ANATOM IC REPORT Rotational Vertebral Artery Occlusion: A Mechanism of Vertebrobasilar Insufficiency Todd A. Kuether, M .D ., Gary M. Nesbit, M .D ., W ayne M. Clark, M .D ., Stanley L. Barnwell, M .D ., Ph.D. Divisions of Neurosurgery (TAK, SLB), Radiology (CMN), Neurology (WMC), and the Dotter Interventional Institute (CMN, SLB), Oregon Health Science University, Portland, Oregon O BJECTIVE: Sym ptom atic dynam ic changes in blood flow secondary to vertebral artery com pression with rotational head motion are evaluated in a series of patients as a cause for posterior circulation transient ischem ic attacks. These cases are classic exam ples of rotational vertebral artery occlusion and allow for the discussion of the anatomic basis, angiographic features, and treatment options. ILLU STRATIVE C A SES: In our series, symptoms of vertebrobasilar insufficiency w ere reproducible with rotational head movement. Com pression of the vertebral artery was demonstrated angiographically. The correct site of occlusion of the vertebral artery was apparent only by dynam ic angiography with progressive head rotation. All of the patients presented in the illustrative cases had occlusion at the C2 level; how ever, one patient had been previously misdiagnosed and another had an additional site of occlusion. The anatom ic course of the vertebral artery is described in addition to the sites of rotational occlusion. C O N C L U S IO N : Rotational vertebral o cclu sio n is an im portant cau se of verteb ro b asilar sym ptom s, w h ich may lead to perm anent n e uro log ical deficit if left undiagnosed. D y n am ic angiography is the established m ethod of diagnosis. G re a t care must be taken to avoid m isdiagnosing the site of o cclu sio n or m issing a second occlu sive site. For this reason, it is c ru c ia l to have a thorough understanding of the an ato m ic co u rse of the vertebral artery and the m u scu lar and tendinous insertions, w h ich may cause rotational o cclu sio n . The decision for treatm ent must be based on the site of o cclu sio n as w ell as the assessm ent of the patient as a surgical can d id ate. A review of the literatu re reveals that surgical treatm ent is effective and must be considered to avoid further m orbidity. (N eurosurgery 4 1 :4 2 7 -4 3 3 , 1997) Key words: Cerebral angiography, Vertebral artery, Vertebrobasilar insufficiency, Vertigo ertebrobasilar insufficiency is a syndrom e charac­ terized by diplopia, dysarthria, visual disturbances, vertigo, and sensory or m otor sym ptom s. Sym ptom s relate to ischemia from atherosclerotic lesions, throm boem ­ bolic events, and m echanical obstruction. In three patients, sympmatic dynam ic changes in blood flow secondary to vertebral artery com pression with rotational head motion are evaluated as a cause for posterior circulation transient ischemic attacks. The purpose of these case reports is not to define a new neurological disorder but rather to serve as examples for discussion of the appropriate diagnostic evaluation and treatm ent options to avoid some of the common pitfalls encountered in patients with vertebrobasi­ lar insufficiency. V ILLU ST R A T IV E CASES Patient 1 This patient, a 49-year-old man, presented with a 1-year history of dizziness when turning his head to the far right. The results of a computed tomographic scan of the brain were normal. An arch aortogram was obtained and demonstrated a normal appearing left vertebral artery up to the C2 vertebral body. The right vertebral artery was hypoplastic. During a selective left vertebral artery injection with the head turned to the right, contrast flow ed to the level of the C 4-C 5 interspace, w hich was thought to be the cause of the sym ptom s (Fig. 1A). The patient underw ent a posterior decom ­ pression of the foram ina transversaria and surrounding soft tissues at the level of C 4-C 5. Postoperatively, there was no im provem ent Neurosurgery, Vol. 41, No. 2, August 1997 427 428 K u e th e r et al. r degenerative disease. The results of a physical examination wen noncontributory. Transcranial doppler ultrasonography indicated