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Cervical Posterior Spinal Artery Syndrome: A Case Report and Literature Review
Case Studies
Cervical Posterior Spinal Artery Syndrome: A Case Report and Literature Review Takeo Sakurai,
MD,
Kenji Wakida,
MD,
and Hiroshi Nishida,
MD
We report a case of left upper cervical posterior spinal artery (PSA) syndrome caused by atherosclerosis of the left vertebral artery. A 70-year-old female experienced sudden dizziness and paralysis of the left upper and lower limbs. Diffusionweighted magnetic resonance imaging (DWI) of the brain showed high signal intensity at the vermis and lower left hemisphere of the cerebellum, and magnetic resonance angiography showed that the entire left vertebral artery was thin. The patient was treated with an intravenous infusion of tissue plasminogen activator 2 hours after symptom onset and made a full recovery. Repeat DWI, fluid-attenuated inversion recovery images, and T2-weighted images showed high signal intensity in the left upper cervical PSA area from the lower medulla oblongata to the C2 level in addition to the cerebellum. Previously reported cases of cervical posterior artery syndrome are reviewed. Key Words: Cervical posterior spinal artery syndrome—tissue plasminogen activator—cerebellar infarction—atherosclerosis. © 2016 National Stroke Association. Published by Elsevier Inc. All rights reserved.
Introduction Spinal cord infarction is rare compared with brain infarction, accounting for 1.2% of all strokes.1 Spinal cord infarction is usually localized to the anterior spinal artery area, while infarction of the posterior spinal artery (PSA) is an uncommon occurrence. In these cases, the thoracic– lumbar region is the most common location for an infarction occurring in the PSA; involvement of the cervical segment is infrequent. We report a case of unilateral upper cervical PSA syndrome, which was successfully treated with tissue From the Department of Neurology, Gifu Prefectural General Medical Center, Gifu, Japan. Received November 26, 2015; revision received January 12, 2016; accepted February 11, 2016. Address correspondence and reprint requests to Takeo Sakurai, MD, Department of Neurology, Gifu Prefectural General Medical Center, 4-6-1 Noisshiki, Gifu 500-8717, Japan. E-mail: sakurai-takeo@ gifu-hp.jp. 1052-3057/$ - see front matter © 2016 National Stroke Association. Published by Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.jstrokecerebrovasdis.2016.02.018
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plasminogen activator (tPA), and review previously reported cases of cervical PSA syndrome.2-16
Case Report A 70-year-old woman experienced sudden dizziness and paralysis of the left upper and lower limbs after washing her face in a washroom at 4:50 am. The patient had a history of rheumatoid arthritis. Neurological findings indicated severe paralysis of the left upper and lower limbs and sensory disturbance of touch sensation and position sensation on the left side of her body from the neck downward, and a National Institutes of Health Stroke Scale (NIHSS) score of 9 points. Laboratory findings showed no obvious abnormalities. Diffusion-weighted magnetic resonance imaging (DWI) of the brain showed faintly high intensity areas at the vermis and lower left hemisphere of the cerebellum, and magnetic resonance angiography (MRA) indicated that the left vertebral artery was generally thin, so-called hypoplasia (Fig 1). The patient had no pain at her neck and MRA showed no intimal flap, double lumen signs, or strings and pearls sign. We
Journal of Stroke and Cerebrovascular Diseases, Vol. 25, No. 6 (June), 2016: pp 1552–1556
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Figure 1. DWI and MRA on admission. (A and B) DWI of the brain showed high signal intensity areas at the vermis and lower left hemisphere of the cerebellum. (C) MRA showed that the entire left vertebral artery was thin, so-called hypoplasia. Abbreviations: DWI, diffusion-weighted magnetic resonance imaging; MRA, magnetic resonance angiography.
Figure 2. Repeat MRI after treatment with tPA. (A-K) Repeat DWI (A-D), axial FLAIR images (E-H), and sagittal T2-weighted images (I and J) showed high signal intensity areas in the left upper cervical posterior spinal artery and at the site of the cerebellar infarction. (K) Findings from brain magnetic resonance angiography did not change following tPA therapy. Abbreviations: DWI, diffusion-weighted magnetic resonance imaging; FLAIR, fluidattenuated inversion recovery; MRI, magnetic resonance imaging; tPA, tissue plasminogen activator.
