Reference / Species (number) / Injury model / Timing of decompression / Study conclusions
Brodkey et al, 1972 [6] / Cats, n = 5 / Weight was applied over the dorsal surface of the spinal cord and intact dura / Time since spinal cord compression and/or aortic clamping to CEP effects / Direct pressure to the spinal cord and hypotension result in additive deficits as recorded by CEP (cortical-evoked potentials)
Croft et al, 1972 [17] / Cats, n = 15 / Weight was applied over the dorsal surface of the spinal cord and intact dura / Graded weight (18-58 g) and graded time (5-20 minutes) / Graded pressure (38 g for 5 to 20 minutes and 58 g for 20 minutes) on the spinal cord produced reversible blocking of SSEP potentials
Thienprasit et al, 1975 [61] / Cats, n = 28 / A Number 3 French Fogarty catheter was passed through a L2-laminectomy extradurally in the cephalic direction for 6 cm and inflated with 0.6-0.9 cc of air and immediately deflated / No treatment versus laminectomy at 6 hours after SCI versus laminectomy at 6 hours after SCI + cooling of spinal cord for 2 hours / In more severely injured animals (based on return of cortical evoked response), surgical decompression and cooling offered improved outcome
Kobrine et al, 1978 [34] / Macaque monkeys, n = 10 / Spinal cord compression (right, lateral) using Fogarty catheter in the epidural space / 1 hour / Results suggested that mechanical forces of compression, rather than ischemia are mainly responsible for the loss of neural conduction in such a model
Kobrine et al, 1979 [35] / Macaque monkeys, n = 18 / Spinal cord compression (right, lateral) using Fogarty catheter in the epidural space / 1, 3, 5, 7, or 15 minutes / These data suggest that the cause for neural dysfunction after balloon compression is physical injury of the neural membrane, irrespective of blood flow changes; recovery is related to length of time of compression
Bohlman et al, 1979 [4] / Dogs, n = 14 / Compression model: transducer; contusion model: Allen weight-drop device / 4 to 8 weeks until neurologic recovery ceased to improve / Of the eight pressure-induced SCIs that recovered, microscopic examination was normal in 2, central gray necrosis occurred in 2, peripheral demyelinization in 2, and lacerations occurred in 3
Pathologic findings associated with significant paralysis: mild anterior horn gray matter necrosis in 2, laceration of the ventral white and gray matter in 3, and no microscopic evidence of cord damage in 1
In this study, the CEP response closely paralleled the degree of initial SCI either from contusion or compression as well as the neurologic recovery of the animals
Dolan et al, 1980 [22] / Rats, n = 91 / Spinal cord clip compression / 3 seconds, 30 seconds, 60 seconds, 300 seconds, or 900 seconds (15 minutes) / Functional recovery decreased as the duration of compression increased and the force of compression increased
Aki and Toya, 1984 [1] / Dogs, n = 33 / Spinal cord compression: weight placement / 30 or 60 minutes / With increasing compressive weights (6 g to 60 g), SEP amplitudes were progressively more reduced and latencies more prolonged
After release of compression, amplitudes and latencies recovered at the lower weights but were more likely to reflect greater conduction deficits with progressively greater weights
Pathologic findings: hemorrhage and necrosis were not found in the gray and white matter in the groups weighted with 6 and 16 g, whereas small petchial hemorrhages and tissue necrosis were observed in the center of the gray matter in the groups weighted with 36 and 60 g
However, there were no distinct findings in the white matter with these higher weights
Guha et al, 1987 [28] / Rats, n = 75 / Spinal cord clip compression / 15 minutes, 60 minutes, 120 minutes, or 240 minutes / The major determinant of recovery was the intensity of compression applied to the spinal cord; the time until decompression also affected recovery, but only for the lighter compression forces (2.3 and 16.9 g)
Nystrom and Berglund, 1988 [47] / Rats, n = 81 / Spinal cord compression: weight placement / 1 minute, 5 minutes, and 10 minutes / Both the amount of weight and the duration of placement affect the animals’ ability to recover, whereby a heavier weight and longer duration of placement are associated with less recovery
Delamarter et al, 1991 [19] / Dogs, n = 30 / Circumferential constriction of the cauda equina with a nylon electrical cable / 2-3 seconds, 1 hour, 6 hours, 24 hours, and 1 week / All 30 dogs developed caudal equina syndrome after constriction and all dogs recovered significant motor function 6 weeks after decompression (recovered to walking (Tarlov Grade 5) with bladder and tail control at 6 weeks after SCI)
Immediately after compression, all 5 groups demonstrated greater than 50% deterioration of the posterior tibial nerve SSEP amplitudes; at 6 weeks after decompression, all 5 groups had a mean amplitude recovery of 20% to 30%; there was no difference in recovery of SSEPs among the groups
All groups demonstrated scattered Wallerian degeneration and axonal regeneration; there were no significant differences in the histologic findings among the 5 groups
