Neurologic Evaluation of the Pelvic Floor

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Virgilio Salanga

Several elegant methods of neurophysiologic assessment of the anal and urethral sphincters exist. Their purpose is to help localize the site of neurologic pathology leading to the disturbance of bowel and bladder continence and evacuation. Although the clinical neurologic examination may sufficiently determine if the lesion involves the muscle or the nerve control to the muscle, a quantitative assessment of the disturbance by neurophysiologic means is often needed for clinical monitoring and treatment planning.

Available neurophysiologic techniques include elec-tromyography of the periurethral and anal sphincter muscles, perineal and pudendal motor conduction studies, sacral reflexes recording, somatosensory evoked response study from the pelvic floor to the cerebral sensory cortex, and transcutaneous spinal cord and cerebral motor cortex stimulation to record an evoked pelvic floor muscle response (Table 3-6.1).

The sacral reflex arc consists of an afferent limb originating in the bladder and urethra along visceral autonomic afferents to the T10-L2 spinal cord, and an efferent limb originating in the S2-S3-S4 ventral nerve roots to the pudendal nerve and its terminal branch, perineal nerve. In response to stimulation of the bladder wall or urethra, pelvic floor muscle contraction occurs. The urethral-anal reflex, bladder-anal reflex, and clitoral-anal reflex are neu-rophysiologically measurable. Abnormalities of the sacral reflexes may be seen in peripheral neuropathy, cauda equina and conus medullaris lesions, pelvic plexus, and pudendal nerve abnormalities.1

Pudendal nerve somatosensory evoked potential recordings provide information on lesions in the spinal cord and brain (central nervous system), but require interpretation in conjunction with pudendal nerve conduction studies.1

Transcutaneous spinal stimulation at two levels of the lumbar spine (L1 and L4) and recording the latencies of the evoked muscle responses from the anal sphincter or pub-orectalis muscle provides information on lesions involving the S2-S3-S4 motor nerve roots, and complements the information derived from pudendal nerve and perineal nerve conduction studies. Transcutaneous cervical spine (spinal cord) and cranial (motor cortex) stimulation and recording motor response from the pelvic floor muscles provide information on upper motor neuron disorders affecting the pelvic floor, when interpreted in conjunction with pudendal nerve or perineal nerve conduction studies.2

In our institution, my colleagues and I have considerable experience in measurement of pudendal nerve terminal motor latencies (PNTML) and external anal sphincter muscle concentric needle electromyography (AEMG), as part of the routine evaluation of bowel evacuatory disorders, especially fecal incontinence. In a 1991 survey of American and British colorectal surgeons, PNTML and AEMG were available only in 15% and 34% of anorectal physiology laboratories, respectively. Neurogenic injury in fecal incontinence was suggested by histometric and single fiber electromyogram (EMG) studies of the anal sphincter. Conditions that promote traction injury to the pudendal nerves (as in childbirth and prolapse) may lead to fecal incontinence. These neurophysiologic techniques provide objective assessment of nerve and/or muscle injury, and allow for optimal treatment approach.3

We perform PNTML studies according to the method described by Kiff and Swash4 using a disposable St. Marks electrode (Dantec, Skovlunde, Denmark) with a Nicolet Viking II (Nicolet, Madison, WI) EMG machine. The St. Marks electrode is mounted onto the gloved index finger of the right hand, which is introduced into the rectum (Figure 3-6.1). The ischial spine and lateral edge of the sacrum are located so that the tip of the finger with the cathode-simulating electrode is in the vicinity of the pudendal nerve. Electrical stimuli are repeatedly delivered as the fingertip is methodically moved until the pudendal nerve is maximally stimulated based on the best amplitude of at least three reproducible and identical compound muscle action potentials recorded from the external anal sphincter muscle. The cathodal stimulating point is at the main trunk of the pudendal nerve; the terminal motor latency represents the conduction time along the inferior

Table 3-6.1. Potential usefulness of electrodiagnostic tests in certain pelvic floor disorders

Pudendal Nerve

Perineal Nerve

Anal Needle

Anal Surface

Sacral Limb

(Motor Latency)

(Motor Latency)

(EMG)

(EMG)

(Reflex)

NCT

SEP

Fecal incontinence

+

-

+

-

-

-

-

Constipation

+

-

+/-

+

-

-

-

Urinary incontinence

+

+

-

-

+

-

-

Pelvic organ prolapse

+

+

+

-

+

-

-

Pelvic trauma

+

+

+

-

+

-

-

Diabetic neuropathy

+

+

+

-

+

+

-

Cauda equine disorder

+

+

+

-

+

+

+

Myelopathy

-

-

-

-

+

-

+

NCT, nerve conduction test; SEP, somatosensory evoked potential.

rectal branch that innervates the external anal sphincter muscle. The other side is similarly done. Patients get a minimum of three recordings on each side to ensure consistency and accuracy in measurements. Based on previously published normative data, we consider PNTML of less than 2.3 ms as normal5 (Figures 3-6.2 and 3-6.3).

