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|LETTERS TO EDITOR
|Year : 2019 | Volume
| Issue : 2 | Page : 571-573
Late changes on magnetic resonance imaging in posterior spinal artery syndrome: A report and literature review
Yuya Kobayashi, Shunichi Sato, Ryota Takamatsu, Rie Watanabe, Kenichi Hoshi, Wataru Ishii, Hiroyuki Yahikozawa
Department of Neurology, Nagano Red Cross Hospital, Nagano, Japan
|Date of Web Publication||13-May-2019|
Dr. Yuya Kobayashi
Department of Neurology, Nagano Red Cross Hospital, 5-22-1, Wakasato, Nagano 380-8582
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Kobayashi Y, Sato S, Takamatsu R, Watanabe R, Hoshi K, Ishii W, Yahikozawa H. Late changes on magnetic resonance imaging in posterior spinal artery syndrome: A report and literature review. Neurol India 2019;67:571-3
|How to cite this URL:|
Kobayashi Y, Sato S, Takamatsu R, Watanabe R, Hoshi K, Ishii W, Yahikozawa H. Late changes on magnetic resonance imaging in posterior spinal artery syndrome: A report and literature review. Neurol India [serial online] 2019 [cited 2021 Jan 27];67:571-3. Available from: https://www.neurologyindia.com/text.asp?2019/67/2/571/258006
Posterior spinal artery syndrome (PSAS) is extremely rare. Spinal cord infarctions represent approximately 1.2% of all strokes, and PSAS accounts for only 3.6% of all spinal cord infarctions. Its diagnosis is often difficult during the acute phase because other spinal cord diseases need to be ruled out. Although magnetic resonance imaging (MRI) is effective for establishing the diagnosis of PSAS, we encountered a case with late MRI changes.
An 82-year old Japanese woman presented to us with motility paralysis of the right lower limb, dysuria, and bilateral paresthesias in areas distal to the umbilicus. The symptoms appeared suddenly in the morning and gradually worsened as the day progressed. The patient was under medication for hypertension, hyperlipidemia, diabetes, atrial fibrillation, and chronic renal dysfunction. At admission, 12 h after the onset of symptoms, we found decreased strength in the right lower limb and decrease in vibration sensation [Figure 1]. She exhibited no symptoms of cranial nerve dysfunction and cerebellar ataxia; however, her Babinski and Chaddock reflexes were positive bilaterally. Spinal cord disease at the thoracic level was suspected on the basis of neurological symptoms. Routine blood tests yielded normal results, and cerebrospinal fluid (CSF) analysis revealed a cell count of 1 cell/μL and the protein content was 50 mg/dL. There were no clinically significant MRI findings in the spine on T2-weighted imaging (T2WI). Diffusion-weighted imaging (DWI) was not performed because 12 h had already lapsed since the onset of symptoms, and we believed that acute changes could be detected from the T2WI images. We prioritized whole spinal imaging to exclude diseases, including hematomas, infections, medial disc herniations, inflammatory diseases, and tumors, which require an immediate treatment. The head MRI revealed no abnormalities. We ruled out an aortic dissection using computed tomography angiography (CTA) considering Adamkiewicz artery infarction. Further, considering the possibility of myelitis including spinal infarction, we administered methylprednisolone (mPSL) 1000 mg/day and ozagrel sodium 160 mg/day. An additional spinal MRI on day 3 did not reveal abnormalities. Other spinal disorders, including multiple sclerosis, neuromyelitis optica, lymphoma, arteriovenous malformation, subacute combined degeneration of spinal cord, collagen diseases, syphilis, sarcoidosis, and parasitoses, were excluded on the basis of additional examinations. On day 11, the right lateral funiculus and bilateral posterior funiculus in the thoracic (T) 8–10 levels revealed a high intensity on the DWI and T2WI MRI [Figure 2]. We diagnosed the patient as having PSAS. The motor deficits gradually improved with therapy; however, dysuria and disturbances in vibration sensation persisted. She was transferred to a rehabilitation facility on day 31.
