Nowa epilepsja po zabiegu chirurgicznym dostępem przez część затylną mózgu: związek z uszkodzeniem płata затylnego i trwałymi zmianami na rezonansie magnetycznym
De novo epilepsy after the occipital transtentorial approach: association with occipital lobe injury and persistent FLAIR lesions
W skrócie
Badanie wykazało, że u pacjentów poddanych zabiegu chirurgicznemu mózgu dostępem przez część затylną, epilepsja pojawiła się u 12,5% chorych. Wszystkie przypadki epilepsji wiązały się z uszkodzeniem korytarza mózgu podczas operacji i trwałymi zmianami widocznymi na obrazach rezonansowych wykonanych po zabiegu. Wyniki wskazują, że ostrożne chronianie naczyń krwionośnych podczas operacji może zmniejszyć ryzyko pojawienia się padaczki po tego typu zabiegu chirurgicznym.
Oryginalny abstract (angielski)
BACKGROUND: The occipital transtentorial approach (OTA) is a useful surgical corridor for deep-seated lesions involving the pineal region, thalamus, ventral temporal structures, and posterior fossa. Although occipital lobe injury is a recognized complication of OTA, its relationship with postoperative epilepsy has not been systematically investigated. We examined the association between postoperative occipital lobe injury and de novo epilepsy following OTA. METHODS: Thirty-two consecutive OTA procedures performed in 31 patients between 2013 and 2025 were retrospectively reviewed. Clinical records, operative videos, and magnetic resonance imaging studies were analyzed. Postoperative occipital injury was assessed using the final follow-up fluid-attenuated inversion recovery (FLAIR) MRI. Patients were classified according to postoperative FLAIR lesion volume (0 mL, < 2 mL, and ≥ 2 mL). Factors associated with de novo epilepsy and postoperative FLAIR lesions ≥ 2 mL were evaluated. RESULTS: De novo postoperative epilepsy developed after 4 of 32 procedures (12.5%). All patients with epilepsy demonstrated intraoperative occipital cortical contusion and postoperative FLAIR lesions ≥ 2 mL. Both factors were significantly associated with epilepsy (p = 0.0058 and p = 0.0010, respectively). Factors associated with postoperative FLAIR lesions ≥ 2 mL included compression of basal occipital veins (p = 0.0044), sacrifice of bridging veins (p = 0.0423), and intraoperative occipital cortical contusion (p = 0.000036). Notably, all FLAIR lesions ≥ 2 mL occurred in procedures complicated by approach-related occipital lobe injury. No patient without a FLAIR lesion ≥ 2 mL developed postoperative epilepsy. CONCLUSIONS: Occipital cortical contusion and persistent postoperative occipital FLAIR lesions ≥ 2 mL were strongly associated with de novo epilepsy following OTA. Venous compromise, including compression of basal occipital veins and sacrifice of bridging veins, was associated with occipital lobe injury. These findings suggest that meticulous preservation of venous structures and avoidance of occipital lobe injury are important surgical principles for reducing postoperative epilepsy after OTA.