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Cryptic Recanalization of Chronic Vertebral Artery Occlusion by Head Rotation
Case Studies
Cryptic Recanalization of Chronic Vertebral Artery Occlusion by Head Rotation Kenji Yagi,
,
MD, PhD,* †
Hiroshi Nakagawa, MD, PhD,‡ Hideo Mure, Shinya Okita, MD,* and Shinji Nagahiro, MD, PhD*
MD, PhD,*
Background: Chronic vertebral artery occlusion (VAO) can be associated with ischemic stroke, as thrombi formed under blood flow stagnation around the stump of the VAO may migrate into the brain. We report a new mechanism of chronic VAOassociated ischemic stroke and a patient with cryptic recanalization of chronic VAO by head rotation. Case description: A 74-year-old man presented with chronic right VAO and repeated ischemic embolic stroke in the posterior circulation despite antiplatelet therapy. He also manifested vertigo with 30° leftward head rotation, indicative of rotational vertebrobasilar insufficiency due to mechanical compression of the patent left vertebral artery (VA) at the C4-C5 level. Surgical decompression of the vessel via the anterior approach resulted in the disappearance of his rotational vertebrobasilar insufficiency. Adequate decompression of the VA on the left side was confirmed on postoperative computed tomography angiography scans obtained with his head rotated more to the left than on preoperative scans. Unexpected partial recanalization of his right chronic VAO was observed at the C5-C6 level. VAO was due to VA compression by osteophytes at neutral head position; it was released by head rotation. We suspected that his repeated brain infarcts were attributable to head rotation-related opening and closing of the VA lumen and these decompressed the left VA by removing the implicated osteophyte via the anterior approach. Conclusions: Cryptic recanalization of chronic VAO by head rotation contributed to repeated infarcts in the posterior circulation and was resolved by surgical decompression. Key Words: Vertebral artery stump syndrome—rotational vetebrobasilar insufficiency—Bow hunter’s syndrome—cervical spondylosis. © 2017 National Stroke Association. Published by Elsevier Inc. All rights reserved.
From the *Department of Neurosurgery, Tokushima University Hospital, Tokushima, Japan; †Department of Neurosurgery, Faculty of Medicine, Fukuoka University, Fukuoka, Japan; and ‡Department of Neurosurgery, Kushiro Kojinkai Memorial Hospital, Kushiro, Japan. Received November 10, 2016; revision received December 26, 2016; accepted December 31, 2016. Financial and material support: This work was partly supported by a Grant-in-Aid for Scientific Research from the Ministry of Education, Science, Sports, and Culture of Japan (C15K10306). Address correspondence to Kenji Yagi, MD, PhD, Department of Neurosurgery, Tokushima University Hospital, 3-18-15 Kuramoto-cho, Tokushima, Japan, 770-8503. E-mail: [email protected]. 1052-3057/$ - see front matter © 2017 National Stroke Association. Published by Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.jstrokecerebrovasdis.2016.12.034
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Vertebral artery occlusion (VAO) can elicit embolic ischemic stroke. Thrombi formed under blood flow stagnation around the stump of the VAO can migrate into the brain, resulting in recurrent stroke, which is called vertebral artery (VA) stump syndrome.1-4 Antegrade flow in the collateral blood flow into the VA can transport these thrombi to intracranial sites.2,3 Here we report another mechanism for VA stump syndrome. A 74-year-old man had suffered a right cerebellar infarct associated with VAO 5 years earlier; he subsequently received antiplatelet therapy. He presented with a visual defect due to repeated infarction elicited by emboli in the bilateral posterior lobes. Computed tomography angiography (CTA) had shown right chronic VAO (Fig 1,
Journal of Stroke and Cerebrovascular Diseases, Vol. 26, No. 4 (April), 2017: pp e60–e61
CRYPTIC RECANALIZATION OF VA OCCLUSION
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Figure 1. (A) At the time of admission, computed tomography angiography (CTA) at neutral head position showed right vertebral artery (VA) occlusion. (B and C) The contralateral left VA was mechanically compressed (arrow) at the level of C4-C5 at 30° leftward head rotation. (D and E) CTA performed at 45° leftward head rotation showed a well-decompressed left VA. There was unexpected partial recanalization of the right VA. Residual stenosis due to mechanical compression by vertebral osteophytes at the right VA was observed at the C5-C6 level (arrow). (F and G) CTA performed at neutral head position after the removal of osteophytes at C5-C6 showed a well-decompressed right VA.
