Adjunctive hyperbaric oxygen therapy for spinal cord ischemia after complex aortic repair.

OBJECTIVE: Spinal cord ischemia (SCI) with paraplegia or paraparesis is a devastating complication of complex aortic repair (CAR). Treatment includes cerebrospinal fluid drainage, maintenance of hemoglobin concentration (>10 g/L), and elevating mean arterial blood pressure. Animal and human case series have reported improvements in SCI outcomes with hyperbaric oxygen therapy (HBOT). We reviewed our center's experience with HBOT as a rescue treatment for spinal cord ischemia post-CAR in addition to standard treatment. METHODS: A retrospective review of the University Health Network's Hyperbaric Medicine Unit treatment database identified HBOT sessions for patients with SCI post-CAR between January 2013 and June 2021. Mean estimates of overall motor function scores were determined for postoperative, pre-HBOT, post-HBOT (within 4 hours of the final HBOT session), and at the final assessment (last available in-hospital evaluation) using a linear mixed model. A subgroup analysis compared the mean estimates of overall motor function scores between improvement and non-improvement groups at given timepoints. Improvement of motor function was defined as either a ≥2 point increase in overall muscle function score in patients with paraparesis or an upward change in motor deficit categorization (para/monoplegia, paraparesis, and no deficit). Subgroup analysis was performed by stratifying by improvement or non-improvement of motor function from pre-HBOT to final evaluation. RESULTS: Thirty patients were treated for SCI. Pre-HBOT, the motor deficit categorization was 10 paraplegia, three monoplegia, 16 paraparesis, and one unable to assess. At the final assessment, 14 patients demonstrated variable degrees of motor function improvement; eight patients demonstrated full motor function recovery. Seven of the 10 patients with paraplegia remained paraplegic despite HBOT. The estimated mean of overall muscle function score for pre-HBOT was 16.6 ± 2.9 (95% confidence interval [CI], 10.9-22.3) and for final assessment was 23.4 ± 2.9 (95% CI, 17.7-29.1). The estimated mean difference between pre-HBOT and final assessment overall muscle function score was 6.7 ± 3.1 (95% CI, 0.6-16.1). The estimated mean difference of the overall muscle function score between pre-HBOT and final assessment for the improved group was 16.6 ± 3.5 (95% CI, 7.5-25.7) vs -4.9 ± 4.2 (95% CI, -16.0 to 6.2) for the non-improved group. CONCLUSIONS: HBOT, in addition to standard treatment, may potentially improve recovery in spinal cord function following SCI post-CAR. However, the potential benefits of HBOT are not equally distributed among subgroups.

Perioperative Blood Transfusion Is Associated with Worse 30-Day Mortality and Complications After Thoracic Endovascular Aortic Repair.

