11 Neural mechanisms in disorders of defaecation

11 Neural mechanisms in disorders of defaecation D. Z. LUBOWSKI M. SWASH M. M. HENRY

Normal defaecation requires a continence mechanism and a process of evacuation. This implies a normal anatomical arrangement of the rectum and anus including a reservoir capacity and a nerve supply which integrates and regulates the complex function of the pelvic floor. Disorders of defaecation therefore consist of alterations in continence or failure to evacuate the rectal contents (Table 1). PHYSIOLOGY

OF CONTINENCE

AND DEFAECATION

Faecal continence is a complex process involving the anal sphincter and pelvic floor muscles. It is largely an unconscious process controlled by spinal and local nerve pathways, but is also regulated by the conscious will. There are a number of components in the continence mechanism (Table 2). The most important are the anal sphincter and the anorectal angle. Anal sphincter The anal sphincter is made up of the internal and external sphincter, which are arranged concentrically around the anal canal; they overlap except in the most distal part of the anal canal in the region of the superficial part of the external sphincter. Continuous electromyographic (EMG) activity may be recorded in the external anal sphincter at rest (Floyd and Walls, 1953) but the external sphincter contributes only lo-15% of the resting anal pressure (Bennett and Duthie, 1964; Duthie and Watts, 1965; Frenckner and von Euler, 1975). An important function of the external anal sphincter is to reflexly contract in response to transient rises in intra-abdominal pressure (Taverner and Smiddy, 1959; Parks et al, 1962). This activity is mediated via a spinal reflex (Melzack and Porter, 1964). The external sphincter also contracts under voluntary control, thus allowing defaecation to be delayed until a socially appropriate Bailli~re’s

Clinical

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1988

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202

D. Z. LUBOWSKI ET AL Table 1. Classification of defaecatory disorders. Incontinence Normal pelvic floor Abnormal pelvic floor Abnormal defaecation Constipation Anismus Total colon dysfunction Rectal prolapse Anterior mucosal prolapse Solitary rectal ulcer syndrome Table 2. Factors related to continence. Pressure zone Internal anal sphincter External anal sphincter Anorectal angle Flap and flutter valves Sensation-rectal, anal Mucosal resistance to opening Rectal capacity Stool consistency Ability to evacuate the rectum

time. The external anal sphincter appears to be particularly important in maintaining continence of solids since voluntary contraction pressures are significantly lower in patients with incontinence to solids and liquids than in patients with incontinence to liquids alone (Read et al, 1984). Resting anal tone is largely due to the internal anal sphincter, which is in a state of tonic partial contraction (Bennett and Duthie, 1964; Duthie and Watts, 1965). The internal anal sphincter is innervated by sympathetic nerves via the hypogastric (presacral) nerves, through visceral efferent fibres derived from the fifth lumbar segment (Schuster, 1968). Its parasympathetic innervation is derived from the sacral outflow via the pelvic plexus. It also receives innervation from the enteric nervous system, consisting of non-cholinergic, non-catecholaminergic nerves, that may utilize purinergic or peptidergic transmitters (Alumets et al, 1978; Burleigh et al, 1979; Burnstock, 1986). The internal anal sphincter relaxes during defaecation straining, and in response to rectal distension (Denny-Brown and Robertson, 1935; Callaghan and Nixon, 1964). The latter response is mediated via a local reflex in the wall of the anorectum, and is independent of extrinsic nerve control (Denny-Brown and Robertson, 1935; Frenckner and Ihre, 1976; Lubowski et al, 1987). Stimulation of the presacral sympathetic nerves in man who results in relaxation of the internal anal sphincter (Shepherd and Wright, 1968; Lubowski et al, 1987). The importance of the internal anal sphincter in the continence mechanism

DISORDERS

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203

seems to vary between individuals, since surgical division of the internal sphincter results in incontinence only in some patients (Marks and Ritchie, 1978). Such incontinence usually consists of mucus leakage, minor faecal leakage, or incontinence to flatus. Conversely, continence may sometimes be preserved when there is neuropathic damage to the external anal sphincter and puborectalis muscles, and when internal sphincter tone is normal (Womack et al, 1986). Anorectal angle

The anorectal angle, produced by the forward pull of the puborectalis muscle, is thought to be crucial in the continence mechanism. Milligan and Morgan (1934) observed that surgical division of the external and internal sphincters did not result in incontinence if the puborectalis was intact, but that division of the puborectalis invariably caused incontinence. Varma and Stephens (1982) noted that continence may be preserved in patients who have a normal anorectal angle but no functioning sphincter, but this must depend on the consistency of the stool. It is hard to envisage how contraction of the puborectalis could by itself maintain continence to liquids, which could seep around the anorectal angle, unless it contracted against a relatively immobile solid object such as the cervix uteri or prostate. Posterior division of puborectalis in the treatment of constipation due to functional pelvic outlet obstruction, however, resulted in incontinence in five of nine patients (Barnes et al, 1985). Loss of the anorectal angle seems to result in incontinence only in the presence of low sphincter pressures (Bartolo et al, 1983~). Flap and flutter valves

