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Micturition Center (micturition + center)
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] Changes in afferent activity after spinal cord injury,NEUROUROLOGY AND URODYNAMICS, Issue 1 2010William C. de Groat Abstract Aims To summarize the changes that occur in the properties of bladder afferent neurons following spinal cord injury. Methods Literature review of anatomical, immunohistochemical, and pharmacologic studies of normal and dysfunctional bladder afferent pathways. Results Studies in animals indicate that the micturition reflex is mediated by a spinobulbospinal pathway passing through coordination centers (periaqueductal gray and pontine micturition center) located in the rostral brain stem. This reflex pathway, which is activated by small myelinated (A,) bladder afferent nerves, is in turn modulated by higher centers in the cerebral cortex involved in the voluntary control of micturition. Spinal cord injury at cervical or thoracic levels disrupts voluntary voiding, as well as the normal reflex pathways that coordinate bladder and sphincter function. Following spinal cord injury, the bladder is initially areflexic but then becomes hyperreflexic due to the emergence of a spinal micturition reflex pathway. The recovery of bladder function after spinal cord injury is dependent in part on the plasticity of bladder afferent pathways and the unmasking of reflexes triggered by unmyelinated, capsaicin-sensitive, C-fiber bladder afferent neurons. Plasticity is associated with morphologic, chemical, and electrical changes in bladder afferent neurons and appears to be mediated in part by neurotrophic factors released in the spinal cord and the peripheral target organs. Conclusions Spinal cord injury at sites remote from the lumbosacral spinal cord can indirectly influence properties of bladder afferent neurons by altering the function and chemical environment in the bladder or the spinal cord. Neurourol. Urodynam. 29: 63,76, 2010. © 2009 Wiley-Liss, Inc. [source] Bladder control, urgency, and urge incontinence: Evidence from functional brain imaging,NEUROUROLOGY AND URODYNAMICS, Issue 6 2008Derek Griffiths Abstract Aim To review brain imaging studies of bladder control in subjects with normal control and urge incontinence; to define a simple model of supraspinal bladder control; and to propose a neural correlate of urgency and possible origins of urge incontinence. Methods Review of published reports of brain imaging relevant to urine storage, and secondary analyses of our own recent observations. Results In a simple model of normal urine storage, bladder and urethral afferents received in the periaqueductal gray (PAG) are mapped in the insula, forming the basis of sensation; the anterior cingulate gyrus (ACG) provides monitoring and control; the prefrontal cortex makes voiding decisions. The net result, as the bladder fills, is inhibition of the pontine micturition center (PMC) and of voiding, together with gradual increase in insular response, corresponding to increasing desire to void. In urge-incontinent subjects, brain responses differ. At large bladder volumes and strong sensation, but without detrusor overactivity (DO), most cortical responses become exaggerated, especially in ACG. This may be both a learned reaction to previous incontinence episodes and the neural correlate of urgency. The neural signature of DO itself seems to be prefrontal deactivation. Possible causes of urge incontinence include dysfunction of prefrontal cortex or limbic system, suggested by weak responses and/or deactivation, as well as abnormal afferent signals or re-emergence of infantile reflexes. Conclusions Bladder control depends on an extensive network of brain regions. Dysfunction in various parts may contribute to urge incontinence, suggesting that there are different phenotypes requiring different treatments. Neurourol. Urodynam. 27:466,474, 2008. © 2007 Wiley-Liss, Inc. [source] Voiding reflex in chronic spinal cord injured cats induced by stimulating and blocking pudendal nerves,,NEUROUROLOGY AND URODYNAMICS, Issue 6 2007Changfeng Tai Abstract Aims To induce efficient voiding in chronic spinal cord injured (SCI) cats. Methods Voiding reflexes induced by bladder distension or by electrical stimulation and block of pudendal nerves were investigated in chronic SCI cats under ,-chloralose anesthesia. Results The voiding efficiency in chronic SCI cats induced by bladder distension was very poor compared to that in spinal intact cats (7.3,±,0.9% vs. 93.6,±,2.0%, P,<,0.05). In chronic SCI cats continuous stimulation of the pudendal nerve on one side at 20 Hz induced large amplitude bladder contractions, but failed to induce voiding. However, continuous pudendal nerve stimulation (20 Hz) combined with high-frequency (10 kHz) distal blockade of the ipsilateral pudendal nerve elicited efficient (73.2,±,10.7%) voiding. Blocking the pudendal nerves bilaterally produced voiding efficiency (82.5,±,4.8%) comparable to the efficiency during voidings induced by bladder distension in spinal intact cats, indicating that the external urethral sphincter (EUS) contraction was caused not only by direct activation of the pudendal efferent fibers, but also by spinal reflex activation of the EUS through the contralateral pudendal nerve. The maximal bladder pressure and average flow rate induced by stimulation and bilateral pudendal nerve block in chronic SCI cats were also comparable to those in spinal intact cats. Conclusions This study shows that after the spinal cord is chronically isolated from the pontine micturition center, bladder distension evokes a transient, inefficient voiding reflex, whereas stimulation of somatic afferent fibers evokes a strong, long duration, spinal bladder reflex that elicits efficient voiding when combined with blockade of somatic efferent fibers in the pudendal nerves. Neurourol. Urodynam. 26:879,886, 2007. © 2007 Wiley-Liss, Inc. [source] Ascending and descending brainstem neuronal activity during cystometry in decerebrate catsNEUROUROLOGY AND URODYNAMICS, Issue 4 2003Kimio Sugaya Abstract Aims This study was undertaken to examine the distribution of pontomedullary neurons related to micturition or urine storage, as well as the connections between the pontine micturition center (PMC), medullary neurons, and the spinal cord. Methods In decerebrate cats, extracellular recording of the rostral pontine and rostral medullary neurons was performed. Firing of each neuron was quantitated during cystometry. Connections between the PMC, medullary neurons, and the spinal cord (L1) were also examined electrophysiologically. Results Ninety-four neurons showed an increase or decrease of the firing rate during micturition. Units with an antidromic response to L1 stimulation and an increased firing rate were located in the nucleus locus coeruleus alpha (LCa; n,=,8) corresponding to the PMC, and in the medial reticular formation (MRF) of the medulla (n,=,14). Units showing a decreased firing rate were located in the nucleus reticularis pontis oralis (PoO; n,=,26) and in the MRF (n,=,11). The latencies of antidromic and orthodromic responses of the LCa units were longer than those of the PoO units. MRF neurons responded antidromically and/or orthodromically to stimulation of the PMC or L1. Conclusions These results suggest that the pathway concerned with urine storage has a faster spinobulbospinal loop than the micturition reflex pathway and that rostral medullary neurons also play an important role in micturition and urine storage. There may be two descending pathways between the PMC and the spinal cord: both a direct pathway and one by means of medullary neurons. Neurourol. Urodynam. 22:343,350, 2003. © 2003 Wiley-Liss, Inc. [source] | ||||||||||