Spinal cord ischemia revealed by a Brown-Sequard syndrome and caused by a calcified thoracic disc extrusion with spontaneous regression: a case report and review of the literature.

BACKGROUND: Thoracic disc herniation is relatively uncommon, accounting for less than 1% of all spinal herniations. Although most often asymptomatic, they may represent a rare cause of spinal cord ischemia. CASE REPORT: We report the case of a healthy 43-year-old North African male who presented with a Brown-Sequard syndrome revealing a spinal cord ischemia caused by a thoracic disc extrusion. The initial MRI revealed a calcified disc extrusion at the level of T5-T6 without significant spinal cord compression or signal abnormality. A pattern consistent with a medullary ischemia only appeared 48 h later. The patient was treated conservatively with Aspirin and Heparin, which were discontinued later because of a negative cardiovascular work-up. The calcified disc extrusion, which was later recognized as the cause of the ischemia, decreased spontaneously over time and the patient recovered within a few months. CONCLUSIONS: Our case highlights the challenge in diagnosing and managing this uncommon condition. We propose a literature review showing the different therapeutic strategies and their corresponding clinical outcomes.

Tube cystostomy is effective for urinary outflow management in dogs with intervertebral disk extrusion and ischemic myelopathy cranial to the L3 spinal cord segment: 61 dogs (2018-2022).

OBJECTIVE: To describe the application and owner experience of tube cystostomy for management of upper motor neuron urinary bladder dysfunction secondary to intervertebral disk extrusion (IVDE) or ischemic myelopathy, and to report complications associated with cystostomy tube management. ANIMALS: 61 dogs. CLINICAL PRESENTATION: Medical records of dogs with IVDE or ischemic myelopathy cranial to the L3 spinal cord segment that underwent tube cystostomy placement via a short, caudal ventral midline celiotomy were reviewed. Days from tube placement to hospital discharge, days from placement to tube removal, and complications were recorded. An owner questionnaire was distributed to ascertain ease of use and perceived time commitment. RESULTS: 58 dogs were diagnosed with IVDE, and 3 dogs were diagnosed with ischemic myelopathy. The modal neurologic grade at cystostomy tube placement was 4 (range, 3 to 5). The median number of days from cystostomy tube placement to hospital discharge was 1 (range, 0 to 3). Follow-up data was available for 56 dogs. The median number of days from cystostomy tube placement until removal was 19 (range, 3 to 74). Fifteen minor and 6 severe postoperative complications were reported, mainly inadvertent removal (n = 11) and peristomal urine leakage (6). Twenty-seven owners responded to the questionnaire and primarily reported that cystostomy tube use was easy (22/27) and perceived time commitment was low or minimal (20/27). CLINICAL RELEVANCE: Tube cystostomy facilitates early hospital discharge and allows at-home, extended urinary management in dogs recovering from upper motor neuron urinary bladder dysfunction secondary to IVDE or ischemic myelopathy. This technique is simple for owners to use.

Git1-PGK1 interaction achieves self-protection against spinal cord ischemia-reperfusion injury by modulating Keap1/Nrf2 signaling.

Spinal cord ischemia-reperfusion (IR) injury (SCIRI) is a significant secondary injury that causes damage to spinal cord neurons, leading to the impairment of spinal cord sensory and motor functions. Excessive reactive oxygen species (ROS) production is considered one critical mechanism of neuron damage in SCIRI. Nonetheless, the molecular mechanisms underlying the resistance of neurons to ROS remain elusive. Our study revealed that the deletion of Git1 in mice led to poor recovery of spinal cord motor function after SCIRI. Furthermore, we discovered that Git1 has a beneficial effect on neuron resistance to ROS production. Mechanistically, Git1 interacted with PGK1, regulated PGK1 phosphorylation at S203, and affected the intermediate products of glycolysis in neurons. The influence of Git1 on glycolysis regulates the dimerization of Keap1, which leads to changes in Nrf2 ubiquitination and plays a role in resisting ROS. Collectively, we show that Git1 regulates the Keap1/Nrf2 axis to resist ROS in a PGK1-dependent manner and thus is a potential therapeutic target for SCIRI.

Intranasal administration of polysulfide prevents neurodegeneration in spinal cord and rescues mice from delayed paraplegia after spinal cord ischemia.

