The devastating losses following traumatic spinal cord injury(SCI) encompass the motor, sensory and autonomic nervous systems. Neurogenic bowel is a slow transit colonic dysfunction marked by constipation, rectal evac...The devastating losses following traumatic spinal cord injury(SCI) encompass the motor, sensory and autonomic nervous systems. Neurogenic bowel is a slow transit colonic dysfunction marked by constipation, rectal evacuation difficulties, decreased anorectal sensation, fecal incontinence or some combination thereof. Furthermore, neurogenic bowel is one of the most prevalent comorbidities of SCI and is recognized by afflicted individuals and caregivers as a lifelong physical and psychological challenge that profoundly affects quality of life. The restoration of post-injury control of movement has received considerable scientific scrutiny yet the daily necessity of voiding the bowel and bladder remains critically under-investigated. Subsequently, physicians and caregivers are rarely presented with consistent, evidence-based strategies to successfully address the consequences of dysregulated voiding reflexes. Neurogenic bowel is commonly believed to result from the interruption of the supraspinal control of the spinal autonomic circuits regulating the colon. In this mini-review, we discuss the clinical challenges presented by neurogenic bowel and emerging pre-clinical evidence that is revealing that SCI also initiates functional remodeling of the colonic wall concurrent with a decrease in local enteric neurons. Since the enteric input to the colonic smooth muscle is the final common pathway for functional contractions of the colon, changes to the neuromuscular interface must first be understood in order to maximize the efficacy of therapeutic interventions targeting colonic dysfunction following SCI.展开更多
The adaptability of the central nervous system has been revealed in several model systems.Of particular interest to central nervous system-injured individuals is the ability for neural components to be modified for re...The adaptability of the central nervous system has been revealed in several model systems.Of particular interest to central nervous system-injured individuals is the ability for neural components to be modified for regain of function.In both types of neurotrauma,traumatic brain injury and spinal cord injury,the primary parasympathetic control to the gastrointestinal tract,the vagus nerve,remains anatomically intact.However,individuals with traumatic brain injury or spinal cord injury are highly susceptible to gastrointestinal dysfunctions.Such gastrointestinal dysfunctions attribute to higher morbidity and mortality following traumatic brain injury and spinal cord injury.While the vagal efferent output remains capable of eliciting motor responses following injury,evidence suggests impairment of the vagal afferents.Since sensory input drives motor output,this review will discuss the normal and altered anatomy and physiology of the gastrointestinal vagal afferents to better understand the contributions of vagal afferent plasticity following neurotrauma.展开更多
基金supported by grants from the National Institutes of Health,No.NINDS 49177(to GMH)Craig H.Neilsen Foundation Senior Research award,No.295319(to GMH)
文摘The devastating losses following traumatic spinal cord injury(SCI) encompass the motor, sensory and autonomic nervous systems. Neurogenic bowel is a slow transit colonic dysfunction marked by constipation, rectal evacuation difficulties, decreased anorectal sensation, fecal incontinence or some combination thereof. Furthermore, neurogenic bowel is one of the most prevalent comorbidities of SCI and is recognized by afflicted individuals and caregivers as a lifelong physical and psychological challenge that profoundly affects quality of life. The restoration of post-injury control of movement has received considerable scientific scrutiny yet the daily necessity of voiding the bowel and bladder remains critically under-investigated. Subsequently, physicians and caregivers are rarely presented with consistent, evidence-based strategies to successfully address the consequences of dysregulated voiding reflexes. Neurogenic bowel is commonly believed to result from the interruption of the supraspinal control of the spinal autonomic circuits regulating the colon. In this mini-review, we discuss the clinical challenges presented by neurogenic bowel and emerging pre-clinical evidence that is revealing that SCI also initiates functional remodeling of the colonic wall concurrent with a decrease in local enteric neurons. Since the enteric input to the colonic smooth muscle is the final common pathway for functional contractions of the colon, changes to the neuromuscular interface must first be understood in order to maximize the efficacy of therapeutic interventions targeting colonic dysfunction following SCI.
基金the National Institutes of Health(NINDS 49177NINDS 105987)+1 种基金Craig H.Neilsen Foundation Senior Research award(295319)to GMHa grant from the National Institutes of Health(NINDS F31 NS 087834)to EMB。
文摘The adaptability of the central nervous system has been revealed in several model systems.Of particular interest to central nervous system-injured individuals is the ability for neural components to be modified for regain of function.In both types of neurotrauma,traumatic brain injury and spinal cord injury,the primary parasympathetic control to the gastrointestinal tract,the vagus nerve,remains anatomically intact.However,individuals with traumatic brain injury or spinal cord injury are highly susceptible to gastrointestinal dysfunctions.Such gastrointestinal dysfunctions attribute to higher morbidity and mortality following traumatic brain injury and spinal cord injury.While the vagal efferent output remains capable of eliciting motor responses following injury,evidence suggests impairment of the vagal afferents.Since sensory input drives motor output,this review will discuss the normal and altered anatomy and physiology of the gastrointestinal vagal afferents to better understand the contributions of vagal afferent plasticity following neurotrauma.