BACKGROUND: It is not uncommon for patients requiring vascular surgery, and in particular aortic surgery, to have increased requirements for blood transfusion. However, studies examining the effects of perioperative transfusion for thoracic endovascular aortic repair (TEVAR) are limited. Using large multicenter data, we aimed to study the impact of perioperative blood transfusion on 30-day mortality and complications after TEVAR. METHODS: A total of 9,263 patients who underwent TEVAR were included in this retrospective study from the multicenter Vascular Quality Initiative cohort spanning 2010-2022. We excluded patients who were post-traumatic, anemic (World Health Organization criteria: hemoglobin < 12 g/dl and < 13 g/dl for females and males respectively), who underwent open conversions or presented with ruptured aneurysms. Primary outcomes were 30-day mortality and stroke. Secondary outcomes were postop congestive heart failure (CHF), respiratory complications, spinal cord ischemia (SCI), myocardial infarction (MI) and any postop complications (composite variable). Poisson regression with robust variance was performed to determine the risk of post op outcomes comparing patients who received red blood cells (RBCs) to those who did not. RESULTS: Comparing patients without any transfusion (n = 8,223), perioperative transfusion of 1-3 units (n = 735) was associated with 3-fold increased risk of 30-day mortality (adjusted relative risk [aRR] 3.30, 95% confidence interval [CI] 2.39,4.57, P < 0.001), almost 2-fold increased risk of stroke (aRR 1.98, 95% CI 1.24,3.15, P = 0.004), 2.7-fold increased risk of SCI (aRR 2.66, 95% CI 1.87-3.77, P < 0.001), 3-fold increased risk of MI (aRR 3.40, 95% CI 2.30, 5.03, P < 0.001), 2-fold increased risk of CHF (aRR 2.04, 95% CI 1.09, 3.83, P = 0.03), 3.5-fold increased risk of respiratory complications (aRR 3.49, 95% CI 2.67, 4.56, P < 0.001), and 2-fold increased risk of any postop complication (aRR 2.36, 95% CI 2.04, 2.73, P < 0.001). These effects were even higher in patients transfused 4 or more units (n = 305) than seen in the effects seen in those transfused 1-3 units; comparing each group to patients who received none. CONCLUSIONS: In hemodynamically stable patients undergoing TEVAR for nonemergent/emergent and nontraumatic indications, transfusion of any amount perioperatively is associated with worse 30-day mortality, stroke, SCI, MI, CHF, and respiratory complications. A conservative transfusion approach and multidisciplinary care to identify complications and rescue TEVAR patients who receive any amount of RBCs perioperatively might help improve outcomes. Future studies to understand the mechanisms of outcomes for transfused patients are needed.

Spinal cord infarction after withdrawal of veno-arterial extracorporeal membrane oxygenation for cardiogenic shock: A case report.

BACKGROUND: Spinal cord infarction is a rare central nervous system angiopathy that impairs motor, sensory, and autonomic nerves and occurs due to various reasons. This study reports a case of spinal cord infarction in a patient following myocardial infarction that was managed by veno-arterial extracorporeal membrane oxygenation (VA-ECMO). CASE SUMMARY: A 78-year-old Japanese man visited the emergency department with a complaint of chest tightness. He had a history of hypertension, dyslipidemia, diabetes, chronic renal failure, and postoperative bladder cancer. Myocardial infarction was diagnosed after ST elevation in lead aVR was identified by electrocardiogram during the visit, and cardiopulmonary arrest occurred twice during our examination and treatment. After percutaneous coronary intervention with an intra-aortic balloon pump and VA-ECMO, the patient was admitted to the intensive care unit. His circulation stabilized, and he was withdrawn from the intra-aortic balloon pump on day 3 of illness and from VA-ECMO on day 4. However, his consciousness remained impaired. When the patient's consciousness improved on day 14, lower limb weakness was identified. Magnetic resonance imaging conducted on the following day revealed spinal cord infarction in the 5th to 12th thoracic vertebrae. CONCLUSION: Spinal cord infarction due to VA-ECMO is extremely rare but has a poor neurological prognosis upon onset. Necessary countermeasures include conducting regular neurological examinations and high blood pressure maintenance, which is very difficult in VA-ECMO patients. Therefore, patient care will benefit from the experiences reported in such cases.

TSG-6 released from adipose stem cells-derived small extracellular vesicle protects against spinal cord ischemia reperfusion injury by inhibiting endoplasmic reticulum stress.

