CASE REPORT CASE REPORT
Surgical Management of a Patient With Thoracic Spinal Cord Herniation: Case Report Eduardo Martinez-delCampo, MD Karam Moon, MD Samuel Kalb, MD Hector Soriano-Baron, MD Nicholas Theodore, MD Division of Neurological Surgery, Barrow Neurological Institute, St. Joseph’s Hospital and Medical Center, Phoenix, Arizona Correspondence: Nicholas Theodore, MD, FACS, c/o Neuroscience Publications, Barrow Neurological Institute, St. Joseph’s Hospital and Medical Center, 350 W Thomas Rd, Phoenix, AZ 85013. E-mail: [email protected] Received, March 20, 2015. Accepted, June 4, 2015. Published Online, June 24, 2015. Copyright © 2015 by the Congress of Neurological Surgeons.
BACKGROUND AND IMPORTANCE: Thoracic spinal cord herniation (TSCH) is rare and likely underdiagnosed. It is characterized by ventral herniation of the spinal cord through a dural defect, effacement of the anterior subarachnoid space, and increased posterior subarachnoid space. We present here a case of TSCH diagnosed and surgically treated at Barrow Neurological Institute, along with supplemental intraoperative video. CLINICAL PRESENTATION: A 61-year-old man with a history of progressive myelopathy causing left lower-extremity weakness with associated numbness, impaired gait, foot drop, incontinence, and sexual impotence was referred without any previous treatment. Computed tomographic myelography and magnetic resonance imaging of the thoracic spine showed ventral spinal cord herniation at T3-T4. Neurological monitoring was recorded preoperatively and intraoperatively. The patient underwent leftsided posterolateral exploration via T3-T4 laminectomies and costotransversectomy for intradural cord release/detethering of the spinal cord with additional superior and inferior extension and repair of the dural defect. Arthrodesis was not considered necessary. After cord release, motor evoked potentials showed immediate improvement from baseline. Dural duplication was considered the cause of TSCH in this case. Total reduction of herniation was evident in postoperative images. The postoperative course was uneventful, and at the last follow-up, the patient had regained ambulation and sphincter control. CONCLUSION: Anterior displacement of the thoracic spinal cord should elicit consideration of herniation to prevent misdiagnosis and inadequate surgery. Surgical cord release and enlargement of the dural defect are safe and associated with good clinical outcomes. KEY WORDS: Anterior, Cord, Herniation, Idiopathic, Spinal, Thoracic Neurosurgery 77:E492–E499, 2015
DOI: 10.1227/NEU.0000000000000860
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horacic spinal cord herniation (TSCH) is a very rare disease, with only about 175 cases reported in the literature in the past 40 years. It was first described by Wortzman et al1 in 1974, who noted the condition while performing a thoracotomy for a herniated thoracic disk. Most described cases were published after 1990, after the advent of WHAT IS THIS BOX? A QR Code is a matrix barcode readable by QR scanners, mobile phones with cameras, and smartphones. The QR Code above links to Supplemental Digital Content from this article.
ABBREVIATIONS: mJOA, modified Japanese Orthopedic Association; TSCH, thoracic spinal cord herniation Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal’s Web site (www.neurosurgery-online.com).
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magnetic resonance imaging. The disease is characterized by a ventral herniation of the spinal cord through a dural defect anywhere in the thoracic spine, usually with a bayonetshaped deformity and expansion of the posterior subarachnoid space. The cause of this disease remains unknown, although it is believed to be congenital or traumatic.2-8 TSCH usually manifests in patients .50 years of age as gradual myelopathy and BrownSéquard syndrome, although some patients may remain asymptomatic.3,4,7,9 This report presents an illustrative case of TSCH treated at Barrow Neurological Institute in 2014, together with diagnostic imaging, intraoperative microscopic video, and follow-up, with
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a discussion of the most recent literature regarding the diagnosis and management of this rare and relatively underdiagnosed pathology.
CLINICAL PRESENTATION A 61-year-old man with a medical history of rheumatic fever, hypertension, hypercholesterolemia, diabetes mellitus, and class I obesity (body mass index = 34.5 kg/m2), without a history of trauma or congenital disease, was referred from an outside hospital as a result of progressive left leg weakness and left foot drop, gait imbalance, bowel/bladder incontinence, and sexual impotence during the previous 6 months. He had not received any treatment before referral. His symptoms became significantly worse during the 2 months before his referral to our center. On physical examination, the patient had full strength in both upper and the right lower extremities and 2/5 throughout the left lower extremity with associated numbness. Gait was shuffling, myelopathic, and significantly impaired by numbness and
weakness. Myelopathy was evaluated with the modified Japanese Orthopedic Association (mJOA) scale; the patient scored 10 of 18 points preoperatively (5 of 5 for upper-extremity motor dysfunction, 2 of 7 for lower-extremity motor dysfunction, 2 of 3 for sensation, and 1 of 3 for sphincter dysfunction). Computed tomographic myelography (Figure 1) and magnetic resonance imaging (Figure 2) of the thoracic spine revealed leftsided tethering of the spinal cord anterolaterally at the T3-4 disk space and an increase in subarachnoid space, without a dorsal cerebrospinal fluid filling defect. The diagnosis of an anterior TSCH, rather than transdural disk herniation or another more insidious process, was made. The spine was marked preoperatively with metal fiducials at the area of interest, and somatosensory evoked potentials and motor evoked potentials were monitored before and during surgery. The patient underwent posterolateral exploration via T3-T4 laminectomies. A T3-T4 costotransversectomy was performed on the left side with a transpedicular approach and intradural exploration under the microscope. The spinal cord was detethered,
FIGURE 1. A, midsagittal computed tomographic myelogram shows anterior displacement of the spinal cord without cerebrospinal fluid flow defect at the T3-4 intervertebral disk space. B and C, axial images show anterior displacement and herniation of the spinal cord through a probable dural defect without evidence of a posterior arachnoid cyst. Used with permission from Barrow Neurological Institute, Phoenix, Arizona.
