P 117 Symptomatic trigeminal neuralgia (TN) – an electrophysiological case study

Abstract

Listen

Translate article

Introduction While idiopathic TN is associated with some delay in P19 response of the cortical trigeminal somatosensory evoked potential (T-SEP) in up to 50 % of patients, the blink reflex (BR) evoked by stimulation of the supraorbital nerve is usually not involved. We present a case of symptomatic TN in which the combination of electrophysiological findings was remarkable. Case report A 74 year-old man had a 3 month history of dull and diffuse pain of the left maxilla. Ten days before admission, he developed short-lasting attacks of severe sudden, sharp and stabbing pain in the left maxilla radiating to the temporal, frontal and mandibular regions of the left face. There were 1 to 4 attacks per day, no triggers could be identified. Neurological examination revealed hypaesthesia in the left face (V1-3) and mild asymmetry of the facial innervation due to peripheral paresis on the left. Other cranial nerve functions were normal, as was the rest of the neurological examination. Electrophysiology T-SEP of the left trigeminal nerve (simultaneous stimulation of upper and lower lip) revealed a delayed P19 response of 24.1 ms versus a normal response on the right of 20.1 ms. Blink reflex studies of the trigeminal and facial nerves were typical of an afferent lesion of the left trigeminal nerve with delays of ipsilateral R1 and ipsi- and contralateral R2 while these potentials were normal on the right ( Fig. 1 ). Electrical stimulation of the facial nerve at the foramen stylomastoideum and magnetic stimulation of the canalicular part of the facial nerve gave normal results, bilaterally. Finally, MRI of the head demonstrated a T1-contrast enhancing mass lesion in the region of the left cavum Meckeli, which reached to the cavernous sinus and the internal carotid artery, presumably of mesenchymal origin (meningeoma? Fig. 2) . Symptomatic pain control was achieved by administration of carbamazepine and pregabaline, and the patient awaited neurosurgical biopsy. Conclusion Our case demonstrates that TN is more likely to be of symptomatic than idiopathic or vascular compressive origin if not only T-SEP but also BR are abnormal, indicating a demyelinating lesion. MRI with thorough examination of the anatomical course of the TN is necessary to guide therapeutic decisions including neurosurgical intervention and biopsy.