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Figure 3. 3D-CTA and BPAS MRA. (A and B) 3D-CTA and BPAS MRA showed that the left vertebral artery was thin. Abbreviations: 3DCTA, 3-dimensional computed tomography angiography; BPAS, basiparallel anatomical scanning; CRA, cranial rotation angle; L, left; LPO, left posterior oblique; MRA, magnetic resonance angiography; P, posterior; S, superior.
therefore concluded that the patient did not have artery dissection. We diagnosed acute brain infarction and treated the patient with an intravenous infusion of tPA at 6:50 am, 2 hours after symptom onset. The patient responded well to treatment and an hour later, her NIHSS score was 4 points, with 2 points attributed to paralysis of the upper and lower left limbs and 2 points attributed to sensory disturbance on the left side of her body. Repeat DWI, fluid-attenuated inversion recovery images, and T2weighted images showed high signal intensity areas in the left upper cervical PSA from the lower medulla oblongata to the C2 level in addition to the site of the cerebellar infarction (Fig 2). Three-dimensional computed tomography angiography and basiparallel anatomical scanning showed that the left vertebral artery was similarly generally thin (Fig 3); therefore, we established that the cause of infarction was not artery dissection and inferred that it was atherosclerotic stenosis. Antiplatelet therapy was administered to the patient and her symptoms gradually improved, with an NIHSS score of 1 point because of slight dysesthesia on the left side of her body.
Discussion Spinal cord infarction is rare compared with brain infarction, and diagnosis during the acute phase is often challenging. Moreover, spinal cord infarction that involves the cervical PSA area is very rare, with 16 reported cases including the case presented herein.2-16 The clinical characteristics of the 16 cases of cervical PSA syndrome are shown in Table 1. The median age was 51 years old, with 9 cases occurring in males (56%). Infarct unilateral lesions were found in 10 cases and bilateral lesions were found in 6 cases. Other locations of lesions found in cervical spinal infarction were those in the medulla oblongata (6 cases, 38%) and the second cerebellum (4 cases, 25%). The most common cause of cervical PSA infarction was atherosclerosis (7 cases, 44%), followed by second artery dissection of the vertebral artery (6 cases, 38%), and trauma (1 case, 6%) and iatrogenic causes (1 case, 6%). Paralysis was frequently observed in patients with cervical PSA syndrome (12 cases, 75%)
in comparison with a small number of cases without any pyramidal signs (3 cases, 19%). The posterior spinal arteries mainly supply the posterior one third of the spinal cord and posterior horn, and the anterior spinal arteries supply the lateral funiculus including the pyramidal tract; therefore, pyramidal tract signs such as muscle weakness are considered atypical of PSA syndrome.17 However, because the PSA area does not have distinct boundaries and may vary between individuals, clinical manifestations can vary, with the pyramidal tract often included as an area in which lesions occur.18 The location of infarct lesions by vertebral level for the 16 cases of cervical PSA syndrome is shown in Figure 4, with a predominance of upper cervical lesions. The anatomy of the PSA at the cervical level is shown in Figure 5. The posterior spinal arteries descend from
Table 1. Cases of cervical posterior spinal artery syndrome (n = 16) Characteristic
N (%)
Median age, years (range) Male sex Infarct lesion Bilateral Unilateral Right Left Other lesions with cervical infarction Medulla oblongata Cerebellum Thoracic spinal cord Cause of cervical infarction Atherosclerosis Artery dissection Trauma Iatrogenic Other Pyramidal symptoms Muscle weakness No pyramidal signs
51 (19-84) 9 (56) 6 (38) 10 (63) 5 (31) 5 (31) 6 (38) 4 (25) 1 (6) 7 (44) 6 (38) 1 (6) 1 (6) 1 (6) 12 (75) 3 (19)
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[Vertebral level]
C1 C2 C3 Figure 4. Location of cervical infarct lesions in reported cases of cervical posterior spinal artery syndrome.
C4
C5 C6 C7 1
2
3
the vertebral artery or the posterior inferior cerebellar arteries and course in the posterior lateral sulcus of the cervical spinal cord.17 The pial plexus is fed mainly by the posterior arteries and exerts a centripetal flow direction primarily on the white matter. In contrast, the central arteries of the anterior spinal artery provide the main
Figure 5.
4
5
6
7
8
9
10
11
12
13
14
15
[Patient No.]
supply to the largest part of the gray matter. Infarction rarely occurs in the spinal cord artery because of the multiple anastomoses. On the other hand, it is thought that there are rarely the examples that many individual variations lead to spinal infarctions. Additionally, the reported cases varied with respect to spinal infarct lesion
Anatomy of posterior spinal artery at the cervical level. Adapted from Benavente and Barnett.17 Abbreviation: A, artery.