BACKGROUND: Spinal cord ischemia reperfusion injury (SCIRI) is a complication of aortic aneurysm repair or spinal cord surgery that is associated with permanent neurological deficits. Mesenchymal stem cell (MSC)-derived small extracellular vesicles (sEVs) have been shown to be potential therapeutic options for improving motor functions after SCIRI. Due to their easy access and multi-directional differentiation potential, adipose-derived stem cells (ADSCs) are preferable for this application. However, the effects of ADSC-derived sEVs (ADSC-sEVs) on SCIRI have not been reported. RESULTS: We found that ADSC-sEVs inhibited SCIRI-induced neuronal apoptosis, degradation of tight junction proteins and suppressed endoplasmic reticulum (ER) stress. However, in the presence of the ER stress inducer, tunicamycin, its anti-apoptotic and blood-spinal cord barrier (BSCB) protective effects were significantly reversed. We found that ADSC-sEVs contain tumor necrosis factor (TNF)-stimulated gene-6 (TSG-6) whose overexpression inhibited ER stress in vivo by modulating the PI3K/AKT pathway. CONCLUSIONS: ADSC-sEVs inhibit neuronal apoptosis and BSCB disruption in SCIRI by transmitting TSG-6, which suppresses ER stress by modulating the PI3K/AKT pathway.

Protective Effect of Mild Hypothermia on Spinal Cord Ischemia-Induced Delayed Paralysis and Spinal Cord Injury.

To explore the mechanism regarding the regulation of spinal cord ischemia (SCI) in rats by mild hypothermia. A SCI rat model was established through aorta occlusion, and in some cases, the rats were intervened with mild hypothermia, after which motor function, microglia activation, and M1/M2 polarization in rats were measured. Also, the expression of inflammatory cytokines (IL-1ß, IL-6 and TNF-α) and neuronal apoptosis were examined. Lipopolysaccharide (LPS)-induced M1 microglia and IL-4-induced M2 microglia were intrathecally injected into rats to evaluate the effect of microglial polarization on SCI. In in vitro experiments, primary microglial cells were treated under hypothermic condition, in which M1/M2 polarization and microglia apoptosis, the levels of iNOS, CD86, CD206, Arg-1 and inflammatory cytokines were assessed. Western blot analysis detected the activation of the TLR4/NF-κB pathway to investigate the role of this pathway in M1/M2 polarization. SCI treatment impaired motor function, induced higher M1 microglia proportion, and increased the levels of pro-inflammatory cytokines in rats, and mild hypothermic treatment attenuated these trends. Moreover, injection of M1 microglia increased M1 microglia proportion and increased the levels of pro-inflammatory cytokines, while injection of M2 microglia induced the reverse results, i.e. decreased M1 microglia proportion and reduced pro-inflammatory cytokine levels. In LPS-induced microglial cells, mild hypothermia treatment increased M2 microglia proportion and decreased pro-inflammatory cytokine levels, relative to normothermia. Mild hypothermia inactivated the TLR4/NF-κB pathway in LPS-treated microglia. TLR4 overexpression reversed the function of mild hypothermia in LPS-stimulated microglia, and under normal condition, TLR4/NF-κB pathway suppressed microglial M2 polarization. Mild hypothermia inhibits TLR4/NF-κB pathway and promotes microglial M2 polarization, thus attenuating SCI-induced injury and inflammation.

Isolated Infarctions of the Conus Medullaris: Clinical Features and Outcomes.

OBJECTIVE: This study aims to describe the clinical features and outcomes of patients with isolated infarctions of the conus medullaris, and to identify factors associated with poor functional outcomes. MATERIALS AND METHODS: We performed a systematic review and retrospective analysis on the clinical characteristics and outcomes of patients with isolated conus medullaris infarctions reported in literature over the past 30 years. RESULTS: We analyzed a total of 19 cases; 18 identified in literature from January 1991 to June 2021, together with our patient. Their median age was 56 years (range 28-79), with twice as many females as males. Pain was prominent at onset (15/19, 79%), only a third had vascular risk factors (7/19, 37%), and half had no significant preceding activities or events (9/19, 47%). Almost all experienced paraplegia or paraparesis (16/19, 84%), in which upper motor neuron features were rare (3/19, 16%). The underlying cause was unknown in half (10/19, 53%). Functional outcomes appeared fair, with nearly half being capable of unassisted ambulation (9/11, 82%). Patients with vascular risk factors (67% vs 13%, p = 0.024) or with identified underlying causes (78% vs 13%, p = 0.007) were less likely to walk unassisted. CONCLUSION: Isolated conus medullaris but should be considered in patients with acute cauda equina syndrome, especially in females. Patients with vascular risk factors, or with known causes of infarction, are less likely to walk unassisted. DWI sequences should be included in conventional MRI sequences when evaluating patients with acute cauda equina syndrome.

