Spinal Cord Infarction Research Articles

Acute spontaneous spinal cord infarction: Utilisation of hyperbaric oxygen treatment, cerebrospinal fluid drainage and pentoxifylline.

Spinal cord infarction (SCI) is a potentially devastating disorder presenting with an acute anterior spinal artery syndrome, accounting for an estimated 1% of stroke presentations. Aetiologies include aortic surgical complications, systemic hypotension, fibrocartilaginous embolism and vascular malformations. Diagnosis is clinical combined with restriction on diffusion-weighted magnetic resonance imaging (MRI). There are no treatment guidelines for non-perioperative cases although there is limited literature regarding potential therapies, including hyperbaric oxygen treatment (HBOT) and cerebrospinal fluid (CSF) drainage. We describe 13 cases of acute SCI, five receiving HBOT, and three also receiving pentoxifylline and drainage of lumbar CSF. Data for all patients with MRI-proven SCI at Fiona Stanley Hospital from 2014-2019 were reviewed. Thirteen patients, median age 57 years (31-74), 54% female, were identified. Aetiologies: two fibrocartilaginous emboli; seven likely atherosclerotic; two thromboembolic; two cryptogenic. All presented with flaccid paraplegia except one with Brown-Sequard syndrome. Levels ranged from C4 to T11. Five patients received HBOT within a median time of 40 hours from symptom onset, with an average 15 treatments (10-20). Three of these received triple therapy (HBOT, pentoxifylline, CSF drainage) and had median Medical Research Council manual muscle testing power of 5, median modified Rankin Score (mRS) of 1 and American Spinal Injury Association (ASIA) score of D on discharge, compared with 2 power, mRS 3.5 and ASIA B in those who did not. SCI can be severely disabling. Triple therapy with pentoxifylline, CSF drainage and HBOT may reduce disability and further prospective trials are required.

754: Cocaine-Induced Acute Spinal Cord Infarction: Case Report

Oli, Sharad1; Patti, Ravi Karan1; Dalsania, Nishil1; Sinha, Ankur1; Somal, Navjot1; Khanal, Resha2; Levin, Ilya1; Seneviratne, Chanaka1; Kupfer, Yizhak1 Author Information

Association of G20210A Prothrombin Gene Mutation and Cerebral Ischemic Stroke in Young Patients.

Ischemic stroke is an acute episode of neurological dysfunction resulting from the focal brain and spinal cord infarction. Many etiologies have been reported and vary significantly with the age of the patients. This study aims to show the association of G20210A prothrombin gene mutation and cerebral ischemic stroke in young patients. The prothrombin gene mutation is the second most common inherited thrombophilia after the factor V mutation. In this single missense mutation, guanine is substituted by adenine base pair in the nucleotide position 20210 of the 3'-untranslated region of the prothrombin gene, resulting in abnormal thrombin production predisposing to both arterial or venous thrombosis. Forty-seven relevant articles were selected after a thorough screening process using a regular keyword ‘G20210A Prothrombin’ and/or ‘Ischemic Stroke’ mostly from the PubMed database. We included the studies that are published in the last 22 years with patients age ≤57 years. This review article depicts the association of G20210A prothrombin gene mutation with ischemic stroke in young patients irrespective of ethnicity and zygosity status of their genotype. However, more multicenter prospective studies are needed to better understand the application of prothrombin gene mutation in predicting the associated risk of ischemic stroke in young patients and its importance in deciding the patients' treatment or prognosis.

Spinal Cord Infarction: A Single Center Experience and the Usefulness of Evoked Potential as an Early Diagnostic Tool.

