Background. Burning mouth syndrome (BMS) is defined as a chronic burning sensation in the oral mucosa that can not be attributed to its pathological findings. Current opinion is that the clinical symptoms of BMS can be attributed to neurological disorders caused by disturbances in the processes of sensory information on various levels of the nervous system. In its etiology, dysfunction of the nigrostriatal dopamine-dependent system is also considered. It has been demonstrated that there are similarities between BMS and Parkinson's disease. Objectives. To evaluate local conditions and disturbances in peripheral nerve conduction in patients with BMS. Material and Methods. The participants of the study were 83 patients; 33 patients with burning mouth syndrome (group I), 20 patients with Parkinson's disease (group II) and 30 controls. Group I: age range 41-82 years (median age 60.4); 27 women, 6 men, group II: age range 51-81 years (median age 65.5 years); 15 women, 5 men. All patients underwent electroneurography. Motor conduction velocity, motor peroneal nerve and ulnar nerve conduction velocity distribution were analyzed. Sensory ulnar and sural nerve conduction velocity tests were also performed. Results. Group I: the authors confirmed a statistically significant decrease of both peroneal nerve amplitude and sural nerve amplitude in patients with BMS compared to controls. In patients with BMS, the prolongation of the ulnar nerve latency of sensory action potential was also proved. Negative correlations were revealed between the age of the patients, type of BMS and most of the parameters evaluated in a standard neurography examination. Group II: we confirmed a statistically significant decrease of the peroneal nerve amplitude of compound muscle action potential in patients with Parkinson's disease, compared to the control group. Conclusions. The findings justify further electrophysiological studies as well as neuropathological studies of the peripheral nervous system in patients with BMS. They could help to determine the role of peripheral changes in the disease's pathogenesis (Adv Clin Exp Med 2011, 20, 6, 753-760).