The Neuroprotective Mechanism of Spinal Cord Stimulation in Spinal Cord Ischemia/Reperfusion Injury.

BACKGROUND: Spinal cord ischemia/reperfusion (I/R) injury following thoracoabdominal aneurysm surgery can lead to severe lower limb neurologic defect. The preliminary result of our study suggested that spinal cord stimulation (SCS) postconditioning effectively protected spinal cord from I/R injury on rabbits. But the mechanism is unknown. In this study, we further investigated the mechanism of SCS postconditioning. METHOD: New Zealand white rabbits were randomly divided into sham, I/R, I/R + 2 Hz SCS, and I/R + 50 Hz SCS group (n = 24/group). Transient spinal cord ischemia was induced by infrarenal aortic balloon occlusion and performed on all rabbits except rabbits of sham group. Rabbits of I/R group received no further intervention. Rabbits of I/R + 2 Hz SCS and I/R + 50 Hz SCS group received 2 Hz or 50 Hz SCS for 30 min at the onset of reperfusion and then daily. The expression of Akt (serine-threonine kinase)/p-Akt, STAT3 (signal transducer and activator of transcription 3)/p-STAT3 and GSK-3ß (glycogen synthase kinase)/p-GSK-3ß of spinal cord were measured by Western blot analysis at 8 h, 1 day, 3 day, and 7 day of reperfusion. RESULT: The Akt expressions of sham, I/R, I/R + 2 Hz SCS, and I/R + 50 Hz SCS group were not significantly different at all prescribed time points, while the p-Akt expression of I/R + 2 Hz SCS group was significantly higher than that of I/R group and sham group at all prescribed time points; The STAT3 and p-STAT3 expression of I/R, I/R + 2 Hz SCS, and I/R + 50 Hz SCS group were not significantly different at all prescribed time points except that at 1day of reperfusion the p-STAT3 expression of I/R + 50 Hz SCS group was significantly lower than I/R group. The GSK-3ß and p-GSK-3ß expressions of I/R, I/R + 2 Hz SCS and I/R + 50 Hz SCS group were not significantly different at all prescribed time points. CONCLUSION: The neuroprotective effect of 2 Hz SCS postconditioning in spinal cord I/R injury is related to Akt activation but not regulation of STAT3 and GSK-3ß phosphorylation.

Transplantation of viable mitochondria attenuates neurologic injury after spinal cord ischemia.

OBJECTIVES: Spinal cord ischemia (SCI) is one of the major concerns of postoperative paraplegia during major vascular or aortic surgery. Since mitochondrial dysfunction develops at the early stage of SCI, this study tested the neuronal protective effect of transplantation of viable mitochondria to the ischemic cord in rats. METHODS: SCI was induced by crossclamping of thoracic aorta at T6 level for 25 minutes, followed by release of vascular clip to restore aortic blood flow in the anesthetized rats. Mitochondria (100 µg) were isolated from freshly harvested soleus muscle and delivered via the internal jugular vein before releasing of vascular clip. The motor function was assessed independently up to 7 days after reperfusion. Spinal cords were harvested and analyzed for molecular and histological changes. RESULTS: Whole-body in vivo images acquired by an in vivo imaging system confirmed the enhancement of MitoTracker fluorescence at the regions below crossclamping and in the ischemic cord. Compared with control vehicles, transplantation of mitochondria significantly improved the lower-limb locomotor function of rats subjected to cord ischemia up to 7 days after surgery. Mitochondrial transplantation suppressed the regional endoplasmic reticulum stress in the ischemic cord by attenuating CCAAT-enhancer-binding protein homologous protein expression and restoring binding immunoglobulin protein levels. In accordance, tissue levels of interleukin-6, tumor necrosis factor-α, and caspase-3 were attenuated in the mitochondrial transplanted group. Histologic examination also showed significant increase in numbers of Nissls bodies in the neurons at the ventral horn of ischemic cord following mitochondrial transplantation. CONCLUSIONS: Our study showed that transplantation of freshly isolated mitochondria during the early stage of spinal cord ischemia-reperfusion injury suppressed the oxidative stress in endoplasmic reticulum of the injured cord, thereby reducing neuroapoptosis and improving locomotor function of rats with SCI.

