Abstracts

Rationale: Intracranial monitoring has evolved as an essential step in identifying the ictal onset zone in epilepsy surgery. However, this process is not devoid of significant risks. Though frequently observed complications associated with electrode placement include extra-axial fluid collections, hemorrhage, infection, infarcts, and edema; cranial nerve complications are not as common (Table 1). To our knowledge, isolated fourth nerve palsy as a result of electrode complications has not been reported. Methods: Here, we report a case of isolated acquired fourth nerve palsy, subsequent to subdural electrode placement that resolved spontaneously over the next six months. Results: A 13 year-old boy with drug-resistant focal epilepsy was evaluated for epilepsy surgery. Seizure onset occurred at age 7 years, with semiology described as brief staring episodes, occasionally with bilateral tonic-clonic activity. MRI brain with gadolinium revealed a left anteromedial temporal lobe lesion with calcifications, cysts, and small foci of enhancement, concerning for glioma (Fig 1A-C). Prenatal, birth, developmental, and family history were unremarkable. Neurological exam, including a detailed neuro-ophthalmologic exam, was also unremarkable. He underwent a Stage I left temporal lesionectomy, followed by placement of a 48-contact fronto-temporal grid, two 4-contact and one 6-contact strip along the temporal resection bed, and one 8-contact depth electrode in the mesial temporal lobe (Fig 1D). Intracranial EEG revealed multifocal epileptiform discharges over the left temporal lobe and the fronto-parieto-temporal grid contacts. As EEG also revealed frequent subclinical seizures with left anterior temporal lobe ictal onsets, he underwent an elective anterior medial temporal lobectomy.Immediate post-operative course was uneventful. Pathology revealed features of a low grade tumor, with features of both ganglioglioma and Dysembryoplastic Neuro-Epithelial Tumor. One week post-operatively, he developed episodic left eye hyper-deviation, with no diplopia or associated visual symptoms. A detailed neuro-ophthalmology evaluation revealed an intact pupillary examination, no afferent pupillary defect, no change in visual acuities, and intact visual fields with no scotoma or hemianopsia. Ocular motility exam revealed intact saccades and pursuits in cardinal directions, and no nystagmus or diplopia in primary position. However, evidence of left hypertropia in attempted left gaze, left superior oblique weakness with overaction of the left inferior oblique, and a subtle head tilt to the right consistent with a left fourth nerve palsy was noted (Fig 1F-G).  A repeat MRI brain was unremarkable. His symptoms spontaneously resolved over the next six months.  Conclusions: In our case, no structural lesions were demonstrated post-operatively. We postulate that the trochlear nerve palsy occurred either as a result of direct electrode placement or from traction injury of the fourth nerve secondary to the temporal lobectomy. We recognize that it is difficult to determine whether one or both of these factors contributed to the fourth nerve palsy in our patient. Nevertheless, no cases of trochlear nerve palsy secondary to either of these causes have been reported in the pediatric population. While a definitive underlying etiology in our case remains speculative, our case highlights that fourth nerve palsies can occur as a complication of intracranial invasive EEG monitoring, and underscores the importance of identifying this for appropriate patient counseling and management. Funding: N/A