• International Neurourology Journal
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• v.22 no.4
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• pp.275-286
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• 2018

Purpose: OnabotulinumtoxinA (BoNT-A) is a promising therapy for treating neurogenic detrusor overactivity (NDO) in individuals with spinal cord injury (SCI). This systematic review and meta-analysis aimed to carry out an in-depth review and to make an objective estimation of the efficacy and safety of BoNT-A on NDO after SCI. Methods: The PubMed, Embase, and Cochrane databases were searched for all relevant articles published from 2001 to 2016 that referred to NDO, SCI, and BoNT-A or botulinum toxin A. All data were recorded in an Excel spreadsheet by 2 individual reviewers. Review Manager version 5.3 was used to carry out the meta-analysis. Results: This analysis included 17 studies involving 1,455 patients. Compared with placebo and baseline, BoNT-A was effective in increasing maximum cystometric capacity, volume at first involuntary detrusor contraction, cystometric bladder capacity (all P<0.00001), compliance (P=0.001), and the number of patients with complete dryness (P=0.0003), and decreasing detrusor pressure, the number of patients with no involuntary detrusor contractions, the maximum flow rate, the incidence of detrusor overactivity (all P<0.00001), and the number of urinary incontinence episodes (P=0.001). There were no statistically significant differences between doses of 200 U and 300 U or between injections into the detrusor and submucosa. There were no life-threatening adverse events. Conclusions: BoNT-A is effective and safe in treating NDO after SCI. There were no statistically significant differences between doses of 200 U and 300 U or between injecting into the detrusor and submucosa. However, more high-quality randomized controlled trials are still needed.

• International Neurourology Journal
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• v.22 no.4
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• pp.268-274
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• 2018

Purpose: To describe a technique for urodynamic diagnosis of detrusor sphincter dyssynergia (DSD) using urethral pressure measurements and examine potential associations between urethral pressure and bladder physiology among patients with DSD. Methods: Multiple sclerosis (MS) and spinal cord injured (SCI) patients with known DSD diagnosed on videourodynamics (via electromyography or voiding cystourethrography) were retrospectively identified. Data from SCI and MS patients with detrusor overactivity (DO) without DSD were abstracted as control group. Urodynamics tracings were reviewed and urethral pressure DSD was defined based on comparison of DSD and control groups. Results: Seventy-two patients with DSD were identified. Sixty-two (86%) had >20 cm $H_2O$ urethral pressure amplitude during detrusor contraction. By comparison, 5 of 23 (22%) of control group had amplitude of >20 cm $H_2O$ during episode of DO. Mean duration of urethral pressure DSD episode was 66 seconds (range, 10-500 seconds) and mean urethral pressure amplitude was 73 cm $H_2O$ (range, 1-256 cm $H_2O$). Longer (>30 seconds) DSD episodes were significantly associated with male sex (81% vs. 50%, P=0.013) and higher bladder capacity (389 mL vs. 219 mL, P=0.0004). Urethral pressure amplitude measurements during DSD were not associated with significant urodynamic variables or neurologic pathology. Conclusions: Urethral pressure amplitude of >20 cm $H_2O$ during detrusor contraction occurred in 86% of patients with known DSD. Longer DSD episodes were associated with larger bladder capacity. Further studies exploring the relationship between urethral pressure measurements and bladder physiology could phenotype DSD as a measurable variable rather than a categorical observation.

• Journal of the Korean Society for Precision Engineering
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• v.29 no.5
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• pp.584-590
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• 2012

The structural and functional disorder of a detrusor induces a bladder hypertrophy and degenerates a bladder muscle gradually by preventing normal urination. Thus, the thickness of the bladder wall has been increased in proportion to the degree of bladder outlet obstruction. In this study, the mechanical characteristics of the detrusor is analyzed for the physical properties and the thickness changes of the bladder muscle using a mathematically analytic method. In order to obtain the mechanical property of the bladder muscle, the tensile test of porcine bladder tissue is performed because its property is similar to that of human. The result of tensile test is applied to the mathematically model as Mooney Rivlin coefficients which represent the hyperelastic material. The model of the bladder is defined as the spherical shape with the initial volume of 50ml. The principal stress and strain according to the thickness are analyzed. Also, computer simulations for three types of the material property for the model of the bladder are performed based on the fact that the stiffness of the bladder is weakened as the progress of the benign prostatic hyperplasia. As a result, the principal stress is 341kPa at the initial thickness of 2.2mm, and is 249kPa at 6.5mm. As the bladder wall thickness increases, the principal stress decreases. The principal stress and strain decrease as the stiffness of the bladder decreases under the same thinkness.

• Journal of Korean Biological Nursing Science
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• v.19 no.2
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• pp.60-68
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• 2017

Purpose: The purpose of this study was to analyze the relationship between lower urinary tract symptoms and urodynamic parameters to investigate the characteristics of mixed urinary incontinence (MUI) and stress urinary incontinence (SUI). Methods: The subjects were 318 women with MUI and 128 women with SUI. Data were collected retrospectively from electronic medical records including Bristol Female Lower Urinary Tract Symptoms-Scored Form (BFLUTS-SF), Incontinence Quality of Life Instrument (I-QOL), voiding diaries, and urodynamic parameters. Results: Compared with the SUI group, the MUI group was older and showed lower I-QOL and more severe urinary tract symptoms. The MUI group had more urinary frequency, more nocturia, and a higher urgency score than the SUI group. In the correlation analysis, the greatest difference between the two groups was that urgency was associated with Qmax, maximal cystometric capacity, and detrusor overactivity only in the MUI group (r = -.175, p= .004; r = -.281, p< .001; r= .232, p< .001, respectively). Conclusion: As a result of this study, we propose that a customized management program that emphasizes the control of urgency for the MUI group, and one that effectively strengthens the weak pelvic floor for the SUI group.

• Journal of The Korean Society of Inherited Metabolic disease
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• v.23 no.1
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• pp.25-30
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• 2023

Leigh syndrome is a rare progressive neurodegenerative mitochondrial disorder with clinical and genetic heterogeneity. Recently, balletic IARS2 variants have been identified in a number of patients presenting broad clinical phenotypes from Leigh and West syndrome to a rare syndrome CAGSSS characterized by cataracts, growth hormone deficiency, sensory neuropathy, sensorineural hearing loss, and skeletal dysplasia syndrome (OMIM#616007). We describe a child with Korean Leigh syndrome with urologic manifestations resulting from a compound heterozygote mutation in IARS2. A 5-year-old girl visited the emergency room with a complaint of abdominal pain accompanied by abdominal distension. Abdominal-pelvic CT showed a markedly distended urinary bladder without definite obstructive lesions. She was diagnosed with neurogenic bladder dysfunction based on a urodynamic study. She had global delayed development due to neurologic regression after 6 months of age and a history of bilateral cataract surgery at the age of 2 years. Her brain magnetic resonance imaging showed symmetrically increased signal intensities in the bilateral putamen and caudate nuclei with diffuse cerebral atrophy. No gene variants were identified through whole-mitochondrial genome analysis. Whole exome sequencing was performed for diagnosis, and compound heterozygous pathogenic variants were identified in IARS2: c.2446C>T (p. Arg816Ter) and c.2450G>A (p. Arg817His). To the best of our knowledge, this is the first case report of bladder dysfunction manifestation in a patient with IARS2-related Leigh syndrome. Thus, it broadens the clinical and genetic spectrum of IARS2-associated diseases.