Sympathetic dysfunction in the overactive bladder etiopathogenesis

The overactive bladder (OAB) is a health problem with high prevalence which has negative effects on quality of life all over the world. In the 2002 International Continence Society (ICS) Terminology Standardization report, OAB is defined as ''urgency, with or without urge incontinence, usually with frequency and nocturia'', after confirming the absence of infections or other local pathological factors. The pathophysiolgy of OAB is still unclear, but various theories have been proposed. Bladder filling depends on an increase in sympathetic activity, concomitant with a decrease in parasympathetic activity. The bladder and sphincter activity is mainly under autonomic nervous system control. So Autonomic dysfunction can have a role in the pathophysiology of OAB. Anticholinergic drugs are the first choice in the treatment of OAB. But these drugs are effective in only % 60 of the patients. It is thought that sympathetic nervous system, nonadrenergic-noncholinergic activation and/or urothelium may have a role in patients unresponsive to anticholinergic therapy. Sympathetic skin responses (SSR) is a simple, safe and non-invasive electrophysiologic tests to assess sympathetic sudomotor function. In this study, we aimed to evaluate the sympathetic dysfunction's role in the etiopathogenesis of OAB using SSR recordings. Meanwhile we investigated the relationship between anticholinergic therapy responses and autonomic dysfunction. Our study group consisted of 40 women who have OAB and 15 healthy women as controls. 20 of the patients had benefited from previous anticholinergic therapy, but the rest had not. We examined hand, foot and genital sympathetic skin response recordings in all subjects. Absence of SSR was considered as abnormal. The absence of genital SSRs were significantly different between the patients and normal controls (p=0,001). Lack of genital SSRs in patients with OAB were found to be much more than normal controls. Genital SSRs could not be obtained from 11 of patients (27.5%). SSRs were obtained from all normal control subjects. Genital SSRs were not obtained in 7 patients (35%) who had not benefit anticholinergic therapy and in 4 patients (20%) who had responded to therapy. There were no statistically significant differences between the two groups (p>0,05). Absence of SSRs in patiens who had not benefited anticholinergic therapy was found significantly higher than normal control group (p=0,01). Hand, foot and genital latencies in patients with OAB were longer than normal control group. Foot and genital amplitudes were lower in patients with OAB than normal controls. Foot amplitude was significantly lower in OAB patients (Right foot p=0,03,Left foot p=0,01). There is a relationship between depression-anxiety and autonomic dysfunction. Based on this relationship we tried to support our investigation by using Hamilton Anxiety Scale. The anxiety scores in the SSR (-) patients were significantly lower than SSR (+) patients (p<0,001). Anxiety levels in patients who had benefited from anticholinergic therapy and in healthy subjects were better than anticholinergic therapy unresponders (p=0,002,p<0,001). There was no significant difference between patients who had benefited from anticholinergic therapy and healthy group (p=0,034). Our findings support that there is a regional sympathetic dysfunction in patients with OAB. We think that it may have a place to explain the etiopathogenesis of OAB. SSR can be use as an accessory test to describe autonomic dysfunction in OAB. But it's routine usage requires further studies using more number of OAB patients. Suffering from OAB and lack of anticholinergic therapy success can cause depression and anxiety. Besides that high anxiety levels can be a factor to diminish response to anticholinergic therapy in OAB. Trials combining anticholinergics with anxiolytic drugs may help to increase therapy responses.