Reply to the letter-to-the-editor: “Prevalence of pelvic floor dysfunction in patients with interstitial cystitis"
We appreciate the thoughtful comments regarding our paper on pelvic floor dysfunction in patients with interstitial cystitis (IC). We agree that many etiologies may be involved in the pain associated with IC and the bladder may be an “innocent bystander” in a more diffuse process. Many patients with IC suffer from other co-morbidities such as fibromyalgia, chronic fatigue syndrome, vulvodynia, and irritable bowel syndrome.1 It is doubtful that pudendal neuropathy alone would account for all of these co-morbidities. Certainly, diffuse hypersensitivity or nerve upregulation may be a central cause of pain and other co-morbidities associated with IC/painful bladder syndrome.
It is our experience that the “taut muscle bands” palpated on exam and trigger points that reproduce the patient's pain are not normal variants. These abnormal areas will often resolve and pain will improve using myofascial release, biofeedback, relaxation techniques, neuromodulation, and so forth. Nerves innervate all muscles and the pudendal nerve may be involved in a component of this syndrome in select patients. We feel that surgical decompression surgery remains controversial and level I evidence is lacking in the literature. However, we have found that pudendal nerve modulation has been effective in our IC population2 and perhaps should be considered prior to more invasive surgical approaches.
The fact we are having this dialogue regarding interstitial cystitis is exciting. Perhaps we will finally move beyond the bladder and improve the evaluation and management of patients suffering from chronic pelvic pain syndrome.