Serotonin receptors associated with the serotonin syndrome development [10, 11, 12].
\\n\\n
Released this past November, the list is based on data collected from the Web of Science and highlights some of the world’s most influential scientific minds by naming the researchers whose publications over the previous decade have included a high number of Highly Cited Papers placing them among the top 1% most-cited.
\\n\\nWe wish to congratulate all of the researchers named and especially our authors on this amazing accomplishment! We are happy and proud to share in their success!
Note: Edited in March 2021
\\n"}]',published:!0,mainMedia:{caption:"Highly Cited",originalUrl:"/media/original/117"}},components:[{type:"htmlEditorComponent",content:'IntechOpen is proud to announce that 191 of our authors have made the Clarivate™ Highly Cited Researchers List for 2020, ranking them among the top 1% most-cited.
\n\nThroughout the years, the list has named a total of 261 IntechOpen authors as Highly Cited. Of those researchers, 69 have been featured on the list multiple times.
\n\n\n\nReleased this past November, the list is based on data collected from the Web of Science and highlights some of the world’s most influential scientific minds by naming the researchers whose publications over the previous decade have included a high number of Highly Cited Papers placing them among the top 1% most-cited.
\n\nWe wish to congratulate all of the researchers named and especially our authors on this amazing accomplishment! We are happy and proud to share in their success!
Note: Edited in March 2021
\n'}],latestNews:[{slug:"webinar-introduction-to-open-science-wednesday-18-may-1-pm-cest-20220518",title:"Webinar: Introduction to Open Science | Wednesday 18 May, 1 PM CEST"},{slug:"step-in-the-right-direction-intechopen-launches-a-portfolio-of-open-science-journals-20220414",title:"Step in the Right Direction: IntechOpen Launches a Portfolio of Open Science Journals"},{slug:"let-s-meet-at-london-book-fair-5-7-april-2022-olympia-london-20220321",title:"Let’s meet at London Book Fair, 5-7 April 2022, Olympia London"},{slug:"50-books-published-as-part-of-intechopen-and-knowledge-unlatched-ku-collaboration-20220316",title:"50 Books published as part of IntechOpen and Knowledge Unlatched (KU) Collaboration"},{slug:"intechopen-joins-the-united-nations-sustainable-development-goals-publishers-compact-20221702",title:"IntechOpen joins the United Nations Sustainable Development Goals Publishers Compact"},{slug:"intechopen-signs-exclusive-representation-agreement-with-lsr-libros-servicios-y-representaciones-s-a-de-c-v-20211123",title:"IntechOpen Signs Exclusive Representation Agreement with LSR Libros Servicios y Representaciones S.A. de C.V"},{slug:"intechopen-expands-partnership-with-research4life-20211110",title:"IntechOpen Expands Partnership with Research4Life"},{slug:"introducing-intechopen-book-series-a-new-publishing-format-for-oa-books-20210915",title:"Introducing IntechOpen Book Series - A New Publishing Format for OA Books"}]},book:{item:{type:"book",id:"194",leadTitle:null,fullTitle:"Laparoscopy - An Interdisciplinary Approach",title:"Laparoscopy",subtitle:"An Interdisciplinary Approach",reviewType:"peer-reviewed",abstract:"Over the last decades an enormous amount of technical advances was achieved in the field of laparoscopy. 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It is characterized by a triad of symptoms that includes neuromuscular hyperactivity, altered mental status and autonomic dysfunction.
The syndrome was first described in 1960 as “Indolamine syndrome” in patients on therapy with monoamine oxidase inhibitors (MAOIs) who develop symptoms of serotonin syndrome after taking tryptophan – a serotonin precursor [1]. Since then, the number of reported cases of serotonin syndrome has increased significantly. The medical community’s attention to serotonin syndrome was drawn in 1984 by the unusual death of 18-year-old Libby Zion in a New York City hospital, which may have been linked to the development of serotonin syndrome after concomitant use of an MAOI and opioid analgesic. The opioid analgesic pethidine was administered to the girl suffering from depression and taking the antidepressant phenelzine, which led to the development of a fatal serotonin syndrome [2, 3].
Of all serotonergic drugs, antidepressants are the most common cause of serotonin syndrome, and recent data suggest that the most common drug combination associated with serotonin syndrome is that between selective serotonin reuptake inhibitors (SSRIs) and opioids [2]. As a relatively rare adverse drug reaction, the incidence of serotonin syndrome is difficult to be calculated during randomized controlled trials [4]. Moreover, it is estimated that over 85% of physicians are unaware of the condition [5]. The non-specific manifestation of the syndrome leads to its difficult recognition and underreporting, which further complicates the determination of its incidence. It is considered that serotonin syndrome occurs in 15% of patients who overdose on selective serotonin reuptake inhibitors. The actual incidence of serotonin syndrome is thought to be significantly higher than reported [6, 7, 8].