A). He also suffered vertigo at 30° leftward head rotation, indicative of rotational vertebrobasilar insufficiency. Mechanical compression of the left VA at C4-C5 (Fig 1, B,C) was surgically decompressed by opening the transverse foramen at C4 via the anterior approach. His vertigo disappeared. Postoperative CTA with his head rotated more to the left than on preoperative images (Fig 1, D,E) showed a decompressed left VA and unexpected partial recanalization of the right VAO. His left VAO at neutral head position was attributed to mechanical compression by osteophytes at C5-C6; it was surgically addressed via the anterior approach. Because of coincident spondylotic myeloradiculopathy, we also performed simultaneous microdiscectomy and anterior fusion at C5-C6. Postoperative CTA showed improved blood flow in the right VA at neutral head position (Fig 1, F,G). We first report a patient with transient recanalization of chronic VAO upon head rotation. This condition is different from rotational vertebrobasilar insufficiency where head rotation induces transient VA stenosis or occlusion.5 We call this phenomenon “cryptic rotational recanalization of VAO” because it is difficult to detect on conventional radiological studies. In patients with VAOassociated brain infarcts and a cervical vertebral deformity due, for example, to the development of osteophytes, cryptic rotational recanalization of VAO should be con-
sidered. We think that in our patient, right chronic VAO with transient blood flow arrest rather than left VA compression was implicated in the elicitation of embolic infarcts. In patients with iterative ischemic stroke associated with VAO, VA stump syndrome should be ruled out. Based on the findings reported here, we suggest “cryptic rotational recanalization of VAO” as another causative factor in the transportation of thrombi formed at the stump of the VAO to intracranial sites.
References 1. Caplan LR, Amarenco P, Rosengart A, et al. Embolism from vertebral artery origin occlusive disease. Neurology 1992;42:1505-1512. 2. Kawano H, Inatomi Y, Hirano T, et al. Vertebral artery stump syndrome in acute ischemic stroke. J Neurol Sci 2013;324:74-79. 3. Kawano H, Inatomi Y, Hirano T, et al. Anticoagulation therapy for vertebral artery stump syndrome. J Neurol Sci 2010;295:125-127. 4. Nguyen TN, Raymond J, Mahmoud M, et al. Vertebral artery stump syndrome. J Neurol Neurosurg Psychiatry 2008;79:91-92. 5. Buchanan CC, McLaughlin N, Lu DC, et al. Rotational vertebral artery occlusion secondary to adjacent-level degeneration following anterior cervical discectomy and fusion. J Neurosurg Spine 2014;20:714-721.
Cryptic Recanalization of Chronic Vertebral Artery Occlusion by Head Rotation Kenji Yagi,
,
MD, PhD,* †
Hiroshi Nakagawa, MD, PhD,‡ Hideo Mure, Shinya Okita, MD,* and Shinji Nagahiro, MD, PhD*
MD, PhD,*
Background: Chronic vertebral artery occlusion (VAO) can be associated with ischemic stroke, as thrombi formed under blood flow stagnation around the stump of the VAO may migrate into the brain. We report a new mechanism of chronic VAOassociated ischemic stroke and a patient with cryptic recanalization of chronic VAO by head rotation. Case description: A 74-year-old man presented with chronic right VAO and repeated ischemic embolic stroke in the posterior circulation despite antiplatelet therapy. He also manifested vertigo with 30° leftward head rotation, indicative of rotational vertebrobasilar insufficiency due to mechanical compression of the patent left vertebral artery (VA) at the C4-C5 level. Surgical decompression of the vessel via the anterior approach resulted in the disappearance of his rotational vertebrobasilar insufficiency. Adequate decompression of the VA on the left side was confirmed on postoperative computed tomography angiography scans obtained with his head rotated more to the left than on preoperative scans. Unexpected partial recanalization of his right chronic VAO was observed at the C5-C6 level. VAO was due to VA compression by osteophytes at neutral head position; it was released by head rotation. We suspected that his repeated brain infarcts were attributable to head rotation-related opening and closing of the VA lumen and these decompressed the left VA by removing the implicated osteophyte via the anterior approach. Conclusions: Cryptic recanalization of chronic VAO by head rotation contributed to repeated infarcts in the posterior circulation and was resolved by surgical decompression. Key Words: Vertebral artery stump syndrome—rotational vetebrobasilar insufficiency—Bow hunter’s syndrome—cervical spondylosis. © 2017 National Stroke Association. Published by Elsevier Inc. All rights reserved.
