Lumbar Synovial or Ganglion Cysts

Neurosurgery ◽  
1986 ◽  
Vol 19 (3) ◽  
pp. 415-420 ◽  
Author(s):  
Terrell D. Kjerulf ◽  
Daniel W. Terry ◽  
Richard J. Boubelik

Abstract Most reports regarding synovial cysts of the spinal canal have been presentations identifying an unusual pathological entity that is to be included in the differential diagnosis of cauda equina compression syndromes. Most of the 26 cases reported represent isolated examples of this pathological process. We present five cases of lumbar synovial cysts encountered in our practice in the past 8 years. Patients with lumbar synovial cysts do not demonstrate any predictable clinical picture. They may present with a unilateral sciatica or neurogenic claudication. Lumbar extension is usually restricted, whereas flexion is full. Mechanical signs of nerve root entrapment or lumbosacral plexus irritation are unimpressive. Neurological deficits are usually mild, if present. Radiological findings include degenerative spondylosis, spondylolisthesis, and a rounded posterolateral extradural mass of low attenuation value adjacent to a facet shown on computed tomographic scan. The etiology of lumbar synovial cysts is not known. Histological findings of myxoid degeneration, microcystic change, calcification, and hemosiderin deposits suggest that chronic microtrauma with occasional focal hemorrhage may play a major role in the etiology of the cysts. With resection of the cyst, the postoperative course is usually uneventful. Recurrences have not yet been encountered in our patients.

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Baasanjav Uranbileg ◽  
Nobuko Ito ◽  
Makoto Kurano ◽  
Daisuke Saigusa ◽  
Ritsumi Saito ◽  
...  

Abstract Cauda equina compression (CEC) is a major cause of neurogenic claudication and progresses to neuropathic pain (NP). A lipid mediator, lysophosphatidic acid (LPA), is known to induce NP via the LPA1 receptor. To know a possible mechanism of LPA production in neurogenic claudication, we determined the levels of LPA, lysophosphatidylcholine (LPC) and LPA-producing enzyme autotaxin (ATX), in the cerebrospinal fluid (CSF) and spinal cord (SC) using a CEC as a possible model of neurogenic claudication. Using silicon blocks within the lumbar epidural space, we developed a CEC model in rats with motor dysfunction. LPC and LPA levels in the CSF were significantly increased from day 1. Importantly, specific LPA species (16:0, 18:2, 20:4) were upregulated, which have been shown to produce by ATX detected in the CSF, without changes on its level. In SC, the LPC and LPA levels did not change, but mass spectrometry imaging analysis revealed that LPC was present in a region where the silicon blocks were inserted. These results propose a model for LPA production in SC and CSF upon neurogenic claudication that LPC produced locally by tissue damages is converted to LPA by ATX, which then leak out into the CSF.


Neurosurgery ◽  
1984 ◽  
Vol 14 (3) ◽  
pp. 287-294 ◽  
Author(s):  
L. Done Stephen ◽  
L. Hayman Anne ◽  
F. J. New Paul ◽  
R. Davis Kenneth ◽  
H. Chapman Paul

Abstract The purpose of this report is to call attention to the clinical, myelographic, and computed tomographic appearance of a very rare type of dural cyst within the lumbosacral spinal canal. We report this condition in three unrelated boys who presented with symptoms of cauda equina compression. Our experience suggests that these cysts are congenital in origin. Anatomically, the cyst wall consisted of a dura-like layer without arachnoid. There was a small ventral defect allowing incomplete communication with the compressed subarachnoid space. Cerebrospinal fluid-like fluid accumulated within the interdural cyst as a result of this communication. Treatment consisted of obliteration of the point of entry between cyst and subarachnoid space in all cases and partial cyst wall excision in one case. After operation, the two patients who had presented with long-standing sphincter disturbance had partial improvement in function and the child with a pain syndrome was completely relieved of symptoms.


1987 ◽  
Vol 66 (4) ◽  
pp. 614-617 ◽  
Author(s):  
Samuel Smith ◽  
Lyal G. Leibrock ◽  
Benjamin R. Gelber ◽  
Eric W. Pierson

✓ Three cases of acute disc herniation causing cauda equina compression syndrome after chemonucleolysis are described. All three patients had myelographic blocks and, despite emergency decompression procedures, were left with residual neurological deficits. Recommendations are made regarding evaluation and therapeutic intervention, and possible etiologies of this problem are reviewed.


2021 ◽  
Vol 12 ◽  
pp. 406
Author(s):  
Wakiko Saruta ◽  
Toshiyuki Takahashi ◽  
Toshihiro Kumabe ◽  
Manabu Minami ◽  
Ryo Kanematsu ◽  
...  