normal flow and velocity in both vertebral arteries and the basilar artery with the head in neutral, far right, and extended positions. Vertebral angiography dem onstrated a hypoplastic right vertebral artery and a n o rm al let vertebral artery with the head in a neutral position. When the pa tient's head was turned to the right, there was significant stenosis ol the left vertebral artery at the foramina transversaria at the C2 verte­ bral body (Fig. 2, A and B). With head rotation, there were n o changein the right vertebral artery. This patient also elected to fo re g o surgi cal treatment and has remained asym ptom atic with voluntary restni tion of head movement. Patient 3 F IG U R E 1. A, angiogram of the left subclavian artery, obtained before surgery (anteroposterior projection, head rotated to the right), dem onstrating flow up the left vertebral artery to the C 5 level (arrow). The contrast m aterial reaches only the level of C 5 , the site at w h ich the lam inectom y w as subsequently perform ed. This does not represent the site of arterial o cclu sion , w hich is higher at the C 2 level. B, angio­ gram of the left vertebral artery, obtained after lam inectom y (lateral projection, head in a neutral position), show ing the left vertebral artery coursing through the foram en transversarium of the C 2 vertebral body (arrow). As the artery This patient, a 39-year-old man, developed episodic tinnitus, haz iness, and blackouts, which were associated with turning his head to the right. There were no focal neurological deficits. The results of angiography of the cervical portions of both vertebral arteries were normal when the patient's head was held in a neutral position. Dynamic angiography with head rotation to the right dem­ onstrated that the left vertebral artery was occluded at the C2 level (Fig. 3A). His right vertebral artery, which was normal in the neutral position (Fig. 3B), occluded at the C 7 level (Fig. 3C) with head rotation to the right. A lateral carotid arteriogram with the patient's head turned sharply to the right showed normal filling of the anterior circulation but no filling of the posterior circulation, indicating that crosses through the foram en transversarium , there is a curve in the vessel but no stenosis. C , angiogram of the left verte­ bral artery (lateral projection, head turned to the right). W ith head turning, there w as progressive stenosis of the left verte­ bral artery at the foram en transversarium of the C 2 vertebral I body (arrow). A small am ount of contrast courses beyond the stenosis into the more distal vertebral artery (curved arrow). ) This stenosis is caused by an ossified or fibrous band across the foram en transversarium at the C 2 level. in the p atient's sym ptom s. He presented to our institution for further evaluation. The findings of a physical examination included immediate onset of dizziness, leading to loss of consciousness, when the patient turned his head 90 degrees to the right. Extreme neck extension also repro­ duced the symptoms. There were no cervical bruits, and the rem ain­ ing neurological examination revealed no focal deficits. Digital subtraction angiograms were obtained of the anteroposte­ rior, Towne's, and Caldwell projections, with the patient's head turned to the right sufficiently to produce dizziness but not loss of consciousness. The left vertebral injection demonstrated a stricture of the left vertebral artery as it entered the C2 foramina. With further head turning, the stenosis became an occlusion (Fig. 1, B and C). The patient refused further surgical treatment, preferring to restrict his head movement to avoid vertebrobasilar insufficiency. F IG U R E 2. A, angiogram of the left vertebral artery (antero­ posterior projectio n), dem onstrating norm al left vertebral and basilar arteries. The vertebral artery, at the point at w hich it enters the foram en transversarium of the C2 verte­ bral body (arrow), show s the norm al anatom ic caliber Patient 2 This patient, a 62-year-old man, presented with a 2-month history of symptoms. He reported that while working on his