Title: Is vestibulodynia a nociplastic pain syndrome? A
commentary
Author : Filippo Murina, MD
Affiliations: Lower Genital Tract Disease Unit, V. Buzzi
Hospital–University of the Study of Milan, Milan, Italy
Corresponding Author: Filippo Murina,filippomurina577@gmail.com,
Via Castelevetro 24-Milan (Italy). Tel number +300257995464-Fax number
+390257995025
Author Orcid. Filippo Murina: 0000-0002-9966-6448
Running title : Is vestibulodynia nociplastic pain?
A recent consensus statement differentiated between persistent vulvar
pain of at least 3-month caused by a specific disorder (e.g.,
inflammatory, neoplastic, traumatic) and vulvodynia, which is vulvar
pain without clear identifiable cause.1 The statement
suggested using a pain-based system to characterize vulvodynia based on
location (localized, generalized, or mixed), situations that elicit the
pain (contact, spontaneous, or mixed), temporal pattern (intermittent or
constant), and onset (primary or secondary).
Vulvodynia is a highly prevalent form of chronic genital pain in women,
to such an extent that prevalence studies estimate ranges from 10% to
28% in reproductive-aged women.2, 3 Localized
provoked vulvodynia at the vestibule, known as vestibulodynia (VBD), is
the most common manifestation of the disease (about
80%).4
Women with VBD often describe vulvar pain as a burning, stinging,
irritation, rawness, and dyspareunia (difficult or painful intercourse).
Most women with VBD described their pain as “hot,” “burning,” or
“pricking” and that the vestibular area is sensitive to the touch
(e.g. during sexual intercourse or tampon use) and that the pain would
be increased by rubbing. The pattern of VBD responses is suggestive of
sensory abnormalities in the form of evoked pain (e.g. hyperalgesia or
allodynia), suggesting sensitization, an underlying manifestation of
neuropathic pain.
This is consistent with biopsy studies that have demonstrated increased
innervation of the vulvar vestibule and an increase in subepithelial
heparinase activity and cytokines that have been linked to
neuroinflammatory processes; patients with VBD also experience body
changes in sensitivity, suggesting that sensory dysregulation might be
involved the expression of this pain condition.5
Furthermore, the discomfort inherent in VBD is always associated with
pelvic floor muscle overactivity.6 This prolonged
pattern can result in decreased tissue perfusion, muscle dysfunctional
overactivity, and the development of myofascial trigger points,
resulting in localized or radiating pain and/or intense tenderness.
Neuropathic pain and hypertonicity can be considered a multifactorial
and complex consequence of maladaptive neuronal
plasticity.7
Neuropathic pain is defined as pain arising as a direct consequence of a
lesion or disease affecting the somatosensory system.8According to this definition, VBD cannot be designated as a neuropathic
pain, because a clear and evident lesion or a disease of the
somatosensory system has not been identified as the cause of VBD pain.
It may be argued that, by excluding VBD from the neuropathic pain
syndrome, there is a risk of stigmatizing this group of patients as
having a somatization disorder, one without a true and demonstrable
abnormality, as opposed to the patients who have a “real” physical
illness. The inability of this pain terminology to harmonize with the
concepts of neuropathic pain has resulted in the use of other
non-defined descriptors of VBD such as “dysfunctional” or
“psychosomatic” pain, which not only give no insight into possible
mechanisms but also carry implications that may stigmatize patients as
only psychologically distressed. The International Association for the
Study of Pain recently introduced the new pain descriptor “nociplastic
pain,” defined as “pain that arises from altered nociception, despite
no clear evidence of actual or threatened tissue damage causing the
activation of peripheral nociceptors or evidence for disease or lesion
of the somatosensory system causing the pain,” meant to cover cases not
properly covered by neuropathic pain definition.8
The descriptor is primarily addressed to patients with chronic pain
conditions characterized by evidence of altered nociceptive processing,
such as VBD, where altered nociception is clinically documented.
Therefore, the new descriptor does not apply to patients reporting pain
without hypersensitivity. As such, it is neither a synonym for
idiopathic pain nor pain of an unknown origin. A multifactorial
aetiology, including infections, hormone disorders, neuroinflammation,
atopic disease, gene polymorphisms that interfere with inflammation, and
psychogenic factors, has been implicated in the development and
maintenance of VBD.8
What is becoming increasingly apparent is that VBD is likely not one
disease but rather several diseases, in which the common end point is
vestibular hypersensitivity and pelvic floor hypertonic dysfunction. In
my experience, VBD represents a summation and overlapping of various
trigger factors (infections, hormonal disturbances, allergies, genetic
aspects, psychological vulnerability, and others) with weight and
predominance varying from patient to patient. It is impossible to say
whether psychosexual factors are involved in the development or
maintenance of VBD or whether they are the consequence of undiagnosed,
persistent, and debilitating pain. Pain modulation by psychological
factors is one of the most complex problems: in patients with VBD,
psycho-neurobiological vulnerability plays a relevant role, and the
experience of pain varies depending on the patient’s psychological
state.
In conclusion, I postulate that VBD results from diverse precipitating
and trigger factors that ultimately promote and maintain a nociplastic
pain syndrome. I believe these considerations provide the impetus for
future work to identify responders of targeted treatments based on
various subgroups of VBD.
Disclosure of interests . None declared.
Contribution to authorship . FM designed and wrote the
manuscript
Details of ethics approval . Ethics approval: N/A.
Funding . None
Acknowledgements . None