The flap valve produced at the anorectal junction appears to be important in the continence process. The flap valve theory proposes that the anterior rectal wall is pushed onto the upper anal canal by the intra-abdominal pressure (Parks et al, 1966). This process is dependent upon the presence of the anorectal angle, which is maintained by the forward pull of the puborectalis muscle. The flap valve theory is supported by the finding that intrarectal pressure is higher than intra-anal canal pressure during coughing in continent subject (Phillips and Edwards, 1965), suggesting that there is a mechanism to counter this recta-anal pressure gradient. Bannister and Read (1987) however, found that the reflex activity in the external anal sphincter caused the anal pressure in normal continent subjects to be maintained above the rectal pressure during graded increases in intra-abdominal pressure. They suggested that this higher pressure would prevent the rectal mucosa being pushed into the anal canal, thereby preventing a flap valve from functioning. The appropriate pressure gradient for a flap valve existed in incontinent patients, but this did not prevent leakage occurring during rises in intra-abdominal pressure. Phillips and Edwards (1965) demonstrated a 0.5 cm long segment of anal canal at the anorectal angle which was rapidly cleared of barium sulphate

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powder. They postulated a zone subjected to greater surrounding forces than other parts of the anal canal and suggested that such a zone might occur at the point at which the anorectum passes through the pelvic floor. They suggested the presence of a flutter valve in this region. This theory is supported by anteroposterior radiographs which show the anal canal to be flattened in the region. The theory of mechanical valves to preserve continence is incompatible with the requirements of defaecation, unless one postulates a mechanism to ‘unlock’ the valve mechanism prior to defaecation. Sensation

The presence of air or stools in the rectum is perceived as a distinct sensation of pelvic ‘fullness’. The rectum accommodates to distension (Ahran et al, 1976; Read and Bannister, 1985) so that this sensation is short-lived. With continued distension a critical volume is reached at which the urge to defaecate is felt. The receptors responsible for this sensation probably lie in the muscles of the pelvic floor rather than in the rectal wall itself. Hence patients with rectal tumours treated by excision of the rectum and cola-anal anastomosis are said to perceive a ‘normal’ sensation of ‘rectal’ filling (Lane and Parks, 1977). Stretch receptors have been identified in the levator muscles (Winkler, 1958) and muscle spindles which might signal stretching have been observed in the external anal sphincter (Walls, 1959) and puborectalis (Swash, 1985). Duthie and Bennett (1963) postulated that rectal contents may be ‘sampled’ by sensory receptors in the anal canal, which are stimulated as rectal contents come into contact with the anus when the internal anal sphincter relaxes in response to rectal distension. Differentiation of flatus from solid stool may also be a function of the differences in afferent discharge from a rectum that is distended with contents that can be displaced or not (Goligher and Hughes, 1951). Even people who have normal anal sensation can find it quite difficult to distinguish between liquid and gas, both of which can be readily displaced. Anal sampling may also be important in discriminating between flatus and stool (Read and Read, 1982). Goligher (1951) found that excision of the rectum, and cola-anal anastomosis by a pull-through technique after excision of the anal mucosa, resulted in inability to discriminate flatus from stool, later developing into incontinence. However, Nicholls and Lubowski (unpublished observations) observed a poor correlation between the ability to differentiate flatus from faeces and continence after rectal excision with cola-anal anastamosis with or without a colonic reservoir. Other factors

Simple surface tension created by apposition of moist mucosal surfaces may aid continence (Duthie, 1975). The presence of a capacitance organ in the pelvis is important and, after proctectomy with straight ileo-anal anastomosis, a significant proportion of patients suffer variable degrees of incontinence

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OF DEFAECATION

(Ravitch, 1948; Martin et al, 1977). The addition of an ileal reservoir greatly improves continence (Nicholls and Pezim, 1985). Defaecation

Normal defaecation requires coordination of abdominal and pelvic muscles and may also involve colorectal propulsion, although this latter aspect remains to be proved. The arrival of faeces into the rectum triggers a desire to defaecate, though the site of the receptors that mediated this sensation is not established and could be in the rectal wall, the anal wall or the pelvic floor. Rectal distension also causes rectal contraction (via a spinal reflex) and internal sphincter relaxation (via an intramural reflex). The squatting position is assumed and abdominal pressure is raised by contraction of the abdominal muscles against a closed glottis. This rise in abdominal pressure is transmitted to the rectum, where the internal anal sphincter relaxes and the anal canal pressure falls sharply. The puborectalis relaxes (Parks et al, 1962; Porter, 1962), widening the anorectal angle. The pelvic floor, however, does not normally descend more than 2 cm (Mahieu et al, 1984), probably due to a compensatory contraction of the levator ani, and the anorectum dilates and assumes a funnel shape as the rectal contents are expelled. At the termination of defaecation the anal canal closes as the internal sphincter regains its tone and the external sphincter contracts transiently (the closing reflex) (Porter 1962).