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FIGURE 2. A, midsagittal magnetic resonance (MR) image shows anterior displacement and a C-shaped kink of the spinal cord, with effacement of the anterior subarachnoid space and increased posterior subarachnoid space at T3-T4. B and C, axial images show anterolateral displacement and herniation of the spinal cord to the left (predominantly in C). Notice that cord herniation or protrusion seen on computed tomography images (Figure 1) is not evident at T3-T4 in any MR image. Used with permission from Barrow Neurological Institute, Phoenix, Arizona.
and a 1- to 2-mm superior and inferior extension of the dural defect was made (Figure 3), with appropriately sized packing of the ventral defect with DuraGen (Integra LifeSciences Co, Plainsboro, New Jersey). At this point, both motor evoked potentials and somatosensory evoked potentials showed an immediate improvement from baseline. The disk space at T3-4 had autofused, and arthrodesis was not considered necessary at that time. Dural duplication was considered to be the cause of TSCH after meticulous review of intraoperative microscopic imaging (Video, Supplemental Digital Content, http://links. lww.com/NEU/A741). Magnetic resonance imaging performed at 7 months postoperatively provided evidence of total reduction without recurrence of the herniated defect, with no evidence of tethering, and with a centrally located spinal cord (Figure 4). Clinical outcome was evaluated with the Benzel mJOA scale, and percent improvement was calculated with the following formula: [(postoperative mJOA score 2 preoperative mJOA score)/preoperative mJOA score] · 100. In the immediate postoperative period,
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strength was regained to 3/5 proximally and 4/5 distally in the left lower extremity. The rest of the postoperative course was uneventful, and the patient was discharged on postoperative day 3. One week after surgery, the patient had no sensory deficit, had regained additional motor function in his left leg, was bladder/bowel continent, and was ambulating with a walker with mild surgicalsite pain under adequate control. The mJOA score at this time was 15 of 18 points. Thus, the patient had an improvement in mJOA score of 5 points, with an improvement of 50%. At the 7-month follow-up, the patient’s mild persistent weakness was gradually improving with physiotherapy. We will continue to follow the patient in the future.
DISCUSSION Pathogenesis and Pathophysiology Spinal cord herniations outside the thoracic spine have been reported in only 7 cases, secondary to surgical procedures.10
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The pathophysiology of TSCH has been proposed to be related to the direct contact between the spinal cord and a pre-existing dural defect in the thoracic spine, leading to the formation of arachnoid adhesions over time. Initially, the cerebrospinal fluid moves unrestrictedly in and out of the defect with each pulsation. The negative pressure in the thoracic extradural space, together with variations in force and amplitude in cerebrospinal fluid pulsations during each heartbeat (ball-valve effect), leads to herniation of an arachnoid membrane, which in turn results in wedging and widening of the dural defect. Eventually, the defect becomes blocked by the spinal cord, which is pulled out by the aforementioned mechanisms into the epidural space. It remains unclear whether the spinal cord herniates into a duplicated or evaginated dural pouch or into the extradural space; however, most authors tend to favor dural duplication.3,4,14 Presenting Symptoms Brown-Séquard syndrome is the most common clinical presentation in idiopathic cases (66%), manifesting as a result of herniation of the lateral spinothalamic tracts. This causes altered pain and temperature sensation, often unilateral and ascending, which might progress to involvement of the corticospinal tracts, with gradual progressive weakness and spasticity. Other presentations include spastic paraparesis in 30% of the patients, tethered cord syndrome, and pure sensory or motor symptoms.3,4,7,9,13,15 Our patient presented with progressive myelopathy.
FIGURE 3. Intraoperative microscopic images of a T3-T4 intradural exploration via left costotransversectomy. The spinal cord was detethered with (A) rostral and (B) caudal dissection, showing the (C) anterior dural defect, with 1to 2-mm superior and inferior extension. Used with permission from Barrow Neurological Institute, Phoenix, Arizona.
Idiopathic or anterior TSCH occurs predominantly between T2 and T8. Several authors have tried to elucidate the pathogenesis and pathophysiology of TSCH, implicating the thoracic spine normal kyphosis and the ventral position of the spinal cord at this region. Congenital causes include dural defects and duplications, ventral dural meningocele, and congenital extradural arachnoid cysts. Other probable causes of TSCH include disk extrusion resulting in shearing and weakening of dural fibers, a posterior arachnoid cyst compressing the spinal cord anteriorly, repeated microtrauma, ischemia, and inflammatory processes. However, in most cases, TSCH is idiopathic.1-4,6,7,11-13
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Imaging In patients with TSCH, T2-weighted sagittal magnetic resonance imaging of the spinal cord provides evidence of a 1- to 3-cm narrowing of the spinal cord with thinning and focal disappearance of the anterior subarachnoid spaces and concomitant posterior enlargement. Some sequences might show spinal cord invagination and focal amputation of cerebrospinal fluid at the point of cord entrapment. Anterolateral tethering is more frequently seen to the left (61.5%) than to the right. A C- or S-shaped kink on sagittal imaging might be considered a pathognomonic finding.2-4,6,7,9,16 In 2009, Imagama et al6 classified TSCH into type K (ventral spinal kinking), type P (protrusion of ventral aspect of the cord, fully effacing the anterior subarachnoid space), and type D (spinal cord disappears at herniated site). They found a duplicated dura in 92% of the cases, without additional evidence of inflammation in any of their patients. TSCH protrusion into the disk space has been reported to range from 67% to 70% of patients compared with 30% with protrusion into the vertebral body, without mention of an additional disk herniation.3,6 It is important to differentiate between TSCH and posterior arachnoid cysts (Figure 5). Misdiagnosis of TSCH was reported in 21% of cases (37 of 174) in a systematic review by Summers et al,8 leading to wrong surgery in 62% (23 of 37) of the misdiagnosed patients. The most common misinterpretation was
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FIGURE 4. Postoperative imaging performed at 7 months. A, midsagittal and (B) axial magnetic resonance images show postoperative changes at T3-T4 without evidence of herniation, recurrence, or tethering of the spinal cord. Used with permission from Barrow Neurological Institute, Phoenix, Arizona.
posterior arachnoid cyst, representing 45% of false diagnoses. However, an association with posterior arachnoid cysts of 20% to 73% has been found in previous reports, although in some cases such an association might not be present. Phase-contrast magnetic resonance imaging and computed tomographic mye-
lography are recommended to assess cerebrospinal fluid flow posterior to the spinal cord to exclude a diagnosis of a cystic lesion. Additionally, axial magnetic resonance imaging allows visualization of the nerve roots traversing the dorsal subarachnoid space in cases of TSCH, in contrast to cases of posterior
FIGURE 5. A, midsagittal magnetic resonance image of a posterior arachnoid cyst in the thoracic spine. Notice the preservation of the anterior subarachnoid space and the spinal roots surrounding the arachnoid cyst posteriorly. B, an axial cut at the dashed line shown in A. The spinal cord is anteriorly displaced and severely compressed; however, the anterior subarachnoid space is patent, and no spinal cord herniation is evident. Used with permission from Barrow Neurological Institute, Phoenix, Arizona.
