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Uncommon ultrasound findings in traumatic extracranial vertebral artery dissection
European Journal of Ultrasound 12 (2001) 227– 231 www.elsevier.com/locate/ejultrasou
Clinical Science: Case Report
Uncommon ultrasound findings in traumatic extracranial vertebral artery dissection N. Cals, G. Devuyst *, D.K. Jung, N. Afsar, G. De Freitas, P-A. Despland, J. Bogousslavsky Department of Neurology, Hopital Uni6ersitaire Vaudois, CHUV, BH 07, 46 Rue du Bugnon, 1011 Lausanne, Switzerland Received 29 June 2000; received in revised form 10 October 2000; accepted 17 October 2000
Abstract We report a case of internal carotid artery dissection (ICAD) associated with contralateral vertebral artery dissection (VAD). The interest of this case is to discuss an unusual Doppler pattern manifesting by a spectrum of an alternating vertebral artery flow suggesting a hemodynamic contribution from the contralateral vertebral artery (VA) and a clear depiction of both antegrade (red) and retrograde (blue) flow within the false and true lumen of the VAD by color Duplex flow imaging. © 2001 Elsevier Science Ireland Ltd. All rights reserved. Keywords: Vertebral artery; Dissection; Color Duplex flow imaging; Blood flow velocities
1. Introduction Although dissection constitutes a frequent cause of strokes in young patients, the early diagnosis of vertebral artery dissection (VAD) is often difficult. Angiography has been considered as the gold standard for diagnosis of VAD but it is invasive and not without risk (Bartels and Flugel, 1996; Auer et al., 1998). The advent of new effective non-invasive methods such as duplex ultrasonography, MRI and MRA may result in * Corresponding author. Tel.: +41-21-3141225; fax: + 4121-3141290. E-mail address: [email protected] (G. Devuyst).
earlier and safe diagnosis of cervical arteries dissection. Although ultrasound seems to be a sensitive and reliable tool in the diagnosis of ICAD, its role in VAD remains equivocal (Sturzenegger et al., 1993). We report a case of ICAD associated with contralateral VAD occurring following chiropractic manipulation. Two lumina in the same vessel and to-and-fro spectrum have already been described in case of VAD by B-mode and Doppler ultrasound, respectively, but in the present case of VAD we could also demonstrate the antegrade (red) and retrograde (blue) flow by color Duplex flow imaging within the false and true lumen. In addition, our case is associated with a vertebral artery alternating flow which is
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N. Cals et al. / European Journal of Ultrasound 12 (2001) 227–231
not related to a subclavian artery and/or proximal VA stenosis but due to a long VAD in our opinion.
2. Case report A 51-year-old woman was admitted because of left hemibody weakness preceded by acute headache. She had no relevant disease in her past except episodes of migraine. Four days after chiropractic maneuvers (with elements of abrupt head rotation), she developed an unusual headache localized to the right frontal region associated with nausea and vomiting with no response to analgesics and aggraving in time. While the pain did not subside, 10 days later she developed a left-sided weakness. On admission, she was oriented and her neurological examination revealed a left facio-brachio-crural hemiparesis with left motor hemineglect. Left Babinski sign was present. There were no cerebellar signs, no sensory dysfunction and no Horner’s syndrome. The examination of cranial nerves was normal. Cardiovascular examination was normal. Routine blood tests did not reveal any abnormality. On continuous wave Doppler and color duplex flow imaging (CDFI) (ATL HDI 5000, Advanced Technologies Laboratories, Seattle, USA), the origin of the left VA (V1 segment) could not be visualized possibly because of a too posterior intrathoracic localization in this patient as described previously (Nicolau et al., 2000). Examination of the V2 segment of the left VA showed a significant decrease in both systolic (18 vs. 40 cm/s on the right VA) and diastolic (4 vs. 15 cm/s on the right VA) blood flow velocities (BFV) with a diameter of 4.4 mm on the left and 3.9 mm on the right, to-and-fro spectrum and double lumen with a red flow (antegrade) and a blue flow (retrograde) on transversal and longitudinal sections between C4 and C5 transverse processes (Fig. 1a and b). No arterial flow could be recorded in V3 segment of left VA as well as by Doppler and CDFI (transverse sections). In the intracranial VA (V4 segment) blood flow was pendulum-like with a retrograde flow in systole and anterograde flow in diastole (Fig. 1c). Left subclavian artery and
