Purpose: To investigate the effectiveness of acotiamide on lower urinary tract dysfunction by using a rat model of neurogenic underactive bladder induced through pelvic nerve crush (PNC) injury. Methods: Bilateral PNC injuries were performed on 8-week-old female Sprague-Dawley rats (PNC group); the sham surgery group was used as control (control group). Two weeks after surgery, awake cystometrography (CMG) was performed, and acotiamide (10 or 100 mg/kg) was subcutaneously administered to the control and PNC groups. Subsequently, CMG parameter values obtained before and after treatment were compared. Results: In baseline CMG, compared to control group, PNC group revealed statistically significant elevations in the intercontraction intervals (ICIs), number of nonvoiding contractions, baseline pressure, threshold pressure, bladder capacity, voided volumes, and postvoid residual. However, contraction amplitudes and voiding efficiency were significantly decreased. In the control group, compared with the baseline values, 10-mg/kg acotiamide resulted in statistically significant elevations in contraction amplitudes. Treatment with 100-mg/kg acotiamide led to statistically significant elevations in contraction amplitudes and decreases in ICI and bladder volume. In the PNC group, there were no statistically significant changes noted in CMG parameters after treatment with 10-mg/kg acotiamide (n=6). Compared with the baseline values, the administration of 100-mg/kg acotiamide significantly decreased ICI (1,025±186 seconds vs. 578±161 seconds; P=0.012), bladder capacity (1,841±323 µL vs. 871±174 µL, respectively; P=0.0059) and postvoid residual (223±46 µL vs. 44±22 µL, respectively; P=0.023), and increased contraction amplitudes (22.09±1.76 cm H2O vs. 43.84±6.87 cm H2O, respectively; P=0.012) and voiding efficiency (0.87±0.02 vs. 0.94±0.03, respectively; P=0.029). Conclusions Acotiamide showed effectiveness in the treatment of underactive bladder, possibly through activation of bladder afferent and detrusor activities.

Purpose: To investigate the effectiveness of acotiamide on lower urinary tract dysfunction by using a rat model of neurogenic underactive bladder induced through pelvic nerve crush (PNC) injury. Methods: Bilateral PNC injuries were performed on 8-week-old female Sprague-Dawley rats (PNC group); the sham surgery group was used as control (control group). Two weeks after surgery, awake cystometrography (CMG) was performed, and acotiamide (10 or 100 mg/kg) was subcutaneously administered to the control and PNC groups. Subsequently, CMG parameter values obtained before and after treatment were compared. Results: In baseline CMG, compared to control group, PNC group revealed statistically significant elevations in the intercontraction intervals (ICIs), number of nonvoiding contractions, baseline pressure, threshold pressure, bladder capacity, voided volumes, and postvoid residual. However, contraction amplitudes and voiding efficiency were significantly decreased. In the control group, compared with the baseline values, 10-mg/kg acotiamide resulted in statistically significant elevations in contraction amplitudes. Treatment with 100-mg/kg acotiamide led to statistically significant elevations in contraction amplitudes and decreases in ICI and bladder volume. In the PNC group, there were no statistically significant changes noted in CMG parameters after treatment with 10-mg/kg acotiamide (n=6). Compared with the baseline values, the administration of 100-mg/kg acotiamide significantly decreased ICI (1,025±186 seconds vs. 578±161 seconds; P=0.012), bladder capacity (1,841±323 µL vs. 871±174 µL, respectively; P=0.0059) and postvoid residual (223±46 µL vs. 44±22 µL, respectively; P=0.023), and increased contraction amplitudes (22.09±1.76 cm H2O vs. 43.84±6.87 cm H2O, respectively; P=0.012) and voiding efficiency (0.87±0.02 vs. 0.94±0.03, respectively; P=0.029). Conclusions Acotiamide showed effectiveness in the treatment of underactive bladder, possibly through activation of bladder afferent and detrusor activities.

