Diagnostic, clinical management, and outcomes in patients with spinal dural arteriovenous fistula.

Background: Spinal dural arteriovenous fistulas (SDAVFs) are rare spinal vascular malformations, but account for 70 to 80% of all spinal arteriovenous malformations. SDAVFs can be treated either surgically or endovascularly, with surgical treatment appearing to lead to higher closure rates. Our aim was to analyze the demographic data, diagnostic history, treatment characteristics and clinical short- and long-term outcomes. Methods: The medical records of 81 patients who underwent surgical (n = 70, 86.4%) and endovascular (n = 11, 13.6%) treatment for SDAVF at a university hospital between 2002 and 2023 were retrospectively analyzed. Results: SDAVF was observed more frequently in men than women (61, 75.3% vs. 20, 24.7%) with a mean age of 63.5 ± 12.7 years and a mean duration of symptoms to diagnosis of 12.0 ± 12.8 months. The most common first symptom was gait disturbance (36, 44.4%), followed by sensory disturbance (24, 29.6%). The location of the fistula point was most common in the lower thoracic region (36, 44.5%), followed by the lumbar region (23, 28.4%). Incomplete or failed occlusion of the fistula occurred in 8 patients (9.9%), with 6 patients (7.4%) undergoing further treatment either surgically or endovascularly. Treatment- or hospital-related complications were observed in 16 patients (19.8%). A single-level laminectomy was the most common approach (31, 44.3%), followed by single-level hemilaminectomy (28, 40.0%), and unilateral interlaminar fenestration (11, 15.7%). Back pain or radiculopathy was observed in 58% of patients (47/81) pre-treatment and had already decreased to 24.7% at hospital discharge (p < 0.001). No significant differences were observed in sensory disturbances (p = 0.681). The median of American Spinal Injury Association motor score (ASIA-MS) was 94 [82.5-100] at admission, 98 [86.5-100] at hospital discharge, 100 [90-100] at the first, second, and third follow-up (p = 0.019). The median modified Aminoff-Logue scale (mALS) was 5 [2-7] at admission, 3 [1-6] at hospital discharge, 2 [1-5] at the first follow-up, 2 [0.5-5] at the second follow-up and 2 [1-7] at the third follow-up (p = 0.006). Conclusions: SDAVF occurs predominantly in men in the 6th decade of life and can be safely and effectively treated surgically and endovascularly, improving symptoms such as pain and motor deficits, gait disturbances as well as bowel and bladder dysfunction, but not sensory disturbances.

Decoding unusual MR findings: Spinal cord edema in atypical cervical spondylotic myelopathy-A case report and literature review.

We report a case of a young man with a slow progression of cervical spondylotic myelopathy (CSM). Cervical magnetic resonance imaging (MRI) revealed a mild cervical discbulging at C5-C6 and an area of atypically enlarged intramedullary high signal intensity extending from C4-C7 (T2-weighted) with contrast enhancement at C5-C6 (T1-weighted). Neurological and radiological diagnoses tend to favor demyelinating diseases, which interfere with the diagnosis of CSM. Patients were followed up and examined by MRI at 3 months, 1 year, and 2 years after surgery. The patient's symptoms improved immediately postoperatively. The functional result according to the modified Japanese Orthopedic Association (JOA) score improved from 10 to 13 within 3 months. He continued to improve neurologically over the first postoperative year. Two years postoperatively, a T2-weighted MRI showed that the edema signal had disappeared completely, and a fat-saturated T2-weighted MRI showed only slight abnormal signal. The numbness and weakness of the extremities had improved, and his JOA score was 16. Spinal cord edema is occasionally seen with CSM. In the case presented, the contrast enhancement was localized at the site of the greatest narrowing of the spinal canal and compression of the spinal cord. This coincidence was the best indicator of a mechanical cause of the spinal cord changes. This feature should increase physician's confidence in distinguishing CSM from intramedullary tumors and myelitis. Surgical decompression may be beneficial in improving neurologic outcomes.

Spinal cord injury induced exacerbation of Alzheimer's disease like pathophysiology is reduced by topical application of nanowired cerebrolysin with monoclonal antibodies to amyloid beta peptide, p-tau and tumor necrosis factor alpha.

