Summary:Purpose: 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 γ -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), microtubuleassociated 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. Key Words: Temporal lobe epilepsy-ParvalbuminImmunocytochemistry.Focal cortical dysplasias (FCDs) result from a disturbance in cortical development and are characterized by focal anomalies of cortical structure. Such malformations are often associated with intractable epilepsy (1), and some of the affected patients are referred for surgical treatment. Some forms of FCD have been clearly defined (2) and, particularly the type IA (architectural) cortical dysplasia, represent an increasingly recognized cause of temporal lobe epilepsy (3). Neuronal hyperexcitability is attributed to lack of balanced excitatory and inhibitory mechanisms (4). Neuropathologic findings suggest that alterations of the γ -aminobutyric acid (GABA)ergic (inhibitory) cortical neuronal system play a role in focal epilepsies secondary to cor-

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