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Overactivity
Kinds of Overactivity Selected AbstractsAnimal Model with Detrusor Overactivity Caused by Cerebral Infarction as a Useful Tool for Pharmacological Therapeutic ApproachesLUTS, Issue 2009Osamu YOKOYAMA Supra-pontine lesions resulting from neurological disorders, such as vascular disease or Parkinson's disease, cause a sense of urgency, frequency, and/or urge incontinence, all of which constitute an overactive bladder. This phenomenon is due in part to the elimination of cortical inhibitory control of the micturition center in the pontine and in part to facilitation of excitatory control. These controls consist of several neurotransmitter systems that include acetylcholine, dopamine, and glutamate. The development of detrusor overactivity following cerebral infarction is mediated by upregulation and downregulation of excitatory and inhibitory inputs of these neurotransmitter systems to the micturition center in the brain, respectively. [source] Adjustment scales for children and adolescents and Native American Indians: Factorial validity generalization for Ojibwe youthsPSYCHOLOGY IN THE SCHOOLS, Issue 6 2006Gary L. Canivez Replication of the core syndrome factor structure of the Adjustment Scales for Children and Adolescents (ASCA; P.A. McDermott, N.C. Marston, & D.H. Stott, 1993) is reported for a sample of 183 Native American Indian (Ojibwe) children and adolescents from North Central Minnesota. The six ASCA core syndromes produced an identical two-factor solution as the standardization data through principal axis analysis using multiple criteria for the number of factors to extract and retain. Varimax, direct oblimin, and promax rotations produced identical results and nearly identical factor-structure coefficients. Coefficients of congruence resulted in an excellent match to the factorial results of the ASCA standardization sample and a large, independent sample. It was concluded that for these Ojibwe students, the ASCA measures two independent dimensions of psychopathology (i.e., Overactivity and Underactivity) that are similar to the conduct problems/externalizing and withdrawal/internalizing dimensions commonly found in the child psychopathology assessment literature. © 2006 Wiley Periodicals, Inc. Psychol Schs 43: 685,694, 2006. [source] Replication of the Adjustment Scales for Children and Adolescents core syndrome factor structurePSYCHOLOGY IN THE SCHOOLS, Issue 2 2004Gary L. Canivez Independent examination and replication of the core syndrome factor structure of the Adjustment Scales for Children and Adolescents (ASCA; McDermott, Marston, & Stott, 1993) is reported. A sample of 1,020 children were randomly selected from their classroom and rated on the ASCA by their teacher. The six ASCA core syndromes produced a two-factor solution through principle axis analysis using multiple criteria for the number of factors to extract and retain. Varimax, direct oblimin, and promax rotations produced identical results and nearly identical factor structure coefficients. It was concluded that the ASCA indeed measures two independent dimensions of psychopathology (Overactivity and Underactivity) that are similar to the conduct problems/externalizing and withdrawal/internalizing dimensions commonly found in the child psychopathology assessment literature (Cicchetti & Toth, 1991; Quay, 1986). © 2004 Wiley Periodicals, Inc. Psychol Schs 41: 191,199, 2004. [source] Construct validity of the adjustment scales for children and adolescents and the preschool and kindergarten behavior scales: Convergent and divergent evidencePSYCHOLOGY IN THE SCHOOLS, Issue 6 2002Gary L. Canivez Construct validity (convergent and divergent) of the Adjustment Scales for Children and Adolescents (ASCA; McDermott, Marston, & Stott, 1993) and the Preschool and Kindergarten Behavior Scales (PKBS; Merrell, 1994a) is presented. Regular classroom teachers (n = 38) randomly selected 5- and 6-year-old children (N = 123) and rated them on the ASCA and PKBS in counterbalanced order. Convergent evidence of construct validity was observed for the PKBS Externalizing Problems scale and the ASCA Overactivity syndrome. Divergent evidence of construct validity was provided for the PKBS Externalizing Problems scale and ASCA Underactivity syndrome. Convergent and divergent evidence of construct validity for the PKBS Internalizing Problems scale and ASCA Overactivity and Underactivity syndromes was mixed. Results were identical to those of Canivez and Bordenkircher (2002). © 2002 Wiley Periodicals, Inc. Psychol Schs 39: 621,633, 2002. [source] Downregulation of glial glutamate transporters after dopamine denervation in the striatum of 6-hydroxydopamine-lesioned ratsTHE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 4 2008E.K.Y. Chung Abstract Overactivity of glutamatergic neurotransmission in the basal ganglia is known to be closely related to the onset and pathogenesis of Parkinson's disease. Glutamate homeostasis around glutamatergic synapses is tightly regulated by two groups of glutamate transporters: glial glutamate transporters GLT1 (EAAT2) and GLAST (EAAT1), and neuronal glutamate transporter EAAC1. In order to investigate the changes of glutamate transporters after the onset of Parkinson's disease, unilateral 6-hydroxydopamine-lesioned rat, an animal model of Parkinson's disease, was employed. By immunofluorescence and Western blot analyses, GLT1 and GLAST proteins were significantly