Electromyography of the external anal sphincter is performed with a bipolar concentric needle electrode, 23-gauge, 25 to 75 mm long. The right and left halves or four quadrants (left,right, anterior, and posterior sectors) of the external anal sphincter muscle are routinely evaluated. Observations are made of muscle electrical activity at rest, during voluntary (squeeze) and reflexive (with a cough) contraction, and simulated defecation. Spontaneous potentials including positive sharp waves, fibrillations, fascicula-

tions, and complex repetitive discharges are looked for (Figure 3-6.4). Alterations in motor unit potential (MUP) amplitude, duration, and polyphasia are observed (Figure 3-6.5). Reduction in MUP recruitment is noted and graded as minimal, moderate, severe, or complete absence of vol-

200 uv

31V 200 uV

200 uV

73 0 UV 200 uV

200 uV

79C iav

200 UV

200 uV

82C uV Left FudendaL Nerve

Figure 3-6.2. External anal sphincter compound muscle action potentials, left pudendal nerve stimulation.

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Figure 3-6.1. St. Mark's electrode.

200 uV

73 0 UV 200 uV

Pudendal Electromyography
Figure 3-6.3. External anal sphincter compound muscle action potentials,right pudendal nerve stimulation.

untarily or reflexively activated MUPs (Figure 3-6.5). Sustained MUP recruitment during simulated defecation, which may indicate paradoxical pelvic floor muscle contraction, is noted.5

In patients with constipation, we use an intra-anal sponge electrode (Dantec) for surface EMG recording of the external anal sphincter muscle, instead of the concentric needle electrode. By avoiding needle-related discomfort, the kinetic activity of the anal sphincter during voluntary and reflexive contraction (squeeze and cough), and during simulated defecation is more accurately assessed, eliminating pain-induced contraction that may mimic paradoxical anal muscle contraction.6

In a prospective study of 225 consecutive patients with fecal incontinence (idiopathic 72, obstetric 45, prolapse 43, trauma 42, neurologic 23), PNTML and AEMG studies showed neurophysiologic evidence of neuromuscular abnormalities in 76% of patients: Reduced MUP recruitment during voluntary contraction (60%), prolonged PNTML (36%), paradoxical anal sphincter contraction during simulated defecation (19%), and assorted abnormalities of MUP morphology, fibrillations/positive waves, and complex repetitive discharges (46%). There was strong correlation between reduced voluntary MUP recruitment and decreased anal manometric pressures. Four-quadrant AEMG"mapping"showed good concordance with endoanal sonography in 35 of41 patients (86%) tested with both techniques. Three patients were found with muscle defects by AEMG that were missed by sonography, and vice versa in another three patients. The two tests are complementary and not redundant. Our data in this group of patients did not clarify the exact role of pudendal neuropathy in the pathogenesis of fecal incontinence, because this was not present in 64%. Nonetheless, the identification of pudendal neuropathy is considered predictive of poor outcome of sphincter surgical repair. These neurophysiologic techniques assisted our colorectal surgeons in assigning the most appropriate therapy based on expected outcome.5

In urinary voiding abnormalities, the integrity of the perineal nerves is assessed by stimulation of the pudendal nerves through the vagina, using the St. Marks electrode, and recording the compound muscle action potential from the periurethral muscle with recording electrodes mounted on a Foley catheter. Simultaneous recording of the compound muscle action potentials from the left and right external anal muscle sphincter muscle is done with a pair of para-anal surface disc electrodes. The pudendal-perineal nerve terminal motor latencies are generally 0.2 to 0.5 msec longer than the pudendal-inferior rectal nerve terminal motor latencies.

Figure 3-6.4. Needle EMG of external anal sphincter: polyphasic MUPs (arrows), positive waves (pw),fibrillations (f), high frequency repetitive discharges (bottom).
Urinary Frequency
Figure 3-6.5. Motor unit potential recruitment, needle EMG of external anal sphincter muscle.

Pelvic organ prolapse potentially leads to traction injury to the pudendal nerves and branches, and to the other pelvic nerves supplying the puborectalis and pubococ-cygeus muscles, and denervation of these pelvic floor muscles and the periurethral and anal sphincter muscles. Pudendal nerve terminal motor latency measurements and needle EMG of these muscles may provide potentially useful information influencing surgical reparative procedures. Severely denervated parts of weakened pelvic floor muscles may not be optimal for pelvic floor repair. Neurologic disorders frequently cause bladder and/or bowel evacuatory dysfunction. Systemic neuropathies, such as diabetic neuropathy, and regional lumbar and sacral radiculopathies, such as in lumbar spine disorders, may involve the somatic and visceral (autonomic) nerve supply to the bladder detrusor muscle, rectal peristaltic muscles, and periurethral and anal sphincter muscles. Nerve conduction tests and EMG in the limbs, and autonomic studies (sympathetic skin response recording, heart rate variability during deep breathing and Valsalva maneuver) may clarify the cause of the neurogenic bladder and/or bowel syndrome in these diseases. Spinal cord disease (myelopa-thy), such as in multiple sclerosis, cervical or thoracic spondylosis, etc., will often cause small-capacity hyper-

reflexic bladder, manifesting as an overactive bladder with frequency and urgency incontinence. Pudendal nerve latencies will be normal in this setting, but lower limb somatosensory evoked potential recording may show delayed conduction along the central somatosensory afferent pathways.

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