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      Depression, Anxiety and the Bladder : Depression and the Bladder

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          Abstract

          Depression and anxiety are common mental illnesses. It is recognized that depression/anxiety causes physical changes, including insomnia, anorexia, and bladder dysfunction. We aimed to delineate bladder dysfunction in patients with depression/anxiety by reviewing the literature. We performed a systematic review of the literature to identify the frequency, lower urinary tract symptoms (LUTS), urodynamic findings, putative underlying pathology, and management of bladder dysfunction in patients with depression/anxiety. From a recent survey of a depression cohort (at a psychiatry clinic), the frequency of bladder dysfunction in depression is lower (up to 25.9%) than that in Parkinson's disease (up to 75%) and stroke (up to 55%), whereas it is significantly higher than that in age-matched controls (around 10%). In both the depression cohort and the psychogenic bladder dysfunction cohort (at a urology clinic), the most common LUTS was overactive bladder (OAB), followed by difficult urination and infrequent voiding. Compared with severe LUTS, urodynamic findings were dissociated; i.e. urodynamic findings were normal except for increased bladder sensation without detrusor overactivity for OAB (50% of all patients), followed by underactive detrusor without post-void residual for difficult urination. The effectiveness of serotonergic or anti-cholinergic medication for ameliorating OAB in the patients awaits further study. In conclusion, although the frequency of LUTS among the depression cohort is not elevated, depression/anxiety is obviously a risk factor for OAB. This finding presumably reflects that the bladder is under emotional control. Amelioration of bladder dysfunction is an important target in treating patients with depression/anxiety.

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          Most cited references60

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          The standardisation of terminology of lower urinary tract function: report from the Standardisation Sub-committee of the International Continence Society.

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            Reduced serotonin type 1A receptor binding in panic disorder.

            Recent animal models suggest that disturbances in serotonin type-1A receptor (5-HT(1A)R) function may contribute to chronic anxiety, although it is not clear at all whether such models constitute relevant models for panic disorder (PD) in humans. The selective 5-HT(1A)R radioligand [18F]trans-4-fluoro-N-2-[4-(2-methoxyphenyl)piperazin-1-yl]ethyl]-N-(2-pyridyl)cyclohexanecarboxamide (FCWAY) permits in vivo assessment of central 5-HT(1A)R binding using positron emission tomography (PET). We studied 16 unmedicated symptomatic outpatients with PD and 15 matched healthy controls. Seven patients had an additional diagnosis of a current major depressive episode, however PD was the primary diagnosis. A 120 min PET study of 5-HT(1A)R binding was acquired using a GE Advance scanner in three-dimensional mode. Using quantitative PET image analysis, regional values were obtained for [18F]-FCWAY volume of distribution (DV), corrected for plasma protein binding, and K1, the delivery rate of [18F]-FCWAY from plasma to tissue. MRI scanning was performed using a GE Signa Scanner (3.0 Tesla) to provide an anatomical framework for image analysis and partial volume correction of PET data. PD patients showed lower DV in the anterior cingulate (t = 4.3; p < 0.001), posterior cingulate (t = 4.1; p < 0.001), and raphe (t = 3.1; p = 0.004). Comparing patients with PD, patients with PD and comorbid depression, and healthy controls revealed that DVs did not differ between PD patients and PD patients with comorbid depression, whereas both patient groups differed significantly from controls. These results provide for the first time in vivo evidence for the involvement of 5-HT(1A)Rs in the pathophysiology of PD.
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              Aberrant supplementary motor complex and limbic activity during motor preparation in motor conversion disorder.

              Conversion disorder (CD) is characterized by unexplained neurological symptoms presumed related to psychological issues. The main hypotheses to explain conversion paralysis, characterized by a lack of movement, include impairments in either motor intention or disruption of motor execution, and further, that hyperactive self-monitoring, limbic processing or top-down regulation from higher order frontal regions may interfere with motor execution. We have recently shown that CD with positive abnormal or excessive motor symptoms was associated with greater amygdala activity to arousing stimuli along with greater functional connectivity between the amygdala and supplementary motor area. Here we studied patients with such symptoms focusing on motor initiation. Subjects performed either an internally or externally generated 2-button action selection task in a functional MRI study. Eleven CD patients without major depression and 11 age- and gender-matched normal volunteers were assessed. During both internally and externally generated movement, conversion disorder patients relative to normal volunteers had lower left supplementary motor area (SMA) (implicated in motor initiation) and higher right amygdala, left anterior insula, and bilateral posterior cingulate activity (implicated in assigning emotional salience). These findings were confirmed in a subgroup analysis of patients with tremor symptoms. During internally versus externally generated action in CD patients, the left SMA had lower functional connectivity with bilateral dorsolateral prefrontal cortices. We propose a theory in which previously mapped conversion motor representations may in an arousing context hijack the voluntary action selection system, which is both hypoactive and functionally disconnected from prefrontal top-down regulation. Copyright © 2011 Movement Disorder Society.
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                Author and article information

                Journal
                LUTS: Lower Urinary Tract Symptoms
                Wiley
                17575664
                September 2013
                September 2013
                March 31 2013
                : 5
                : 3
                : 109-120
                Affiliations
                [1 ]Division of Neurology, Department of Internal Medicine, Sakura Medical Center; Toho University; Sakura; Japan
                [2 ]Division of Neurology; Chiba University; Chiba; Japan
                [3 ]Continence Center; Dokkyo Medical College; Tochigi; Japan
                [4 ]Mental Health Clinic, Sakura Medical Center; Toho University; Sakura; Japan
                Article
                10.1111/luts.12018
                26663445
                8008b1c9-739f-47ac-bd89-820db060f59e
                © 2013

                http://doi.wiley.com/10.1002/tdm_license_1.1

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