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LETTER TO EDITOR
Year : 2014  |  Volume : 62  |  Issue : 4  |  Page : 471-472

Role of diffusion-weighted MR imaging in diagnosis of spinal cord stroke following aorto-iliac bypass: Case report and review of literature


1 Department of Radiology, All India Institute of Medical Sciences, New Delhi, India
2 Department of Surgical Discipline, All India Institute of Medical Sciences, New Delhi, India

Date of Web Publication19-Sep-2014

Correspondence Address:
Chandan J Das
Department of Radiology, All India Institute of Medical Sciences, New Delhi
India
Chandan J Das
Department of Radiology, All India Institute of Medical Sciences, New Delhi
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.141294

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How to cite this article:
Singh A, Das CJ, Dhar A, Gupta A K, Singh A, Das CJ, Dhar A, Gupta A K. Role of diffusion-weighted MR imaging in diagnosis of spinal cord stroke following aorto-iliac bypass: Case report and review of literature . Neurol India 2014;62:471-2

How to cite this URL:
Singh A, Das CJ, Dhar A, Gupta A K, Singh A, Das CJ, Dhar A, Gupta A K. Role of diffusion-weighted MR imaging in diagnosis of spinal cord stroke following aorto-iliac bypass: Case report and review of literature . Neurol India [serial online] 2014 [cited 2019 Aug 22];62:471-2. Available from: http://www.neurologyindia.com/text.asp?2014/62/4/471/141294


Sir,

Spinal cord stroke is a rare event and due to non-specific symptoms and lack of awareness, diagnosis often remains clinically elusive. The report presents a case of acute spinal cord stroke following aortoiliac bypass and discusses the place of diffusion-weighted image (DWI) magnetic resonance imaging (MRI) in the diagnostic evaluation of cases of acute myelopathy.

A 27-year-old female presented with sudden onset of paraplegia with bladder and bowel incontinence. She had undergone aortoiliac bypass under spinal anesthesia for severe aortic narrowing just proximal to aortic bifurcation. On examination, patient was afebrile with blood pressure of 120/80 mmHg. Neurological examination revealed flaccid paralysis (motor power 2/5 in the hip flexors and 0/5 in the distal muscles) with absent deep tendon reflexes and no plantar response. Cerebrospinal fluid (CSF) analysis was normal. MRI of dorsolumbar spine revealed focal cord enlargement from T9-L1 vertebral levels [Figure 1]a and b and abnormal signal intensity in the form of T1 hypo and T2 hyperintensity [Figure 1]a and b. DWI revealed progressively increased diffusion restriction appearing as hyperintensity from b-0 to b-1000 [Figure 1]c and d with hypointensity on corresponding apparent diffusion coefficient (ADC) maps [Figure 1]e suggesting acute nature of cord ischemia.
Figure 1: T2W sagittal (a) image of spinal cord showing increased cord volume and hyperintensity extending from T9-L1 level, predominantly central, better appreciated on T2W axial (b). Sagittal (c) and axial (d) DWI images (b-1000)- shows diffusion restriction involving the cord. ADC axial image (e) showing corresponding hypointensity suggesting acute nature of stroke

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Spinal cord blood supply is by three longitudinally coursing arteries: single anterior spinal artery and paired posterior spinal artery. [1] Each spinal segment is further reinforced with collateral supply. Posterior spinal artery receives 12 unpaired radicular collateral branches whereas anterior spinal artery has more vicarious blood supply, receiving only 7-10 unpaired radicular collaterals. Dorsolumbar segment usually from T9 to cauda equina receives a large radiculomeullary collateral called "artery of Adamkiewicz. [1] Anterior spinal artery is narrowest at T8 level, making it most susceptible for neurovascular complications. [2]

Spinal cord infarct is an uncommon cause (5-8%) of acute myelopathy. Overall incidence of spinal cord infarct as a cause of stroke is merely 1-2%. [2],[3] In the absence of history of trauma or constitutional symptoms, vascular cause should be suspected. [3]. Most common cause of spinal cord stroke is atherosclerosis followed by aortic pathologies (traumatic or non-traumatic), degenerative, hypoperfusion, embolism and idiopathic. [1],[3]

