Different strategies for surgical approaches in TLE result in equally good outcomes. Seizure outcome is mainly dependent on the diagnosis and clinical factors, whereas the neuropsychological results are more beneficial after resections limited to an epileptogenic lesion and focus.

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The etiology and pathogenesis of complex focal lesions associated with chronic, intractable epilepsy are largely unknown. Some data indicate that malformative changes of the central nervous system may precede the development of gangliogliomas and other epilepsy-associated neoplasms. In the present immunhistochemical study, we have examined epilepsy-associated lesions for CD34, a stem cell marker transiently expressed during early neurulation. Surprisingly, most tissue samples from patients with chronic epilepsy (n = 262) revealed neural cells immunoreactive for CD34. Prominent immunoreactivity was detected in gangliogliomas (74%), low-grade astrocytomas (62%) and oligodendrogliomas (59%). Only 52% of non-neoplastic, malformative pathologies, such as glio-neuronal hamartias or hamartomas showed solitary or small clusters of CD34-immunoreactive cells. None of the adult control tissues (n = 22), none of the specimens obtained from the developing human brain (n = 44) and none of those tumor samples from patients without epilepsy (n = 63) contained CD34-immunoreactive neural cells. However, a malignant teratoma with microscopic features of early neural differentiation displayed a focal CD34-immunoreactive staining pattern. The majority of CD34-immunoreactive cells co-localized with S-100 protein and a small subpopulation was also immunoreactive for neuronal antigens. CD34 may, thus, represent a valuable marker for the diagnostic evaluation of neoplastic and/or malformative pathological changes in epilepsy patients. The CD34 immunoreactivity of these lesions indicates an origin from dysplastic or atypically differentiated neural precursors. Further studies may elucidate the functional significance of CD34 expression during the pathogenesis of epilepsy-related focal lesions as well as during neurogenesis.

Summary: Background and Purpose: Focal cortical dysplasia of Taylor's balloon-cell type (FCD-BC) are a frequent cause of pharmacoresistant epilepsy in young patients. In order to characterize FCD-BC, we coupled MRI and histopathology, and analyzed the clinical outcome following epilepsy surgery.Methods: From an epilepsy data bank with 547 histological specimens, 17 FCD-BC were re-evaluated of which high resolution MRI was available. Five additional FCD-BC were prospectively identified by MRI. Histopathological and immunohistochemical features were related to MRI. Outcome following lesionectomy was analyzed as determined on routine examinations 3, 6 and 12 months following surgery.Results: All but one lesion were located outside the temporal lobe. A markedly hyperintense funnel-shaped subcortical zone tapering towards the lateral ventricle was the characteristic finding on FLAIR MRI. Histopathologically, the subcortical zone of the FCD-BC displayed hypomyelinated white matter with radially oriented balloon cells and gliosis. Dysplastic neurons were found in the adjacent, disorganized cortex. All patients with complete lesionectomy were seizure free one year following surgery. Conclusion: Focal cortical dysplasias of Taylor's ballooncell type (FCD-BC) have characteristic MRI and histopathological findings. MRI recognition is important, since outcome following resective surgery is favorable. Key words: focal cortical dysplasia-balloon cells-epilepsy surgery-MRI Malformations of the cerebral cortex are a frequent cause of pharmacoresistant epilepsies and developmental disorders (1). Various terms have been introduced to classify the underlying pathology such as cortical dysgenesis (2,3), focal cortical dysplasias (4) or glioneuronal hamartias/hamartomas (5,6). Unfortunately, the nomenclature is not uniform, and different diagnostic terms are even used for malformative lesions that appear identical on histological specimens. One of these peculiar lesions is characterized by focal cortical disorganization with enlarged, dysplastic neurons and the presence of bizarre balloon cells within the cortex and subcortical white matter. Taylor et al. first described it in 1971 (7) detailing the history of ten patients suffering from longstanding epilepsy: Six of ten lesions contained "grotesque cells, probably of glial origin," within the cortex and subcortical white matter, and four lesions did not.Both lesion types were initially merged and denominated as focal cortical dysplasia of Taylor. Other neuropathological terms for the lesions containing balloon cells include focal cortical dysplasia (2), focal transmantle cortical dysplasia (8), focal cortical dysplasia of Taylor, balloon cell subtype (9), severe cortical dysplasia, type II (10), type II focal cortical dysplasia (11), forme fruste of tuberous sclerosis or type III focal cortical dysplasia (11), balloon cell changes (4) and glioneuronal hamartoma with TS cells (5).With the recent progress in magnetic resonance imaging (MRI), malformations of the cerebral cortex are i...