Psychogenic urinary dysfunction: a uro-neurological assessment.

AIMS: The diagnosis of psychogenic urinary dysfunction (PUD) is one of exclusion, particularly from urologic and neurologic causes, and is usually accompanied by more obvious psychologic/ psychiatric features. We here describe patients with PUD who were diagnosed in our uro- neurological laboratory. MATERIALS AND METHODS: We reviewed the digitized records of 2,300 urodynamic cases treated in the past 6 years to identify patients who fulfilled the diagnostic criteria of PUD. All 2,300 patients had completed a urinary questionnaire and undergone both electromyography (EMG)-cystometry and a detailed neurological examination. In addition, pressure-flow analysis, neurophysiology tests including sphincter EMG analysis, and MRI of the brain and spinal cord were performed as applicable. RESULTS: PUD was seen in 16 cases (0.7%): 6 men, 10 women, mean age 37 years. Lower urinary tract symptoms (LUTS) included overactive bladder (OAB) alone in 5, difficult urination alone in one, and both in 10. LUTS commonly occurred in particular situations, for example, OAB only while riding the train. Some patients showed extremely infrequent toileting. The urodynamic findings were normal except for increased bladder sensation (50%) for OAB and acontractile detrusor (31%) for difficulty. The final diagnosis was conversion reaction in six followed by anxiety in four. CONCLUSIONS: PUD patients experienced the situational occurrence of OAB and/or difficult urination and, in some patients, extremely infrequent toileting. The main urodynamic abnormalities were increased bladder sensation and acontractile detrusor. However, even in cases suggestive of PUD, a non-PUD pathology behind the symptoms should be explored.

Bladder sensation in peripheral nerve lesions.

OBJECTIVE: To present bladder sensory data of three common peripheral nerve lesions (e.g., distal, intermediate/focal, and proximal). METHODS: We measured first sensation (FS) and bladder capacity (BC) (not exceeding 600 ml) in 71 patients with peripheral nerve lesions: 35 diabetic neuropathy (D group), 6 post-pelvic surgery (S), and 27 cauda equina syndrome due to lumbar spondylosis (L). We excluded those with detrusor overactivity or low compliance that might affect bladder sensation. RESULTS: The mean FS was 301.7 ml (D), 271.3 ml (S), and 189.4 ml (L), with the largest being in the D group (P < 0.05); the mean BC was 495.2, 475.4, and 391.4 ml, with the largest being in the D group (P < 0.05); who commonly had less frequent toileting. The mean post-void residual volume was 106.5, 29.0, and 42.0 ml; the values tended to increase along with BC. In the D group, the mean FS in patients with skin hypoalgesia as detected by pin prick and in those without it was 407.8 and 210.0 ml. The percentage of patients with FS < 100 ml was 5.7%, 0%, and 7.4%, respectively, who commonly had urinary urgency and frequency. CONCLUSIONS: Bladder sensation is affected in diabetic neuropathy more severely than in intermediate/proximal lesions, together with somatic sensory disturbance. Bladder sensory disturbance leads to less frequent toileting, resulting in bladder over-distension and large post-void residuals. A small proportion of patients with peripheral nerve lesions develop urinary urgency, presumably reflecting irritation of the afferent nerve fibers or the urothelium.

Pyridostigmine in autonomic failure: can we treat postural hypotension and bladder dysfunction with one drug?

In a 66-year-old man with autonomic failure, pyridostigmine (180 mg/day orally) improved both postural hypotension and underactive detrusor bladder dysfunction. Acetylcholinesterase inhibition may be useful in the management of orthostatic hypotension and bladder dysfunction in autonomic failure patients.

Urinary dysfunction and autonomic control in amyloid neuropathy.

Uro-neurological assessment was performed in four patients with small-fiber neuropathy due to amyloidosis (2 transthyretin-type/2 immunoglobulin light-chain-type). Voiding difficulties were due to detrusor weakness and impaired bladder sensation. In two patients cholinesterase inhibition treatment caused urge incontinence, indicating detrusor denervation supersensitivity. The underlying mechanisms of urinary dysfunction seem to involve postganglionic cholinergic and afferent somatic nerves.