Dr Marinkovic and his colleagues carried out an extensive review on the management of interstitial cystitis (IC) stressing that although original descriptions of IC date back to the nineteenth century for the past several decades, IC has been thought of as an uncommon disease in women. More recent studies, however, have shown that this disease complex is much more prevalent than initially reported. The prevalence of IC is much higher in women than men. Patients with IC have suprapubic pain or discomfort, accompanied by urinary symptoms including urgency, frequency, and dysuria. Diagnosis of IC requires exclusion of other urologic or gynecologic disease processes. It is very interesting the hypothesis from RM Maskell that emerging pathogenicity of commensal organisms in patients who have been treated with broad- spectrum antibiotics, might have a role in the pathogenesis of IC. The response by Richard G Fiddian-Green led us to some further comments on this interesting topic. Hypertonic pelvic floor dysfunction and myofascial pain syndrome is present in as many as 85% of patients with IC and/or chronic pelvic pain syndromes (1). The matter is: which came first: the bladder organic lesions or the pelvic floor hyperactivity ? Trying to answer this question we may start from the IC definition. According to the last ICS standardization of terminology, IC is a clinical diagnosis primarily based on symptoms of urgency/frequency and pain in the bladder and or pelvis (2). ICS prefers the term “Painful Bladder Syndrome (PBS) reserving the diagnosis of IC to patients with typical cystoscopic and histological features. These syndromes are functional abnormalities for which a precise cause has not been defined. It is presumed that routine assessment (history taking, physical examination, and other appropriate investigations) has excluded obvious local pathologies such as those that are infective, neoplastic, metabolic or hormomal in nature (2). As stressed by Marinkovic, in the clinical setting of early IC, bladder forceps biopsy pathology may be normal and is not therefore useful as a confirmatory test; moreover, despite extensive scientific effort, the precise etiology of PBS/IC is still an enigma. In order to find a suitable reading key to better know the wide spectrum of PBS/IC with its gynecologic, urologic and colon-proctologic presentations, it is important to understand the neuropathology due to any prolonged inflammatory or noxious stimuli and the self-perpetuating aspects of these visceral pain syndromes (1). Changes in urothelial permeability, increased mast cell activity, neuro-immune abnormalities, neuroplasticity of the nervous system and infectious etiologies are all purposed pathogenetic causes of PBS/IC. Any one may in fact be the trigger for an individual patient (3). Tissue injury due to any of the above mentioned etiologies triggers the release of chemicals giving rise to an inflammatory reaction which in turn results in pain signals that travel from the periphery to the dorsal horn of the spinal cord and then upwards into the cortex of the brain. A special group of C fibers (“silent afferents”) have the potential to transmit pain, but do not unless they are activated by a prolonged or particularly noxious insult; 30-80% of all afferent nerves traveling from the viscera are of this silent type and the bladder is particularly rich in them being the most neurally dense organ in the pelvis (3). As already stated by Markenson (4), these neuropathic changes lead to an up-regulation of the dorsal horn. This dorsal horn barrage of noxious stimuli results in metabolic, biochemical and electrophysiological changes resulting first in an acute pain and then in a chronic visceral pain syndrome. NMDA receptor activation, loss of dorsal horn neurons inhibition and decrease in the threshold of these nocioreceptive nerves result in a reduction of the amount of stimuli necessary to be perceived as a painful stimulus clinically causing the so called allodynia. This dysregulation of normal processing of sensory information together with the neuropathic up-regulation are responsible for a neurogenic inflammation, hyperalgesia and dysreflexia, causing a self-perpetuating state leading to the chronic visceral pain syndrome (5). The dorsal root reflex induces the afferent nerves to fire backward down the sensory nerves, releasing NGF and substance P in the periphery. This centrally mediated neurogenic inflammation may result in cystitis, vaginal pain, vulvar hyperalgesia leading to viscero-visceral hyperalgesia and than chronic pelvic pain syndrome. This neuropathic output state resulting from altered “cross-talk” of pelvic viscera with shared nerve supply may easily explains the association