BACKGROUND: Delayed paraplegia is a devastating complication of thoracoabdominal aortic surgery. Hydrogen sulfide (H2S) was reported to be protective in a mouse model of spinal cord ischemia and the beneficial effect of H2S has been attributed to polysulfides. The objective of this study was to investigate the effects of polysulfides on delayed paraplegia after spinal cord ischemia. METHODS AND RESULTS: Spinal cord ischemia was induced in male and female C57BL/6J mice by clamping the aortic arch and the left subclavian artery. Glutathione trisulfide (GSSSG), glutathione (GSH), glutathione disulfide (GSSG), or vehicle alone was administered intranasally at 0, 8, 23, and 32 h after surgery. All mice treated with vehicle alone developed paraplegia within 48 h after surgery. GSSSG, but not GSH or GSSG, prevented paraplegia in 8 of 11 male mice (73%) and 6 of 8 female mice (75%). Intranasal administration of 34S-labeled GSSSG rapidly increased 34S-labeled sulfane sulfur species in the lumbar spinal cord. In mice treated with intranasal GSSSG, there were increased sulfane sulfur levels, and decreased neurodegeneration, microglia activation, and caspase-3 activation in the lumbar spinal cord. In vitro studies using murine primary cortical neurons showed that GSSSG increased intracellular levels of sulfane sulfur. GSSSG, but not GSH or GSSG, dose-dependently improved cell viability after oxygen and glucose deprivation/reoxygenation (OGD/R). Pantethine trisulfide (PTN-SSS) also increased intracellular sulfane sulfur and improved cell viability after OGD/R. Intranasal administration of PTN-SSS, but not pantethine, prevented paraplegia in 6 of 9 male mice (66%). CONCLUSIONS: Intranasal administration of polysulfides rescued mice from delayed paraplegia after transient spinal cord ischemia. The neuroprotective effects of GSSSG were associated with increased levels of polysulfides and sulfane sulfur in the lumbar spinal cord. Targeted delivery of sulfane sulfur by polysulfides may prove to be a novel approach to the treatment of neurodegenerative diseases.

Spinal cord ischemia as intraoperatory complication in shoulder surgery positioned in beach chair: case report.

Spinal cord infarction is an uncommon phenomenon, which can be caused by different etiologies, constituting a real diagnostic challenge which can lead to devastating consequences. General anesthesia in beach chair positioning with intraoperative hypotension in order to avoid surgical bleeding are associated with hypoperfusion and potential neurological ischemia-related complications. We present a case of spinal cord ischemia in the context of shoulder surgery in a beach chair position.

Spinal cord ischemia as intraoperatory complication in shoulder surgery positioned in beach chair: case report

Abstract Spinal cord infarction is an uncommon phenomenon, which can be caused by different etiologies, constituting a real diagnostic challenge which can lead to devastating consequences. General anesthesia in beach chair positioning with intraoperative hypotension in order to avoid surgical bleeding are associated with hypoperfusion and potential neurological ischemia-related complications. We present a case of spinal cord ischemia in the context of shoulder surgery in a beach chair position.

Long-segment spinal cord infarction complicated with multiple cerebral infarctions: a case report.

BACKGROUND: Spinal cord infarction is a rare disorder, constituting only 1% to 2% of all neurological vascular emergencies (making it less frequent than ischaemic brain injury); however, it is severe. A case of long-segment spinal cord infarction complicated with multiple cerebral infarctions has not been reported to date. CASE PRESENTATION: Here, we describe one such case: a patient with spinal cord infarction from the cervical 7 (C7) to thoracic 6 (T6) vertebrae, along with anterior spinal artery syndrome and complicated by multiple cerebral infarctions. A 65-year-old farmer experienced sudden onset of severe pain in his chest, back and upper limbs while unloading heavy objects. Subsequently, both his lower limbs became weak and hypoaesthetic, and he was unable to walk. Spinal magnetic resonance imaging (MRI) revealed equal T1 and long T2 signals centred on the anterior horn of the spinal cord. The axial slice of these signals was shaped like an owl's eye. After receiving drug treatment and active rehabilitation treatment, the patient's ability to walk was restored. CONCLUSIONS: Long-segment spinal cord infarction is rare and can be complicated with cerebral infarction. The specific aetiology is worth exploring.

[Xenon post-conditioning protects against spinal cord ischemia-reperfusion injury in rats by downregulating mTOR pathway and inhibiting endoplasmic reticulum stress-induced neuronal apoptosis].

