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).