Hypometabolism in the Posteromedial Temporal and Medial Occipital Cortex on Preoperative 2-Deoxy-2-(18F) Fluoro-D-Glucose Positron Emission Tomography Suggests Exacerbation of Visual Field Defects After Surgery for Temporal Lobe Epilepsy: A Retrospective Long-Term Follow-Up Study.

OBJECTIVE: Surgery is a good treatment option for drug-resistant temporal lobe epilepsy (TLE). 2-deoxy-2-(18F) fluoro-D-glucose (FDG) positron emission tomography (PET) is used to detect epileptic foci as hypometabolic lesions in presurgical evaluation. Visual field defects (VFDs) in the contralateral homonymous upper quadrant are common postoperative complications in TLE. This study aimed to quantify VFDs using pattern deviation probability plots (PDPPs) and examine the effect of hypometabolism in FDG-PET on VFDs. METHODS: This study included 40 patients. Both visual fields were assessed using the Humphrey field analyzer preoperatively and 3 months and 2 years postoperatively. PDPPs with <0.5% confidence level counted in the contralateral homonymous upper quadrant. FDG-PET results were compared between groups with (15 patients) and without (24 patients) hypometabolism in the optic radiation. RESULTS: All 40 patients were evaluated by Humphrey field analyzer at 3 months postoperatively and 39 at 2 years postoperatively. The incidence of VFDs 3 months postoperatively was 35/40 (87.5%), and 17/40 (42.5%) patients had severe VFDs. In cases of surgery on the left temporal lobe, ipsilateral eyes appeared to be more significantly affected than contralateral eyes. VFDs were more severe in patients with FDG hypometabolism than in those without hypometabolism in posteromedial temporal and medial occipital cortex (P < 0.01); however, 85% of patients with FDG hypometabolism had a reduced VFD 2 years postoperatively. CONCLUSIONS: PDPP counting is useful for quantifying VFDs. Preoperative dysfunction indicated by preoperative FDG-PET in the posteromedial temporal and medial occipital cortex could enhance VFDs early after TLE surgery.

Extratemporal abnormalities in phosphorus magnetic resonance spectroscopy of patients with mesial temporal sclerosis / Anormalidades extratemporais na espectroscopia de fósforo por ressonância magnética em pacientes com esclerose mesial temporal

ABSTRACT Objective We evaluated extratemporal metabolic changes with phosphorus magnetic resonance spectroscopy (31P-MRS) in patients with unilateral mesial temporal sclerosis (MTS). Method 31P-MRS of 33 patients with unilateral MTS was compared with 31 controls. The voxels were selected in the anterior, posterior insula-basal ganglia (AIBG, PIBG) and frontal lobes (FL). Relative values of phosphodiesters- PDE, phosphomonoesters-PME, inorganic phosphate - Pi, phosphocreatine- PCr, total adenosine triphosphate [ATPt = γ- + a- + b-ATP] and the ratios PCr/ATPt, PCr/γ-ATP, PCr/Pi and PME/PDE were obtained. Results We found energetic abnormalities in the MTS patients compared to the controls with Pi reduction bilaterally in the AIBG and ipsilaterally in the PIBG and the contralateral FL; there was also decreased PCr/γ-ATP in the ipsilateral AIBG and PIBG. Increased ATPT in the contralateral AIBG and increased γ-ATP in the ipsilateral PIBG were detected. Conclusion Widespread energy dysfunction was detected in patients with unilateral MTS.

RESUMO Objetivo Nós avaliamos as alterações metabóblicas através da espectroscopia de fósforo por ressonância magnética (31P-MRS) em pacientes com esclerose mesial temporal (EMT) unilateral. Método 31P-MRS de 33 pacientes com EMT unilateral foram comparadas aos de 31 controles. Foram selecionados os voxels nas regiões insulonuclear anterior e posterior (RINA e RINP) e frontal (RF). Os valores relativos de fosfodiésteres – PDE, fosfomonoésteres- PME, fosfato inorgânico- Pi, fosfocreatina –PCr, adenosina trifosfato total [ATPt = γ- + a- + b-ATP] e as razões PCr/ATPt, PCr/γ-ATP, PCr/Pi e PME/PDE foram obtidas. Resultados Nós encontramos anormalidades em pacientes com EMT em comparação aos controles. Redução de Pi nas RINA bilateralmente, RINP ipsilateral e RF contralateral, redução de PCr/γ-ATP nas RINA e RINP ipsilaterais foram detectadas. Aumentos de ATPT na RINA contralateral e aumento de γ-ATP na RINP ipsilateral também foram encontradas. Conclusão Disfunção energética difusa foi encontrada em pacientes com EMT unilateral.