Hallmark of Alzheimer's disease include amyloid beta peptide and phosphorylated tau deposition in brain that could be aggravated following traumatic of concussive head injury. However, amyloid beta peptide or p-tau in spinal cord following injury is not well known. In this investigation we measured amyloid beta peptide and p-tau together with tumor necrosis factor-alpha (TNF-α) in spinal cord and brain following 48 h after spinal cord injury in relation to the blood-spinal cord and blood-brain barrier, edema formation, blood flow changes and cell injury in perifocal regions of the spinal cord and brain areas. A focal spinal cord injury was inflicted over the right dorsal horn of the T10-11 segment (4 mm long and 2 mm deep) and amyloid beta peptide and p-tau was measured in perifocal rostral (T9) and caudal (T12) spinal cord segments as well as in the brain areas. Our observations showed a significant increase in amyloid beta peptide in the T9 and T12 segments as well as in remote areas of brain and spinal cord after 24 and 48 h injury. This is associated with breakdown of the blood-spinal cord (BSCB) and brain barriers (BBB), edema formation, reduction in blood flow and cell injury. After 48 h of spinal cord injury elevation of amyloid beta peptide, phosphorylated tau (p-tau) and tumor necrosis factor-alpha (TNF-α) was seen in T9 and T12 segments of spinal cord in cerebral cortex, hippocampus and brain stem regions associated with microglial activation as seen by upregulation of Iba1 and CD86. Repeated nanowired delivery of cerebrolysin topically over the traumatized segment repeatedly together with monoclonal antibodies (mAb) to amyloid beta peptide (AßP), p-tau and TNF-α significantly attenuated amyloid beta peptide, p-tau deposition and reduces Iba1, CD68 and TNF-α levels in the brain and spinal cord along with blockade of BBB and BSCB, reduction in blood flow, edema formation and cell injury. These observations are the first to show that spinal cord injury induces Alzheimer's disease like symptoms in the CNS, not reported earlier.

Co-Administration of Nanowired Monoclonal Antibodies to Inducible Nitric Oxide Synthase and Tumor Necrosis Factor Alpha Together with Antioxidant H-290/51 Reduces SiO2 Nanoparticles-Induced Exacerbation of Pathophysiology of Spinal Cord Trauma.

Military personnel are often exposed to silica dust during combat operations across the globe. Exposure to silica dust in US military or service personnel could cause Desert Strom Pneumonitis also referred to as Al Eskan disease causing several organs damage and precipitate autoimmune dysfunction. However, the effects of microfine particles of sand inhalation-induced brain damage on the pathophysiology of traumatic brain or spinal cord injury are not explored. Previously intoxication of silica nanoparticles (50-60 nm size) is shown to exacerbates spinal cord injury induces blood-spinal cord barrier breakdown, edema formation and cellular changes. However, the mechanism of silica nanoparticles-induced cord pathology is still not well known. Spinal cord injury is well known to alter serotonin (5-hydroxytryptamine) metabolism and induce oxidative stress including upregulation of nitric oxide synthase and tumor necrosis factor alpha. This suggests that these agents are involved in the pathophysiology of spinal cord injury. In this review, we examined the effects of combined nanowired delivery of monoclonal antibodies to neuronal nitric oxide synthase (nNOS) together with tumor necrosis factor alpha (TNF-α) antibodies and a potent antioxidant H-290/51 to induce neuroprotection in spinal cord injury associated with silica nanoparticles intoxication. Our results for the first time show that co-administration of nanowired delivery of antibodies to nNOS and TNF-α with H-290/51 significantly attenuated silica nanoparticles-induced exacerbation of spinal cord pathology, not reported earlier.

Diagnostic Accuracy of Magnetic Resonance Imaging With 3-Dimensional T2-SPACE Techniques for Preganglionic Injury of the Brachial Plexus.