basilar artery flow were normal. MRI (Magnetom –Symphony, diffusion, T1 and T2 weighted images) revealed multiple lesions in the right anterior borderzone hemispheric distribution (preferentially involving subcortical white matter). Brain stem and cerebellum were normal. The right internal carotid artery (ICA) and the left VA on MRI exhibited characteristic features of a dissection with presence of a narrowed eccentric signal void surrounded by a semilunar hyperintensity (on T2weighted images) within the vessel wall (Fig. 1d). MRA (Angio-TOF sequences) showed long dissection with tapering high-grade stenosis of the right ICA and irregularity of the left VA beginning at the V2 portion to the level of proximal V3 segment. A high-grade irregular stenosis of distal V2 segment was observed (Fig. 2). MRA with bolus contrast-enhanced acquisitions showed retrograde opacification of the left V4 segment from the right V4 segment characterized by a better opacification and a larger diameter of the left V4 segment. The other arteries were normal without sign of fibromuscular dysplasia. According to our diagnosis of a right ICA and left VA dissections, the patient received anticoagulant therapy. The neurological recovery was good and the patient presented only a mild disability at discharge.
3. Discussion Diagnosis of VAD is based classically on angiographic criteria such as string sign, tapering narrowing, double lumen and intimal flaps (Touboul et al., 1987). These findings on cerebral angiography are pathognomonic but are infrequent in VAD (Hoffmann et al., 1993; Sturzenegger et al., 1993). More often, irregular stenosis or occlusion of the vertebral artery is found, which is less specific for VAD and may be detected in atherosclerotic or partially recanalized embolic occlusion of the vertebral artery (Hoffmann et al., 1993). In addition, a long stenosis of the vertebral artery may be mistaken for a hypoplasia, and if the vessel is occluded, the etiology of the occlusion may not be recognized (Sturzenegger et al., 1993). Until recently, the role of ultrasound in VAD was not established for several reasons:
N. Cals et al. / European Journal of Ultrasound 12 (2001) 227–231
firstly, it is more difficult to detect VA pathologies than ICA because the deep localization of VA, and secondly, the hemodynamics of vertebro-basilar diseases are different from those of the carotid system. During the last decade with the advent of new ultrasound technologies such as CDFI, some authors (Bartels and Flugel, 1996) have suggested that the new methods appear promising to improve the non-invasive diagnosis of VAD. Doppler is a very sensitive method, from 79 to 90% according to the series (Rother et al., 1995; Bartels and Flugel, 1996; Auer et al., 1998) of detecting VA pathologies but one drawback is the lack of specificity for VAD (Rother et al., 1995). The typical ultrasonographic findings of VAD described in the literature (Touboul et al., 1987; Rother et al., 1995; Bartels and Flugel, 1996)
229
include irregular stenosis, tapering stenosis with distal occlusion, hemodynamic signs of stenosis or occlusion such as decreased flow velocities and/or decreased pulsatility and high resistive pattern, localized increase in diameter of the artery associated with decreased pulsatility, presence of intravascular echoes, a pseudoaneurysm formation, an intramural hematoma (appearing as echolucent formation), a dissecting membrane with true and false lumen and a to-and-fro spectrum. These findings in VAD are encountered less frequently than in ICAD. All of them are not always simultaneously present in individual case of VAD and for instance, slosh phenomenon in VAD described as synchronous forward-and-backward components during systole is detected approximately in only one-third of cases (Hennerici and Neuer-
Fig. 1. Continuous wave Doppler with a to-and-fro spectrum with decreased systolic and diastolic blood flow velocities in V2 segment, as well as a double lumen with a red flow (antegrade) and a blue flow (retrograde) on: (a) longitudinal and (b) transversal sections between C4 and C5 transverse processes. (c) Demonstrates an alternating blood flow with retrograde flow in systole and antegrade flow in diastole in V4 segment. (d) T2-weighted axial MRI image shows VAD with narrowing eccentric signal void surrounded by a semilunar hyperintensity.
