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CASE REPORT |
From the Departments of Urology (B.v.H., L.H.), Psychotherapy (R.S.), and Neurosurgery (H.W.B.), Westfälische Wilhelms-Universität, Münster, Germany.
Address reprint requests to: Burkhard von Heyden, MD, PhD, Department of Urology, Friederikenstift Hannover, Humboldtstrasse 5, 30169 Hannover, Germany. Email: sekretariat.uro{at}friederikenstift.de
ABSTRACT
OBJECTIVE: This case report describes the use of sacral neuromodulation to treat urinary retention after sexual abuse.
METHODS: Sacral neuromodulation was added to therapeutic regimen of a 38-year-old woman in whom chronic, complete urinary retention developed after psychological and sexual abuse during childhood.
RESULTS: The combination of psychotherapy and neuromodulation restored the patient’s ability to void, whereas psychotherapy alone had not.
CONCLUSIONS: Although a multifactorial etiology of retention cannot be ruled out in this patient, neuromodulation might effectively treat urinary retention in cases of a conversion disorder after sexual abuse.
Key Words: neural conduction • urinary retention • sexual abuse • epilepsy.
Sexual and psychological abuse may cause urinary retention (1, 2). Somatic treatment will be difficult as long as the psychological origin is not recognized; likewise, psychotherapy alone may be ineffective. We report the case of a woman with urinary retention as a late result of sexual and psychological abuse in whom an interdisciplinary approach proved successful.
CASE REPORT
In 1993, a 33-year-old nun presented with recurrent urinary tract infections caused by an inability to empty her bladder completely (residual volume, 150–250 ml). The voiding difficulties had begun in 1979 with no apparent cause. In 1989, the patient had been taught at another institution to perform self-catheterization, which she performed three times per day. Also in 1989, fasciculation of the right arm and leg had prompted a neurologic examination. The woman’s reflex status was normal, and no paralysis was seen. Computed tomography and magnetic resonance imaging of the brain ruled out encephalitis disseminata. The electroencephalogram showed no specific focus. Because the results of a spinal fluid puncture 2 years earlier had been normal, this invasive test was not repeated.
At presentation to our institution in 1993, the results of the urologic workup were inconclusive. Urethral calibration and cystoscopic parameters were normal. Radiographic imaging showed no neurogenic bladder deformation or reflux of contrast medium into ureters or kidneys. Bladder position was normal, and no diverticula were seen. The sensation of bladder filling was impaired, with a slight sensation beginning at a bladder volume of 500 ml. Measurement of bladder and urethral pressure during filling and emptying revealed an enlarged, hypotonic bladder with residual volumes of up to 750 ml and increased muscle tone of the urethral sphincter and pelvic floor. The urinary flow was interrupted, requiring abdominal straining, and accompanied by pelvic floor dyssynergia. Attempts to strengthen the bladder with bethanechol (3 x 25 mg) or to relax the pelvic floor with baclofen (3 x 10 mg) and phenoxybenzamine (3 x 5 mg) did not restore micturition. Five years later, in 1998 at age 38, she returned to our institution with a complete inability to void. Her social history, related by her psychotherapist, suggested a psychological cause.
Psychological Background
The patient was one of seven children of a farming family. In early childhood she began experiencing nocturnal epileptic seizures, which she later tried to conceal from her family. Between ages 4 and 6, she was sent to live with her grandmother, where she was treated as a household servant. When she was 11, her 15-year-old brother began to abuse her sexually. She failed elementary school and learned sewing. At 18 years of age, she fell from a tractor and did not regain consciousness for 2 days. The sexual abuse by her older brother continued until she left home at the age of 20 to enter a convent.
As a nun she received her high school diploma and successfully completed training as a tailor and instructor for disabled children; both professions she practiced. Despite these achievements her self-esteem remained low and symptoms of a posttraumatic personality disorder developed. Insomnia with nightmares, chronic nervousness, distrust, feelings of estrangement, emptiness, and paranoia resulted in social retreat. She gained weight, and gradually an inability to empty her bladder completely developed.
At age 32 years she started drinking. Aggravated by her epilepsy, alcohol addiction developed within months. At age 34 an epileptic seizure occurred in public. The frequency of these attacks increased, and her alcohol addiction worsened. Medical treatment for epilepsy failed because she did not take her medication regularly. When she lost her instructor’s position, her convent urged her to seek psychotherapy, for which she was hospitalized from August to November 1997.
In the beginning she was distrustful, almost hostile; only gradually could her trust be gained. Initially she discussed her alcohol abuse and later her epileptic seizures, which her superiors had incorrectly attributed to intoxication. The order had taken her driver’s license and put her under constant surveillance, both inside and outside the convent. She did not contest these restrictions but instead withdrew into the passive role of victim. She mentioned her inability to void only as a mechanical impediment, and when she spoke of her psychological and physical abuse, it was superficially and without emotion.
Antiepileptic drugs were instituted, but with the recurrence of her alcohol addiction, treatment was interrupted for an alcohol withdrawal regimen and was reinstated on an ambulatory basis in May 1998. Contact with the psychotherapist was maintained through regular telephone conversations.
Psychotherapy was aimed at restructuring her depressive self-perception and building her social competence. She learned to reject the role of victim, and she developed self-reliance. She took responsibility within the order and garnered respect. However, her epilepsy, voiding dysfunction, and looming alcohol addiction continued to undermine her position. She suffered from occasional epileptic seizures because she refused to take her medication for fear of addiction, and this refusal was interpreted by her superiors as disobedience. Intermittent self-catheterization (three to four times per day), accompanied by recurrent urinary tract infections, evoked the memory of the chronic sexual abuse of her youth. This was the psychological background when, at the end of 1998, she presented with a complete inability to void and sacral neuromodulation was offered by the urologist.
