Posttraumatic Syringomyelia and Spinal Cord Tethering

✓Myelopathy caused by a spinal cord infection is typically related to an adjacent compressive lesion such as an epidural abscess. The authors report a case of progressive high cervical myelopathy from spinal cord tethering caused by arachnoiditis related to an adjacent C-2 osteomyelitis. This 70-year-old woman initially presented with a methicillin-sensitive Staphylococcus aureus osteomyelitis involving the C-2 odontoid process. She was treated with appropriate antibiotic therapy but, over the course of 4 weeks, she developed progressive quadriparesis. A magnetic resonance image revealed near-complete resolution of the C-2 osteomyelitis, but new ventral tethering of the cord was observed at the level of the odontoid tip. She subsequently underwent open surgical decompression and cord detethering. Postoperatively she experienced improvement in her symptoms and deficits, which continued to improve 1 year after her surgery. To the authors’ knowledge, this is the first reported case of progressive upper cervical myelopathy due to arachnoiditis and cord tethering from an adjacent methicillin-sensitive S. aureus C-2 osteomyelitis.

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Posttraumatic spinal cord tethering and syringomyelia: surgical treatment and long-term outcome

Journal of Neurosurgery Spine ◽

10.3171/2009.4.spine09333 ◽

2009 ◽

Vol 11 (4) ◽

pp. 445-460 ◽

Cited By ~ 43

Author(s):

Scott P. Falci ◽

Charlotte Indeck ◽

Daniel P. Lammertse

Keyword(s):

Spinal Cord ◽

Spinal Injury ◽

Treatment Center ◽

Term Outcome ◽

Repeat Surgery ◽

Long Term Outcome ◽

Progressive Myelopathy ◽

Cord Injury ◽

Spinal Cord Tethering

Object Permanent neurological loss after spinal cord injury (SCI) is a well-known phenomenon. There has also been a growing recognition and improved understanding of the pathophysiological mechanisms of late progressive neurological loss, which may occur after SCI as a result of posttraumatic spinal cord tethering (SCT), myelomalacia, and syringomyelia. A clinical study of 404 patients sustaining traumatic SCIs and undergoing surgery to arrest a progressive myelopathy caused by SCT, with or without progressive myelomalacia and cystic cavitation (syringomyelia) was undertaken. Both objective and subjective long-term outcomes were evaluated. To the authors' knowledge, this is the first series of this size correlating long-term patient perception of outcome with long-term objective outcome analyses. Methods During the period from January 1993 to November 2003, 404 patients who had previously sustained traumatic SCIs underwent 468 surgeries for progressive myelopathies attributed to tethering of the spinal cord to the surrounding spinal canal, with or without myelomalacia and syrinx formation. Forty-two patients were excluded because of additional pathological entities that were known to contribute to a progressive myelopathy. All surgeries were performed by the same neurosurgeon at a single SCI treatment center and by using a consistent surgical technique of spinal cord detethering, expansion duraplasty, and when indicated, cyst shunting. Results Outcome data were collected up to 12 years postoperatively. Comparisons of pre- and postoperative American Spinal Injury Association sensory and motor index scores showed no significant change when only a single surgery was required (86% of patients). An outcome questionnaire and phone interview resulted in > 90% of patients self-assessing arrest of functional loss; > 50% of patients self-assessing improvement of function; 17 and 18% self-assessing improvement of motor and sensory functions to a point greater than that achieved at any time postinjury, respectively; 59% reporting improvement of spasticity; and 77% reporting improvement of hyperhidrosis. Conclusions Surgery for spinal cord detethering, expansion duraplasty, and when indicated, cyst shunting, is a successful treatment strategy for arresting a progressive myelopathy related to posttraumatic SCT and syringomyelia. Results suggest that surgery leads to functional return in ~ 50% of patients, and that in some patients posttraumatic SCT limits maximal recovery of spinal cord function postinjury. A patient's perception of surgery's failure to arrest the progressive myelopathy corresponds closely with the need for repeat surgery because of retethering, cyst reexpansion, and pseudomeningocele formation.

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2 Normal Spinal Cord Development and the Embryogenesis of Spinal Cord Tethering Malformations

Tethered Cord Syndrome in Children and Adults ◽

10.1055/b-0034-80500 ◽

2010 ◽

Keyword(s):

Spinal Cord ◽

Spinal Cord Development ◽

Spinal Cord Tethering

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Spinal development and spinal dysraphism

Oxford Textbook of Neurological Surgery ◽

10.1093/med/9780198746706.003.0085 ◽

2019 ◽

pp. 983-992

Author(s):

Dominic Thompson

Keyword(s):

Spinal Cord ◽

Spinal Dysraphism ◽

Radical Resection ◽

Management Plan ◽

Congenital Disorders ◽

Spinal Cord Development ◽

Precise Diagnosis ◽

Over Time ◽

Spinal Cord Tethering

The term spinal dysraphism encompasses a group of congenital disorders of spinal cord development. This potentially confusing array of conditions is best understood from an embryological perspective, and a unifying method of classification is presented. Spinal dysraphism is associated with neurological, urological, and orthopaedic deficits, these may be present at birth or may evolve over time due to the effects of spinal cord tethering. Precise diagnosis is essential to formulating an appropriate surgical management plan in order to optimize long-term neurological outcome. Contemporary and controversial surgical advances in the field are discussed including electrophysiology directed radical resection for spinal lipomas and antenatal surgery for myelomeningocele.