Serotonin syndrome results from an increase in intrasynaptic serotonin levels caused by overstimulation of both central and peripheral serotonin receptors [9, 10]. Theoretically, serotonin syndrome can occur as a result of stimulation of any receptor of all seven serotonin receptor families [11]. However, the role of 5-HT1A and 5-HT2A is most often mentioned [6, 7, 11, 12]. Moreover, the 5-HT2A receptor is thought to mediate the most serious consequences of the serotonin syndrome (Table 1).
Receptor | Function related to serotonin toxicity | |
---|---|---|
Type | Subtype | |
5-HT1 | 5-HT1A | neuronal inhibition, thermoregulation, hyperactivity associated with anxiety, hypoactivity associated with depression |
5-HT1D | locomotion, muscle tone | |
5-HT2 | 5-HT2A | neuronal excitation, vasoconstriction, platelet aggregation |
5-HT2B | smooth muscle contraction | |
5-HT3 | — | nausea and vomiting |
5-HT4 | — | increased GIT motility |
Some authors suggest that the development of serotonin syndrome requires the accumulation of a critical amount of serotonin. However, studies show that this level of serotonin is probably different for each patient. Experimental studies in animal models of serotonin syndrome have shown that other neurotransmitters such as noradrenaline (NA), N-methyl-D-aspartate (NMDA), gamma-aminobutyric acid (GABA) and dopamine may also play a role in the development of serotonin syndrome but their role is not fully understood [6, 13].
It is shown that in serotonin syndrome CNS serotonin levels increase between 40 and 140 times. At the same time, dopamine levels are increased 10 to 44 times [14, 15]. Other studies indicate overactivation of the noradrenergic system with a rise in NA levels up to 15.9 times in serotonin syndrome, but the cause remains unknown. Some authors explain this increase in NA levels with activation of 5-HT2A receptors. This is supported by the fact that no significant increase in NA was observed with prior administration of ritanserin and pipamperone which act as antagonists of these receptors. On the other hand, there is evidence of the involvement of 5-HT1A receptors, although the administration of 5-HT1A antagonists does not prevent the increase in NA levels [14, 15]. The degree of NA increase may be related to the prognosis of serotonin syndrome, although it is not fully understood. At the same time, some of the observed symptoms of autonomic instability may be due to an overactivated noradrenergic system [14].
Drugs and substances that increase serotonin levels are known as serotonergic, and a mechanism by which they do that are as follows:
Increased serotonin synthesis
Increased serotonin release
Activation of serotonergic receptors
Serotonin reuptake inhibition
Inhibition of serotonin metabolism
The full list of all serotonergic substances is long, but antidepressants and, in recent years, some opioids take the central place. It is important to note that substances with serotonergic activity include not only antidepressants and opioids but also a number of other drugs used in everyday medical practice – some antibiotics, antiemetics, anxiolytics, antipsychotics, as well as over-the-counter drugs (OTC), dietary supplements, some illicit drugs and more [5, 6, 7, 16, 17, 18, 19].
Some of the antidepressants, opioids, and other drugs reported in the literature causing serotonin syndrome, as well as the mechanisms by which they increase serotonin levels are listed in Table 2.
Mechanism | Implicated drugs |
---|---|
Increased serotonin synthesis | |
Increased serotonin release | |
Activation of serotonergic receptors | |
Serotonin reuptake inhibition | |
Inhibition of serotonin metabolism |
The term “serotonin syndrome” in animals was first used in 1979 by Hwang and Van Woert [20, 21]. Manifestation of serotonin toxicity has been described in various animal species, however, most literature data, respectively most studies, are available on the development of serotonin syndrome in mice and rats [20].
In contrast to humans, in whom the symptoms of serotonin syndrome are well defined, the literature describes a wide variety of manifestations and different combinations of responses characterizing the development of serotonin syndrome in rodents.
There is considerable heterogeneity in the animal models reported in the literature. The use of different assessment methods, different response sets and different scales in assessing the effects of increased serotonergic tone limits quantitative comparisons of laboratory results. In this regard, Haberzettl et al. [20] conducted a systematic literature review of the described models of serotonin syndrome in rats and mice and evaluated the observed behavioral and autonomic manifestations. Based on the frequency of behavioral manifestations, the team divides them into traditional and additional, distinguishing those that reliably characterize the development of serotonin syndrome in rodents. The described behavioral and autonomic symptoms of serotonin syndrome in rats are presented in Table 3.
Behavioral manifestations | Autonomic manifestations | |
---|---|---|
Traditional | Additional | |
forepaw treading head weaving hind limb abduction low body posture Straub phenomenon tremor backward walking | body twitches chewing head shakes head twitches hyperactivity hyperreactivity locomotor activity (increased or decreased) myoclonus rearing wet dog shake | body temperature (increased or decreased) lower lip retraction penile erection pyloric erection salivation |
Serotonin syndrome manifestation in rats.