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characteristics, such as bilateral or unilateral type and length of lesion, which makes it difficult to determine any patterns. The main causes of cervical PSA syndrome are atherosclerosis and artery dissection. In the present case, the patient had no symptoms such as neck pain and headache, and there was no evidence of artery dissection on MRA, basiparallel anatomical scanning, and 3-dimensional computed tomography angiography. Additionally, cervical posterior spinal ischemia may have been caused by hypoplasia complicated by atherosclerosis because the entire left vertebral artery is thin. Acute brain infarction was diagnosed and the patient was treated with intravenous tPA therapy. Repeat DWI, fluid-attenuated inversion recovery images, and T2weighted images revealed cervical PSA syndrome, thereby showing that tPA may be useful in the treatment of spinal infarction. There are no previous reports of treating spinal cord infarction with tPA, and our case report therefore describes a suggestive use for this intervention. However, further evidence is needed to support the use of tPA for spinal infarction.
References 1. Sandson TA, Friedman JH. Spinal cord infarction. Report of 8 cases and review of the literature. Medicine (Baltimore) 1989;68:282-292. 2. Pryse-Phillips W. Infarction of the medulla and cervical cord after fitness exercises. Stroke 1989;20:292294. 3. Gutowski NJ, Murphy RP, Beale DJ. Unilateral upper cervical posterior spinal artery syndrome following sneezing. J Neurol Neurosurg Psychiatry 1992;55:841843. 4. Fukuda H, Kitani M. Unilateral posterior spinal artery syndrome of the upper cervical cord associated with vertebral artery occlusion. Rinsho Shinkeigaku 1994;34:1171-1174. 5. Bergqvist CA, Goldberg HI, Thorarensen O, et al. Posterior cervical spinal cord infarction following vertebral artery dissection. Neurology 1997;48:1112-1115.
T. SAKURAI ET AL. 6. Manabe Y, Murase T, Iwatsuki K, et al. Infarct presenting with a combination of Wallenberg and posterior spinal artery syndromes. J Neurol Sci 2000;176:155-157. 7. Masson C, Colombani JM. Unilateral infarct in the posterior spinal artery territory presenting as a ‘clumsy hand’. J Neurol 2002;249:1327-1328. 8. Reich P, Müller-Schunk S, Liebetrau M, et al. Combined cerebellar and bilateral cervical posterior spinal artery stroke demonstrated on MRI. Cerebrovasc Dis 2003; 15:143-147. 9. Mandrioli J, Zini A, Cavalleri F, et al. Bilateral posterior medullary and cervical stroke: a case report. Neurol Sci 2006;27:281-283. 10. Iwanaka Y, Okada K, Tanaka Y, et al. Unilateral upper cervical cord infarct restricted to the right funiculus cuneatus. Intern Med 2008;47:479. 11. An JY, Song IU, Kim WJ, et al. Posterior cervical spinal cord infarction following thyrocervical trunk embolization. Eur Neurol 2008;59:200-201. 12. Wang CM, Tsai WL, Lo YL, et al. Unilateral right occipital condyle to C2 level spinal cord infarction associated with ipsilateral vertebral artery stenosis and contralateral vertebral artery dissection: a case report. J Spinal Cord Med 2011;34:118-121. 13. Vuillier F, Tatu L, Camara A, et al. Unusual sensory disturbances revealing posterior spinal artery infarct. Case Rep Neurol 2012;4:23-27. 14. Murata K, Ikeda K, Muto M, et al. A case of posterior spinal artery syndrome in the cervical cord: a review of the clinicoradiological literature. Intern Med 2012;51:803807. 15. Matsubayashi J, Tsuchiya K, Shimizu S, et al. Posterior spinal artery syndrome showing marked swelling of the spinal cord: a clinico-pathological study. J Spinal Cord Med 2013;36:31-35. 16. Richard S, Abdallah C, Chanson A, et al. Unilateral posterior cervical spinal cord infarction due to spontaneous vertebral artery dissection. J Spinal Cord Med 2014;37:233-236. 17. Benavente O, Barnett HJM. Spinal cord ischemia. In: Barnett HJM, Mohr JP, Stein BA, et al., eds. Stroke. New York: Churchill Livingstone, 1998:751-765. 18. Lazorthes G. Pathology, classification and clinical aspects of vascular diseases of the spinal cord. In: Vinken PJ, Bruyn GW, eds. Handbook of clinical neurology, vol. 12. Oxford: North-Holland, 1972:492-506.