Intravenous delivery of mesenchymal stem cells protects both white and gray matter in spinal cord ischemia.

Ischemic spinal cord injury (iSCI) is a devastating complication of aortic surgery, with few strategies for prevention. Intravenous infusion of mesenchymal stem cells (MSCs) for iSCI has been shown to provide functional improvement through protection of gray matter. The purpose of this study was to investigate additional mechanisms which may exert therapeutic efficacy in iSCI. Severe iSCI was created to occlude the descending aorta, which was cross-clamped 5 mm distal to the left subclavian artery for 16 min. One day after iSCI induction, iSCI rats were randomized into two groups: one received intravenous infusion of MSCs (MSC-group), the other received vehicle (no cells; vehicle-group). Locomotor function and in vivo MRI were recorded. H&E, Nissl and toluidine blue stainings, immunohistochemical analysis, diffusion tensor imaging (DTI), and the assessment of blood-spinal cord barrier (BSCB) stability were performed. MSC treated animals exhibited gradual improvement in hind-limb locomotor function during the 4-week study period; however the vehicle-treated group displayed persistent motor deficits. In the MSC-treated group we observed the protection of white and gray matter volume reduction of axonal and neuronal loss or degeneration and preservation of microvasculature including BSCB function. Intravenous infusion of MSCs may provide therapeutic efficacy to improve functional outcomes in a rat model of severe iSCI via protection of white and gray matter.

Quadriplegia and quadriparesis after endovascular aortic procedures: a catastrophic and under-reported complication?

In this study are presented three cases of spinal cord ischemia (SCI) involving the cervical-dorsal level and leading to quadriplegia and quadriparesis, following thoraco-abdominal aortic aneurysm (TAAA) endovascular repair. A 79-year-old woman with an extent III TAAA was scheduled for a multi-step fenestrated/branched endovascular aortic repair. Immediately after the first step, consisting of standard proximal thoracic stent-graft implantation, she developed quadriplegia that did not resolve despite all therapeutic actions, and died therefore on postoperative day 32. A 72-year old male with an extent IV TAAA underwent endovascular repair, using a customized fenestrated aortic stent-graft. Five hours after the procedure, he developed an asymmetric quadriparesis, that progressively resolved after spinal fluid drainage and arterial pressure increase, even if signs of SCI were documented at magnetic resonance imaging (MRI). A 79-year old man, referred for a type II TAAA with rapid enlargement, underwent a one-stage endovascular repair, using a customized branched aortic stent-graft. As soon as the procedure was completed, the patient presented inferior limbs paralysis and upper limbs paresis. Although no signs of SCI were documented at MRI, the patient did not recover and died therefore three months after the procedure. Although rare, cervical-dorsal SCI may develop during TAAA endovascular aortic repair. This possibly catastrophic event should be considered in the decisional process of TAAA repair and considered to allow prompt recognition and treatment.

Hypogastric Artery Stenting for Chronic Intermittent Spinal Cord Ischemia After Thoracic Endovascular Aortic Repair.

