Arteriovenous fistula and pseudoaneurysm of the anterior spinal artery caused by an epidural needle in a 5-year-old patient

2013 ◽  
Vol 11 (3) ◽  
pp. 340-345 ◽  
Author(s):  
Ibrahim Alnaami ◽  
Fred C. Lam ◽  
Graham Steel ◽  
Bryan Dicken ◽  
Cian J. O'Kelly ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Arteriovenous Fistula ◽  
Neurological Deficits ◽  
Anterior Spinal Artery ◽  
Epidural Needle ◽  
Needle Stick Injury ◽  
Neuraxial Blockade ◽  
Spinal Arteriovenous Fistula ◽  
Cord Injury ◽  
Repeat Angiography

Authors present the case of a 5-year-old patient with a spinal arteriovenous fistula (AVF) and pseudoaneurysm of the anterior spinal artery (ASA) caused by a traumatic epidural needle stick injury. A discussion and relevant review of the literature follow. The boy had a remote history of a liver transplant and required neuraxial blockade for an unrelated abdominal surgical procedure. Initial insertion of the epidural needle at the T9–10 interspace yielded blood. A second attempt at T10–11 was successful. Delayed left leg weakness developed on postoperative Day 8, with an MR image showing a track injury through the cord and a ventral subarachnoid hematoma. Laminectomies from T-9 to T-11were performed emergently to decompress the spinal cord. The dura mater was opened, the ventral hematoma was evacuated, and brisk venous bleeding was controlled with cauterization. Postoperative spinal angiography demonstrated an AVF and pseudoaneurysm of the ASA. Repeat angiography at postoperative Week 4 demonstrated complete resolution of the AVF and pseudoaneurysm, probably due to intraoperative cauterization of the draining vein. The patient underwent a short course of rehabilitation and had no clinical or electrophysiological evidence of spinal cord damage at the 20-month follow-up. One should be cognizant of the possibility of a cord injury in a patient with new-onset neurological deficits following an interventional spine procedure. Neuroimaging is essential for prompt diagnosis and treatment.

Clipping of an anterior spinal artery aneurysm using an endoscopic fluorescence imaging system for craniocervical junction epidural arteriovenous fistula: technical note

2019 ◽  
Vol 31 (2) ◽  
pp. 279-284 ◽  
Author(s):  
Ahmed Mansour ◽  
Toshiki Endo ◽  
Tomoo Inoue ◽  
Kenichi Sato ◽  
Hidenori Endo ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Arteriovenous Fistula ◽  
Fluorescence Imaging ◽  
Imaging System ◽  
Artery Aneurysm ◽  
Craniocervical Junction ◽  
Anterior Spinal Artery ◽  
Posterolateral Approach ◽  
Fluorescence Imaging System ◽  
Ventral Spinal Cord

The authors report the case of a 78-year-old man with a craniocervical junction epidural arteriovenous fistula who presented with subarachnoid hemorrhage from a ruptured anterior spinal artery (ASA) aneurysm. Because endovascular embolization was difficult, a posterolateral approach was chosen and a novel endoscopic fluorescence imaging system was utilized to clip the aneurysm. The fluorescence imaging system provided clear and magnified views of the ventral spinal cord simultaneously with the endoscope-integrated indocyanine green videoangiography, which helped safely obliterate the ASA aneurysm. With the aid of this novel imaging system, surgeons can appreciate and manipulate complex vascular pathologies of the ventral spinal cord through a posterolateral approach, even when the lesion is closely related to the ASA.