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arachnoid cysts in which the nerve roots are seen at the periphery of the cyst. Other diseases that may cause space-occupying intradural lesions that could be confused with TSCH include epidermoid cysts, spinal abscesses, thoracic disk herniations, transverse myelitis, arachnoiditis, intradural mass, and extradural compressive lesions.2-4,8,15,17 Differential diagnoses of TSCH and disk herniation were considered in our patient, and the definite diagnosis of TSCH was based on surgical findings. Surgical Management Most authors advocate surgical treatment for patients with TSCH (91.4%, 159 of 174 cases reported in the literature), although 15 cases of TSCH (8.6%) were reported to be treated conservatively. Although the authors state that nonsurgical patients had unchanged neurological status at the last follow-up (33 months; range, 1-96 months),8 Prada et al18 reported that 3 of their patients who were initially treated conservatively had worsening neurological symptoms that prompted surgical intervention. The goals of surgery are to release the strangulated spinal cord, to restore normal intradural position, and to prevent the recurrence of herniation in order to stop—and ideally reverse— neurological deterioration. Somatosensory evoked potentials are often unchanged because the anterior spinal tracts are predominantly affected by the herniation and might be affected in type D TSCH. Our patient showed immediately improved motor evoked potentials after cord release/detethering. Conservative management should be tried initially in patients without deficits or progressive myelopathy because clinical presentation might be nonspecific and neurological deterioration may not occur. Posterior instrumentation is usually not required. Most cases require a single-level approach without significant destabilization of the thoracic spine; however, each case should be evaluated individually.3,6-8,13 Most frequently, surgical procedures include detethering of the spinal cord via posterolateral approaches with laminectomy, costotransversectomy, and lateral durotomy to provide direct anterior visualization and less manipulation of the spinal cord compared with purely posterior approaches. A posterior approach is less ideal than a posterolateral approach because with the former it is necessary to rotate the spinal cord posterolaterally to reduce the herniation and to expose the dural defect after the dentate ligaments are cut. A right vs left approach should be decided on the basis of the location of the defect and symptomatology of the patient. Although long-term follow-up studies are very scarce,19,20 recurrence has been reported, and different techniques have been described to prevent them. An actual recurrence rate has not been calculated in any of the large systematic reviews or meta-analyses.3,8,13 Anterior dural patching with fascia and pericardium, suturing, and grafting with glue have been recommended to prevent recurrences. However, some dural defects may be very large, requiring extensive manipulation of the spinal cord, and thus it may not be technically feasible to create a dural patch, which adds a potentially avoidable neurovascular risk to the procedure. On the other hand, widening or extending the ventral dural defect by resection of the dural ring
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around the cord is associated with higher rates of neurological improvement and prevention of future reherniation while being less technically demanding than anterior dural patching. Recurrence may be attributed to incomplete cord release, reherniation, inadequate widening of the ventral dural defect, or induction of arachnoid scarring by graft material.3,4,7-9,13,21 Clinical Outcomes In several case reports and small series, 20% of patients with TSCH remain unchanged, and 7% to 10% worsen with conservative management.3-5,8,9,13 In a systematic review of 174 patients from 2013 and a meta-analysis of 126 patients from 2009, Summers et al8 and Groen et al3 found clinical improvement rates ranging from 73% to 85%. They found that spinal cord release was most strongly associated with improved motor function postoperatively (75%) compared with those without cord release (45.5%) and that patients with widening of the dural defect had statistically significantly better outcomes (81.8% improved and 18.5% were unchanged/worsened) than those with anterior dural patch (64.3% improved and 35.7% were unchanged/worsened). Of clinical importance, patients with Brown-Séquard syndrome, patients with TSCH at T3-T4 or T8-T9, and those with evidence of dural duplication had a statistically significant improvement in motor function after surgery compared with patients with paraparesis, TSCH at different levels, or evidence of a posterior arachnoid cyst at surgery. Patients with lesions found between T5 and T7 usually have unfavorable outcomes as a result of ischemia arising from watershed zones in the midthoracic areas. Good clinical outcomes, defined as unchanged or improved symptoms, are reported to range from 86% to 93% of surgically treated patients.3,4,9 Our patient presented with T3-T4 TSCH and had satisfactory cord release/detethering and repair of the dural defect. Clinical outcomes reported in the TSCH literature are generally categorized as improved, unchanged, or worse,8 and only 2 series have used standardized outcome scores. Nakamura et al20 reported their experience with 16 patients with a mean follow-up of 9.6 years. Clinical outcomes were reported preoperatively and postoperatively with mean JOA scores of 5.3 and 7.4 points, respectively (full score, 11 points), and the mean recovery rate was 29.4%. Imagama et al6 reported 12 patients with preoperative and postoperative mean JOA scores of 5.3 and 8.1 points, respectively, and a mean recovery rate of 34.5%. Similarly, our patient had an increase of 5 points in mJOA score, with an improvement of 50%. Complications Complication rates have not been reported in most publications, including the large systematic reviews and meta-analyses.3,8,18 A review of 51 patients from case reports and series,4,6,7,13,14,16,19,20,22-31 including our own, resulted in a calculated complication rate of 7.8% (4 of 50), including 1 patient with evidence of meningocele in postoperative imaging requiring external lumbar drainage and another patient with neurological deterioration, both of whom required revision
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surgery (3.9%). One case (1.9%) of spasticity in the immediate postoperative period resulting from spinal cord biopsy was reported, as was 1 patient (1.9%) with superficial wound infection 1 week after surgery. Limitations This is a case report with short follow-up and a review of the literature using information dating from 1974 to 2014. Results presented in this article may not be reproducible in different clinical or radiological scenarios. Important metrics such as followup period length and complication rates were not detailed in all of the studies. Data in retrospective studies require mining, and inconsistencies are present because all of the information to be studied may not be readily available across studies.
CONCLUSION Despite advanced imaging technologies, TSCH remains a very rare and underdiagnosed spinal pathology, even in high-volume tertiary referral institutions such as our own. Although BrownSéquard syndrome is the initial presentation of more than twothirds of the patients with TSCH, thoracic myelopathy and isolated motor or sensory deficits should raise concerns that lead to further diagnostic imaging studies. Whenever an anterior displacement of the spinal cord is evident in the thoracic spine, high suspicion for TSCH should prevent misdiagnosis and inadequate surgical procedures. Surgical cord release and enlargement of the dural defect are associated with good clinical outcomes with acceptable complication rates. Disclosure The authors have no personal, financial, or institutional interest in any of the drugs, materials, or devices described in this article.
