Trigeminal neuropathy following orthognathic surgery

Abstract

Traumatic trigeminal neuropathy occupies a special place in the pain continuum. The clarification of genesis and clinical and neurophysiological findings makes it possible to perform differentiation treatment.Objective: to evaluate the clinical and neurophysiological efficiency of repetitive magnetic stimulation (RMS) and vitamin B complex therapy for traumatic trigeminal neuropathy.Patients and methods. The investigation enrolled 36 patients (26 women and 10 men) aged 25 to 35 years with inferior alveolar neuropathy following bilateral sagittal split osteotomy. The DN4 questionnaire was used to identify a neurogenic pain component. The intensity of pain syndrome was assessed using a visual analogue scale. A neurophysiological examination involving the recording of brainstem auditory evoked potentials (BAEPs) and trigeminal evoked potentials (TEPs) was made using a Neuro-MEP device (Neurosoft, Russia). Therapy including vitamin B complex was performed in 12 patients. Twenty-four patients received low-frequency pulsed magnetic field therapy using a Neuro-MS magnetic stimulator.Results and discussion. The clinical picture in patients with traumatic inferior alveolar neuropathy after corrective mandible surgery is characterized by the polymorphism of pain sensations and sensory disorders. The development of pain syndrome is due to a neuropathic component. The 10-day vitamin group B therapy cycle had no substantial impact on the time course of clinical and neurophysiological changes. After the 10-day RMS cycle, there were reductions in swelling and the intensity of pain syndrome and the severity of sensory disorders in the lower lip, chin, and mandible. The data on BAEPs showed shortening in the interpeak intervals III–V; those on TEPs demonstrated a decrease in the P1–N1 amplitude.Conclusion. Unlike vitamin B complex therapy, the RMS cycle in patients with traumatic trigeminal neuropathy makes it possible to reduce the intensity of pain syndrome and the severity of sensory disorders, as well as excitability of the nonspecific structures of the brainstem and the central structures of the trigeminal system.