NEUROMUSCULAR INJURY TO THE PELVIC FLOOR DUE TO VAGINAL DELIVERY

Many studies using different techniques have demonstrated neurogenic and structural damage to the PFM and sphincter muscles as a consequence of vaginal delivery (Vodušek 2002b). Other lesion mechanisms, such as muscle ischaemia, may also be operative during childbirth. As a consequence, the PFM would become weak; such weakness has indeed been demonstrated (Verelst & Leivseth 2004). The sphincter mechanisms and pelvic organ support become functionally impaired, with SUI and prolapse being a logical consequence.

Although muscle weakness may be a common consequence of childbirth injury, there seem to be further pathophysiological possibilities for deficient PFM function; it is not only the strength of muscle contraction that defines its functional integrity. Normal neural control of muscle activity leads to coordinated and timely responses to ensure appropriate muscle function as required. Muscular ‘behavioural’ patterns have been studied by kinesiological EMG recording. Changes in muscular behaviour may originate from minor and repairable neuromuscular pelvic floor injury. In nulliparous healthy women two types of behavioral patterns named as tonic and phasic pattern, respectively, can be found:

• the tonic pattern consists of a crescendo–decrescendo type of activity (probably derived from grouping of slow motor units) that may be the expression of constant (‘tonic’) reflex input parallel to the breathing pattern;

• the phasic pattern, probably related to fast-twitch motor unit activation, is motor unit activity seen only during activation maneuvers, either voluntary contraction or coughing. With respect to these muscle activation patterns parous women with SUI are subject to a number of possible changes, such as a significant reduction of duration of motor unit recruitment, unilateral recruitment of reflex response in the pubococcygeal muscle, and paradoxical inhibition of continuous firing of motor units in PFM activation on coughing.

The reasons for such persisting abnormalities are not clear and are diffi cult to explain by muscle denervation (which has been amply studied) alone. Although not proven in studies, it is reasonable to assume that motor denervation is accompanied also by sensory denervation of the PFM. In addition to denervation injury there may be some further temporary ‘inhibitors’ of PFM activity, such as periods of pain and discomfort after childbirth (e.g. perineal tears, episiotomy), increased by attempted PFM contraction. All above mentioned factors may lead to a temporary disturbance of PFM neural control after childbirth. This, in combination with a particularly vulnerable pelvic floor neural control (which only evolved in its complexity phylogenetically after the attainment of the upright stance), might become persistent, even if the factors originally leading to the problem disappear.