Thoracic Spinal Cord Herniation Research Articles

Idiopathic Thoracic Spinal Cord Herniation: Two Case Reports of a Frequently Misdiagnosed Pathology

Idiopathic Thoracic Spinal Cord Herniation: Two Case Reports of a Frequently Misdiagnosed Pathology

Long term follow up of surgery for thoracic spinal cord herniation :early and late outcome

Long term follow up of surgery for thoracic spinal cord herniation :early and late outcome

Thoracic Anterior Spinal Cord Herniation: Treatment and Prognosis Outcome of Seven Patients

This study aimed to investigate the diagnosis and treatment of thoracic anterior spinal cord herniation, a rare condition. Clinical data of 7 patients diagnosed with thoracic anterior spinal cord herniation were analyzed. All patients were diagnosed with a complete preoperative examination and scheduled for surgical treatment. In addition, regular follow-up was performed after the surgery, and the operation's efficacy was evaluated according to clinical symptoms, imaging findings, and improvement in neurologic function. All patients underwent spinal cord release with an anterior dural patch. Notably, no severe postoperative surgical complications were observed. All patients were followed up for 12-75months, with an average duration of approximately 46.5months. Post-operative pain symptoms were controlled, neurological dysfunction and related symptoms improved to varying degrees, and anterior spinal cord herniation did not recur. The modified Japanese Orthopedic Association score at the last follow-up was significantly higher than the preoperative score. Clinicians should avoid misdiagnosing patients with thoracic anterior spinal cord herniation with intervertebral disc herniation, arachnoid cysts, and other related diseases, and patients should undergo surgical treatment as early as possible. In addition, surgical treatment can protect the neurologic function of patients and effectively prevent the aggravation of clinical symptoms.

Dural repair with fat patch for idiopathic spinal cord herniation: operative technique and a review of seven cases.

BackgroundIdiopathic ventral thoracic spinal cord herniation is a rare disease presented with progressive myelopathy or Brown Séquard syndrome, causing neurological deficits. There is no consensus on etiology and surgical strategy. The purpose of the present study is to report the case series using fat patch for the repair of the ventral dural defect with clinical follow up.MethodsA retrospective review of all cases of idiopathic spinal cord herniation (ISCH) at our institution was performed between January 2017 and June 2021. Clinical data were reviewed including patients' demographic information, symptoms, imaging, operative details, perioperative and postoperative courses, and clinical outcomes, and complications. Japanese Orthopedic Association (JOA) score was calculated preoperatively and postoperatively for the comparison of outcomes.ResultsA total of 7 patients were included. Fat patch was applied in all cases, and artificial dural patch was also used in 2 cases. Average operating time and estimated blood loss were 3 hours and 24 minutes and 88.6 mL, respectively. Five of 7 patients improved and 2 patients remained unchanged during follow up (average, 23.4 months; range, 9–42 months). The mean recovery rate (RR) of JOA score was 17.9%. One patient experienced cerebrospinal fluid (CSF) leakage, and 1 patient suffered from surgical related spinal canal stenosis.ConclusionsSurgical treatment using fat patch is an effective strategy for the ventral dural defect repair of ISCH.

Repair of Thoracic Spinal Cord Herniation: 2-Dimensional Operative Video.

Spinal cord herniation is an uncommon surgically treatable cause of thoracic myelopathy and progressive paraplegia. The thoracic spinal cord focally protrudes through a defect in the dura, resulting in progressive weakness, numbness, and spasticity affecting the lower extremities, in addition to possible urinary symptoms. In this video, we present the case of a 69-yr-old female who presented with 3 yr of progressive thoracic myelopathy due to a thoracic spinal cord herniation at T4-T5. We demonstrate the surgical steps to lyse arachnoid webs, mobilize the spinal cord, reduce the spinal cord herniation, and repair the dural defect. Appropriate patient consent was obtained.

Novel Strategy of Ventral Dural Repair for Idiopathic Thoracic Spinal Cord Herniation: Report of Outcomes and Review of Techniques.