reduced in the striatum with lesion. No change in GLT1 and GLAST protein was found in the substantia nigra. The reduction of GLT1 protein in the striatum was more prominent than that of GLAST protein (,40% vs. 20%). In addition, EAAC1 protein was found to be increased in the substantia nigra pars reticulata of the lesioned rats but not in the striatum. The present results indicate that reductions of GLT1 and GLAST may impair glutamate homeostasis around glutamatergic synapses in the striatum and contribute to over-spills of glutamate in the system. An increase in the EAAC1 level in the substantia nigra pars reticulata may increase GABA synthesis and enhance GABAergic neurotransmission. These results indicate that there are differential and distinct modulations of glutamate transporters after dopamine denervation in the 6-hydroxydopamine-lesioned rat. J. Comp. Neurol. 511:421,437, 2008. © 2008 Wiley-Liss, Inc. [source] Intrauterine exposure to caffeine and inattention/overactivity in childrenACTA PAEDIATRICA, Issue 6 2010M Bekkhus Abstract Aim:, To determine the association between intrauterine exposure to timing and sources of caffeine and inattention/overactivity, suggesting ADHD in the child. Method:, This study used prospectively collected data from the large population-based study, The Norwegian Mother and Child Cohort Study (MoBa). Participants were 25 343 mothers and their 18-month-old children. Mothers reported on consumption of a number of caffeine sources at the 17th week and 30th week of gestation, as well as child inattention/overactivity at 18 months. Data were analysed using univariate analyses of covariance (ancova). Results:, Once we controlled for confounders, there was a small effect of caffeine intake at 17th week of gestation on inattention/overactivity combined, and both 17th and 30th week of gestation on overactivity, when investigated separately from inattention. Surprisingly, the caffeine effect was only found for soft drinks, not tea or coffee. Conclusion:, Intrauterine exposure to soft drinks rather than coffee, the traditional focus, is associated with maternal reports of overactive behaviour in children aged 18 months. [source] Pregnancy-induced sympathetic overactivity: a precursor of preeclampsia,EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 6 2004T. Fischer Abstract Background, Preeclampsia has been shown to constitute a state of sympathetic overactivity. However, it remains unclear if the sympathetic activity precedes preeclampsia or represents only a secondary phenomenon. To further investigate this issue, we performed a prospective study in pregnant women considered to be at increased risk for preeclampsia owing to preeclampsia during a preceding pregnancy. Materials and methods, Twenty-two women with a history of preeclampsia were longitudinally studied on three occasions: twice during pregnancy (M1: 22 ± 4, M2: 33 ± 5 weeks) and once postpartum (M3: 26 ± 6 weeks postpartum). We measured muscle sympathetic nerve activity (MSNA), forearm blood flow, and blood pressure at rest and during reactive hyperaemia after forearm occlusion. Results, At M1 and M2, none of the subjects was hypertensive, however, muscle sympathetic nerve activity levels were significantly augmented, compared with their postpartum values (M1: 21 ± 9, M2: 29 ± 14, M3: 9 ± 5 bursts min,1; P < 0·05). Forearm vascular resistance did not significantly change from M1 through M3 (M1: 16 ± 9, M2: 15 ± 7, M3: 16 ± 7 U; P = NS). Gestational muscle sympathetic nerve activity values did not differ significantly among the subjects with subsequent preeclampsia compared with those who remained normotensive [with preeclampsia (n = 6): M1: 21 ± 5, M2: 27 ± 6, M3: 7 ± 4 bursts min,1; without preeclampsia (n = 16): M1: 21 ± 11, M2: 30 ± 16, M3: 9 ± 6 bursts min,1; P = NS]. Conclusion, Invariably, all women at risk for preeclampisa showed a pregnancy-induced increase in MSNA (pregnancy-induced sympathetic overactivity, PISO), which normalized after delivery. Most importantly, PISO is not necessarily associated with peripheral vasoconstriction and hypertension. Furthermore, only a subset of patients developed preeclampsia later on. Therefore, we hypothesize that PISO constitutes a precursor of preeclampsia which is physiologically compensated for by vasodilating mechanisms, leading to preeclampsia only when they fail. [source] The pathophysiology of spasticityEUROPEAN JOURNAL OF NEUROLOGY, Issue 2002G. Sheean Spasticity is only one of several components of the upper motor neurone (UMN) syndrome, known collectively as the `positive' phenomena, that are characterized by muscle overactivity. Other components include tendon hyper-reflexia, clonus, the clasp-knife phenomenon, flexor and extensor spasms, a Babinski sign, and spastic dystonia. Spasticity is a form of hypertonia due to hyperexcitable tonic stretch reflexes. It is distinguished from rigidity by its dependence upon the speed of the muscle stretch and by the presence of other positive UMN signs. Hyperactive spinal reflexes mediate most of these positive phenomena, while others are due to disordered control of voluntary movement or abnormal efferent drive. An UMN lesion disturbs the balance of supraspinal inhibitory and excitatory inputs, producing a state of net disinhibition of the spinal reflexes. These include proprioceptive (stretch) and nociceptive (flexor withdrawal and extensor) reflexes. The clinical syndrome resulting from an UMN lesion depends more