The second urodynamic study (3 months after starting 15 mg/day pilocarpine) showed a first sensation

at 50 mL and a bladder capacity of 195 mL, but no detrusor overactivity. On voiding, although his post-void residual decreased significantly, urodynamic parameters did not change (Schafer grade 2, a weak detrusor and low Watts factor of 7.71 watts/m2). The clinical manifestations of our case were mostly the same as those in previously reported SCA31 cases.[4-6] Our case was unique in that he developed partial urinary retention; and a urodynamic study revealed weak detrusor and neurogenic change of MUPs in the external sphincter muscles. Prostatic hyperplasia is the most common disease that produces urinary retention in older men (he was 73 years old). His prostate volume (26 mL) indicated mild prostate enlargement (BPE). However, R788 cell line regarding the result of Schafer’s nomogram (no obstruction), we considered that mild BPE in this patient can not affect his voiding disorder significantly. Even though, in the presence of poor detrusor contractility, the possibility of an additional element of outflow obstruction cannot be excluded completely. Also, he did not have neurologic comorbidities such as lumbar spondylosis or diabetes. A weak detrusor originates from various lesion sites anti-PD-1 monoclonal antibody in the neural axis, for example, either a

lower motor neuron lesion or upper motor neuron lesion.[9] However, our case showed no apparent pyramidal signs such as exaggerated reflexes, spasticity or extensor plantar responses. Rather, he showed sphincter EMG abnormality, which indicates a nuclear or infra-nuclear lesion in the pudendal nerves.[1] Although no spinal cord pathology is available in SCA31,[4-6] the weak detrusor and sphincter EMG abnormality in our case

indicates that the sacral spinal cord might be Adenylyl cyclase affected in this case. This feature mimics that of MSA-C,[1] which prompts particular caution when performing sphincter EMG in patients with cerebellar ataxia. Neurogenic urinary retention in SCA31 can be listed in the clinical differential diagnosis of cerebellar ataxia. Three months administration of 15 mg/day pilocarpine lessened his post-void residual significantly. Pilocarpine acts primarily as a muscarinic agonist, and it non-selectively stimulates muscarinic receptors. It is experimentally known that muscarinic stimulation relaxes posterior urethra via nitric oxide (NO) pathways[10, 11] and muscarinic M3 stimulation contracts the bladder wall. Therefore, similar mechanism might have underlain this amelioration although we could not see significant changes in the urodynamic parameters. In conclusion, we report a man with SCA31 in whom urodynamic study showed a weak detrusor and sphincter EMG abnormality, indicating involvement of the sacral spinal cord. Neurogenic urinary retention in SCA31 can be listed in the clinical differential diagnosis of cerebellar ataxia.