Spinal cord infarct is categorized into various clinical subtypes depending upon the vascular territory involved. Anterior and posterior spinal artery syndrome occur as a result of radicular artery involvement whereas generalised hypoperfusion leads to central and transverse cord stroke. [4] In cases of myelopathy, plain radiographs and computed tomography (CT) help to evaluate extra or intradural extramedullary lesions, which may miss intramedullary lesions in as high as more than 50% of cases. [3] MRI is the modality of choice for evaluation of myelopathy. In acute spinal cord infarct, evolution of findings varies with the severity. In early cases, only central gray matter is affected, but with progression, entire gray matter may be involved. [5] Immediately after the ischemic insult, MRI findings may be normal, similar to cerebral ischemia. [5] Findings are well established after 1-2 days. [5] In early stages, T1WI may be either normal or may show slightly bulky cord. [3] T2WI shows abnormal intramedullary hyperintensity due to edema. On DWI, there is restricted diffusion with corresponding ADC hypointensity. In later stages, there may be enhancement of affected gray matter. [3],[5] DWI is the most useful sequence to diagnose infarct. However, technical factors like susceptibility artifacts and small spinal cord volume limit its widespread use with limited study so far. [6],[7],[8] If the arterial involvement is proximal to the origin of vertebral artery, vertebral stroke may also occur, further reinforcing the diagnosis. [3] Other causes of acute myelopathy include acute transverse myelitis, demyelinaton, tumours etc., However, sudden onset and MRI findings of central gray matter predilection help in excluding these differentials. [3]

Few cases of spinal cord infarct following surgeries have been reported, citing it to be multifactorial, the exact etiology being unknown. Nonetheless, in post operative setting, hypotension is postulated to be the most likely reason. Associated cardiovascular co-morbidities further compound the scenario. [1] Irreversibility of spinal cord infarct, especially in post operative setting calls for the prevention to be the best management. Any hypotensive or hypovolemic episode in peri-operative period should be treated aggressively. [1]

Recovery in such cases may not be complete; however, the recovery may depend on time factor. Like cerebral stroke, earlier the diagnosis, better is the prognosis. Due to its rarity, diagnosis is often missed and hence prognosis is extremely poor. In addition, prognosis also depends upon the extent of neurological deficit at presentation. Severe neurological deficit and female gender carry poor prognosis. [9] In our case, however, there was no known hypotensive episode and patient was managed conservatively. At 2-months follow-up motor recovery was still incomplete (power 3/5).

Through this case report, we wish to highlight that this clinical entity should be strongly suspected in any case of sudden onset paraplegia which is non-traumatic and without any systemic symptoms. We emphasize that all cases of sudden onset paraplegia should be evaluated by MRI spine. Diagnostic accuracy and specificity can be increased by DWI-MR imaging.

 
  References Top

1.Cekic G, Kock MD, Kremer Y, Sholtes JL. Paraplegia after combined general and epidural anesthesia: A case report. Acta Anaesthesiol Belg 2008;59:95-8.  Back to cited text no. 1
    
2.El-Osta B, Ghoz A, Singh VK, Saed E, Abdunabi M. Spontaneous spinal cord infarction secondary to embolism from an aortic aneurysm mimicking as cauda equina due to disc prolapse: A case report. Cases J 2009;2:7460.  Back to cited text no. 2
    
3.Murugan KS, Kalpana KR. Spinal cord and vertebral body infarction in a patient with thoracic aortic dissection: A case report. Indian J Radiol Imaging 2008;18:135-7.  Back to cited text no. 3
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4.Novy J, Carruzzo A, Maeder P, Bogousslavsky J. Spinal cord ischemia: Clinical and imaging patterns, pathogenesis, and outcomes in 27 patients. Arch Neurol 2006;63:1113-20.  Back to cited text no. 4
    
5.Alblas CL, Bouvy WH, Lycklama À Nijeholt GJ, Boiten J. Acute spinal-cord ischemia: Evolution of MRI findings. J Clin Neurol 2012;8:218-23.  Back to cited text no. 5
    
6.Thurnher MM, Bammer R. Diffusion-weighted MR imaging (DWI) in spinal cord ischemia. Neuroradiology 2006;48:795-801.  Back to cited text no. 6
    
7.Küker W, Weller M, Klose U, Krapf H, Dichgans J, Nägele T. Diffusion-weighted MRI of spinal cord infarction-high resolution imaging and time course of diffusion abnormality. J Neurol 2004;251:818-24.  Back to cited text no. 7
    
8.Loher TJ, Bassetti CL, Lövblad KO, Stepper FP, Sturzenegger M, Kiefer C, et al. Diffusion-weighted MRI in acute spinal cord ischae-mia. Neuroradiology 2003;45:557-61.  Back to cited text no. 8
    
9.Nedeltchev K, Loher TJ, Stepper F, Arnold M, Schroth G, Mattle HP, et al. Long-term outcome of acute spinal cord ischemia syndrome. Stroke 2004;35:560-5.  Back to cited text no. 9
    


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