Upper thoracic spinal cord herniation after traumatic nerve root avulsion

2003 ◽  
Vol 99 (3) ◽  
pp. 306-309 ◽  
Author(s):  
Victor R. Dasilva ◽  
Mubarak Al-Gahtany ◽  
Rajiv Midha ◽  
Dipanka Sarma ◽  
Perry Cooper

✓ Transdural herniation of the spinal cord, a rare but well-documented entity, has been reported sporadically for more than 25 years as a possible cause for various neurological signs and symptoms ranging from isolated sensory or motor findings to myelopathy and Brown—Séquard syndrome. The authors report, to the best of their knowledge, the first case of upper thoracic spinal cord herniation occurring after traumatic nerve root avulsion.

2004 ◽  
Vol 16 (5) ◽  
pp. 306-309
Author(s):  
Victor R. DaSilva ◽  
Mubarak Al-Gahtany ◽  
Rajiv Midha ◽  
Dipanka Sarma ◽  
Perry Cooper

✓ Transdural herniation of the spinal cord, a rare but well-documented entity, has been reported sporadically for more than 25 years as a possible cause for various neurological signs and symptoms ranging from isolated sensory or motor findings to myelopathy and Brown–Séquard syndrome. The authors report, to the best of their knowledge, the first case of upper thoracic spinal cord herniation occurring after traumatic nerve root avulsion.


2004 ◽  
Vol 1 (2) ◽  
pp. 223-227 ◽  
Author(s):  
Ryder Gwinn ◽  
Fraser Henderson

✓ Anterior spinal cord herniation is a well-documented condition in which the thoracic cord becomes tethered within a defect in the anterior dura mater. Typical procedures have involved a posterior approach with direct manipulation of the thoracic cord to expose and blindly release its point of tethering. The authors report three cases in which a novel approach for the treatment of anterior thoracic cord herniation was performed, cord manipulation and traction are minimized, and direct dural repair of the defect is performed.


2007 ◽  
Vol 17 (S2) ◽  
pp. 263-266 ◽  
Author(s):  
Masato Tanaka ◽  
Hisanori Ikuma ◽  
Kazuo Nakanishi ◽  
Yoshihisa Sugimoto ◽  
Haruo Misawa ◽  
...  

Spinal Cord ◽  
2009 ◽  
Vol 47 (11) ◽  
pp. 829-831 ◽  
Author(s):  
K Ijiri ◽  
K Hida ◽  
S Yano ◽  
S Komiya ◽  
Y Iwasaki

1973 ◽  
Vol 39 (5) ◽  
pp. 645-647 ◽  
Author(s):  
M. Peter Heilbrun ◽  
David O. Davis

✓ A case of spastic paraplegia secondary to constriction of the upper thoracic spinal cord by the dura, which was associated with the juvenile onset of diabetes mellitus, is described.


2012 ◽  
Vol 312 (1-2) ◽  
pp. 170-172 ◽  
Author(s):  
Giorgio B. Boncoraglio ◽  
Elena Ballabio ◽  
Alessandra Erbetta ◽  
Francesco Prada ◽  
Mario Savoiardo ◽  
...  

2007 ◽  
Vol 68 (4) ◽  
pp. 461-463 ◽  
Author(s):  
Cumhur Kilinçer ◽  
Levent Öztürk ◽  
M. Kemal Hamamcioglu ◽  
Emre Altunrende ◽  
Sebahattin Çobanoglu

1991 ◽  
Vol 75 (6) ◽  
pp. 911-915 ◽  
Author(s):  
Thomas H. Milhorat ◽  
David E. Adler ◽  
Ian M. Heger ◽  
John I. Miller ◽  
Joanna R. Hollenberg-Sher

✓ The pathology of hematomyelia was examined in 35 rats following the stereotactic injection of 2 µl blood into the dorsal columns of the thoracic spinal cord. This experimental model produced a small ball-hemorrhage without associated neurological deficits or significant tissue injury. Histological sections of the whole spinal cord were studied at intervals ranging from 2 hours to 4 months after injection. In acute experiments (2 to 6 hours postinjection), blood was sometimes seen within the lumen of the central canal extending rostrally to the level of the fourth ventricle. Between 24 hours and 3 days, the parenchymal hematoma became consolidated and there was an intense proliferation of microglial cells at the perimeter of the lesion. The cells invaded the hematoma, infiltrated its core, and removed erythrocytes by phagocytosis. Rostral to the lesion, the lumen of the central canal was found to contain varying amounts of fibrin, proteinaceous material, and cellular debris for up to 15 days. These findings were much less prominent in the segments of the canal caudal to the lesion. Healing of the parenchymal hematoma was usually complete within 4 to 6 weeks except for residual hemosiderin-laden microglial cells and focal gliosis at the lesion site. It is concluded that the clearance of atraumatic hematomyelia probably involves two primary mechanisms: 1) phagocytosis of the focal hemorrhage by microglial cells; and 2) drainage of blood products in a rostral direction through the central canal of the spinal cord.


1978 ◽  
Vol 48 (6) ◽  
pp. 1002-1007 ◽  
Author(s):  
Stephen E. Rawe ◽  
William A. Lee ◽  
Phanor L. Perot

✓ The early sequential histopathological alterations following a concussive paraplegic injury to the posterior thoracic spinal cord in cats were studied. The lack of significant progression of hemorrhages over a 4-hour period after injury indicates that most hemorrhages probably occur within the first hour. The marked enhancement or retardation of hemorrhages in the post-injury period, when the blood pressure was increased or decreased, respectively, demonstrates the loss of autoregulation of spinal cord vasculature at the trauma site after a concussive paraplegic injury. Progressive edema formation was evident over a 4-hour period following injury, and it could be enhanced or retarded by elevation or reduction of the systemic blood pressure.


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