REFERENCES 1. Wortzman G, Tasker RR, Rewcastle NB, Richardson JC, Pearson FG. Spontaneous incarcerated herniation of the spinal cord into a vertebral body: a unique cause of paraplegia: case report. J Neurosurg. 1974;41(5):631-635. 2. Cosnard G. Tips and traps in spinal cord pathology. Diagn Interv Imaging. 2012; 93(12):975-984. 3. Groen RJ, Middel B, Meilof JF, et al. Operative treatment of anterior thoracic spinal cord herniation: three new cases and an individual patient data meta-analysis of 126 case reports. Neurosurgery. 2009;64(3 suppl):ons145-ons159; discussion ons159-ons160. 4. Gwinn R, Henderson F. Transdural herniation of the thoracic spinal cord: untethering via a posterolateral transpedicular approach: report of three cases. J Neurosurg Spine. 2004;1(2):223-227. 5. Hassler W, Al-Kahlout E, Schick U. Spontaneous herniation of the spinal cord: operative technique and follow-up in 10 cases. J Neurosurg Spine. 2008;9(5):438-443. 6. Imagama S, Matsuyama Y, Sakai Y, et al. Image classification of idiopathic spinal cord herniation based on symptom severity and surgical outcome: a multicenter study. J Neurosurg Spine. 2009;11(3):310-319. 7. Kasliwal MK, O’Toole JE, Deutsch H. Unilateral paramedian transpedicular approach for repair of anterior transdural spinal cord herniation: report of a case and literature review. Asian Spine J. 2012;6(1):55-59. 8. Summers JC, Balasubramani YV, Chan PC, Rosenfeld JV. Idiopathic spinal cord herniation: clinical review and report of three cases. Asian J Neurosurg. 2013;8(2): 97-105. 9. Marshman LA, Hardwidge C, Ford-Dunn SC, Olney JS. Idiopathic spinal cord herniation: case report and review of the literature. Neurosurgery. 1999;44(5):1129-1133.
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10. Iencean SM, Poeata I. Late postoperative cervical spinal cord herniation. Spine J. 2014;14(5):856-857. 11. Hausmann ON, Moseley IF. Idiopathic dural herniation of the thoracic spinal cord. Neuroradiology. 1996;38(6):503-510. 12. Quencer RM. Transdural spinal cord herniation: acquired or developmental? AJNR Am J Neuroradiol. 1998;19(7):1185. 13. Sasani M, Ozer AF, Vural M, Sarioglu AC. Idiopathic spinal cord herniation: case report and review of the literature. J Spinal Cord Med. 2009;32(1):86-94. 14. Kumar R, Taha J, Greiner AL. Herniation of the spinal cord: case report. J Neurosurg. 1995;82(1):131-136. 15. Haber MD, Nguyen DD, Li S. Differentiation of idiopathic spinal cord herniation from CSF-isointense intraspinal extramedullary lesions displacing the cord. Radiographics. 2014;34(2):313-329. 16. Massicotte EM, Montanera W, Ross Fleming JF, et al. Idiopathic spinal cord herniation: report of eight cases and review of the literature. Spine (Phila Pa 1976). 2002;27(9):E233-E241. 17. Barrenechea IJ, Lesser JB, Gidekel AL, Turjanski L, Perin NI. Diagnosis and treatment of spinal cord herniation: a combined experience. J Neurosurg Spine. 2006;5(4):294-302. 18. Prada F, Saladino A, Giombini S, et al. Spinal cord herniation: management and outcome in a series of 12 consecutive patients and review of the literature. Acta Neurochir (Wien). 2012;154(4):723-730. 19. Selviaridis P, Balogiannis I, Foroglou N, Hatzisotiriou A, Patsalas I. Spontaneous spinal cord herniation: recurrence after 10 years. Spine J. 2009;9(3):e17-e19. 20. Nakamura M, Fujiyoshi K, Tsuji O, et al. Long-term surgical outcomes of idiopathic spinal cord herniation. J Orthop Sci. 2011;16(4):347-351. 21. Shin JH, Krishnaney AA. Idiopathic ventral spinal cord herniation: a rare presentation of tethered cord. Neurosurg Focus. 2010;29(1):E10. 22. Arts MP, Lycklama a Nijeholt G, Wurzer JA. Surgical treatment of idiopathic transdural spinal cord herniation: a new technique to untether the spinal cord. Acta Neurochir (Wien). 2006;148(9):1005-1009. 23. Aydin AL, Sasani M, Erhan B, Sasani H, Ozcan S, Ozer AF. Idiopathic spinal cord herniation at two separate zones of the thoracic spine: the first reported case and literature review. Spine J. 2011;11(8):e9-e14. 24. Brugieres P, Malapert D, Adle-Biassette H, Fuerxer F, Djindjian M, Gaston A. Idiopathic spinal cord herniation: value of MR phase-contrast imaging. AJNR Am J Neuroradiol. 1999;20(5):935-939. 25. Chaichana KL, Sciubba DM, Li KW, Gokaslan ZL. Surgical management of thoracic spinal cord herniation: technical consideration. J Spinal Disord Tech. 2009;22(1):67-72. 26. Ellger T, Schul C, Heindel W, Evers S, Ringelstein EB. Idiopathic spinal cord herniation causing progressive Brown-Séquard syndrome. Clin Neurol Neurosurg. 2006;108(4):388-391. 27. Haque A, Morgan H. Thoracic transdural spinal cord herniation at a level caudal to prior discectomy. Acta Neurochir (Wien). 2010;152(11):1985-1989. 28. Karadeniz-Bilgili MY, Castillo M, Bernard E. Transdural spinal cord herniation: pre- and postoperative MRI findings. Clin Imaging. 2005;29(4):288-290. 29. Spissu A, Peltz MT, Matta G, Cannas A. Traumatic transdural spinal cord herniation and the nuclear trail sign: case report. Neurol Sci. 2004;25(3):151-153. 30. Tekkok IH. Spontaneous spinal cord herniation: case report and review of the literature. Neurosurgery. 2000;46(2):485-491; discussion 491-482. 31. Vallee B, Mercier P, Menei P, et al. Ventral transdural herniation of the thoracic spinal cord: surgical treatment in four cases and review of literature. Acta Neurochir (Wien). 1999;141(9):907-913.
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COMMENTS
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he authors present a case report of a surgically managed patient with thoracic spinal cord herniation and a review of the corresponding literature. Thoracic spinal cord herniation is a relatively rare entity, and when it occurs, the diagnosis may not be readily apparent. Cursory review of a thoracic magnetic resonance imaging may not demonstrate the anticipated evidence of direct spinal cord compression; instead, a detailed
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review may be required to detect the more subtle appearance of a spinal cord herniation. As illustrated in this case report, the neurological findings of this condition may be significant, and appreciating the diagnosis and providing appropriate and timely treatment are important. Effective surgical management of this condition can be challenging. The accompanying video of the surgical technique used by the authors is outstanding. This report is a useful reminder to the spine community of the diagnosis of thoracic spinal cord herniation and provides an excellent description and video presentation of its surgical management.
he authors report their experience in the management of a patient with spinal cord herniation at T3-T4. Spinal cord herniation is a rare entity, which, because of its rarity, can be mistaken for a dorsal arachnoid cyst. This is an exceptional case report, with excellent illustrations and video. What is new in this report is the authors’ use of a more lateral approach via costotransversectomy and the use of 1- to 2-mm rostral and caudal extension of the dural defect to help mobilize the cord from its point of herniation. I commend the authors for this outstanding contribution to the literature.
