Effect of durotomy in dogs with thoracolumbar disc herniation and without deep pain perception in the hind limbs.

OBJECTIVE: To determine the effectiveness of durotomy as an adjunct to surgical decompression in dogs with thoracolumbar intervertebral disc herniation (TL-IVDH) and loss of deep pain perception (DPP) in the hind limbs. STUDY DESIGN: Retrospective study. ANIMALS: Dogs (n = 116) with TL-IVDH and loss of DPP treated with hemilaminectomy. METHODS: Signalment, surgical site, recovery rate, incidence of progressive myelomalacia (PMM), time elapsed from onset of paraplegia of the hind limbs to surgery (TPS), and the length of area of hyperintensity of the spinal cord on magnetic resonance T2-weighted images compared with L2 vertebral body length (LHT2) were compared between dogs treated with hemilaminectomy alone and those treated with adjunct durotomy. Multivariate logistic regression analyses were used to test the association between outcomes and the external view of the spinal cord parenchyma after durotomy. RESULTS: The percentage of dogs regaining ambulation was greater when durotomy was performed (56.9%) than when dogs were treated with hemilaminectomy alone (38.5%; P = .04). In the hemilaminectomy group, 14 dogs died of suspected PMM, while no PMM was detected in the durotomy group. Durotomy, breed, surgical site, and LHT2 influenced recovery. No association was detected between age, sex, body weight, and TPS and recovery. CONCLUSION: Performing a durotomy in combination with decompression improved the return to function and prevented PMM in our clinical setting. CLINICAL SIGNIFICANCE: Surgeons should consider durotomy in dogs with TL-IVDH and loss of DPP in hind limbs to improve surgical outcome.

Vertebral fixation does not affect recovery or recurrence of cervical intervertebral disc herniation in small dogs (< 15 kg).

OBJECTIVE: To compare the prognosis of small dogs with cervical intervertebral disc herniation (C-IVDH) when treated with ventral slot decompression (VSD) alone or with concomitant vertebral fixation (VF). ANIMALS: Small dogs (n = 303) weighing < 15 kg diagnosed with C-IVDH and treated with VSD. PROCEDURES: We recorded signalment, cervical myelopathy grade, surgical site, use of VF, degree of adjacent disc degeneration, recovery, recurrence, recurrence site, and postoperative course, including the time elapsed from recovery to recurrence. We examined factors associated with recovery and recurrence during the 30-month postoperative period using multivariate logistic regression analysis. RESULTS: VF did not affect recovery (P = .79). However, nonchondrodystrophic breeds had poorer recovery (OR, 5.89; P = .023) than chondrodystrophic breeds, and a higher preoperative cervical myelopathy grade (grade 3 or 4) was associated with poorer recovery (OR, 7.09 or 3.46, respectively; P = .019 or .042, respectively), compared with grade 1. VF did not affect recurrence (P = .79); however, increasing age was associated with recurrence (OR, 1.79; P = .001). CLINICAL RELEVANCE: In small dogs weighing < 15 kg, there was no difference in postoperative recovery and recurrence rates after VSD with or without concomitant VF. Therefore, in small dogs with C-IVDH, even if the slot volume is increased to remove sufficient disc material during VSD, a good prognosis can be achieved with or without VF.

Effect of PCB-126 on intracellular accumulation and transepithelial transport of vinblastine in LLC-PK1 and its transformant cells expressing human P-glycoprotein.

The effects of 3, 3', 4, 4', 5-pentachlorobiphenyl (PCB-126), which is the most toxic congener of coplanar polychlorinated biphenyls (Co-PCBs), on intracellular accumulation and transepithelial transport of vinblastine were examined in porcine kidney cells, LLC-PK1, and its transformant cells expressing human P-glycoprotein (LLC-MDR1). The accumulation decreased less than one-tenth in LLC-MDR1 compared to LLC-PK1. In both cells, the accumulation increased with the addition of PCB-126 and cyclosporine A (CYA), which are P-glycoprotein modulators, though the magnitudes were different in these two cell groups as well as for these two chemicals. Thus, PCB-126 might inhibit extrusion of vinblastine through the drug extrusion system as does CYA. In both the cells, there might be an endogenous drug extrusion system other than P-glycoprotein that was inhibited by CYA or PCB-126. The net basal-to-apical transepithelial transport of vinblastine increased 1.7-fold more in LLC-MDR1 than in LLC-PK1. By adding PCB-126 on the apical side, the transport was greatly decreased by -76% in the monolayer of both cells. By adding PCB-126 and CYA on the basal side in LLC-MDR1 monolayer, the transports increased -1.7-fold, so that PCB-126 might inhibit the extrusion of vinblastine on both the apical and basal sides. One of the causes to be considered for the adverse effects of Co-PCBs, in addition to the binding with an aryl hydrocarbon receptor, might be the modification of drug transport by its interaction with the drug transport system.