Cervical Posterior Spinal Artery Syndrome: A Case Report and Literature Review Takeo Sakurai,
MD,
Kenji Wakida,
MD,
and Hiroshi Nishida,
MD
We report a case of left upper cervical posterior spinal artery (PSA) syndrome caused by atherosclerosis of the left vertebral artery. A 70-year-old female experienced sudden dizziness and paralysis of the left upper and lower limbs. Diffusionweighted magnetic resonance imaging (DWI) of the brain showed high signal intensity at the vermis and lower left hemisphere of the cerebellum, and magnetic resonance angiography showed that the entire left vertebral artery was thin. The patient was treated with an intravenous infusion of tissue plasminogen activator 2 hours after symptom onset and made a full recovery. Repeat DWI, fluid-attenuated inversion recovery images, and T2-weighted images showed high signal intensity in the left upper cervical PSA area from the lower medulla oblongata to the C2 level in addition to the cerebellum. Previously reported cases of cervical posterior artery syndrome are reviewed. Key Words: Cervical posterior spinal artery syndrome—tissue plasminogen activator—cerebellar infarction—atherosclerosis. © 2016 National Stroke Association. Published by Elsevier Inc. All rights reserved.
Introduction Spinal cord infarction is rare compared with brain infarction, accounting for 1.2% of all strokes.1 Spinal cord infarction is usually localized to the anterior spinal artery area, while infarction of the posterior spinal artery (PSA) is an uncommon occurrence. In these cases, the thoracic– lumbar region is the most common location for an infarction occurring in the PSA; involvement of the cervical segment is infrequent. We report a case of unilateral upper cervical PSA syndrome, which was successfully treated with tissue From the Department of Neurology, Gifu Prefectural General Medical Center, Gifu, Japan. Received November 26, 2015; revision received January 12, 2016; accepted February 11, 2016. Address correspondence and reprint requests to Takeo Sakurai, MD, Department of Neurology, Gifu Prefectural General Medical Center, 4-6-1 Noisshiki, Gifu 500-8717, Japan. E-mail: sakurai-takeo@ gifu-hp.jp. 1052-3057/$ - see front matter © 2016 National Stroke Association. Published by Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.jstrokecerebrovasdis.2016.02.018
1552
plasminogen activator (tPA), and review previously reported cases of cervical PSA syndrome.2-16
Case Report A 70-year-old woman experienced sudden dizziness and paralysis of the left upper and lower limbs after washing her face in a washroom at 4:50 am. The patient had a history of rheumatoid arthritis. Neurological findings indicated severe paralysis of the left upper and lower limbs and sensory disturbance of touch sensation and position sensation on the left side of her body from the neck downward, and a National Institutes of Health Stroke Scale (NIHSS) score of 9 points. Laboratory findings showed no obvious abnormalities. Diffusion-weighted magnetic resonance imaging (DWI) of the brain showed faintly high intensity areas at the vermis and lower left hemisphere of the cerebellum, and magnetic resonance angiography (MRA) indicated that the left vertebral artery was generally thin, so-called hypoplasia (Fig 1). The patient had no pain at her neck and MRA showed no intimal flap, double lumen signs, or strings and pearls sign. We
Journal of Stroke and Cerebrovascular Diseases, Vol. 25, No. 6 (June), 2016: pp 1552–1556
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Figure 1. DWI and MRA on admission. (A and B) DWI of the brain showed high signal intensity areas at the vermis and lower left hemisphere of the cerebellum. (C) MRA showed that the entire left vertebral artery was thin, so-called hypoplasia. Abbreviations: DWI, diffusion-weighted magnetic resonance imaging; MRA, magnetic resonance angiography.
Figure 2. Repeat MRI after treatment with tPA. (A-K) Repeat DWI (A-D), axial FLAIR images (E-H), and sagittal T2-weighted images (I and J) showed high signal intensity areas in the left upper cervical posterior spinal artery and at the site of the cerebellar infarction. (K) Findings from brain magnetic resonance angiography did not change following tPA therapy. Abbreviations: DWI, diffusion-weighted magnetic resonance imaging; FLAIR, fluidattenuated inversion recovery; MRI, magnetic resonance imaging; tPA, tissue plasminogen activator.
