Intermittent vertebral artery compression: a new syndrome. Surgery. 1961; 49: 257-64.
  59. PUCA A, SCOGNA A, ROLLO M. Craniovertebral junction malformation and rotational occlusion of the vertebral artery. Br J Neurosurg. 2000; 14 (4): 361-4.
  60. REUTER U, HAMLING M, KAVUK I, EINHAUPL KM, SCHIELKE E. Vertebral artery dissections after chiropractic neck manipulation in Germany over three years. J Neurol. 2006; 253 (6): 724-30.
  61. ROCK EH. Vascular dizziness and transcranial Doppler ultrasonography. Ann Otol Rhinol Laryngol Suppl. 1989; 141:1-24.
  62. RUBINSTEIN SM, PEERDEMAN SM, VAN TULDER MW, RIPHAGEN I, HALDEMAN S. A systematic review of the risk factors for cervical artery dissection. Stroke. 2005; 36(7): 1575-80.
  63. SAKAGUCHI M, KITAGAWA K, HOUGAKU H, HASHIMOTO H, NAGAI Y, YAMAGAMI H, OHTSUKI T, OKU N, HASHIKAWA K, MATSUSHITA K, MATSUMOTO M, HORI M. Mechanical compression of the extracranial vertebral artery during neck rotation. Neurology. 2003; 61(6): 845-7.
  64. SAKAIDA H, OKADA M, YAMAMOTO A. Vascular reconstruction of a vertebral artery loop causing cervical radiculopathy and vertebrobasilar insufficiency. Case report. J Neurosurg. 2001; 94 (1Suppl): 145-9.
  65. SAWLANI V, BEHARI S, SALUNKE P, JAIN VK, PHADKE RV. ‘Stretched loop sign’ of the vertebral artery: a predictor of vertebrobasilar insufficiency in atlantoaxial dislocation. Surg Neurol. 2006; 66: 298-304.
  66. SELMONOSKY CA. A neglected cause of dizziness and neck pain. BMJ 2007; 334: 600-6.
  67. SHEEHAN S, BAUER RB, MEYER JS. Vertebral artery compression in cervical spondylosis. Neurology. 1960; 10: 968-86.
  68. SIMON H, NIEDERKORN K, HORNER S, DUFT M, SCHROCKENFUCHS M. [Effect of head rotation on the vertebrobasilar system. A transcranial Doppler ultrasound contribution to the physiology][Article in German] . HNO. 1994; 42 (10): 614-8.
  1. SITKO S, HONRUBIA V. Differential effect of ischemia on spontaneous and sinusoidal-evoked activity in semicircular canal afferents in the bullfrog. Acta Otolaryngol (Stockh). 1986; 102: 179-85.
  2. SMITH DR, VANDERARK GD, KEMPE LG. Cervical spondylosis causing vertebrobasilar insufficiency: A surgical treatment. J Neurol Neurosurg Psychiatry. 1971; 34: 388-92.
  3. SORENSEN BF. Bow hunter’s stroke. Neurosurgery. 1978; 2: 259-61.
  4. STREK P, RERON E, MAGA P, MODRYZEYEWSHI M, SZYBIST N. A possible correlation between vertebral artery insufficiency and degenerative changes in cervical spine. Eur Arch Otorhinolaryngol. 1998; 255: 437-40.
  5. SULLIVAN HG, HARBISON JW, VINES FS, BECKER D. Embolic posterior cerebral artery occlusion secondary to spondylotic vertebral artery compression. J Neurosurg. 1975; 2: 259-61.
  6. SWARTZ R, LONGWELL P. Treatment of vertigo. Am Fam Physician. 2005; 71(6): 1115-22.
  7. TSUTSUMI S, ITO M, YASUMOTO Y. Simultaneous bilateral vertebral artery occlusion in the lower cervical spine manifesting as bow hunter’s syndrome. Neurol Med Chir (Tokyo). 2008; 48(2): 90-4.
  8. UEMURA K, NOZUE M. [Vertigo-their typical clinical pictures from neurosurgical standpoints]. No Shinkei Geka 1983; 11(3): 229-42.
  9. VATES GE, WANG KC, BONOVICH D, DOWD CF, LAWTON MT. Bow hunter stroke caused by cervical disc herniation. Case report
    8. J Neurosurg. 2002; 96 (1 Suppl): 90-3.
  10. VELAT GJ, REAVEY-CANTWELL JF, ULM AJ, LEWIS SB. Intraoperative dynamic angiography to detect resolution of Bow Hunter’s syndrome: Technical case report. Surg Neurol. 2006; 66(4): 420-3.
  11. VILELA MD, GOODKIN R, LUNDIN DA, NEWELL DW. Rotational vertebrobasilar ischemia: hemodynamic assessment and surgical treatment. Neurosurgery. 2005; 56 (1): 36-43.
  12. WEINTRAUB MI, KHOURY A. Use of quantitative magnetic resonance angiography to stratify stroke risk in symptomatic vertebrobasilar disease.
    Stroke. 2005; 36(11): 2341-2.
  13. WEINTRAUB MI, KHOURY A. Mechanical compression of the extracranial vertebral artery during neck rotation. Neurology. 2004; 62(11): 2143.
  14. WEINTRAUB MI, KHOURY A. Cerebral hemodynamic changes induced by simulated tracheal intubation: a possible role in perioperative stroke? Magnetic resonance angiography and flow analysis in 160 cases. Stroke. 1998; 29(8): 1644-9.
  15. WEINTRAUB MI. Stroke after visit to the hairdresser. Lancet. 1997; 350 (9093): 1777-8.
  16. WEINTRAUB MI, KHOURY A. Critical neck position as an independent risk factor for posterior circulation stroke. A magnetic resonance angiographic analysis. J Neuroimaging. 1995a; 5 (1): 16-22.
  17. WEINTRAUB MI, KHOURY A. Transcranial Doppler assessment of positional vertebrobasilar ischemia. Stroke. 1995b; 26 (2): 330-2.
  18. WEINTRAUB MI. Beauty parlor stroke syndrome: report of five cases. JAMA. 1993; 269 (16): 2085-6.
  19. WELSH LW, WELSH JJ, LEWIN B. Basilar artery and vertigo. Ann Otol Rhinol Laryngol. 2000; 109(7): 615-22.
  20. YAMAGUCHI S, SAKATA K, NAKAYAMA K, SHIGEMORI M. [A case of embolic infarction originating from extracranial vertebral artery stenosis by cervical spondylosis at C5/6: its pathogenesis and surgical treatment]. No Shinkei Geka. 2003; 31 (10): 1111-6.
  21. YOUNG YO, CHEN CH. Acute Vertigo Following Cervical Manipulation. Laryngoscope. 2003; 113(4): 659-62.
  22. ZALEWSKI P, KONOPKA W, PIETKIEWICZ P. [Analysis of vascular vertigo due to cervical spondylosis and vertebro-basilar insufficiency based on sex and age in clinical materials]. Otolaryngol Pol 2004; 58 (1): 97-100.

© 2002-2018 African Journal of Neurological Sciences.
All rights reserved. Terms of use.
Tous droits réservés. Termes d'Utilisation.
ISSN: 1992-2647