Colocalización de proteínas proepileptogénicas en sinapsis hipocampales después de convulsiones / Colocalization of proepileptogenic proteins on hippocampal sinapsis after seizure

INTRODUCCIÓN: La epilepsia del lóbulo temporal se desarrolla como consecuencia de insultos cerebrales como trauma, infartos, infección o convulsiones. Los circuitos neuronales del lóbulo temporal, incluyendo al hipocampo, se reorganizan generando redes hiperexcitables, el foco epiléptico, proceso denominado epileptogénesis; en cambio, la corteza cerebral es más resistente a la reorganización. La epileptogénesis en el hipocampo está mediada en parte por óxido nítrico, sintetizado por la óxido nítrico sintasa neuronal y por la neurotrofina BDNF, cuyo receptor es TrkB. Estas proteínas están localizadas en las sinapsis excitadoras y podrían estar implicadas en la sensibilidad diferencial entre el hipocampo y corteza cerebral a la epileptogénesis. OBJETIVO: Lograr un acercamiento a los mecanismos que participan en la sensibilidad diferencial a la epileptogénesis entre el hipocampo y la corteza, después de convulsiones. MATERIAL Y MÉTODO: Se indujeron convulsiones en ratas mediante inyección de kainato. Se obtuvieron membranas sinápticas reselladas (sinaptosomas) de corteza e hipocampo. En ellas, se cuantificó la co-localización de óxido nítrico sintasa neuronal, TrkB y un marcador de sinapsis excitadoras (Prosap2) mediante técnicas inmunohistoquímicas. Los resultados expresados como por ciento promedio +/- error estándar se sometieron a prueba de t-student. RESULTADOS: TrkB y óxido nítrico sintasa neuronal aumentaron de 20,6 +/- 3,5 por ciento a 35,7 +/- 2,6 por ciento (p = 0,0008) y de 32,4 +/- 3,8 por ciento a 51,5 +/- 3,5 por ciento (p = 0,0003), respectivamente, en sinaptosomas excitadores hipocampales después de convulsiones. En sinaptosomas excitadoras de cerebro corteza no se observaron cambios significativos. DISCUSIÓN: óxido nítrico sintasa neuronal y TrkB se asocian a sinapsis excitadoras hipocampales después de convulsiones, pudiendo contribuir así a la epileptogénesis. La cerebrocorteza es resistente a esta reorganización molecular.

INTRODUCTION: Temporal lobe epilepsy develops as a consequence of brain insults such as trauma, stroke, infection, or seizures. The temporal lobe circuit, including the hippocampus, reorganizes generating hyper-excitable networks and, therefore, the epileptic focus, process called epileptogenesis. Where as, the cerebral cortex is more resistant to the reorganization. Temporal lobe epileptogenesis is mediated partly by neuronal nitric oxide synthase and the neurotrophin BDNF with its receptor TrkB. These proteins are localized at excitatory synapses and might be involved in the differential sensitivity of the hippocampus and cerebral cortex to epileptogenesis. OBJECTIVE: Getting closer to mechanisms involved in epileptogenesis differential sensitivity between the hippocampus and cortex after seizures. MATERIAL AND METHOD: Seizures were induced in rats by injection of kainic acid. Resealed synaptic membranes (synaptosomes) were obtained from cortex and hippocampus. Then the co-localization of neuronal nitric oxide synthase, TrkB and a marker of excitatory synapses (Prosap2/Shank3) was quantified by immunohistochemistry. The results were expressed as mean +/- standard error and subjected to t-student test. RESULTS: TrkB and neuronal nitric oxide synthase increased from 20.6 +/- 3.5 percent to 35.7 +/- 2.6 percent (p = 0.0008) and from 32.4 +/- 3.8 percent to 51.5 +/- 3.5 percent (p = 0.0003), respectively in excitatory hippocampal synaptosomes after seizures. In excitatory cerebrocortical synaptosomes no significant changes were observed. DISCUSSION: neuronal nitric oxide synthase and TrkB associate to excitatory hippocampal synapses after seizures, thereby probably contributing to epileptogenesis. The cerebral cortex is resistant to this molecular reorganization.