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Peer-reviewedCC BY-NC-ND 4.0Acta Neurochirurgica

De novo epilepsy after the occipital transtentorial approach: association with occipital lobe injury and persistent FLAIR lesions

  • Hajime Handa1
  • Toshihiro Kumabe1
  • Takahiro Ono2
  • Daisuke Yamamoto1
  • Hiroyuki Koizumi1
  • Ichiyo Shibahara1
  1. 1Department of Neurosurgery, Kitasato University School of Medicine, 1-15-1 Kitasato, Minami-Ku, Sagamihara, Kanagawa 252-0374 Japan
  2. 2Department of Neurosurgery, Akita University Graduate School of Medicine, Akita, Akita Japan
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Abstract

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.

Supplementary Information: The online version contains supplementary material available at https://doi.org/10.1007/s00701-026-07003-1.

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BibTeXRIS
BibTeX
@article{handa2026novo,
  title = {{De novo epilepsy after the occipital transtentorial approach: association with occipital lobe injury and persistent FLAIR lesions}},
  author = {Hajime Handa and Toshihiro Kumabe and Takahiro Ono and Daisuke Yamamoto and Hiroyuki Koizumi and Ichiyo Shibahara},
  journal = {Acta Neurochirurgica},
  year = {2026},
  month = aug,
  doi = {10.1007/s00701-026-07003-1},
  url = {https://doi.org/10.1007/s00701-026-07003-1},
  note = {CC BY-NC-ND 4.0},
}
RIS
TY  - JOUR
TI  - De novo epilepsy after the occipital transtentorial approach: association with occipital lobe injury and persistent FLAIR lesions
AU  - Hajime Handa
AU  - Toshihiro Kumabe
AU  - Takahiro Ono
AU  - Daisuke Yamamoto
AU  - Hiroyuki Koizumi
AU  - Ichiyo Shibahara
PY  - 2026
DA  - 2026/08/08
JO  - Acta Neurochirurgica
DO  - 10.1007/s00701-026-07003-1
UR  - https://doi.org/10.1007/s00701-026-07003-1
AB  - 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.  Supplementary Information: The online version contains supplementary material available at https://doi.org/10.1007/s00701-026-07003-1.
SN  - 0001-6268
SN  - 0942-0940
ER  -