Justin S. Smith Charlottesville, Virginia
Craig H. Rabb Oklahoma City, Oklahoma
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Surgical Management of a Patient With Thoracic Spinal Cord Herniation: Case Report Eduardo Martinez-delCampo, MD Karam Moon, MD Samuel Kalb, MD Hector Soriano-Baron, MD Nicholas Theodore, MD Division of Neurological Surgery, Barrow Neurological Institute, St. Joseph’s Hospital and Medical Center, Phoenix, Arizona Correspondence: Nicholas Theodore, MD, FACS, c/o Neuroscience Publications, Barrow Neurological Institute, St. Joseph’s Hospital and Medical Center, 350 W Thomas Rd, Phoenix, AZ 85013. E-mail: [email protected] Received, March 20, 2015. Accepted, June 4, 2015. Published Online, June 24, 2015. Copyright © 2015 by the Congress of Neurological Surgeons.
BACKGROUND AND IMPORTANCE: Thoracic spinal cord herniation (TSCH) is rare and likely underdiagnosed. It is characterized by ventral herniation of the spinal cord through a dural defect, effacement of the anterior subarachnoid space, and increased posterior subarachnoid space. We present here a case of TSCH diagnosed and surgically treated at Barrow Neurological Institute, along with supplemental intraoperative video. CLINICAL PRESENTATION: A 61-year-old man with a history of progressive myelopathy causing left lower-extremity weakness with associated numbness, impaired gait, foot drop, incontinence, and sexual impotence was referred without any previous treatment. Computed tomographic myelography and magnetic resonance imaging of the thoracic spine showed ventral spinal cord herniation at T3-T4. Neurological monitoring was recorded preoperatively and intraoperatively. The patient underwent leftsided posterolateral exploration via T3-T4 laminectomies and costotransversectomy for intradural cord release/detethering of the spinal cord with additional superior and inferior extension and repair of the dural defect. Arthrodesis was not considered necessary. After cord release, motor evoked potentials showed immediate improvement from baseline. Dural duplication was considered the cause of TSCH in this case. Total reduction of herniation was evident in postoperative images. The postoperative course was uneventful, and at the last follow-up, the patient had regained ambulation and sphincter control. CONCLUSION: Anterior displacement of the thoracic spinal cord should elicit consideration of herniation to prevent misdiagnosis and inadequate surgery. Surgical cord release and enlargement of the dural defect are safe and associated with good clinical outcomes. KEY WORDS: Anterior, Cord, Herniation, Idiopathic, Spinal, Thoracic Neurosurgery 77:E492–E499, 2015
DOI: 10.1227/NEU.0000000000000860
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horacic spinal cord herniation (TSCH) is a very rare disease, with only about 175 cases reported in the literature in the past 40 years. It was first described by Wortzman et al1 in 1974, who noted the condition while performing a thoracotomy for a herniated thoracic disk. Most described cases were published after 1990, after the advent of WHAT IS THIS BOX? A QR Code is a matrix barcode readable by QR scanners, mobile phones with cameras, and smartphones. The QR Code above links to Supplemental Digital Content from this article.
ABBREVIATIONS: mJOA, modified Japanese Orthopedic Association; TSCH, thoracic spinal cord herniation Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal’s Web site (www.neurosurgery-online.com).
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magnetic resonance imaging. The disease is characterized by a ventral herniation of the spinal cord through a dural defect anywhere in the thoracic spine, usually with a bayonetshaped deformity and expansion of the posterior subarachnoid space. The cause of this disease remains unknown, although it is believed to be congenital or traumatic.2-8 TSCH usually manifests in patients .50 years of age as gradual myelopathy and BrownSéquard syndrome, although some patients may remain asymptomatic.3,4,7,9 This report presents an illustrative case of TSCH treated at Barrow Neurological Institute in 2014, together with diagnostic imaging, intraoperative microscopic video, and follow-up, with
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a discussion of the most recent literature regarding the diagnosis and management of this rare and relatively underdiagnosed pathology.
CLINICAL PRESENTATION A 61-year-old man with a medical history of rheumatic fever, hypertension, hypercholesterolemia, diabetes mellitus, and class I obesity (body mass index = 34.5 kg/m2), without a history of trauma or congenital disease, was referred from an outside hospital as a result of progressive left leg weakness and left foot drop, gait imbalance, bowel/bladder incontinence, and sexual impotence during the previous 6 months. He had not received any treatment before referral. His symptoms became significantly worse during the 2 months before his referral to our center. On physical examination, the patient had full strength in both upper and the right lower extremities and 2/5 throughout the left lower extremity with associated numbness. Gait was shuffling, myelopathic, and significantly impaired by numbness and
weakness. Myelopathy was evaluated with the modified Japanese Orthopedic Association (mJOA) scale; the patient scored 10 of 18 points preoperatively (5 of 5 for upper-extremity motor dysfunction, 2 of 7 for lower-extremity motor dysfunction, 2 of 3 for sensation, and 1 of 3 for sphincter dysfunction). Computed tomographic myelography (Figure 1) and magnetic resonance imaging (Figure 2) of the thoracic spine revealed leftsided tethering of the spinal cord anterolaterally at the T3-4 disk space and an increase in subarachnoid space, without a dorsal cerebrospinal fluid filling defect. The diagnosis of an anterior TSCH, rather than transdural disk herniation or another more insidious process, was made. The spine was marked preoperatively with metal fiducials at the area of interest, and somatosensory evoked potentials and motor evoked potentials were monitored before and during surgery. The patient underwent posterolateral exploration via T3-T4 laminectomies. A T3-T4 costotransversectomy was performed on the left side with a transpedicular approach and intradural exploration under the microscope. The spinal cord was detethered,
FIGURE 1. A, midsagittal computed tomographic myelogram shows anterior displacement of the spinal cord without cerebrospinal fluid flow defect at the T3-4 intervertebral disk space. B and C, axial images show anterior displacement and herniation of the spinal cord through a probable dural defect without evidence of a posterior arachnoid cyst. Used with permission from Barrow Neurological Institute, Phoenix, Arizona.