car, he felt as though he were going to pass out when he extended his head back­ ward. After that, he experienced daily events of near fainting when he turned his head backward and to the right. The events rapidly re­ solved whenever he turned his head to a neutral position. His medical history was notable for hypothyroidism and cervical spondylotic change w ithout significant stenosis. B, angiogram of the left vertebral artery (anteroposterior projection, head turned to the right), show ing com pression of the left vertebral artery (arrow), producing m arkedly d ecreased flow through the m ore distal vertebral artery (curved arrow). In the more proxim al vertebral artery, there is stasis of contrast, a ccount ing for the increased density. Neurosurgery, Vol. 41, No. 2, August 1997 R o tatio n al V e rte b ra l O c c lu s io n 429 At this time, the number of causes of this syndrome has grown to include many activities. Vertebral artery compres­ sion has resulted from chiropractic manipulation, surgical positioning, rheumatoid subluxation, a multitude of physical activities, and sports. There have also been numerous ac­ counts of embolic complications related to vertebral compres­ sion. However, the true incidence of this disorder is not known. In an early study of 43 asymptomatic male volunteers with a mean age of 47 years, Farris et al. (5) observed angio­ graphic evidence of vertebral artery occlusion with head ro­ tation in 4 of the volunteers (9%). Anatom ic relationships FIG U R E 3. A, angiogram of the left vertebral artery (lateral projection, head rotated to the right), show ing occlu sion of the artery at the foram en transversarium of the C 2 vertebral body (arrow ). B, angiogram show ing right subclavian artery injection (anteroposterior projection, head in a neutral posi­ tion) and dem onstrating flow in the right vertebral artery to the C5 vertebral body (arrow). C, w ith head rotation to the right, a high-grade stenosis of the right vertebral artery developed at the C 7 level (arrow). there was no flow through the posterior communicating arteries. The patient reported having symptoms during that part of the examina­ tion. He elected to treat this conservatively and has remained asymptomatic. D ISC U SSIO N What was referred to as cervical vertigo (17) in 1955 was a syndrome characterized by vertigo, dizziness, and blurred vision with head rotation. Tatlow and Bammer (24) postu­ lated, in 1957, that head rotation compressed the vertebral arteries, which led to these symptoms of vertebrobasilar in­ sufficiency. In studies performed on a single cadaver, com­ pressions of the vertebral arteries were identified at the C 1-C 2 and the C 5-C 6 levels when the head was rotated. These observations were based on work performed 20 years earlier by DeKleyn and Versteegh (4), who described a decrease in vertebral circulation on one side when the head was turned backward and to the opposite side. Toole and Tucker (25) later observed, in a study of 20 cadavers, that 75% of the cases demonstrated significantly compromised blood flow in one or both vertebral arteries with head rotation. Cervical spondylosis provided the initial model for verte­ bral artery compression. Sheehan et al. (19), in I960, published reports of a series in which 5 of 26 patients with cervical spondylosis and symptoms of vertigo and blurred vision with head rotation demonstrated vertebral artery compression as revealed by angiography. Powers et al. (16) then described a similar syndrome related to intermittent compression of the vertebral artery by the anterior scalene muscle. Since then, there have been more than 100 cases of symptoms related to compression of the vertebral artery, which has recently been named bow hunter's syndrome (22). We do know that the vertebral arteries are susceptible to mechanical compression with head rotation because of their anatomic relationship with neighboring bone, muscle, liga­ ments, and fascia. As each vertebral artery branches from the first part of its respective subclavian artery, it ascends and enters the foramina transversaria of C6. At this entry