PURPOSE: An accurate diagnosis of the site and severity of a brachial plexus injury is imperative for selecting the appropriate management. Conventional magnetic resonance imaging (MRI) does not allow for the precise interpretation of preganglionic injuries (pre-GIs), especially intravertebral canal injuries. We developed 4 MRI sequences of conventional 1.5-tesla 3-dimensional T2-weighted turbo spin echo sampling perfection with the application of optimized contrasts using different flip angles evolution (T2-SPACE) images to clearly visualize each component of the brachial plexus. The purpose of this study was to introduce basic normal and pathologic findings of our current MRI approach, focusing on its diagnostic accuracy for pre-GIs. METHODS: We initially examined 119 patients with brachial plexus injuries who underwent surgical exploration by MRI using 4 sequences of the 1.5-tesla 3-dimensional T2-SPACE technique. We obtained coronal, transverse, coronal oblique, and coronal cuts of T2 short time inversion recovery. The images of 595 roots were interpreted by multiple-image synchronizing techniques of the 4 views to precisely interpret the presence of spinal cord edema, numbers of anterior and posterior rootlets, sites of ganglions, meningeal cysts, and the "black line sign" (displaced ruptured dura or bundles of ruptured rootlets). We assessed the accuracy, sensitivity, and specificity of these abnormal findings with regard to diagnosing pre-GIs by comparing surgical exploration. RESULTS: The absence or decreased numbers of anterior and posterior rootlets and displacement of ganglions were definitive evidence of pre-GIs and the other findings, like spinal cord edema, meningeal cysts, and black line signs, were predictive signs. CONCLUSIONS: The synchronizing techniques of the four 1.5-tesla 3-dimensional T2-SPACE images provided high diagnostic accuracy of pre-GIs. TYPE OF STUDY/LEVEL OF EVIDENCE: Diagnostic II.

Diagnosis and Treatment of a Dural Arteriovenous Fistula Involving the Superior Petrosal Vein.

OBJECTIVE: A dural arteriovenous fistula involving the superior petrosal vein (SPV DAVF) is an extremely rare condition. Therefore, its clinical presentation, imaging characteristics, treatment methods, and risk factors remain unclear. In this study, we discuss and analyze the aforementioned features of an SPV DAVF. METHODS: We retrospectively reviewed 30 patients with SPV DAVFs, with a 1-year follow-up rate of 96.67% (29 of 30). The neurological function of the patients was assessed using the modified Aminoff-Logue scale and the modified Rankin Scale score. The risk factors before and after treatment were established using univariate and multivariate logistic regression analyses. Additionally, treatments involving 3 distinct SPV DAVF drainage patterns were presented. RESULTS: Of the 30 patients, 24 were men (80.0%). Besides, the angiography images were reexamined 12 months after surgery. Univariate analyses indicated that the extent of edema (odds ratio 1.889, 95% confidence interval 1.132-3.154) and the number of draining veins (≤2) (odds ratio 10.833, 95% confidence interval 1.961-59.834) were risk factors for pretreatment modified Rankin Scale score ≥3. However, multivariate analyses revealed no statistically significant differences (P = 0.051, P = 0.055). Following the multivariate analyses, steroid pulse (odds ratio 12.153 95% confidence interval 1.080-136.772) was found to be the only significant risk factor for post-treatment difference between pretreatment and 1-year follow-up modified Rankin Scale score ≥2. CONCLUSIONS: A DAVF with SPV drainage is an uncommon type of intracranial vascular malformation. Most lesions involve the brain stem or high cervical spinal cord, thereby posing a higher risk of disability or death. Moreover, neuronal damage from persistent venous hypertension is permanent. Therefore, precise diagnosis and timely treatment are key to a good patient prognosis.

Surgical Obliteration of a Posterior Fossa Dural Arteriovenous Fistula Presenting with Exclusive Spinal Signs and Symptoms Caused by Spinal Cord Venous Hypertension.

Vascular malformations in the dura of the spinal root sleeve in the thoracic or lumbar region can cause venous hypertension with resultant spinal cord edema and neurologic deterioration. However, occasionally an intracranial vascular malformation can have venous drainage into the spinal canal causing symptoms, signs, and radiographic appearance that can mimic spinal lesions. Herein, we present the case of a 73-year-old man who developed lower extremity weakness and loss of sensation. The patient initially underwent L4-L5 diskectomy elsewhere, but the symptoms progressed. Spinal magnetic resonance imaging revealed serpiginous vessels in the spinal subarachnoid space and spinal cord edema (Video 1). Diagnostic spinal and cerebral angiogram showed no evidence of spinal vascular malformations yet did reveal early venous shunting arising from the posterior fossa consistent with a dural arteriovenous fistula (dAVF). The venous drainage from this lesion was inferiorly directed into the spinal canal, causing venous hypertension of the spinal cord, which explained the patient's symptoms. An asymptomatic second dAVF of the petrous apex was also discovered. Surgical obliteration of both dAVFs in 1 sitting using a right far-lateral suboccipital craniotomy was planned. The dural drainage of each dAVF was identified and coagulated. Postoperative angiography confirmed complete obliteration of both dAVFs, and the patient's neurologic function improved shortly after surgery. This case highlights the importance of complete investigation of the spinal and cranial vasculature in the hunt for the cause of venous hypertension in the spinal cord.

Spinal cord swelling in patients with cervical compression myelopathy.