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FIGURE 2. A, midsagittal magnetic resonance (MR) image shows anterior displacement and a C-shaped kink of the spinal cord, with effacement of the anterior subarachnoid space and increased posterior subarachnoid space at T3-T4. B and C, axial images show anterolateral displacement and herniation of the spinal cord to the left (predominantly in C). Notice that cord herniation or protrusion seen on computed tomography images (Figure 1) is not evident at T3-T4 in any MR image. Used with permission from Barrow Neurological Institute, Phoenix, Arizona.
and a 1- to 2-mm superior and inferior extension of the dural defect was made (Figure 3), with appropriately sized packing of the ventral defect with DuraGen (Integra LifeSciences Co, Plainsboro, New Jersey). At this point, both motor evoked potentials and somatosensory evoked potentials showed an immediate improvement from baseline. The disk space at T3-4 had autofused, and arthrodesis was not considered necessary at that time. Dural duplication was considered to be the cause of TSCH after meticulous review of intraoperative microscopic imaging (Video, Supplemental Digital Content, http://links. lww.com/NEU/A741). Magnetic resonance imaging performed at 7 months postoperatively provided evidence of total reduction without recurrence of the herniated defect, with no evidence of tethering, and with a centrally located spinal cord (Figure 4). Clinical outcome was evaluated with the Benzel mJOA scale, and percent improvement was calculated with the following formula: [(postoperative mJOA score 2 preoperative mJOA score)/preoperative mJOA score] · 100. In the immediate postoperative period,
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strength was regained to 3/5 proximally and 4/5 distally in the left lower extremity. The rest of the postoperative course was uneventful, and the patient was discharged on postoperative day 3. One week after surgery, the patient had no sensory deficit, had regained additional motor function in his left leg, was bladder/bowel continent, and was ambulating with a walker with mild surgicalsite pain under adequate control. The mJOA score at this time was 15 of 18 points. Thus, the patient had an improvement in mJOA score of 5 points, with an improvement of 50%. At the 7-month follow-up, the patient’s mild persistent weakness was gradually improving with physiotherapy. We will continue to follow the patient in the future.
DISCUSSION Pathogenesis and Pathophysiology Spinal cord herniations outside the thoracic spine have been reported in only 7 cases, secondary to surgical procedures.10
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The pathophysiology of TSCH has been proposed to be related to the direct contact between the spinal cord and a pre-existing dural defect in the thoracic spine, leading to the formation of arachnoid adhesions over time. Initially, the cerebrospinal fluid moves unrestrictedly in and out of the defect with each pulsation. The negative pressure in the thoracic extradural space, together with variations in force and amplitude in cerebrospinal fluid pulsations during each heartbeat (ball-valve effect), leads to herniation of an arachnoid membrane, which in turn results in wedging and widening of the dural defect. Eventually, the defect becomes blocked by the spinal cord, which is pulled out by the aforementioned mechanisms into the epidural space. It remains unclear whether the spinal cord herniates into a duplicated or evaginated dural pouch or into the extradural space; however, most authors tend to favor dural duplication.3,4,14 Presenting Symptoms Brown-Séquard syndrome is the most common clinical presentation in idiopathic cases (66%), manifesting as a result of herniation of the lateral spinothalamic tracts. This causes altered pain and temperature sensation, often unilateral and ascending, which might progress to involvement of the corticospinal tracts, with gradual progressive weakness and spasticity. Other presentations include spastic paraparesis in 30% of the patients, tethered cord syndrome, and pure sensory or motor symptoms.3,4,7,9,13,15 Our patient presented with progressive myelopathy.
FIGURE 3. Intraoperative microscopic images of a T3-T4 intradural exploration via left costotransversectomy. The spinal cord was detethered with (A) rostral and (B) caudal dissection, showing the (C) anterior dural defect, with 1to 2-mm superior and inferior extension. Used with permission from Barrow Neurological Institute, Phoenix, Arizona.
Idiopathic or anterior TSCH occurs predominantly between T2 and T8. Several authors have tried to elucidate the pathogenesis and pathophysiology of TSCH, implicating the thoracic spine normal kyphosis and the ventral position of the spinal cord at this region. Congenital causes include dural defects and duplications, ventral dural meningocele, and congenital extradural arachnoid cysts. Other probable causes of TSCH include disk extrusion resulting in shearing and weakening of dural fibers, a posterior arachnoid cyst compressing the spinal cord anteriorly, repeated microtrauma, ischemia, and inflammatory processes. However, in most cases, TSCH is idiopathic.1-4,6,7,11-13
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Imaging In patients with TSCH, T2-weighted sagittal magnetic resonance imaging of the spinal cord provides evidence of a 1- to 3-cm narrowing of the spinal cord with thinning and focal disappearance of the anterior subarachnoid spaces and concomitant posterior enlargement. Some sequences might show spinal cord invagination and focal amputation of cerebrospinal fluid at the point of cord entrapment. Anterolateral tethering is more frequently seen to the left (61.5%) than to the right. A C- or S-shaped kink on sagittal imaging might be considered a pathognomonic finding.2-4,6,7,9,16 In 2009, Imagama et al6 classified TSCH into type K (ventral spinal kinking), type P (protrusion of ventral aspect of the cord, fully effacing the anterior subarachnoid space), and type D (spinal cord disappears at herniated site). They found a duplicated dura in 92% of the cases, without additional evidence of inflammation in any of their patients. TSCH protrusion into the disk space has been reported to range from 67% to 70% of patients compared with 30% with protrusion into the vertebral body, without mention of an additional disk herniation.3,6 It is important to differentiate between TSCH and posterior arachnoid cysts (Figure 5). Misdiagnosis of TSCH was reported in 21% of cases (37 of 174) in a systematic review by Summers et al,8 leading to wrong surgery in 62% (23 of 37) of the misdiagnosed patients. The most common misinterpretation was
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FIGURE 4. Postoperative imaging performed at 7 months. A, midsagittal and (B) axial magnetic resonance images show postoperative changes at T3-T4 without evidence of herniation, recurrence, or tethering of the spinal cord. Used with permission from Barrow Neurological Institute, Phoenix, Arizona.
posterior arachnoid cyst, representing 45% of false diagnoses. However, an association with posterior arachnoid cysts of 20% to 73% has been found in previous reports, although in some cases such an association might not be present. Phase-contrast magnetic resonance imaging and computed tomographic mye-
lography are recommended to assess cerebrospinal fluid flow posterior to the spinal cord to exclude a diagnosis of a cystic lesion. Additionally, axial magnetic resonance imaging allows visualization of the nerve roots traversing the dorsal subarachnoid space in cases of TSCH, in contrast to cases of posterior
FIGURE 5. A, midsagittal magnetic resonance image of a posterior arachnoid cyst in the thoracic spine. Notice the preservation of the anterior subarachnoid space and the spinal roots surrounding the arachnoid cyst posteriorly. B, an axial cut at the dashed line shown in A. The spinal cord is anteriorly displaced and severely compressed; however, the anterior subarachnoid space is patent, and no spinal cord herniation is evident. Used with permission from Barrow Neurological Institute, Phoenix, Arizona.