point, the artery must pass near tendinous insertions of the longus colli, scalenus anterior, and scalenus medius muscles (Fig. 4). Fibers arising from the lateral rim of the vertebral canal cross medially to join the longus colli. In addition, fibers from the medial rim cross laterally to join the scalenus anterior and me­ dius. Powers et al. (16), in 1960, were the first to publish reports of a series of patients whom they treated by performing scalenotomies. Reports of more than 50 cases have been published relating to external compression of the vertebral artery by liga­ mentous insertions or deep fascia at the "scalenovertebral angle" (3, 8, 10-12). The artery next passes through the foramina transversaria of the cervical vertebrae at C 6-C2. At that point, the artery is susceptible to compression by osteophytes and other degen­ erative changes of cervical spondylosis (Fig. 5). There have been more than 30 published reports of cases of vertebral compression by osteophytes at all levels (1, 13, 19, 21). When the head is rotated toward the side with the osteophyte, the ipsilateral vertebral artery is compressed against the osteo- Neurosurgery, Vol. 41, No. 2, August 1997 F IG U R E 4. Illustration of the left vertebral artery as it passes near the tendinous insertions of longus colli (arrow), scalenus anterior (curved arrow), and scalenus medius ( arrow head). 430 K u e th e r et al. lies that led to cerebral ischemia or infarction with heac rotation (9). F IG U R E 5. Illustration of the left cervical osteophyte (arrow) show ing com pression of the vertebral artery at the foram ina. phyte and the contralateral artery is compressed at the foramina. The vertebral artery then passes obliquely to the C l foram­ ina. At the atlantoaxial joint, the artery can be compressed by fibers from the obliquus capitis inferior muscle, intertransversarius muscle, membrane hypertrophy, or vertebral subluxa­ tion (7) (Fig. 6). Selecki (18) demonstrated, using cadavers in 1969, that kinking and stretching of the contralateral vertebral artery can be observed at this site with 30 degrees of head rotation and becomes well marked at 45 degrees. Beyond 45 degrees, kinking and stretching at the foramina transversaria was seen in both arteries. After passing through the C l foramina, the artery bends posteriorly at right angles and winds around the superior part of the lateral mass of the atlas. The vertebral artery pierces the posterior atlanto-occipital membrane. At that point, the artery may finally be compressed (15, 26). The arteries then pierce the dura mater and arachnoid to enter the subarachnoid space of the cerebellomedullary cistern and unite to form the basilar artery. One last hypothesis concerning the cause of these vertebro­ basilar symptoms involves the formation of thrombus within the vertebral arteries during the time when the flow is oc­ cluded. These thrombi then embolize to result in either transient ischemic attacks or cerebral vascular accidents (6, 15, 20, 23). In many of these cases, the patient had one hypoplastic vertebral artery. Symptoms resulted from occlusion of flow in the normal artery with insufficient collateral flow through the opposite vertebral. There were also cases of vascular anomaF IG U R E 6. Illustration of the left atlantoo ccipital m em brane (arrow), left intertransversarius m uscle (curved arrow), and right obliquus capitis inferior m uscle (arrow head) in relation to the vertebral arteries. Diagnosis and Treatm ent Although there are many causes of vertebrobasilar svmp toms with head rotation, these cases demonstrate that d\ namic angiography is necessary for diagnosis. One must vi­ sualize the compression of the artery with head rotation Credibility is added to the examination if the patient's symptoms are reproduced. In any case, great care must be taken to avoid diagnosing an occlusion lower than the actual constric tion. If the patient's head is turned, producing occlusion of flow, and the contrast has not yet reached the occlusive site then the level of occlusion may be incorrectly identified, as demonstrated in the first