PATHOGENESIS

AND

CLINICAL

FEATURES

Faecal incontinence

Faecal incontinence may be defined as minor incontinence, in which there is partial soiling or occasional incontinence to flatus or watery stool, or major incontinence with loss of control of stool of normal consistency. This clinical differentiation is important when assessing the incontinent patient as it provides an important clue to aetiology. Faecal incontinence is a common condition. The estimated prevalence is 4.2/1000; the known prevalence in the over 65-year age group is about S/l000 and the estimated prevalence in this group is over lO/lOOO (Thomas et al, 1984). In geriatric and psychiatric wards the incidence is 26% and 3 1% respectively (Clarke et al, 1979). There are numerous causes of faecal incontinence (Table 3). Incontinence may occur in normal subjects in the presence of diarrhoea when the normal continence mechanism is inadequate to cope with large volumes of watery stool. A proportion of patients with incontinence have a local anorectal disorder (Table 3). Corrective surgical treatment in these cases may result in marked functional improvement. In most patients the pathophysiological basis for incontinence is damage to the pelvic nerves which innervate the muscles of the pelvic floor and the external anal sphincter (Parks et al, 1977; Beersiek et al, 1979; Swash, 1982).

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Table 3. Causes of faecal incontinence. Diarchoea Infection Inflammatory bowel disease Small bowel resection Local anorectal conditions Haemorrhoids Fissure Fistula Mucosal prolapse Abnormal Minor

sphincter incontinence

Internal sphincter deficiency Anal surgery Prolapse-haemorrhoidal -rectal Faecal impaction Old age Severe constipation Mental disorder Major

incontinence

Congenital abnormalities of the anorectum Childhood incontinence-Encopresis Trauma Obstetric Anal surgery Impalement, gunshot Pelvic fracture Violation Neurological and neuromuscular UMN Cerebral--stroke, tumours, trauma Spinal-multiple sclerosis, tumours, vitamin Btl deficiency LMN Cauda equina-disc prolapse, tumours Pelvic tumours Multiple sclerosis Tabes dorsalis, diabetes, alcohol Polymyositis, scleroderma Rectal carcinoma Anorectal sepsis-hidradenitis, lymphogranuloma Idiopathic (neurogenic) Rectal prolapse

The external sphincter is innervated by the pudendal nerves, deriving fibres from the primary rami of the second, third and fourth sacral nerves and supplying the muscle from its perineal aspect (Percy et al, 1981). The pelvic floor muscles are innervated on their pelvic aspect by direct branches from the third and fourth motor roots (Lawson, 1974; Percy et al, 1981; Snooks and Swash, 1986). Damage to these nerves may occur in a number of ways.

DISORDERS

207

OF DEFAECATION Childbirth

Childbirth

Cauda

Equina

Urinary Incontinence

Anorectal Incontinence

Perineal

Descent

t

Excessive Defaecation,’ Straiping-Solitary

,/

Complete

Rectal

Yap\

?Aetiology Rectal

Ulcer

t Constipation

Figure

1. Algorithm

to show

pathogenesis

of faecal

incontinence.

From

Swash

et al, 1985.

Perineal descent and incontinence

The central factor relating to pelvic nerve damage is abnormal descent of the pelvic floor (Figure 1) (Henry et al, 1982). Pelvic floor descent was first described as the syndrome of the descending perineum (Parks et al, 1966). This clinical syndrome consists of a sensation of incomplete rectal evacuation, with a constant desire to bear down, pelvic discomfort, anal bleeding and mucous discharge. It is thought to be caused by incomplete rectal emptying. The latter results in excessive straining at stool and prolapse of the anterior rectal mucosa into the anal canal. We now regard perineal descent as a physical sign rather than as a discrete syndrome, since descent of the pelvic floor is seen as part of a variety of disease processes, including constipation, solitary rectal ulcer syndrome and faecal incontinence. Abnormal perineal descent results in stretching of the pudendal nerves. Since the pudendal nerve is fixed at the point at which it passes around the ischial spine, this stretch affects only the distal part of the nerve, that is, the part distal to the ischial spine (Kiff and Swash, 1984a). Normal nerves are vulnerable to stretch injury of greater than 12% of their length (Sunderland, 1978). Excessive stretching of the pudendal nerves results in denervation of the external anal sphincter. Histological studies of the external anal sphincter and puborectalis in patients with perineal descent and faecal incontinence have shown changes of denervation and reinnervation in these muscles (Parks et al, 1977; Beersiek et al, 1979; Parks and Swash, 1979). Electrophysiological studies in these patients using single fibre EMG (Neil1 and Swash, 1980; Neil1 et al, 1981) and concentric needle EMG (Bartolo et al, 1983a) techniques have shown evidence of neurogenic damage consistent with the histological findings. Studies of motor conduction in the terminal part of the pudendal nerve (Kiff and Swash, 1984a; Snooks et al, 1984b; Jones et al, 1987a) have shown

