+1 Recommend
0 collections
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Will repeated botulinum toxin A improve detrusor overactivity and bladder compliance in patients with chronic spinal cord injury?


      Read this article at

          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.


          Chronic spinal cord injury (SCI) can induce neurogenic detrusor overactivity (NDO), leading to urinary incontinence and renal damage due to low bladder compliance and high detrusor pressure during the storage and voiding of urine. In 2011, Botox ® (onabotulinumtoxinA, botulinum neurotoxin serotype A [BoNT-A]) was approved by the Food and Drug Administration for the treatment of NDO. Intradetrusor injection of BoNT-A has been shown to have clinical utility for the treatment of urinary incontinence, with consequent improvements in quality of life for patients. In the past 20 years, this treatment has been shown to be an effective treatment for patients with SCI refractory to antimuscarinic medication. The present review focused on publications in MEDLINE/PubMed relating to botulinum toxin to evaluate the treatment outcomes of repeated injection of BoNT-A, the mechanisms of action, results of clinical and urodynamic studies, and adverse effects.

          Related collections

          Most cited references 66

          • Record: found
          • Abstract: found
          • Article: found

          Incidence of Spinal Cord Injury Worldwide: A Systematic Review

          Background: Incidence studies of spinal cord injury (SCI) are important for health-care planning and epidemiological research. This review gives a quantitative update on SCI epidemiology worldwide through a statistical evaluation of incidence rates. Methods: A systematic review was conducted. For each study, the crude rate ratio was calculated and, when possible, age- and gender-adjusted incidence rate ratios with 95% CI were determined by direct adjustment or using Poisson regression. Results: Thirteen studies were included. Annual crude incidence rates in traumatic SCI varied from 12.1 per million in The Netherlands to 57.8 per million in Portugal. Compared to the Portuguese reference study, incidence rates showed a 3-fold variation, with the highest rates in Canada and Portugal. Most traumatic SCI studies showed a bimodal age distribution. The first peak was found in young adults between 15 and 29 years and a second peak in older adults (mostly ≧65 years). Motor vehicle accidents and falls were the most prevalent causes of injury accounting for nearly equal percentages. In contrast, another age pattern in non-traumatic SCI reflected steadily increasing incidence with advancing age. Conclusions: The results show significant variation in SCI incidence with changing epidemiological patterns. A trend towards increased incidence in the elderly was observed, likely due to falls and non-traumatic injury.
            • Record: found
            • Abstract: found
            • Article: not found

            Altered urinary bladder function in mice lacking the vanilloid receptor TRPV1.

            In the urinary bladder, the capsaicin-gated ion channel TRPV1 is expressed both within afferent nerve terminals and within the epithelial cells that line the bladder lumen. To determine the significance of this expression pattern, we analyzed bladder function in mice lacking TRPV1. Compared with wild-type littermates, trpv1(-/-) mice had a higher frequency of low-amplitude, non-voiding bladder contractions. This alteration was accompanied by reductions in both spinal cord signaling and reflex voiding during bladder filling (under anesthesia). In vitro, stretch-evoked ATP release and membrane capacitance changes were diminished in bladders excised from trpv1(-/-) mice, as was hypoosmolality-evoked ATP release from cultured trpv1(-/-) urothelial cells. These findings indicate that TRPV1 participates in normal bladder function and is essential for normal mechanically evoked purinergic signaling by the urothelium.
              • Record: found
              • Abstract: found
              • Article: not found

              Regulation of calcitonin gene-related peptide secretion from trigeminal nerve cells by botulinum toxin type A: implications for migraine therapy.

              To determine the effect of botulinum toxin type A on calcitonin gene-related peptide secretion from cultured trigeminal ganglia neurons. The ability of botulinum toxins to cause muscle paralysis by blocking acetylcholine release at the neuromuscular junction is well known. Previous studies and clinical observations have failed to demonstrate sensory changes related to botulinum toxins or the disease of botulism. Recent studies, however, have suggested that botulinum toxin type A injected into pericranial muscles may have a prophylactic benefit in migraine. This observation has renewed the debate of a mechanism of sensory inhibition mediated by botulinum toxin type A. Primary cultures of rat trigeminal ganglia were utilized to determine whether botulinum toxin type A could directly decrease the release of calcitonin gene-related peptide, a neuropeptide involved in the underlying pathophysiology of migraine. Untreated cultures or cultures stimulated with a depolarizing stimulus (potassium chloride) or capsaicin, an agent known to activate sensory C fibers, were treated for 3, 6, or 24 hours with clinically effective doses of botulinum toxin type A or a control vehicle. The amount of calcitonin gene-related peptide secreted into the culture media following the various treatments was determined using a specific radioimmunoassay. A high percentage (greater than 90%) of the trigeminal ganglia neurons present in 1- to 3-day-old cultures was shown to express calcitonin gene-related peptide. Treatment with depolarizing stimuli (potassium chloride), a mixture of inflammatory agents, or capsaicin caused a marked increase (4- to 5-fold) in calcitonin gene-related peptide released from the trigeminal neurons. Interestingly, overnight treatment of trigeminal ganglia cultures with therapeutic concentrations of botulinum toxin type A (1.6 or 3.1 units) did not affect the amount of calcitonin gene-related peptide released from these neurons. The stimulated release of calcitonin gene-related peptide following chemical depolarization with potassium chloride or activation with capsaicin, however, was greatly repressed by the botulinum toxin, but not by the control vehicle. A similar inhibitory effect of overnight treatment with botulinum toxin type A was observed with 1.6 and 3.1 units. These concentrations of botulinum toxin type A are well within or below the range of tissue concentration easily achieved with a local injection. Incubation of the cultures with toxin for 24, 6, or even 3 hours was very effective at repressing stimulated calcitonin gene-related peptide secretion when compared to control values. These data provide the first evidence that botulinum toxin type A can directly decrease the amount of calcitonin gene-related peptide released from trigeminal neurons. The results suggest that the effectiveness of botulinum toxin type A in the treatment of migraine may be due, in part, to its ability to repress calcitonin gene-related peptide release from activated sensory neurons.

                Author and article information

                Tzu Chi Med J
                Tzu Chi Med J
                Tzu-Chi Medical Journal
                Wolters Kluwer - Medknow (India )
                Apr-Jun 2021
                29 July 2020
                : 33
                : 2
                : 101-107
                [1]Department of Urology, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation and Tzu Chi University, Hualien, Taiwan
                Author notes
                [* ] Address for correspondence: Dr. Hann-Chorng Kuo, Department of Urology, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, 707, Section 3, Chung-Yang Road, Hualien, Taiwan. E-mail: hck@ 123456tzuchi.com.tw
                Copyright: © 2020 Tzu Chi Medical Journal

                This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms.

                Review Article


                Comment on this article