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N. Cals et al. / European Journal of Ultrasound 12 (2001) 227–231
Fig. 2. MRA with bolus contrast-enhanced acquisition of cervical and cerebral arteries showed irregularity of the left VA beginning at the V2 portion to the level of proximal V3 segment, a high-grade irregular stenosis of distal V2 segment, a retrograde opacification of the left V4 segment from the right V4 segment characterized by a better opacification and a larger diameter of the left V4 segment.
burg-Heusler, 1998). On this basis and because the too small series, the exact sensitivity and specificity of each sign are not known. In our case, V2 segment examination showed pathognomonic signs of dissection namely slosh phenomenon and double lumen with simultaneously red (antegrade) and blue (retrograde) flow. It is the first time to our knowledge that this finding is so clearly demonstrated in VAD by CDFI. As reported for carotid artery dissection (Bluth et al., 1989; Tratting et al., 1995), we believe that red antegrade and blue retrograde flow may represent the true lumen and the false lumen of the VAD, respectively. In our case, the missing signs of the high resistance flow pattern in the upper Doppler spectrum in the V2 segment of the left vertebral artery may be explained by an overestimation of the degree of V2/V3 stenosis by MRA on one hand, and by the mobilization of collateral supply which is difficult to demonstrate by both ultrasound and MRA on the other hand. These two possible factors, particularly a good collateral supply, could also taken into consideration to
explain why the patient did not experience any neurological deficit (TIA or stroke) in the vertebrobasilar circulation, but only symptoms depending on the right internal carotid dissection. The marked decrease of systolic and diastolic BFV in the V2 segment could be explained by a stenosis in V2/V3 suggesting a resistive flow as suggested previously by Steinke et al. (1994) in ICAD who have demonstrated that long ICAD was not associated with an increase of blood flow velocities. In our case, the dissection of the left VA was considered as long because including V2 and V3 segments. No flow could be detected in V3 segment presumably because of a subocclusion of the vertebral artery at this level, or because it is not always possible to insonate this V3 segment of the vertebral artery (Sturzenegger et al., 1993; Ries et al., 1998). In the V4 segment of the VAD, we had an alternating flow. Although this sign is frequently associated with severe subclavian steal syndrome and severe stenosis at the ostium of VA (Cattin and Bonneville, 1995), these abnormalities were excluded by MRA in our patient. Our hypothesis of a high-grade stenosis on V2/V3 segments of the left VA together with a vertebro –vertebral reflux from the contralateral VA was confirmed by MRA with bolus which showed an increased flow and diameter of V4 segment in comparison with non-injected sequences of MRA. This is a rare finding in VAD, recently reported by Ringelstein (1996) in a patient who had left VAD with VA occlusion at the level of the atlas loop and supplied by right VA and cervical collateral pathways. In our case, one explanation could be a characteristic collateralization pattern to supply the posterior inferior cerebellar artery territory on the affected side. This hypothesis could be also taken into account in the observation that the alternating flow was only restricted to the downstream segment — V4 of the left VA — and not distributed equally over the total length of the affected VA as in the case of subclavian steal syndrome. In conclusion, our findings suggest that: firstly, typical signs of dissection often seen in ICAD may be found in VAD, particularly in the presence of both red and blue flow at the same level of the artery. Secondly, a severe stenosis of V2 or/
N. Cals et al. / European Journal of Ultrasound 12 (2001) 227–231
and V3 segment must be considered if an alternating flow is present in the V4 segment without severe stenosis of the V1 segment or subclavian artery.
