Dysfunction Of Infravesical Mechanisms

The dysfunction of infravesical mechanisms (DIVM) encompasses the dysfunction of the striated urethral sphincter and that of the pelvic floor. Either dysfunction may occur alone or in combination. DIVM has been inconsistently reported in variable numbers,3,22,24,36 including its complete absence.13 Correlation with clinical symptomatology is frequently inadequate or lacking,3,22,24 and therefore its clinical significance is unclear. Different kinds of dysfunctions have been described. In some cases, the descriptions are poorly characterized and may not be confirmed again in other reports.

* Detrusor hyperreflexia with impaired contractile function was defined as an overactive bladder with uninhibited detrusor contractions associated with low maximum detrusor pressure during the voiding phase of less than 40 cm of water with a slow pressure increase and a large post-void residual volume.6

The presence of DIVM was suggested by a number of early reports where an elevated urethral pressure profile was noted in a proportion of PD patients. Eighteen per cent of patients (2/11) in a series of PD patients with urinary symptoms had evidence of increased urethral resistance at the external sphincter level.22 Adequate correlation with symptoms was not presented in this particular report.

Berger et al.7,8 performed uroflow studies in 15 uro-logically symptomatic patients and demonstrated decreased flow in 10 (less than 12 ml per second). Only in 5 of these 10 patients was there evidence of an obstructive uropathy. A clear clinical correlation with obstructive symptoms or other manifestations was not available in this report. Although the possibility could be raised that the other five patients may have harbored a DIVM, no such activity was documented on sphincter EMG testing during voluntary detrusor contraction.

Raz was able to demonstrate changes in urethral pressure profile as a result of dopaminergic treatment in 66% (10/15) of a group of PD patients with urinary symptoms who were off anticholinergics and free of BPH.27 Treatment with L-dopa reduced the closure pressure of the urethra as measured by urethral pressure. Interruption of treatment for a week resulted in an increase in the urethral pressure profile. Raz proposed that outlet dysfunction played an important role in the urinary symptomatology of PD by way of an increased tone of the external sphincter, the absence of a well coordinated pelvic floor relaxation during micturition and the lack of normal external sphincter function during interruption of micturition.

The most consistent DIVM consists of delayed relaxation of the striated urethral sphincter and pelvic floor, also known as sphincter bradykinesia. To understand this phenomenon, one must first understand that there is a normal guarding reflex where there is an increase in striated muscle activity during vesical filling before the onset of detrusor contraction. Sphincter bradykinesia would be an abnormality where involuntary EMG activity persists through at least the initial part of the expulsive phase of the CMG.24

In the Pavlakis et al. series,24 11% (3/28) had sphincter bradykinesia. Galloway15 reported that 42% (5/12) of his urologically symptomatic patients were unable to relax the external urethral sphincter with voiding and were associated with low flow rates. Andersen et al.3 studied 24 urologically symptomatic patients with parkin-sonism (the words "Parkinson's disease" are not used). The same authors subsequently revised their data in a subsequent article.5 They reported electromyographic findings in these 24 PD patients. The authors did not specify whether all 24 patients were symptomatic. Twenty-one per cent (5/24) had impaired sphincter control defined as poor ability to contract or relax the sphincter on command.

Pavlakis et al.24 also found pseudodyssynergia in two patients. This phenomenon was defined as "an attempt at continence by voluntary contraction of the pelvic musculature during an involuntary detrusor contraction."35 These two patients were part of a group of ten in which the maximum flow rate was decreased. The clinical role of this phenomenon was not defined because of coexistent prostatic obstruction. Pseudodyssynergia has not been reported in any of the subsequent articles of this review. Sphincter "tremor," described in 11/12 patients of Galloway's series,15 has also not been confirmed in subsequent reports.

While Pavlakis et al.24 called attention to the absence of vesicosphinter dyssynergia, Andersen et al.3,5 also reported two patients with an abnormality they initially called "dyssynergia" in their first article3 but later labeled "spasticity."5 In the Araki et al.6 series of 70 PD patients referred for urological evaluation and who were free of obstructive etiologies, they found 2 patients (3%) who had both hyperreflexia and detrusor-sphincter dyssyner-gia (2/70).

DIVM may also be asymptomatic. Berger et al.7,8 studied 29 PD patients (24 men and 5 women) who were urologically symptomatic. They reported sporadic involuntary electromyography activity of the external sphincter during involuntary detrusor contractions in 61% (14/23 patients so tested) without any case resulting in obstruction. They termed this phenomenon involuntary sphinc-teric activity. Because the phenomenon was not associated with radiographic or manometric evidence of obstruction at the level of the membranous urethra, the authors concluded that it did not meet criteria for the definition of detrusor sphincter dyssynergia. This activity is reminiscent of pseudodyssynergia in that both occur in response to involuntary detrusor contractions, but pseudodyssyner-gia is seen as a voluntary or conscious act.

Stocchi et al.36 studied 30 PD patients irrespective of presence of urological symptoms. They found that 27% (8/30) had an inability to relax the perineal muscles immediately and completely when asked to initiate micturition. This was their only abnormal finding (they had normal cystometrics). Not a single one is described with hesitancy or weak urinary stream. This subgroup of 8 patients had more severity and longer duration of disease than 11 patients with totally normal findings. An additional three patients (10%) had the same abnormality but associated with detrusor hyperreflexia. One of the three patients had urinary incontinence, diurnal and nocturnal, but the authors do not specify if preceded by urge incontinence (no mention of hesitancy or weak urinary stream).

Pavlakis et al.24 reported "neuropathic potentials" in two of their patients. Andersen et al.5 also reported two patients as having a "sphincter paralysis" in their 1976 report and as "flaccid sphincter" in their 1985 report. These cases most likely represent multiple system atrophy rather than PD.

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