Architectural (Type IA) focal cortical dysplasia and parvalbumin immunostaining in temporal lobe epilepsy.
OBJECTIVE
We analyzed 26 surgically treated patients operated on for intractable epilepsy associated with type IA (architectural) cortical dysplasia, to investigate neuropathologic and immunocytochemical features, particularly of the gamma-aminobutyric acid (GABA)ergic system, and to compare the findings with those observed in normal cortex.


METHODS
Routinely stained slides and serial sections immunostained for neurofilaments (SMI 311), microtubule-associated protein-2 (MAP-2), neuron-specific nuclear protein (NeuN), glial fibrillary acidic protein (GFAP), parvalbumin (PV), calbindin (CB), and calretinin (CR) were processed. Some sections were processed by using single-immunoperoxidase procedures; others were processed for double immunofluorescence labelling and observed by confocal microscopy. The density of inhibitory PV-immunoreactive interneurons was quantitatively assessed in all patients and control cases by using a two-dimensional cell-counting technique on PV immunostained sections.


RESULTS
The density of PV-immunoreactive interneurons was significantly reduced in this group of patients, whereas CB- and CR- positivity appeared similar to those in normal cortex. In five cases, architectural abnormalities, in addition to those that defined type 1A dysplasia, were present and characterized by abnormal clusters of neurons and laminar cellular loss in superficial cortical laminate.


CONCLUSIONS
The reduction of PV expression in type IA cortical dysplasia suggests an impairment of the GABAergic system as a possible mechanism for the epileptogenicity; in addition, PV immunoreactivity can be helpful in the neuropathologic characterization of this form of cortical dysplasia.
Garbelli
Rita
R
Department of Experimental Neurophysiology, National Neurological Institute C. Besta,, Milano, Italy.
Meroni
Alessandra
A
Magnaghi
Giuseppina
G
Beolchi
Maria Sana
MS
Ferrario
Arianna
A
Tassi
Laura
L
Bramerio
Manuela
M
Spreafico
Roberto
R
D000293:Adolescent; D000328:Adult; D034961:Antigens, Nuclear / Q000276:immunology / Q000378:metabolism; D064032:Calbindin 2; D064026:Calbindins; D002452:Cell Count; D004833:Epilepsy, Temporal Lobe / Q000175:diagnosis* / Q000473:pathology* / Q000601:surgery; D005455:Fluorescent Antibody Technique; D006801:Humans; D007124:Immunoenzyme Techniques; D007150:Immunohistochemistry; D007395:Interneurons / Q000378:metabolism / Q000473:pathology; D018613:Microscopy, Confocal; D008869:Microtubule-Associated Proteins / Q000276:immunology / Q000378:metabolism; D008875:Middle Aged; D009419:Nerve Tissue Proteins / Q000276:immunology / Q000378:metabolism; D010320:Parvalbumins / Q000276:immunology / Q000378:metabolism; D010640:Phenothiazines / Q000378:metabolism; D064030:S100 Calcium Binding Protein G / Q000276:immunology / Q000378:metabolism; D013194:Staining and Labeling; D013702:Temporal Lobe / Q000002:abnormalities* / Q000473:pathology* / Q000601:surgery
D034961:Antigens, Nuclear; C576764:CALB2 protein, human; D064032:Calbindin 2; D064026:Calbindins; C489788:MAP2 protein, human; D008869:Microtubule-Associated Proteins; D009419:Nerve Tissue Proteins; D010320:Parvalbumins; D010640:Phenothiazines; D064030:S100 Calcium Binding Protein G; C506808:neuronal nuclear antigen NeuN, human; C009469:thionine