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This chapter discusses the role of the cortical and subcortical areas in the control of pelvic organs. It presents case histories, the lesion literature, effects of injury or disease at focal sites. The results of diffuse cortical and subcortical diseases are then considered. The temporal lobes have little or no apparent influence on bladder or bowel control but a major role in determining sexual behavior. Cerebrovascular disease is often accompanied by bladder dysfunction. The severity, extent and site of brain damage following brain injury are so variable that generalizations about the effect of traumatic brain injury on pelvic organ dysfunction are impossible. Recommendations have been made to treat specific aspects of sexual dysfunction following traumatic brain injury. An expected correlation is seen between the occurrence of a neurogenic bladder and the severity and extent of brain damage so that urodynamic abnormalities have been associated with motor deficits.
Based on observations under laboratory conditions of over 300 couples, Masters and Johnson identified four discrete phases of the human sexual response as arousal (excitement), plateau, orgasm and satisfaction. This sequence was subsequently modified to include the phase of sexual drive: Kaplan proposed a triphasic response model, each phase with a distinct underlying neurophysiological basis. Libido is defined as the biological need for sexual activity (sex drive) and depends upon hypothalamic and temporal lobe functioning. This chapter outlines the roles of the subcortical and cortical regions, spinal connections and peripheral innervation involved in the phases of the human sexual cycle, with reference to the experimental animal literature and mention of the dysfunctions that can result from neurological disease at each level. Findings from recent functional imaging experiments are discussed in the context of the role of the cortical regions in human neurological control of sexual function.
Based on observations under laboratory conditions of over 300 couples, Masters and Johnson identified four discrete phases of the human sexual response as arousal (excitement), plateau, orgasm and satisfaction. This sequence was subsequently modified to include the phase of sexual drive: Kaplan proposed a triphasic response model, each phase with a distinct underlying neurophysiological basis. Libido is defined as the biological need for sexual activity (sex drive) and depends upon hypothalamic and temporal lobe functioning. This chapter outlines the roles of the subcortical and cortical regions, spinal connections and peripheral innervation involved in the phases of the human sexual cycle, with reference to the experimental animal literature and mention of the dysfunctions that can result from neurological disease at each level. Findings from recent functional imaging experiments are discussed in the context of the role of the cortical regions in human neurological control of sexual function.
This chapter discusses the role of the cortical and subcortical areas in the control of pelvic organs. It presents case histories, the lesion literature, effects of injury or disease at focal sites. The results of diffuse cortical and subcortical diseases are then considered. The temporal lobes have little or no apparent influence on bladder or bowel control but a major role in determining sexual behavior. Cerebrovascular disease is often accompanied by bladder dysfunction. The severity, extent and site of brain damage following brain injury are so variable that generalizations about the effect of traumatic brain injury on pelvic organ dysfunction are impossible. Recommendations have been made to treat specific aspects of sexual dysfunction following traumatic brain injury. An expected correlation is seen between the occurrence of a neurogenic bladder and the severity and extent of brain damage so that urodynamic abnormalities have been associated with motor deficits.
Symptoms of colorectal and anal sphincter dysfunction are common in patients with neurological disorders. The most frequent symptoms of neurogenic bowel dysfunction (NBD) are constipation, fecal incontinence, and abdominal pain. Bowel dysfunction should be viewed in relation to other complications following spinal cord injury (SCI). The international bowel function SCI data sets were developed to collect data on bowel symptoms after SCI in a common format. Most clinicians prefer to support the history with more objective investigations. The technique most often used to study colorectal functions in patients with neurological diseases is radiographically determined colorectal transit time (CTT). Physical evaluation should be performed in all patients. Perianal inspection should be performed to detect pressure sores, hemorrhoids, anal fissures, rectal prolapse or signs of soiling. Anorectal digitations should be performed to assess anorectal sensibility, anal tone and voluntary contraction.
Afferent nerve endings in the bladder wall are important in conveying the sensations associated with degrees of bladder fullness and also bladder pain to the spinal cord. This chapter discusses the peripheral control of micturition, cellular signaling pathways in normal bladder function, spinal control of bladder function, and interoceptive sensations. Acetylcholine (ACh) and adenosine triphosphate (ATP) are released by the bladder urothelium during urine storage, in increasing concentrations as the bladder wall distends. Muscarinic, nicotinic and purinergic receptors have been identified in the bladder urothelium and/or suburothelium in human or animal studies. In normal adults information about the bladder is passed from the periaqueductal gray (PAG) to higher regions of the brain. This type of interoception is mediated by afferent input through small-diameter fibers in lamina 1 of the spinal cord. A number of spinal reflex mechanisms are involved in the control of the urethro-vesical unit.