BACKGROUND: Intramedullary hyperintense lesions associated with spinal cord edema on T2-weighted MR images (T2WI) are rare findings in patients with cervical spondylosis and are poorly characterized. We investigated the clinical characteristics of spinal cord edema due to cervical spondylosis (SCECS). METHODS: In total, 214 patients with cervical spondylotic myelopathy who underwent surgery between April 2007 and March 2017 were divided into SCECS and non-SCECS groups with SCECS defined as follows: (1) intramedullary signal intensity (ISI) of the cervical spinal cord in sagittal T2WI extending to more than one vertebral body height; (2) "fuzzy" ISI, recognized as a faint intramedullary change with a largely indistinct and hazy border; and (3) a larger sagittal diameter of the spinal cord segment with ISI just above or below the cord compression area compared with areas of the cervical spine without ISI. Radiographic parameters, demographic characteristics, and the Japanese Orthopedic Association (JOA) surgical outcomes score were compared between the groups. RESULTS: Seventeen patients (7.9%) were diagnosed with SCECS. These patients were younger than those in the non-SCECS group [median (interquartile range), 64 (20) vs. 69 (15) years, respectively, p = 0.016], and the disease duration from onset to surgery was significantly shorter in the SCECS group than in the non-SCECS group [6 (7) vs. 20 (48) months, respectively]. No significant difference was observed between groups with respect to sex, radiologic findings, or surgical outcomes. CONCLUSION: The disease showed an earlier onset and more rapid progression in the patients with SCECS than in those without SCECS.

First case of neurofibromatosis with posterior reversible encephalopathy syndrome showing spinal cord involvement.

Posterior reversible encephalopathy syndrome (PRES) is a well-documented pathology of the brain in systemic upsets. Majority of PRES cases present with edema in the cerebrum, most commonly in the territory of posterior circulation. It has been reported to show spinal cord involvement in a rare subgroup known as PRES with spinal cord involvement (PRES-SCI), with very limited existing literature even in adult patients. Our institution recently encountered a pediatric case with neurofibromatosis type I (NF 1) showing PRES with extensive reversible spinal cord changes. This case illustrates the features of this rare entity in the pediatric group of patients, and is the first reported case in NF 1 patients.

Spinal cord edema with contrast enhancement mimicking intramedullary tumor in patient with cervical myelopathy: A case report and a brief literature review.

BACKGROUND: Cervical myelopathy (CM) is a clinical diagnosis that may be associated with hyperintense areas on T2-weighted magnetic resonance imaging (MRI) scan. The use of contrast enhancement in such areas to differentiate between neoplastic and degenerative disease has rarely been described. CASE DESCRIPTION: We present a 41-year-old female with a 5-month course of progressive CM. The cervical MRI revealed spinal cord swelling, stenosis, and a hyperintense signal at the C5-C6 and C5-C7 levels. Both the neurologic and radiologic examinations were consistent with an intramedullary cervical cord tumor. To decompress the spinal canal, an anterior cervical discectomy and fusion was performed from C5 to C7 level. This resulted in immediate and significant improvement of the myelopathy. Postoperatively, over 1.5 years, the hyperintense, enhancing intramedullary lesion gradually regressed on multiple postoperative MRI scans. CONCLUSION: Spinal cord edema is occasionally seen on MR studies of the cervical spine in patients with degenerative CM. Contrast-enhanced MR studies may help differentiate hyperintense cord signals due to edema vs. atypical intramedullary tumors. Routine successive postoperative MRI evaluations are crucial to confirm the diagnosis of degenerative vs. neoplastic disease.

The value of intraoperative ultrasound in the recognition of pseudo-swelling of the spinal cord.

We present the case of a woman who presented with weakness of both legs due to a low grade tumor of the spinal cord. Excision of the tumor was performed and confirmed with intraoperative ultrasound. Prior to dural closure the spinal cord was found to be pushed dorsally with herniation of the cord through the dural defect. Intraoperative ultrasound showed a collection of cerebrospinal fluid in an anterior pocket giving the impression of the cord being swollen. Once cerebrospinal fluid was drained, the cord settled within the thecal space and closure of the dural defect was performed. Surgery for an intramedullary spinal cord tumor can cause a significant amount of swelling and either a duroplasty is required or the dura is left open with meticulous closure of the wound. Ultrasound is helpful to identify pathology anterior to the cord and prevents the potential complications associated with duroplasty or leaving the dura open.

