© Springer International Publishing AG 2018
Philip M. Hanno, Jørgen Nordling, David R. Staskin, Alan J. Wein and Jean Jacques Wyndaele (eds.)Bladder Pain Syndrome – An Evolutionhttps://doi.org/10.1007/978-3-319-61449-6_1515. Neuro-Urologic Evaluation in Interstitial Cystitis
(1)
Department of Urology, Antwerp University, GGW, Wilrijk, Antwerp, Belgium
There has been quiet an evolution about knowledge of BPS since Ed McGuire wrote this chapter.
The terminology has changed, the value of different tests has become clearer. The international understanding of BPS as “symptom syndrome” and not “disease” has opened new perspectives, and created new challenges.
As BPS is a syndrome with symptoms found in many different conditions, a stepwise diagnosis is needed, which starts with the clinical possibility that the patient suffers from BPS, the performance of consequent tests to exclude confusable diseases, putting all data together in order to define which type of BPS pathology is present and leading to the best decision for what should be the primary treatment, and eventually further steps.
It is a fact that pain is the major symptom. Sensation is subjective, and pain sensation per definition will show very different levels and localisations depending on the individual. Is it nociceptive pain or rather neuropathy? Its subjectivity does not mean that symptom reporting is unreliable or not valid. It is the main thing available to indicate that there is a pain causing condition in the pelvic region. Problematic may be that tests can grade and better define the pain but not prove that pain actually exists.
15.1 What Did We Get Right?
Neuro-urological diagnostic techniques have so far fairly little to offer in the investigation of BPS patients, beside for excluding other conditions.
That differential diagnosis with Overactive Bladder can be important in patients complaining of urgency and frequency, and discomfort is correct.
It has been shown that hyperactivity of the striated pelvic muscles/urethral sphincter is present in many BPS patients. It remains uncertain if this is cause, consequence or both.
That BPS patients mostly show discomfort when the bladder is filled to smaller than considered normal volumes is correct. But not in all patients such a relation can be seen. Though several pathophysiological mechanisms have been hypothesized the exact cause of this increased sensation remains uncertain.
It is likely that different types of sensory innervation play and that sensory information which leads to bladder contraction is different from the pain related mechanisms.
The limited role of urodynamic tests is accepted by many, though considered important in the differential diagnosis with OAB.
Patients with BPS but with normal bladder capacity under anaesthesia are not rare. There is no evidence that the cases with general macroscopic pathology of the bladder wall or with Hunner lesion relate to different neurologic dysfunctions. It needs to be better studied if patients with different diagnostic findings need to be treated differently. That treatment does anything more than influence the symptomatic expression of the disease rather than cure the condition is likely. If spontaneous cure may happen is uncertain.
15.2 Where Were We off Base?
The neuro-urologic evaluation as described highlights some important reflexions, but focus, based on the knowledge at that time, was somewhat missing. Since publication quite a lot of new knowledge has been acquired.
The terminology “sensory urgency “and “motor urgency “has been abandoned. The latest terminology reports [1, 2] describe genitourinary pain syndromes as constellations, or varying combinations of symptoms, which cannot be used for precise diagnosis.
All bladder pain syndromes are chronic in their nature. Pain is the major complaint but concomitant complaints are of LUT, bowel, sexual or gynecological nature. The suprapubic pain may be related to bladder filling, accompanied by other symptoms such as increased daytime and night-time frequency, in the absence of proven urinary infection or other obvious pathology.
The knowledge on the innervation related to BPS in primary order, second order, third order neurons and in the brain has been extensively described [3]. The different stages in development of the pain: local >peripheral > central > cerebral, known for a long time in other pain conditions [4] are present also in BPS. The importance of making an early diagnosis follows from this, as well as the need to study the influence of duration of the disease on different treatment success. Combination treatments for peripheral and central can be worthwhile [5].
An oversimplified view on the different neurogenic structures involved in BPS pain is not valid anymore. Several things can be mentioned: myelinated mechanoreceptive fibers in the bladder wall also possess chemoreceptive properties [6]; mechanoinsensitive C fibers may become mechanosensitive during inflammation, probably providing a substrate for hypersensitivity (pain, urgency) at lower bladder content [7]. The innervation related to signaling pain from the pelvic region runs not only in the pelvic plexus, but also in the hypogastric nerves [8]. It need to be explored if such animal findings are also happening in humans with BPS. The effects of intravesical vanilloids, and of oxybutinin give credit to this hypothesis [9, 10]. It needs to be developed further how the increased knowledge in basic findings can help improving the phenotyping and choice of treatment modalities.
Best ways to diagnose have been looked at in International Guidelines (as AUA, mentioned here). “Recommended are a basic assessment including a careful history, physical examination, and laboratory examination in order to rule in symptoms that characterize IC/BPS and rule out other confusable disorders. Baseline voiding symptoms and pain levels should be obtained in order to measure subsequent treatment effects. Cystoscopy and/or urodynamics should be considered as an aid to diagnosis only for complex presentations”.