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.

Plasticity After Spinal Cord Injury: Relevance to Recovery and Approaches to Facilitate It

“…Additionally, the chABC injection site may have played a role. Rat locomotion recovers to lesser extents following excitotoxic and contusion SCI at the rostral lumbar spinal cord [127][128][129]. Wheel running alone also did not improve locomotion recovery; however, task-specific and general rehabilitation alone each had positive, negative, or no effects on forelimb functional recovery [57].…”

A New Acute Impact-Compression Lumbar Spinal Cord Injury Model in the Rodent

“…17 If the injury was made one vertebral level caudal at the T12-T13 level, the injury would represent a caudal lumbar SCI, with animals recovering almost full function of the hindlimbs. 6 Therefore, significant efforts were taken to ensure a consistent and accurate landmarking procedure.…”

“…3,4 Only a small number of models have been described for this location, however. [5][6][7][8][9][10] Injuries to the thoracolumbar region of the spine differ from injuries to the midthoracic or cervical regions because each results in distinct motor and sensory deficits. 3,4 It has been shown that interneurons involved in the hindlimb central pattern generator (CPG) are predominantly localized in the L1 and L2 spinal cord segments of the rat, 11 with injuries to this region resulting in significant locomotor deficits.…”

“…15 With respect to lumbar SCI, several models have been described in the literature. Magnuson and associates 6 in 2005 investigated behavioral and histological outcomes after weight-drop contusion injury to various lumbar segments in the rat and provided the first description of traumatic SCI to the lumbar cord. The authors described moderately severe (12.5 g-cm) versus severe injuries (25 g-cm) with the NYU impactor at T13-L1, L2, and L3-L4 segments of the spinal cord.…”

“…Two other groups investigated variations of the weight-drop mechanism and found similar results to those of Magnuson and associates. 6,7,14 Chemical injuries to the rat lumbar cord at the L2 spinal cord segment have been reported, although they are not considered clinically relevant. 5,8 In contrast to the clip impact-compression model, which simultaneously applies dorsal-ventral forces that likely includes the spinal roots, contusion-only models cause trauma to the dorsal CNS alone.…”