Chiari I: edema medular y aumento de la siringomielia luego de la descompresión cráneo espinal con plástica meníngea. reporte de un caso / Chiari I: medullary edema and increased syringomyelia after decompression spinal skull with meningeal plastic. report a case

Objetivo: Describir y analizar un caso de Chiari I con edema medular y aumento de la siringomielia (SM), luego de una descompresión cráneo espinal (DCE). Descripción: una mujer de 57 años consultó por cefaleas agravadas por maniobras de Valsalva, hipo, disfagia e hipoestesia distal del miembro superior izquierdo. La Resonancia Magnética (RM) mostró una malformación de Chiari tipo I con SM. Intervención: en abril del 2009 se efectuó una DCE (occipital + atlas) con plástica meníngea (dura artificial). En el postoperatorio inmediato notó aumento de su cefalea, y además se produjo una fístula de LCR que se trató con un drenaje lumbar externo. Como sus síntomas pre y postoperatorios mejoraron fue externada. En la RM realizada a los 15 días se observó un pseudomeningocele (PM) con edema medular. Los controles posteriores mostraron la desaparición del edema y el PM, con un aumento en el tamaño de la SM. En marzo del 2011 se hizo una laminectomía del axis sin reducción de la SM. Luego de un acceso de tos apareció un dolor neuropático en el brazo izquierdo. La nueva RM mostró que la SM no se había reducido y que la plástica meníngea se había retraído obstruyendo la cisterna magna. En diciembre del 2011 se realizó una nueva plástica meníngea con periostio y la RM de marzo del 2012 mostró una desaparición de la SM. Conclusión: en este caso, el edema medular y el PM se redujeron espontáneamente pero la SM no mejoró hasta eliminar todas las causas de obstrucción en la circulación del LCR a nivel del foramen magno.

Objective: To describe and analyze a Chiari I malformation with spinal cord edema and syrinx increase after craneospinal decompression (CED).Description: a 57 years-old female referred a history of headaches after Valsalva maneuvers, hiccup, dysphagia and left distal upper limb hypoesthesia. Magnetic Resonance Imaging (MRI) showed a Chiari I malformation with syringomyelia.Intervention: during April 2009 a CED (occipital + atlas) with a non autologous duraplasty were performed. In the immediate postoperative period headaches increased and also appeared an external CSF fistula that was treated successfully with an external lumbar drainage. As the pre and postoperative symptoms improved she was discharged. After 15 days MRI revealed a pseudomeningocele (PMC) with spinal cord edema. Further controls showed the disappearance of the PMC and the edema with syrinx increase. In March 2011 a laminectomy of the axis was performed without reduction of the syrinx. A few months later and after a cough attack a neuropathic pain developed in the left upper limb. MRI showed a larger syrinx with retraction of the duraplasty. In December 2011 a new duraplasty with autologous pericranium was performed. Three months latter a postoperative MRI showed syrinx resolution. Conclusion: in this case the spinal cord edema and PMC resolved spontaneously but syringomyelia improved only after removing all the causes that obstructed the normal CSF circulation at the foramen magnum.

Spinal cord swelling with abnormal gadolinium-enhancement mimicking intramedullary tumors in cervical spondylosis patients: Three case reports and review of the literature.

OBJECTIVE: Spinal cord swelling with abnormal gadolinium (Gd) enhancement is a rare preoperative radiological finding in patients with cervical spondylosis. In the presence of progressive myelopathy, timely surgical decompression can be curative. CASE PRESENTATION: We report 3 patients with cervical spondylotic myelopathy. Preoperative magnetic resonance imaging (MRI) revealed spondylotic changes and intramedullary lesions in the cervical spine. We noted cervical cord swelling with high intensity on T2-weighted MRI and abnormal Gd-DTPA enhancement. Laminoplasty resulted in marked improvement of their neurological condition and postoperative MRI revealed gradual regression of the intramedullary lesions during the first year. CONCLUSION: We posit that the intramedullary lesions in our patients were reflective of spinal cord edema with blood-brain-barrier disturbance in the cervical cord, possibly due to minor recurrent spinal cord injury and disturbed venous circulation. Spinal cord edema is a rare condition in patients with cervical spondylosis and an accurate diagnosis and timely surgery are necessary for cure. Therefore, this unusual condition must be considered in spondylosis patients manifesting as intramedullary lesions on MRI of the cervical spinal cord. Careful evaluation of the postoperative course can be used to confirm the diagnosis and help in selecting a subsequent therapeutic strategy.