upon its location and extent, and the time since it occurred, than on the pathology of the lesion. However, the change in spinal reflex excitability cannot simply be due to an imbalance in supraspinal control. The delayed onset after the lesion and the frequent reduction in reflex excitability over time, suggests plasticity in the central nervous system. Knowledge of the electrophysiology and neurochemistry of spinal reflexes, together with the action of antispasticity drugs, helps us to understand the pathophysiology of spasticity. [source] Botulinum toxin injection therapy in the management of lower urinary tract dysfunctionINTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 2006A. K. PATEL Summary We have great pleasure in introducing this supplement containing a collection of articles reviewing the contemporary clinical management of functional disorders of the lower urinary tract (LUT) with particular emphasis on the potential role of botulinum toxin injection therapy. Detrusor sphincter dyssynergia (DSD), detrusor overactivity (DO), painful bladder syndrome (PBS) and LUT symptoms consequent on bladder outflow obstruction (LUTS/BPH) have all been treated by the injection of botulinum toxin. This treatment can be administered as a minimally invasive, outpatient procedure which on the initial trials for DO (particularly of neurogenic aetiology) shows a remarkable efficacy with effects lasting up to a year after a single treatment with few significant side effects. Success has been reported with the management of detrusor sphincter dyssynergia and preliminary series report positive outcomes in the management of PBS and LUTS/BPH. However, most of the studies to date include small numbers and have a recruitment bias with few randomised controlled trials having been reported. The answers to some of the key questions are addressed with reference to our contemporary knowledge. It is clear that considerable work both clinical and basic science still needs to be performed to answer the many remaining questions with regard to this treatment modality but undoubtedly it will be a major future treatment option in those with intractable symptoms or those unable to tolerate medications. Currently, all botulinum toxin use for urological conditions is off-label and unlicensed, therefore caution should be exercised until future large randomised studies are reported. [source] Withdrawal syndrome following cessation of antihypertensive drug therapyINTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 5 2005G. N. Karachalios Summary In this study, a review of the available information concerning abrupt withdrawal of antihypertensive drug therapy is presented. Abrupt withdrawal of these drugs can produce a syndrome of sympathetic overactivity that includes nervousness, tachycardia, headache, agitation and nausea 36,72 h after cessation of the drug. A withdrawal syndrome may occur after discontinuation of almost all types of antihypertensive drugs, but mostly occurs with clonidine, ,-blockers, methyldopa and guanabenz. Less commonly can produce a rapid increase of the blood pressure to pre-treatment levels or above, or both and/or myocardial ischaemia. Although the exact incidence of the syndrome is not known, it appears to be rare, at least in patients receiving standard doses of the above antihypertensive drugs. The best treatment is prevention. In this study regarding the withdrawal syndrome that follows cessation of antihypertensive drugs therapy, a reference to the abrupt discontinuation of the main categories of antihypertensive drugs is also attempted. [source] The bitter truth: Sensitivity to saccharin's bitterness predicts overactivity in highly arousable female dietersINTERNATIONAL JOURNAL OF EATING DISORDERS, Issue 1 2003Melynda L. Craig Abstract Objective The interaction between taste sensitivity and emotionality in rats provides a provocative view of hyperactivity. Rats that have been bred selectively for their reactivity to saccharin exhibit characteristic emotionality. When placed on restrictive diets, these rats exhibit excessive activity levels, relative to rats that are not sensitive to saccharin. Because humans who are highly arousable (i.e., reactive to environmental stimuli) also exhibit an increase in sensitivity to saccharin's bitterness, the current study evaluated whether women who are highly arousable, currently dieting, and sensitive to saccharin's bitterness engage in excessive exercise. Method Participants completed a questionnaire packet, which assessed emotionality, eating patterns, and exercise patterns. On another occasion, they completed a body contour drawings handout, and their weight and height were measured. They also rated saccharin's bitterness and sweetness following a stressful event. Results and Discussion As hypothesized, sensitivity to saccharin's bitterness predicted overactivity in highly arousable female dieters, which reveals the multidimensionality of activity anorexia. © 2003 by Wiley Periodicals, Inc. Int J Eat Disord 34: 71,82, 2003. [source] Autism spectrum disorders and low body weight: Is there really a systematic association?INTERNATIONAL JOURNAL OF EATING DISORDERS, Issue 3 2002Sven Bölte Abstract Objective To examine the relationship between autism spectrum disorders and low body weight. Method The effect of maladaptive social and communicative behavior as well as stereotyped features on the normative body mass index (BMI) was analyzed in 103 subjects with