Neurogenic Causes of Detrusor Underactivity

Kadow, Brian T.; Tyagi, Pradeep; Chermansky, Christopher

doi:10.1007/s11884-015-0331-6

Cited by 28 publications

(12 citation statements)

References 69 publications

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“…Having been shown to result in a complex cascade of pathophysiological and neurochemical events, TBI concerns adversities towards both recovery and stress level, and therefore warrants attention [ 36 , 37 ]. Disruption of neural connections between the cerebral cortex and the brainstem due to TBI frequently impairs bladder control [ 38 ]. This is consistent with the high rate of genitourinary comorbidities in older males and females in our study.…”

Section: Main Textmentioning

confidence: 99%

Clinical profile and comorbidity of traumatic brain injury among younger and older men and women: a brief research notes

et al. 2017

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ObjectiveComorbid disorders influence the course and outcomes of rehabilitation following traumatic brain injury (TBI), yet sex- and age-related disparities in the frequency distribution of these disorders remain poorly understood. We aimed to describe comorbid disorders by the International Classification of Diseases in patients with TBI undergoing inpatient rehabilitation in Ontario, Canada over a 3-year period, by sex and age, and discuss their potential impact on rehabilitation outcomes.ResultsThe percentage of TBI patients with one or more comorbid disorder is higher among older (≥65 years) men and women than among those who are younger or middle-aged (<65 years). Among younger and middle-aged patients, multiple injuries and trauma, mental health conditions, and nervous system disorders were the most prevalent comorbidities. In older patients, circulatory, endocrine, nutritional, metabolic, and immune disorders were the most prevalent comorbidities. Our results suggest that a multisystem view of rehabilitation of men and women with TBI across age categories is needed to reflect the complex clinical profile of TBI patients undergoing rehabilitation.Electronic supplementary materialThe online version of this article (doi:10.1186/s13104-017-2682-x) contains supplementary material, which is available to authorized users.

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Section: Main Textmentioning

confidence: 99%

Clinical profile and comorbidity of traumatic brain injury among younger and older men and women: a brief research notes

et al. 2017

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“…As they aged more, both male and female GM2 Synthase KO mice showed a decrease in the numbers of void spots produced in urinary pattern tests. By 19–20 months, GM2 Synthase KO mice also developed bladder enlargement that paralleled the decrease in void spots, which is consistent with hyporeflexia and/or urinary retention due to detrusor underactivity (Cockayne et al, 2000) a dysfunction that is common in patients with PD (Kadow et al, 2015). We had anticipated that such dysfunction may have resulted from PD-like aggregation of aSyn and Lewy body/Lewy neurite formation in neurons in the brain micturition centers or in bladder.…”

Section: Discussionmentioning

confidence: 62%

Parkinsonian GM2 synthase knockout mice lacking mature gangliosides develop urinary dysfunction and neurogenic bladder