OBJECTIVE: The purpose of this study was to determine whether xenon post-conditioning affects mTOR signaling as well as endoplasmic reticulum stress (ERS)-apoptosis pathway in rats with spinal cord ischemia/reperfusion injury. METHODS: Fifty male rats were randomized equally into sham-operated group (Sham group), I/R model group (I/R group), I/R model+ xenon post-conditioning group (Xe group), I/R model+rapamycin (a mTOR signaling pathway inhibitor) treatment group (I/R+ Rapa group), and I/R model + xenon post- conditioning with rapamycin treatment group (Xe + Rapa group).. In the latter 4 groups, SCIRI was induced by clamping the abdominal aorta for 85 min followed by reperfusion for 4 h. Rapamycin (or vehicle) was administered by daily intraperitoneal injection (4 mg/kg) for 3 days before SCIRI, and xenon post-conditioning by inhalation of 1∶1 mixture of xenon and oxygen for 1 h at 1 h after initiation of reperfusion; the rats without xenon post-conditioning were given inhalation of nitrogen and oxygen (1∶ 1). After the reperfusion, motor function and histopathologic changes in the rats were examined. Western blotting and real-time PCR were used to detect the protein and mRNA expressions of GRP78, ATF6, IRE1α, PERK, mTOR, p-mTOR, Bax, Bcl-2 and caspase-3 in the spinal cord. RESULTS: The rats showed significantly lowered hind limb motor function following SCIRI (P < 0.01) with a decreased count of normal neurons, increased mRNA and protein expressions of GRP78, ATF6, IRE1α, PERK, and caspase-3, and elevated p-mTOR/mTOR ratio and Bax/Bcl-2 ratio (P < 0.01). Xenon post-conditioning significantly decreased the mRNA and protein levels of GRP78, ATF6, IRE1α, PERK and caspase-3 (P < 0.05 or 0.01) and reduced p-mTOR/mTOR and Bax/Bcl-2 ratios (P < 0.01) in rats with SCIRI; the mRNA contents and protein levels of GRP78 and ATF6 were significantly decreased in I/R+Rapa group (P < 0.01). Compared with those in Xe group, the rats in I/R+Rapa group and Xe+Rapa had significantly lowered BBB and Tarlov scores of the hind legs (P < 0.01), and caspase-3 protein level and Bax/Bcl-2 ratio were significantly lowered in Xe+Rapa group (P < 0.05 or 0.01). CONCLUSION: By inhibiting ERS and neuronal apoptosis, xenon post- conditioning may have protective effects against SCIRI in rats. The mTOR signaling pathway is partially involved in this process.

Evaluating the risk of spinal cord ischemia in zone 2 frozen elephant trunk replacement.

BACKGROUND: The appropriate stent length in frozen elephant trunk replacements (FET) remains debated relative to the risk for paraplegia. However, landing the distal end of the stent beyond the curve of the arch facilitates distal reintervention, which is commonly beyond the 10 cm stent coverage when deployed proximal to the left subclavian artery. The aim of this study was to evaluate outcomes following the use of 15 cm stent grafts in zone 2 (z2, distal to the left common carotid). METHODS: Using our single institution-maintained database, 103 zone 2 FET performed from 2016 to 2020 were reviewed. RESULTS: Of the 103 z2, a 15 cm stent graft was used in 51 operations. The indications for FET included acute and chronic aortic dissection, arch aneurysms, and pseudoaneurysms. The incidence of SCI was 0%. Seven deaths (13.7%) occurred. CONCLUSIONS: The data demonstrates the incidence of post-operative paraplegia to be 0% with 15 cm z2 FET. The understanding of SCI in FET should not only include the stent length but also from where it begins.

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.

Spinal cord ischaemia following the gluteal injection of Benzathine benzylpenicillin.

INTRODUCTION: Spinal cord injury is a devastating complication, though rare but possible following the intramuscular injection of the Penicillin. The spinal cord injury can be permanent, leaving the patient with paralysis, bowel and bladder incontinence, and with other associated morbidities. CASE PRESENTATION: We report a 25-year-old gentleman who developed anterior spinal cord syndrome following the benzathine benzylpenicillin injection. In this case report, we discuss the clinical details, possible hypothesis behind spinal cord ischaemia and literature review. DISCUSSION: Spinal cord ischaemia or infarction occurs due to embolism of the Penicillin products. The products following injection are carried as emboli retrogradely through the superior gluteal artery and can cause infarction to the cord's anterior part.

Is Surfer's myelopathy an acute hyperextension-induced myelopathy? A systematic synthesis of case studies and proposed diagnostic criteria.