Zhang et al, 1993 [64] / Rats, N = not disclosed / Spinal cord compression (graded weight compression) / 5 minutes of compression with varied weight: group 1 (no compression, control), group 2 (9 g weight), group 3 (35 g weight), and group 4 (50 g weight) / In groups 2 and 3, lactate levels increased 6 to 7 times the basal levels in the first fraction; group 2 levels normalized within approximately 30 minutes, whereas group 3 levels were a lot slower in recovering
Group 4 lactate levels increased 10x in the second fraction; only partial recovery was seen in the 2-hour period
No significant change in pyruvate levels was seen in any of the groups
Inosine levels rose 0.7-0.9 uM in groups 2 and 3 and 1.4 uM in the Group 4
Inosine recovery was faster than lactate with group 4 recovering completely in approximately 40 minutes
Recovery of hypozanthine was more delayed compared with other metabolites; complete recovery took almost 80 minutes
Delamarter et al, 1995 [18] / Dogs, n = 30 / Circumferential constriction of the caudal spinal cord with a nylon electrical cable to 50% of the diameter of the spinal canal. / 2-3 seconds, 1 hour, 6 hours, 24 hours, and 1 week / The dogs with immediate decompression generally recovered neurologic function within 2 to 5 days; animals that were compressed for 6 hours or more showed no significant motor recovery after decompression of spinal cord
Discrete areas of Wallerian degeneration and demyelination were seen in the spinal cord of animals decompressed either immediately or at 1 hour; in contrast, there was severe central necrosis in the spinal cord of animals that were decompressed at 6 hours or later
Carlson et al, 1997 [9] / Dogs, n = 12 / Spinal cord compression: hydraulic loading piston / 5 minutes, 3 hours / Regional spinal cord blood flow was reduced at the site of piston compression; in the sustained compression group, no recovery of SSEP occurred and blood flow remained significantly lower than baseline at 30 and 180 minutes after maximum compression; spinal cord decompression was associated with an early recovery of blood flow and SSEP recovery; by 3 hours, blood flow was similar in both the compressed and decompressed groups, although SSEP recovery occurred only in the decompressed group
Carlson et al, 1997 [10] / Dogs, n = 21 / Cord compression / Spinal cord displacement was maintained for 30 minutes (n = 7), 60 minutes (n = 8), or 180 minutes (n = 6) after lower extremity SEP amplitudes were reduced by 50% of baseline / SEP recovery was seen in 6 of 7 dogs in 30-minute, 5 of 8 dogs in 60-minute, and 0 of 6 of the dogs in 180-minute compression group
Regional spinal cord blood flow at baseline decreased after stopping dynamic compression; reperfusion flows after decompression was inversely related to duration of compression
Reperfusion flows measured as the interval change in blood flow between the time dynamic compression was stopped to 5, 15, or 180 minutes after decompression were significantly greater in those dogs that recovered SEP (p < 0.05)
Spinal cord decompression within 1 hour of SEP loss resulted in significant electrophysiological recovery after 3 hours of monitoring
Dimar et al, 1999 [21] / Rats, n = 42 / Contusion injury: impactor / 0, 2 hours, 6 hours, 24 hours, and 72 hours / There was a progressively more severe central and dorsal cavitation as the time of spinal cord compression increased
Midsagittal sections demonstrated progressive cephalad and caudal cord necrosis and cavitation, which worsened the longer the duration of compression; these changes were most severe in the 24- and 72-hour specimens
Carlson et al, 2003 [8] / Dogs, n = 16 / Spinal cord compression: hydraulic piston / Spinal cord displacement was maintained for 30 minutes (n = 8) or 180 minutes (n = 8) after SSEP amplitudes were reduced by 50% of baseline / A shorter time of compression was associated with better neurologic function at both early and late time points
Lesion volumes as assessed with MRI were smaller in the 30-minute compression group than the 180-minute compression group (p = 0.04)
The 30-minute compression group showed smaller lesion volume (p < 0.001) and greater percentage of residual white matter (p = 0.005) than the 180-minute compression group
Hejcl et al, 2008 [30] / Rats, n = 23 / Spinal cord transection / HEMA-MOETACl hydrogel was inserted right away after SCI (acute group) or 1 week after SCI (delayed group) / There was no significant difference in histopathologic examination of spinal cord between the acute and delayed implantation groups; there were no significant differences between the two treatment groups with regard to the BBB scores
Rabinowitz et al, 2008 [50] / Dogs, n = 18 / Circumferential constriction of the thoracolumbar junction with a nylon electrical cable / Group 1: decompression at 6 hours + methylprednisolone
Group 2: decompression at 6 hours + sham
Group 3: methylprednisolone only / Decompression within 6 hours (groups 1 and 2) showed significant neurologic improvement when compared with the no decompression (group 3); methylprednisolone did not significantly affect outcome; there was no statistical difference in the percentage of cord involvement histologically among the 3 groups; group 3 did show greater involvement below the level of the lesion
SCI = spinal cord injury; SEP = sensory-evoked potential; SSEP = somatosensory-evoked potential