References Auer A, Felber S, Schmidauer C, et al. Magnetic resonance angiographic and clinical features of extracranial vertebral artery dissection. J Neurol Neurosurg Psychiatry 1998;64:474–81. Bartels E, Flugel KA. Evaluation of extracranial vertebral artery dissection with duplex color-flow imaging. Stroke 1996;27:290–5. Bluth EI, Shyn PB, Sullivan MA, et al. Doppler color flow imaging of carotid artery dissection. J Ultrasound Med 1989;8:149–53. Cattin F, Bonneville JF. Echo-Doppler des Arteres Carotides et Vertebrales, Aspects Pratiques. Paris: Masson, 1995:73. Hennerici M, Neuerburg-Heusler D. Vascular Diagnosis with Ultrasound. Stuttgart: Thieme, 1998:81. Hoffmann M, Sacco R, Chan S, Mohr JP. Noninvasive detection of vertebral artery dissection. Stroke 1993;24:815– 9.
.
231
Nicolau C, Gilabert R, Chamorro A, et al. Doppler sonography of the intertransverse segment of the vertebral artery. J Ultrasound Med 2000;19:47– 53. Ries S, Steinke W, Devuyst G, et al. Power Doppler imaging and color Doppler flow imaging for the evaluation of normal and pathological vertebral arteries. J Neuroimaging 1998;8:71– 4. Ringelstein EB. Cerebrovascular diseases. In: Tegeler C, Babikian V, Gomez C, editors. Neurosonology. St. Louis: Mosby-Year Book, 1996:172– 88. Rother J, Schwartz A, Rautenberg W, et al. Magnetic resonance angiography of spontaneous vertebral artery dissection suspected on Doppler ultrasonography. J Neurol 1995;242:430– 6. Steinke W, Rautenberg W, Schwartz A, et al. Noninvasive monitoring of internal carotid artery dissection. Stroke 1994;25:998– 1005. Sturzenegger M, Mattle HP, Rivoir A, et al. Ultrasound findings in spontaneous extracranial vertebral artery dissection. Stroke 1993;24:1910– 21. Touboul PJ, Mas JL, Bousser MG, et al. Duplex scanning in extracranial vertebral artery dissection. Stroke 1987;18:116– 21. Tratting S, Rand T, Thurnher M, et al. Color-coded Doppler sonography of common carotid artery dissection. Neuroradiology 1995;37:124– 6.
Clinical Science: Case Report
Uncommon ultrasound findings in traumatic extracranial vertebral artery dissection N. Cals, G. Devuyst *, D.K. Jung, N. Afsar, G. De Freitas, P-A. Despland, J. Bogousslavsky Department of Neurology, Hopital Uni6ersitaire Vaudois, CHUV, BH 07, 46 Rue du Bugnon, 1011 Lausanne, Switzerland Received 29 June 2000; received in revised form 10 October 2000; accepted 17 October 2000
Abstract We report a case of internal carotid artery dissection (ICAD) associated with contralateral vertebral artery dissection (VAD). The interest of this case is to discuss an unusual Doppler pattern manifesting by a spectrum of an alternating vertebral artery flow suggesting a hemodynamic contribution from the contralateral vertebral artery (VA) and a clear depiction of both antegrade (red) and retrograde (blue) flow within the false and true lumen of the VAD by color Duplex flow imaging. © 2001 Elsevier Science Ireland Ltd. All rights reserved. Keywords: Vertebral artery; Dissection; Color Duplex flow imaging; Blood flow velocities
1. Introduction Although dissection constitutes a frequent cause of strokes in young patients, the early diagnosis of vertebral artery dissection (VAD) is often difficult. Angiography has been considered as the gold standard for diagnosis of VAD but it is invasive and not without risk (Bartels and Flugel, 1996; Auer et al., 1998). The advent of new effective non-invasive methods such as duplex ultrasonography, MRI and MRA may result in * Corresponding author. Tel.: +41-21-3141225; fax: + 4121-3141290. E-mail address: [email protected] (G. Devuyst).
earlier and safe diagnosis of cervical arteries dissection. Although ultrasound seems to be a sensitive and reliable tool in the diagnosis of ICAD, its role in VAD remains equivocal (Sturzenegger et al., 1993). We report a case of ICAD associated with contralateral VAD occurring following chiropractic manipulation. Two lumina in the same vessel and to-and-fro spectrum have already been described in case of VAD by B-mode and Doppler ultrasound, respectively, but in the present case of VAD we could also demonstrate the antegrade (red) and retrograde (blue) flow by color Duplex flow imaging within the false and true lumen. In addition, our case is associated with a vertebral artery alternating flow which is
0929-8266/01/$ - see front matter © 2001 Elsevier Science Ireland Ltd. All rights reserved. PII: S 0 9 2 9 - 8 2 6 6 ( 0 0 ) 0 0 1 1 4 - 2
228
N. Cals et al. / European Journal of Ultrasound 12 (2001) 227–231
not related to a subclavian artery and/or proximal VA stenosis but due to a long VAD in our opinion.
