Incontinence in individuals with Angelman syndrome: A comparative study.
Res Dev Disabil. 2013 Sep 25;34(11):4184-4193
Authors: Radstaake M, Didden R, Giesbers S, Korzilius H, Peters-Scheffer N, Lang R, von Gontard A, Curfs LM
Abstract Frequency and type of incontinence and variables associated with incontinence were assessed in individuals with Angelman syndrome (AS; n=71) and in a matched control group (n=69) consisting of individuals with non-specific intellectual disability (ID). A Dutch version of the "Parental Questionnaire: Enuresis/Urinary Incontinence" (Beetz, von Gontard, & Lettgen, 1994) was administered and information on primary caretakers' perspectives regarding each individual's incontinence was gathered. Results show that diurnal incontinence and fecal incontinence during the day more frequently occurred in the control group than in the AS group. In both groups, nocturnal enuresis was the most common form of incontinence. More incontinence was seen in individuals with AS who were younger, had a lower level of adaptive functioning and/or had epilepsy. Individuals with AS were able to stay dry for longer periods of time than the controls and often showed both in-toilet urination and urinary accidents during the day, whereas accidents and correct voids during the day were more set apart in the control group. Also, persons with AS had a lower micturition frequency implying possible voiding postponement. Both groups showed high rates of LUTS (lower urinary tract symptoms) possibly indicative of functional bladder disorders such as voiding postponement, dysfunctional voiding, or even an underactive bladder. In general, most primary caretakers reported severe intellectual disability as the main cause for urinary incontinence. Based on these results incontinence does not appear to be part of the behavioral phenotype of Angelman syndrome. Therefore, pediatric or urologic diagnostics and treatment are recommended for all persons with incontinence and intellectual disability. Further implications for practice and research are given.
PMID: 24076983 [PubMed - as supplied by publisher]
Neurogenic bladder and disc disease:A brief review.
Curr Med Res Opin. 2013 May 24;
Authors: Siracusa G, Sparacino A, Lentini V
Abstract Abstract Objective Neurogenic bladder refers to morphofunctional alterations of bladder-sphincter complex secondary to central or peripheral neurological lesions. Discal etiology can be suggested by clinical observation in patients complaining classical lower back pain, but not excluded even without musculoskeletal pain. This review provides a brief overview of associations between neurogenic bladder and disc disease, analyzing neuroanatomy, pathophysiology, clinical and urodynamic findings. Therapy is revised focusing on aetiological treatments. Methods The literature search has been performed on PubMed, Medline and Google scholar using the following keywords: 'neurogenic bladder', 'disc herniation', 'disc prolapse', 'disc protrusion', 'cauda equina syndrome', 'treatment', 'surgery', 'urodynamic', either alone or in combination using "AND" or "OR". The reference lists of articles retrieved were examined to capture other potentially relevant articles. The search has been restricted to articles published between 1970 and 2012. 79 papers have been found, but only 42 have been reviewed and summarized. Findings The literature revised confirmed correlations between neurogenic bladder and disc disease. Approximately 40% of patients with lumbar disc disease haveabnormal urodynamic testing, and even larger proportion complain voiding symptoms. The most common urodynamic finding is detrusor areflexia, but underactive or overactive detrusor can also be observed. Electromiography can reveal perineal floor muscle innervation abnormalities. Chronic nervous damage induces reduction of bladder sensitivity and detrusor atrophy. A overdistension of bladder follows, with global and circumferential thinning of thickness. Overactive detrusor is related to early nerve roots stretching causing irritative state responsible for overstimulation and neurogenic overactivity. Correlated anatomical deformations could be represented by detrusor hypertrophy. Conclusions Benefits for neurogenic bladder obtained through disc disease treatment should be studied in more detail, especially conservative therapies, not yet discussed in literature. Spine surgery effectiveness on voiding function should be valued in the light of the latest surgical techniques, considering the controversial results reported after laminectomy.
PMID: 23701600 [PubMed - as supplied by publisher]
AIMS: Bombesin receptors (BB receptors) and bombesin related peptides are expressed in the lower urinary tract of rodents. Here we investigated whether in vivo activation of BB receptors can contract the urinary bladder and facilitate micturition in sham rats and in a diabetic rat model of voiding dysfunction.
MATERIAL AND METHODS: In vivo cystometry experiments were performed in adult female Sprague-Dawley rats under urethane anesthesia. Diabetes was induced by streptozotocin (STZ; 65mg/kg, i.p.) injection. Experiments were performed 9 and 20weeks post STZ-treatment. Drugs included neuromedin B (NMB; BB1 receptor preferring agonist), and gastrin-releasing peptide (GRP; BB2 receptor preferring agonist).
KEY FINDINGS: NMB and GRP (0.01 - 100μg/kg in sham rats; 0.1 - 300μg/kg in STZ-treated rats, i.v.) increased micturition frequency, bladder contraction amplitude and area under the curve dose dependently in both sham and STZ-treated rats. In addition, NMB (3, 10μg/kg i.v.) triggered voiding in >80% of STZ-treated rats when the bladder was filled to a sub-threshold voiding volume. NMB and GRP increased mean arterial pressure and heart rate at the highest doses, 100 and 300μg/kg.
SIGNIFICANCE: Activation of bombesin receptors facilitated neurogenic bladder contractions in vivo. Single applications of agonists enhanced or triggered voiding in sham rats as well as in the STZ-treated rat model of diabetic voiding dysfunction. These results suggest that BB receptors may be targeted for drug development for conditions associated with poor detrusor contraction such as underactive bladder.
PMID: 24496039 [PubMed - as supplied by publisher]