PURPOSE: To report a case of chronic intermittent spinal cord ischemia (SCI) after thoracic endovascular aortic repair (TEVAR) and its successful treatment using hypogastric artery stenting. CASE REPORT: A 79-year-old patient presented in May 2013 with a thoracic aortic aneurysm (TAA) and a contained rupture. He urgently underwent TEVAR that covered 274 mm of descending thoracic aorta without immediate postoperative signs of acute SCI. At 3-month follow-up, he reported repeating incidents of sudden lower extremity weakness leading to a fall with a humerus fracture. A neurological consultation revealed the tentative diagnosis of intermittent SCI caused by TEVAR and initially recommended a conservative approach. During the following year there was no clinical improvement of the symptoms. Computed tomography angiography showed a high-grade stenosis of the right hypogastric artery, which was stented in November 2014 to improve the collateral network of spinal cord perfusion. Following treatment, the patient had no further neurological symptoms; at 32 months after the reintervention, the imaging follow-up documented a patent stent and continued exclusion of the TAA. CONCLUSION: Intermittent neurological symptoms after TEVAR should be suspected as chronic intermittent SCI. The improvement of collateral networks of the spinal cord by revascularization of the hypogastric artery is a viable treatment option.

Spinal Cord Ischemia Rescue after Hybrid Total Arch Repair with Frozen Elephant Trunk: A Case Report.

Frozen elephant trunk repair is a technique described to simplify total arch repair for Stanford type A aortic dissection. Spinal cord ischemia is a devastating complication after frozen elephant trunk repair. In this report, we describe a case of spinal cord ischemia resulting in paralysis after frozen elephant trunk repair. Our spinal cord ischemia protocol was implemented and rescued patients from paraplegia. We report a dedicated spinal cord ischemia protocol that can rescue patients from paraplegia after hybrid arch repair with frozen elephant trunk.

Incidence, predictors, and outcomes of spinal cord ischemia in elective complex endovascular aortic repair: An analysis of health insurance claims.

OBJECTIVE: This study aimed to determine predictors and outcomes associated with spinal cord ischemia (SCI) after elective fenestrated or branched endovascular aneurysm repair (F/BEVAR) of thoracoabdominal aortic aneurysm (TAAA), abdominal aortic aneurysm (AAA), or aortic dissection. METHODS: Health insurance claims data of Germany's third largest insurance provider, DAK-Gesundheit, were used to investigate SCI in elective F/BEVAR performed between 2008 and 2017. The International Classification of Diseases and German Operation and Procedure Classification System were used. We stratified the results into F/BEVAR with one or two (AAA) vs three or more (TAAA) fenestrations or branches. RESULTS: A total of 877 patients (18.9% female; 5.8% with SCI) matching the inclusion criteria were identified during the study period. SCI occurred more often after F/BEVAR of TAAA vs AAA (10.7% vs 3.0%; P < .001). SCI was associated with female sex in the AAA group (odds ratio, 3.87; 95% confidence interval [CI], 1.25-11.15; P = .014) and with cardiac arrhythmias in the TAAA group (odds ratio, 2.98; 95% CI, 1.24-7.06; P = .013). Compared with patients without SCI, SCI patients were more likely to suffer from drug use disorders (eg, opioids, cannabinoids, sedatives) in the TAAA group (17.6% vs 2.1%; P < .05). After F/BEVAR of TAAA, the occurrence of SCI was associated with higher 90-day mortality (14.7% vs 1.1%; P < .05), longer postoperative hospital stay (22 vs 9 days; P < .05), and severe adverse events, such as acute respiratory insufficiency (44.1% vs 12.7%), acute renal failure (35.3% vs 11.3%), and pneumonia (29.4% vs 4.9%; all P < .05). In adjusted analyses, SCI was associated with worse long-term survival after F/BEVAR for TAAA (hazard ratio, 2.54; 95% CI, 1.37-4.73; P < .003). CONCLUSIONS: Female AAA patients and TAAA patients with cardiac arrhythmias are at highest risk for development of SCI after F/BEVAR. The occurrence of this event was strongly associated with higher major complication rates and worse short-term and long-term survival. This emphasizes a need to further illuminate the value of spinal cord protection protocols in F/BEVAR.

