OBJECTIVE In acute traumatic brain injury, decompressive craniectomy is a common treatment that involves the removal of bone from the cranium to relieve intracranial pressure. The present study investigated whether neurological function following a severe spinal cord injury improves after utilizing either a durotomy to decompress the intradural space and/or a duraplasty to maintain proper flow of cerebrospinal fluid. METHODS Sixty-four adult female rats (n = 64) were randomly assigned to receive either a 3- or 5-level decompressive laminectomy (Groups A and B), laminectomy + durotomy (Groups C and D), or laminectomy + duraplasty with graft (Group E and F) at 24 hours following a severe thoracic contusion injury (200 kilodynes). Duraplasty involved the use of DuraSeal, a hydrogel dural sealant. Uninjured and injured control groups were included (Groups G, H). Hindlimb locomotor function was assessed by open field locomotor testing (BBB) and CatWalk gait analysis at 35 days postinjury. Bladder function was analyzed and bladder wall thickness was assessed histologically. At 35 days postinjury, mechanical and thermal allodynia were assessed by the Von Frey hair filament and hotplate paw withdrawal tests, respectively. Thereafter, the spinal cords were dissected, examined for gross anomalies at the injury site, and harvested for histological analyses to assess lesion volumes and white matter sparing. ANOVA was used for statistical analyses. RESULTS There was no significant improvement in motor function recovery in any treatment groups compared with injured controls. CatWalk gait analysis indicated a significant decrease in interlimb coordination in Groups B, C, and D (p < 0.05) and swing speed in Groups A, B, and D. Increased mechanical pain sensitivity was observed in Groups A, C, and F (p < 0.05). Rats in Group C also developed thermal pain hypersensitivity. Examination of spinal cords demonstrated increased lesion volumes in Groups C and F and increased white matter sparing in Group E (p < 0.05). The return of bladder automaticity was similar in all groups. Examination of the injury site during tissue harvest revealed that, in some instances, expansion of the hydrogel dural sealant caused compression of the spinal cord. CONCLUSIONS Surgical decompression provided no benefit in terms of neurological improvement in the setting of a severe thoracic spinal cord contusion injury in rats at 24 hours postinjury. Decompressive laminectomy and durotomy did not improve motor function recovery, and rats in both of these treatment modalities developed neuropathic pain. Performing a durotomy also led to increased lesion volumes. Placement of DuraSeal was shown to cause compression in some rats in the duraplasty treatment groups. Decompressive duraplasty of 3 levels does not affect functional outcomes after injury but did increase white matter sparing. Decompressive duraplasty of 5 levels led to neuropathic pain development and increased lesion volumes. Further comparison of dural repair techniques is necessary.

Objective The aim of the study was to investigate differences between flail limb syndrome and amyotrophic lateral sclerosis. Design A retrospective chart review identified 16 cases of amyotrophic lateral sclerosis and 16 of flail limb syndrome. Revised Amyotrophic Lateral Sclerosis Functional Rating Scale, compound muscle action potential amsplitudes, and rate of loss of vital capacity were compared. Results Comparing amyotrophic lateral sclerosis and flail limb syndrome patients, rate of loss of vital capacity was 5.26% ± 0.33% versus 0.54% ± 0.06%, respectively (P < 0.05). No patient in the flail limb syndrome group had a rate of loss of vital capacity more than 0.65% per month. No patient in the amyotrophic lateral sclerosis group had a rate of loss of vital capacity less than 4.6% per month. The average ulnar nerve compound muscle action potential amplitudes were significantly lower in flail limb syndrome (P < 0.05). No significant difference was observed in the rate of Revised Amyotrophic Lateral Sclerosis Functional Rating Scale decline or average peroneal, tibial, and median nerve compound muscle action potential amplitudes. Conclusions In flail limb syndrome, an average monthly decrease in vital capacity exceeding 0.65% may suggest a spread of motor neuron loss to higher cervical anterior horn areas and raise the possibility of progression to amyotrophic lateral sclerosis. Larger prospective studies are needed to investigate the rate of VC decline in flail limb syndrome and limb-onset amyotrophic lateral sclerosis and to establish whether a cutoff score combining rate of loss of vital capacity and compound muscle action potential amplitude mainly of the ulnar nerve might predict progression of flail limb syndrome to amyotrophic lateral sclerosis, the knowledge of which can facilitate appropriate patient counseling.