Unilateral Anterior Spinal Artery Syndrome following Spinal Anesthesia for Cesarian Section: A Case Report.

Introduction: Spinal cord infarction is a rare but serious neurologic complication of spinal anesthesia. Direct vessel injury, intra-arterial anesthetic injection, and anesthetic-induced local hypotension are potential mechanisms of infarction during this procedure. The proximity of the artery of Adamkiewicz to the spinal levels used for spinal anesthesia may also play a role. This case of unilateral anterior spinal artery syndrome highlights the potential for an atypical pattern of injury and deficits due to the complexity of the spinal cord's anterior circulation. Case Presentation: We present a 38-year-old female patient who presented with left lower extremity weakness, loss of temperature sensation, and urinary retention following spinal anesthesia for cesarian section. Magnetic resonance imaging of the spine demonstrated T2 hyperintensities in the left central spinal cord from T8 to the conus medullaris. A diagnosis of spinal cord infarction was made after lumbar puncture testing showed no evidence of inflammatory myelitis. The patient was treated with steroids empirically until lumbar puncture testing showed no inflammation. The patient was discharged on daily aspirin with persistent left lower extremity weakness and loss of temperature sensation. A plan for outpatient physical therapy was made for rehabilitation. Conclusion: Awareness of the potential for spinal cord infarction secondary to spinal anesthesia must increase among anesthesiologists, obstetricians, and neurologists. The risk of systemic hypotension during and after spinal anesthesia is important to recognize for both primary and secondary prevention of this complication. The hyperacute onset of myelopathic symptoms should point neurologists to investigate an ischemic etiology in the proper clinical context.

[Ischemia-related compartment syndromes in vascular surgery]. / Ischämisch bedingte Kompartmentsyndrome in der Gefäßchirurgie.

Even after the endovascular revolution, acute compartment syndrome (CS) remains an important and frequently present differential diagnosis after many operations. Based on a qualitative review this article gives an overview of the most frequent forms of CS as well as some less frequent entities that require attention in the routine clinical practice. Additionally, the pathophysiology, diagnostics and treatment as well as current research topics for CS, especially concerning the lower leg, are dealt with in detail. In summary, nothing has essentially changed ever since the first description of CS in that the clinical estimation remains the gold standard. The detection and the adequate treatment especially of abdominal CS and CS of the lower leg remain a key competence of vascular surgeons.

Veno-arterial extracorporeal membrane oxygenation (ECMO VA) as part of a multimodal approach for the protection of spinal cord ischemia in surgical repair of a thoracoabdominal aneurysm.

Spinal cord ischaemia leading to paraplegia or paraparesis is one of the most devastating complications of aortic surgery. The risk of ischaemia is particularly high in repairs involving both the thoracic and abdominal segments, because in these cases blood flow to the spinal arteries can be interrupted. Multimodal protocols have now been developed to reduce the incidence of this complication, and include measures such as cerebrospinal fluid (CSF) drainage, avoidance of hypotension and anaemia, systemic hypothermia, neuromonitoring, maintaining distal perfusion during proximal clamping of the aorta, and reimplantation of intercostal or lumbar arteries, whenever feasible. We describe a case in which, due to the special characteristics of the surgery, veno-arterial extracorporeal membrane oxygenation (VA ECMO) was used to maintain distal blood flow in the lumbar, inferior mesenteric, and hypogastric arteries during aortic clamping. This approach reduced the risk of spinal cord and visceral ischaemia, and also eliminated the need for thoracotomy because partial left bypass was not required.

Small Thoracic Disk Herniation without Spinal Stenosis Presenting with Acute Myelopathy: Three Case Reports.

We herein describe three patients with thoracic disk herniation (TDH) that presented with acute myelopathy at the Tokyo Metropolitan Neurological Hospital between 2014 and 2021 (age range, 45-76 years; male/female ratio = 1:2), with a focus on the mechanisms underlying their development. All patients had sudden-onset gait disturbance due to acute nontraumatic paraparesis. The specialties of the doctors at the first hospital were neurology and orthopedic surgery. TDH was overlooked at the first hospital, and the patients were referred to our hospital. The TDH in all cases was of the central type; however, since they were small, no spinal stenosis was observed. The key feature of all three cases is the small anterior deformation of the spinal cord, making a vascular etiology for the symptoms more plausible than a compressive etiology. After a follow-up of several months or years, two out of three patients underwent surgery with the use of the transfacet pedicle-sparing approach due to residual symptoms. Intraoperative ultrasonography showed that the spinal cord was anchored to TDH by the dural attachment of dentate ligaments. The physical relationship between the dentate ligaments and TDH may be associated with the vascular cause of the symptoms of small TDH.

Possible Transient Anterior Spinal Artery Syndrome After a Celiac Plexus Neurolytic Block.