It is widely believed that 5-HT1A receptors mediate most behavioral manifestations of serotonin syndrome in rats [22, 23, 24, 25, 26, 27, 28, 29, 30, 31]. In support of this are studies demonstrating the induction of serotonin syndrome behaviors by the administration of 5-HT1A agonists [26, 32, 33] and the induction of a narrower spectrum of manifestations such as hind limb abduction, a Straub phenomenon and low body posture, from the partial 5-HT1A-agonist buspirone [31].
Other behavioral responses such as head weaving and wet dog shake, are mediated by 5-HT2A receptors [22, 34, 35, 36, 37]. For example, head weaving in rats induced by the administration of the non-selective MAO inhibitor phenelzine and the SSRI paroxetine was dose-dependently antagonized by 5-HT2 antagonists [35, 37]. In addition, head weaving caused by the administration of a 5-HT2A/2C agonist has been antagonized by the administration of a 5-HT2A antagonist, but not by a 5-HT2C/2B antagonist [38].
The analysis of Haberzettl et al. showed that the most common autonomic dysregulation manifestation observed in rats with serotonin syndrome is the change in the body temperature. The hyperthermic reaction observed is thought to be mainly related to the activation of 5-HT2A receptors [14, 39]. Experimental studies confirmed the involvement of 5-HT1A and 5-HT2A receptors in thermoregulation in rats. For example, blockade of 5-HT2 receptors by ketanserin or pirenperone causes a decrease in body temperature, while blockade of 5-HT1A receptors by pindolol results in an increase in body temperature [40].
Although not a mandatory manifestation of serotonin syndrome, hyperthermia is one of the leading causes of observed mortality in experimental serotonin syndrome. In both animals and humans, it is hyperthermia that mainly causes complications. Such complications in humans could include seizures, rhabdomyolysis, myoglobinuria, metabolic acidosis, renal failure, acute respiratory distress syndrome, respiratory failure, disseminated intravascular coagulation (DIC syndrome), coma and death [6].
The manifestation of serotonin syndrome observed in rodents resembles the manifestation of serotonin syndrome in humans (Table 4). For example, neuromuscular manifestations such as tremor and muscle rigidity have been observed in both humans and rodents. Myoclonus, which is a clinical symptom of serotonin syndrome in humans, in rodents may manifest as head twitches and forepaw treading. The Straub phenomenon observed in rodents may refer to the muscle rigidity observed in humans [21]. According to autonomic dysregulation manifestation, changes in body temperature occur in both rodents and humans.
Symptoms/manifestations of serotonin syndrome | Humans | Rodents |
---|---|---|
Neuromuscular disorders | clonus tremor hyperreflexia muscle rigidity myoclonus | head weaving tremor hind limb abduction Straub phenomenon low body posture backward walking |
Autonomic dysfunction | diaphoresis hyperthermia (>38 °C) diarrhea shivering | change in body temperature (increase or decrease) |
Mental status changes | agitation confusion hyperactivity hypomania anxiety | hyperactivity hyperreactivity |
Symptoms and manifestations of serotonin syndrome in humans and rodents – Comparison.
The most difficult to differentiate in animals is the third group of symptoms typical for the manifestation of serotonin syndrome in humans - mental status changes. However, hyperactivity and to some extent the hyperreactivity observed in rodents are associated with agitation observed in humans. Moreover, it is important to note that the current criteria for diagnosing serotonin syndrome in humans, Hunter’s criteria, do not include as a mandatory diagnostic criterion changes in mental status, which confirms the validity and applicability of the animal model of serotonin syndrome [21].
Two classical models of serotonin syndrome in rats have been described in the literature induced by concomitant administration of serotonergic substances with different mechanisms of action: 5-HTP (100 mg/kg i.p.) - a precursor of serotonin and clorgyline (2 mg/kg i.p.) - selective MAO-A inhibitor [14] and fluoxetine (10 mg/kg i.p.) - a selective serotonin reuptake inhibitor and tranylcypromine (3.5 mg/kg, i.p.) - a non-selective MAO inhibitor [12].
Many central neurotransmitters, such as serotonin, norepinephrine, dopamine, acetylcholine, GABA and glutamate, are involved in the thermoregulation. GABA is a major central inhibitory neurotransmitter involved in thermoregulatory processes. The role of GABA as a thermoregulatory neurotransmitter or modulator is suggested by the good distribution of the mediator in the hypothalamus, confirmed by autoradiographic and immunohistochemical studies [41, 42, 43] and its central action. In addition, GABA-ergic neurons, as well as postsynaptic GABAA-ergic receptors have been identified in PO/AH (preoptic area/anterior hypothalamus) [44, 45, 46].
