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Pelvic and pudendal nerve injury can occur during extirpative visceral surgery such as radical hysterectomy.1 2 Many of these patients develop severe chronic pelvic pain and bladder symptoms, and are often referred to neurologists with suspicion of lumbosacral plexus lesions or disc disease. There are few or no signs on examination, and patients are often considered to be “hysterical”, despite having severe symptoms. Here, we describe two patients in whom severe pelvic pain and bladder dysfunction developed after hysterectomy, and who demonstrated detrusor and rectal hyperreflexia with cocontractions, features usually associated with lesions of the CNS. Whereas spinal cord sensitisation is well recognised after somatic nerve injury, our studies provide the first clear evidence for its development after visceral nerve injury in humans, and a method for its detection using ambulatory urorectodynamics.
Patient 1, a 42 year old woman, was diagnosed as having carcinoma of the cervix 5 years previously and underwent Wertheim's hysterectomy, followed by chemotherapy and pelvic irradiation. She developed severe persistent vaginal pain and hypersensitivity, which prevented her from having sexual intercourse, and subsequently bladder dysfunction, which required intermittent selfcatheterisation. She received several analgesic drugs without benefit. Neurological and pelvic examination and spinal imaging, were normal. An ambulatory urorectodynamics study (after prior written informed consent) showed vesical instability associated with unstable urethral function; simultaneous abnormal rectal contractions and an associated fall in anal pressure were also recorded (figure). A repeat ambulatory study confirmed these findings, which showed clear temporal correlation with her symptoms.
Patient 2, a 69 year old woman, had had vaginal hysterectomy for prolapse with bladder repair 23 years previously. She developed severe persistent pelvic pain, exacerbated during micturition. She reported that her vagina and rectum felt continuously stretched, “as if sitting on a baby's head”, and found it difficult to sit without discomfort. She developed progressive urinary and rectal urgency. Neurological examination and anal tone were normal. Vaginal examination showed exquisite tenderness on the left. Nerve conduction study showed prolonged pudendal nerve latency (left 2.7 ms, right 2.4 ms; normal range 2.0 ± 0.2 ms).
Magnetic resonance imaging of the spine and pelvis were normal, as was flexible cystoscopy. An ambulatory urorectodynamic study (after prior written informed consent) showed urethral instability, unstable vesical contractions with simultaneous abnormal rectal contractions, and falls in anal pressure.
These patients had severe symptoms but no clinical signs, and abnormalities were detected only after pudendal nerve conduction and urorectodynamic studies, which disclosed visceral hyperreflexia in both cases. Patient 1 probably had injury to the pelvic nerves, which is well recognised after extensive hysterectomy.1 Patient 2 had pudendal nerve damage, supported by the nerve conduction study. Our patients did not have neurological signs suggestive of CNS lesions, but demonstrated features usually associated with such lesions, namely detrusor and rectal hyperreflexia. Visceral hyperreflexia can occur after spinal cord lesions and in the absence of obvious neurogenic lesions but its occurrence after peripheral nerve damage is not well recognised.3 4
The likely explanation for visceral hyperreflexia in our patients is increased barrage originating from injured sensory nerves, leading to spinal cord sensitisation; this mechanism is well established after somatic peripheral nerve injury, but rarely considered after pelvic surgery.5 Persistent visceral noxious input to the spinal cord could lead to reflex activation of the intermediolateral cell column,6 the increased output of which may in turn increase bladder and rectal contractions. Other relevant evidence of spinal cord disinhibition in our patients is the loss of the normal inhibition of urinary bladder contraction induced by rectal and vaginal stimulation7 and the development of bladder and rectum cocontractions, which have not been reported previously.
Our cases show how pelvic surgery could be complicated by persistent neuropathic pain and bladder and bowel hypersensitivity, and further studies of spinal cord excitability are needed to clarify underlying mechanisms. Early recognition and initiation of analgesic treatment for neuropathic pain isessential to prevent the condition becoming intractable.
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