Background: There have been many reports on the clinical, radiographic, and surgical management of thoracolumbar burst fractures attributed to high-energy trauma. Interestingly, few reports have described how to extract bone fragments associated with these injuries protruding into the spinal canal contributing to significant neurological deficits. Methods: An 18-year-old male presented with a severe L3-level paraparesis (i.e., loss of motor/sensory function below L3 lower extremity hyporeflexia, and sphincter dysfunction: American Spinal Injury Association [ASIA] Impairment Scale B) following a high-speed crash. The computed tomography and magnetic resonance studies revealed a L3 burst fracture with bone fragments protruding into the spinal canal causing marked cauda equina compression. Following a L3-L4 laminectomy, and opening of the dorsal dura, the bone fragments were ventrally impacted into the fractured L3 vertebral body a pedicle/screw L1-L5 fusion was then completed. Results: One month later, the patient recovered to an ASIA Scale of C, (i.e., residual proximal 3/5 and distal 2/5 motor deficits, with partial sensory sparing). Conclusion: Transdural ventral impaction of protruded bone fragments attributed to high speed lumbar burst fractures contributing to significant cauda equina compression can be safely/effectively accomplished.


2021 ◽  
Vol 12 ◽  
pp. 7
Author(s):  
Abiodun Idowu Okunlola ◽  
Tesleem Olayinka Orewole ◽  
Cecilia Kehinde Okunlola ◽  
Olakunle Fatai Babalola ◽  
Akinola Akinmade

Background: The most common cause of cauda equina compression in the elderly is lumbar spinal stenosis. Epidural lipomatosis is an additional known but rare cause of cauda equina compression readily diagnosed on MR studies. Notably, spinal canal decompression and direct excision of the epidural fat effectively manage this combined pathology. Case Description: A 70-year-old male presented with progressive truncal obesity associated with refractory lumbar neurogenic claudication. The lumbar magnetic resonance imaging (MRI) showed excessive epidural fat extending from L4 to S2 resulting in thecal sac compression; this was confirmed on the MRI myelogram study. Following a decompressive laminectomy, the patient’s cauda equina syndrome resolved. Conclusion: Recent weight gain with increased neurogenic claudication and the onset of a cauda equina syndrome may herald the presence of significant lumbar epidural lipomatosis. Here, laminectomy for excision of the excessive epidural fat resolved the patient’s symptomatic spinal stenosis.


1989 ◽  
Vol 70 (4) ◽  
pp. 514-518 ◽  
Author(s):  
Benjamin H. Venger ◽  
Richard K. Simpson ◽  
Raj K. Narayan

✓ Associated injuries to the neck, chest, or abdomen are found in approximately one-quarter of all civilians with penetrating spinal cord or cauda equina injuries. While the value of and indications for general surgical exploration and repair of these injuries are fairly self-evident, the value of neurosurgical intervention in terms of neurological outcome and infection prophylaxis remains the subject of debate. To study this issue, 160 civilian patients with penetrating spinal injuries and neurological deficits were retrospectively reviewed. Associated injuries of the esophagus, trachea, bronchi, or bowel were seen in 107 individuals (67%); 33 (31%) of these patients had abdominal injuries, 25 (23%) had neck injuries, 23 (21%) had thoracic injuries, and 26 (24%) had injuries occurring at multiple sites. Of these 107 patients, 67 (63%) had complete neurological injuries and the remaining 40 (37%) demonstrated incomplete deficits. All 107 patients underwent surgical exploration and repair of their visceral injuries; in 19 of them a neurosurgical procedure was also performed for decompression of the neural elements and/or debridement of the wound. Regardless of the presence of associated visceral injuries, the mechanism of injury, and the extent of the neurological deficit, no statistically significant difference in neurological outcome was found in patients with or without neurosurgical intervention. Complications associated with neurological injury were reported in 17 (11%) of the total group of 160 patients. Four (21%) of the 19 patients who had neurosurgical intervention suffered a related complication, compared to only six (7%) of the 88 patients who were managed conservatively (p < 0.05). Within the limitations of a retrospective review, the results of this study do not clearly support the value of routine neurosurgical intervention as an adjunct to general surgical repair in cases of spinal injury associated with penetrating visceral trauma.


1997 ◽  
Vol 79-B (4) ◽  
pp. 670-674 ◽  
Author(s):  
F. E. Sayegh ◽  
G. A. Kapetanos ◽  
P. P. Symeonides ◽  
G. Anogiannakis ◽  
M. Madentzidis

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