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ET AL

slowed conduction in this part of the nerve. The terminal motor latency is measured after stimulation of the pudendal nerve at the ischial spine and the evoked compound muscle action potential is recorded in the external anal sphincter muscle (Kiff and Swash, 1984a). This implies that the pudendal nerve has been damaged in the distal part of its course. The severity of nerve damage is related to the amount of perineal descent (Jones et al, 1987). Conduction in the proximal part of this innervation, assessedby measurement of the motor latency to the external anal sphincter after transcutaneous electrical stimulation of the cauda equina at the Ll and L4 vertebral levels, is normal in the majority ofpatients (Kiff and Swash, 1984b; Snooks et al, 1985). Similar studies on the innervation of the puborectalis muscle, that is, the direct pelvic branches of the third and fourth sacral motor roots (Percy et al, 1981) have shown that the distal, and not the proximal, part of this innervation is abnormal (Snooks et al, 1984a). This evidence therefore suggests that damage to the innervation of the external anal sphincter and puborectalis has occurred in the distal part of the innervation of these muscles. Perineal descent with neurogenic faecal incontinence is largely a disorder of women. The majority of these women have borne children (Parks et al, 1977; Kiff and Swash, 1984a) and 40 to 50% report a difficult childbirth, usually with a prolonged second stage of labour, forceps delivery, perineal tear or high infant birth weight. Prospective evaluation of women after vaginal delivery has shown evidence of nerve damage, with prolongation of pudendal nerve terminal motor latency and increase in fibre density in the external anal sphincter muscle (Snooks et al, 1984; 1986). These changes are usually reversible within 2 months of vaginal delivery, although they may be permanent, particularly in multiparous subjects (Snooks et al, 1986). No evidence of nerve damage is found in subjects undergoing caesarean section, suggesting that it is the vaginal delivery itself that causes the nerve damage. Perineal descent is a major feature of these patients, and in the absence of perineal descent histological evidence of denervation is not found (Henry et al, 1982). It is likely that vaginal delivery results in nerve damage as a result of a marked straining effort with prolonged perineal descent, as well as by direct damage to the sacral nerves during the passage of the fetal head through the pelvis. Clinical evidence also suggests that repeated and prolonged straining during defaecation is a risk factor in the development of pelvic nerve damage (Parks et al, 1977). Stress urinary and faecal incontinence

About 10% of patients with faecal incontinence presenting for surgical repair also suffer from stress urinary incontinence. Corresponding prevalence figures for faecal incontinence in patients presenting for surgical repair or genuine stress urinary incontinence are not available. Stress incontinence of urine is due to weakness of the anterior pelvic floor musculature, and of the sphincter musculature of the bladder neck. The latter consists of a smooth internal sphincter component and two striated components. The periurethral striated sphincter muscle is a group of muscle fibres innervated by the perineal branch of the pudendal nerve. The intramural component of the striated sphincter

DISORDERS

OF DEFAECATION

209

system, situated within the wall of the urethra at the urethrovesical angle is innervated like the puborectalis, by direct pelvic branches derived from the S2 motor roots (Snooks and Swash, 1986). In patients with faecal incontinence and perineal descent the perineal nerve terminal motor latency is increased, and if there is coincidental stress urinary incontinence the perineal nerve terminal motor latency is further increased above the mean value for normal subjects (Snooks and Swash, 1984a). In patients with genuine stress urinary incontinence, without faecal incontinence, the perineal nerve terminal motor latency is increased to a similar extent as in patients with double incontinence. These observations suggest that stress urinary incontinence resembles neurogenie faecal incontinence in its pathogenesis. The physiological abnormalities and the changes in the bladder, urethra, and urethrovesical angle may thus be due to weakness of the striated musculature of the anterior pelvic floor. The latter leads to secondary changes in smooth muscle function from disruption and distortion of these structures. Incontinence from neurological disease

Diseases of the nervous system can cause incontinence from damage to the sphincter mechanisms at a supranuclear or infranuclear level. Infranuclear lesions

Lower motor lesions cause denervation of the pelvic floor striated sphincters and therefore incontinence. In addition to the damage to the innervation of these muscles from distal lesions, as described above, damage to the sacral nerve roots at their exit foramina, or within the cauda equina can similarly cause denervation of these muscles and incontinence. Cauda equina disease commonly results from lumbar or sacral spondylosis and spinal canal narrowing, or from disc prolapse or other intraspinal lesions such as neoplasms. Trauma, either from fracture or penetrating wounds is also well recognized. These disorders can be recognized electrophysiologically by measuring the motor latency from stimulation of the cauda equina nerve roots at the Ll and L4 levels, and recording from the external anal sphincter, puborectalis, or external urinary sphincter muscles (Snooks and Swash, 1984b). Other electrophysiological techniques include EMG of the pelvic floor muscles (Snooks and Swash, 1986) and the use of F wave responses. The F wave (F = foot) is a response in a leg muscle derived from antidromic firing of anterior horn cells induced by electrical stimulation of a motor nerve. Its latency is a measure of conduction from the point of stimulation to the lumbosacral spinal cord, activation of the anterior horn cell and conduction to the muscle. F wave latencies are much used in the electrophysiological diagnosis of lumbosacral root disorders (Eisen et al, 1911; Kimura, 1983). Disease in the pelvis itself may damage the same pelvic nerves in the lumbosacral plexus as in the retroperitoneal space. Investigation of proximal lesions of these types usually involves X-rays of the lumbosacral spine, computerized tomography (CT) scanning of the spine and pelvis, and CT myelography. In primary autonomic failure, a degenerative disorder of the autonomic nervous