autism or Asperger syndrome. Statistics were controlled for medication, neurological signs, overactivity, and general intelligence. Results Twenty-eight percent of the male individuals had a BMI in the fifth percentile or below. Except for hyperactive behavior, none of the predictors showed a significant association with BMI. None of the subjects met diagnostic criteria for anorexia nervosa. Discussion Although low body weight is often present in male subjects with autism or Asperger syndrome, results indicate that this link is inconsistent and partly mediated by hyperactivity. The co-occurrence of autism spectrum disorders and anorexia nervosa is probably due to chance. © 2002 by Wiley Periodicals, Inc. Int J Eat Disord 31: 349,351, 2002; DOI 10.1002/eat.10015 [source] Changes of bladder activity and glycine levels in the lumbosacral cord after partial bladder outlet obstruction in ratsINTERNATIONAL JOURNAL OF UROLOGY, Issue 9 2008Minoru Miyazato Objectives: We investigated the time course of changes in bladder activity as well as in spinal and serum levels of glutamate and glycine after partial bladder outlet obstruction (BOO) in rats. Methods: A total of 36 female rats were divided into six groups: sham operation (control); 3 days, 14 days, and 28 days after BOO; 3 days and 28 days after relief of BOO. Under urethane anesthesia, isovolumetric cystometry was carried out in each group. Then, spinal and serum levels of glutamate and glycine were measured. Results: The interval between bladder contractions was shorter in all of the groups compared with the control group. The amplitude and duration of bladder contractions was decreased at 3 days, 14 days, and 28 days after BOO, and at 3 days after relief of BOO. Spinal and serum glutamate levels showed no changes. However, the spinal glycine level was decreased at 14 days and 28 days after BOO, and at 28 days after relief of BOO. Serum glycine level was also decreased at 28 days after BOO and 28 days after relief of BOO. Conclusions: Detrusor overactivity during the chronic phase of partial BOO is partly caused by a decrease of glycinergic neuronal activity in the lumbosacral cord. A 3-day period of BOO produces detrusor overactivity, which might be due to an irreversible decrease of spinal glycinergic neuronal activity. [source] Urodynamic findings in children with cerebral palsyINTERNATIONAL JOURNAL OF UROLOGY, Issue 8 2005M IHSAN KARAMAN Abstract Aim: More than one-third of children with cerebral palsy are expected to present with dysfunctional voiding symptoms. The voiding dysfunction symptoms of the cerebral palsy patients in the present study were documented. Methods: Of the study group, 16 were girls and 20 were boys (mean age: 8.2 years). Children with cerebral palsy were evaluated with urodynamics consisting of flow rate, filling and voiding cystometry, and electromyography findings of the external urethral sphincter to determine lower urinary tract functions. Treatment protocols were based on the urodynamic findings. Anticholinergic agents to reduce uninhibited contractions and to increase bladder capacity were used as a treatment. Clean intermittent catheterization and behavioral modification were used for incomplete emptying. Results: Of the children, 24 (66.6%) were found to have dysfunctional voiding symptoms. Daytime urinary incontinence (47.2%) and difficulty urinating (44.4%) were the most common symptoms. Urodynamic findings showed that neurogenic detrusor overactivity (involuntary contractions during bladder filling) with a low bladder capacity was present in 17 (47.2%) children, whereas detrusor,sphincter dyssynergia was present in four patients (11%). The mean bladder capacity of patients with a neurogenic bladder was 52.2% of the expected capacity. Conclusions: The present study concluded that voiding dysfunction was seen in more than half of the children with cerebral palsy, which is a similar result to other published studies. We propose that a rational plan of management of these patients depends on the evaluation of the lower urinary tract dysfunction with urodynamic studies. These children benefit from earlier referral for assessment and treatment. [source] Urodynamic effects and safety of modified intravesical oxybutynin chloride in patients with neurogenic detrusor overactivity: 3 years experienceINTERNATIONAL JOURNAL OF UROLOGY, Issue 8 2004MOTOAKI SAITO Abstract Background:, Intravesical oxybutynin chloride with hydroxypropylcellulose (HPC) (modified intravesical oxybutynin) has been reported to be effective for treatment of overactive bladder. We reported the short-term effects of modified intravesical oxybutynin previously. In the present article, we detail the results of a 3-year follow-up study of patients from our previous analysis and report the efficacy and side-effects of modified intravesical oxybutynin. Methods:, Modified intravesical oxybutynin (5 mg/10 mL, twice a day) was applied for more than 3 years to six neurogenic overactive detrusor patients (three men and three women, average age 53.3 years) who were not satisfied with oral anticholinergic agents or the other therapy. A cystometogram (CMG) was performed before, 1 week after and 3 years after the start of modified intravesical oxybutynin treatment. We evaluated the patient's satisfaction of this treatment after 4 weeks and again after 3 years. We compared the patients' answers before and after the therapy (excellent, good, fair, unchanged and worse). We also