[Disjunction patterns: the morphological and ultrastructural bases of bladder instability in the male]

To apply the new protocols and recent contributions on detrusor ultrastructural morphology in order to standardize criteria and evaluate our findings relative to the ultrastructural morphology, the presence of a dysfunction pattern, changes in nerve supply and formation of a chained cellular syncytium in hyperactive detrusor bladder instability in the male.

We studied 480 ultrastructural preparations of detrusor muscle from 32 male patients with bladder outlet obstruction with and without urodynamically demonstrated bladder hyperactivity. Bladder biopsies were obtained from the anterior aspect of the bladder and prepared according to the standard procedures for ultrastructural study. Semiquantitative nerve supply ultrastructural patterns, syncytial composition, and complete and incomplete disjunction were analyzed.

Lower urinary tract obstruction was demonstrated in all patients; 6 of these patients had involuntary phasic detrusor contractions during filling. No significant decrease in nerve supply was found in isolated obstruction or in bladder hyperactivity. No axonal degeneration was observed in any of the patients and the myelin sheath structure was normal. Nerve effector endings were also normal. Four patients with hyperactive detrusor showed complete and two incomplete disjunction pattern. Incomplete disjunction pattern was also demonstrated in two patients with isolated obstruction.

The change in the properties of the detrusor muscle in the unstable bladder is due to a complete reduction in excitatory nerve relation to smooth muscle. Having established the concept of common final myogenic pathway that explains involuntary detrusor contraction, complete dysfunction ultrastructural patterns have been defined with univocal relation to hyperactive detrusor. These patterns indicate the existence of a syncytium of chained muscle cells with changes in the excitation threshold that are absent in the normal stable detrusor. Two ultrastructural components sustain this hypothesis: 1) the major loss observed in intermediate cellular unions that are thought to mediate in the mechanical coupling of cellular contraction and 2) the presence in all the microscopic fields of abutments in the narrow cellular unions like gap-junctions, which mediate the electrical coupling. In the present study we have found this pattern in 4 out of 6 patients with hyperactive detrusor, and congruent with other studies, the incomplete disjunction pattern could be the prelude of bladder hyperactivity.