case. For this reason, it is imperative to see the contrast extend to the level of the foramen magnum before making a final decision regarding the location of the stenosis. Once an accurate diagnosis is made of rotational vertebral artery occlusion, then the patient has the option of conserva­ tive or surgical treatment. The conservative approach consists of anticoagulation or neck immobilization, either by instrucling the patient to refrain from head turning or by the use of a collar. Surgical treatm ent must be tailored to the likely cause of the compression. Simple exploration with fascial decom­ pression may be all that is needed. For obstructions relating to foraminal compression, either a midline approach with discectomy and osteophyte removal or a posterior lateral ap­ proach with partial transversectomy and unroofing of the foramina may be performed. Fusion has been advocated by some individuals but has not been shown to comparatively improve the postoperative course (1, 21). There are certainly those cases, such as vertebral compression related to sublux­ ation, in which fusion is indicated. O utcom e Regardless of the surgical procedure, a postoperative dy­ namic angiogram is required to substantiate that the rota­ tional compression has been corrected. Listed in Table 1 is a review of the published reports of cases of rotational vertebral artery obstruction. The average age of the patients was 4q years, and the most common presenting symptoms were ver­ tigo and vision changes. The method of diagnosis was angiog­ raphy in every case. However, some of the earlier published reports did not include the use of dynamic angiography. The surgical treatment depended on the cause of the extrinsic compression. The overall success rate for surgery based on relief of symptoms was 85%. Of those treated conservatively, nearly 50% went on to infarct or had residual neurological deficits. For this reason,!1 is crucial to discuss potential risks with patients when seeking informed consent. Most patients prefer not to have su rg en but they must be aware of the potential complications of more conservative treatment. The three patients presented in th>s article elected to treat their rotational compression conserva­ tively despite the risks and our recommendations for surgical intervention. Neurosurgery, Vol. 41, No. 2, August 1997 R o tatio n al V e rte b ra l O c c lu s io n 431 TABLE 1. R eview of Cases in Literature'1 Series (Ref. No.) No. of Average Patients Age (yr) Presenting Symptom Method of Diagnosis Imaging Dynamic Angio­ graphy Treatment Cause Outcome Asymptomatic at 6 mo Medullary infarct in one patient Asymptomatic postoperatively Postoperative Angiography Normal + Decompression, ant fusion C5-C6 osteophyte + None C1-C2 vertebral occlusion CT + Ant scalenotomy, section of longus colli tendon Vertebral occlusion near origin Angiography CT + Anticoagulation C1-C2 vertebral occlusion Cerebellar infarct Weakness, vertigo, nausea Angiography CT + Decompressive transverse foramenectomy C1-C2 vertebral occlusion 58 Dizziness, syncope, dysarthria Angiography + Ant scalenotomy and fascial decompression, section of thyrocervical trunk, suture fixation of subclavian artery Vertebral occlusion origin to C5 Asymptomatic, 2-yr f/u in one case Asymptomatic, 13 of 15 1 16 Headache, vision, ataxia Angiography None Cerebral infarct Hypoplastic left vertebral, absent left posterior communicating artery Husni et al., 1966 (10) 20 40 Dizziness Angiography C5-C6 vertebral occlusion Asymptomatic, 19 of 20; avg f/u, 2 yr Kojima et al., 1985 (11) 1 64 Vertigo with head turning Angiography CT + Ant scalenotomy, section of longus colli tendon, interposing fat pedicle Decompression, C6 transverse process unroofed Longus colli, ant scalene Asymptomatic; f/u, 18 mo Normal Mapstone and Spetzler, 1982 (12) 1 54 Vertigo with head turning Angiography CT + Decompression Longus colli Postoperative resolution Normal Nagashima, 1970 (13) 20 52 Vertigo, dizziness, blurred vision Angiography 3 34 Paralysis, ataxia Angiography Myelogram 72% asymptomatic Residual weakness and ataxia 13 of 20 Normal