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ET AL

system characterized by hypotension, impotence, incontinence, sweating disorders, Parkinsonism, constipation, pupillary disturbances, and abnormalities of cardiovascular reflexes, there is associated degeneration of the somatic efferent motor fibres innervating the pelvic floor sphincter muscles from the Onuf nuclei in the spinal cord.

Supranuclear lesions Faecal and urinary incontinence are common in patients with upper motor neurone lesions resulting from disorders such as multiple sclerosis or multifocal vascular disease. In addition, incontinence may result from bilateral damage to the corticospinal pathways containing the efferent and afferent nerve fibres subserving the urinary and anorectal systems, and this may occur at any level, including the spinal cord. Thus spinal trauma, or other spinal disease, such as multiple sclerosis, limited to the cervical region, may cause incontinence as an early presenting symptom. Disease of the orbitofrontal cerebral cortex is particularly likely to present with incontinence since the central representation of sphincter control, at its highest level, is contained at this region. Diffuse diseases of the brain such as dementias are commonly accompanied by incontinence. In patients with tabes dorsalis incontinence also occurs, but it is uncertain whether this results primarily from damage to the efferent system, or whether it is due to a limited sensory disturbance resulting in the afferent defects so characteristic of this disorder. Some disorders, especially motor neurone disease, are striking by the occurrence of widespread muscular wasting, but relative preservation of the striated sphincter musculature of the pelvic floor. This is accompanied by sparing of the motor neurones in the Onuf nuclei in the anterior horns of the S2-4 segments of the spinal cord that innervate these sphincter muscles (Mannen et al, 1982). Constipation A definition of constipation must include delay in colonic emptying as well as problems in evacuating a full rectum (namely, straining). The definition supplied by Drossman et al (1982) appears to meet these criteria; a patient is defined as constipated if he or she strains at stool for more than 25% of defaecating time or, alternatively, passes two or fewer stools per week. The implication from the above definition is that this disorder is the consequence of pelvic floor dysfunction or of delay in transit of faecal matter through the colon. Much interest has been focused recently on the former, following the description of a clearly defined group of patients whose constipation appeared to be exemplified by a failure to expel previously inserted balloons from the rectum (Barnes and Lennard Jones, 1985; Read et al, 1986), such balloons having been readily expelled in a control population. Evidence in favour of pelvic floor dysfunction was further provided by radiological studies in which a balloon filled with 100 ml of barium was used to outline the impression made by the puborectalis muscle, so enabling

DISORDERS

OF DEFAECATION

211

measurement of the anorectal angle to be made. The angle was noted to be constant during a straining effort in patients with constipation, implying that the puborectalis had displayed inappropriate or ‘paradoxical’ contraction instead of relaxing, thus allowing an increased angle as seen in the normal population (Preston et al, 1984a). Paradoxical contraction of the pelvic floor may be associated with pelvic outlet obstruction and constipation, but this electrophysiological finding per se does not seem to be specific for this disease (Jones et al, 1987b); the phenomenon may be observed in control subjects and in patients with perineal pain and solitary rectal ulcer syndrome. Further evidence which suggests that pelvic floor dysfunction is not the principal factor in constipation is suggested by the failure of surgical division of the puborectalis muscle to improve these patients (Barnes et al, 1985). Some authorities believe that overactivity of the internal anal sphincter may be a factor in the causation of constipation and have claimed good results from sphincterotomy or myotomy (Duhamel, 1969; Yoshioka anmd Keighly, 1987). High resting anal pressures have been recorded in patients with anal fissure (Hancock, 1977) and in patients with haemorrhoids (Hancock and Smith, 1975). Although internal anal sphincter dysfunction may play a role in these anal disorders there is no evidence that constipation is causally related. The evidence that colonic dysfunction leading to a reduction in the vis a rergo is the fundamental factor in many patients with constipation is impressive. Lennard-Jones and his coworkers (Hinton et al, 1969) showed that in patients with constipation given radio-opaque markers 80% of the markers had not been voided within 10 days whereas normally this number should be voided within 4 days. Although no specific motor abnormality has been demonstrated in these patients, in some cases the functional abnormality is associated with an especially long colon or even with megacolon. It is important to identify these patients since they may benefit from colectomy and ileorectal anastomosis (Preston et al, 1984b). Other factors related to constipation are outlined in Table 4. Colonic motility is generally enhanced by food, particularly by fats, whereas inhibition may be seen as a late response to lipids or to amino acids (Holdstock et al, 1970). Colonic motor function may also be impaired by damage to the extrinsic innervation (e.g. diabetes mellitus) or to the intrinsic innervation (e.g. Hirschsprung’s disease). Damage to the myenteric plexus may rarely be associated with laxative abuse but is most commonly seen worldwide as the sequel to infection with T. cruzii. Constipation, denervation and faecal incontinence