BACKGROUND: Surfer's myelopathy is a rare complication of spinal hyperextension originally described in novice surfers. However, reports from patients practicing different activities had risen. AIM: To systematically synthesize the epidemiological and clinical evidence on acute hyperextension-induced myelopathy ("Surfer's myelopathy") and propose new diagnostic criteria. METHODS: We systematically searched four databases for all observational and case studies on the topic. We performed a narrative synthesis to propose diagnostic criteria and tested the criteria retrospectively on the included cases. A case report is also presented. RESULTS: Forty-two articles reporting 104 cases (median age 19 years, slightly male predominance) were included. All cases reported a nontraumatic hyperextension event (58% after surfing). All of the cases presented pain of hyperacute onset. The most frequent clinical feature was bladder or bowel dysfunction (84%). The thoracic region was the most frequently affected (87%) with longitudinal involvement until the conus (67%). At discharge or follow-up, 52% partially recovered. We propose five diagnostic criteria with three levels of certainty (definite, probable, and possible): (1) nontraumatic spine hyperextension activity (in individuals with no pre-existent spinal disease); (2) hyperacute onset (with acute pain onset); (3) spinal cord injury clinic (motor, sensory, or autonomic deficit); (4) MRI findings with central spinal cord abnormalities (multiple segments); and (5) no other alternative diagnosis. We identified 88% definite and 12% probable/possible cases. CONCLUSION: The acute hyperextension-induced myelopathy could occur not only during surfing but also during other activities. Therefore, increased awareness and education among sports communities and general physicians are needed.

Stress-induced phosphoprotein 1 restrains spinal cord ischaemia-reperfusion injury by modulating NF-κB signalling.

Spinal cord injury (SCI), a major cause of disability, causes high global disease and economic burdens. Stress-induced phosphoprotein 1 (STIP1) has been identified to be involved in spinal cord ischaemia-reperfusion injury (SCII); however, the effect of STIP1 on SCII remains unclear until now. This study aimed to examine the role of STIP1 in SCII and unravel the possible mechanisms. Western blotting and immunohistochemical staining showed that STIP1 expression rapidly increased and then decreased in rat spinal cord following SCII treatment. Neurological function scoring, HE staining, immunohistochemical staining and Western blotting revealed that STIP1 overexpression alleviated SCII-induced motor dysfunction of hind limbs, neuronal loss and inflammation in spinal cord, and inhibited activity of nuclear factor kappa B (NF-κB) signalling in rats. Immunoprecipitation identified that STIP1 was co-located with Iba-1. In addition, STIP1 was found to ameliorate oxygen and glucose deprivation (OGD)-induced inflammation and activation of NF-κB signalling in mouse microglia BV2 cells, and STIP1 resulted in decrease of heat shock protein family A member 8 (HSPA8), increase of IκBß expression and reduced binding of IκBß to HSPA8 in BV2 cells. The results of the present study demonstrate that STIP1 alleviates ischaemia/reperfusion-induced neuronal injury and inflammation in rat spinal cord and mouse microglial cells by deactivating NF-κB signalling. These findings may provide novel insights for the clinical diagnosis and treatment of SCI.

Astragalin Protects against Spinal Cord Ischemia Reperfusion Injury through Attenuating Oxidative Stress-Induced Necroptosis.

Spinal cord ischemia/reperfusion (SCI/R) injury is a devastating complication usually occurring after thoracoabdominal aortic surgery. However, it remains unsatisfactory for its intervention by using pharmacological strategies. Oxidative stress is a main pharmacological process involved in SCI/R, which will elicit downstream programmed cell death such as the novel defined necroptosis. Astragalin is a bioactive natural flavonoid with a wide spectrum of pharmacological activities. Herein, we firstly evaluated the effect of astragalin to oxidative stress as well as the possible downstream necroptosis after SCI/R in mice. Our results demonstrated that astragalin improves the ethological score and histopathological deterioration of SCI/R mice. Astragalin mitigates oxidative stress and ameliorates inflammation after SCI/R. Astragalin blocks necroptosis induced by SCI/R. That is, the amelioration of astragalin to the motoneuron injury and histopathological changes. Indicators of oxidative stress, inflammation, and necroptosis after SCI/R were significantly blocked. Summarily, we firstly illustrated the protection of astragalin against SCI/R through its blockage to the necroptosis at downstream of oxidative stress.