Nagler, 1973 (14) Okawara and Nibbelink, 1974 (15) 1 43 Headache ataxia Angiography Transverse C4-C7 foramenectomy compression Cervical C1-C2 vertebral laminectomy in occlusion in one case one case Steroids C1-C2 vertebral occlusion Powers et al., 1961 (16) 28 Vertigo, tinnitus, deafness, bruit Angiography Decompressive scalenotomy and section of thyrocervical trunk 17 of 28 ant scalene Asymptomatic, 16 of 17 Sheehan et al., 1960 (19) 26 53 Vertigo, dizziness, blurred vision Angiography Bed rest, limit head motion Cervical spondylosis Shimizu et al., 1988 (20) 1 37 Dizziness, diplopia, Angiography nausea + Decompressive transverse foramenectomy Asymptomatic; f/u, 24 mo Normal Smith et al., 1971 (21) 2 52 Headache, syncope, vertigo Angiography - Decompressive foraminotomy, ant fusion C1-C2 vertebral occlusion with embolism C5-C6 osteophyte Asymptomatic Normal Sullivan et al., 1975 (23) 1 37 Headache vision loss Angiography CT - Decompression, ant fusion Residual visual field defect Normal Yanget al., 1985 (26) 2 58 Angiography Vision loss, ataxia, and dizziness with head turning CT + C5-C6 osteophyte with embolism C1-C2 fusion/ observation C1-C2 vertebral occlusion Asymptomatic; f/u, 6 and 18 mo Normal Bakay and Leslie, 1965 (1) 2 44 Dizziness Barton and Margolis, 1975 (2) Dadsetan and Skerhut, 1990 (3) 2 50 Dizziness, Angiography blackouts, vertigo 1 56 Vertigo, decreased vision Angiography Grossman and Davis, 1982 (6) 1 19 Vertigo, diplopia, ataxia Hanakita et al., 1988 (7) 3 58 Hardin and Poser, 1963 (8) 15 Hope et al., 1983 (9) ■*CT, computed tomography; + , performed; Angiography Myelogram CT + CT CT - not performed; ant, anterior; f/u, follow-up. Neurosurgery, Vol. 41, No. 2, August 1997 Normal Normal Residual ataxia 432 K u e th e r et al. Postoperative angiography was performed in 20% of the cases. In the majority of patients, angiography was performed in the immediate postoperative period. Only four patients were reported with angiographic follow-up 3 to 8 months after surgery. Regardless of timing, all postoperative angiog­ raphy revealed complete resolution of the rotational compres­ sion. Nagashima (13) reported that in 10 of 13 patients, al­ though the compression was relieved, there remained some evidence of a retained kink in the artery. C O N C L U S IO N Rotational vertebral occlusion is an important cause of vertebrobasilar symptoms. As many prior case reports have demonstrated, this may lead to permanent neurological defi­ cit if left undiagnosed. A thorough understanding of the anatomic course of the vertebral artery and the muscular and tendinous insertions that may result in rotational occlusion is imperative in the treatment of this disorder. These three cases are classic examples of vertebral compression with head ro­ tation. Misdiagnosis must be avoided by the use of dynamic angiography if this entity is suspected. Dynamic angiography is not a new concept but can be misinterpreted if not per­ formed correctly. The decision regarding the appropriate type of treatment must be based on the site of occlusion as well as the assessment of the patient as a surgical candidate. A review of the literature reveals that surgical treatment is effective and should be considered to avoid further morbidity. Received, August 5, 1996. Accepted, February 28, 1997. Reprint requests: Todd A. Kuether, M.D., Division of Neurosurgery, L-472, Oregon Health Sciences University, 3181 S.W. Sam Jackson Park Road, Portland, OR 97201. REFEREN CES 1. Bakay L, Leslie EV: Surgical treatment of vertebral artery insuf­ ficiency caused by cervical spondylosis. J Neurosurg 23:596-602, 1965. 2. Barton JW , M argolis MT: Rotational obstruction of the vertebral artery at the atlantoaxial joint. Neuroradiology 9:117-120, 1975. 3. Dadsetan MR, Skerhut HE: Rotational vertebrobasilar insuffi­ ciency secondary to vertebral artery occlusion from fibrous band of the longus colli muscle. Neuroradiology 32:514-515, 1990. 4. DeKleyn A, Versteegh C: Uber verschiedene Formen von Menieres Syndrom. Dtsch Z Nervenheilkd 132:157-189, 1933. 