A study conducted in 24 women with chronic constipation revealed evidence of denervation in the puborectalis and external anal sphincter muscles (Snooks et al, 1985). It seems likely that nerve damage occurs secondarily in response to repeated straining, particularly if there is abnormal perineal descent (see below). The latter abnormality was demonstrated in 20 of the 24 patients studied and in all of these there was evidence of neuronal damage. Continence is maintained presumably because, the stool is usually solid and hard, and despite damage to the pelvic floor innervation, the puborectalis or

212

D.

Table

4. Causes

No structural abnormality Diet Pregnancy Ageing Slow transit Related to irritable bowel

Z. LUBOWSKI

ET AL

of constipation.

syndrome

Stroctoral disease of anus, rectum or colon Anal pain or anal stenosis Colonic stricture Aganglionosis Hirschsprung’s disease Chagas’ disease East-African megacolon Pseudo-obstruction Idiopathic megarectum + / - megacolon Extracolonic abnormality Endocrine and metabolic Hypothyroidism Hypercalcaemia Porphyria Neurological Damage to sacral outflow or spinal cord Central nervous disorders Pain on straining, e.g. sciatic root compression Systemic sclerosis and other connective tissue disorders Psychological Depression Anorexia nervosa Drug side-effects After

Lennard-Jones,

1985.

external anal sphincter muscles are functioning adequately. In addition, incontinence is unlikely to develop in those constipated patients who display paradoxical puborectalis contraction. Prolapse and perineal descent

Evidence of denervation can be detected in the puborectalis and external anal sphincter muscles of patients with complete rectal prolapse (Neil1 et al, 1981), or in some patients with partial prolapse, associated with abnormal descent of the pelvic floor (Henry et al, 1982). Constipation and repeated straining are characteristic features in both diseases, the nerve damage probably a consequence of a stretch injury to the nerves supplying the pelvic floor caused by abnormal perineal descent (an abnormality also found in patients with rectal prolapse). Defaecation difficulties may be aggravated in the descending perineum syndrome because prolapse of the anterior rectal wall mucosa

DISORDERS

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OF DEFAECATION

occurs and this can lead to secondary obstruction to the passage of the faecal bolus. Mucosa prolapsed into the anal canal may lie in contact with sensory receptors at the dentate line and give rise to the mistaken impression of faecal matter in the anal canal, so causing the patient to make futile attempts to defaecate. Investigation of disorders of abnormal defaecation

Tests of motor function are usually unhelpful in most cases of constipation, with the exception of ‘shape’ studies (Hinton et al, 1969). The absence of normal rectal ganglia in Hirschsprung’s disease leads to failure of the locally-mediated reflex which induces internal anal sphincter relaxation in response to rectal distension (Callaghan and Nixon, 1964). This is therefore a quick and relatively non-invasive technique enabling this disease to be excluded in a patient (including an infant) with constipation. Falsepositive results can be excluded in patients with megarectum if sufficient air is introduced into the rectal balloon to cause rectal distension; this may require up to 400 ml. More recently, Womack et al (1985) have described a dynamic study of pelvic floor function applied to a group of 16 patients with constipation. The technique involves radiological visualization of the rectum during voiding with synchronous computer-linked intrarectal pressures and integrated sphincter EMG superimposed onto the video record. The technique has the advantage of showing the events which attend defaecation as a dynamic system rather than as a static event. METHODS

OF ANORECTAL

PHYSIOLOGY

The methods we use at St Mark’s Hospital for the investigation of pelvic floor disorders have been described in detail elsewhere (Snooks et al, 1984a; 1984b; Snooks et al, 1985; Henry et al, 1985). They are important since they are quantitative, reproducible and directly relevant to the causative underlying disorders. Transcutaneous spinal stimulation

Direct electrical stimulation of the cauda equina is achieved using a modification (Snooks et al, 1985) of the technique devised by Merton and colleagues (1982). The patient is placed in the left lateral position and a separate ground electrode is connected from the right upper thigh to the preamplifier of the EMG apparatus. A single impulse of 500 to 1500 V, of 0.5 ms duration, and decaying with a time constant of 50 ps, is delivered through two saline-soaked pad electrodes with the cathode applied to the skin at the level of the spine of the first lumbar vertebra. The anode is directed cranially. An initial 200 V stimulus is applied and increased in 200 V increments until the amplitude and latency of the evoked muscle response in the external anal

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D. Z. LUBOWSKI ET AL

I

,2ms,

.Figure 2. Transcutaneous spinal stimulation showing evoked responses in the external anal sphincter after stimulation at the Ll and L4 vertebral levels.