Potentiation of the central inhibitory effect of GABA is achieved by several different mechanisms, including allosteric modulation of GABA receptors (benzodiazepines, barbiturates, Z-hypnotics, propofol and fospropofol), direct GABA- or GABA-receptor agonist action (respectively muscimol, baclofen), increased synthesis of GABA (e.g., gabapentin, pregabalin, sodium valproate), inhibition of enzymatic degradation of GABA (e.g., vigabatrin, sodium valproate) and inhibition of neuronal or glial uptake of GABA (e.g., tiagabine).
Benzodiazepines mediate their pharmacological effects by enhancing the inhibitory effect of GABA on the CNS by binding to a specific modulating site on GABAA-ergic receptors containing 1, 2, 3 or 5 alpha-subunits. Benzodiazepines have no affinity for receptor complexes containing 4 or 6 alpha-subunits [47]. Activation of specific benzodiazepine receptors by diazepam or other benzodiazepines increase the frequency of GABAA-associated chloride channel opening [48].
The pharmacological activity of valproic acid is expressed in potentiation of GABA-ergic neurotransmission and prolongation of the inactivation of voltage-dependent neuronal sodium channels [49]. Sodium valproate is thought to increase brain GABA concentration by the following mechanisms: (1) inhibition of GABA-transaminase enzyme activity and decreased GABA degradation [50] 2) stimulating GAD activity [51] and increasing GABA synthesis; (3) decreased GABA turnover [52]. Vigabatrin (gamma-vinyl GABA) is a vinyl-substituted analogue of GABA that selectively and irreversibly inhibits the activity of the enzyme GABA-transaminase (GABA-T) and significantly increases the concentration of GABA in the brain [53].
After central and systemic administration of diazepam, sodium valproate, and vigabatrin dose-dependent decreases of body temperature in rats is observed [54, 55, 56, 57]. GABA-induced hypothermia has been suggested to be mediated by GABAA and/or GABAB receptor activation [58, 59]. The hypothermic effect of sodium valproate and vigabatrin occurs later than diazepam-induced hypothermia, which can be explained by their indirect mechanism of potentiation of GABA-ergic mediation.
These results are further confirmed in our studies, where we found that substances with a GABA-ergic mechanism of action such as diazepam, sodium valproate and vigabatrin effectively reduced the hyperthermic response in experimental serotonin syndrome in rats induced by concomitant administration of 5-HTP (100 mg/kg i.p.) - a precursor of serotonin and clorgyline (2 mg/kg i.p.) - selective MAO-A inhibitor [14]. The reduction in serotonergic-induced hyperthermia with pretreatment of GABA-mimetic drugs is most likely due to an increase in central GABA-ergic neurotransmission through activation of GABAA receptors (e.g., diazepam) as well as through indirect action by increasing GABA concentration (e.g., sodium valproate, vigabatrin). These results on the hyperthermia associated with serotonin syndrome support the hypothesis of an interaction between the GABA-ergic and serotoninergic systems in thermoregulatory processes.
In our studies, after the concomitant administration of 5-HTP (100 mg/kg i.p.) and clorgyline (2 mg/kg i.p.), a model of serotonin syndrome with typical behavioral and autonomic manifestations developed. Tremor occurs 10 minutes after injection, the hyperthermic reaction develops at 30 minutes, and the maximum value is observed 60 minutes after injection of the substances. All animals in this group died between 60 and 90 minutes after injection of serotonin. Pretreatment with diazepam at a dose of 5 mg/kg i.p. reduced the hyperthermic reaction at 30 and 60 min compared to the group with a model of serotonin syndrome, in which saline was administered prior to the injection of serotonergic agent. Administration of sodium valproate at a dose of 300 mg/kg i.p. reduced the hyperthermic reaction at 30 and 60 min compared to the group with a model of serotonin syndrome, in which saline was administered before the injection of serotonergic substances [56, 60]. Additionally, in another of our experiments, we used a modified model of serotonin syndrome induced by the concomitant administration of fluoxetine (10 mg/kg i.p.) - a selective serotonin reuptake inhibitor and clorgyline (2 mg/kg i.p.) - selective MAO-A inhibitor. Vigabatrin at a dose of 300 mg/kg i.p. significantly decreased the hyperthermic response between 150 and 300 min in rats with a serotonin syndrome model, compared to the group with a model of serotonin syndrome in which only saline was administered before the injection of the serotonergic substances [57, 61].
In summary pretreatment with diazepam (5 mg/kg i.p.), sodium valproate (300 mg/kg i.p.), and vigabatrin (300 mg/kg i.p.) decreased hyperthermia in different experimental models of the serotonin syndrome. These results suggest involvement of interactions between GABA-ergic and serotonergic systems in the processes of thermoregulation.
We assume that in addition to direct GABA-ergic mechanisms, interactions between neurotransmitters or mediator systems are involved in the influence of hyperthermia in serotonin syndrome by GABA-ergic substances. Presynaptic GABAB receptors affect the release of norepinephrine, dopamine, and 5-hydroxytryptamine [62]. Expression of predominantly GABAB receptors has been found in most of the serotonin and catecholamine neurons in the nuclei of the brainstem, which are involved in the regulation of autonomic functions [63]. Interactions between the GABA-ergic and serotonergic systems are mediated by presynaptic heteroreceptor GABAB-inhibition of 5-HT release or by G-protein-coupled interaction between 5-HT1A and GABAB-ergic receptors [64].