Celiac plexus blocks have been utilized to treat chronic abdominal pain of various etiologies that are refractory to medication management. This procedure is considered relatively safe; however, one rare complication is anterior spinal artery syndrome, which can result in temporary or permanent paralysis of the lower extremities. A 67-year-old male with a history of metastatic esophageal adenocarcinoma and chronic pain refractory to high doses of opioids presented for a celiac plexus neurolytic block. The block was performed successfully with a test block containing 2% lidocaine and 0.5% bupivacaine, after which neurolysis with alcohol was completed. The patient had a syncopal episode in the post-anesthesia care unit (PACU), which resolved with fluid resuscitation without requiring advanced cardiovascular life support (ACLS). He was then discharged. On the evening of discharge, the patient had progressive lower extremity weakness to the point where he was unable to walk even with significant assistance from a family member. He went to the emergency department where a complete spine MRI was done which did not show any spinal cord defect. His physical exam showed preserved proprioception and vibration sensation with upper motor neuron exam signs. The remainder of his sensory exam was inconsistent with both reported intact sensation to pinprick and temperature with intermittently reported hyperalgesia in his lower extremities. Over the next day of admission, his weakness slowly improved. Unfortunately, the patient developed a bowel perforation during hospitalization that was non-operable, and he passed away on hospital day five. This patient likely had anterior spinal artery vasospasm causing temporary lower extremity weakness. Given his overall debility, his physical exam was difficult, although he had intact proprioception and vibration sensation with upper motor neuron exam findings suggestive of an anterior cord process. Vasospasm could be secondary to needle placement near the artery of Adamkiewicz, alcohol, or epinephrine. This case emphasizes the importance of recognizing anterior spinal artery syndrome despite its rarity in patients undergoing celiac plexus neurolysis. Regardless of the rarity of various complications, it is imperative that physicians discuss potential devastating complications of procedures with patients to allow for individualized decision-making. Additionally, there should be a low threshold for overnight admission after celiac plexus neurolytic blocks in patients with severe underlying systemic disease processes.

Unraveling the enigma of Adamkiewicz: exploring the prevalence, anatomical variability, and clinical impact in spinal embolization procedures for bone metastases.

BACKGROUND: The artery of Adamkiewicz (AKA) is vital for spinal cord blood supply. Its role in embolization procedures for bone metastases can cause serious complications. We explored its prevalence, anatomical variation, and effect on spinal embolization using N-butyl cyanoacrylate (NBCA) in patients with bone metastases. PURPOSE: To understand the impact and variability of AKA in spinal embolizations in cases of bone metastases to reduce complications and improve patient outcomes. MATERIAL AND METHODS: We examined data from 454 patients who underwent spinal embolization with NBCA between 2009 and 2018. The presence, anastomoses, and tumor features of AKA were assessed via pre-procedure imaging and angiography. Complications were classified per the CIRSE Classification System. RESULTS: AKA was found in 22.8% of patients, predominantly left-sided and originating from T8 to L1. Direct and indirect anastomoses were present in 66.6% and 33.4% of patients, respectively. Extra-compartmental invasion was linked with direct anastomosis (P = 0.004). High-grade complications were rare but included one instance of bilateral lower limb paralysis. Partial embolization was necessary in 22.8% of cases due to AKA. CONCLUSION: The study underscores the need for rigorous preoperative evaluation of AKA origin and anastomoses in patients undergoing spinal embolization for bone metastases. Given the significant presence of AKA and related anastomoses, especially with renal extra-compartmental tumors, caution is advised to reduce complications and optimize patient outcomes. Further research is required for best practice guidelines involving bone metastases and AKA.

Incomplete Anterior Spinal Artery Syndrome Responsive to Intrathecal Baclofen.

Anterior cord syndrome (ACS) occurs as a result of ischemia in the territory of the anterior spinal artery (ASA). Although spinal cord strokes are rare, the ASA is the most commonly affected vessel in the spinal cord. The typical presentation of an ASA stroke is paraparesis or paraplegia, bilateral loss of pain and temperature sensation, and fecal or urinary incontinence; the underlying neural structures responsible for these symptoms include the corticospinal tracts and anterior horns, anterolateral spinothalamic tracts, and lateral horns, respectively. ACS is a feared complication of aortic procedures and has been well-documented to occur during or after endovascular abdominal aortic aneurysm revascularization (EVAR). We report a case of incomplete or partial ACS presenting with delayed-onset spasticity and instability several months following EVAR, who was subsequently treated with intrathecal baclofen. We hypothesize that this patient's ischemia selectively damaged descending white matter tracts responsible for modulating the stretch receptor reflex, including damage to the corticospinal tract, which likely also impaired positional stability.

Spinal Cord Infarct Due to Fibrocartilaginous Embolism in an Adolescent Boy: A Case Report and Literature Review.

