**1. Introduction**

The normal functioning of the urinary system is closely related to the functional integrity of the central nervous system (CNS). Neuro-urological symptoms may be caused by a variety of diseases and events affecting the nervous system controlling the lower urinary tract (LUT). The resulting neuro-urological symptoms depend predominantly on the location and the extent of the neurological lesion. There are no exact figures on the overall prevalence of neurourological disorders in the general population, but data are available on the prevalence of the underlying conditions and the relative risk of these for the development of neuro-urological

© 2016 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2018 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

symptoms. The majority of the data show a very wide range of prevalence/incidence. This reflects the variability in the cohort (e.g. early or late stage disease) and the frequently small sample sizes, resulting in a low level of evidence in most published data. Spinal cord injury patients may be the most studied group among neurogenic patients.

The physiological function of the lower urinary tract is characterized by the central control of the urinary reflexes (inhibition or removal of reflex inhibition) from the upper cortical centers of the cortex. Urine concentration within the bladder results in an increase in intravesical pressure that causes stimulation of the thoracic-lymphatic sympathetic center (T10-L2) via transient and adductor nerve fibers. Adjacent nerve fibers transfer the stimulus to the breech centers of urination and from there to the upper centers of the cerebral cortex. Then, if there is no central depression, the urinary reflex is manifested through the contraction of the detrusor resulting in the sympathetic nerves. However, if urination is undesirable, this reflex is inhibited as cationic signals inhibit sympathetic stimulation at the level of the thoracic-lumbar sympathetic center and increase the muscular tone of the external sphincter by suture from the pelvic neural mesh formed by the S2–S4 level. From the above, it is clear that any damage at any level of SC results in disorders of lower urinary function. These disorders vary according to level [11, 12], the degree (complete or incomplete) [13] and the extent of the damage.

Urinary Tract Infections in Neuro-Patients http://dx.doi.org/10.5772/intechopen.79690 63

Neurogenic urinary tract dysfunction characterized by increased intravesical pressures and/ or urine residual [14]. These patients have decreased microorganism removal capacity [15]. Both incomplete emptying of the bladder [16] and high intravesical pressure [17, 18] are accompanied by an increased risk of UTI. Patients who have been using Credé maneuver for a long time to empty their bladder have had severe complications in the upper urinary tract (82% pyuria, 60% ureter dilation, 35% hydronephrosis, and 16% renal failure). Men appeared more susceptible to upper urinary tract damage than to women [19]. According to Esclarin De Ruz et al [20] in patients with SCI with detrusor overactivity, the coexistence of detrusor-

Under normal circumstances, the ureterovesical junction allows urine to enter the bladder but prevents urine from regurgitating into the ureter and the kidney. This results in the kidney being protected from high pressure in the bladder and from contamination by vesical bacteria. In this way, vesicoureteral reflux is considered to be an important factor in urinary tract infection [20]. It occurs in 10% of patients over 4 years of SCI [21]. Although the reflux is the result of high intravesical pressure, it must be controlled by another neurological mechanism since patients with a T10- L2 lesion exhibit more regressive effects than patients who have a level of damage above or below this level [22]. The damage at this level is probably related to the ureteral peristaltic mechanisms.

Intermittent catheterization (IC) during the recovery period appears to reduce the rate of urinary tract infections and substantially eliminate many of the complications associated with the use of an indwelling catheter [23, 24]. However, IC may also present certain

sphincter dyssynergia duplicates the risk of urinary tract infections.