monitored systemic and topical side-effects in these patients during this period. Results:, CMG studies showed that two of six patients no longer exhibited uninhibited contraction 1 week after the treatment and that the cystocapacity of patients before, 1 week after and 3 years after the initial modified intravesical oxybutynin was 129.7 ± 19.4, 283.5 ± 40.4 and 286.8 ± 38.1 mL, respectively. For the evaluation of patients' satisfaction with this treatment, four patients considered the therapy excellent and one patient described it as good after both 4 weeks and after 3 years. Two patients dropped out of the study; one developed left ureteral cancer (2.25 years) and the other developed ileus (1.5 years). Dry mouth and acute cystitis were observed in both patients. Conclusion:, Modified intravesical oxybutynin is an effective and relatively safe option of therapy for overactive bladder patients. However, this therapy requires careful observation for emergent side-effects. [source] Solifenacin-induced small bowel pseudo-obstructionJOURNAL OF HOSPITAL MEDICINE, Issue 2 2008Naveen Pemmaraju MD Abstract An 89-year-old woman was admitted to Johns Hopkins Hospital with a small bowel obstruction and symptoms of urinary retention. She had been started on solfenacin for bladder overactivity 10 days prior to her presentation. Withdrawal of the solfenacin resulted in a full recovery, which has persisted for greater than 6 months without surgical intervention. This is the first reported case report of small bowel pseudo-obstruction due to solifenacin. Journal of Hospital Medicine 2008;3:176,178. © 2008 Society of Hospital Medicine. [source] Elimination disorders in people with intellectual disabilityJOURNAL OF INTELLECTUAL DISABILITY RESEARCH, Issue 10 2008E. Van Laecke Incontinence in children with intellectual and physical disabilities is an underestimated problem in paediatric urology. Literature is scarce, often limited to the incidence and urodynamics, and seldom focused on treatment and prevention. Lack of interest and knowledge of this population are the major reasons why urologists know so little. Very often continence difficulties are accepted and even expected in children with intellectual disabilities. The published prevalence of urinary incontinence in children with intellectual and physical disabilities varies between 23% and 86%. In our experience the prevalence ranges from 60% to 65%. The vast majority of these children have bladder dysfunction, showing overactive detrusor and sphincter dyssynergia on video-urodynamic examination. The uroflow pattern is disturbed in over 65% of these children but is not correlated with the degree of urinary incontinence. Over 70% of the children have reduced bladder capacity. This is due to low bladder compliance and restricted fluid intake which effects urinary incontinence and is an important cause of constipation. Constipation is a common problem in intellectual and physical disabled children and there is a correlation between constipation and urinary incontinence. Children with intellectual disability, particularly those with a greater degree of disability need more time to become continent than typically developing children. Children with mild intellectual disability do not differ significantly from typically developing children with regard to nocturnal enuresis and faecal continence but they are more prone to urinary incontinence during the day. Greater mobility is associated with a higher incidence of continence. Some factors that influence continence, such as intellectual and motor capacity cannot easily be influenced but others, such as bladder capacity, detrusor overactivity and fluid intake, are treatable. It is importance that children with intellectual and physical disabilities suffering urinary incontinence are referred for assessment and treatment to increase their quality of life. [source] Factors affecting the risk of behaviour problems in children with severe intellectual disabilityJOURNAL OF INTELLECTUAL DISABILITY RESEARCH, Issue 2 2000O. Chadwick In order to examine the importance of a range of potential risk factors for behaviour problems in children with severe intellectual disability, a sample was identified by the administration of a screening version of the Vineland Adaptive Behaviour Scales (VABS) to the parents of children aged 4,11years attending six special needs schools in three adjacent inner London boroughs. Parents whose children had a VABS standard score of 50 were interviewed using the Disability Assessment Schedule and both parents and teachers completed the Aberrant Behaviour Checklist. Most behaviour problems were more common in ambulant children, but problems less dependent on the ability to walk, such as sleeping difficulties, screaming and self-injury, were equally common in ambulant and non-ambulant children. Among ambulant children, there were few significant associations between the severity of the child's behaviour problems and the age or sex of the child, the presence or absence of epilepsy, and various indices of socio-economic disadvantage. Sleeping difficulties, overactivity, self-injury, destructive behaviour and autistic features, such as social withdrawal and stereotypies, were strongly associated with skills deficits, but aggression, temper tantrums and general disruptive behaviour were not. Limitations in daily living skills were better predictors of behaviour problems than were poor communication skills. [source] Nigrostriatal denervation does not affect glutamate transporter mRNA expression but subsequent levodopa treatment selectively increases GLT1 mRNA and protein expression in the rat striatumJOURNAL OF NEUROCHEMISTRY, Issue 4 2001J.