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arachnoid cysts in which the nerve roots are seen at the periphery of the cyst. Other diseases that may cause space-occupying intradural lesions that could be confused with TSCH include epidermoid cysts, spinal abscesses, thoracic disk herniations, transverse myelitis, arachnoiditis, intradural mass, and extradural compressive lesions.2-4,8,15,17 Differential diagnoses of TSCH and disk herniation were considered in our patient, and the definite diagnosis of TSCH was based on surgical findings. Surgical Management Most authors advocate surgical treatment for patients with TSCH (91.4%, 159 of 174 cases reported in the literature), although 15 cases of TSCH (8.6%) were reported to be treated conservatively. Although the authors state that nonsurgical patients had unchanged neurological status at the last follow-up (33 months; range, 1-96 months),8 Prada et al18 reported that 3 of their patients who were initially treated conservatively had worsening neurological symptoms that prompted surgical intervention. The goals of surgery are to release the strangulated spinal cord, to restore normal intradural position, and to prevent the recurrence of herniation in order to stop—and ideally reverse— neurological deterioration. Somatosensory evoked potentials are often unchanged because the anterior spinal tracts are predominantly affected by the herniation and might be affected in type D TSCH. Our patient showed immediately improved motor evoked potentials after cord release/detethering. Conservative management should be tried initially in patients without deficits or progressive myelopathy because clinical presentation might be nonspecific and neurological deterioration may not occur. Posterior instrumentation is usually not required. Most cases require a single-level approach without significant destabilization of the thoracic spine; however, each case should be evaluated individually.3,6-8,13 Most frequently, surgical procedures include detethering of the spinal cord via posterolateral approaches with laminectomy, costotransversectomy, and lateral durotomy to provide direct anterior visualization and less manipulation of the spinal cord compared with purely posterior approaches. A posterior approach is less ideal than a posterolateral approach because with the former it is necessary to rotate the spinal cord posterolaterally to reduce the herniation and to expose the dural defect after the dentate ligaments are cut. A right vs left approach should be decided on the basis of the location of the defect and symptomatology of the patient. Although long-term follow-up studies are very scarce,19,20 recurrence has been reported, and different techniques have been described to prevent them. An actual recurrence rate has not been calculated in any of the large systematic reviews or meta-analyses.3,8,13 Anterior dural patching with fascia and pericardium, suturing, and grafting with glue have been recommended to prevent recurrences. However, some dural defects may be very large, requiring extensive manipulation of the spinal cord, and thus it may not be technically feasible to create a dural patch, which adds a potentially avoidable neurovascular risk to the procedure. On the other hand, widening or extending the ventral dural defect by resection of the dural ring
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around the cord is associated with higher rates of neurological improvement and prevention of future reherniation while being less technically demanding than anterior dural patching. Recurrence may be attributed to incomplete cord release, reherniation, inadequate widening of the ventral dural defect, or induction of arachnoid scarring by graft material.3,4,7-9,13,21 Clinical Outcomes In several case reports and small series, 20% of patients with TSCH remain unchanged, and 7% to 10% worsen with conservative management.3-5,8,9,13 In a systematic review of 174 patients from 2013 and a meta-analysis of 126 patients from 2009, Summers et al8 and Groen et al3 found clinical improvement rates ranging from 73% to 85%. They found that spinal cord release was most strongly associated with improved motor function postoperatively (75%) compared with those without cord release (45.5%) and that patients with widening of the dural defect had statistically significantly better outcomes (81.8% improved and 18.5% were unchanged/worsened) than those with anterior dural patch (64.3% improved and 35.7% were unchanged/worsened). Of clinical importance, patients with Brown-Séquard syndrome, patients with TSCH at T3-T4 or T8-T9, and those with evidence of dural duplication had a statistically significant improvement in motor function after surgery compared with patients with paraparesis, TSCH at different levels, or evidence of a posterior arachnoid cyst at surgery. Patients with lesions found between T5 and T7 usually have unfavorable outcomes as a result of ischemia arising from watershed zones in the midthoracic areas. Good clinical outcomes, defined as unchanged or improved symptoms, are reported to range from 86% to 93% of surgically treated patients.3,4,9 Our patient presented with T3-T4 TSCH and had satisfactory cord release/detethering and repair of the dural defect. Clinical outcomes reported in the TSCH literature are generally categorized as improved, unchanged, or worse,8 and only 2 series have used standardized outcome scores. Nakamura et al20 reported their experience with 16 patients with a mean follow-up of 9.6 years. Clinical outcomes were reported preoperatively and postoperatively with mean JOA scores of 5.3 and 7.4 points, respectively (full score, 11 points), and the mean recovery rate was 29.4%. Imagama et al6 reported 12 patients with preoperative and postoperative mean JOA scores of 5.3 and 8.1 points, respectively, and a mean recovery rate of 34.5%. Similarly, our patient had an increase of 5 points in mJOA score, with an improvement of 50%. Complications Complication rates have not been reported in most publications, including the large systematic reviews and meta-analyses.3,8,18 A review of 51 patients from case reports and series,4,6,7,13,14,16,19,20,22-31 including our own, resulted in a calculated complication rate of 7.8% (4 of 50), including 1 patient with evidence of meningocele in postoperative imaging requiring external lumbar drainage and another patient with neurological deterioration, both of whom required revision
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surgery (3.9%). One case (1.9%) of spasticity in the immediate postoperative period resulting from spinal cord biopsy was reported, as was 1 patient (1.9%) with superficial wound infection 1 week after surgery. Limitations This is a case report with short follow-up and a review of the literature using information dating from 1974 to 2014. Results presented in this article may not be reproducible in different clinical or radiological scenarios. Important metrics such as followup period length and complication rates were not detailed in all of the studies. Data in retrospective studies require mining, and inconsistencies are present because all of the information to be studied may not be readily available across studies.
CONCLUSION Despite advanced imaging technologies, TSCH remains a very rare and underdiagnosed spinal pathology, even in high-volume tertiary referral institutions such as our own. Although BrownSéquard syndrome is the initial presentation of more than twothirds of the patients with TSCH, thoracic myelopathy and isolated motor or sensory deficits should raise concerns that lead to further diagnostic imaging studies. Whenever an anterior displacement of the spinal cord is evident in the thoracic spine, high suspicion for TSCH should prevent misdiagnosis and inadequate surgical procedures. Surgical cord release and enlargement of the dural defect are associated with good clinical outcomes with acceptable complication rates. Disclosure The authors have no personal, financial, or institutional interest in any of the drugs, materials, or devices described in this article.