Protective Effect of Contralateral, Ipsilateral, and Bilateral Remote Ischemic Preconditioning on Spinal Cord Ischemia Reperfusion Injury in Rats.

AIM: To evaluate the effect of different remote ischemic preconditioning (RIPC) methods in spinal cord ischemia-reperfusion (IR) injury. MATERIAL AND METHODS: A total of 36 rats were distributed to the 6 groups: sham surgery, control (only spinal cord IR), unilateral (hind limb RIPC before spinal cord IR), bilateral (hind limbs RIPC before spinal cord IR), ipsilateral (hind and fore limbs RIPC to the right before spinal cord IR), contralateral (right hind limb and left fore limb as RIPC before spinal cord IR). Thirty minutes after RIPC, the spinal cord was subjected to ischemia for 60 minutes. Seventy two hours after IR, all rats were evaluated by neurological function, histological and biochemical examinations. RESULTS: The mean Motor Deficit Index (MDI) scores in the ipsilateral, contralateral, and bilateral groups were lower than that of the unilateral group (p < 0.05). The mean malondialdehyde (MDA) in ipsilateral group was lower than were control group (p < 0.05). The mean total antioxidant capacity (TAC) and the mean number of normal motor neurons in the experimental groups were significantly higher than increased control group (p < 0.05). The mean plasma levels of catalase in the contralateral, ipsilateral, and bilateral groups were significantly increased compared to control group (p < 0.05). The mean scores of white matter damage in contralateral, bilateral, and unilateral groups were lower than control group (p < 0.05). CONCLUSION: The results of this study show that contralateral, ipsilateral, and bilateral limb RIPC may reduce the complications of spinal cord ischemic injury.

The etiologies and prognosis associated with spinal cord infarction.

BACKGROUND: This study aims to investigate the etiology and prognosis of spinal cord infarction (SCI). METHODS: Over a period of 16 years, we retrospectively analyzed 31 patients with SCI. Demographic features and symptom presentations were carefully documented. Etiology-specific MRI features, such as the length and distribution of the lesions and owl's eyes sign, were recorded and analyzed to determine their associations with the clinical signs/symptoms. RESULTS: In total, seven patients had aortic or vertebral artery dissections. We divided the patients with SCI into two groups: those with or without vessel dissection. Among SCI patients, the onset age was younger, and the proportion of patients with long-segment lesions and posterior pattern involvement on axial view was higher in the group with dissection than in the group without dissection (all P < 0.05). The lesions were frequently located in the upper cervical or lower thoracic-lumbar regions, and the lengths of the lesions were associated with 1-month outcomes, suggesting that artery dissection may contribute to the longitudinal and posterior extension of SCI. In contrast, among patients without dissection, the range of longitudinal extensions of in spans of vertebral bodies was broader (range, 1-8). A higher proportion of patients had focal pain adjacent to the lesion (P = 0.05) and a poorer 1-month outcome (P = 0.04) in the long-segment lesion group than in the short-segment lesion group. CONCLUSIONS: A detailed history and the use of modern imaging tools may help clinicians search for vessel dissection and other etiologies, evaluate the spatial extension of lesions in SCI, and predict prognosis.

Successful reversal of isolated delayed spinal cord ischemia following endovascular abdominal aneurysm repair.

A 74-year-old patient presented with isolated fecal incontinence 6 weeks following endovascular aneurysm repair. The delayed presentation of spinal cord ischemia was precipitated by commencement of alpha-blockers for benign prostatic hyperplasia. This case stresses that vulnerability to spinal cord perfusion is not limited to the perioperative period. In addition, systemic arterial pressure should be closely monitored in cases of marginal vascular insufficiency of the spinal cord.

