Status epilepticus is a life-threatening neurological emergency with high mortality and disability rates. If not treated promptly and effectively, it can lead to severe brain damage or even death. Currently, diagnosis and prognosis assessment mainly rely on electroencephalogram (EEG) and clinical manifestations, which have delays and subjectivity. Therefore, the search for biomarkers that can rapidly, objectively, and accurately assist in the diagnosis, classification, treatment guidance, and prognosis judgment of status epilepticus has become a research hotspot. Biomarkers can reflect the occurrence and development process of the disease at the molecular level, bringing new hope for the precise diagnosis and treatment of status epilepticus. This review aims to systematically elaborate on potential biomarkers in the field of SE.
The pathological state of "epileptic heart" induced by epilepsy has shattered the perception that epilepsy is an isolated neurological disorder, reflecting the synergistic damage between chronic epilepsy and cardiac bioelectrical activity as well as mechanical function. Autonomic nervous system dysfunction is the core mediating link, which regulates the expression of myocardial ion channels and induces risks such as arrhythmias. In the long term, it also drives structural remodeling and functional impairment including left atrial enlargement and myocardial fibrosis. This kind of damage is influenced by factors such as classification of epilepsy, disease duration, and antiepileptic drugs—for instance, patients with drug resistant epilepsy or those on long-term polypharmacy suffer more significant damage. This article systematically reviews recent research progress, summarizes consensus and controversies, provides a basis for the precision management of cardiovascular risks in epilepsy patients, and contributes to reducing the incidence of SUDEP and improving long-term quality of life.
Currently, approximately one-third of epilepsy patients exhibit resistance to anti-seizure medications (Anti-seizure medications, ASMs), which can only alleviate symptoms, but cannot completely cure the condition. Consequently, the development of new ASMs from an understanding of epilepsy pathogenesis has emerged as an urgent social issue. The role of neuroinflammation in various neurological diseases has garnered significant attention as a popular research topic both domestically and internationally. Numerous studies have corroborated the involvement of neuroinflammation in the onset and progression of epilepsy. The biological target, Translocator protein 18 kDa (TSPO), is considered as a marker of neuroinflammation and is intricately involved in the entire neuroinflammatory response. Investigating the function of TSPO in epilepsy neuroinflammation can potentially uncover new treatment targets. At present, the exact mechanism of TSPO in epilepsy neuroinflammation remains unclear, thus necessitating a comprehensive summary and overview. This article reviewed the advancements made in TSPO research within the realm of neuroinflammation and its role in epileptic neuroinflammation, aiming to contribute novel insights for the identification of related targets and pathways for epilepsy treatment.