of a given chronic pelvic pain syndrome with other hyperalgesic or dysfunctional pelvic viscera (3,6). Moreover, these neuropathogenetic changes elicitate a viscero-muscolar reflex resulting in muscular instability and a hypertonic contracted state within the muscles of the pelvic floor. The consequent decrease in muscle function and development of myofascial trigger points cause myofascial pain and new pain generators (3). Myofascial pelvic pain is due to a hypertonus of the levator any group muscles producing pain poorly localized to the perivaginal and perirectal areas (7). Pain may also be felt in the abdominal lower quadrants, suprapubic areas, coccyx, and posterior thigh. This disorders involve a high resting tone in the muscles and fascia that attach to the bony pelvis (7). Thus IC and visceral pelvic pain syndromes in general may contribute to the pain associated with these conditions. We completely agree with Butrick (3) in stating that the up-regulation of the dorsal horn is the first step in the cascade of events resulting in self-perpetuating, multisite visceral pain syndromes. Thus a functional disorder may cause an organic lesion and vice versa. 1. Weiss JM. Pelvic floor myofascial trigger points: manual therapy for interstitial cystitis and the urgency-frequency syndrome. J Urol 2001, 166: 2226-2231. 2. Abrams P, Cardozo L, Fall M, et al. the Standardisation of terminology in lower urinary tract function: report from the standardisation sub-committee of the International Continence Society. Urology 2003; 61: 37-49. 3. Butrick CW. Interstitial cystitis and chronic pelvic pain: new insights in neuropathology, diagnosis, and treatment. Clin Obstet Gynecol 2003; 46(4):811–823 4. Markenson JA. Mechanisms of Chronic Pain. Am J Med 1996; 101 (suppl 1A): 6S-18S. 5. Melzack R. From the gate to the neuromatrix. Pain Supplement 6 (1999); S121-S126. 6. Pezzone MA, Liang R, Fraser MO. A model of neural cross-talk and irritation in the pelvis: implications for the overlap of chronic pelvic pain disorders. Gastroenterology 2005; 128:1953–1964. 7. Simons DG, Dommerholt J. Myofascial pain sindrome – Trigger points. J Obstet Gynaecol Can 2005; 27(9): 869-887.

Interstitial cystitis - pelvic floor activity and bladder organic lesions: which came first, the chicken or the egg?

CERRUTO, Maria Angela;MANTOVANI, William
2009-01-01

Abstract

Dr Marinkovic and his colleagues carried out an extensive review on the management of interstitial cystitis (IC) stressing that although original descriptions of IC date back to the nineteenth century for the past several decades, IC has been thought of as an uncommon disease in women. More recent studies, however, have shown that this disease complex is much more prevalent than initially reported. The prevalence of IC is much higher in women than men. Patients with IC have suprapubic pain or discomfort, accompanied by urinary symptoms including urgency, frequency, and dysuria. Diagnosis of IC requires exclusion of other urologic or gynecologic disease processes. It is very interesting the hypothesis from RM Maskell that emerging pathogenicity of commensal organisms in patients who have been treated with broad- spectrum antibiotics, might have a role in the pathogenesis of IC. The response by Richard G Fiddian-Green led us to some further comments on this interesting topic. Hypertonic pelvic floor dysfunction and myofascial pain syndrome is present in as many as 85% of patients with IC and/or chronic pelvic pain syndromes (1). The matter is: which came first: the bladder organic lesions or the pelvic floor hyperactivity ? Trying to answer this question we may start from the IC definition. According to the last ICS standardization of terminology, IC is a clinical diagnosis primarily based on symptoms of urgency/frequency and pain in the bladder and or pelvis (2). ICS prefers the term “Painful Bladder Syndrome (PBS) reserving the diagnosis of IC to patients with typical cystoscopic and histological features. These syndromes are functional abnormalities for which a precise cause has not been defined. It is presumed that routine assessment (history taking, physical examination, and other appropriate investigations) has excluded obvious local pathologies such as those that are infective, neoplastic, metabolic or hormomal in nature (2). As stressed by Marinkovic, in the clinical setting of early IC, bladder forceps biopsy pathology may be normal and is not therefore useful as a confirmatory test; moreover, despite extensive scientific effort, the precise etiology of PBS/IC is still an enigma. In order to find a suitable reading key to better know the wide spectrum of PBS/IC with its gynecologic, urologic and colon-proctologic presentations, it is