ObjectiveTo explore the clinical and video EEG features of patients with post-stroke epilepsy (PSE).MethodsThe clinical data of 68 patients with epilepsy after cerebral infarction and 33 patients with epilepsy after cerebral hemorrhage were analyzed retrospectively from January 2015 to June 2018 in the Affilated Hospital of Jining Medical University. There were 5 cases of early-onset epilepsy, and the rest were late-onset epilepsy. There were 68 cases of cerebral infarction (1 case showed post-infarction hemorrhagic transformation), 33 cases of cerebral hemorrhage; 51 females, 50 males (f∶m = 1.02∶1); the onset age was 45 ~ 101 years, with an average of (68.10 ± 10.26) years.ResultsThe time from seizure to stroke in 101 cases was (28.92 ± 35.61) months, 60 cases (59.40%) ≤ 1 year, 26 cases (25.74%) 1 ~ 5 years, and 15 cases (14.85%) 5 ~ 10 years. Post-stroke epilepsy had no relation to gender (P>0.05). The age of onset is mostly in 60 to 75 years old (62.38%). Seizure often happen within 1 year after stroke (59.4%). The type of attack is focal seizure (77.23%). Cortical infarction (77.94%), cerebral artery stenosis (83.82%), hypertension, diabetes, and atrial fibrillation are risk factors for epilepsy after infarction. The abnormal rate of EEG for PSE is 90.1%, which was manifested as slow wave in the lesion side, epileptic wave in the lesion side or contralateral side.ConclusionsThe location, duration, age and severity of cerebral artery stenosis in patients with PSE are closely related to the occurrence of seizure. VEEG plays an important role in the diagnosis, treatment and prognosis of epilepsy.
Epilepsy is a disorder of the brain in which sudden abnormal discharges of neurons cause transient dysfunction and is a common disorder of the nervous system. Although most patients experience remission of symptoms with medication, about 20 ~ 30% of patients still have poor outcomes with medication and progress to refractory epilepsy. The etiology of epilepsy is complex and the exact pathogenesis is not yet clear. Current research has explored the pathophysiological mechanisms underlying epileptogenesis, thus providing a basis for identifying potential therapeutic targets for epilepsy and advancing the precision treatment of epilepsy. p38 Mitogen-activated protein kinase (MAPK) signalling pathway is a conserved class of kinases involved in many physiological/pathological processes by regulating intracellular gene expression levels, cell division, differentiation and apoptosis in response to various extracellular stimuli in order to mediate intracellular signalling cascades. The p38 MAPK signalling pathway is one of the subfamilies of MAPK that mediates inflammatory responses, apoptosis, tissue edema and other biological processes involved in the development of central nervous system diseases. The p38 MAPK signalling pathway is now reviewed for its involvement in the development of epilepsy through unused pathways, in order to identify new potential targets for epilepsy treatment and provide clinical precision.
Epilepsy is a complex disease spectrum, because of long-term recurrent seizures and seriously affect the quality of life of patients, it is of great significance to explore the pathogenesis of epilepsy and actively seek new therapeutic targets. In this paper, the pathogenesis of epilepsy related to mitochondrial pathway was discussed from the aspects of energy depletion, oxidative stress damage, impaired calcium homeostasis, increased glutamic acid release, mitochondrial DNA mutation, Coenzyme Q10 deficiency, abnormal mitochondrial movement and change, and relevant therapeutic ideas were proposed. This paper shows that mitochondrial function affects the onset of epilepsy from various ways. Further understanding of the relationship between mitochondria and the onset of epilepsy is beneficial to find new therapeutic targets and develop new therapies beyond the control of epilepsy.
Epilepsy is one of the most common neurological disorders, and status epilepticus (SE) can lead to permanent neuronal brain damage in the central nervous system, but the mechanism is not clear. Solving this problem will help to find more SE therapeutic targets, benefiting tens of millions of epilepsy patients. The pathway of SE leading to neuronal damage in the brain has made new progress in neuroinflammation, autophagy, apoptosis and pyroptosis, glial cell hyperplasia and category transformation, and changes in neurotransmitters in the brain, which will be beneficial to the discovery of new targets for the treatment of SE, thus laying a foundation for the development of new anti-epileptic drugs.