Unlike skeletal striated muscle, the detrusor, because of its postganglionic system, is capable of some contractions, although imperfect, after complete destruction of the sacral segments of the spinal cord. Isolation of the sacral cord centers (transverse lesions of the cord above the sacral levels) and their peripheral nerves permits contractions of the detrusor muscle, but they still do not empty the bladder completely; patients with such lesions usually develop dyssynergia of the detrusor and external sphincter muscles (see later), indicating that coordination of these muscles must occur at supraspinal levels (Blaivas). With acute transverse lesions of the upper cord, the function of sacral segments is abolished for several weeks in the same way as the motor neurons of skeletal muscles (the state of spinal shock).
The storage of urine and the efficient emptying of the bladder are possible only when the spinal segments, together with their afferent and efferent nerve fibers, are connected with the so-called micturition centers in the pontomesencephalic tegmentum. In experimental animals, this center (or centers) lies within or adjacent to the locus ceruleus. A medial region triggers micturition, while a lateral area seems more important for continence. These neurons receive afferent impulses from the sacral cord segments; their efferent fibers course downward via the reticulospinal tracts in the lateral funiculi of the spinal cord and activate cells in the nucleus of Onuf, as well as in the intermediolateral cell groups of the sacral segments (Holstege and Tan). In cats, the pontomesencephalic centers receive descending fibers from anteromedial parts of the frontal cortex, thalamus, hypothalamus, and cerebellum, but the brainstem centers and their descending pathways have not been precisely defined in humans. Other fibers from the motor cortex descend with the corticospinal fibers to the anterior horn cells of the sacral cord and innervate the external sphincter. According to Ruch, the descending pathways from the midbrain tegmentum are inhibitory and those from the pontine tegmentum and posterior hypothalamus are facilitatory. The pathway that descends with the corticospinal tract from the motor cortex is inhibitory. Thus the net effect of lesions in the brain and spinal cord on the micturition reflex, at least in animals, may be either inhibitory or facilitatory (DeGroat).
Almost all of this information has been inferred from animal experiments; there is little human pathologic material to corroborate the role of brainstem nuclei and cortex in bladder control. What information is available is reviewed extensively by Fowler, whose article is recommended. Also of interest here is the study by Blok and colleagues, who performed positron emission tomography (PET) studies in volunteer subjects during micturition. Increased blood flow was detected in the right pontine tegmentum, periaqueductal region, hypothalamus, and right inferior frontal cortex. When the bladder was full but subjects were prevented from voiding, increased activity was seen in the right ventral pontine tegmentum. The meaning of these lateralized findings is unclear, but the study supports the presumption that pontine centers are involved in the act of voiding.