Surgical histopathologic findings of 232 Chinese children cases with drug-resistant seizures

Abstract

Objectives: The drug-resistant seizures are characterized by frequent and severe onset of seizures in childhood. There is only little literature had extensively explored the types of pathological brain damage in Chinese children cases. The present study aims to investigate the histopathologic findings and seizure outcomes of drug-resistant seizures in cases of 0-14-year-old children.

Materials and methods: About 232 children cases were retrospectively who underwent epilepsy surgery. The medical records, onset age, age of surgery, disease course, seizure type, pathological reports, and seizure outcomes of these patients were retrospectively analyzed.

Results: The most common categories were malformations of cortical development (focal cortical dysplasia (FCD) was the most common type (94.36%, 67/71), found in 30.60% of the patients, tumors in 18.11%, glial scar in 12.50%, and encephalitis in 11.63%). It was found that the effective seizure outcome of FCD cases with shorter duration of epilepsy (<2 years, 87.23%) was better than that with longer duration (≥2 years, 60.00%) and the difference was statistically significant (χ² = 4.76, p < .05). Patients with FCD I, FCD II, and tumor showed the relatively better postsurgical seizure outcome than patients with other pathological types.

Conclusion: The malformations of cortical development (MCD) (most FCD) were the most common pathological type for children cases in China with drug-resistant seizures. It was speculated further that the FCD patients with shorter duration of epilepsy before surgery seem to have a higher ratio of being seizure-free after surgery.

Keywords: drug-resistant seizures; focal cortical dysplasia; histopathologic findings; seizure outcome.

Figure 1

Histopathology of FCD type I and FCD type II. (a) Abnormal cortical architecture with columnar disorganization (HE, ×100); (b) abnormal cortical architecture with dyslamination disorganization (HE, ×200); (c) neurons with abnormal morphology and nucleus (HE, ×400); (d) neurons with abnormal morphology marked by NF (×400); (e) BCs: the nucleus were offset or absent, and excess cytoplasm was stained in homogeneous pink (HE × 400); (f) Nestin staining of BCs (×400)

Figure 2

Histopathology of tumors (GG and DNT). (a and b) (GG) showed the hyperplasia of gliocyte. Some cells were in mild dysplasia. Numbers of neurons with different size and shape were distributed among hyperplastic gliocytes (HE × 100, ×200). (c) NeuN staining of the neurons (×100); (d) abundant CD34‐positive tumor aggregates can be identified within adjacent neocortex. (×100); (e and f) (DNT) showed that oligodendrocyte‐like cells were distributed like trees; some myxoid tiny cysts were formed, and neurons were floated in the cyst (E: HE × 100; F: HE × 200); (g) Olig‐2‐positive oligodendrocyte‐like cells (×200); (h) NeuN‐positive neurons floated in the cyst (×200)

Figure 3

Histopathology of glial scars and encephalitis. (a) Focal cortex was missing, and glial scars were formed (HE × 100); (b) persistent perivascular T cell; (c) microglial nodule was formed (HE × 200)