Primary burning mouth syndrome (BMS) is defined as an "intraoral burning or 
dysaesthetic sensation, recurring daily… more than 3 months, without clinically 
evident causative lesions" (IHS 2013). In addition to pain, taste alterations 
are frequent (dysgeusia, xerostomia). Although lacking clinical signs of 
neuropathy, more accurate diagnostic methods have shown neuropathic involvement 
at various levels of the neuraxis in BMS: peripheral small fiber damage (thermal 
quantitative sensory testing, electrogustatometry, epithelial nerve fiber 
density), trigeminal system lesions in the periphery or the brainstem (brainstem 
reflex recordings, trigeminal neurography, evoked potentials), or signs of 
decreased inhibition within the central nervous system (deficient brainstem 
reflex habituation, positive signs in quantitative sensory testing, 
neurotransmitter-positron emission tomography findings indicative of deficient 
striatal dopamine function). Abnormalities in electrogustatometry indicate the 
involvement of the small Aδ taste afferents, in addition to somatosensory small 
fibers. According to these findings, the clinical entity of BMS can be divided 
into 2 main subtypes compatible with either peripheral or central neuropathic 
pain, which may overlap in individual patients. The central type does not 
respond to local treatments and associates often with psychiatric comorbidity 
(depression or anxiety), whereas the peripheral type responds to peripheral 
lidocaine blocks and topical clonazepam. Burning mouth syndrome is most 
prevalent in postmenopausal women, having led to a hypothesis that BMS is 
triggered as a consequence of nervous system damage caused by neurotoxic factors 
affecting especially vulnerable small fibers and basal ganglia in a setting of 
decrease in neuroprotective gonadal hormones and increase in stress hormone 
levels, typical for menopause.