-C. Liévens There is growing evidence that the loss of the nigrostriatal dopaminergic neurones induces an overactivity of the corticostriatal glutamatergic pathway which seems to be central to the physiopathology of parkinsonism. Moreover, glutamatergic mechanisms involving NMDA receptors have been shown to interfere with the therapeutical action of levodopa. Given the key role played by uptake processes in glutamate neurotransmission, this study examined the effects of nigrostriatal deafferentation and of levodopa treatment on the striatal expression of the glutamate transporters GLT1, GLAST and EAAC1 in the rat. No significant changes in striatal mRNA levels of these transporters were detected after either levodopa treatment (100 mg/kg; i.p., twice a day for 21 days) or unilateral lesion of the nigrostriatal pathway by intranigral 6-hydroxydopamine injection. In contrast, animals with the lesion subsequently treated with levodopa showed a selective increase (36%) in GLT1 mRNA levels in the denervated striatum versus controls. These animals also showed increased GLT1 protein expression, as assessed by immunostaining and western blotting. These data provide the first evidence that levodopa therapy may interfere with striatal glutamate transmission through change in expression of the primarily glial glutamate transporter GLT1. We further suggest that levodopa-induced GLT1 overexpression may represent a compensatory mechanism preventing neurotoxic accumulation of endogenous glutamate. [source] Tension-free vaginal tape-obturator procedure for treatment of severe urodynamic stress incontinence: Subjective and objective outcomes during 2 years of follow-upJOURNAL OF OBSTETRICS AND GYNAECOLOGY RESEARCH (ELECTRONIC), Issue 6 2009Tsung-Hsien Su Abstract Aim:, To report our experience of the tension-free vaginal tape-obturator (TVT-O) procedure for the treatment of severe female urodymanic stress incontinence (USI) during 2 years of follow-up. Methods:, Between January 2005 and June 2007, 67 women with severe USI who underwent the TVT-O procedure were enrolled in the study. Pelvic examination, pad test, urodynamic study, and quality of life (QoL) assessment were performed pre- and post-operatively. Regular follow-up was arranged for analysis. Results:, The median duration of follow-up was 24 months. The objective cure rate was 76.2%. The postoperative pad test revealed significant reduction of leakage. The subjective cure rate was 83.5%, and improvement occurred in 14.9%. The postoperative QoL showed significant improvement. One (1.5%) extrusion of tape occurred and three cases of de novo detrusor overactivity were detected. Three patients (4.4%) had immediate postoperative urine retention. No major complications occurred. Conclusion:, Our results show that the TVT-O procedure is an effective and safe surgical procedure for severe female USI with satisfactory outcomes, significant improvement in quality of life, and few complications during 2 years of follow-up. [source] Novel Biomarkers for Diagnosis and Therapeutic Assessment of Overactive Bladder: Urinary Nerve Growth Factor and Detrusor Wall ThicknessLUTS, Issue 2009Hann-Chorng KUO Clinical diagnosis of overactive bladder (OAB) varies greatly and is based on subjective symptoms. A better way to diagnose and assess therapeutic outcome in patients who present with OAB needs to be developed. Evidence has shown that urinary proteins, such as nerve growth factor (NGF) and prostaglandin E2 (PGE2) levels increase in patients with OAB, bladder outlet obstruction (BOO) and detrusor overactivity (DO). Urinary NGF level increases physiologically in normal subjects at urge to void, but increases pathologically in OAB patients at small bladder volume and at urgency sensation. Patients with OAB dry and OAB wet have significantly higher urinary NGF levels compared to controls and patients with increased bladder sensation. Urinary NGF levels decrease after antimuscarinic therapy and further decrease after detrusor botulinum toxin injections in refractory OAB. A higher urinary NGF level could be a biomarker for sensory nerve-mediated DO. Urinary NGF levels could be a potential biomarker for diagnosis of OAB and serve for the assessment of the therapeutic effect of antimuscarinic therapy. Another potential biomarker for the diagnosis of OAB is detrusor wall thickness. It has been hypothesized that the bladder wall increases in thickness in patients with OAB. The thickened detrusor wall might decrease in response to antimuscarinic treatment, and measurement of detrusor wall thickness might be a useful biomarker for the evaluation of OAB. However, current investigations do not yet provide a uniform observation among various studies. [source] Animal Model with Detrusor Overactivity Caused by Cerebral Infarction as a Useful Tool for Pharmacological Therapeutic ApproachesLUTS, Issue 2009Osamu YOKOYAMA Supra-pontine lesions resulting from neurological disorders, such as vascular disease or Parkinson's disease, cause a sense of urgency, frequency, and/or urge incontinence, all of which constitute an overactive bladder. This phenomenon is due in part to the elimination of cortical inhibitory control of the micturition center in the pontine and in part to facilitation