**2. Associated risk factors**

**2.2. Vesicoureteral reflux**

**2.3. Intermittent catheterization**

**2.1. Increased intravesical pressures**

Spinal cord injury (SCI) is a damage to the spinal cord from traumatic or nontraumatic etiology, as defined by the International Spinal Cord Society (ISCoS) [1]. It is difficult to accurately calculate the worldwide prevalence and incidence of SCI due to the lack of standardized methods of assessment across regions and limited information in the data collected. The incidence varies from 12 to more than 65 cases/million per year. Data from Olmsted County, Minnesota, United States, from 1975 to 1981, showed an age- and sex-adjusted incidence rate of 71 spinal cord injuries/million [2]. The annual incidence of SCI reported for the year 1991 was around 30.0–32.1 persons/million population in the United States, meaning 7500 and 8000 new cases per year at that time [3]. In 2016, the estimated annual incidence of SCI was approximately 54 cases/million population or 17,000 new SCI cases each year [4]. The annual incidence varies widely by country. From 27 per million persons in Japan, 8–13.4 in Switzerland, 12.7 in France, and 16.7 in South Africa [5]. A systematic review in 2010 by Van den Berg et al. showed up to threefold variation in incidence rates between developed countries. The highest rates reported in Canada and Portugal. Most traumatic SCI studies show a bimodal age distribution. The first peak was found in young men between 15 and 29 years of age and the second peak in older adults (mostly ≥65 years old and women) [6]. The National Spinal Cord Injury Statistical Center at the University of Alabama at Birmingham reported approximately 12,000 new cases each year, with 4:1 male-to-female ratio. The average age at injury was 40 years. The most common injury was incomplete tetraplegia at 30%, followed by 25.6% for complete paraplegia, 20.4% for complete tetraplegia, and 18.5% for incomplete paraplegia. In the past, the leading cause of death among SCI patients was the renal failure while nowadays, is pneumonia, pulmonary emboli, and septicemia supersede renal failure. SCI patients seem to have a higher prevalence of several comorbidities than the general population. It is reported high blood pressure (49% vs. 26%, respectively), high cholesterol (47% vs. 30%), and diabetes (19% vs. 7%). Obesity is also a significant problem for individuals with SCI (25%).

Spinal cord injury (SCI) patients clinically face urinary incontinence during the bladder filling phase and incomplete emptying during the micturition phase. The main aggravating factors are the increased intravesical pressure and the residual urine. These may result in vesicoureteral reflux, bladder diverticula, and urinary stones formation. These conditions also lead to an increased risk of urinary tract infection (UTI) [7, 8]. Despite improved treatment methods, UTI is considered the second leading cause of death in SCI patients [9]. It is known that UTIs are the most common hospital infections with known repercussions for the patient and the national economy. Approximately 5–10% of patients admitted to hospital are infected during their hospitalization and UTIs account for the highest (40–50%) [10, 11]. In addition, SCI patients usually have asymptomatic bacteriuria. In this way, positive urine culture is not the foundation stone for the diagnosis of urinary tract infection. The clinical signs and symptoms of urinary tract infection are differentiated in these individuals as the neural sensation is affected or absent. The review of the following literature aims to highlight the specificities of urinary tract infections in people with SCI or other neurogenic conditions in order to prevent and treat the infections and recognize asymptomatic bacteriuria without treatment necessity.

The physiological function of the lower urinary tract is characterized by the central control of the urinary reflexes (inhibition or removal of reflex inhibition) from the upper cortical centers of the cortex. Urine concentration within the bladder results in an increase in intravesical pressure that causes stimulation of the thoracic-lymphatic sympathetic center (T10-L2) via transient and adductor nerve fibers. Adjacent nerve fibers transfer the stimulus to the breech centers of urination and from there to the upper centers of the cerebral cortex. Then, if there is no central depression, the urinary reflex is manifested through the contraction of the detrusor resulting in the sympathetic nerves. However, if urination is undesirable, this reflex is inhibited as cationic signals inhibit sympathetic stimulation at the level of the thoracic-lumbar sympathetic center and increase the muscular tone of the external sphincter by suture from the pelvic neural mesh formed by the S2–S4 level. From the above, it is clear that any damage at any level of SC results in disorders of lower urinary function. These disorders vary according to level [11, 12], the degree (complete or incomplete) [13] and the extent of the damage.