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Figure 3. 3D-CTA and BPAS MRA. (A and B) 3D-CTA and BPAS MRA showed that the left vertebral artery was thin. Abbreviations: 3DCTA, 3-dimensional computed tomography angiography; BPAS, basiparallel anatomical scanning; CRA, cranial rotation angle; L, left; LPO, left posterior oblique; MRA, magnetic resonance angiography; P, posterior; S, superior.
therefore concluded that the patient did not have artery dissection. We diagnosed acute brain infarction and treated the patient with an intravenous infusion of tPA at 6:50 am, 2 hours after symptom onset. The patient responded well to treatment and an hour later, her NIHSS score was 4 points, with 2 points attributed to paralysis of the upper and lower left limbs and 2 points attributed to sensory disturbance on the left side of her body. Repeat DWI, fluid-attenuated inversion recovery images, and T2weighted images showed high signal intensity areas in the left upper cervical PSA from the lower medulla oblongata to the C2 level in addition to the site of the cerebellar infarction (Fig 2). Three-dimensional computed tomography angiography and basiparallel anatomical scanning showed that the left vertebral artery was similarly generally thin (Fig 3); therefore, we established that the cause of infarction was not artery dissection and inferred that it was atherosclerotic stenosis. Antiplatelet therapy was administered to the patient and her symptoms gradually improved, with an NIHSS score of 1 point because of slight dysesthesia on the left side of her body.
Discussion Spinal cord infarction is rare compared with brain infarction, and diagnosis during the acute phase is often challenging. Moreover, spinal cord infarction that involves the cervical PSA area is very rare, with 16 reported cases including the case presented herein.2-16 The clinical characteristics of the 16 cases of cervical PSA syndrome are shown in Table 1. The median age was 51 years old, with 9 cases occurring in males (56%). Infarct unilateral lesions were found in 10 cases and bilateral lesions were found in 6 cases. Other locations of lesions found in cervical spinal infarction were those in the medulla oblongata (6 cases, 38%) and the second cerebellum (4 cases, 25%). The most common cause of cervical PSA infarction was atherosclerosis (7 cases, 44%), followed by second artery dissection of the vertebral artery (6 cases, 38%), and trauma (1 case, 6%) and iatrogenic causes (1 case, 6%). Paralysis was frequently observed in patients with cervical PSA syndrome (12 cases, 75%)
in comparison with a small number of cases without any pyramidal signs (3 cases, 19%). The posterior spinal arteries mainly supply the posterior one third of the spinal cord and posterior horn, and the anterior spinal arteries supply the lateral funiculus including the pyramidal tract; therefore, pyramidal tract signs such as muscle weakness are considered atypical of PSA syndrome.17 However, because the PSA area does not have distinct boundaries and may vary between individuals, clinical manifestations can vary, with the pyramidal tract often included as an area in which lesions occur.18 The location of infarct lesions by vertebral level for the 16 cases of cervical PSA syndrome is shown in Figure 4, with a predominance of upper cervical lesions. The anatomy of the PSA at the cervical level is shown in Figure 5. The posterior spinal arteries descend from
Table 1. Cases of cervical posterior spinal artery syndrome (n = 16) Characteristic
N (%)
Median age, years (range) Male sex Infarct lesion Bilateral Unilateral Right Left Other lesions with cervical infarction Medulla oblongata Cerebellum Thoracic spinal cord Cause of cervical infarction Atherosclerosis Artery dissection Trauma Iatrogenic Other Pyramidal symptoms Muscle weakness No pyramidal signs
51 (19-84) 9 (56) 6 (38) 10 (63) 5 (31) 5 (31) 6 (38) 4 (25) 1 (6) 7 (44) 6 (38) 1 (6) 1 (6) 1 (6) 12 (75) 3 (19)
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[Vertebral level]
C1 C2 C3 Figure 4. Location of cervical infarct lesions in reported cases of cervical posterior spinal artery syndrome.
C4
C5 C6 C7 1
2
3
the vertebral artery or the posterior inferior cerebellar arteries and course in the posterior lateral sulcus of the cervical spinal cord.17 The pial plexus is fed mainly by the posterior arteries and exerts a centripetal flow direction primarily on the white matter. In contrast, the central arteries of the anterior spinal artery provide the main
Figure 5.
4
5
6
7
8
9
10
11
12
13
14
15
[Patient No.]
supply to the largest part of the gray matter. Infarction rarely occurs in the spinal cord artery because of the multiple anastomoses. On the other hand, it is thought that there are rarely the examples that many individual variations lead to spinal infarctions. Additionally, the reported cases varied with respect to spinal infarct lesion
Anatomy of posterior spinal artery at the cervical level. Adapted from Benavente and Barnett.17 Abbreviation: A, artery.
