Assess and manage vulvodynia and chronic vulvar pain

In one line

Vulvodynia is vulvar pain of at least three months' duration with no clear identifiable cause — a diagnosis reached only after a specific disorder has been excluded — and it is managed not with a single drug but with a multimodal, multidisciplinary plan built around a credible biopsychosocial explanation, because no monotherapy reliably beats placebo.

The groundwork — the anatomy of the vestibule, the differential of vulvar pain and the basics of provoked vestibulodynia — is the Intermediate vestibulitis chapter (FCOG Intermediate, General gynaecology → "Vestibulitis"); this builds on it. The consultant task here is the harder one: to separate true vulvodynia from the long list of conditions that mimic it, to construct a defensible formulation when the evidence base is thin, and to argue treatment choices from trials that are mostly small, mostly negative against placebo, and honest about it.

Mechanism & pathophysiology

The single most important conceptual move, fixed by the 2015 ISSVD/ISSWSH/IPPS consensus terminology, is the split between vulvar pain caused by a specific disorder and vulvodynia itself. Vulvar pain caused by a specific disorder has a name and a treatment: candidiasis, herpes, lichen sclerosus or lichen planus, a fissure, a fixed drug eruption, a pudendal neuralgia, an oestrogen-deficient atrophic vestibule, a desquamative inflammatory vaginitis. Vulvodynia is what is left when all of those have been excluded — vulvar pain of ≥3 months with no clear identifiable cause. It is therefore, by definition, a diagnosis of exclusion, and the commonest reason a "refractory vulvodynia" fails treatment is that it was never vulvodynia: a low-grade candidal vestibulitis, an under-recognised lichen sclerosus, or a vaginal atrophy was driving the pain all along.

The 2015 framework also gives the descriptors that organise the rest of the reasoning. Pain is classified by site (localised — most often the vestibule, provoked vestibulodynia, formerly "vulvar vestibulitis"; generalised — the whole vulva; or mixed), by provocation (provoked by contact/penetration, spontaneous, or mixed), by onset (primary, present from the first attempt at penetration or tampon use, versus secondary, acquired after a period of pain-free function), and by temporal pattern (intermittent, persistent, constant, immediate, delayed). The terminology deliberately appends a list of associated factors rather than causes — comorbid pain conditions, musculoskeletal and pelvic-floor dysfunction, inflammatory and infectious triggers, neurological mechanisms, hormonal factors, structural and psychosocial contributors — because the honest position is that vulvodynia is a final common pathway, not one disease.

The mechanistic core a consultant must hold is that vulvodynia behaves like a chronic neuropathic and central-sensitisation pain syndrome localised to the vulva, not like ongoing tissue injury. Three layers stack:

• Peripheral sensitisation. Biopsy and quantitative-sensory-testing studies of provoked vestibulodynia show increased density of vestibular nociceptive C-fibre and A-delta free nerve endings — a neural hyperplasia in the vestibular mucosa — together with a local low-grade inflammatory and immune signature (increased mast-cell numbers and degranulation, raised pro-inflammatory cytokines, and upregulated nociceptor transducers such as TRPV1) in a vestibule that often looks entirely normal. The embryology matters here: the vestibule is endodermal in origin, distinct from the ectodermal vulvar skin lateral to Hart's line, which is part of why pain localises to this precise zone. The result is allodynia — light touch (a cotton swab, a tampon, penetration) is read as pain — with the mucosa intact. This is why "there is nothing to see" never excludes the diagnosis.
• Central sensitisation. As in other chronic pain, repeated nociceptive input amplifies dorsal-horn and central processing, lowers pain thresholds at sites remote from the vulva, and explains the strong overlap with other central-sensitivity syndromes — irritable bowel, fibromyalgia, interstitial cystitis/bladder pain syndrome, temporomandibular disorder, chronic fatigue and migraine. A patient with several of these has a centrally sensitised nervous system, and that prediction shapes both the explanation you give and the drugs you reach for.
• Pelvic-floor hypertonicity. Pain provokes a protective reflex tightening of the levator ani; the hypertonic, tender pelvic floor then becomes an independent pain generator and a barrier to penetration, closing a self-sustaining loop of pain → guarding → more pain. This is why pelvic-floor physiotherapy is mechanistic treatment, not adjunct comfort.