of excitatory control. These controls consist of several neurotransmitter systems that include acetylcholine, dopamine, and glutamate. The development of detrusor overactivity following cerebral infarction is mediated by upregulation and downregulation of excitatory and inhibitory inputs of these neurotransmitter systems to the micturition center in the brain, respectively. [source] Restless legs syndrome: Evidence for nocturnal hypothalamic-pituitary-adrenal system activation,MOVEMENT DISORDERS, Issue 8 2010Claudia Schilling MD Abstract Epidemiological studies consistently point to a relationship between restless legs syndrome (RLS) and cardiovascular disease. The mechanism underlying this association is unclear. Activation of the hypothalamic-pituitary-adrenal (HPA) system has been shown to contribute to the metabolic syndrome and an enhanced cardiovascular risk. We investigated cortisol levels as an indicator of HPA system activity in RLS during the nighttime, when RLS symptoms are at their maximum. We assessed nocturnal urinary cortisol excretion in 73 patients with RLS and 34 healthy controls, controlling for age and gender. Urine sampling was paralleled by polysomnographic recordings. We found significantly enhanced nocturnal cortisol excretion in RLS, demonstrating nocturnal HPA system overactivity in RLS. HPA system overactivity is a possible mechanism contributing to the enhanced load of cardiovascular disease in RLS patients. Nocturnal cortisol release showed weak correlations with some polysomnographic parameters of disturbed sleep, making a potential contribution of RLS-induced sleep disruption to HPA system activation conceivable. © 2010 Movement Disorder Society [source] Genitourinary dysfunction in Parkinson's disease,MOVEMENT DISORDERS, Issue 1 2010Ryuji Sakakibara MD Abstract Bladder dysfunction (urinary urgency/frequency) and sexual dysfunction (erectile dysfunction) are common nonmotor disorders in Parkinson's disease (PD). In contrast to motor disorders, genitourinary autonomic dysfunctions are often nonresponsive to levodopa treatment. The brain pathology causing the bladder dysfunction (appearance of overactivity) involves an altered dopamine-basal ganglia circuit, which normally suppresses the micturition reflex. By contrast, hypothalamic dysfunction is mostly responsible for the sexual dysfunction (decrease in libido and erection) in PD, via altered dopamine-oxytocin pathways, which normally promote libido and erection. The pathophysiology of the genitourinary dysfunction in PD differs from that in multiple system atrophy; therefore, it might aid in differential diagnosis. Anticholinergic agents are used to treat bladder dysfunction in PD, although these drugs should be used with caution particularly in elderly patients who have cognitive decline. Phosphodiesterase inhibitors are used to treat sexual dysfunction in PD. These treatments might be beneficial in maximizing the patients' quality of life. © 2010 Movement Disorder Society [source] Normal interhemispheric inhibition in persistent developmental stuttering,MOVEMENT DISORDERS, Issue 5 2009Martin Sommer MD Abstract Imaging studies suggest a right hemispheric (pre)motor overactivity in patients with persistent developmental stuttering (PDS). The interhemispheric inhibition (IHI) studied with transcranial magnetic stimulation is an established measure of the interplay between right and left motor areas. We assessed IHI in 15 young male adults with PDS and 15 age-matched fluent-speaking subjects. We additionally studied the ipsilateral silent period (iSP) duration. We found no significant between-group difference for IHI or for iSP duration. We conclude that the interplay between the primary motor cortices is normal in patients with PDS. The abnormal right motor and premotor activity observed in functional imaging studies on PDS are not likely to reflect altered primary motor cortex excitability, but are likely to have a different origin. © 2009 Movement Disorder Society [source] Incomplete emptying and urinary retention in multiple-system atrophy: When does it occur and how do we manage it?MOVEMENT DISORDERS, Issue 6 2006Takashi Ito MD Abstract Neurogenic urinary retention can be a major cause of morbidity in multiple-system atrophy (MSA). However, the timing of its appearance has not been entirely clear, and neither have the medical and surgical modalities for managing patients. We present the data obtained from our uroneurological assessment and therapeutic interventions at various stages of MSA. We recruited 245 patients with probable MSA. We measured postvoid residuals (PVR) and performed EMG cystometry in all patients. The grand average volume of PVR was 140 mL (range, 0,760) in our patients. The average PVR volume was 71 mL in the first year, increasing to 129 mL in the second year and 170 mL by the fifth year. The percentages of patients with complete urinary retention, acontractile detrusor, and detrusor,sphincter dyssynergia (DSD) also increased. The increase in PVR resulted in a decrease in functional bladder capacity, together with an increase in detrusor overactivity and neurogenic sphincter EMG. Clean intermittent self-catheterization (CISC) was introduced in most patients. Bladder-oriented therapy (cholinergic agents) had a limited value, whereas urethra-oriented therapy benefited patients with DSD (surgery) for up to 2 years, but syncope occurred in a subset of patients (,-blockers). MSA patients present with large