UNASSIGNED: Delayed @entity16 in the absence of direct cord insult following surgical removal and cord decompression is a rare but severe @entity260 in a small subset of @entity1 with @entity1653 . To date, the underlying pathophysiology of such a finding remains unclear and @entity63 -reperfusion injury (IRI) is considered as the potential etiology in the literature. However, no experimental research has been reported to prove this hypothesis. The present study investigated whether IRI occurs following decompression surgery using an experimental @entity35 model of chronic compressive @entity1566 ( @entity1566 ). A chronic @entity1745 model was developed with various sizes of polymer sheets (mild and severe compression) that were microsurgically implanted underneath the T8-9 laminae, and occurrence of IRI in the spinal cord following decompression was determined by measuring @entity224 dismutase (SOD) level and @entity1234 ( @entity1865 ) concentration. In the mild compression groups, after decompression SOD activities significantly increased along with a reduction in @entity1865 content compared with the non-decompression group (P<0.05), which exhibited diminishment of lipid peroxidation and relief of the secondary injury. These findings indicated that decompression is effective to improve neurological recovery and may deliver improved outcomes for chronic mild compression of the spinal cord. However, in severe compression groups, after decompression, SOD activities markedly reduced further along with a significant increase in @entity1865 content compared with non-decompression group (P<0.05). The results indicated that lipid peroxidation increased immediately after decompression surgery which resulted from reperfusion of the spinal cord. These findings demonstrated IRI may occur as a result of chronic severe compression of the spinal cord. In clinical practice, sudden cord expansion and reperfusion may have lead to disruption in the blood spinal cord barrier, and triggered a cascade of IRI resulting in postoperative @entity16 . Recognition of this @entity16 following removal for @entity1653 may improve preoperative @entity1 counseling and merits further study for determination of the precise pathophysiology.

Delayed XXXX after surgery for @entity1653 : Ischemia-reperfusion injury in a @entity35 model.

@entity1 :: ('9606', 'Species') :: ['patients', 'patient'] @entity63 :: ('MESH:D007511', 'Disease') :: ['ischemia'] @entity16 :: ('MESH:D009422', 'Disease') :: ['neurological deterioration', 'neurologic deterioration'] @entity260 :: ('MESH:D011183', 'Disease') :: ['postoperative complication'] @entity1653 :: ('MESH:D008579', 'Disease') :: ['intraspinal meningiomas'] @entity1745 :: ('MESH:D013117', 'Disease') :: ['spinal cord compression'] @entity1234 :: ('MESH:D008315', 'Chemical') :: ['malondialdehyde'] @entity1566 :: ('MESH:D013119', 'Disease') :: ['spinal cord injury', 'SCI'] @entity35 :: ('10116', 'Species') :: ['rat'] @entity224 :: ('MESH:D013481', 'Chemical') :: ['superoxide'] @entity1865 :: ('CHEBI:566274', 'Chemical') :: ['MDA']
@entity16 :: (MESH:D009422,Disease) :: ['neurological deterioration']