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Treatment of posttraumatic syringomyelia: evidence from a systematic review

Acta Neurochirurgica ◽

10.1007/s00701-020-04529-w ◽

2020 ◽

Vol 162 (10) ◽

pp. 2541-2556

Author(s):

Andrea Kleindienst ◽

Francisco Marin Laut ◽

Verena Roeckelein ◽

Michael Buchfelder ◽

Frank Dodoo-Schittko

Keyword(s):

Spinal Cord ◽

English Language ◽

Spinal Cord Injuries ◽

Case Reports ◽

Treatment Options ◽

Sensory Function ◽

Time Interval ◽

Eligibility Criteria ◽

Cord Injury ◽

Posttraumatic Syringomyelia

Abstract Background Following spinal cord injury (SCI), the routine use of magnetic resonance imaging (MRI) resulted in an incremental diagnosis of posttraumatic syringomyelia (PTS). However, facing four decades of preferred surgical treatment of PTS, no clear consensus on the recommended treatment exists. We review the literature on PTS regarding therapeutic strategies, outcomes, and complications. Methods We performed a systematic bibliographic search on (“spinal cord injuries” [Mesh] AND “syringomyelia” [Mesh]). English language literature published between 1980 and 2020 was gathered, and case reports and articles examining syrinx due to other causes were excluded. The type of study, interval injury to symptoms, severity and level of injury, therapeutic procedure, duration of follow-up, complications, and outcome were recorded. Results Forty-three observational studies including 1803 individuals met the eligibility criteria. The time interval from SCI to the diagnosis of PTS varied between 42 and 264 months. Eighty-nine percent of patients were treated surgically (n = 1605) with a complication rate of 26%. Symptoms improved in 43% of patients postoperatively and in 2% treated conservatively. Stable disease was documented in 50% of patients postoperatively and in 88% treated conservatively. The percentage of deterioration was similar (surgery 16%, 0.8% dead; conservative 10%). Detailed analysis of surgical outcome with regard to symptoms revealed that pain, motor, and sensory function could be improved in 43 to 55% of patients while motor function deteriorated in around 25%. The preferred methods of surgery were arachnoid lysis (48%) and syrinx drainage (31%). Conclusion Even diagnosing PTS early in its evolution with MRI, to date, no satisfactory standard treatment exists, and the present literature review shows similar outcomes, regardless of the treatment modality. Therefore, PTS remains a neurosurgical challenge. Additional research is required using appropriate study designs for improving treatment options.

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Role of the blood-spinal cord barrier in posttraumatic syringomyelia

Journal of Neurosurgery Spine ◽

10.3171/2009.6.spine08564 ◽

2009 ◽

Vol 11 (6) ◽

pp. 696-704 ◽

Cited By ~ 21

Author(s):

Sarah J. Hemley ◽

B. Biotech ◽

Jian Tu ◽

Marcus A. Stoodley

Keyword(s):

Spinal Cord ◽

Spinal Cord Injury ◽

Amino Acid ◽

Vascular Permeability ◽

Neurological Deficits ◽

Time Points ◽

Functional Integrity ◽

Cord Injury ◽

Posttraumatic Syringomyelia ◽

Blood Spinal Cord Barrier

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

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Association Between Symptomatic Giant Sacral Meningeal Diverticulum and Spinal Cord Tethering With Thickened Lipomatous Filum

Spine ◽

10.1097/brs.0b013e31820e4720 ◽

2011 ◽

Vol 36 (18) ◽

pp. E1230-E1232 ◽

Cited By ~ 2

Author(s):

Frank Feigenbaum ◽

Susan Hale

Keyword(s):

Spinal Cord ◽

Spinal Cord Tethering

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Microcystic spinal cord degeneration causing posttraumatic myelopathy

Journal of Neurosurgery ◽

10.3171/jns.1988.68.3.0466 ◽

1988 ◽

Vol 68 (3) ◽

pp. 466-471 ◽

Cited By ~ 32

Author(s):

Robert L. Macdonald ◽

J. Max Findlay ◽

Charles H. Tator

Keyword(s):

Spinal Cord ◽

Spinal Cord Injury ◽

Magnetic Resonance ◽

Magnetic Resonance Image ◽

Cervical Spinal Cord ◽

Content Type ◽

Progressive Myelopathy ◽

Cord Injury ◽

Posttraumatic Syringomyelia ◽

Bull's Eye

✓ Two cases of progressive myelopathy occurring years after incomplete cervical spinal cord injury are presented. In both patients, the clinical features, as well as the “bull's-eye” appearance of the delayed computerized tomography (CT) myelography study and the circumscribed low density of the magnetic resonance image, were consistent with posttraumatic syringomyelia, but surgical exploration including intraoperative spinal sonography failed to reveal a syrinx. Although arachnoiditis was present in both patients, the striking abnormality found at surgery was the softened appearance and the microcystic degeneration of the cord. The microcystic spinal cord degeneration found in these cases represents a previously undescribed cause of late deterioration after spinal cord injury that may mimic the clinical, CT-myelographic, and magnetic resonance features of posttraumatic syringomyelia.

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