Hyperthermia is the most common cause of complications of life-threatening forms of serotonin syndrome in humans and is one of the leading causes of mortality reported in experimental models of serotonin syndrome [6, 7].
As already mentioned, several studies indicate the role of 5-HT2A receptors in the development of a hyperthermic response in rats. In this regard, the effect of a number of 5-HT2 antagonists in influencing the hyperthermic response in experimental serotonin syndrome has been studied. Some of the serotonin antagonists investigated are cyproheptadine, ritanserin, ketanserin, mirtazapine, some antipsychotics such as chlorpromazine, risperidone and olanzapine [8, 11, 12, 13, 14, 15]. Results demonstrate a significant involvement of the 5-HT2A receptors in the development of hyperthermic response in experimental serotonin syndrome [65].
Studies have shown that cyproheptadine effectively affects the hyperthermic response in an experimental model of serotonin syndrome. Moreover, a comparative study demonstrates that, unlike other 5-HT2 antagonists, it prevents both the development of serotonin syndrome and the mortality of experimental animals [14, 66].
The role of atypical antipsychotics in the treatment of serotonin syndrome has been increasingly discussed in the last few years, given that most atypical antipsychotics work primarily by blocking 5-HT2 receptors [67].
Moreover, temperature dysregulation is a documented side effect of antipsychotic drugs [68, 69, 70, 71, 72]. That most often manifests in the development of hyperthermia, a life-threatening symptom characteristic of the malignant neuroleptic syndrome (MNS). Data from various clinical cases, summarized in recent years by van Marum [68] and Zonnenberg [69, 70], show that the use of classical or atypical antipsychotics carries the risk of developing another, less well-documented adverse drug reaction, namely hypothermia. In humans, hypothermia is defined as a body temperature below 35 ° C, distinguishing three degrees: mild (33–35 ° C), moderate (28–33 ° C) and severe (<28 ° C) hypothermia [69].
Although the hypothermic effect of antipsychotics is less known than the hyperthermic one expressed in MNS, analysis of the literature data shows that there are almost equal reports of hypothermia (480 cases) and hyperthermia (524 cases) associated with the use of antipsychotics. Zonnenberg et al. consider that the actual incidence of hypothermia associated with the use of antipsychotics is at least 10 times higher than the documented [69]. For the first time, the development of hypothermia after the use of antipsychotic drugs was described by Loughnane in a 26-year-old patient on chlorpromazine therapy [73].
The analyzes of van Marum et al. and Zonnenberg et al. indicate that hypothermia most often occurs one week after starting antipsychotic therapy or after increasing the dose. They also indicated that the use of atypical antipsychotics was more common (approximately 55% of cases), with risperidone being the most commonly reported [68, 69, 74]. Mild hypothermia associated with low-dose risperidone has also been observed in a child with verbal and physically aggressive behavior [75].
Analyzes by van Marum and Zonnenberg show that antipsychotics with a higher affinity for blocking 5-HT2A than D2 receptors are more often associated with the development of hypothermia [68, 69]. This is also confirmed by experimental and clinical studies which demonstrate that the atypical antipsychotics olanzapine and risperidone cause a decrease in body temperature indicating that the mechanism of hypothermic action is associated with blockade of 5-HT2 receptors [72, 74, 75, 76].
From all data reported thus far, it can be concluded that 5-HT2 receptors and the GABA system are strongly involved in the development of hyperthermia in serotonin syndrome and the mortality associated with it.
Drug-induced hyperthermia is resistant to the action of classical antipyretics therefore their use is not recommended. The use of acetylsalicylic acid and other classical antipyretics not only has no effect in the case of drug-induced hyperthermia but may even cause a worsening of the course of the hyperthermic reaction. In our opinion, due to the proven hypothermic effect of the mentioned GABA-ergic drugs and 5-HT2-antagonists, their use in the therapeutic regimen of hyperthermia in specific hyperthermic syndromes is appropriate.
The similarity in the manifestation of the syndrome in rats and humans can serve as a basis for further elucidation of the mechanism of development of serotonin syndrome in humans. The animal model of serotonin syndrome can be used to study drugs and drug combinations that pose a potential risk of developing serotonin syndrome in humans and the possibilities for its prevention.
