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We sincerely thank our colleagues for their thoughtful and detailed commentary on our recent study, and we appreciate their recognition of the importance of dedicated imaging protocols, postprocessing and integrating clinical data into MRI interpretation for patients with drug-resistant focal epilepsy.
We note with interest the comparison to their 1993–1998 cohort, which revealed a similar rate of interpretation errors (33%) as observed in our study (31.5%). Despite the passage of time and advances in MRI technology, this similarity underscores the persistent diagnostic challenges in epilepsy imaging and highlights that improved protocols must be matched by refined interpretation strategies.
As the authors rightly point out, the landscape of commonly missed lesions has shifted. Whereas hippocampal sclerosis (HS) was the most frequent missed finding in earlier studies, we observed a markedly lower rate of missed mesial temporal sclerosis (MTS) in our cohort—only 6%. This likely reflects the growing routine use of high-resolution coronal T2-weighted and FLAIR imaging acquired perpendicular to the hippocampal axis, which has improved sensitivity for MTS detection.
The evolving discussion around “no hippocampal sclerosis/gliosis only” lesions—without clear neuronal loss—is well taken. As we agree, such findings remain a diagnostic gray zone, both radiologically and histopathologically. Continued refinement of MRI criteria and correlation with histopathological subtypes will be critical in better characterizing these ambiguous entities.
We also share the authors’ concern regarding focal cortical dysplasias (FCD), which have become the predominant category of overlooked lesions in our cohort. The identification of FCD remains one of the most challenging aspects of epilepsy imaging—even with optimized sequences and experienced readers. We fully endorse the necessity of post-processing approaches, such as surface-based morphometry and voxel-based analyses, with the caveat that these may be difficult to implement in clinical routines.
We appreciate the authors’ observations on amygdala enlargement, which can be related to prior seizures but also has been shown to be a primary epileptogenic lesion. Regression of this lesion over time as well as its occurence in temporal proximity to a prior seizure are the key indicators to differentiate the secondary enlargement from the primary epileptogenic lesions, and we echo the call for vigilance in interpreting such findings in context.
Finally, the debated significance of malrotated hippocampi in epilepsy is an important reminder of the nuanced nature of radiological interpretation. As with any morphologic variant, correlation with clinical, electrographic, and surgical data remains essential.
In conclusion, we wholeheartedly agree with the commentary's emphasis on the need for a comprehensive diagnostic approach. Our findings, alongside theirs, reinforce the importance of epilepsy-dedicated imaging protocols, expert review, and interdisciplinary case discussions. Crucially, they also support the integration of quantitative post-processing methods as a vital adjunct in identifying subtle cortical malformations.