Idiopathic ventral thoracic spinal cord herniation is a rare condition that usually presents with progressive myelopathy or Brown-Séquard syndrome. More than 100 cases have been reported with significant variance in surgical treatment strategies and likewise, significant variance in patient outcomes. Although laminectomy has often been used, to date, there is no consensus regarding the optimal surgical approach or strategy for ventral dural repair. To report and illustrate a novel approach to repair the ventral dural defect with more than 2 yr of clinical follow-up. The specific approach and graft used are both detailed. A retrospective chart review of all known cases of idiopathic spinal cord herniation at the Cleveland Clinic over the last 15 yr was performed. Postoperative outcome scores (including the Japanese Orthopedic Association score, European Myelopathy score, and Nurick) were calculated preoperatively and postoperatively. A total of 5 patients were identified. Four of five patients improved clinically after surgery and 1 patient remained unchanged at last follow-up (average 23.2 mo, range 12-60 mo). There were no complications. All patients had postoperative magnetic resonance imaging demonstrating realignment of the spinal cord and no recurrence of tethering. A unilateral dorsolateral, transpedicular approach combined with laminectomy provides excellent exposure for ventral or ventrolateral dural defects associated with idiopathic spinal cord herniation and minimizes spinal cord manipulation. A collagen matrix graft used as an onlay between the spinal cord and ventral dural defect is a safe and effective option for ventral dural repair.

Factors Affecting the Severity of Neurological Disorders in Thoracic Idiopathic Spinal Cord Herniation.

Retrospective multicenter case-controlled study. The objective of this study was to quantitatively examine imaging findings of idiopathic spinal cord herniation (ISCH) and determine the relationship between the image findings and the severity of pre- and postoperative neurological symptoms. Many radiographic types of ISCH have been identified with regard to the location of the hernial opening or amount of herniated spinal cord. However, few previous studies have investigated the relationship between radiographic findings and the severity of neurological symptoms. Of 30,469 patients who underwent spinal surgery at 7 hospitals, 18 patients who underwent surgery for ISCH were identified. Their preoperative neurological severity, disease duration, magnetic resonance imaging findings, computed tomography myelography findings, surgical findings, and postoperative improvements were retrospectively examined. The spinal cord kink angle and minimum cord occupancy rate within the dural tube were measured. In addition, herniation was classified according to the location of the hiatus as either central (type C) or lateral (type L) type. A negative correlation was found between the spinal cord kink angle and the minimum cord occupancy rate. Patient age was significantly higher in the severe paralysis group than in the mild paralysis group. In addition, the number of patients with type C herniation and the kink angle were significantly higher in the severe paralysis group. The number of patients with type L herniation was higher in the significant recovery group than in the mild recovery group; however, the difference was not significant. Patients with a large spinal cord kink angle had a smaller spinal cord occupancy rate within the dural tube, and this resulted in severe preoperative conditions. Type C ISCH cases had a severe preoperative neurological deficit and poor postoperative neurological recovery, and the spinal cord in such cases might be damaged irreversibly. 4.

Clinical and Radiographical Differences Between Thoracic Idiopathic Spinal Cord Herniation and Spinal Arachnoid Cyst.

A retrospective, multicenter, case-controlled study. The aim of this study was to investigate the clinical and radiographical differences between thoracic idiopathic spinal cord herniation (ISCH) and spinal arachnoid cyst (SAC). ISCH and SAC are relatively rare diseases. Preoperative misdiagnose was frequently reported in both; however, these clinical and radiographical differences remain unclear. Of 30,469 patients who underwent spinal surgery, 18 (0.059%) and 22 (0.072%) patients were diagnosed as ISCH or SAC at nine hospitals, respectively, and their clinical and radiographical data were retrospectively evaluated. The spinal cord kink angle was measured on magnetic resonance or computed tomography myelography sagittal images; the kink angle was the exterior angle formed between the two tangents to the dorsal-side inflection points at the maximally affected level. There were no significant differences in age, gender, and duration of symptoms. Preoperative motor deficit was significantly higher (94.4%) and severer (manual muscle testing: 3.1 ± 1.1) in ISCH. Brown-Séquard syndrome was observed in 38.9% of ISCH, while no patients in SAC. In addition, leg sensory disorder and bladder rectal disorder were significantly more common in ISCH, while back pain was significantly frequent in SAC. With respect to radiographical findings, the length of disease (5.1 ± 2.7 levels) and altered cerebrospinal flow (CSF) (81.8%) in the lesion was significantly longer and more common in SAC. On the contrary, the kink angle was significantly greater in ISCH (54.0 ± 23.1°) than in SAC (14.1 ± 12.0°) (P < 0.001). The cut-off value of the kink angle to distinguish ISCH and SAC was 32.8°. Patients with ISCH commonly had severe preoperative neurological deficit, Brown-Séquard syndrome, and higher kink angle, while patients with SAC had back pain, longer length of disease, and altered CSF in the lesion. 4.

