Rationale:
Although EEG artifacts are commonly encountered and generally recognizable, rare cases exist where true electrographic activity mimics artifact, potentially delaying diagnosis. We present a case of highly, and atypically, focal seizures initially confined to a single electrode, illustrating the diagnostic challenges such patterns pose. This underscores the importance of meticulous EEG interpretation and suggests that higher-density electrode arrays or neuroimaging correlation may aid in timely and accurate diagnosis, and early initiation of aggressive management, in such cases.
Methods:
We report the case of a 78-year-old man with a history of traumatic brain injury (TBI) and bifrontal craniectomy who presented with generalized tonic-clonic seizures (GTCS) approximately 8 months post-injury. Following his seizures, he was intubated and admitted to the ICU in coma state. Initial EEG tracing revealed highly focal, rhythmic, stereotyped discharges localized, almost exclusively, to the left anterior temporal (F7) electrode (Figure 1 A-C). Started as 20-30 Hz activity, progressively increasing in amplitude and decreasing in frequency to 5 to 8 hertz sharply contoured discharges, before dissipating-off. Despite clear evolution in frequency, there was no spread to the surrounding electrodes and no associated clinical signs. These discharges lasted 30-45 seconds and were seen up to 10-15 times each hour. These activities were thought to be artifact, or breach rhythm, particularly in the setting of prior cranioplasty and underlying metal hardware. The concern that these are artifacts was even supported by the lack of clinical and EEG response to antiseizure medications, for which the patient was initially treated non-aggressively. On day 2-3, MRI revealed diffusion restriction involving medial frontal lobes and orbital frontal gyri (Figure 2 A&B). Careful review of electrographic onset demonstrated that this rhythm, although still first seen in the left anterior temporal region (F7), progressed rapidly to the left frontopolar (Fp1) and central (C3), followed by spread to the left frontal region (F3) (Figure 1 D).
Diagnosis was delayed due to the atypical, focal nature of the electrographic patterns, initially mistaken for artifact. After confirming the non-convulsive status epilepticus, aggressive treatment started. Despite escalation of antiepileptic therapy and use of anesthetic agents, seizures remained refractory (there was reduction in electrographic seizure burden after introducing Ketamine and Phenobarbital). Ultimately, care was withdrawn per family wishes, and the patient was transitioned to hospice.
Results: .
Conclusions:
This case carries an important lesson for the neurophysiologist: Focal electrographic discharges recorded near a skull defect should not be dismissed as artifacts without further investigation. The use of extended EEG arrays, such as the 10–10 montage or additional anterior temporal electrodes, or imaging modalities such as MRI, may help resolve this diagnostic challenge. This is particularly crucial in the context of aggressive treatment of status epilepticus, as delays in treatment may potentially lead to poor response and increased morbidity.
Funding: none