5. Farris AA, Poser CM, W ilmore DW, Agnew CH: Radiologic vi­ sualization of neck vessels in healthy men. Neurology 13:386-396, 1963. 6. Grossman RI, Davis KR: Positional occlusion of the vertebral artery: A rare cause of embolic stroke. Neuroradiology 23:227230, 1982. 7. Hanakita J, Miyake H, Nagayasu S, Nishi S, Suzuki T: Angio­ graphic examination and surgical treatment of bow hunter's stroke. J Neurosurg 23:228-232, 1988. 8. Hardin CA, Poser CM: Rotational obstruction of the vertebral artery due to redundancy and extraluminal cervical fascial bands. Ann Surg 158:133-137, 1963. 9. Hope EE, Bodensteiner JB, Barnes P: Cerebral infarction related to neck position in an adolescent. Pediatrics 72:335-337, 1983. 10. Husni EA, Bell HS, Storer J: Mechanical occlusion of the vertebral artery. JA M A 196:475-478, 1966. 11. Kojima N, Tamaki N, Fujita K, M atsumoto S: Vertebral arten occlusion at the narrowed "scalenovertebral angle": Mechanical vertebral occlusion in the distal first portion. Neurosurgery If, 672-674, 1985. 12. M apstone T, Spetzler RF: Vertebrobasilar insufficiency secondary to vertebral artery occlusion from a fibrous band. J Neurosurg 56:581-583, 1982/ 13. Nagashima C: Surgical treatment of vertebral artery insufficiency caused by cervical spondylosis. J Neurosurg 32:512-521, 1970. 14. Nagler W: Vertebral artery obstruction by hyperextension of the neck: Report of three cases. Arch Phys Med Rehabil 54:237-240, 1973. !< 15. Okawara S, Nibbelink D: Vertebral artery occlusion following hyperextension and rotation of the head. Stroke 5:640-642,1974 16. Powers SR, Drislane TM, Nevins S: Intermittent vertebral arten compression: A new syndrome. Surgery 49:257-264, 1961. 17. Ryan GM, Cope S: Cervical vertigo. Lancet 2:1355-1358, 1955. 18. Selecki BR: The effects of rotation of the atlas on the axis: Exper imental work. Med J Austr 1:1012-1015, 1969. 19. Sheehan S, Bauer RB, Meyer JS: Vertebral artery compression in cervical spondylosis. N eurology 10:968-986, 1960. 20. Shimizu T, Waga S, Kojima T, Shigehiko N: Decompression of the vertebral artery for bow -hunter's stroke. J Neurosurg 69:127— 131 1988. 21. Smith DR, Vanderark GD, Kempe LG: Cervical spondylosis caus­ ing vertebrobasilar insufficiency: A surgical treatment. J Neurol Neurosurg Psychiatry 34:388-392, 1971. 22. Sorensen BF: Bow hunter's stroke: J Neurosurg 2:259-261, 1978 23. Sullivan HG, Harbison JW , Vines FS, Becker D: Embolic posterior cerebral artery occlusion secondary to spondylitic vertebral artery compression. J N eurosurg 43:618-622, 1975. 24. Tatlow WFT, Bammer HG: Syndrom e of vertebral artery com­ pression. N eurology 7:331-340, 1957. 25. Toole JF, Tucker SH: Influence of head position on cerebral cir­ culation. Arch Neurol 2:616-623, 1960. 26. Yang PJ, Latack JT, Gabrielsen TO, Knake JE, Gebarsk SS Chandler WF: Rotational vertebral artery occlusion at C1-C2. AJN R Am J Neuroradiol 6:98-100, 1985. CO M M EN TS The authors provide a very concise summary of a peculiar clinical syndrome: rotational vertebral artery occlusion with vertebrobasilar ischemic symptoms. The reader should pay particular attention to the illustrative case of Patient 1 and Figure 1 of the article. This case report clearly demonstrates a mechanism by which the cause of the patient's symptoms can be misdiagnosed and treatment directed at the wrong site The use of dynamic angiography in these cases is critical, because transcranial doppler ultrasonography or angiogra­ phy performed in the neutral position will routinely miss the diagnosis. The authors summarize the available data and provide insight into various surgical and medical treatment alternatives for patients with compression syndromes arising from the various anatomic sites. H . H u n t Batjer Chicago, Win®* This article demonstrates the angiographic feature of rota­ tional occlusion of the vertebral artery in the neck. A w areness Neurosurgery, Vol. 41, No. 2, August 1997 1 i R o tatio n al V e rte b ra l O c c lu s io n of this phenomena is important in clinical practice when evaluating transient ischemia of the posterior circulation. It would be helpful to know the potential effects of surgical