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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.
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.
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