4
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Predictors of urinary or fecal incontinence in dogs with thoracolumbar acute non‐compressive nucleus pulposus extrusion

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Background

          Urinary (UI) and fecal (FI) incontinence occur in up to 7.5% and 32% of dogs, respectively, after thoracolumbar acute noncompressive nucleus pulposus extrusion (ANNPE).

          Hypotheses/Objectives

          To investigate clinical, diagnostic, and therapeutic predictors of UI and FI in dogs with ANNPE affecting the T3‐L3 spinal cord segments.

          Animals

          Hundred and eighty‐seven dogs with T3‐L3 ANNPE diagnosed based on clinical and MRI findings.

          Methods

          Multicenter retrospective study. Data were obtained from medical records and telephone questionnaires and analyzed by logistic regression.

          Results

          UI and FI were reported in 17 (9.1%) and 44 (23.5%) dogs, respectively. Paraplegic dogs were 3 times (95% CI = 1.25, 10.87) more likely to develop UI ( P = .018) and 4 times (95% CI = 1.94, 12.56) more likely to develop FI ( P = .001) compared to nonparaplegic dogs. Dogs with an intramedullary hyperintensity greater than 40% of the cross‐sectional area of the spinal cord at the same level on transverse T2‐weighted MRI images were 4 times more likely to develop UI (95% CI = 1.04, 21.72; P = .045) and FI (95% CI = 1.56, 10.39; P = .004) compared to dogs with smaller lesions. FI was 3 times (95% CI = 1.41, 7.93) more likely in dogs that were not treated with nonsteroidal anti‐inflammatory drugs (NSAIDs) after diagnosis compared to dogs administered NSAIDs ( P = .006) and 2 times (95% CI = 1.12, 5.98) more likely in dogs presented with clinical signs compatible with spinal shock compared to dogs without ( P = .026).

          Conclusion and Clinical Importance

          The identification of clinical, diagnostic, and therapeutic predictors of UI and FI in dogs with T3‐L3 ANNPE can help to approach these autonomic dysfunctions occurring after spinal cord injury.

          Related collections

          Most cited references36

          • Record: found
          • Abstract: found
          • Article: not found

          Spinal shock revisited: a four-phase model.

          Spinal shock has been of interest to clinicians for over two centuries. Advances in our understanding of both the neurophysiology of the spinal cord and neuroplasticity following spinal cord injury have provided us with additional insight into the phenomena of spinal shock. In this review, we provide a historical background followed by a description of a novel four-phase model for understanding and describing spinal shock. Clinical implications of the model are discussed as well.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Nonsteroidal anti-inflammatory drugs can lower amyloidogenic Abeta42 by inhibiting Rho.

            A subset of nonsteroidal anti-inflammatory drugs (NSAIDs) has been shown to preferentially reduce the secretion of the highly amyloidogenic, 42-residue amyloid-beta peptide Abeta42. We found that Rho and its effector, Rho-associated kinase, preferentially regulated the amount of Abeta42 produced in vitro and that only those NSAIDs effective as Rho inhibitors lowered Abeta42. Administration of Y-27632, a selective Rock inhibitor, also preferentially lowered brain levels of Abeta42 in a transgenic mouse model of Alzheimer's disease. Thus, the Rho-Rock pathway may regulate amyloid precursor protein processing, and a subset of NSAIDs can reduce Abeta42 through inhibition of Rho activity.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Nonsteroidal anti-inflammatory drugs promote axon regeneration via RhoA inhibition.

              After a CNS injury in the adult mammals, axonal regeneration is very limited because of the reduced intrinsic growth capacity and nonpermissive environment for axonal elongation. The growth inhibitions from CNS myelin and astroglial chondroitin sulfate proteoglycans partially account for the lack of CNS repair. Here, we show that the nonsteroidal antiinflammatory drugs (NSAIDs) ibuprofen and indomethacin, the drugs widely used as pain relievers in the clinic, can surmount axon growth restrictions from myelin and proteoglycans by potently inhibiting their downstream pathway RhoA signal. Similar to Rho and Rock inhibitors C3 transferase or Y27632 [(R)-(+)-trans-N-(4-pyridyl)-4-(1-aminoethyl)-cyclohexanecarboxamide], both NSAID drugs stimulate a significant neurite growth in the cultured dorsal root ganglion neurons exposed to the inhibitory substrates. Systemic administration of ibuprofen to spinal cord-lesioned rodents reverses the active RhoA signal around injury area measured via Rho-GTP binding assay. Subcutaneous injections of ibuprofen via minipumps to rats with a thoracic spinal cord transection or contusion injury result in substantial corticospinal and serotonergic axon sprouting in the caudal spinal cord and promote locomotor functional recovery, even delaying the treatment 1 week after trauma. In contrast, the non-RhoA-inhibiting NSAID naproxen does not have the axon growth-promoting effects on cultured or lesioned neurons. These studies demonstrate the therapeutic potential of RhoA-inhibiting NSAIDs in treating CNS injuries characterized by axonal disconnection including spinal cord injury.
                Bookmark

                Author and article information

                Contributors
                lorenzo.mari@hotmail.com
                Journal
                J Vet Intern Med
                J. Vet. Intern. Med
                10.1111/(ISSN)1939-1676
                JVIM
                Journal of Veterinary Internal Medicine
                John Wiley & Sons, Inc. (Hoboken, USA )
                0891-6640
                1939-1676
                31 October 2019
                Nov-Dec 2019
                : 33
                : 6 ( doiID: 10.1111/jvim.v33.6 )
                : 2693-2700
                Affiliations
                [ 1 ] Department of Neurology/Neurosurgery Centre for Small Animal Studies, Animal Health Trust Newmarket Suffolk UK
                [ 2 ] Neurology/Neurosurgery Service Willows Veterinary Centre and Referral Services Solihull UK
                [ 3 ] Diagnostic Imaging Unit, Centre for Small Animal Studies, Animal Health Trust Newmarket Suffolk UK
                [ 4 ] Department of Small Animal Clinical Science Institute of Veterinary Science, University of Liverpool Neston Cheshire UK
                [ 5 ] School of Veterinary Medicine University of Surrey Guildford Surrey UK
                Author notes
                [*] [* ] Correspondence

                Lorenzo Mari, Department of Neurology/Neurosurgery, Centre for Small Animal Studies, Animal Health Trust, Newmarket, Newmarket, Suffolk, UK.

                Email: lorenzo.mari@ 123456hotmail.com

                Author information
                https://orcid.org/0000-0002-5732-1011
                https://orcid.org/0000-0003-2353-9028
                Article
                JVIM15626
                10.1111/jvim.15626
                6872617
                31674064
                53646fb2-4efd-46e0-affe-6bfeab116d19
                © 2019 The Authors. Journal of Veterinary Internal Medicine published by Wiley Periodicals, Inc. on behalf of the American College of Veterinary Internal Medicine.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

                History
                : 29 April 2019
                : 05 September 2019
                Page count
                Figures: 0, Tables: 2, Pages: 8, Words: 6648
                Categories
                Standard Article
                SMALL ANIMAL
                Standard Articles
                Neurology
                Custom metadata
                2.0
                jvim15626
                November/December 2019
                Converter:WILEY_ML3GV2_TO_NLMPMC version:5.7.2 mode:remove_FC converted:21.11.2019

                Veterinary medicine
                high‐velocity intervertebral disc extrusion,neurogenic bowel dysfunction,nonsteroidal anti‐inflammatory drugs,spinal cord injury,spinal shock,traumatic intervertebral disc extrusion

                Comments

                Comment on this article