Background: Spinal cord infarction (SCI) is a rare disease and its early diagnosis is challenging. Here, we described the clinical features and imaging findings of SCI, and assessed the results of evoked potential (EP) studies to elucidate their diagnostic role in the early stage of SCI.Methods: We retrospectively analyzed 14 patients who had spontaneous SCI. The demographic, neurological, and temporal profiles of the SCI patients were identified. We reviewed the imaging findings and assessed the changes in them over time. To review EP, central motor conduction time (CMCT) and somatosensory evoked potential (SEP) values were obtained. We also enrolled 15 patients with transverse myelitis (TM), and compared the clinical, radiological and electrophysiological features between SCI and TM patients.Results: The ages of the SCI patients ranged from 54 to 73 years. Nine patients (64.3%) showed nadir deficits within 6 h. The most common type of clinical visit was via the emergency center. Nine patients (64.3%) presented with peri-onset focal pain. The median initial modified Rankin scale score was 3. For 9 patients (64.3%), initial T2 imaging findings were negative, but subsequent diffusion weighed imaging (DWI) showed diffusion restriction. Vertebral body infarction was observed in 5 patients (35.7%). EP data were available for 10 SCI patients. All 8 patients who had their CMCT measured showed abnormalities. Among them, motor evoked potentials were not evoked in 6 patients at all. SEP was measured in 10 patients, and 9 of them showed abnormalities; one of them showed no SEP response. For 5 patients, the EP studies were done prior to DWI, and all the patients showed definite abnormalities. The abnormalities in the EP findings of the SCI patients were more profound than those of the TM patients, even though the duration from the onset to the start of the study was much shorter for SCI patients.Conclusion: SCI can be diagnosed based on typical clinical manifestations and appropriate imaging studies. Our study also indicates that immediate sensory and motor EP study can have an adjuvant diagnostic role in the hyperacute stage of SCI, and can improve the accuracy of diagnosis.

Hyperacute extensive spinal cord infarction and negative spine magnetic resonance imaging: a case report and review of the literature

Rationale:Spinal cord infarction (SCI) accounts for only 1% to 2% of all ischemic strokes and 5% to 8% of acute myelopathies. Magnetic resonance imaging (MRI) holds a role in ruling out non-ischemic etiologies, but the diagnostic accuracy of this procedure may be low in confirming the diagnosis, even when extensive cord lesions are present. Indeed, T2 changes on MRI can develop over hours to days, thus accounting for the low sensitivity in the hyperacute setting (ie, within 6 hours from symptom onset). For these reasons, SCI remains a clinical diagnosis. Despite extensive diagnostic work-up, up to 20% to 40% of SCI cases are classified as cryptogenic. Here, we describe a case of cryptogenic longitudinally extensive transverse myelopathy due to SCI, with negative MRI and diffusion-weighted imaging at 9 hours after symptom onset.Patient concerns:A 51-year-old woman presented to our Emergency Department with acute severe abdominal pain, nausea, vomiting, sudden-onset of bilateral leg weakness with diffuse sensory loss, and paresthesias on the trunk and legs.Diagnoses:On neurological examination, she showed severe paraparesis and a D6 sensory level. A 3T spinal cord MRI with gadolinium performed at 9 hours after symptom onset did not detect spinal cord alterations. Due to the persistence of a clinical picture suggestive of an acute myelopathy, a 3T MRI of the spine was repeated after 72 hours showing a hyperintense “pencil-like” signal mainly involving the grey matter from T1 to T6 on T2 sequence, mildly hypointense on T1 and with restricted diffusion.Interventions:The patient was given salicylic acid (100 mg/d), prophylactic low-molecular-weight heparin, and began neuromotor rehabilitation.Outcomes:Two months later, a follow-up neurological examination revealed a severe spastic paraparesis, no evident sensory level, and poor sphincteric control with distended bladder.Lessons:Regardless of its relatively low frequency in the general population, SCI should be suspected in every patient presenting with acute and progressive myelopathic symptoms, even in the absence of vascular risk factors. Thus, a clinical presentation consistent with a potential vascular syndrome involving the spinal cord overrides an initially negative MRI and should not delay timely and appropriate management.

Pediatric spinal cord infarction following a minor trauma: a case report.

