Involvement of GABA in mirror focus: a case report
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Updated: Jun 12, 2026
Electrophoretic Delivery of γ-aminobutyric Acid (GABA) into Epileptic Focus Prevents Seizures in Mice
Published on: May 16, 2019
Marco Bortolato1, Luigi Barberini, Monica Puligheddu
1Department of Neurological and Cardiovascular Sciences, University of Cagliari, Monserrato (CA), Italy.
Abstract:
Mirror focus (MF) is a cortical epileptogenic lesion that is posited to develop in the contralateral site to a cortical primary focus (PF) by secondary epileptogenic mechanisms. Previous animal evidence supports the implication of gamma-aminobutyric acid (GABA) in this phenomenon, but this contention has not yet been substantiated by clinical findings. Here we report for the first time clinical evidence suggesting the involvement of GABAergic cortical transmission in MF pathogenesis, in a 37-year-old man affected by a lesional PF in the right frontal lobe and a homotopic MF in the contralateral hemisphere, triggered by hyperventilation. One year after surgical excision of the PF, the electric activity of the MF remained unchanged, but was accompanied by a significant increase in the density of GABA(A)/benzodiazepine receptor binding in the left frontal lobe, as measured by (123)I-Iomazenil SPECT. These results extend previous evidence on the involvement of GABAergic signaling in MF pathophysiology.
Insights
This study provides clinical evidence that gamma-aminobutyric acid (GABA) signaling is involved in mirror focus (MF) development. Increased GABA(A)/benzodiazepine receptor binding was observed in the contralateral hemisphere of a patient with epilepsy.
Area of Science:
- Neuroscience
- Epileptology
- Molecular Imaging
Background:
- Mirror focus (MF) is a secondary epileptogenic lesion contralateral to a primary focus (PF).
- Animal studies suggest gamma-aminobutyric acid (GABA) involvement, but clinical evidence is lacking.
- Understanding MF pathogenesis is crucial for epilepsy treatment.
Observation:
- A 37-year-old male patient presented with a right frontal lobe PF and a contralateral left frontal lobe MF, triggered by hyperventilation.
- Following surgical excision of the PF, the MF's electrical activity persisted.
- Iomazenil SPECT revealed a significant increase in GABA(A)/benzodiazepine receptor binding in the left frontal lobe.
Findings:
- The study presents the first clinical evidence linking GABAergic cortical transmission to MF pathogenesis.
- Increased GABA(A)/benzodiazepine receptor binding in the contralateral hemisphere suggests a compensatory or pathological role in MF.
- Persistent MF activity despite PF removal highlights the complex mechanisms of secondary epileptogenesis.
Implications:
- These findings support the role of GABAergic signaling in the development and maintenance of mirror foci.
- This research may inform future therapeutic strategies targeting GABAergic pathways for epilepsy management.
- Further clinical studies are warranted to elucidate the precise mechanisms of GABAergic involvement in MF.
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