PVR by the second year of illness, and that large PVR secondarily causes urinary frequency. CISC is the recommended treatment for most patients. Urethra-oriented medication and surgery benefit patients who would have difficulty performing CISC, although careful consideration of the short-term efficacy and potential adverse effects of these alternatives is mandatory. © 2006 Movement Disorder Society [source] Pathophysiology of spastic paresis.MUSCLE AND NERVE, Issue 5 2005II: Emergence of muscle overactivity Abstract In the subacute and chronic stages of spastic paresis, stretch-sensitive (spastic) muscle overactivity emerges as a third fundamental mechanism of motor impairment, along with paresis and soft tissue contracture. Part II of this review primarily addresses the pathophysiology of the various forms of spastic overactivity. It is argued that muscle contracture is one of the factors that cause excessive responsiveness to stretch, which in turn aggravates contracture. Excessive responsiveness to stretch also impedes voluntary motor neuron recruitment, a concept termed stretch-sensitive paresis. None of the three mechanisms of impairment (paresis, contracture, and spastic overactivity) is symmetrically distributed between agonists and antagonists, which generates torque imbalance around joints and limb deformities. Thus, each may be best treated focally on an individual muscle-by-muscle basis. Intensive motor training of the less overactive muscles should disrupt the cycle of paresis,disuse,paresis, and concomitant use of aggressive stretch and focal weakening agents in their more overactive and shortened antagonists should break the cycle of overactivity,contracture,overactivity. Muscle Nerve, 2005 [source] Botulinum toxins in neurological diseaseMUSCLE AND NERVE, Issue 5 2004Cynthia L. Comella MD Abstract Botulinum toxins are among the most potent neurotoxins known to humans. In the past 25 years, botulinum toxin has emerged as both a potential weapon of bioterrorism and as a powerful therapeutic agent, with growing applications in neurological and non-neurological disease. Botulinum toxin is unique in its ability to target peripheral cholinergic neurons, preventing the release of acetylcholine through the enzymatic cleavage of proteins involved in membrane fusion, without prominent central nervous system effects. There are seven serotypes of the toxin, each with a specific activity at the molecular level. Currently, serotypes A (in two preparations) and B are available for clinical use, and have been shown to be safe and effective for the treatment of dystonia, spasticity, and other disorders in which muscle overactivity gives rise to symptoms. This review focuses on the pharmacology, electrophysiology, immunology, and application of botulinum toxin in selected neurological disorders. Muscle Nerve 29: 628,644, 2004 [source] Urodynamic effects of silodosin, a new ,1A -adrenoceptor selective antagonist, for the treatment of benign prostatic hyperplasia,,NEUROUROLOGY AND URODYNAMICS, Issue 4 2010Tomonori Yamanishi Abstract Aims To investigate urodynamically the effects of silodosin, a new ,1A -adrenoceptor-selective antagonist, in the treatment of benign prostatic hyperplasia (BPH). Methods Thirty six male patients with BPH (69.9,±,7.3 years), who were referred as candidates for surgery, were treated with silodosin (4,mg twice daily). The total International Prostate Symptom Score (IPSS) was 20.7,±,7.4, maximum flow rate (Qmax) was 6.7,±,3.0,ml/sec, and prostate volume was 45.6,±,24.5,ml. Results Total IPSS, storage and voiding symptom subscores and QOL score decreased significantly, and Qmax increased significantly after 1,12 months of therapy (all P,<,0.05). In urodynamic study (n,=,29), maximum cystometric capacity increased significantly (P,=,0.0027), and detrusor overactivity disappeared in 8 of 20 patients (40%) and improved (bladder capacity increased more than 50%) in 7 (35%) after the therapy. In pressure/flow studies (n,=,27), the obstruction grade was improved in 15 patients (56%). Detrusor opening pressure, detrusor pressure at Qmax, bladder outlet obstruction index, and Schäfer's obstruction class decreased significantly after therapy (all P,<,0.01). After 12 months, 16 patients (44%) are still on silodosin for 23.3,±,7.0 (range 12,36) months, and the improvements in IPSS and Qmax were stable. Twenty patients withdrew because of insufficient effectiveness in 13 patients (12 patients underwent surgery), side effects in 3, and unknown reasons in 4. Conclusion Silodosin appears to improve detrusor overactivity and obstruction grade in patients with BPH. With silodosin treatment, LUTS could be managed effectively for more than a year in at least 44% of the patients. Neurourol. Urodynam. 29:558,562, 2010. © 2009 Wiley-Liss, Inc. [source] Urgency: All or none phenomenon?,NEUROUROLOGY AND URODYNAMICS, Issue 4 2010Stefan De Wachter Abstract Urgency is the key symptom of a very prevalent symptom complex, the overactive bladder syndrome. Addressing urgency as a hallmark for detrusor overactivity is for physicians very comfortable, but appears to be an oversimplification of a very complex symptom entity. This overview tries to put the relevant literature on urgency against the question whether urgency is an all or none phenomenon, and summarizes the current views on how urgency is perceived. Neurourol. Urodynam. 29:616,617, 2010. © 2010 Wiley-Liss, Inc. [source] | ||||||||||||||||||||||||||||||||||