Stereoisomers of the monoterpene epoxycarvone (EC), namely (+)-cis-EC, (−)-cis-EC, (+)-trans-EC, and (−)-trans-EC, were comparatively evaluated for anticonvulsant activity in specific methodologies. In the pentylenetetrazole (PTZ)-induced anticonvulsant test, all of the stereoisomers (at 300 mg/kg) increased the latency to seizure onset, and afforded 100% protection against the death of the animals. In the maximal electroshock-induced seizures (MES) test, prevention of tonic seizures was also verified for all of the isomers tested. However, the isomeric forms (+) and (−)-trans-EC showed 25% and 12.5% inhibition of convulsions, respectively. In the pilocarpine-induced seizures test, all stereoisomers demonstrated an anticonvulsant profile, yet the stereoisomers (+) and (−)-trans-EC (at 300 mg/kg) showed a more pronounced effect. A strychnine-induced anticonvulsant test was performed, and none of the stereoisomers significantly increased the latency to onset of convulsions; the stereoisomers probably do not act in this pathway. However, the stereoisomers (+)-cis-EC and (+)-trans-EC greatly increased the latency to death of the animals, thus presenting some protection. The four EC stereoisomers show promise for anticonvulsant activity, an effect emphasized in the isomers (+)-cis-EC, (+)-trans-EC, and (−)-trans-EC for certain parameters of the tested methodologies. These results serve as support for further research and development of antiepileptic drugs from monoterpenes.

Imidazolidine derivatives, or hydantoins, are synthetic compounds with different therapeutic applications. Many imidazolidine derivatives have psychopharmacological properties, such as phenytoin, famous for its anticonvulsant efficacy, but also effective in the treatment of neuropathic pain. The hydantoin, 3-phenyl-5-(4-ethylphenyl)-imidazolidine-2,4-dione (IM-3), synthesized from the amino acid, glycine, was selected for psychopharmacological studies in mice on the basis of its chemical and structural similarity with phenytoin. The first step of this study was to define the LD₅₀, which determined the doses of 50, 100 and 200 mg/kg for subsequent tests. The results obtained from the behavioral screening indicated that IM-3 produces decreased ambulation and analgesia in mice. Motor coordination and anxiety behavior were not affected by treatment with IM-3, as observed in the rotarod and elevated plus-maze tests, respectively. Regarding its antinociceptive properties, IM-3 showed efficacy in the acetic acid-induced writhing test by increasing the latency of the first writhe and reducing the number of writhes, as well as reducing the paw licking time in the second phase of the formalin test. The behavior of treated animals exposed to the hot plate test, however, did not differ from that of the control group. These data suggest that IM-3 has antinociceptive effects in mice, which is probably mediated by anti-inflammatory mechanisms.

Dificuldades na socialização e comunicação, em consonância com comportamentos repetitivos e estereotipados são características básicas para o diagnóstico autista. As bases fisiopatológicas de sua etiologia compreendem uma gama de fatores neurobiológicos comuns à outras patologias como a epilepsia. Devido à farmacorresistência, alternativas terapêuticas não convencionais estão em ascensão, das quais o CBD (canabidiol), fitocanabinóide extraído da Cannabis sativa, apresenta-se como forte candidato à terapêutica de pacientes epilépticos e com Perturbações do Espectro Autista (PEA). Pretendeu-se demonstrar as correlações fisiopatológicas entre o autismo e a epilepsia, atreladas à possibilidade de tratamento com o CBD. Realizou-se uma pesquisa nas bases de dados PubMed, ScieLo e ScienceDirect, observando os critérios de inclusão e exclusão: escolha do tema e categorização dos estudos, incluindo artigos em: inglês, português e espanhol, publicados entre os anos de 2012 a 2019, utilizando estratégias de busca com os seguintes descritores: autism and epilepsy, autism and cannabidiol e autism and treatment. Conclui-se que alterações genéticas e neuroquímicas estão fortemente ligadas às similaridades fisiopatológicas entre as PEA e epilepsia, visto que mutações em genes codificadores de receptores e neurotransmissores responsáveis pelas sinapses, contribuem para problemas no neurodesenvolvimento e disfunções na comunicação neuronal, ocasionando quadros clínicos comuns à essas neuropatologias.