scholarly journals Cauda equina schwannoma presenting with subarachnoid and subdural hemorrhage: Its underlying mechanism

2021 ◽  
Vol 12 ◽  
pp. 462
Author(s):  
Keitaro Shiraishi ◽  
Takahiro Tomita ◽  
Takuya Akai ◽  
Satoshi Kuroda

Background: A patient presented with a spinal subarachnoid hemorrhage (SAH) and subdural hematoma (SDH) attributed to a spinal schwannoma at the T12-L1 level. Case Description: A 67-year-old male acutely presented with severe back pain and L1 paraparesis/sensory loss, with urinary incontinence. CT/MR studies showed a spinal SAH and SDH within a likely T12-L1 schwannoma. At surgery, the hemorrhage within the tumor was continuous through the lower pole of the tumor into the subarachnoid and subdural spaces; tumor was dissected away from the surrounding tissues and totally removed. The postoperative course was uneventful, and the preoperative neurological deficits gradually resolved. Histopathologically, the lesion was a schwannoma with intratumoral hemorrhage. Conclusion: This case demonstrates the rare acute presentation of a T12-L1 schwannoma with an accompanying intratumoral hemorrhage resulting in both a SDH/SAH.

2009 ◽  
Vol 49 (6) ◽  
pp. 255-257 ◽  
Author(s):  
Tsutomu ICHINOSE ◽  
Toshihiro TAKAMI ◽  
Naoki YAMAMOTO ◽  
Naohiro TSUYUGUCHI ◽  
Kenji OHATA

1984 ◽  
Vol 61 (5) ◽  
pp. 975-980 ◽  
Author(s):  
Karl W. Swann ◽  
Allan H. Ropper ◽  
Paul F. J. New ◽  
Charles E. Poletti

✓ Two patients with spontaneous spinal subarachnoid hemorrhage are presented to emphasize the clinical and radiological features of this uncommon illness. Both had severe back pain at the onset. One patient had a subdural hematoma that compressed the conus medullaris and cauda equina, and was drained percutaneously; the other had clots in the subarachnoid space. The cerebrospinal fluid showed a polymorphonuclear pleocytosis that simulated septic meningitis. Complete spinal angiography failed to reveal a cause for the hemorrhages.


Neurosurgery ◽  
1987 ◽  
Vol 20 (2) ◽  
pp. 281-285 ◽  
Author(s):  
Edward C. Benzel ◽  
Theresa A. Hadden ◽  
James Edward Coleman

Abstract We evaluated 42 patients with neurological deficits after civilian gunshot wounds to the spine. Thirty-five of these patients (the study population presented here) received their initial and follow-up care at Louisiana State University Medical Center in Shreveport over a 4-year period. Each patient had incurred a single gunshot wound to the spinal cord or cauda equina with an accompanying neurological deficit. The patient population was divided into three groups. Group 1 patients had incurred a complete motor and sensory loss below the injury (20 patients (57%)). Group 2 patients had incurred incomplete spinal cord injuries (9 patients (26%)), whereas Group 3 patients had cauda equina injuries (6 patients (17%)). Myelography was performed for all Group 2 and 3 patients as well as Group 1 patients in whom the trajectory of the bullet did not explain a higher level of neurological injury (3 patients (15%)). A decompressive operation was performed in the patients whose myelography showed neural compression. Three patients in Group 1 (15%), 5 patients in Group 2 (56%), and 5 Group 3 patients (83%) underwent operation. All 3 Group 1 patients who underwent operation had some improvement of nerve root function postoperatively. All operated Group 2 and 3 patients had improvement of myelopathic or radicular function postoperatively. All began improving within several days of operation, implying a cause and effect relationship. None of the 17 nonoperated Group 1 patients improved neurologically, whereas 3 of the 4 nonoperated Group 2 patients improved. The single nonoperated Group 3 patient improved neurologically. It is concluded that patients with incomplete neurological injuries after civilian gunshot wounds to the spine can expect radicular or myelopathic improvement. Decompressive operation is indicated in selected cases with unexpected radicular injuries or incomplete myelopathic injuries with myelographic evidence of neural compression. A stepwise improvement in neurological function over that expected without operation should be realized in these cases.


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.


