Incontinence is the inability to control excretory function. The term is generally used in reference to the inability to control normal bladder or rectal function, leading to urinary or fecal incontinence respectively. By comparison, urinary incontinence is more variable in its clinical presentation, and as a result, is classified according to its dominant features as either stress, urge, mixed, neurogenic or continuous incontinence. Of these types of urinary incontinence, stress incontinence is the most common, and depending upon the age of the individual occurs in approximately 15-45% of women but only 1.5-5% of men.
With stress incontinence urinary loss occurs as a result of any type of activity that has the effect of raising the intra-abdominal pressure (and hence, pressure within the bladder) beyond the point where the urethral sphincter is able to restrain and prevent urinary loss. As a result, the high pressure within the bladder forces urine past the urethral sphincter causing incontinence to occur. Common examples of activities that can raise the intra-abdominal pressure sufficiently to result in urinary loss include coughing, sneezing, straining, bending, lifting and, if the condition is severe enough, even just a change in body position. There are several factors that can contribute to the development of urinary incontinence, but the most common involve injury or damage to the musculature and/or nerves of the pelvic floor that serve to maintain normal support necessary to preserve normal bladder function and urinary control.
Pregnancy, childbirth, accidents and falls are common events or mechanisms that can cause injury to these muscles and nerves, and are also common mechanisms for causing the type of spinal disorder leading to urinary incontinence that develops in the PPOD syndrome patient. While stress incontinence is the most common type of urinary incontinence that occurs overall, it is also the most common type of urinary loss seen in the PPOD syndrome patient. However, urge, mixed, neurogenic and overflow incontinence are also found in the PPOD syndrome patient, and generally respond every bit as well as does stress urinary incontinence to PPOD syndrome therapeutic protocols. See cases 4, 10, 15 and 16 for examples of the response of urinary incontinence to PPOD syndrome treatment.
Fecal or anorectal incontinence occurs in approximately 10% of both men and women, however, in individuals who suffer symptoms of irritable bowel syndrome, it’s prevalence rises to approximately 20%. In the PPOD syndrome patient fecal incontinence is usually caused by damage to the nerves that control normal pelvic floor and anal sphincter muscle function. The nerve damage that occurs in these cases is the result of an underlying spinal disorder which results in weakness of the muscles that normally restrain and prevent passage of stool from the rectum. In this weakened state, the normal peristaltic activity of the large bowel can force stool past the anal sphincter and result in fecal incontinence.
There are generally two variations of fecal incontinence as it typically occurs in the PPOD syndrome patient. In the first instance nerve damage is confined to the nerves that initiate contraction of the muscles that prevent incontinence from occurring. In these cases, because sensory nerve function to the rectum remains intact, the individual finds that they are able to consciously sense the leakage of stool as it occurs. However, because of the weakness of the pelvic floor and anal sphincter, they are unable to contract these muscles with sufficient strength to prevent fecal incontinence from occurring. In the other variation, some PPOD patients with fecal incontinence have additionally lost normal sensory perception of the lower portion of the rectum and anal canal, and as a result cannot tell when the rectum is full or when they are passing stool. In these cases fecal incontinence can occur without their consciousness awareness of the event having occurred. Refer to cases 8, 15 and 16 for examples of the response of fecal incontinence to PPOD therapeutic protocols.