Fibrocartilaginous embolism (FCE) is one of the rare causes of acute spinal cord infarction. We report the case of a previously healthy 14-year-old boy with this condition. A few hours after lifting heavy objects, he developed sudden quadriparesis. On examination, he had asymmetric hypotonic quadriparesis and normal dorsal column function but absent spinothalamic function in all limbs with sensory level to shoulder. Magnetic resonance imaging (MRI) of the spine confirmed the diagnosis of spinal infarction secondary to FCE. The patient initially received methylprednisolone and plasma exchange. A follow-up visit after neurorehabilitation showed improvement but with residual neurological deficit. Although FCE is rare, it should be kept as one of the differential diagnoses of an acute neurological deficit of the spinal cord.

Fibrocartilaginous embolism: a rare cause leading to spinal cord infarction?

PURPOSE: Fibrocartilaginous nucleus pulposus components herniation and embolism rarely causes acute ischaemic events involving the spinal cord. Few reports have suggested this as a mechanism leading to anterior spinal artery syndrome. The purpose of this study was to evaluate the topography and pattern of this rare myelopathy by MRI. METHODS: A retrospective observational case series of patients, admitted to our Institute between 2008 and 2021, with a diagnosis of fibrocartilaginous embolism based on typical clinical and radiological features. RESULTS: Five patients were identified (2 men and 3 women; range 13-38 years). No one had pre-existing vascular risk factors. All referred potential precipitating event in the 24 h prior to symptom onset. MRI findings showed increased signal intensity of the spinal cord on T2-weighted images in all cases and degenerative disc changes opposite to it in four of them. The outcome was poor: three showed only partial sensitivity and motor improvement (mRs 4, 3, and 2, respectively); one completely recovered except for isolated hand paresis (mRs 1); and one remained severely neurologically affected (mRs 5). CONCLUSIONS: Fibrocartilaginous embolism must be a differential diagnosis in case of otherwise unexplained spinal cord infarction in adult and paediatric low risk population. Neuroradiological findings such as abnormal spinal cord signal intensity and degenerative disc changes can aid in early diagnosis of this rare myelopathy. The prevalent myelopathy location was thoracic. All signal alterations were detected in the anterior region of the spinal cord in the territories of the anterior spinal artery.

Two-year follow-up after treatment of an aortic transection in the presence of an aberrant right subclavian artery.

OBJECTIVES: An aberrant right subclavian artery (ARSA) is one of the most common anatomic variants of the aortic arch. The combination of an ARSA and a transection is naturally rare. METHODS: This case report describes the treatment of a transection in the presence of an ARSA and the follow-up of two years. RESULTS: We successfully treated the contained rupture with a stentgraft. Both subclavian arteries had to be covered in the emergency setting. At the two-year follow-up, the patient did not suffer from any neurological impairment. CONCLUSIONS: In emergency settings, primary cover of both subclavian arteries with a stentgraft can be performed in individual cases after risk assessment. Severe complications such as development of upper limb ischaemia, ASAS or reduced perfusion of the posterior cerebral circulation should be considered in treatment planning.

The Role of Folate Deficiency as a Potential Risk Factor for Nontraumatic Anterior Spinal Artery Syndrome in an Adolescent Girl.

Nontraumatic anterior spinal artery syndrome (ASAS) is an extremely rare clinical condition in pediatric populations with a mostly unknown underlying etiology. Here we discuss the case of a previously healthy 14-year-old girl presenting with sudden onset acute flaccid paralysis to the emergency department. A spinal STIR/DWI MRI revealed hyperintensities extending from cervical vertebrae C3-6, consistent with the diagnosis of ASAS. In order to determine any precipitating causes of ASAS, we also extensively investigated established potential risk factors for ASAS in our patient and noticed that she had a marked folate deficiency requiring folic acid supplementation to prevent future episodes of ASAS as well as to repair the patient's injured spinal cord. Interestingly, the patient did not display elevated levels of homocysteine nor did she possess the three pathogenic MTHFR mutations characteristic of ASAS. Although her folate deficiency did not cause responsive hyperhomocysteinemia, and she did not have pathogenic MTHFR mutations that impair the function of methylenetetrahydrofolate reductase in folate cycle, we suggest that isolated folate deficiency may play a role in adolescent cases of ASAS that, once identified, would require prompt identification and early intervention to improve the prognosis of these patients.

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.

Anterior Spinal Artery Syndrome Occurring after One Level Segmental Artery Ligation during Spinal Surgery.