1996 ◽  
Vol 19 (2) ◽  
pp. 113-117 ◽  
Author(s):  
Gabriele Wurm ◽  
Peter Pogady ◽  
Karin Lungenschmid ◽  
Johannes Fischer

2021 ◽  
Vol 15 (1) ◽  
Author(s):  
Chanil Deshan Ekanayake ◽  
Deepal Weerasekera ◽  
Dilini Dissanayake ◽  
Ranga Wickramarachchi ◽  
Saman Pushpakumara ◽  
...  

Abstract Background Cauda equina syndrome is a rare clinical condition that requires prompt diagnosis and timely surgical decompression with postoperative rehabilitation to prevent devastating complications. Case presentation A 55-year-old Sinhalese woman presented with a vulval abscess, with a history of involuntary leakage of urine for the last 7 years. Her sexual activity has been compromised due to coital incontinence, and she had also been treated for recurrent urinary tract infections during the last 7 years. On examination, a distended bladder was found. Neurological examination revealed a saddle sensory loss of S2–S4 dermatomes. There was no sensory loss over the lower limbs. Bladder sensation was absent, but there was some degree of anal sphincter tone. Motor functions and reflexes were normal in the limbs. Magnetic resonance imaging revealed L5–S1 spondylolisthesis. Ultrasound imaging confirmed the finding of a distended bladder, in addition to bilateral hydroureters with hydronephrosis. An incision and drainage with concomitant intravenous antibiotics were started for the vulval abscess. An indwelling catheter was placed to decompress the bladder and to reduce vulval excoriations due to urine. Bilateral ureteric stenting was performed later for persistent hydronephrosis and hydroureter despite an empty bladder. Conclusion This is a tragic case that illustrates the devastating long-term sequelae that ensues if cauda equina syndrome is left undiagnosed. It reiterates the importance of prompt referral and surgical decompression.


1999 ◽  
Vol 51 (4) ◽  
pp. 373-375 ◽  
Author(s):  
Teoman Cordan ◽  
Ahmet Bekar ◽  
Osman Yaman ◽  
Şahsine Tolunay

1980 ◽  
Vol 25 (4) ◽  
pp. S41-S43
Author(s):  
J. Marshall

The residual neurological deficits after stroke are discussed in this article. The main problems are weakness, spasticity and rigidity. Weakness may be amenable to help with a variety of physical aids and mobility maintained with a wheelchair. Spasticity is defined in terms of the neurological defect and its consequences examined in the clinical context of the stroke patient. The place of antispastic drugs and their method of use is described. The importance of sensory loss in the production of functional disability is also discussed.


Neurosurgery ◽  
2011 ◽  
Vol 68 (6) ◽  
pp. 1500-1519 ◽  
Author(s):  
Dachling Pang ◽  
John Zovickian ◽  
Greg S. Moes

Abstract BACKGROUND: Formation of the caudal spinal cord in vertebrates is by secondary neurulation, which begins with mesenchyme-epithelium transformation within a pluripotential blastema called the tail bud or caudal cell mass, from thence initiating an event sequence proceeding from the condensation of mesenchyme into a solid medullary cord, intrachordal lumen formation, to eventual partial degeneration of the cavitatory medullary cord until, in human and tailless mammals, only the conus and filum remain. OBJECTIVE: We describe a secondary neurulation malformation probably representing an undegenerated medullary cord that causes tethered cord symptoms. METHOD: We present 7 patients with a robust elongated neural structure continuous from the conus and extending to the dural cul-de-sac, complete with issuing nerve roots, which, except in 2 infants, produced neurological deficits by tethering. RESULTS: Intraoperative motor root and direct cord stimulation indicated that a large portion of this stout neural structure was “redundant” nonfunctional spinal cord below the true conus. Histopathology of the redundant cord resected at surgery showed a glioneuronal core with ependyma-lined lumen, nerve roots, and dorsal root ganglia, corroborating the picture of a blighted spinal cord. CONCLUSION: We propose that these redundant spinal cords are portions of the medullary cord normally destined to regress but are here retained because of late arrest of secondary neurulation before the degenerative phase. Because programmed cell death almost certainly plays a central role during degeneration, defective apoptosis may be the underlying mechanism.


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