Mystery Case: Brown-Séquard syndrome caused by idiopathic spinal cord herniation.

A 48-year-old man developed numbness in the left leg, which progressed gradually to paresis and urinary incontinence. Neurologic examination revealed a left Brown-Sequard syndrome with leg paresis, mild spasticity, reduced proprioception, and contralateral thermal and painful hypoesthesia below T6. MRI revealed a thoracic spinal cord herniation (SCH) (figure). Idiopathic SCH is relatively rare. Pathogenesis involves a dura mater defect (see video on the Neurology ® Web site at [Neurology.org][1]); herniation develops over a progressive pressure gradient through the dural fissure.2 Surgical reduction is typically performed if symptoms progress, but mild symptoms may be eligible for conservative treatment and monitoring. Surgical spinal reduction and dural repair usually reverses neurologic deficits. [1]: http://neurology.org/lookup/doi/10.1212/WNL.0000000000002886

Surgical management of thoracic idiopathic spinal cord herniation. Technical case report and review

Idiopathic spinal cord herniation (ISCH) is a rare spinal disease, in which chronic cerebrospinal fluid pulsations push the arachnoid and adjacent thoracic spinal cord region through an antero-lateral dural defect of congenital, post-traumatic, or inflammatory/erosive origin. Symptomatic patients commonly present around the 5th decade of life with slowly progressive myelopathy. Diagnosis relies on high-resolution magnetic resonance imaging. Stable mild cases may be observed, whereas in progressive symptomatic situations, surgical spinal cord reposition and dural defect repair with a dural patch is the preferred treatment. We present a case of ISCH at T5/6 and a review the literature.

Spontaneous Anterior Thoracic Spinal Cord Herniation through Dura Defect: A Case Report.

Thoracic spinal cord herniation is a rare disease cause of progressive myelopathy. Magnetic resonance image is a useful tool to diagnose preoperatively. Operation is a treatment of option. Sixty-six-year-old female visited Dong-A University Medical Center for progressive gait disturbance with falling tendency to right side. She had radiating pain and tingling sense on both leg. Sense of touch and temperature was decreased below T6 level. Both hip and knee motor power were grade IV. Magnetic resonance imaging scan showed anterior displacement of the spinal cord at T4-T5 vertebral level. Under the diagnosis of thoracic spinal cord herniation with dura defect, operation was performed for the patient with intraoperative neuromonitoring. Laminectomy at T4 and T5 level was done, and intradural exploration of the spinal cord revealed dura defect about 25mm×8mm in size. Spinal cord was released under microscope and dura defect was repaired with Lyoplant. The patient's symptom improved after the surgical procedure, but touch and temperature sense under T6 level had unchanged.

Posterior Trans-Dural Repair of Iatrogenic Spinal Cord Herniation after Resection of Ossification of Posterior Longitudinal Ligament.

Iatrogenic spinal cord herniation is a rare complication following spinal surgery. We introduce a posterior trans-dural repair technique used in a case of thoracic spinal cord herniation through a ventral dural defect following resection of ossification of the posterior longitudinal ligament (OPLL) in the cervicothoracic spine. A 51-year-old female was suffering from paraplegia after laminectomy alone for cervicothoracic OPLL. Magnetic resonance imaging revealed a severely compressed spinal cord with pseudomeningocele identified postoperatively. Cerebrospinal fluid leak and iatrogenic spinal cord herniation persisted despite several operations with duroplasty and sealing agent. Finally, the problems were treated by repair of the ventral dural defect with posterior trans-dural duroplasty. Several months after surgery, the patient could walk independently. This surgical technique can be applied to treat ventral dural defect and spinal cord herniation.

Symptomatic thoracic spinal cord herniation: case series and technical report.