Pediatric spinal cord infarction is a rare entity that presents a diagnostic challenge at the emergency department. Ischemic spinal cord infarction can occur in the setting of trauma, cardiovascular malformation, or postoperatively. We report a case of anterior spinal artery infarction following seemingly minor trauma in an otherwise healthy 14-year-old male. A 14-year-old male presented with unprovoked sudden-onset stabbing back pain earlier that day. The patient then demonstrated bilateral lower extremities weakness while at the emergency department. After extensive diagnostic workup, the patient was diagnosed with anterior spinal artery territory infarction involving the thoracic spinal cord. Minor trauma to the thoracic spinal cord was detected on imaging and was believed to be the culprit of this event. Given the rarity of spinal cord ischemia, a high index of suspicion and extensive workup of patients presenting with clinical weakness are needed for accurate diagnosis and to avoid the eventual poor outcome. With so few reports in the literature regarding spinal cord ischemia in the pediatric population, accurate diagnosis is often delayed until after irreversible events have already taken place. Our case report of anterior spinal artery distribution thoracic cord infarct following a minor trauma was diagnosed by axial thin-slice DWI MRI with an otherwise negative workup.

Complications Associated with Lumbar Transforaminal Epidural Steroid Injections.

Low back pain with radicular symptoms is a common cause of disability in the adult population in the USA. Lumbar transforaminal epidural steroid injection (TFESI) is one of the most frequently used intervention for lumbar radiculitis. The purpose of this review is to evaluate complications associated with lumbar TFESI. Based on the literature review, the reported rate of minor complications was between 2.4 and 9.6%. The major complications including spinal abscess, spinal cord infarct, and epidural hematoma were documented as case reports. Some patients with spinal cord infarct had permanent neurologic deficits, while the other patients had recovery of neurological function after surgical or medical intervention. This review identifies both the minor and major complications related to lumbar transforaminal epidural steroid injections. According to this review, most complications are minor. Lumbar TFESI can be considered a safe treatment in the management of lumbar radicular pain. However, pain specialists should be aware of the potentially devastating major complications. Early recognition and treatment of complications are crucial for improving the outcome.

Spinal cord infarction associated to retinal vein occlusion in a patient with chronic kidney disease.

A 70-year-old man presented to the emergency department with blood hypotension associated to a sudden paraplegia and thermalgesic analgesia. He had an history of colic and prostatic adenocarcinoma, hypertension and non-dialyzed Chronic Kidney Disease (CKD) related to an idiopathic membranous glomerulonephritis type 1 discovered 9 years ago. Magnetic resonance imaging confirmed a diagnosis of Spinal Cord Infarction (SCI). Few months later, he presented a blurred vision due to central Retinal Vein Occlusion (RVO), which was improved by Anti-VEGF therapy. This is the first reported case of a concomitance of retinal vascular event and SCI highlights the links between the central nervous system and retinal vascularization despite separate involvement of the two events in the arterial and venous systems. Additionally, CKD worsened the risk of cardiovascular incidents by induced oxidative stress, thrombophilia, chronic inflammation, and endothelial dysfunction. SCI occurrence indicates severe vascular dysfunction and elevates the risk of additional vascular disorders.

Severe Unilateral Proprioceptive Loss in Medullary-rostral Spinal Cord Infarction. A Posterior Spinal Artery Syndrome

Introduction. The symptoms and signs found in patients with lateral medullary infarction have been described for more than 200 years. The major symptoms are vestibulo-cerebellar and dysphagia and dysphonia attributable to structures innervated by the ambiguous nucleus. Sensory symptoms and signs are often present in the ipsilateral face and contralateral limbs and trunk and sometimes the face. Case Report. A 29 year old woman had headache and left neck pain during weeks. Her left side suddenly became “completely dead and lacked feeling.” She saw double and was dizzy. Her right side remained normal. MRI showed infarction in the left lateral caudal medulla extending into the medulla-spinal junction. Vascular imaging showed a dissection of the left vertebral artery . Second case is A retired man with his neurological symptoms and signs developed in steps. He first noticed while shaving that his left face was numb, A week later, while showering, he became unsteady and had discomfort behind his left ear and in his left neck. MRI showed an infarct limited to the caudo-medial portion of the left dorsolateral medulla that extended into the rostral spinal cord. Discussion. Loss of position sense in the limbs ipsilateral to a medullary infarct has only rarely been reported. Lesions of the vertebral artery just above or below dural penetration are most likely to cause medullary infarcts that are tegmental rather than basal and to cause rostral spinal cord infarction. This region of the vertebral artery is rarely affected by atherosclerosis and the commonest lesion is dissection.