2. Case report A 51-year-old woman was admitted because of left hemibody weakness preceded by acute headache. She had no relevant disease in her past except episodes of migraine. Four days after chiropractic maneuvers (with elements of abrupt head rotation), she developed an unusual headache localized to the right frontal region associated with nausea and vomiting with no response to analgesics and aggraving in time. While the pain did not subside, 10 days later she developed a left-sided weakness. On admission, she was oriented and her neurological examination revealed a left facio-brachio-crural hemiparesis with left motor hemineglect. Left Babinski sign was present. There were no cerebellar signs, no sensory dysfunction and no Horner’s syndrome. The examination of cranial nerves was normal. Cardiovascular examination was normal. Routine blood tests did not reveal any abnormality. On continuous wave Doppler and color duplex flow imaging (CDFI) (ATL HDI 5000, Advanced Technologies Laboratories, Seattle, USA), the origin of the left VA (V1 segment) could not be visualized possibly because of a too posterior intrathoracic localization in this patient as described previously (Nicolau et al., 2000). Examination of the V2 segment of the left VA showed a significant decrease in both systolic (18 vs. 40 cm/s on the right VA) and diastolic (4 vs. 15 cm/s on the right VA) blood flow velocities (BFV) with a diameter of 4.4 mm on the left and 3.9 mm on the right, to-and-fro spectrum and double lumen with a red flow (antegrade) and a blue flow (retrograde) on transversal and longitudinal sections between C4 and C5 transverse processes (Fig. 1a and b). No arterial flow could be recorded in V3 segment of left VA as well as by Doppler and CDFI (transverse sections). In the intracranial VA (V4 segment) blood flow was pendulum-like with a retrograde flow in systole and anterograde flow in diastole (Fig. 1c). Left subclavian artery and
basilar artery flow were normal. MRI (Magnetom –Symphony, diffusion, T1 and T2 weighted images) revealed multiple lesions in the right anterior borderzone hemispheric distribution (preferentially involving subcortical white matter). Brain stem and cerebellum were normal. The right internal carotid artery (ICA) and the left VA on MRI exhibited characteristic features of a dissection with presence of a narrowed eccentric signal void surrounded by a semilunar hyperintensity (on T2weighted images) within the vessel wall (Fig. 1d). MRA (Angio-TOF sequences) showed long dissection with tapering high-grade stenosis of the right ICA and irregularity of the left VA beginning at the V2 portion to the level of proximal V3 segment. A high-grade irregular stenosis of distal V2 segment was observed (Fig. 2). MRA with bolus contrast-enhanced acquisitions showed retrograde opacification of the left V4 segment from the right V4 segment characterized by a better opacification and a larger diameter of the left V4 segment. The other arteries were normal without sign of fibromuscular dysplasia. According to our diagnosis of a right ICA and left VA dissections, the patient received anticoagulant therapy. The neurological recovery was good and the patient presented only a mild disability at discharge.