Purpose: To investigate the effectiveness of acotiamide on lower urinary tract dysfunction by using a rat model of neurogenic underactive bladder induced through pelvic nerve crush (PNC) injury. Methods: Bilateral PNC injuries were performed on 8-week-old female Sprague-Dawley rats (PNC group); the sham surgery group was used as control (control group). Two weeks after surgery, awake cystometrography (CMG) was performed, and acotiamide (10 or 100 mg/kg) was subcutaneously administered to the control and PNC groups. Subsequently, CMG parameter values obtained before and after treatment were compared. Results: In baseline CMG, compared to control group, PNC group revealed statistically significant elevations in the intercontraction intervals (ICIs), number of nonvoiding contractions, baseline pressure, threshold pressure, bladder capacity, voided volumes, and postvoid residual. However, contraction amplitudes and voiding efficiency were significantly decreased. In the control group, compared with the baseline values, 10-mg/kg acotiamide resulted in statistically significant elevations in contraction amplitudes. Treatment with 100-mg/kg acotiamide led to statistically significant elevations in contraction amplitudes and decreases in ICI and bladder volume. In the PNC group, there were no statistically significant changes noted in CMG parameters after treatment with 10-mg/kg acotiamide (n=6). Compared with the baseline values, the administration of 100-mg/kg acotiamide significantly decreased ICI (1,025±186 seconds vs. 578±161 seconds; P=0.012), bladder capacity (1,841±323 µL vs. 871±174 µL, respectively; P=0.0059) and postvoid residual (223±46 µL vs. 44±22 µL, respectively; P=0.023), and increased contraction amplitudes (22.09±1.76 cm H2O vs. 43.84±6.87 cm H2O, respectively; P=0.012) and voiding efficiency (0.87±0.02 vs. 0.94±0.03, respectively; P=0.029). Conclusions Acotiamide showed effectiveness in the treatment of underactive bladder, possibly through activation of bladder afferent and detrusor activities.

Syndrome of the trephined (SoT) is a complication that develops weeks to months after decompression craniotomy. Previous studies have reported cases in which paralysis, disturbance of consciousness, and cognitive impairment associated with the primary disease worsened, and cases in which new neurological symptoms appeared in addition to the primary disease. It is known that cranioplasty rapidly improves these symptoms, but there are few reports on rehabilitation treatment for SoT. In this report, we describe a case of paralysis limited to the right hand due to SoT. The patient was a 34-year-old male who underwent decompression craniotomy for a left acute subdural hematoma on day X-180. No paralysis or cognitive impairment were observed. He was discharged home on day X-106, but paralysis of the right hand appeared around day X-100. The cause was unknown, but it was suspected to be due to the decompression craniotomy. He received cranioplasty on day X, and was referred to the rehabilitation department on day X+1. We considered that the paralysis was influenced by SoT, and a task-oriented training and electrical stimulation therapy approach was applied. The paralysis improved rapidly and the patient recovered completely on day X+29. This case suggests that SoT resulting in paralysis limited to the fingers may have a good prognosis and that high goals can be set in rehabilitation treatment.

Syndrome of the trephined (SoT) is a complication that develops weeks to months after decompression craniotomy. Previous studies have reported cases in which paralysis, disturbance of consciousness, and cognitive impairment associated with the primary disease worsened, and cases in which new neurological symptoms appeared in addition to the primary disease. It is known that cranioplasty rapidly improves these symptoms, but there are few reports on rehabilitation treatment for SoT. In this report, we describe a case of paralysis limited to the right hand due to SoT. The patient was a 34-year-old male who underwent decompression craniotomy for a left acute subdural hematoma on day X-180. No paralysis or cognitive impairment were observed. He was discharged home on day X-106, but paralysis of the right hand appeared around day X-100. The cause was unknown, but it was suspected to be due to the decompression craniotomy. He received cranioplasty on day X, and was referred to the rehabilitation department on day X+1. We considered that the paralysis was influenced by SoT, and a task-oriented training and electrical stimulation therapy approach was applied. The paralysis improved rapidly and the patient recovered completely on day X+29. This case suggests that SoT resulting in paralysis limited to the fingers may have a good prognosis and that high goals can be set in rehabilitation treatment.