Spinal neurovascular complications with anterior thoracolumbar spine surgery: a systematic review and review of thoracolumbar vascular anatomy.

Spinal cord infarction due to interruption of the spinal vascular supply during anterior thoracolumbar surgery is a rare but devastating complication. Here, the authors sought to summarize the data on this complication in terms of its incidence, risk factors, and operative considerations. They also sought to summarize the relevant spinal vascular anatomy. They performed a systematic literature review of the PubMed, Scopus, and Embase databases to identify reports of spinal cord vascular injury related to anterior thoracolumbar spine procedures as well as operative adjuncts and considerations related to management of the segmental artery ligation during such anterior procedures. Titles and abstracts were screened, and studies meeting inclusion criteria were reviewed in full. Of 1200 articles identified on the initial screening, 16 met the inclusion criteria and consisted of 2 prospective cohort studies, 10 retrospective cohort studies, and 4 case reports. Four studies reported on the incidence of spinal cord ischemia with anterior thoracolumbar surgery, which ranged from 0% to 0.75%. Eight studies presented patient-level data for 13 cases of spinal cord ischemia after anterior thoracolumbar spine surgery. Proposed risk factors for vasculogenic spinal injury with anterior thoracolumbar surgery included hyperkyphosis, prior spinal deformity surgery, combined anterior-posterior procedures, left-sided approaches, operating on the concavity side of a scoliotic curve, and intra- or postoperative hypotension. In addition, eight studies analyzed operative considerations to reduce spinal cord ischemic complications in anterior thoracolumbar surgery, including intraoperative neuromonitoring and preoperative spinal angiography. While spinal cord infarction related to anterior thoracolumbar surgery is rare, it warrants proper consideration in the pre-, intra-, and postoperative periods. The spine surgeon must be aware of the relevant risk factors as well as the pre- and intraoperative adjuncts that can minimize these risks. Most importantly, an understanding of the relevant spinal vascular anatomy is critical to minimizing the risks associated with anterior thoracolumbar spine surgery.

Endovascular Repair for Retrograde Type A Intramural Haematoma with Intimal Tear in the Descending Thoracic Aorta

The current treatment for acute retrograde type A intramural haematoma (IMH) remains challenging. Aortic remodelling in both the ascending aorta (AA) and descending thoracic aorta (DTA) was evaluated and the 30 day and mid term outcomes were determined in patients who underwent thoracic endovascular aneurysm repair (TEVAR) for retrograde type A IMH with a primary intimal tear or ulcer like projection in the DTA METHODS: This was a retrospective, multicentre observational study. Clinical data, including post-operative mortality and adverse event, aorta related re-intervention, aortic remodelling, and the survival rate of 18 non-consecutive patients with acute retrograde type A IMH undergoing TEVAR between June 2006 and March 2018 were reviewed. The median age at repair was 58.1 years (range 38-86) and 14 (78%) were men. Eight patients (44%) presented with haemopericardium, and 10 (56%) underwent TEVAR within 24h. The mean IMH thickness and AA diameter were 10.4±3.6 and 45.7±4.6mm, respectively. Among all patients with acute retrograde type A IMH, 11 patients presented with classical type B aortic dissection and seven with type B IMH. All procedures were technically successful. The median follow up was 28.7 months (range 7-78). No 30 day mortality was observed. Three patients developed post-procedure adverse events. Of these, two patients had neurological events, with one each having cerebrovascular and spinal cord infarction individually, and the third patient required long term haemodialysis with ventilator support. The overall survival rate was 100%. The maximum diameter of the AA and the IMH in the AA significantly decreased after TEVAR. Aortic remodelling was also observed in the DTA along the length of TEVAR coverage. In selected patients with acute retrograde type A IMH, TEVAR offered a treatment alternative to open surgical grafting and medical follow up.