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characteristics, such as bilateral or unilateral type and length of lesion, which makes it difficult to determine any patterns. The main causes of cervical PSA syndrome are atherosclerosis and artery dissection. In the present case, the patient had no symptoms such as neck pain and headache, and there was no evidence of artery dissection on MRA, basiparallel anatomical scanning, and 3-dimensional computed tomography angiography. Additionally, cervical posterior spinal ischemia may have been caused by hypoplasia complicated by atherosclerosis because the entire left vertebral artery is thin. Acute brain infarction was diagnosed and the patient was treated with intravenous tPA therapy. Repeat DWI, fluid-attenuated inversion recovery images, and T2weighted images revealed cervical PSA syndrome, thereby showing that tPA may be useful in the treatment of spinal infarction. There are no previous reports of treating spinal cord infarction with tPA, and our case report therefore describes a suggestive use for this intervention. However, further evidence is needed to support the use of tPA for spinal infarction.
References 1. Sandson TA, Friedman JH. Spinal cord infarction. Report of 8 cases and review of the literature. Medicine (Baltimore) 1989;68:282-292. 2. Pryse-Phillips W. Infarction of the medulla and cervical cord after fitness exercises. Stroke 1989;20:292294. 3. Gutowski NJ, Murphy RP, Beale DJ. Unilateral upper cervical posterior spinal artery syndrome following sneezing. J Neurol Neurosurg Psychiatry 1992;55:841843. 4. Fukuda H, Kitani M. Unilateral posterior spinal artery syndrome of the upper cervical cord associated with vertebral artery occlusion. Rinsho Shinkeigaku 1994;34:1171-1174. 5. Bergqvist CA, Goldberg HI, Thorarensen O, et al. Posterior cervical spinal cord infarction following vertebral artery dissection. Neurology 1997;48:1112-1115.
T. SAKURAI ET AL. 6. Manabe Y, Murase T, Iwatsuki K, et al. Infarct presenting with a combination of Wallenberg and posterior spinal artery syndromes. J Neurol Sci 2000;176:155-157. 7. Masson C, Colombani JM. Unilateral infarct in the posterior spinal artery territory presenting as a ‘clumsy hand’. J Neurol 2002;249:1327-1328. 8. Reich P, Müller-Schunk S, Liebetrau M, et al. Combined cerebellar and bilateral cervical posterior spinal artery stroke demonstrated on MRI. Cerebrovasc Dis 2003; 15:143-147. 9. Mandrioli J, Zini A, Cavalleri F, et al. Bilateral posterior medullary and cervical stroke: a case report. Neurol Sci 2006;27:281-283. 10. Iwanaka Y, Okada K, Tanaka Y, et al. Unilateral upper cervical cord infarct restricted to the right funiculus cuneatus. Intern Med 2008;47:479. 11. An JY, Song IU, Kim WJ, et al. Posterior cervical spinal cord infarction following thyrocervical trunk embolization. Eur Neurol 2008;59:200-201. 12. Wang CM, Tsai WL, Lo YL, et al. Unilateral right occipital condyle to C2 level spinal cord infarction associated with ipsilateral vertebral artery stenosis and contralateral vertebral artery dissection: a case report. J Spinal Cord Med 2011;34:118-121. 13. Vuillier F, Tatu L, Camara A, et al. Unusual sensory disturbances revealing posterior spinal artery infarct. Case Rep Neurol 2012;4:23-27. 14. Murata K, Ikeda K, Muto M, et al. A case of posterior spinal artery syndrome in the cervical cord: a review of the clinicoradiological literature. Intern Med 2012;51:803807. 15. Matsubayashi J, Tsuchiya K, Shimizu S, et al. Posterior spinal artery syndrome showing marked swelling of the spinal cord: a clinico-pathological study. J Spinal Cord Med 2013;36:31-35. 16. Richard S, Abdallah C, Chanson A, et al. Unilateral posterior cervical spinal cord infarction due to spontaneous vertebral artery dissection. J Spinal Cord Med 2014;37:233-236. 17. Benavente O, Barnett HJM. Spinal cord ischemia. In: Barnett HJM, Mohr JP, Stein BA, et al., eds. Stroke. New York: Churchill Livingstone, 1998:751-765. 18. Lazorthes G. Pathology, classification and clinical aspects of vascular diseases of the spinal cord. In: Vinken PJ, Bruyn GW, eds. Handbook of clinical neurology, vol. 12. Oxford: North-Holland, 1972:492-506.