title: Functional consequences of lumbar spinal cord contusion injuries in the adult rat.
abstract: Our understanding of the substrates of locomotion, and hence our understanding of the causes of deficits following spinal cord injury, is still incomplete. While severe locomotor deficits can be induced by either contusion or laceration injuries or demyelination of thoracic spinal cord ventral and ventrolateral white matter, loss of mid-thoracic gray matter (intraspinal kainic acid injection) has no impact on locomotion. In contrast, loss of gray matter from the rostral lumbar segments induces severe locomotor deficits. This study examines the histological and locomotor outcomes following contusion injuries involving the rostral segments of the lumbar enlargement in the adult rat. Adult Sprague-Dawley rats received contusion injuries centered on the T13/L1, L2, or L3/4 spinal cord segments. Moderately severe injuries centered on the T13/L1 and L2 spinal cord segments induced more severe locomotor deficits than those centered on the L3/4 segments, despite a significantly smaller total gray matter volume loss (1.7 vs. 2.7 mm3). Moderately-severe injuries at T13/L1, L2, and L3/4 showed 21%, 31%, and 39% white matter sparing, respectively, with 6-week BBB scores of 10, 10, and 15.7, respectively. These data suggest that moderately-severe contusion injuries centered on the rostral segments of the lumbar enlargement induce more severe locomotor deficits than would be predicted by the histological outcome (spared white matter), suggesting that gray matter loss may play a role in functional deficits following some lumbar contusion injuries.
authors.affiliation: Departments of Neurological Surgery, University of Louisville School of Medicine, Louisville, Kentucky, USA. dsmagn01@gwise.louisville.edu
authors.forename: David S K
authors.initials: DS
authors.lastname: Magnuson
authors.forename: Rachael
authors.initials: R
authors.lastname: Lovett
authors.forename: Carree
authors.initials: C
authors.lastname: Coffee
authors.forename: Rebecca
authors.initials: R
authors.lastname: Gray
authors.forename: Yingchun
authors.initials: Y
authors.lastname: Han
authors.forename: Y Ping
authors.initials: YP
authors.lastname: Zhang
authors.forename: Darlene A
authors.initials: DA
authors.lastname: Burke
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D018450:Disease Progression; D020233:Gait Disorders, Neurologic / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology; D008159:Lumbar Vertebrae; D008297:Male; D009069:Movement Disorders / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology; D009413:Nerve Fibers, Myelinated / Q000473:pathology; D009434:Neural Pathways / Q000473:pathology* / Q000503:physiopathology; D009474:Neurons / Q000473:pathology; D010243:Paralysis / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013116:Spinal Cord / Q000473:pathology* / Q000503:physiopathology; D013119:Spinal Cord Injuries / Q000473:pathology* / Q000503:physiopathology