sphincter or puborectalis muscles does not change with further stimulus increments, thus indicating that the stimulus is supramaximal. Application of the same stimulus to the spine at the level of the fourth lumbar vertebral spine enables a latency between the Ll and L4 levels to be measured, thus allowing calculation of conduction time in the motor roots of the cauda equina (Snooks et al, 1985) (Figure 2). External anal sphincter response The response in the external anal sphincter muscle is recorded with an anal plug surface electrode containing two parallel steel wires which are lubricated with electrode jelly, placed in the anal canal and connected to ground. The onset of the stimulus triggers the oscilloscope of the EMG apparatus. The latency of the responses following five consecutive supramaximal stimuli delivered at 1 second intervals is measured from the onset of the stimulus to the onset of the response on the paper print-out. Using the same technique of transcutaneous spinal stimulation, the latency of the response to the puborectalis muscle is measured. The compound muscle action potential evoked in the puborectalis muscle is recorded using a rubber finger stall with two circular steel surface electrode-plates, placed 1 cm apart, positioned at its tip (Kiff and Swash, 1984b; Snooks et al, 1985). The finger

DISORDERS

215

OF DEFAECATION

t

.---,

,-

1

I

2ms Figure

3. Pudendal

nerve

stimulation

with

evoked

response

in the external

anal sphincter.

bearing this device is inserted into the rectum so that the recording surfaces are in contact with the puborectalis muscle bar, i.e. the recording surfaces face posteriorly. The contraction response of the puborectalis muscle, which can be palpated with the finger, is displayed on the EMG apparatus and the latency measured in the same way as that for the external anal sphincter.

Urethral striated sphincter response The response of this muscle to the same spinal stimulus is recorded using an intraurethral surface electrode (DANTEC 21Lll) mounted on a Foley catheter.

Pudendal and perineal nerve terminal motor latencies These methods were developed from the technique of electroejaculation described by Brindley (1981) for use in men with impotence due to paraplegia. These methods have been described in detail (Kiff and Swash, 1984a; Henry et al, 1985). The pudendal nerve can be stimulated near the ischial spine through the wall of the rectum using a pair of electrodes mounted on the tip of a rubber finger stall similar to that used for clinical examination of the rectum. Two steel surface electrodes mounted at the base of the finger stall, 3.5 cm from the cathodal stimulating electrode, are used to record the response in the external anal sphincter muscle (Figure 3). The latter can be felt by the examiner and the tip of the finger stall moved slightly in the rectum to achieve the best response. Square wave stimuli of 0.1 ms duration and up to 50 V are given at 1 second intervals. The same stimulus can be used to record the compound muscle action potential evoked in the periurethral striated sphincter muscle, using the catheter-mounted electrode described above. Latencies to supramaximal responses are measured on paper print-outs of these responses (Snooks and Swash, 1984a) and, since the apparatus is standardized, a set of normal values for the pudendal (PNTML) and perineal (PerNTML) nerve terminal motor

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latencies has been obtained (Kiff and Swash, 1984a; 1984b; Snooks et al, 1984a; Snooks and Swash, 1984a). These electrophysiological studies have allowed separate evaluation of the anal and urinary sphincter musculature and their innervation. During transrectal stimulation of the pudendal nerve to measure the pudendal nerve terminal motor latency (PNTML) in control subjects no contraction of the puborectalis is felt by the examiner’s finger. This suggests that the puborectalis muscle is not activated by electrical stimulation of the pudendal nerves at the level of the ischial spines. The latencies of the compound muscle action responses in the external anal sphincter and periurethral striated sphincter muscles, which are both innervated by the pudendal nerves, differ by 0.5 f 0.2 ms, a difference consistent with the additional length of the perineal branch of the pudendal nerve innervating the latter muscle (approximately 2.5 cm at a nerve conduction velocity of 50 m/s). Spinal stimulation at the level of the Ll vertebral spine produces recordable muscle action potentials in the puborectalis, external anal sphincter and urethral striated sphincter muscles. The difference in latency between the compound muscle action potential evoked in the external anal sphincter and in the urethral striated sphincter muscles after spinal stimulation at Ll is 0.6kO.2 ms. The compound muscle action potential recorded in the puborectalis muscle after this stimulus is evoked 0.7 + 0.4 ms earlier than that in the external anal sphincter muscle, suggesting that the innervation of the puborectalis from the point of stimulation at Ll is about 3.5 cm shorter than that to the external anal sphincter (assuming a conduction velocity of 50 m/s). Electromyography

(EMG)

EMG depends upon the recording of electrical activity generated in muscle fibres. The external anal sphincter and pelvic floor muscles are unique striated muscles in having continuous activity at rest, even during sleep (Floyd and Walls, 1953). This activity is derived from activity in the Onuf nucleus. EMG activity may therefore be recorded at rest or during voluntary contraction of these muscles. The motor unit The term ‘motor unit’ refers to the anterior horn cell, its axon and axonal branches, and the motor end plates and muscle fibres innervated by this cell. The number of muscle fibres in the motor unit varies between different muscles and, in the external anal sphincter numbers around 20-30. Concentric needle EMG The concentric needle electrode consists of a steel wire 0.1 mm in diameter contained within a thin pointed cannula resembling a hypodermic needle. The recording is made from the oval tip of the electrode at the cannula tip and the reference electrode is the haft of the cannula. Since the uptake area of the electrode is relatively small, it can be stated with confidence that any electrical

