Cortical neuronal densities and lamination in focal cortical dysplasia.

Focal cortical dysplasia (FCD) is considered to represent a malformation due to abnormal cortical development (MCD) and is an important cause of focal epilepsy. The histopathological features include abnormal laminar architecture, the presence of hypertrophic and dysmorphic neurones in FCD type IIA...

Ամբողջական նկարագրություն

Մատենագիտական մանրամասներ
Հիմնական հեղինակներ: Thom, M, Martinian, L, Sen, A, Cross, J, Harding, B, Sisodiya, S
Ձևաչափ: Journal article
Լեզու:English
Հրապարակվել է: 2005
_version_ 1826300538830979072
author Thom, M
Martinian, L
Sen, A
Cross, J
Harding, B
Sisodiya, S
author_facet Thom, M
Martinian, L
Sen, A
Cross, J
Harding, B
Sisodiya, S
author_sort Thom, M
collection OXFORD
description Focal cortical dysplasia (FCD) is considered to represent a malformation due to abnormal cortical development (MCD) and is an important cause of focal epilepsy. The histopathological features include abnormal laminar architecture, the presence of hypertrophic and dysmorphic neurones in FCD type IIA and additional balloon cells in FCD type IIB. The events causing these sporadic lesions are unknown, but abnormal progenitor cell proliferation occurring late in corticogenesis has been proposed. FCD-like lesions have, however, also been described following a cerebral injury early in life. We carried out a stereological assessment on 15 cases of FCD on NeuN- and Nissl-stained sections from patients with a wide age range, and identified a significant reduction in the neuronal density in all cases in the region of dysplasia compared to the adjacent unaffected cortex (mean neuronal densities 19.2x10(3)/mm3 in the region of dysplasia; 42.8x10(3)/mm3 in the adjacent cortex). Relative differences in neuronal density and size in FCD cases between the superficial (layer I and II) and deep cortical laminae (layer V and VI) were similar to that observed in other pathologies including mild MCD, temporal neocortex adjacent to hippocampal sclerosis as well as in a non-epilepsy surgical control group. The lower overall neuronal densities observed in FCD may reflect neuropil expansion, a local failure of neuronal migration, proliferation or secondary neuronal loss. The preservation of relative differences in neuronal densities between cortical layers and laminar patterns of neurofilament staining in FCD would support the view that the temporal sequence of lamination is not affected.
first_indexed 2024-03-07T05:18:41Z
format Journal article
id oxford-uuid:de20defc-6037-485c-8b72-9989549cb579
institution University of Oxford
language English
last_indexed 2024-03-07T05:18:41Z
publishDate 2005
record_format dspace
spelling oxford-uuid:de20defc-6037-485c-8b72-9989549cb5792022-03-27T09:29:59ZCortical neuronal densities and lamination in focal cortical dysplasia.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:de20defc-6037-485c-8b72-9989549cb579EnglishSymplectic Elements at Oxford2005Thom, MMartinian, LSen, ACross, JHarding, BSisodiya, SFocal cortical dysplasia (FCD) is considered to represent a malformation due to abnormal cortical development (MCD) and is an important cause of focal epilepsy. The histopathological features include abnormal laminar architecture, the presence of hypertrophic and dysmorphic neurones in FCD type IIA and additional balloon cells in FCD type IIB. The events causing these sporadic lesions are unknown, but abnormal progenitor cell proliferation occurring late in corticogenesis has been proposed. FCD-like lesions have, however, also been described following a cerebral injury early in life. We carried out a stereological assessment on 15 cases of FCD on NeuN- and Nissl-stained sections from patients with a wide age range, and identified a significant reduction in the neuronal density in all cases in the region of dysplasia compared to the adjacent unaffected cortex (mean neuronal densities 19.2x10(3)/mm3 in the region of dysplasia; 42.8x10(3)/mm3 in the adjacent cortex). Relative differences in neuronal density and size in FCD cases between the superficial (layer I and II) and deep cortical laminae (layer V and VI) were similar to that observed in other pathologies including mild MCD, temporal neocortex adjacent to hippocampal sclerosis as well as in a non-epilepsy surgical control group. The lower overall neuronal densities observed in FCD may reflect neuropil expansion, a local failure of neuronal migration, proliferation or secondary neuronal loss. The preservation of relative differences in neuronal densities between cortical layers and laminar patterns of neurofilament staining in FCD would support the view that the temporal sequence of lamination is not affected.
spellingShingle Thom, M
Martinian, L
Sen, A
Cross, J
Harding, B
Sisodiya, S
Cortical neuronal densities and lamination in focal cortical dysplasia.
title Cortical neuronal densities and lamination in focal cortical dysplasia.
title_full Cortical neuronal densities and lamination in focal cortical dysplasia.
title_fullStr Cortical neuronal densities and lamination in focal cortical dysplasia.
title_full_unstemmed Cortical neuronal densities and lamination in focal cortical dysplasia.
title_short Cortical neuronal densities and lamination in focal cortical dysplasia.
title_sort cortical neuronal densities and lamination in focal cortical dysplasia
work_keys_str_mv AT thomm corticalneuronaldensitiesandlaminationinfocalcorticaldysplasia
AT martinianl corticalneuronaldensitiesandlaminationinfocalcorticaldysplasia
AT sena corticalneuronaldensitiesandlaminationinfocalcorticaldysplasia
AT crossj corticalneuronaldensitiesandlaminationinfocalcorticaldysplasia
AT hardingb corticalneuronaldensitiesandlaminationinfocalcorticaldysplasia
AT sisodiyas corticalneuronaldensitiesandlaminationinfocalcorticaldysplasia