Spinal Cord Infarction after Transcatheter Embolization of Pelvic Arteriovenous Malformation.

An 80-year-old woman presented with abdominal and right lower limb pain. Radiological examination revealed pelvic arteriovenous malformations (pAVMs). Although transarterial embolization was repeated, dilation of the common iliac vein worsened. Four sessions of embolization were performed for the internal iliac vein. Paraplegia gradually occurred a day after the final procedure. Magnetic resonance imaging revealed thoracic spinal cord edema and paraspinal vasodilatation, suggesting spinal cord infarction. Additional angiography revealed a radiculomedullary vein draining into the spinal canal from the pAVM; hence, surgical interruption was performed. Incomplete venous embolization of the pAVM caused spinal cord congestion and infarction.

Spinal cord infarction due to fibrocartilaginous embolism

Spinal cord infarction due to fibrocartilaginous embolism

Detection of the common origin of the radiculomedullary artery with the feeder of spinal dural arteriovenous fistula using slab maximum intensity projection image.

Endovascular therapy to the spinal dural arteriovenous fistula (SDAVF) with a common origin of the radiculomedullary artery and the feeder of the shunt has the risk of spinal cord infarction. This study aimed to retrospectively assess the detection rate of normal spinal arteries from the feeder of SDAVF. We retrospectively collected the angiographic and clinical data of SDAVFs. This study included 19 patients with 20 SDAVF lesions admitted to our department between January 2007 and December 2018. We assessed the detection rate of normal radiculomedullary artery branched from the feeder of SDAVF between the period using the image intensifier (II) and flat panel detector (FPD) and evaluated the treatment results. The detection rates of the radiculomedullary artery branched from the feeder of SDAVF were 10% (1/10 lesions) during the II period and 30% (3/10 lesions) during the FPD period. During the FPD period, all normal radiculomedullary arteries branched from the feeder were only detected on slab maximum intensity projection (MIP) images of rotational angiography, and we could not detect them in 2D or 3D digital subtraction angiography. All lesions that had a common origin of a normal radiculomedullary artery and the feeder were completely obliterated without complications. There was no recurrence during the follow-up period. The flat panel detector and slab MIP images seem to show the common origin of the normal radiculomedullary arteries from the feeder more accurately. With detailed analyses, SDAVF can be safety treated.

Nucleus Polposus Embolism Causing Anterior Spinal Artery Occlusion: A Rare but Possible Cause of Fibrocartilaginous Embolic Myelopathy.

Fibrocartilaginous embolic myelopathy (FCEM) is a rare cause of spinal cord infarction. It has been confirmed by autopsy in postmortem cases. Herein we describe a case of FCEM diagnosed based on clinical grounds. A 58-year-old man presented with acute onset of complete paraplegia with bladder and bowel involvement developing a few hours after a trivial trauma. There were no upper motor neuron signs. His magnetic resonance imaging (MRI) was suggestive of longitudinally extensive transverse myelitis from T5 to the conus. There was left paracentral disc protrusion at the T4-T5 level. However, no features of inflammatory, infectious, or autoimmune etiology were found on history, on examination, or in blood or cerebrospinal fluid analysis, and there was no contrast enhancement on MRI. A diagnosis of anterior spinal artery occlusion was made based on clinical examination with sparing of posterior column sensations in the lower limbs, predominant involvement of anterior half of the spinal cord on MRI, and accompanying new onset of back pain with rapid symptom progression to nadir as opposed to inflammatory etiology. Fibrocartilaginous embolism was suspected after ruling out all other causes of vascular compromise and presence of disc herniation at T4-T5. He was managed with rehabilitation and showed no signs of recovery. FCEM, though rare, should be kept in mind as a differential diagnosis of acute medical myelopathy when no other cause can be identified.