Sacral Neuromodulation
Sacral neuromodulation has been reported to restore micturition in patients with idiopathic urinary retention (3). Square pulses of 12 Hz are applied to one of the sacral spinal nerves (S3 or S4) on one or both sides, depending on the results of test stimulation. If voiding is restored during this subchronic stimulation period, a permanent stimulator can be implanted. The stimulator is switched off by the patient to initiate voiding and is switched on again thereafter. How permanent stimulation, interrupted only to void, can restore micturition is as yet unknown.
At the time a test of neuromodulation was offered to the patient, her creatinine was normal (0.7 mg/dl). Cystography showed an initial sensation at 500 ml, an urge to void at 650 ml, and a capacity of 700 ml. Coughing did not provoke a bladder contraction, and the bladder configuration was normal. When another urodynamic examination was planned, the patient asked her psychotherapist to urge the urologist not to repeat unnecessary tests that might enhance her memory of the sexual trauma.
With the patient under full anesthesia, a marked contraction of the levator ani muscle at 2 V indicated the integrity of the peripheral nerves at S3 bilaterally (12 Hz, Medtronic test stimulator, Düsseldorf, Germany). As is standard during test stimulation, the wire was not fixed near the sacral nerve but only covered with adhesive pads on the skin. The patient (now weighing 90 kg; her height was 168 cm) had a subcutaneous fat layer of 7 cm, and although care was taken to maintain the wire’s position when she was transferred back into her bed from the operating table, both stimulating wires became dislodged. The procedure was repeated 2 days later. This time the wires were looped in a subcutaneous pocket before exiting. Despite this precaution, complete displacement occurred on the left side. The right wire was partially displaced (12 mm) and evoked a sensation at 10 V in the right gluteus muscle with projections to the perineum and vagina. Every 3 to 4 hours the patient was asked to switch off the stimulator and void. One to two minutes after the cessation of stimulation, the patient was able to empty her bladder partially. Several urinary flow measurements showed a voided volume ranging from 340 to 485 ml with residual volumes between 200 and 500 ml. Despite a residual of 50%, which would necessitate self-catheterization, the patient requested a third test stimulation. The partially displaced right wire was removed, and complete inability to void recurred.
In March 1999 the third test stimulation was done. This time the wire was fixed at the fascial layer with absorbable 3-0 suture and did not dislodge. When the stimulation was switched off, voiding began without delay. Initial voiding volumes ranged from 400 to 800 ml with residuals of 90 to 250 ml. The patient was asked to void more often to keep the voiding volume below 500 ml, and the residuals remained below 100 ml. The flow characteristics reflected an intact bladder muscle.
At the end of March 1999 a permanent stimulator was implanted at S3 on the right side (Medtronic IPG stimulator model 3023) (Figure 1). The radio transmitter enabled the patient to turn the stimulator on and off and to change the amplitude within a programmed range. The stimulation parameters were 0.5 to 1.7 V amplitude, 13 Hz frequency, and monopolar stimulation with the stimulator positive and the electrode position No. 1 negative. Six days after implantation the voided volume ranged from 320 to 730 ml, with residual volumes at or below 30%. Wound healing occurred uneventfully.
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Bladder neuromodulation boosted the patient’s progress in psychotherapy. This experience demonstrated to her for the first time that an "organic" impairment could be "healed," and this encouraged her to comply with her prescribed antiepileptic drug regimen. The workup of her past sexual trauma could finally be integrated because the need to catheterize (which had revived the trauma) was abolished. Her relationships with members of her family and her order changed owing to her growing self-confidence, and she began to dress with greater care as her attitude toward her body improved as well. She is now contemplating a college education.
DISCUSSION
In children the "lazy bladder syndrome" is well known. Excessive toilet training or fear of strange bathrooms (4) may cause infrequent voiding, resulting in gradual overdistension of the bladder with loss of the filling sensation (5). Residual urine with recurrent urinary tract infections may ensue. A similar mechanism may be postulated in our patient, in whom sexual abuse was followed initially by an inability to relax the pelvic floor properly during voiding and later by a complete inability to void. In a previous report by Kroll et al. (1), a 14-year-old girl from a pathologic family setting presented in urinary retention with a bladder capacity of 1300 ml. Medication could not restore micturition, but after 10 days’ rest in a sanatorium, spontaneous voiding resumed. It is interesting to note that in our patient, when the ability to void was partially restored during test stimulation, the residual volume correlated with the malposition of the stimulating electrode. This finding indicates the unlikeliness of a placebo effect. Thus, the indications for neuromodulation can be broadened to include not only idiopathic (3) or iatrogenic (6) urinary retention but also that after sexual or psychological abuse in the absence of permanent physical trauma. Prerequisites for success seem to be the presence of intact nerves running from the pelvic plexus to the bladder and pelvic floor and a viable bladder muscle that has not been overdistended. However, it cannot be ruled out that the epilepsy, the history of unconsciousness, and the history of alcohol dependence also play a role in the etiology of this patient’s retention. Therefore, we can only say that the probable psychophysiological contribution of the sexual abuse to urinary retention was overcome by neuromodulation.
From a psychotherapeutic point of view, the urinary retention in this case seems to be a psychophysiological dysfunction comparable to posttraumatic vaginismus. Although both the urologist and patient were initially skeptical of neuromodulation, seeing it as a mechanistic approach to a psychological problem, the outcome proved that it was worth a try, especially because each self-catheterization exacerbated the patient’s memory of her sexual abuse. Although it cannot be predicted whether further progress in psychotherapy will make neuromodulation unnecessary, as it is now the patient’s quality of life has significantly improved since the introduction of sacral neuromodulation in an interdisciplinary approach.
Received for publication June 28, 2000.
REFERENCES
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