Lower urinary tract dysfunction (LUTD) can result from a wide range of neurological conditions. This chapter provides the clinician with an approach to neurogenic bladder dysfunction based on the history, physical examination and investigations, in order to optimize patient management and follow-up. Classification helps with understanding the functional disturbances occurring in neurogenic LUTD. Understanding the underlying dysfunction is paramount before starting treatment. History-taking should address potential dysfunction in both the storage and voiding phases of micturition. Several symptom scales have been validated for the evaluation of urinary disorders, but none are specific for neurogenic LUTD. Physical examination should include neurological, urological, gynecological, abdominal and rectal examination. History, bladder diary and clinical examination may not always be sufficient for understanding the nature of LUTD. Urodynamic tests involve functional and dynamic assessment of the lower urinary tract and are used to assess detrusor and bladder outlet function.
Sexual function is recognized as an important factor determining quality of life and dysfunction in neurological patients may significantly add to the burden of their disease. Any disruption in the sexual response cycle results in sexual dysfunction (SD). Laboratory testing should be tailored according to patient symptoms and risk factors. Fasting glucose and lipid profile may be measured to assess atherosclerotic risk factors for erectile dysfunction (ED). Oral drugs should be considered as first-line therapy for neurogenic ED. There are fewer evidence-based therapeutic options for treatment of female SD. However it is an area of increasing interest and marketing of therapies by pharmaceutical companies. Therapies relate to treatment of sexual desire, arousal, orgasm and/or sexual pain. The term hypoactive sexual desire disorder (HSDD) is used to describe low sexual desire and distress, and many therapies aim to address this aspect of female sexual function.
Pelvic Organ Dysfunction in Neurological Disease describes the neurological control of human bladder, bowel and sexual function and then details the dysfunctions which may arise as a consequence of various neurological diseases. Easy to read, the book will be of value to any healthcare professional managing patients in whom pelvic organ functions have been compromised by neurological disease. The book provides a structured approach to present day understanding of the neurological control of pelvic organs and the investigation and management of each type of organ dysfunction. A unique feature of this book is that it addresses the impact of specific neurological disorders on all three functions. The authors have all been associated with the Department of Uro-Neurology at the National Hospital for Neurology and Neurosurgery, London since it was established 20 years ago. This book is a timely review of their accumulated knowledge and the latest literature.
Lower urinary tract dysfunction (LUTD) can result from a wide range of neurological conditions. This chapter provides the clinician with an approach to neurogenic bladder dysfunction based on the history, physical examination and investigations, in order to optimize patient management and follow-up. Classification helps with understanding the functional disturbances occurring in neurogenic LUTD. Understanding the underlying dysfunction is paramount before starting treatment. History-taking should address potential dysfunction in both the storage and voiding phases of micturition. Several symptom scales have been validated for the evaluation of urinary disorders, but none are specific for neurogenic LUTD. Physical examination should include neurological, urological, gynecological, abdominal and rectal examination. History, bladder diary and clinical examination may not always be sufficient for understanding the nature of LUTD. Urodynamic tests involve functional and dynamic assessment of the lower urinary tract and are used to assess detrusor and bladder outlet function.
Urodynamic investigations in patients with multiple system atrophy (MSA) commonly show detrusor overactivity (DO) as the underlying cause of decreased bladder volumes at first sensation, reduced bladder capacity and urgency incontinence. Incomplete bladder emptying is a significant feature of MSA and worsens with the progression of illness. The bladder neck, also known as the internal urethral sphincter, is an important component in the maintenance of continence and receives sympathetic innervation from the hypogastric nerve. Careful analysis of bladder abnormalities can be helpful in distinguishing between MSA-P and Parkinson's disease (PD), although DO causing urgency and frequency occurs in both conditions, patients with MSA are more likely to have a high PVR, detrusorsphincter dyssynergia and an open bladder neck at the start of bladder filling on videocystometrogram and a neurogenic electromyography (EMG) of the anal sphincter.