Spinal Cord Infarction due to Fibrocartilaginous Embolism: A Report of 3 Cases.

Fibrocartilaginous embolism (FCE) is an uncommon cause of spinal cord infarction often misdiagnosed as transverse myelitis. The mechanism of ischemia is suspected to be due to retrograde embolization of nucleus pulposus material originating from Schmorl's nodes to the spinal vessels following acute disk herniation. We describe the clinical and imaging findings of FCE in 3 healthy young women with history of trivial spinal cord trauma, and recommend that FCE should be considered in the differential diagnosis of acute myelopathy.

Abdominal Aortic Transplantation of Bone Marrow Mesenchymal Stem Cells Regulates the Expression of Ciliary Neurotrophic Factor and Inflammatory Cytokines in a Rat Model of Spinal Cord Ischemia-Reperfusion Injury.

BACKGROUND This study aimed to investigate the effects of abdominal aortic transplantation of bone marrow mesenchymal stem cells (BMMSCs) on the expression of inflammatory cytokines in a rat model of spinal cord ischemia-reperfusion injury. MATERIAL AND METHODS Adult female Sprague-Dawley rats (N=160) were divided into five groups: the sham operation group (N-32); the control group (N=32); the BMMSC transplanted group (N=32); the anti-ciliary neurotrophic factor (CNTF)-treated BMMSC transplanted group (N=32); and the CNTF small interfering RNA (siRNA)-treated BMMSC transplanted group (N=32). Motor behavior was assessed using the Basso, Beattie, and Bresnahan (BBB) locomotor scale. Motor evoked potentials (MEPs) and cortical somatosensory evoked potentials (CSEPs) were measured. Immunohistochemistry, quantitative real-time polymerase chain reaction (qRT-PCR), and Western blot analysis evaluated the expression of spinal inflammatory cytokines. RESULTS Following surgery, compared with the control group the findings in the BMMSC transplant groups included significantly increased BBB scores; the latency and the amplitude of MEP and CSEP were reduced and increased, respectively; spinal neuronal necrosis was reduced; the number of normal neurons increased; CNTF mRNA and protein expression levels increased; expression levels of interleukin-6 (IL-6) were reduced and IL-10 levels were significantly increased (P<0.05). The effects of abdominal aortic BMMSC transplantation were at least partially reversed by both anti-CNTF and CNTF siRNA treatment. CONCLUSIONS In a rat model of spinal cord ischemia-reperfusion injury, abdominal aortic transplantation of BMMSCs increased the expression of CNTF, which improved hindlimb locomotor recovery by regulating the expression of IL-6 and IL-10 to reduce inflammation of the spinal cord.

Spinal Cord Ischemia after Endovascular Aortic Repair of a Unilateral Iliac Artery Dissecting Aneurysm: A Case Report.

PURPOSE: Spinal cord ischemia (SCI) is a rare complication of endovascular repair of abdominal aortic aneurysm that is attributed to the variable anatomy of the artery of Adamkiewicz, embolization of the collateral circulation, or hypoperfusion of cord structures secondary to hypotension. CASE REPORT: A hypertensive 83-year-old male with chronic obstructive pulmonary disease presented with a 2.3-cm right iliac artery dissecting aneurysm. Paraplegia occurred on the first day after endovascular repair of iliac artery aneurysm. Postoperative magnetic resonance imaging showed multiple foci of spinal cord ischemia involvement from T10 to L1. Neither arterial pressure augmentation nor steroid therapy was effective. We hypothesized that the compromised blood flow from the artery of Adamkiewicz, combined with the transient hypotension and embolism, resulted in spinal cord infarction. The patient was eventually transferred to a nursing facility, with no improvement in his neurological status. CONCLUSIONS: SCI after endovascular aortic repair is an extremely rare and unpredictable complication. Physicians should pay more attention to the patients with comorbidities of atherosclerosis, chronic obstructive pulmonary disease, or peripheral artery occlusive disease.