<![CDATA[Febrile seizures are the result of complex interactions between multiple molecular components in the child's central nervous system, including changes in neurotransmitters, neuronal activity, and the brain's inflammatory response. When a child has a fever, there is an increase in body temperature, which triggers a series of molecular changes in the brain, affecting electrical signaling pathways and triggering characteristic seizures. The literature search process was carried out on various databases (PubMed, Web of Sciences, EMBASE, Cochrane Libraries, and Google Scholar) regarding studies of molecular aspects of febrile seizures. This study follows the preferred reporting items for systematic reviews and meta-analysis (PRISMA) recommendations. An increase in body temperature (fever) is the main trigger for febrile seizures. Fever can result in changes in brain chemistry, including changes in neurotransmitters and inflammatory responses, which can affect the molecular pathways that trigger seizures. Glutamate is the main neurotransmitter that plays a role in triggering seizures. Increased glutamate release during fever can trigger excessive activity in neurons. On the other hand, GABA, a neurotransmitter that plays a role in dampening neuronal activity, may also be involved, and an imbalance between glutamate and GABA may occur during seizures. Genetic factors play a role in susceptibility to febrile seizures. Several genes, such as SCN1A and GABRG2, have been identified as potentially increasing the risk of febrile seizures, especially those of a complex nature. Febrile seizures usually do not cause permanent changes in brain structure. However, in some very rare cases, such as EASIFE, temporary changes in brain structure may occur.]]>