From the *Department of Neurosurgery, Tokushima University Hospital, Tokushima, Japan; †Department of Neurosurgery, Faculty of Medicine, Fukuoka University, Fukuoka, Japan; and ‡Department of Neurosurgery, Kushiro Kojinkai Memorial Hospital, Kushiro, Japan. Received November 10, 2016; revision received December 26, 2016; accepted December 31, 2016. Financial and material support: This work was partly supported by a Grant-in-Aid for Scientific Research from the Ministry of Education, Science, Sports, and Culture of Japan (C15K10306). Address correspondence to Kenji Yagi, MD, PhD, Department of Neurosurgery, Tokushima University Hospital, 3-18-15 Kuramoto-cho, Tokushima, Japan, 770-8503. E-mail: [email protected]. 1052-3057/$ - see front matter © 2017 National Stroke Association. Published by Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.jstrokecerebrovasdis.2016.12.034
e60
Vertebral artery occlusion (VAO) can elicit embolic ischemic stroke. Thrombi formed under blood flow stagnation around the stump of the VAO can migrate into the brain, resulting in recurrent stroke, which is called vertebral artery (VA) stump syndrome.1-4 Antegrade flow in the collateral blood flow into the VA can transport these thrombi to intracranial sites.2,3 Here we report another mechanism for VA stump syndrome. A 74-year-old man had suffered a right cerebellar infarct associated with VAO 5 years earlier; he subsequently received antiplatelet therapy. He presented with a visual defect due to repeated infarction elicited by emboli in the bilateral posterior lobes. Computed tomography angiography (CTA) had shown right chronic VAO (Fig 1,
Journal of Stroke and Cerebrovascular Diseases, Vol. 26, No. 4 (April), 2017: pp e60–e61
CRYPTIC RECANALIZATION OF VA OCCLUSION
e61
Figure 1. (A) At the time of admission, computed tomography angiography (CTA) at neutral head position showed right vertebral artery (VA) occlusion. (B and C) The contralateral left VA was mechanically compressed (arrow) at the level of C4-C5 at 30° leftward head rotation. (D and E) CTA performed at 45° leftward head rotation showed a well-decompressed left VA. There was unexpected partial recanalization of the right VA. Residual stenosis due to mechanical compression by vertebral osteophytes at the right VA was observed at the C5-C6 level (arrow). (F and G) CTA performed at neutral head position after the removal of osteophytes at C5-C6 showed a well-decompressed right VA.
A). He also suffered vertigo at 30° leftward head rotation, indicative of rotational vertebrobasilar insufficiency. Mechanical compression of the left VA at C4-C5 (Fig 1, B,C) was surgically decompressed by opening the transverse foramen at C4 via the anterior approach. His vertigo disappeared. Postoperative CTA with his head rotated more to the left than on preoperative images (Fig 1, D,E) showed a decompressed left VA and unexpected partial recanalization of the right VAO. His left VAO at neutral head position was attributed to mechanical compression by osteophytes at C5-C6; it was surgically addressed via the anterior approach. Because of coincident spondylotic myeloradiculopathy, we also performed simultaneous microdiscectomy and anterior fusion at C5-C6. Postoperative CTA showed improved blood flow in the right VA at neutral head position (Fig 1, F,G). We first report a patient with transient recanalization of chronic VAO upon head rotation. This condition is different from rotational vertebrobasilar insufficiency where head rotation induces transient VA stenosis or occlusion.5 We call this phenomenon “cryptic rotational recanalization of VAO” because it is difficult to detect on conventional radiological studies. In patients with VAOassociated brain infarcts and a cervical vertebral deformity due, for example, to the development of osteophytes, cryptic rotational recanalization of VAO should be con-
sidered. We think that in our patient, right chronic VAO with transient blood flow arrest rather than left VA compression was implicated in the elicitation of embolic infarcts. In patients with iterative ischemic stroke associated with VAO, VA stump syndrome should be ruled out. Based on the findings reported here, we suggest “cryptic rotational recanalization of VAO” as another causative factor in the transportation of thrombi formed at the stump of the VAO to intracranial sites.
References 1. Caplan LR, Amarenco P, Rosengart A, et al. Embolism from vertebral artery origin occlusive disease. Neurology 1992;42:1505-1512. 2. Kawano H, Inatomi Y, Hirano T, et al. Vertebral artery stump syndrome in acute ischemic stroke. J Neurol Sci 2013;324:74-79. 3. Kawano H, Inatomi Y, Hirano T, et al. Anticoagulation therapy for vertebral artery stump syndrome. J Neurol Sci 2010;295:125-127. 4. Nguyen TN, Raymond J, Mahmoud M, et al. Vertebral artery stump syndrome. J Neurol Neurosurg Psychiatry 2008;79:91-92. 5. Buchanan CC, McLaughlin N, Lu DC, et al. Rotational vertebral artery occlusion secondary to adjacent-level degeneration following anterior cervical discectomy and fusion. J Neurosurg Spine 2014;20:714-721.