ObjectiveImpaired breathing during and following seizures is an important cause of sudden unexpected death in epilepsy (SUDEP), but the network mechanisms by which seizures impair breathing have not been thoroughly investigated. Progress would be greatly facilitated by a model in which breathing could be investigated during seizures in a controlled setting. MethodRecent work with an acute Long-Evans rat model of limbic seizures has demonstrated that depression of brainstem arousal systems may be critical for impaired consciousness during and after seizures. We now utilize the same rat model to investigate breathing during partial seizures with secondary generalization. ResultBreathing is markedly impaired during seizures(P < 0.05;n=21), and that the severity of breathing impairment is strongly correlated with the extent of seizure propagation (Pearson R=-0.73;P < 0.001;n=30). ConclusionSeizure propagation could increase the severity of breathing impairment caused by seizures. Based on these results, we suggest that this animal model would help us to improve understanding of pathways involved in impairment of breathing caused by seizures and this is an important initial step in addressing this significant cause of SUDEP in people living with epilepsy.
ObjectiveSeizure-related respiratory or cardiac dysfunction was once thought to be the direct cause of sudden unexpected death in epilepsy (SUDEP), but both may be secondary to postictal cerebral inhibition. An important issue that has not been explored to date is the neural network basis of cerebral inhibition. Our aim was to investigate the features of neural networks in patients at high risk for SUDEP using a blood oxygen level-dependent (BOLD) resting-state functional MRI (Rs-fMRI) technique. MethodsRs-fMRI data were recorded from 13 patients at high risk for SUDEP and 12 patients at low risk for SUDEP. The amplitude of low-frequency fluctuations (ALFF) values were compared between the two groups to decipt the regional brain activities. ResultsCompared with patients at low risk for SUDEP, patients at high risk exhibited significant ALFF reductions in the right superior frontal gyrus, the left superior orbital frontal gyrus, the left insula and the left thalamus; and ALFF increase in the right middle cigulum gyrus, the right supplementary motor area and the left thalamus. ConclusionsThese findings highlight the need to understand the fundamental neural network dysfunction in SUDEP, which may fill the missing link between seizure-related cardiorespiratory dysfunction and SUDEP, and provide a promising neuroimaging biomarker for risk prediction of SUDEP.
Objectives To investigate the changes of serum monoamine neurotransmitters and myocardial enzymes in patients with refractory epilepsy (RE), and the possible effects on the cardiovascular system, which would contribute to provide help and guidance to the early warming and prevention to the sudden unexpected death in epilepsy (SUDEP). Methods We collected sixty patients with RE who admitted to Neurological department of First Hospital of Jilin University from December 2015 to December 2016. According to the exclusion criteria, we selected thirty-two patients into the study. The study included 21 males and 11 females patients. Epinephrine (EPI), norepinephrine (NE), dopamine (DA), 5-hydroxytryptamine (5-HT), creatine kinase isoenzyme (CKMB), lactate dehydrogenase (LDH) and hydroxybutyrate dehydrogenase (HBDH) were measured in peri-ictal period and the interictal period in the patients. All the data were analyzed by SPSS17.0 statistical software. Results ① Thirty two patients were eligiblefor this study and the maleto female ratio is 21:11; The age ranged from 15 to 85 years old, with the average age of 50.9±17.6 years old. Twelve (37.5%) were older than 60 years old and 20 (62.5%) were under 60 years old. The epilepsy history ranged from 1 year to 14 years, with an average of 3.75±3.12 years; ② Comparing the levels of monoamine neurotransmitters in peri-ictal period and the interictal period in the patients with RE, we found that the level of EPI and LDH was significantly lower than that in interictal period, while the levels of NE and DA were significantly increased; ③ The results showed that EPI, NE and DA levels in patients under 60 were higher than over 60; ④ Patients were divided into four groups according to the etiology of the disease: idiopathic epilepsy group (10 cases, 31.25%), post-encephalitic epilepsy group (7 cases, 21.88%), post-stroke epilepsy group (9 cases, 28.12%) and epilepsy after brain injury group (6 cases, 18.75%). The results showed that the levels of EPI, NE and DA in the post-strokeepilepsy group were significantly lower than those in the other three groups. The level of CKMB in the idiopathic epilepsy group was higher than that in post-stroke epilepsy and epilepsy induced by brain injury patients. Conclusions RE patients have a higher level of serum NE and DA interictal period, suggesting that seizures may increase sympathetic nervous excitability. The patients under 60 years-old with RE release more catecholamines than young patients, suggesting that the latterwith intractable epilepsy may have higher sympathetic nerve excitability. And it may be associated with the higher incidence of SUDEP in young patients. Post-stroke epilepsyrelease less catecholamine than others, suggesting that the sympathetic nervous excitability is relatively low, and it may have relatively little damage to heart.