|Figure 1: Graphical representation of the area of vibration sensation decrease (gray shadow)|
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|Figure 2: At admission (a and f), a herniated disc was detected at L4/5 level. However, no abnormalities were observed in the spine on T2WI MRI. DWI was not performed on admission. Follow-up MRI on day 3 (b, c, g and i) showed no abnormalities. MRI on day 13, DWI (e and j), and T2WI (d and h) revealed abnormalities in the right lateral funiculus and bilateral posterior funiculus at the thoracic 8–10 levels. (T2WI: T2-weighted imaging, DWI: Diffusion-weighted imaging)|
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PSAS is caused by infarction of the posterior spinal artery. One anterior spinal artery supplies two-thirds of the spinal cord on the ventral side, and two posterior spinal arteries supply the dorsal one-third of the spinal cord. These three vessels anastomose and form a complicated vascular meshes on the surface of the spinal cord., PSAS can cause various symptoms such as profound proprioceptive deficits, motor deficits, superficial sensory loss, and ataxia. Our patient exhibited signs of posterior funiculus involvement, including dysuria and motor deficit. On admission, we suspected spinal cord dysfunction, but the lack of MRI findings and symptoms other than that pertaining to the posterior cord did not support the diagnosis of a single posterior spinal artery infarction. Although posterior spinal arteries exist on both the sides, patients with PSAS usually develop bilateral significant sensory disturbances (only 2 PSAS patients had unilateral involvement out of a reported total of 27 cases), and we should have noted it. This may be because blood vessels in the posterior spinal artery are frequently anastomosed and supply both the sides. Additionally, the two posterior spinal arteries become discontinuous in some portions and distribute blood to the contralateral side. Thus, the blocking of blood flow on one side may affect the contralateral side. Moreover, involvement of the corticospinal tract may develop.
Generally, a high signal on DWI is observed at an early stage of cerebral infarction, and spinal cord infarctions exhibit the same change on DWI approximately 3 h after the onset in some cases; however, four out of 28 cases were reported to have normal MRI findings (on day 1 in one patient and on day 2 in three others) on T2WI. Further, bone marrow changes on MRI can also reflect spinal cord infarction because the same artery also supplies the vertebral body and the spinal cord. However, the vertebral body is not always associated with spinal cord infarction, and this evidence for establishing the radiologic diagnosis of PSAS may be absent, as was seen in our case. Our patient did not show any pathological MRI findings on days 1 and 3 after the onset of symptoms, but only after day 11, and there may be two reasons for this. First, the spinal cord tissue has lower oxygen demands than the brain and is more resistant to ischemia. Second, complete ischemia had not occurred and was still gradually developing because of the presence of collateral circulation. As an explanation for these facts, the range of symptoms did not change, but the intensity of the symptoms worsened over a week. Thus, in cases of suspected PSAS, MRI should be repeated over time.
As our patient had risk factors for arteriosclerosis with the presence of hypertension, hyperlipidemia, and diabetes, an arteriosclerotic mechanism was considered. A frequent (23.6%) cause of spinal cord ischemia is arteriosclerosis. We performed a computed tomographic angiography (CTA) but could not implicate a specific artery. An arteriovenous malformation was not detected. There is no consensus on the treatment of spinal cord infarction, and it has not been proven that the early administration of thrombolytic agents improves outcome. Eleven percent of spinal cord infarctions are caused by aortic dissections, and therefore, careful judgment is necessary before antithrombolytic treatment is adminstered.
Taking all these facts into consideration as well as referring to our own experience, establishing the diagnosis of PSAS can be difficult, and the exclusion of other possible diseases is required. To uncover delayed findings, such as those seen in our case, the evaluation of progressive clinical symptoms should lead the search for a lesion site by repeated imaging over time.
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Conflicts of interest
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[Figure 1], [Figure 2]