Rehabilitation of the canine patient following spinal cord injury: a practical guide

2021 ◽  
Vol 26 (1) ◽  
pp. 1-6
Author(s):  
Cheryl Corral
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Spinal Injury ◽  
Neurological Deficits ◽  
Practical Guide ◽  
Cord Injury ◽  
Physical Therapies

This article forms part of a series exploring the rehabilitation of the canine shoulder, elbow, back, hip and stifle following injury or disease. Discussed here are different rehabilitation techniques used to address neurological deficits, pain and weakness following spinal injury, including physical therapies, electrotherapies and acupuncture.

scholarly journals Local Serpin Treatment via Chitosan-Collagen Hydrogel after Spinal Cord Injury Reduces Tissue Damage and Improves Neurologic Function

2020 ◽  
Vol 9 (4) ◽  
pp. 1221 ◽  
Author(s):  
Jacek M. Kwiecien ◽  
Liqiang Zhang ◽  
Jordan R. Yaron ◽  
Lauren N. Schutz ◽  
Christian J. Kwiecien-Delaney ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Tissue Damage ◽  
Low Dose ◽  
Dorsal Column ◽  
Neurological Deficits ◽  
Sustained Delivery ◽  
Post Surgery ◽  
Cord Injury ◽  
Anti Inflammatory

Spinal cord injury (SCI) results in massive secondary damage characterized by a prolonged inflammation with phagocytic macrophage invasion and tissue destruction. In prior work, sustained subdural infusion of anti-inflammatory compounds reduced neurological deficits and reduced pro-inflammatory cell invasion at the site of injury leading to improved outcomes. We hypothesized that implantation of a hydrogel loaded with an immune modulating biologic drug, Serp-1, for sustained delivery after crush-induced SCI would have an effective anti-inflammatory and neuroprotective effect. Rats with dorsal column SCI crush injury, implanted with physical chitosan-collagen hydrogels (CCH) had severe granulomatous infiltration at the site of the dorsal column injury, which accumulated excess edema at 28 days post-surgery. More pronounced neuroprotective changes were observed with high dose (100 µg/50 µL) Serp-1 CCH implanted rats, but not with low dose (10 µg/50 µL) Serp-1 CCH. Rats treated with Serp-1 CCH implants also had improved motor function up to 20 days with recovery of neurological deficits attributed to inhibition of inflammation-associated tissue damage. In contrast, prolonged low dose Serp-1 infusion with chitosan did not improve recovery. Intralesional implantation of hydrogel for sustained delivery of the Serp-1 immune modulating biologic offers a neuroprotective treatment of acute SCI.

scholarly journals Nogo receptor decoy promotes recovery and corticospinal growth in non-human primate spinal cord injury

Brain ◽  
2020 ◽  
Vol 143 (6) ◽  
pp. 1697-1713 ◽  
Author(s):  
Xingxing Wang ◽  
Tianna Zhou ◽  
George D Maynard ◽  
Pramod S Terse ◽  
William B Cafferty ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Recovery Of Function ◽  
Neurological Deficits ◽  
Vehicle Group ◽  
Post Injury ◽  
Nogo Receptor ◽  
Human Dose ◽  
Cord Injury ◽  
Human Primate

