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Drug-refractory epilepsy remains a significant challenge in neurological care, affecting 30 to 40% of individuals with epilepsy and significantly impairing quality of life.[1] In such cases, surgical intervention is often pursued either to resect the epileptogenic focus (curative procedures) or to disrupt the propagation of seizure activity (disconnection procedures). Temporo-parieto-occipital (TPO) disconnection is a relatively rare surgical procedure. It is reserved for seizures originating from the posterior quadrant of the cerebral hemisphere (temporal, parietal, and occipital lobes). While considered safe and motor-sparing, known complications include cognitive and sensory integration deficits.[2] Facial nerve palsy—specifically, upper motor neuron (UMN) type—has not previously been documented as a postoperative complication of this procedure.

We present the case of a 36-year-old right-handed female with drug-refractory epilepsy who underwent right TPO disconnection surgery. She had a long history of seizures, which were uncontrolled despite adherence to three antiepileptic drugs. Preoperative evaluations revealed right-sided encephalomalacia, gliosis, medial temporal sclerosis, and abnormal electrical activity predominantly in the right posterior regions. Based on these findings, right-sided TPO disconnection was performed under general anesthesia. Neuronavigation was used throughout the procedure. The surgery lasted approximately 7 hours. Due to the prolonged duration, the patient was electively ventilated postoperatively in the neuro-intensive care unit.

The patient maintained stable vitals with a full Glasgow Coma Scale and was extubated the next morning. However, a neurological examination revealed a deviation of the mouth to the right and drooling from the left ([Fig. 1]). The presence of forehead wrinkling bilaterally, preserved gag reflex, and normal swallowing assessments (performed using the Gugging Swallowing Screen) further supported the diagnosis of UMN-type facial nerve weakness. Postoperative blood investigations were within normal limits. Postoperative computed tomography and magnetic resonance imaging of the brain with a dedicated stroke protocol were obtained, and these detected only postoperative changes with no new abnormalities.

Fig. 1 On postoperative day 5, panel (A) shows the deviation of the angle of the mouth to the right side (black arrow). Panel (B) shows the ability to wrinkle the forehead bilaterally (red arrow), confirming right side upper motor neuron type facial nerve palsy.

An extensive literature review revealed only two previous cases of facial palsy following epilepsy surgery, lower motor neuron (LMN) type, and associated with temporal lobectomy.[3] [4] These were attributed to direct mechanical or thermal injury to the facial nerve or ganglion. The UMN-type facial palsy reported here suggests a different etiology. The UMN of the facial nerve is located in the primary motor cortex of the frontal lobe. The UMN axons then descend ipsilaterally as the corticobulbar tract via the internal capsule and reach the facial nucleus in the pons to synapse with LMNs.

It is possible that subtle surgical trauma, localized edema, perioperative ischemia, microvascular compromise, cortical retraction, or transient ischemia affected the motor cortex or the corticobulbar tract. In epilepsy, even the plasticity of the brain can shift the motor cortical presentation.[5] In the absence of intraoperative neuromonitoring, these deficits went unnoticed. The use of intraoperative neuromonitoring could have identified or potentially prevented this complication. The absence of imaging abnormalities underscores the likelihood of transient or microscopic disruption of cortical-subcortical pathways rather than gross anatomical damage.

The patient was managed conservatively with supportive therapy, appropriate counselling, and outpatient follow-up to monitor nerve functional recovery. In similar LMN cases, recovery occurred over 6 to 8 weeks. A similar prognosis was observed in our case, where the deficit was transient and spontaneously recovered with the House–Brackmann scale of two after a 3-month follow-up.

To our knowledge, this is the first reported incidence of UMN-type facial palsy following TPO disconnection surgery. Awareness of such a rare postoperative complication is critical for understanding the vulnerability of the supranuclear facial nerve tract and the vital role of intraoperative neuromonitoring. It also reinforces the importance of detailed neurological assessments in the postoperative period to capture subtle deficits that might otherwise go unnoticed.

Article published online:
25 March 2026

© 2026. The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution License, permitting unrestricted use, distribution, and reproduction so long as the original work is properly cited. (https://creativecommons.org/licenses/by/4.0/)

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