Hormonal and psychosexual layers sit on top. A subset of provoked vestibulodynia is associated with combined hormonal contraception: suppressed ovarian oestradiol and testosterone plus a raised sex-hormone-binding globulin lower free androgen and oestrogen at the vestibule, thinning the epithelium and, on the prevailing hypothesis, sensitising the nociceptors — a state that can be partly reversed by stopping the pill and applying topical oestrogen/testosterone. A further subset overlaps the genitourinary syndrome of menopause. Both blur into "specific disorder" territory and both are treatable, which is why a hormonal history and an oestrogen assessment of the vestibule are part of the work-up rather than an afterthought. There is also a heritable and immunogenetic thread — familial clustering, an association with a history of recurrent candidiasis, and polymorphisms in inflammatory genes (for example in the interleukin-1 receptor antagonist and mannose-binding lectin pathways) have been reported — consistent with a primed, hyper-reactive local immune response in predisposed women, though none of this is yet a clinical test. The psychosexual layer — anxiety, hypervigilance, catastrophising, fear-avoidance, relationship distress, and a history of sexual trauma in some women — is not a competing "psychological cause" to be set against the "physical" one; it is a modulator of the same nociceptive system, descending facilitation and arousal amplifying the very spinal processing that peripheral sensitisation feeds, and treating it (CBT, sex therapy) measurably moves pain. Holding the biopsychosocial model as one mechanism, rather than a polite list, is what separates a consultant answer from a registrar's.

Assessment

The assessment has one job before all others: to decide whether this is vulvodynia or vulvar pain caused by something specific and treatable. Everything below serves that exclusion, then the biopsychosocial formulation.

• Structured history. Characterise the pain in the 2015 descriptors — localised or generalised, provoked or spontaneous, primary or secondary, and its temporal pattern — because the descriptor predicts the management (provoked vestibulodynia is the physiotherapy-and-topical-and-CBT phenotype; generalised spontaneous vulvodynia is the neuromodulator-led, pain-clinic phenotype). Ask specifically about dyspareunia (entry versus deep), tampon use, the relationship to the menstrual cycle and to contraception, and the impact on the relationship and on mood.
• Screen for the central-sensitivity comorbidities explicitly — IBS, bladder pain syndrome, fibromyalgia, migraine, TMJ, chronic fatigue. Their presence both supports the diagnosis and steers you towards centrally-acting drugs.
• Drug and hormonal history. Combined hormonal contraception, aromatase inhibitors, and the menopausal transition all produce a hypo-oestrogenic vestibule that mimics or causes provoked pain.
• Psychosocial history, sensitively taken: anxiety and depression screening, fear-avoidance and catastrophising, relationship dynamics, and — asked safely and without assuming — any history of sexual violence, which in the South African setting is common enough that it must be enquired about, with a clear pathway to support if disclosed.
• Inspection to exclude a dermatosis or infection: the architecture of lichen sclerosus (pallor, atrophy, loss of architecture, fissuring) or lichen planus (Wickham striae, erosions, a desquamative vaginitis), fissures, ulcers, erythema, atrophic change. A vulva that looks abnormal points away from vulvodynia and towards a specific disorder.
• The cotton-swab (Q-tip) test, the single most useful examination manoeuvre. Map light-touch allodynia systematically around the vestibule (a clock-face), the labia, the perineum and the interlabial sulci. In classic provoked vestibulodynia the allodynia is sharply localised to the vestibule, often maximal posteriorly (5 and 7 o'clock), with normal sensation on the labia majora — a positive, reproducible map on an otherwise normal-looking vestibule is the clinical signature.
• Pelvic-floor assessment. Palpate the levator ani and obturator internus for resting hypertonicity, tenderness and trigger points, and assess the patient's ability to relax and contract — the hypertonic, tender pelvic floor is both diagnostic and a treatment target, and missing it under-treats the patient.
• Exclude infection and treat the treatable. A vaginal pH, microscopy and culture (including for candida — recurrent or low-grade candidiasis is a classic mimic), and a low threshold to swab for herpes if the history fits. Vulvar biopsy is not routine for vulvodynia (the point is that there is nothing to biopsy); reserve it for a visible lesion, suspected dermatosis, or anything atypical or non-healing — never to "confirm" vulvodynia, which has no histological diagnosis.
• Assess for a neuralgia. A unilateral, dermatomal, burning pain in the pudendal distribution, worse on sitting and relieved by standing or sitting on a toilet seat, suggests pudendal neuralgia rather than vulvodynia — a different entity with a different work-up (and one of the "specific disorders" the terminology carves out).