Abstract After CNS trauma such as spinal cord injury, the ability of surviving neural elements to sprout axons, reorganize neural networks and support recovery of function is severely restricted, contributing to chronic neurological deficits. Among limitations on neural recovery are myelin-associated inhibitors functioning as ligands for neuronal Nogo receptor 1 (NgR1). A soluble decoy (NgR1-Fc, AXER-204) blocks these ligands and provides a means to promote recovery of function in multiple preclinical rodent models of spinal cord injury. However, the safety and efficacy of this reagent in non-human primate spinal cord injury and its toxicological profile have not been described. Here, we provide evidence that chronic intrathecal and intravenous administration of NgR1-Fc to cynomolgus monkey and to rat are without evident toxicity at doses of 20 mg and greater every other day (≥2.0 mg/kg/day), and far greater than the projected human dose. Adult female African green monkeys underwent right C5/6 lateral hemisection with evidence of persistent disuse of the right forelimb during feeding and right hindlimb during locomotion. At 1 month post-injury, the animals were randomized to treatment with vehicle (n = 6) or 0.10–0.17 mg/kg/day of NgR1-Fc (n = 8) delivered via intrathecal lumbar catheter and osmotic minipump for 4 months. One animal was removed from the study because of surgical complications of the catheter, but no treatment-related adverse events were noted in either group. Animal behaviour was evaluated at 6–7 months post-injury, i.e. 1–2 months after treatment cessation. The use of the impaired forelimb during spontaneous feeding and the impaired hindlimb during locomotion were both significantly greater in the treatment group. Tissue collected at 7–12 months post-injury showed no significant differences in lesion size, fibrotic scar, gliosis or neuroinflammation between groups. Serotoninergic raphespinal fibres below the lesion showed no deficit, with equal density on the lesioned and intact side below the level of the injury in both groups. Corticospinal axons traced from biotin-dextran-amine injections in the left motor cortex were equally labelled across groups and reduced caudal to the injury. The NgR1-Fc group tissue exhibited a significant 2–3-fold increased corticospinal axon density in the cervical cord below the level of the injury relative to the vehicle group. The data show that NgR1-Fc does not have preclinical toxicological issues in healthy animals or safety concerns in spinal cord injury animals. Thus, it presents as a potential therapeutic for spinal cord injury with evidence for behavioural improvement and growth of injured pathways in non-human primate spinal cord injury.

Evaluation of experimental spinal cord injury using cortical evoked potentials

1973 ◽  
Vol 39 (1) ◽  
pp. 75-81 ◽  
Author(s):  
Stephen H. Martin ◽  
James R. Bloedel
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Cortical Response ◽  
Neurological Deficits ◽  
Cystic Degeneration ◽  
Post Injury ◽  
Content Type ◽  
Cord Injury ◽  
Cortical Responses ◽  
Control Response

✓ Experiments were performed to determine if changes in cortical evoked responses could be used to predict the extent of the neurological deficits following spinal cord injury by sudden inflation of a Fogarty balloon in the epidural space cephalad to a laminectomy. The cortical responses to stimulation of the posterior tibial nerve were recorded over the sigmoid gyrus at various times following the lesion and compared with the control response. Severe, irreversible neurological deficits occurred in cats in which the cortical response either could not be evoked immediately after injury or disappeared rapidly during this period. At the end of at least 6 weeks following injury, all of these animals were paraplegic and showed severe cystic degeneration of the spinal cord. In animals in which the post-injury cortical response did not completely disappear, only mild changes were observed in a spinal cord 6 weeks following injury. This technique may be helpful in ascertaining the severity and irreversibility of a traumatic spinal cord lesion; because the technique is simple, the method may prove helpful in the clinical management of patients with spinal cord injury.

scholarly journals Neurological recovery after surgical intervention of a complete spinal cord injury secondary to a chronic untreated odontoid neck fracture: a lesson in patient prognostication

2020 ◽  
Vol 13 (1) ◽  
pp. e233077
Author(s):  
Patricio III Espinoza Dumlao ◽  
Samuel Grozman
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Spinal Injury ◽  
Neurological Deficits ◽  
Posterior Decompression ◽  
Clear Cut ◽  
Cord Injury ◽  
Neck Fracture ◽  
Complete Spinal Cord Injury

Odontoid fractures are injuries that can either be benign or devastatingly progress to quadriplegia and significant morbidity and mortality. Management is not clear cut for patients who already present late and with severe neurological deficits. We present a case of a type 2 odontoid fracture with associated complete spinal cord injury (American Spinal Injury Association A) initially untreated for 3 months but was subsequently managed with posterior decompression, instrumentation and occipitocervical fusion. The patient fully recovered all deficits and is independent of activities of daily living.