Tat-p27 Ameliorates Neuronal Damage Reducing α-Synuclein and Inflammatory Responses in Motor Neurons After Spinal Cord Ischemia.

p27Kip1 (p27) regulates the cell cycle by inhibiting G1 progression in cells. Several studies have shown conflicting results on the effects of p27 against cell death in various insults. In the present study, we examined the neuroprotective effects of p27 against H2O2-induced oxidative stress in NSC34 cells and against spinal cord ischemia-induced neuronal damage in rabbits. To promote delivery into NSC34 cells and motor neurons in the spinal cord, Tat-p27 fusion protein and its control protein (Control-p27) were synthesized with or without Tat peptide, respectively. Tat-p27, but not Control-27, was efficiently introduced into NSC34 cells in a concentration- and time-dependent manner, and the protein was detected in the cytoplasm. Tat-p27 showed neuroprotective effects against oxidative stress induced by H2O2 treatment and reduced the formation of reactive oxygen species, DNA fragmentation, and lipid peroxidation in NSC34 cells. Tat-p27, but not Control-p27, ameliorated ischemia-induced neurological deficits and cell damage in the rabbit spinal cord. In addition, Tat-p27 treatment reduced the expression of α-synuclein, activation of microglia, and release of pro-inflammatory cytokines such as interleukin-1ß and tumor necrosis factor-α in the spinal cord. Taken together, these results suggest that Tat-p27 inhibits neuronal damage by decreasing oxidative stress, α-synuclein expression, and inflammatory responses after ischemia.

The Potential Causes of Paraplegia after Coronary Artery Bypass Grafting: A Literature Review.

Paraplegia is an unpredictable neurologic complication after coronary artery bypass grafting (CABG) surgery. It is rare but fatal, and the mechanism still is unclear. We aimed to make a summary of the possible causes of paraplegia after CABG. Pubmed database was searched from January 1, 1978 to December 31, 2019, and 14 studies were finally included. Paraplegia after CABG is a multifactorial consequence, but spinal cord ischemia is the key pathological factor to postoperative paraplegia.

[A case of spinal cord infarction accompanied with neuromyelitis optica spectrum pathophysiology].

We report a 60-year-old woman who developed spinal cord infarction (SCI) with anti-aquaporin (AQP) 4 antibody seropositive. She was admitted to our hospital with acute onset of flaccid paraparesis and urinary disturbances that completed within a few minutes after acute pain in her lower back. Neurological examination revealed flaccid paraparesis, bladder and bowel dysfunction and dissociated sensory loss below the level of Th11 spinal cord segment. Diffusion weighted imaging (DWI) and T2-wighted imaging (T2WI) of thoracic spine MRI showed high signal intensity in the spinal cord between Th9 and Th12 vertebral levels with decreased apparent diffusion coefficient (ADC). We diagnosed her as having SCI. Thereafter the serum examination on admission was reported as positive for anti-aquaporin 4 (AQP4) antibody. Cerebrospinal fluid (CSF) analysis revealed pleocytosis, and the spinal cord lesions became enlarged in MRI on 12 days after the onset. We, therefore, suspected that the pathophysiology of neuromyelitis optica spectrum disorder (NMOSD) accompanied SCI. The patient underwent two courses of high dose intravenous methylprednisolone (IVMP) for three days (1 g/day). Her neurological symptoms did not improve significantly, but the size of T2WI MRI high signal lesion improved to that of the initial MRI scan. Anti-AQP4 antibody seropositivity may have modified the SCI pathology in the present patient.

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

INTRODUCTION: 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. CASE PRESENTATION: 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. DISCUSSION: 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.

Conus Medullaris Infarction Involving the Paraspinal Muscles and Nerve Roots.

Spinal cord infarctions account for less than 1% of all strokes. The segmental artery supplies the spinal cord, vertebrae, nerve roots, and paraspinal muscles. To our knowledge, this is the first case of spinal cord infarction involving multiple distinct infarcts at various sites, including the lumbar vertebrae, conus medullaris, dorsal thoracolumbar spinal cord, paraspinal muscles, and nerve roots.

Clinical, neuroimaging, and nerve conduction characteristics of spontaneous Conus Medullaris infarction.

BACKGROUND: Spontaneous conus medullaris infarction is a rare disease. We describe two patients with spontaneous conus medullaris infarction presenting as acute cauda equina syndrome and their unique electromyography (EMG) findings. CASE PRESENTATION: Two patients developed acute low back pain with mild asymmetric paraparesis, loss of perianal sensation and sphincter dysfunction. Ankle deep tendon reflexes were reduced in bilaterally. Neither patient had cardiovascular risk factors. Magnetic Resonance imaging showed infarction in the conus medullaris. Functional recovery was good in both patients, but progressive asymmetric calf wasting and sphincter dysfunction remained. EMG studies at follow-up of at least 3 years demonstrate active denervation at the muscles innervated by the first sacrum anterior horn cells. CONCLUSION: Spontaneous conus medullaris infarction can occur in healthy individuals and presents as cauda equina syndrome. Findings of needle EMG studies indicate a progressive course of sacrum anterior horn cell disorder during long-term follow-up.