3. Discussion Diagnosis of VAD is based classically on angiographic criteria such as string sign, tapering narrowing, double lumen and intimal flaps (Touboul et al., 1987). These findings on cerebral angiography are pathognomonic but are infrequent in VAD (Hoffmann et al., 1993; Sturzenegger et al., 1993). More often, irregular stenosis or occlusion of the vertebral artery is found, which is less specific for VAD and may be detected in atherosclerotic or partially recanalized embolic occlusion of the vertebral artery (Hoffmann et al., 1993). In addition, a long stenosis of the vertebral artery may be mistaken for a hypoplasia, and if the vessel is occluded, the etiology of the occlusion may not be recognized (Sturzenegger et al., 1993). Until recently, the role of ultrasound in VAD was not established for several reasons:
N. Cals et al. / European Journal of Ultrasound 12 (2001) 227–231
firstly, it is more difficult to detect VA pathologies than ICA because the deep localization of VA, and secondly, the hemodynamics of vertebro-basilar diseases are different from those of the carotid system. During the last decade with the advent of new ultrasound technologies such as CDFI, some authors (Bartels and Flugel, 1996) have suggested that the new methods appear promising to improve the non-invasive diagnosis of VAD. Doppler is a very sensitive method, from 79 to 90% according to the series (Rother et al., 1995; Bartels and Flugel, 1996; Auer et al., 1998) of detecting VA pathologies but one drawback is the lack of specificity for VAD (Rother et al., 1995). The typical ultrasonographic findings of VAD described in the literature (Touboul et al., 1987; Rother et al., 1995; Bartels and Flugel, 1996)
229
include irregular stenosis, tapering stenosis with distal occlusion, hemodynamic signs of stenosis or occlusion such as decreased flow velocities and/or decreased pulsatility and high resistive pattern, localized increase in diameter of the artery associated with decreased pulsatility, presence of intravascular echoes, a pseudoaneurysm formation, an intramural hematoma (appearing as echolucent formation), a dissecting membrane with true and false lumen and a to-and-fro spectrum. These findings in VAD are encountered less frequently than in ICAD. All of them are not always simultaneously present in individual case of VAD and for instance, slosh phenomenon in VAD described as synchronous forward-and-backward components during systole is detected approximately in only one-third of cases (Hennerici and Neuer-
Fig. 1. Continuous wave Doppler with a to-and-fro spectrum with decreased systolic and diastolic blood flow velocities in V2 segment, as well as a double lumen with a red flow (antegrade) and a blue flow (retrograde) on: (a) longitudinal and (b) transversal sections between C4 and C5 transverse processes. (c) Demonstrates an alternating blood flow with retrograde flow in systole and antegrade flow in diastole in V4 segment. (d) T2-weighted axial MRI image shows VAD with narrowing eccentric signal void surrounded by a semilunar hyperintensity.
230
N. Cals et al. / European Journal of Ultrasound 12 (2001) 227–231
Fig. 2. MRA with bolus contrast-enhanced acquisition of cervical and cerebral arteries showed irregularity of the left VA beginning at the V2 portion to the level of proximal V3 segment, a high-grade irregular stenosis of distal V2 segment, a retrograde opacification of the left V4 segment from the right V4 segment characterized by a better opacification and a larger diameter of the left V4 segment.
burg-Heusler, 1998). On this basis and because the too small series, the exact sensitivity and specificity of each sign are not known. In our case, V2 segment examination showed pathognomonic signs of dissection namely slosh phenomenon and double lumen with simultaneously red (antegrade) and blue (retrograde) flow. It is the first time to our knowledge that this finding is so clearly demonstrated in VAD by CDFI. As reported for carotid artery dissection (Bluth et al., 1989; Tratting et al., 1995), we believe that red antegrade and blue retrograde flow may represent the true lumen and the false lumen of the VAD, respectively. In our case, the missing signs of the high resistance flow pattern in the upper Doppler spectrum in the V2 segment of the left vertebral artery may be explained by an overestimation of the degree of V2/V3 stenosis by MRA on one hand, and by the mobilization of collateral supply which is difficult to demonstrate by both ultrasound and MRA on the other hand. These two possible factors, particularly a good collateral supply, could also taken into consideration to