Role of the blood-spinal cord barrier in posttraumatic syringomyelia

2009 ◽  
Vol 11 (6) ◽  
pp. 696-704 ◽  
Author(s):  
Sarah J. Hemley ◽  
B. Biotech ◽  
Jian Tu ◽  
Marcus A. Stoodley
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Amino Acid ◽  
Vascular Permeability ◽  
Neurological Deficits ◽  
Time Points ◽  
Functional Integrity ◽  
Cord Injury ◽  
Posttraumatic Syringomyelia ◽  
Blood Spinal Cord Barrier

Object Posttraumatic syringomyelia produces a significant burden of pain and neurological deficits in patients with spinal cord injury. The mechanism of syrinx formation is unknown and treatment is often ineffective. A possible explanation for syrinx formation is fluid leakage from the microcirculation in the presence of a compromised blood-spinal cord barrier (BSCB). The aim of this study was to investigate the structural and functional integrity of the BSCB in a model of posttraumatic syringomyelia. Methods The excitotoxic amino acid and arachnoiditis model of syringomyelia was used in 27 Sprague-Dawley rats. Structural integrity of the BSCB was assessed using immunoreactivity to endothelial barrier antigen (EBA), and loss of functional integrity was assessed by extravasation of intravascular horseradish peroxidase. Animals were studied after 3 days, or at 1, 3, 6, or 12 weeks after surgery. There were laminectomy-only and saline injection control animals for comparison at each time point. Results Syrinxes formed in 16 of the 17 animals injected with excitotoxic amino acid. Loss of structural and functional integrity of the BSCB in syrinx animals was noted at all time points. Disruption of the BSCB was most dramatic in tissue adjacent to the syrinx, and in the central and dorsal gray matter. Changes in EBA expression generally corresponded with altered vascular permeability, although in the acute stages, widespread vascular permeability occurred without a corresponding decrease in EBA expression. At the later time points (3–12 weeks) EBA expression was often absent, although no vascular leakage was observed. Conclusions This study demonstrated a prolonged structural and functional disruption of the BSCB in this model of posttraumatic syringomyelia. Loss of functional integrity of the BSCB, with fluid entering the interstitial space of the spinal cord, may contribute to initial cyst formation after spinal cord injury and subsequent enlargement of the cyst, to produce posttraumatic syringomyelia.

Intrathecal baclofen for intractable spasticity of spinal origin: results of a long-term multicenter study

1993 ◽  
Vol 78 (2) ◽  
pp. 226-232 ◽  
Author(s):  
Robert J. Coffey ◽  
David Cahill ◽  
William Steers ◽  
T. S. Park ◽  
Joe Ordia ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Intrathecal Baclofen ◽  
Neurological Deficits ◽  
Pump System ◽  
Postoperative Score ◽  
Long Term Treatment ◽  
Cord Injury

✓ A total of 93 patients with intractable spasticity due to either spinal cord injury (59 cases), multiple sclerosis (31 cases), or other spinal pathology (three cases) were entered into a randomized double-blind placebocontrolled screening protocol of intrathecal baclofen test injections. Of the 88 patients who responded to an intrathecal bolus of 50, 75, or 100 µg of baclofen, 75 underwent implantation of a programmable pump system for chronic therapy. Patients were followed for 5 to 41 months after surgery (mean 19 months). No deaths or new permanent neurological deficits occurred as a result of surgery or chronic intrathecal baclofen administration. Rigidity was reduced from a mean preoperative Ashworth scale score of 3.9 to a mean postoperative score of 1.7. Muscle spasms were reduced from a mean preoperative score of 3.1 (on a fourpoint scale) to a mean postoperative score of 1.0. Although the dose of intrathecal baclofen required to control spasticity increased with time, drug tolerance was not a limiting factor in this study. Only one patient withdrew from the study because of a late surgical complication (pump pocket infection). Another patient received an intrathecal baclofen overdose because of a human error in programming the pump. The results of this study indicate that intrathecal baclofen infusion can be safe and effective for the long-term treatment of intractable spasticity in patients with spinal cord injury or multiple sclerosis.

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