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There are many microbial agents which may cause UTIs. Enterobacteriaceae family members are recognized as important UTI bacterial causative agents. Among them, uropathogenic Escherichia coli (UPEC) pathotypes are considered as the most important bacterial agents of UTIs. Today, genomics and bioinformatics explain us why UPEC strains are so considerable pathogens regarding UTIs. There is a diversity of E. coli strains involving commensal and pathogenic strains. Genomics shows that commensal strains of E. coli encompass the minimal amount of genome and genetic elements among E. coli populations, whereas the pathotypes of E. coli possess the maximal or a big portion of genomic elements. Previous studies confirm the presence of a vast range of virulence genes within the pool of E. coli pathotypes like UPEC. So, the pool of virulence genes (virulome) belonging to UPEC enables UPEC pathotypes to have huge genomes with the ability of different levels of pathogenesis. The more virulence factors, the more pathogenicity. Due to the presence of a mass of virulence factors within UPEC cellular structures, well-known fimbrial adhesins in UPEC pathotypes are discussed in this chapter.",book:{id:"6147",slug:"urinary-tract-infection-the-result-of-the-strength-of-the-pathogen-or-the-weakness-of-the-host",title:"Urinary Tract Infection",fullTitle:"Urinary Tract Infection - The Result of the Strength of the Pathogen, or the Weakness of the Host"},signatures:"Payam Behzadi",authors:[{id:"45803",title:"Ph.D.",name:"Payam",middleName:null,surname:"Behzadi",slug:"payam-behzadi",fullName:"Payam Behzadi"}]},{id:"34718",doi:"10.5772/33742",title:"Epidemiology of Urinary Incontinence in Pregnancy and Postpartum",slug:"epidemiology-of-urinary-incontinence-during-pregnancy-and-postpartum",totalDownloads:3724,totalCrossrefCites:1,totalDimensionsCites:10,abstract:null,book:{id:"1448",slug:"urinary-incontinence",title:"Urinary Incontinence",fullTitle:"Urinary Incontinence"},signatures:"Stian Langeland Wesnes, Steinar Hunskaar and Guri Rortveit",authors:[{id:"96897",title:"Dr.",name:"Stian Langeland",middleName:null,surname:"Wesnes",slug:"stian-langeland-wesnes",fullName:"Stian Langeland Wesnes"},{id:"97544",title:"Prof.",name:"Steinar",middleName:null,surname:"Hunskaar",slug:"steinar-hunskaar",fullName:"Steinar Hunskaar"},{id:"97545",title:"Prof.",name:"Guri",middleName:null,surname:"Rortveit",slug:"guri-rortveit",fullName:"Guri Rortveit"}]},{id:"45363",doi:"10.5772/55371",title:"Problem of Catheter Associated Urinary Tract Infections in Sub–Saharan Africa",slug:"problem-of-catheter-associated-urinary-tract-infections-in-sub-saharan-africa",totalDownloads:2571,totalCrossrefCites:4,totalDimensionsCites:8,abstract:null,book:{id:"3313",slug:"recent-advances-in-the-field-of-urinary-tract-infections",title:"Recent Advances in the Field of Urinary Tract Infections",fullTitle:"Recent Advances in the Field of Urinary Tract Infections"},signatures:"Mohamed Labib and Nenad Spasojevic",authors:[{id:"155793",title:"Prof.",name:"Mohamed",middleName:null,surname:"Labib",slug:"mohamed-labib",fullName:"Mohamed Labib"},{id:"158764",title:"Dr.",name:"Nenad",middleName:null,surname:"Spasojevic",slug:"nenad-spasojevic",fullName:"Nenad Spasojevic"}]},{id:"23987",doi:"10.5772/22951",title:"Tunica Albuginea Urethroplasty",slug:"tunica-albuginea-urethroplasty",totalDownloads:2442,totalCrossrefCites:0,totalDimensionsCites:6,abstract:null,book:{id:"369",slug:"current-concepts-of-urethroplasty",title:"Current Concepts of Urethroplasty",fullTitle:"Current Concepts of Urethroplasty"},signatures:"RK Mathur",authors:[{id:"49936",title:"Dr.",name:"Rajkumar",middleName:null,surname:"Mathur",slug:"rajkumar-mathur",fullName:"Rajkumar Mathur"}]}],mostDownloadedChaptersLast30Days:[{id:"71493",title:"Pelvic Organ Prolapse: Examination and Assessment",slug:"pelvic-organ-prolapse-examination-and-assessment",totalDownloads:1102,totalCrossrefCites:0,totalDimensionsCites:0,abstract:"Pelvic organ prolapse (POP) is a common, benign condition in women, and patient can present with complaints of vaginal bulge and pressure, voiding and defecatory, and sexual dysfunction, which may adversely affect quality of life. Although POP can occur in younger women, it is commonly seen in aging population with a prevalence of 45–50%. Older terms describing pelvic organ prolapse (e.g., cystocele, urethrocele, rectocele) have been replaced because they do not provide complete information regarding the structures on the other side of the vaginal bulge, especially