REFERENCES 1. Wortzman G, Tasker RR, Rewcastle NB, Richardson JC, Pearson FG. Spontaneous incarcerated herniation of the spinal cord into a vertebral body: a unique cause of paraplegia: case report. J Neurosurg. 1974;41(5):631-635. 2. Cosnard G. Tips and traps in spinal cord pathology. Diagn Interv Imaging. 2012; 93(12):975-984. 3. Groen RJ, Middel B, Meilof JF, et al. Operative treatment of anterior thoracic spinal cord herniation: three new cases and an individual patient data meta-analysis of 126 case reports. Neurosurgery. 2009;64(3 suppl):ons145-ons159; discussion ons159-ons160. 4. Gwinn R, Henderson F. Transdural herniation of the thoracic spinal cord: untethering via a posterolateral transpedicular approach: report of three cases. J Neurosurg Spine. 2004;1(2):223-227. 5. Hassler W, Al-Kahlout E, Schick U. Spontaneous herniation of the spinal cord: operative technique and follow-up in 10 cases. J Neurosurg Spine. 2008;9(5):438-443. 6. Imagama S, Matsuyama Y, Sakai Y, et al. Image classification of idiopathic spinal cord herniation based on symptom severity and surgical outcome: a multicenter study. J Neurosurg Spine. 2009;11(3):310-319. 7. Kasliwal MK, O’Toole JE, Deutsch H. Unilateral paramedian transpedicular approach for repair of anterior transdural spinal cord herniation: report of a case and literature review. Asian Spine J. 2012;6(1):55-59. 8. Summers JC, Balasubramani YV, Chan PC, Rosenfeld JV. Idiopathic spinal cord herniation: clinical review and report of three cases. Asian J Neurosurg. 2013;8(2): 97-105. 9. Marshman LA, Hardwidge C, Ford-Dunn SC, Olney JS. Idiopathic spinal cord herniation: case report and review of the literature. Neurosurgery. 1999;44(5):1129-1133.
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10. Iencean SM, Poeata I. Late postoperative cervical spinal cord herniation. Spine J. 2014;14(5):856-857. 11. Hausmann ON, Moseley IF. Idiopathic dural herniation of the thoracic spinal cord. Neuroradiology. 1996;38(6):503-510. 12. Quencer RM. Transdural spinal cord herniation: acquired or developmental? AJNR Am J Neuroradiol. 1998;19(7):1185. 13. Sasani M, Ozer AF, Vural M, Sarioglu AC. Idiopathic spinal cord herniation: case report and review of the literature. J Spinal Cord Med. 2009;32(1):86-94. 14. Kumar R, Taha J, Greiner AL. Herniation of the spinal cord: case report. J Neurosurg. 1995;82(1):131-136. 15. Haber MD, Nguyen DD, Li S. Differentiation of idiopathic spinal cord herniation from CSF-isointense intraspinal extramedullary lesions displacing the cord. Radiographics. 2014;34(2):313-329. 16. Massicotte EM, Montanera W, Ross Fleming JF, et al. Idiopathic spinal cord herniation: report of eight cases and review of the literature. Spine (Phila Pa 1976). 2002;27(9):E233-E241. 17. Barrenechea IJ, Lesser JB, Gidekel AL, Turjanski L, Perin NI. Diagnosis and treatment of spinal cord herniation: a combined experience. J Neurosurg Spine. 2006;5(4):294-302. 18. Prada F, Saladino A, Giombini S, et al. Spinal cord herniation: management and outcome in a series of 12 consecutive patients and review of the literature. Acta Neurochir (Wien). 2012;154(4):723-730. 19. Selviaridis P, Balogiannis I, Foroglou N, Hatzisotiriou A, Patsalas I. Spontaneous spinal cord herniation: recurrence after 10 years. Spine J. 2009;9(3):e17-e19. 20. Nakamura M, Fujiyoshi K, Tsuji O, et al. Long-term surgical outcomes of idiopathic spinal cord herniation. J Orthop Sci. 2011;16(4):347-351. 21. Shin JH, Krishnaney AA. Idiopathic ventral spinal cord herniation: a rare presentation of tethered cord. Neurosurg Focus. 2010;29(1):E10. 22. Arts MP, Lycklama a Nijeholt G, Wurzer JA. Surgical treatment of idiopathic transdural spinal cord herniation: a new technique to untether the spinal cord. Acta Neurochir (Wien). 2006;148(9):1005-1009. 23. Aydin AL, Sasani M, Erhan B, Sasani H, Ozcan S, Ozer AF. Idiopathic spinal cord herniation at two separate zones of the thoracic spine: the first reported case and literature review. Spine J. 2011;11(8):e9-e14. 24. Brugieres P, Malapert D, Adle-Biassette H, Fuerxer F, Djindjian M, Gaston A. Idiopathic spinal cord herniation: value of MR phase-contrast imaging. AJNR Am J Neuroradiol. 1999;20(5):935-939. 25. Chaichana KL, Sciubba DM, Li KW, Gokaslan ZL. Surgical management of thoracic spinal cord herniation: technical consideration. J Spinal Disord Tech. 2009;22(1):67-72. 26. Ellger T, Schul C, Heindel W, Evers S, Ringelstein EB. Idiopathic spinal cord herniation causing progressive Brown-Séquard syndrome. Clin Neurol Neurosurg. 2006;108(4):388-391. 27. Haque A, Morgan H. Thoracic transdural spinal cord herniation at a level caudal to prior discectomy. Acta Neurochir (Wien). 2010;152(11):1985-1989. 28. Karadeniz-Bilgili MY, Castillo M, Bernard E. Transdural spinal cord herniation: pre- and postoperative MRI findings. Clin Imaging. 2005;29(4):288-290. 29. Spissu A, Peltz MT, Matta G, Cannas A. Traumatic transdural spinal cord herniation and the nuclear trail sign: case report. Neurol Sci. 2004;25(3):151-153. 30. Tekkok IH. Spontaneous spinal cord herniation: case report and review of the literature. Neurosurgery. 2000;46(2):485-491; discussion 491-482. 31. Vallee B, Mercier P, Menei P, et al. Ventral transdural herniation of the thoracic spinal cord: surgical treatment in four cases and review of literature. Acta Neurochir (Wien). 1999;141(9):907-913.
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COMMENTS
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he authors present a case report of a surgically managed patient with thoracic spinal cord herniation and a review of the corresponding literature. Thoracic spinal cord herniation is a relatively rare entity, and when it occurs, the diagnosis may not be readily apparent. Cursory review of a thoracic magnetic resonance imaging may not demonstrate the anticipated evidence of direct spinal cord compression; instead, a detailed
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T
review may be required to detect the more subtle appearance of a spinal cord herniation. As illustrated in this case report, the neurological findings of this condition may be significant, and appreciating the diagnosis and providing appropriate and timely treatment are important. Effective surgical management of this condition can be challenging. The accompanying video of the surgical technique used by the authors is outstanding. This report is a useful reminder to the spine community of the diagnosis of thoracic spinal cord herniation and provides an excellent description and video presentation of its surgical management.
he authors report their experience in the management of a patient with spinal cord herniation at T3-T4. Spinal cord herniation is a rare entity, which, because of its rarity, can be mistaken for a dorsal arachnoid cyst. This is an exceptional case report, with excellent illustrations and video. What is new in this report is the authors’ use of a more lateral approach via costotransversectomy and the use of 1- to 2-mm rostral and caudal extension of the dural defect to help mobilize the cord from its point of herniation. I commend the authors for this outstanding contribution to the literature.
Justin S. Smith Charlottesville, Virginia
Craig H. Rabb Oklahoma City, Oklahoma
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