Idiopathic spinal cord herniation (ISCH) is an uncommon condition located predominantly in the thoracic spine and often associated with a remote history of a major traumatic injury. ISCH has an incompletely described presentation and unknown etiology. There is no consensus on the treatment algorithm and surgical technique, and there are few data on clinical outcomes. In this case series and technical report, we describe the atypical myelopathy presentation, remote history of traumatic injury, radiographic progression, treatment, and outcomes of 5 patients treated at Washington University for symptomatic ISCH. A video showing surgical repair is presented. In contrast to classic compressive myelopathy symptomatology, ISCH patients presented with an atypical myelopathy, characterized by asymmetric motor and sensory deficits and early-onset urinary incontinence. Clinical deterioration correlated with progressive spinal cord displacement and herniation observed on yearly spinal imaging in a patient imaged serially because of multiple sclerosis. Finally, compared with compressive myelopathy in the thoracic spine, surgical treatment of ISCH led to rapid improvement despite a long duration of symptoms. Symptomatic ISCH presents with atypical myelopathy and slow temporal progression and can be successfully managed with surgical repair.

A Rare Case of Anterior Transdural Thoracic Spinal Cord Herniation: Magnetic Resonance Imaging Features

Idiopathic transdural thoracic spinal cord herniation is a rare cause of thoracic myelopathy. The cord herniates or prolapses through an anterior or anterolateral defect of the dura mater. Magnetic resonance imaging is the gold standard investigation for this condition as the imaging features are diagnostic. We report on a patient with thoracic myelopathy due to idiopathic transdural thoracic spinal cord herniation. Radiologists should be able to recognise this condition as increased awareness may result in early diagnosis. To the authors’ knowledge, this is the first report of idiopathic transdural thoracic spinal cord herniation in Hong Kong.

Dorsal thoracic spinal cord herniation: report of an unusual case and review of the literature

Spinal cord herniation is a rare but well-documented condition that has been associated with tethering through the dural defect. Both spinal cord herniation and cord tethering result in progressive myelopathy that can be improved or stabilized with surgical intervention. Most cases of herniation are caused by dural defects in the ventral or ventrolateral thoracic spine, rarely occurring through the dorsal dura. This is the first reported case of a spontaneous dorsal herniation. To describe a unique case of thoracic tethered cord resulting from a dorsal dural defect through which there is spinal cord herniation. A case report and review of the literature. A 55-year-old man presented with progressive low back pain, paresthesias, and weakness in his left lower extremity that was exacerbated by walking. Imaging revealed a dorsal dural defect with tethering and herniation of the spinal cord at T7. The patient underwent a T6-T7 laminoplasty to release the tethered cord and repair the dural defect. At 1-year follow-up, the patient noted improvement in strength and back spasticity. Spinal cord herniation through a dural defect is an uncommon but important cause of symptomatic tethered cord in adults. Surgical intervention can significantly alter the course and prevent further disability.

Spinal cord herniation: management and outcome

Spinal cord herniation: management and outcome

Idiopathic Thoracic Spinal Cord Herniation: Retrospective Analysis Supporting a Mechanism of Diskogenic Dural Injury and Subsequent Tamponade: Fig 1.

tSCH in the absence of spinal trauma or surgery is a rare disorder for which numerous mechanisms have been proposed. Here, we have conducted an analysis of images in all published reports of idiopathic tSCH and identified evidence supporting a pathogenesis in which anterior dural erosion at thoracic levels generates a CSF leak that pushes adjacent spinal tissue to tamponade the dural defect, causing progressive myelopathy. Additionally, we describe a case of tSCH in which postural headache was a significant symptom before myelopathy. This finding suggests that tSCH pathogenesis may be related to spontaneous intracranial hypotension. Published imaging from all available prior case reports in the scientific literature was reviewed to determine whether tSCH occurred at the disk or bone level. The presence of EDF, HNP, or an osteophyte in the spinal canal was determined from review of published images. Additionally, 3 previously unreported cases from the teaching files of our department were assessed by using these criteria. In greater than two-thirds (47 of 67) of identified cases with published images, tSCH occurred at a disk level. When assessment was possible, EDF, HNP, and osteophytes were present in 26.8%, 30.7%, and 26.2% of cases, respectively. Overall, 52.3% of cases with published images demonstrated evidence of these abnormalities. Our analysis of published imaging indicates that tSCH occurs preferentially at spinal levels and with imaging findings consistent with dural injury that support the proposed etiology of this disorder.