treatment. St Shigeaki Kobayashi Matsumoto, Japan This study presents three patients with posterior circulation transient ischemic attacks in whom dynamic angiography during rotational head movements confirmed vertebral artery compression. The authors emphasize that the use of dynamic angiography is critical to making the diagnosis and delineat­ ing the precise site of vertebral artery compression. The artery is susceptible to mechanical compression during head rotar; tion, particularly because of compression from muscle, liga­ ment, and fascial insertions along the ascent of the vertebral artery in the cervical spine. Although the topic of mechanical vertebral artery compres­ sion and head rotation causing posterior circulation transient ischemic attacks has been reviewed previously (1), the strength of this article lies in the demonstration of the useful­ 43 3 ness of dynamic angiography for establishing the diagnosis and site of rotational vertebral artery occlusion. The authors provide a thorough literature review and conclude that the overall success rate for surgical treatment of this problem is high. We have also achieved gratifying clinical outcomes after surgical decompression of the cervical vertebral artery in similar patients with posterior circulation transient ischemic attacks and angiographic confirmation of vertebral artery compression with head turning. In all of our cases, the con­ tralateral vertebral artery was absent, was hypoplastic, or ended in the posteroinferior cerebellar artery. Gary K. Steinberg Reid C. Thompson Neuroscientist Stanford, California 1. Bauer RB: Mechanical compression of the vertebral arteries, in Berguer R, Bauer RB (eds): Vertebrobasilar Arterial Occlusive Dis­ ease: M edical and Surgical Management. New York, Raven Press, 1984, pp 45-71. A N N O U N CEM EN T et Foundation for International Education in Neurosurgery Update and Request for Volunteers The Foundation for International Education in Neurosurgery (FIENS) continues to develop activities that are primarily designed to foster education in developing areas of the world. These initiatives are coordinated with the activities of the World Federation of Neurosurgical Societies, which, through its Education Committee, has sponsored a number of regional educational programs for neurosurgeons in developing areas. The Foundation assists in providing faculty for these larger educational efforts. The major current activities of FIENS consist of programs in Africa. The Foundation has worked with neurosurgeons in Ghana in an attempt to help develop an indigenous neurosur­ gical training program there. This has involved sending senior level residents and faculty for varying periods of time, usually 3 to 6 months for residents and 2 to 4 weeks for faculty support. FIENS has supported a program in Zimbabwe to provide neuro­ surgical assistance to the program already in place in that country, and it has supported an African trainee, who currently is a resident at Yale, in the initial steps to develop a neuroscience initiative for Southern Africa. She has been a liaison with the Panafrican Neurosurgical Association, which strongly supports this concept, and we anticipate rapid development. Another new project involves a Senior Neurosurgical Interchange with Peru under the guidance of Dr. Anselmo Pineda and the Peruvian-American Neurosurgical Society. Opportunities exist for volunteer neurosurgeons to go to Peru and visit and work in a number of different medical centers around the country. FIENS maintains a roster of neurosurgeons interested in serving as volunteers. For volunteer experiences of at least 4 to 6 weeks, the Foundation will support the volunteer's air travel expenses. The host country is ordinarily able to underwrite most of the volun­ teer's expenses incurred at work. Further information and volunteer request forms can be obtained from the Office of the Secretary of the Foundation, Dr. David Fairholm: Division of Neurosurgery, Department of Surgery, Room 3100, 910 W. 10th Avenue, Vancouver, BC, Canada V5Z 4E3. tfi \d Neurosurgery, Vol. 41, No. 2, August 1997