Gil-Tommee

Vidal-Martinez

Reyes

et al. 2019

Experimental Neurology

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Parkinson’s disease is a neurodegenerative disorder that reduces a patients’ quality of life by the relentless progression of motor and non-motor symptoms. Among the non-motor symptoms is a condition called neurogenic bladder that is associated with detrusor muscle underactivity or overactivity occurring from neurologic damage. In Parkinson’s disease, Lewy-body-like protein aggregation inside neurons typically contributes to pathology. This is associated with dopaminergic neuron loss in substantia nigra pars compacta (SNc) and in ventral tegmental area (VTA), both of which play a role in micturition. GM1 gangliosides are mature glycosphingolipids that enhance normal myelination and are reduced in Parkinson’s brain. To explore the role of mature gangliosides in vivo, we obtained GM2 Synthase knockout (KO) mice, which develop parkinsonian pathology including a loss of SNc dopaminergic neurons, which we reconfirmed. However, bladder function and innervation have never been assessed in this model. We compared GM2 Synthase KO and wild type (WT) littermates’ urination patterns from 9–19 months of age by counting small and large void spots produced during 1 hour tests. Because male and female mice had different patterns, we evaluated data by sex and genotype. Small void spots were significantly increased in 12–16 month GM2 Synthase KO females, consistent with overactive bladder. Similarly, at 9–12 month GM2 KO males tended to have more small void spots than WT males. As GM2 Synthase KO mice aged, both females and males had fewer small and large void spots, consistent with detrusor muscle underactivity. Ultrasounds confirmed bladder enlargement in GM2 Synthase KO compared to WT mice. Tyrosine hydroxylase (TH) immunohistochemistry revealed significant dopaminergic loss in GM2 Synthase KO VTA and SNc, and a trend toward TH loss in GM2 KO periaqueductal gray (PAG) micturition center. Levels of the nerve growth factor precursor, proNGF, were significantly increased in GM2 Synthase KO bladders and transmission electron micrographs established atypical myelination of pelvic ganglion innervation in GM2 Synthase KO bladders. Cumulatively, our findings provide the first evidence that mature ganglioside loss affects micturition center TH neurons as well as proNGF dysregulation and innervation of the bladder. Thus, identifying therapies that will counteract these effects could be beneficial for those suffering from Parkinson’s disease and related disorders.

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“…DESD is defined as a spontaneous contraction of the external urethral sphincter over an involuntary detrusor contraction, and the PMC plays a vital role in synchronizing external urethral relaxation prior to it. DESD leads to a circumstance of high storage pressure and incomplete bladder emptying [22]. Significantly increased levels of ICI were observed in TBI rats compared to NC rats.…”

Section: Discussionmentioning

confidence: 99%

Cystometric Measurements in Rats with an Experimentally Induced Traumatic Brain Injury and Voiding Dysfunction: A Time-Course Study

et al. 2019

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Traumatic brain injuries (TBIs) are a serious public health issue worldwide with increased mortality as well as severe disabilities and injuries caused by falls and road accidents. Unfortunately, there is no approved therapy for TBIs, and bladder dysfunction is a striking symptom. Accordingly, we attempted to analyze bladder dysfunction and voiding efficiency in rats with a TBI at different time-course intervals. Time-dependent analyses were scheduled from the next day until four weeks after a TBI. Experimental animals were grouped and analyzed under the above conditions. Cystometric measurements were used for this analysis and were further elaborated as external urethral sphincter electromyographic (EUS-EMG) activity and cystometrogram (CMG) measurements. Moreover, magnetic resonance imaging (MRI) studies were conducted to investigate secondary injury progression in TBI rats, and results were compared to normal control (NC) rats. Results of EUS-EMG revealed that the burst period, active period, and silent period in TBI rats were drastically reduced compared to NC rats, but they increased later and reached a stagnant phase. Likewise, in CMG measurements, bladder function, the voided volume, and voiding efficiency decreased immediately after the TBI, and other parameters like the volume threshold, inter-contraction interval, and residual volume drastically increased. Later, those levels changed, and all observed results were compared to NC rats. MRI results revealed the prevalence of cerebral edema and the progression of secondary injury. All of the above-stated results of the experiments were extensively substantiated. Thus, these innovative findings of our study model will surely pave the way for new therapeutic interventions for TBI treatment and prominently highlight their applications in the field of neuroscience in the future.

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Neurogenic Causes of Detrusor Underactivity

Cited by 28 publications

References 69 publications

Clinical profile and comorbidity of traumatic brain injury among younger and older men and women: a brief research notes

Clinical profile and comorbidity of traumatic brain injury among younger and older men and women: a brief research notes

Parkinsonian GM2 synthase knockout mice lacking mature gangliosides develop urinary dysfunction and neurogenic bladder

Cystometric Measurements in Rats with an Experimentally Induced Traumatic Brain Injury and Voiding Dysfunction: A Time-Course Study

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