[Bladder Dysfunction and Neurology: How to Assess Neurogenic Bladder Dysfunction?]

Here we reviewed bladder dysfunction in neurological diseases. Diseases of the brain cause overactive bladder (OAB); peripheral neuropathy including lumbar spondylosis results in postvoid residual; and spinal cord diseases cause a combination of OAB and postvoid residual. Multiple system atrophy mimics bladder dysfunction related to spinal cord disease. Conversely, in cases of bladder dysfunction of unknown etiologies, the underlying disease can be identified by the bladder dysfunction pattern. Aging also causes nocturnal polyuria. The collaboration between neurologists and urologists is highly recommended to maximize the quality of life of neurological patients.

[Urinary dysfunction in idiopathic normal pressure hydrocephalus].

Urinary incontinence (UI) is a significant burden in the elderly and their caregivers when assessed by quality-of-life measures, early institutionalization, or health economics. UI is well known as a clinical triad for the diagnosis of normal pressure hydrocephalus (NPH). However, other than UI, NPH patients commonly have urinary urgency/frequency (overactive bladder: OAB), and less commonly, voiding difficulty. Fourteen percent of the patients (either women or men) have post-void residual > 100 ml. The most common urodynamic abnormality is detrusor overactivity (DO), which was noted in 95% of patients. The underlying pathophysiology for OAB/DO in patients with NPH seems to be decreased cerebral blood flow in the right frontal cortex, and to a lesser extent, altered basal ganglia function. Functional UI can overlap the OAB/DO due secondary to impaired cognition/initiative, immobility, or disturbed consciousness in this disorder.

Mechanism of bladder dysfunction in idiopathic normal pressure hydrocephalus.

AIM: To elucidate the mechanism of bladder dysfunction in idiopathic normal pressure hydrocephalus (iNPH) by a urodynamic study. METHODS: Forty-two patients with possible iNPH, who were diagnosed by clinical symptoms/signs (gait, cognitive, and urinary disorders) with typical imaging features (ventricular enlargement) and normal cerebrospinal fluid pressure, were enrolled. The subjects included 36 men and 6 women; mean age, 72 years (62-83 years). All patients underwent a urodynamic test according to the definitions and methods proposed by the International Continence Society. RESULTS: Lower urinary tract symptoms were seen in 93% of the patients, with storage symptoms (93%) being more common than voiding symptoms (71%); and urinary urgency (overactive bladder) (64%)/frequency (64%) being more common than urinary incontinence (57%). The mean values for the maximum flow rate and post-void residual (PVR) volume were 11.7 ml/sec and 42.1 ml, respectively. PVR >100 ml was noted in six patients (three men, three women; range, 100-228 ml). Although the majority of patients had normal bladder volume at the first sensation (mean 134 ml), bladder capacity was small (mean 200 ml) and detrusor overactivity was seen in 95% of patients. CONCLUSIONS: While incontinence can result secondarily from gait disturbance or dementia, detrusor overactivity mostly underlies urinary urgency/frequency and incontinence in iNPH.

Different mechanism of vocal cord paralysis between spinocerebellar ataxia (SCA 1 and SCA 3) and multiple system atrophy.

While multiple system atrophy (MSA) is frequently associated with vocal cord paralysis (VCP) causing severe respiratory failure, it is still unknown whether hereditary types of spinocerebellar degeneration develop similar laryngeal paralysis. We analyzed the laryngeal function from the viewpoints of fiberoptic laryngoscopy and laryngeal myopathology and then attempted to clarify the difference of the mechanism of VCP among the patients with spinocerebellar ataxia type 1 (SCA 1), type 3 (SCA 3), and MSA. Seven patients with SCA 1, nineteen with SCA 3, and eleven with MSA were studied. Vocal cord movement was analyzed by fiberoptic laryngoscopy during wakefulness and diazepam-induced sleep (sleep load test). Paraffin-embedded sections or cryosections of the intrinsic laryngeal muscles from five autopsied cases (one with SCA 1 and four with SCA 3) were histologically examined. VCP was found in two of the seven SCA 1 patients (29%), three of the nineteen SCA 3 patients (16%), and in nine of the eleven MSA patients (82%). VCP observed in SCA 1 and SCA 3 was various in the severity and showed no exacerbation on sleep load test in all of the eight patients but one SCA 3 patient. In this patient, the findings of fiberoptic laryngoscopy were quite similar to those found in MSA. All the intrinsic laryngeal muscles including cricothyroid (CT), interarytenoid (IA), and posterior cricoarytenoid (PCA) muscles showed neurogenic atrophy in one autopsied SCA 1 and four SCA 3 patients. Our conclusion is that VCP in SCA 1 and SCA 3 contrasts with that in MSA in its occurrence, response to the sleep load test, and the distribution of the neurogenic abnormalities among the intrinsic laryngeal muscles.