in women who have had previous pelvic organ prolapse surgery. Therefore, a thorough history and performing a careful physical examination with dignity and care, using some basic tools that aid in the accurate evaluation of anatomical and functional defects, should be conducted. A standardized assessment system has been used to document findings which should explain everything in understandable terms.",book:{id:"7957",slug:"lower-urinary-tract-dysfunction-from-evidence-to-clinical-practice",title:"Lower Urinary Tract Dysfunction",fullTitle:"Lower Urinary Tract Dysfunction - From Evidence to Clinical Practice"},signatures:"Priyanka Bhadana",authors:[{id:"287080",title:"Associate Prof.",name:"Priyanka",middleName:null,surname:"Bhadana",slug:"priyanka-bhadana",fullName:"Priyanka Bhadana"}]},{id:"53697",title:"Physiotherapy in Women with Urinary Incontinence",slug:"physiotherapy-in-women-with-urinary-incontinence",totalDownloads:2377,totalCrossrefCites:2,totalDimensionsCites:2,abstract:"Urinary incontinence is a complex and serious condition that can affect all age groups around the world. It is not only a serious medical condition but also an undeniable psychosocial problem creating embarrassment and negative self‐perception, and it has a severe impact on a patient's quality of life. Today, there are wide different treatment options in urinary incontinence from surgery to conservative modalities. Among these, conservative management approaches are recommended as the first‐line treatment to manage with urinary incontinence. The choice of the most suitable option to treat for urinary incontinence differs according to the underlying pathophysiological mechanism defining subtypes of urinary incontinence and severity of symptoms. In this chapter, we addressed the different components of physiotherapy management of urinary incontinence, including pelvic floor muscle training, electrical stimulation, biofeedback, vaginal cones, mechanical devices and magnetic stimulation. We concluded that the optimal physiotherapy care should be individualised to ensure applicability the clinic setting for each patient.",book:{id:"5352",slug:"synopsis-in-the-management-of-urinary-incontinence",title:"Synopsis in the Management of Urinary Incontinence",fullTitle:"Synopsis in the Management of Urinary Incontinence"},signatures:"Özlem Çinar Özdemir and Mahmut Surmeli",authors:[{id:"185712",title:"Ph.D.",name:"Özlem",middleName:null,surname:"Çinar Özdemir",slug:"ozlem-cinar-ozdemir",fullName:"Özlem Çinar Özdemir"},{id:"193852",title:"Mr.",name:"Mahmut",middleName:null,surname:"Surmeli",slug:"mahmut-surmeli",fullName:"Mahmut Surmeli"}]},{id:"43981",title:"Functional Anatomy of the Vesicoureteric Junction: Implication on the Management of VUR/ UTI",slug:"functional-anatomy-of-the-vesicoureteric-junction-implication-on-the-management-of-vur-uti",totalDownloads:3625,totalCrossrefCites:0,totalDimensionsCites:2,abstract:null,book:{id:"3313",slug:"recent-advances-in-the-field-of-urinary-tract-infections",title:"Recent Advances in the Field of Urinary Tract Infections",fullTitle:"Recent Advances in the Field of Urinary Tract Infections"},signatures:"Vivian Yee-Fong Leung and Winnie Chiu-Wing Chu",authors:[{id:"53633",title:"Prof.",name:"Winnie Chiu Wing",middleName:null,surname:"Chu",slug:"winnie-chiu-wing-chu",fullName:"Winnie Chiu Wing Chu"},{id:"55589",title:"Dr.",name:"Vivian Yee-fong",middleName:null,surname:"Leung",slug:"vivian-yee-fong-leung",fullName:"Vivian Yee-fong Leung"}]},{id:"53692",title:"Assessment of Urinary Incontinence (UI) in Adult Patients",slug:"assessment-of-urinary-incontinence-ui-in-adult-patients",totalDownloads:2023,totalCrossrefCites:3,totalDimensionsCites:4,abstract:"The diagnosis and assessment of urinary incontinence (UI) are variable. In general, diagnosis is made in primary care using clinical evaluation (a good history and physical examination), bladder diary and validated symptom scales. Condition-specific diagnosis is made in secondary care, and it often involves interventional tools such as urodynamic studies. The evidence available on the accuracy and acceptability of the assessment of UI is inconsistent and variable. A structured data collection tool was used for initial assessment of UI. Some key questions are required for initial assessment of UI in order to diagnose the type of UI. This chapter includes a gender-specific evaluation based on history and clinical examination. Pelvic organ prolapse (POP) in female patients is associated with UI and POP diagnosis, and staging is made by clinical examination