explain why the patient did not experience any neurological deficit (TIA or stroke) in the vertebrobasilar circulation, but only symptoms depending on the right internal carotid dissection. The marked decrease of systolic and diastolic BFV in the V2 segment could be explained by a stenosis in V2/V3 suggesting a resistive flow as suggested previously by Steinke et al. (1994) in ICAD who have demonstrated that long ICAD was not associated with an increase of blood flow velocities. In our case, the dissection of the left VA was considered as long because including V2 and V3 segments. No flow could be detected in V3 segment presumably because of a subocclusion of the vertebral artery at this level, or because it is not always possible to insonate this V3 segment of the vertebral artery (Sturzenegger et al., 1993; Ries et al., 1998). In the V4 segment of the VAD, we had an alternating flow. Although this sign is frequently associated with severe subclavian steal syndrome and severe stenosis at the ostium of VA (Cattin and Bonneville, 1995), these abnormalities were excluded by MRA in our patient. Our hypothesis of a high-grade stenosis on V2/V3 segments of the left VA together with a vertebro –vertebral reflux from the contralateral VA was confirmed by MRA with bolus which showed an increased flow and diameter of V4 segment in comparison with non-injected sequences of MRA. This is a rare finding in VAD, recently reported by Ringelstein (1996) in a patient who had left VAD with VA occlusion at the level of the atlas loop and supplied by right VA and cervical collateral pathways. In our case, one explanation could be a characteristic collateralization pattern to supply the posterior inferior cerebellar artery territory on the affected side. This hypothesis could be also taken into account in the observation that the alternating flow was only restricted to the downstream segment — V4 of the left VA — and not distributed equally over the total length of the affected VA as in the case of subclavian steal syndrome. In conclusion, our findings suggest that: firstly, typical signs of dissection often seen in ICAD may be found in VAD, particularly in the presence of both red and blue flow at the same level of the artery. Secondly, a severe stenosis of V2 or/
N. Cals et al. / European Journal of Ultrasound 12 (2001) 227–231
and V3 segment must be considered if an alternating flow is present in the V4 segment without severe stenosis of the V1 segment or subclavian artery.
References Auer A, Felber S, Schmidauer C, et al. Magnetic resonance angiographic and clinical features of extracranial vertebral artery dissection. J Neurol Neurosurg Psychiatry 1998;64:474–81. Bartels E, Flugel KA. Evaluation of extracranial vertebral artery dissection with duplex color-flow imaging. Stroke 1996;27:290–5. Bluth EI, Shyn PB, Sullivan MA, et al. Doppler color flow imaging of carotid artery dissection. J Ultrasound Med 1989;8:149–53. Cattin F, Bonneville JF. Echo-Doppler des Arteres Carotides et Vertebrales, Aspects Pratiques. Paris: Masson, 1995:73. Hennerici M, Neuerburg-Heusler D. Vascular Diagnosis with Ultrasound. Stuttgart: Thieme, 1998:81. Hoffmann M, Sacco R, Chan S, Mohr JP. Noninvasive detection of vertebral artery dissection. Stroke 1993;24:815– 9.
.
231
Nicolau C, Gilabert R, Chamorro A, et al. Doppler sonography of the intertransverse segment of the vertebral artery. J Ultrasound Med 2000;19:47– 53. Ries S, Steinke W, Devuyst G, et al. Power Doppler imaging and color Doppler flow imaging for the evaluation of normal and pathological vertebral arteries. J Neuroimaging 1998;8:71– 4. Ringelstein EB. Cerebrovascular diseases. In: Tegeler C, Babikian V, Gomez C, editors. Neurosonology. St. Louis: Mosby-Year Book, 1996:172– 88. Rother J, Schwartz A, Rautenberg W, et al. Magnetic resonance angiography of spontaneous vertebral artery dissection suspected on Doppler ultrasonography. J Neurol 1995;242:430– 6. Steinke W, Rautenberg W, Schwartz A, et al. Noninvasive monitoring of internal carotid artery dissection. Stroke 1994;25:998– 1005. Sturzenegger M, Mattle HP, Rivoir A, et al. Ultrasound findings in spontaneous extracranial vertebral artery dissection. Stroke 1993;24:1910– 21. Touboul PJ, Mas JL, Bousser MG, et al. Duplex scanning in extracranial vertebral artery dissection. Stroke 1987;18:116– 21. Tratting S, Rand T, Thurnher M, et al. Color-coded Doppler sonography of common carotid artery dissection. Neuroradiology 1995;37:124– 6.