The concept of Painful Uterine Syndrome (PUS):
It is based on the principle of central sensitization, described by Woolf in 1983 (10).
Central sensitization is defined as a decrease in cortical nociceptive thresholds (10-13). This is responsible for a variety of problems such as neuropathic pain, muscle spasms, autonomic nervous system disorders, and visceral sensitization.
Abdominal visceral sensitization is known to occur in irritable bowel syndrome (14-17). The same applies at the pelvic level, where painful bladder syndrome (PBS) also appears to be related to the central sensitization mechanisms (18-21).
The existence of uterine sensitization is, therefore, very likely. This hypothesis has become increasingly evident in recent years, with publications by Iacovides in 2013 (22) and 2015 (23), Giamberardino in 2016 (24), and finally, Jarell in 2016 (25 and 26), which confirm a significant reduction in central pain thresholds in dysmenorrheic patients.
The concept of PUS allows us to better understand pelvic pain, whose symptomatic pattern appears to be uterine, with a negative anatomical evaluation, associating primary dysmenorrhoea and painful symptoms related to episodes of violent and inappropriate uterine myometrial contractions. Muscle hypercontractility is a common occurrence in sensitization. Several cine magnetic resonance (cine MRI) studies confirm the significant increase in uterine myometrial peristalsis in dysmenorrheic patients (27-29).
In 2011, we published a diagnostic score for uterine adenomyosis (30), which allowed for a positive diagnosis with a sensitivity of 98% and specificity of 90%. This diagnostic score is usefully applied in PUS cases (Table 1) and is defined by a particular type of complaint where the pain, located in the pelvis, is typical for uterine pain, including cramping and contractions, dysmenorrhoea, and deep dyspareunia. A physical examination reveals a painful uterine pain trigger that reproduces the pain.
The concept of PUS not only provides us with a better understanding of the painful symptoms, but it also allows us to better understand how to treat these symptoms and the treatment options available. This validates the suppression of menstrual function as one of the important, primary focus areas in the treatment of dysmenorrhoea, whether or not it is caused by endometriosis (24 and 25).
If this fails, there are few conservative treatment options available.
The logical connection with PBS and overactive bladder (OAB), as well as the importance of myometrial hypercontractility mechanisms led us to consider the use of Botulinum Toxin (BTX) injections for treating PUS. BTX injections have been shown to be effective in patients with an overactive bladder, where detrusor hypercontractility is the main symptom (31). While BTX’s effectiveness is somewhat less evident in PBS, it is an attractive treatment option that has been confirmed by recent randomised controlled studies or meta-analysis (32 and 33).