In treating the ventral pathology of spine, ligating the segmental vessels is sometimes necessary. This may cause spinal cord ischemia, and concerns of neurologic injury have been presented. However, spinal cord ischemic injury after sacrificing segmental vessels during spine surgery is very rare. Reports of this have been scarce in the literature and most of these complications occur after multi-level segmental vessel ligation. Here we report a case of a patient with postoperative anterior spinal artery syndrome, which occurred after ligating one level segmental vessels during spinal surgery for a T8 vertebral pathologic fracture. Despite its rarity, the risk of spinal cord ischemic injury after segmental vessel ligation is certainly present. Surgeons must keep in mind such risk, and surgery should be planned under a careful risk-benefit consideration.

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

BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSION: FCEM, though rare, should be kept in mind as a differential diagnosis of acute medical myelopathy when no other cause can be identified.

Anterior Spinal Artery Syndrome: Rare Precedented Reason of Postoperative Plegia After Spinal Deformity Surgery: Report of 2 Cases.

BACKGROUND: Complications in spinal deformity surgery vary from insignificant to severe. Apart from direct mechanical insult, ischemia can also cause spinal cord injury. Ischemic injury may be detected during surgery or may manifest itself postoperatively. We present 2 cases of anterior spinal artery syndrome. CASE DESCRIPTION: In the first case, a 12-year-old girl developed anterior spinal artery syndrome resulting in total quadriplegia 8 hours after spinal deformity surgery. She was treated with a steroid, immunoglobulin, and low-molecular-weight heparin. She showed complete recovery at 1 year postoperatively both clinically and radiographically. In the second case, a 62-year-old woman experienced sudden loss of motor evoked potentials intraoperatively during dural tear repair after sagittal and coronal alignment was established. The paraplegic patient was diagnosed with anterior spinal artery syndrome at the thoracic level postoperatively. She was treated with a steroid and heparin. At 1 year postoperatively, she has gained much of her strength and has myelomalacia in her spinal cord. CONCLUSIONS: Anterior spinal artery syndrome is a serious condition with a generally poor prognosis. Though treatment should be directed at the underlying cause, the best strategy is to prevent it from occurring. Peroperative blood pressure control, intraoperative neuromonitoring, avoidance from mechanical stress during surgery, and close neurologic and hemodynamic monitorization postoperatively should be performed.

Retroperitoneal approach for the treatment of diaphragmatic crus syndrome: technical note.

OBJECTIVE: Myelopathy selectively involving the lower extremities can occur secondary to spondylotic changes, tumor, vascular malformations, or thoracolumbar cord ischemia. Vascular causes of myelopathy are rarely described. An uncommon etiology within this category is diaphragmatic crus syndrome, in which compression of an intersegmental artery supplying the cord leads to myelopathy. The authors present the operative technique for treating this syndrome, describing their experience with 3 patients treated for acute-onset lower-extremity myelopathy secondary to hypoperfusion of the anterior spinal artery. METHODS: All patients had compression of a lumbar intersegmental artery supplying the cord; the compression was caused by the diaphragmatic crus. Compression of the intersegmental artery was probably producing the patients' symptoms by decreasing blood flow through the artery of Adamkiewicz, causing lumbosacral ischemia. RESULTS: All patients underwent surgery to transect the offending diaphragmatic crus. Each patient experienced substantial symptom improvement, and 2 patients made a full neurological recovery before discharge. CONCLUSIONS: Diaphragmatic crus syndrome is a rare or under-recognized cause of ischemic myelopathy. Patients present with episodic acute-on-chronic lower-extremity paraparesis, gait instability, and numbness. Angiography confirms compression of an intersegmental artery that gives rise to a dominant radiculomedullary artery. Transecting the offending diaphragmatic crus can produce complete resolution of neurological symptoms.

Anterior Spinal Artery Syndrome in a Patient with Cervical Spondylosis Demonstrated by CT Angiography.

A few published reports have described anterior spinal artery syndrome (ASAS) with cervical spondylosis based on clinical presentation and/or MRI study, but no photographs of anterior spinal arteries were provided in these studies. Here we present a case of ASAS with cervical spondylosis in a CT angiography (CTA) study. A previously healthy 31-year-old man was diagnosed with acute ASAS with cervical spondylosis. Neurological examination revealed four-limb weakness predominant in the distal part of the upper limbs and superficial sensory impairment below the cervical region. T2-weighted images on MRI showed an area of hyperintensity in the gray matter of the cervical cord from C3 to C5 with a disc herniation at the C4,5 vertebral level. CTA demonstrated that ASA was occluded at level C4,5 , which coincided with the location of disc herniation. Anterior spinal cord decompression and fusions were performed. The patient tolerated the procedure well and had complete resolution of his exertionally dependent myelopathic symptoms 1 week later. In conclusion, although ASAS with cervical spondylosis is rare, it can be diagnosed based on clinical symptoms and MRI and identified by CTA of ASA. A good neurological prognosis is anticipated after anterior spinal cord decompression and fusion is performed if disc herniation is responsible for ASA occlusion.