The value of intraoperative motor evoked potential monitoring during surgical intervention for thoracic idiopathic spinal cord herniation

Thoracic idiopathic spinal cord herniation (TISCH) is a rare neurological disorder characterized by an incarceration of the spinal cord at the site of a ventral dural defect. The disorder is associated with clinical signs of progressive thoracic myelopathy. Surgery can withhold the natural clinical course, but surgical repair of the dural defect bears a significant risk of additional postoperative motor deficits, including permanent paraplegia. Intraoperative online information about the functional integrity of the spinal cord and warning signs about acute functional impairment of motor pathways could contribute to a lower risk of permanent postoperative motor deficit. Motor evoked potential (MEP) monitoring can instantly and reliably detect dysfunction of motor pathways in the spinal cord. The authors have applied MEPs during intraoperative neurophysiological monitoring (IOM) for surgical repair of TISCH and have correlated the results of IOM with its influence on the surgical procedure and with the functional postoperative outcome. The authors retrospectively reviewed the intraoperative neurophysiological data and clinical records of 4 patients who underwent surgical treatment for TISCH in 3 institutions where IOM, including somatosensory evoked potentials and MEPs, is routinely used for spinal cord surgery. In all 4 patients the spinal cord was reduced from a posterior approach and the dural defect was repaired using a dural graft. Motor evoked potential monitoring was feasible in all patients. Significant intraoperative changes of MEPs were observed in 2 patients. The changes were detected within seconds after manipulation of the spinal cord. Monitoring of MEPs led to immediate revision of the placement of the dural graft in one case and to temporary cessation of the release of the incarcerated spinal cord in the other. Changes occurred selectively in MEPs and were reversible. In both patients, transient changes in intraoperative MEPs correlated with a reversible postoperative motor deficit. Patients without significant changes in somatosensory evoked potentials and MEPs demonstrated no additional neurological deficit postoperatively and showed improvement of motor function during follow-up. Surgical repair of the dural defect is effected by release and reduction of the spinal cord and insertion of dural substitute over the dural defect. Careful monitoring of the functional integrity of spinal cord long tracts during surgical manipulation of the cord can detect surgically induced impairment. The authors' documentation of acute loss of MEPs that correlated with reversible postoperative motor deficit substantiates the necessity of IOM including continuous monitoring of MEPs for the surgical treatment of TISCH.

Superficial siderosis due to dural defect with thoracic spinal cord herniation

Superficial siderosis (SS) of the central nervous system is a rare disorder caused by chronic or recurrent hemorrhages into the subarachnoid space with hemosiderin and ferritin deposition, which leads to neuronal damage. The source of bleeding remains unknown in 50% of cases. Recently, attention has been focused on fluid-filled collection in the spinal canal, suggesting the presence of a dural defect which may be the bleeding point. We present a patient with SS and spinal extradural fluid collection due to midthoracic dural defect with spinal cord herniation. The reduction of the spinal cord herniation and the repair of the dural defect resulted in the disappearance of the fluid collection and cerebrospinal fluid abnormalities. The case here reported is, to our knowledge, the first case of spinal cord herniation presenting with SS and confirms the key role played by dural lacerations in the pathogenesis of both SS and spinal cord herniation. The search for dural lacerations should be one of the primary aims in patients with SS.

Thoracic spinal cord herniation in a patient with long-standing ankylosing spondylitis

The objective of this study was to describe an adult male patient with ankylosing spondylitis (AS) associated with thoracic spinal cord herniation (TSCH). TSCH is a scarce entity presented as a displacement of thoracic cord through an anterior or anterolateral dural defect. More importantly, the co-occurrence of AS and thoracic spinal cord herniation is exceptional. To date, only one case of SCH in association with AS has been reported in the literature. A 56-year-old male patient presented with the progressive difficulty in walking and numbness of both lower limbs for the past 18months. The patient was diagnosed as AS when he was 30years old. Sagittal MRI of thoracic spine showed dural defect of the posterior aspect of T11 and 12 vertebral bodies. Axial T2-weighted MRI demonstrated that spinal cord was displaced ventrally and to the right. The diagnosis of TSCH with AS was established. The prognosis was explained to the patient. We recommended duraplasty for dural repair to the patient, but he refused surgery. The results demonstrated that TSCH associated with long-standing AS was very uncommon, and MRI is recommended to rule out SCH in the long-standing AS patients with neurologic symptoms. The SCH in AS might be caused by inflammation, and thoracolumbar hyperkyphosis results from AS might be associated with the development of SCH.