only, while male patients are examined for prostate obstructive urinary symptoms. Basic evaluation includes bladder diary in cases of overactive bladder and stress test, for stress urinary incontinence. Other diagnostic tests include urine analysis, uroflowmetry and measurement of post-void residual volume in cases of neurogenic bladder and benign prostate hypertrophy. Patients referred to specialist require further assessment of UI using urodynamic testing, electrophysiological test and imaging.",book:{id:"5352",slug:"synopsis-in-the-management-of-urinary-incontinence",title:"Synopsis in the Management of Urinary Incontinence",fullTitle:"Synopsis in the Management of Urinary Incontinence"},signatures:"Raheela M. Rizvi and Mohammad Hammad Ather",authors:[{id:"88868",title:"Prof.",name:"M Hammad",middleName:null,surname:"Ather",slug:"m-hammad-ather",fullName:"M Hammad Ather"},{id:"185970",title:"Dr.",name:"Raheela",middleName:"Mohsin",surname:"Rizvi",slug:"raheela-rizvi",fullName:"Raheela Rizvi"}]},{id:"45043",title:"Developments Regarding Dysfunctional Voiding and Urinary Tract Infections in Children",slug:"developments-regarding-dysfunctional-voiding-and-urinary-tract-infections-in-children",totalDownloads:2286,totalCrossrefCites:0,totalDimensionsCites:0,abstract:null,book:{id:"3313",slug:"recent-advances-in-the-field-of-urinary-tract-infections",title:"Recent Advances in the Field of Urinary Tract Infections",fullTitle:"Recent Advances in the Field of Urinary Tract Infections"},signatures:"Yusuf Kibar and Faysal Gok",authors:[{id:"51399",title:"Dr.",name:"Yusuf",middleName:null,surname:"Kibar",slug:"yusuf-kibar",fullName:"Yusuf Kibar"}]}],onlineFirstChaptersFilter:{topicId:"1162",limit:6,offset:0},onlineFirstChaptersCollection:[],onlineFirstChaptersTotal:0},preDownload:{success:null,errors:{}},subscriptionForm:{success:null,errors:{}},aboutIntechopen:{},privacyPolicy:{},peerReviewing:{},howOpenAccessPublishingWithIntechopenWorks:{},sponsorshipBooks:{sponsorshipBooks:[],offset:0,limit:8,total:null},allSeries:{pteSeriesList:[{id:"14",title:"Artificial Intelligence",numberOfPublishedBooks:9,numberOfPublishedChapters:89,numberOfOpenTopics:6,numberOfUpcomingTopics:0,issn:"2633-1403",doi:"10.5772/intechopen.79920",isOpenForSubmission:!0},{id:"7",title:"Biomedical Engineering",numberOfPublishedBooks:12,numberOfPublishedChapters:104,numberOfOpenTopics:3,numberOfUpcomingTopics:0,issn:"2631-5343",doi:"10.5772/intechopen.71985",isOpenForSubmission:!0}],lsSeriesList:[{id:"11",title:"Biochemistry",numberOfPublishedBooks:31,numberOfPublishedChapters:314,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2632-0983",doi:"10.5772/intechopen.72877",isOpenForSubmission:!0},{id:"25",title:"Environmental Sciences",numberOfPublishedBooks:1,numberOfPublishedChapters:11,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2754-6713",doi:"10.5772/intechopen.100362",isOpenForSubmission:!0},{id:"10",title:"Physiology",numberOfPublishedBooks:11,numberOfPublishedChapters:141,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2631-8261",doi:"10.5772/intechopen.72796",isOpenForSubmission:!0}],hsSeriesList:[{id:"3",title:"Dentistry",numberOfPublishedBooks:8,numberOfPublishedChapters:129,numberOfOpenTopics:2,numberOfUpcomingTopics:0,issn:"2631-6218",doi:"10.5772/intechopen.71199",isOpenForSubmission:!0},{id:"6",title:"Infectious Diseases",numberOfPublishedBooks:13,numberOfPublishedChapters:113,numberOfOpenTopics:3,numberOfUpcomingTopics:1,issn:"2631-6188",doi:"10.5772/intechopen.71852",isOpenForSubmission:!0},{id:"13",title:"Veterinary Medicine and Science",numberOfPublishedBooks:11,numberOfPublishedChapters:105,numberOfOpenTopics:3,numberOfUpcomingTopics:0,issn:"2632-0517",doi:"10.5772/intechopen.73681",isOpenForSubmission:!0}],sshSeriesList:[{id:"22",title:"Business, Management and Economics",numberOfPublishedBooks:1,numberOfPublishedChapters:19,numberOfOpenTopics:2,numberOfUpcomingTopics:1,issn:"2753-894X",doi:"10.5772/intechopen.100359",isOpenForSubmission:!0},{id:"23",title:"Education and Human Development",numberOfPublishedBooks:0,numberOfPublishedChapters:5,numberOfOpenTopics:1,numberOfUpcomingTopics:1,issn:null,doi:"10.5772/intechopen.100360",isOpenForSubmission:!0},{id:"24",title:"Sustainable Development",numberOfPublishedBooks:0,numberOfPublishedChapters:14,numberOfOpenTopics:5,numberOfUpcomingTopics:0,issn:null,doi:"10.5772/intechopen.100361",isOpenForSubmission:!0}],testimonialsList:[{id:"13",text:"The collaboration with and support of the technical staff of IntechOpen is fantastic. 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