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Rest

Squeeze

Figure 4. Concentric puborectalis muscle voluntary contraction,

0.5sec 1

I

Strain

needle EMG; 100 msjcm. The two upper traces show activity in the at rest. The lower trace (left) shows the increase in EMG activity during and (right) the reduced activity during simulated defaecation straining.

activity recorded is derived from the muscle into which the needle electrode has been inserted. With a slow sweep of the oscilloscope trace (100 ms/division) and freerunning visualization of the trace, the compound muscle action potentials representing discharging motor units may be recorded to show the muscle activity at rest and during voluntary contraction (Figure 4). This technique is useful in mapping the external anal sphincter when a sphincter defect is present in order to determine the position of the muscle ends prior to sphincter repair. Individual motor unit potentials may be assessed, not during free-running visualization of the trace, but with a trigger-delay line, and using a rapid oscilloscope sweep (2 ms/division). The trigger-delay line allows the isolation of individual potentials by triggering the trace at a preset amplitude level and displaying the potential after a short delay so that the earliest parts of the triggered potential are seen. Filter settings of 20 Hz for the high pass and 5 kHz for the low pass filter are used. With denervation and reinnervation of a muscle there is an increase in the proportion of polyphasic motor unit potentials which are of abnormally long duration (Stalberg and Thiele, 1975; Swash and Schwartz, 1981). This technique has been applied to the external anal sphincter and puborectalis muscles (Bartolo et al, 1983a; 1983b) and to the urethral striated sphincter (Fowler and Kirby, 1986). Increasing the level of the high pass filter through 500 Hz or 1000 Hz results in sharpening of the action potential, but in loss of low frequency components of these action potentials. However, changing the filter characteristics in this manner allows the recognition of the contribution of individual muscle fibre action potentials in complex motor unit action potentials of increased duration. This process is better investigated using the technique of single fibre EMG. Single fibre EMG The single fibre needle electrode consists of a central wire which opens on the shaft of the needle electrode in a small leading-off surface of 25 pm diameter.

218 (a) : i

(b)

D. Z. LUBOWSKI

:

: :

: :f

Single

i;

Single

fi

bre

1;;:;

ET AL

j’

Fi bre

Figure 5. Single fibre EMG in the external anal sphincter. (a) Normal subject. Traces from two different motor units showing monophasic and biphasic action potentials; (b) Incontinent subject. Traces from two different motor units. The top polyphasic action potential contains six components.

The radius uptake of the electrode is 270 pm’. An oscilloscope sweep of 2 ms/ division and a trigger-delay line are used with low pass filter cut-off of 500 Hz and high pass 2 kHz. Using this technique the activity of individual muscle fibres is recorded (Figure 5). The technique is particularly useful as it lends itself to quantification by calculating fibre density. This provides an accurate assessment of the degree of reinnervation in the external anal sphincter or puborectalis muscles. The fibre density consists of the mean number of phases of single muscle fibre action potentials recorded within the uptake area of the single fibre electrode in 20 different positions within the muscle (Stalberg and Thiele, 1975). This usually requires between two and four skin insertions of the

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electrode, with small adjustments of the position of the electrode during the process of recording. In normal subjects the fibre density in most muscles is less than 1.6 (Stalberg and Trontelj, 1979) although after the age of 60 years the value increases slightly. In the external anal sphincter muscle, the normal fibre density is 1.5 + 0.16 (Neil1 and Swash, 1980). By convention, in limb muscles, components used for triggering must be greater than 150 PV in amplitude but, because of the smaller size of the muscle fibres in the pelvic sphincter muscles, potentials of greater than 100 PV are accepted. During the process of reinnervation and fibre-type grouping, with increasing compaction of the muscle fibres within individual motor units, the fibre density will increase because there are more fibres within the uptake area of the electrode innervated by an individual axon or its branches. Measurement of the fibre density is thus a useful parameter for assessing reinnervation. It is important to stress that all potentials in which a component is greater than 100 PV must be included in the calculation of the mean derived from the 20 recordings. Thus, single recordings must all be included. It is tempting during the recording to discard single recordings in favour of the more visually exciting multiple-phase action potentials and so to obtain a falsely high value for the fibre density. It is our practice to record all the action potentials recorded on the paper print-out of the EMG machine and to calculate the fibre density from 20 sequential action potentials. This method enables the fibre density to be checked by several observers from the paper print-outs. Acknowledgements We would like to thank the grant-giving agencies who have supported our work the last 10 years and, especially, the Research Fellows who have so enthusiastically loped our ideas on pelvic floor function.

during deve-

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Walls