Proposed caudal appendage classification system; spinal cord tethering associated with sacrococcygeal eversion

2016 ◽  
Vol 33 (1) ◽  
pp. 69-89 ◽  
Author(s):  
C. Corbett Wilkinson ◽  
Arianne J Boylan
2021 ◽  
pp. bmjmilitary-2021-001931
Author(s):  
Daniel Llewellyn Mills ◽  
O O'Sullivan ◽  
E Sellon ◽  
S Dharm-Datta

2007 ◽  
Vol 6 (1) ◽  
pp. 64-67 ◽  
Author(s):  
Sharad Rajpal ◽  
Krisada Chanbusarakum ◽  
Praveen R. Deshmukh

✓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.


2009 ◽  
Vol 11 (4) ◽  
pp. 445-460 ◽  
Author(s):  
Scott P. Falci ◽  
Charlotte Indeck ◽  
Daniel P. Lammertse

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.


Author(s):  
Dominic Thompson

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.


2002 ◽  
Vol 347 (4) ◽  
pp. 256-259 ◽  
Author(s):  
Catherine A. Mazzola ◽  
A. Leland Albright ◽  
Leslie N. Sutton ◽  
Gerald F. Tuite ◽  
Ronald L. Hamilton ◽  
...  

2000 ◽  
Vol 8 (3) ◽  
pp. 1-6 ◽  
Author(s):  
Thomas H. Milhorat

Syringomyelia poses special challenges for the clinician because of its complex symptomatology, uncertain pathogenesis, and multiple options of treatment. The purpose of this study was to classify intramedullary cavities according to their most salient pathological and clinical features. Pathological findings obtained in 175 individuals with tubular cavitations of the spinal cord were correlated with clinical and magnetic resonance (MR) imaging findings in a database of 927 patients. A classification system was developed in which the morbid anatomy, cause, and pathogenesis of these lesions are emphasized. The use of a disease-based classification of syringomyelia facilitates diagnosis and the interpretation of MR imaging findings and provides a guide to treatment.


2002 ◽  
Vol 96 (2) ◽  
pp. 145-156 ◽  
Author(s):  
Robert F. Spetzler ◽  
Paul W. Detwiler ◽  
Howard A. Riina ◽  
Randall W. Porter

The literature on spinal vascular malformations contains a great deal of confusing terminology. Some of the nomenclature is inconsistent with the lesions described. Based on the experience of the senior author (R.F.S.) in the treatment of more than 130 spinal cord vascular lesions and based on a thorough review of the relevant literature, the authors propose a modified classification system for spinal cord vascular lesions. Lesions are divided into three primary or broad categories: neoplasms, aneurysms, and arteriovenous lesions. Neoplastic vascular lesions include hemangioblastomas and cavernous malformations, both of which occur sporadically and familially. The second category consists of spinal aneurysms, which are rare. The third category, spinal cord arteriovenous lesions, is divided into arteriovenous fistulas and arteriovenous malformations (AVMs). Arteriovenous fistulas are subdivided into those that are extradural and those that are intradural, with intradural lesions categorized as either dorsal or ventral. Arteriovenous malformations are subdivided into extradural-intradural and intradural malformations. Intradural lesions are further divided into intramedullary, intramedullary-extramedullary, and conus medullaris, a new category of AVM. This modified classification system for vascular lesions of the spinal cord, based on pathophysiology, neuroimaging features, intraoperative observations, and neuroanatomy, offers several advantages. First, it includes all surgical vascular lesions that affect the spinal cord. Second, it guides treatment by classifying lesions based on location and pathophysiology. Finally, it eliminates the confusion produced by the multitude of unrelated nomenclatural terms found in the literature.


2005 ◽  
Vol 102 (3) ◽  
pp. 311-313 ◽  
Author(s):  
John Sherman Cole ◽  
Thomas Pittman

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