Neuromyelitis Optica Spectrum Disorder (NMOSD) Misdiagnosed as Spinal Cord Infarction (5394)

Neuromyelitis Optica Spectrum Disorder (NMOSD) Misdiagnosed as Spinal Cord Infarction (5394)

A rare presentation of perinatal spinal cord infarct (646)

A rare presentation of perinatal spinal cord infarct (646)

Brown-Sequard Syndrome Caused by a Cocaine-Induced Spinal Cord Infarct: A Case Report (2515)

Brown-Sequard Syndrome Caused by a Cocaine-Induced Spinal Cord Infarct: A Case Report (2515)

Delayed quadriparesis after posterior spinal fusion for scoliosis: a case series.

A multicenter retrospective IRB exempt case series analyzing clinical and radiographical data of patients treated by three surgeons over the past two decades was conducted. To examine the factors involved in the development of quadriparesis in patients who underwent posterior spinal fusion for scoliosis. Delayed spinal cord infarcts usually present at the region of instrumentation according to reports from the Scoliosis Research Society. Nonetheless, there is a lack of data regarding factors associated with delayed quadriparesis following posterior spinal fusion METHODS: Evaluated variables were age, Cobb angle, blood loss, and curve correction percentage. Postoperative imaging was also evaluated to determine factors indicative of the etiology of the quadriparesis. Eight patients presented delayed postoperative quadriparesis. All patients had a postoperative examination equal to that of baseline. The first patient deteriorated at 6h postoperatively and the most delayed patient presented 4days postoperatively. Six patients had neuromuscular disorders and 2 had adolescent idiopathic scoliosis. Mean age was 13.7, mean curve magnitude was 78.7°, mean percent curve correction was 71% and the mean estimated blood loss was 1185cc. Seven of eight patients had documented peri- or postoperative hypotension. Cervical infarction is the likely cause of delayed quadriparesis after posterior spinal fusion. Even though the underlying etiology continues to be unclear, postoperative hypotension, curve magnitude, percent curve correction, and the presence of cervical kyphosis/stenosis may be contributory and need to be closely evaluated. IV, Case Series.

Experimental Study on the Role of Apelin-13 in Alleviating Spinal Cord Ischemia Reperfusion Injury Through Suppressing Autophagy.

BackgroundThis study aimed to explore the effect of Apelin-13 in protecting rats against spinal cord ischemia reperfusion injury (SCIR), as well as the related molecular mechanisms.MethodsOne week prior to the experiment, experimental Sprague–Dawley rats were injected with Apelin-13 and the autophagy activator rapamycin through the tail vein once a day for 7 consecutive days. The SCIR rat model was prepared through the abdominal aorta clamping method. At 72 h after injury, the spinal cord tissue water content, infarct volume, and normal neuron count were determined to evaluate the degree of spinal cord tissue injury in the rats. The Basso–Beattie–Bresnahan scoring standard was adopted for functional scoring of the rat hind leg, to reflect the post-injury motor function. At 72 h after injury, changes in mitochondrial membrane potential, reactive oxygen species content, and mitochondrial ATP were detected. ELISA was carried out to detect the malonaldehyde content, as well as catalase, superoxide dismutase, and glutathione catalase activities in spinal cord tissues at 72 h after injury. Quantitative chemistry was conducted to examine the contents of nitric oxide (NO) and endothelial nitric oxide synthase (eNOS) in spinal cord tissues. Finally, the expression of autophagy-related proteins, Beclin1, ATG5, and LC3, in spinal cord tissues was detected through the Western blotting assay.ResultsApelin-13 pretreatment alleviated SCIR, promoted motor function recovery, suppressed mitochondrial dysfunction, resisted oxidative stress, and inhibited autophagy in spinal cord tissues following ischemia reperfusion injury.ConclusionApelin-3 exerts protection against SCIR by suppressing autophagy.