important to understand the neuropathology due to any prolonged inflammatory or noxious stimuli and the self-perpetuating aspects of these visceral pain syndromes (1). Changes in urothelial permeability, increased mast cell activity, neuro-immune abnormalities, neuroplasticity of the nervous system and infectious etiologies are all purposed pathogenetic causes of PBS/IC. Any one may in fact be the trigger for an individual patient (3). Tissue injury due to any of the above mentioned etiologies triggers the release of chemicals giving rise to an inflammatory reaction which in turn results in pain signals that travel from the periphery to the dorsal horn of the spinal cord and then upwards into the cortex of the brain. A special group of C fibers (“silent afferents”) have the potential to transmit pain, but do not unless they are activated by a prolonged or particularly noxious insult; 30-80% of all afferent nerves traveling from the viscera are of this silent type and the bladder is particularly rich in them being the most neurally dense organ in the pelvis (3). As already stated by Markenson (4), these neuropathic changes lead to an up-regulation of the dorsal horn. This dorsal horn barrage of noxious stimuli results in metabolic, biochemical and electrophysiological changes resulting first in an acute pain and then in a chronic visceral pain syndrome. NMDA receptor activation, loss of dorsal horn neurons inhibition and decrease in the threshold of these nocioreceptive nerves result in a reduction of the amount of stimuli necessary to be perceived as a painful stimulus clinically causing the so called allodynia. This dysregulation of normal processing of sensory information together with the neuropathic up-regulation are responsible for a neurogenic inflammation, hyperalgesia and dysreflexia, causing a self-perpetuating state leading to the chronic visceral pain syndrome (5). The dorsal root reflex induces the afferent nerves to fire backward down the sensory nerves, releasing NGF and substance P in the periphery. This centrally mediated neurogenic inflammation may result in cystitis, vaginal pain, vulvar hyperalgesia leading to viscero-visceral hyperalgesia and than chronic pelvic pain syndrome. This neuropathic output state resulting from altered “cross-talk” of pelvic viscera with shared nerve supply may easily explains the association of a given chronic pelvic pain syndrome with other hyperalgesic or dysfunctional pelvic viscera (3,6). Moreover, these neuropathogenetic changes elicitate a viscero-muscolar reflex resulting in muscular instability and a hypertonic contracted state within the muscles of the pelvic floor. The consequent decrease in muscle function and development of myofascial trigger points cause myofascial pain and new pain generators (3). Myofascial pelvic pain is due to a hypertonus of the levator any group muscles producing pain poorly localized to the perivaginal and perirectal areas (7). Pain may also be felt in the abdominal lower quadrants, suprapubic areas, coccyx, and posterior thigh. This disorders involve a high resting tone in the muscles and fascia that attach to the bony pelvis (7). Thus IC and visceral pelvic pain syndromes in general may contribute to the pain associated with these conditions. We completely agree with Butrick (3) in stating that the up-regulation of the dorsal horn is the first step in the cascade of events resulting in self-perpetuating, multisite visceral pain syndromes. Thus a functional disorder may cause an organic lesion and vice versa. 1. Weiss JM. Pelvic floor myofascial trigger points: manual therapy for interstitial cystitis and the urgency-frequency syndrome. J Urol 2001, 166: 2226-2231. 2. Abrams P, Cardozo L, Fall M, et al. the Standardisation of terminology in lower urinary tract function: report from the standardisation sub-committee of the International Continence Society. Urology 2003; 61: 37-49. 3. Butrick CW. Interstitial cystitis and chronic pelvic pain: new insights in neuropathology, diagnosis, and treatment. Clin Obstet Gynecol 2003; 46(4):811–823 4. Markenson JA. Mechanisms of Chronic Pain. Am J Med 1996; 101 (suppl 1A): 6S-18S. 5. Melzack R. From the gate to the neuromatrix. Pain Supplement 6 (1999); S121-S126. 6. Pezzone MA, Liang R, Fraser MO. A model of neural cross-talk and irritation in the pelvis: implications for the overlap of chronic pelvic pain disorders. Gastroenterology 2005; 128:1953–1964. 7. Simons DG, Dommerholt J. Myofascial pain sindrome – Trigger points. J Obstet Gynaecol Can 2005; 27(9): 869-887.
2009
Interstitial cystitis; painful bladder; chronic pelvic pain
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11562/334215
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