Reversible Splenial Lesion Syndrome (RESLES) After Chemotherapy of Oral Tegafur-uracil in a Female With Locally Rectal Adenocarcinoma.

A 42-year-old woman with reversible splenial lesion syndrome (RESLES) and rectal adenocarcinoma presented with sudden-onset delirium after the sixth cycle of her chemotherapy drug, oral tegafur-uracil (300 mg/m/day, days 1-14, with treatment cycle repeated every 21 days). Accompanied by the anti-CV2 antibody, paraphasia, and a loss of bimanual coordination, the patient's etiology and clinical manifestations of RESLES are unlike those of other reported cases of RESLES. Tegafur-uracil is an oral fluoropyrimidine that has a similar effect to 5-fluorouracil as an adjuvant treatment for colorectal cancer. The possibility that the toxicity of chemotherapeutic drugs may play a role in the pathogenesis of cytotoxic edema in the splenium of the corpus callosum and extracallosal white matter should be investigated further.

Brivaracetam Prevents the Over-expression of Synaptic Vesicle Protein 2A and Rescues the Deficits of Hippocampal Long-term Potentiation In Vivo in Chronic Temporal Lobe Epilepsy Rats.

BACKGROUND: Patients with temporal lobe epilepsy (TLE) usually suffer from cognitive deficits and recurrent seizures. Brivaracetam (BRV) is a novel anti-epileptic drug (AEDs) recently used for the treatment of partial seizures with or without secondary generalization. Different from other AEDs, BRV has some favorable properties on synaptic plasticity. However, the underlying mechanisms remain elusive. OBJECTIVE: The aim of this study was to explore the neuroprotective mechanism of BRV on synaptic plasticity in experimental TLE rats. METHODS: The effect of chronic treatment with BRV (10 mg/kg) was assessed on Pilocarpine induced TLE model through measurement of the field excitatory postsynaptic potentials (fEPSPs) in vivo. Differentially expressed synaptic vesicle protein 2A (SV2A) were identified with immunoblot. Then, fast phosphorylation of synaptosomal-associated protein 25 (SNAP-25) during long-term potentiation (LTP) induction was performed to investigate the potential roles of BRV on synaptic plasticity in the TLE model. RESULTS: An increased level of SV2A accompanied by a depressed LTP in the hippocampus was shown in epileptic rats. Furthermore, BRV treatment continued for more than 30 days improved the over-expression of SV2A and reversed the synaptic dysfunction in epileptic rats. Additionally, BRV treatment alleviates the abnormal SNAP-25 phosphorylation at Ser187 during LTP induction in epileptic ones, which is relevant to the modulation of synaptic vesicles exocytosis and voltagegated calcium channels. CONCLUSION: BRV treatment ameliorated the over-expression of SV2A in the hippocampus and rescued the synaptic dysfunction in epileptic rats. These results identify the neuroprotective effect of BRV on TLE model.