scholarly journals Dysfunctional Brain Networking among Autonomic Regulatory Structures in Temporal Lobe Epilepsy Patients at High Risk of Sudden Unexpected Death in Epilepsy

2017 ◽  
Vol 8 ◽  
Author(s):  
Luke A. Allen ◽  
Ronald M. Harper ◽  
Rajesh Kumar ◽  
Maxime Guye ◽  
Jennifer A Ogren ◽  
...  
2019 ◽  
Vol 121 (1) ◽  
pp. 177-187 ◽  
Author(s):  
Isabel D. Derera ◽  
Katalin Cs. Smith ◽  
Bret N. Smith

Sudden unexpected death in epilepsy (SUDEP) is among the leading causes of death in people with epilepsy. Individuals with temporal lobe epilepsy (TLE) have a high risk for SUDEP because the seizures are often medically intractable. Neurons in the nucleus tractus solitarii (NTS) have been implicated in mouse models of SUDEP and play a critical role in modulating cardiorespiratory and autonomic output. Increased neuronal excitability of inhibitory, GABAergic neurons in the NTS develops during epileptogenesis, and NTS dysfunction has been implicated in mouse models of SUDEP. In this study we used the pilocarpine-induced status epilepticus model of TLE (i.e., pilo-SE mice) to investigate the A-type voltage-gated K+ channel as a potential contributor to increased excitability in GABAergic NTS neurons during epileptogenesis. Compared with age-matched control mice, pilo-SE mice displayed an increase in spontaneous action potential frequency and half-width 9–12 wk after treatment. Activity of GABAergic NTS neurons from pilo-SE mice showed less sensitivity to 4-aminopyridine. Correspondingly, reduced A-type K+ current amplitude was detected in these neurons, with no change in activation or inactivation kinetics. No changes were observed in Kv4.1, Kv4.2, Kv4.3, KChIP1, KChIP3, or KChIP4 mRNA expression. These changes contribute to the increased excitability in GABAergic NTS neurons that develops in TLE and may provide insight into potential mechanisms contributing to the increased risk for cardiorespiratory collapse and SUDEP in this model. NEW & NOTEWORTHY Sudden unexpected death in epilepsy (SUDEP) is a leading cause of death in epilepsy, and dysfunction in central autonomic neurons may play a role. In a mouse model of acquired epilepsy, GABAergic neurons in the nucleus tractus solitarii developed a reduced amplitude of the A-type current, which contributes to the increased excitability seen in these neurons during epileptogenesis. Neuronal excitability changes in inhibitory central vagal circuitry may increase the risk for cardiorespiratory collapse and SUDEP.


1995 ◽  
Vol 53 (3b) ◽  
pp. 619-624 ◽  
Author(s):  
L.M. Li ◽  
J. Roche ◽  
J.W.A.S. Sander

Changes in cardiac rhythm may occur during epileptic seizures and this has been suggested as a possible mechanism for sudden unexpected death amongst patients with chronic epilepsy (SUDEP). We have studied ECG changes during 61 complex partial seizures of temporal lobe origin in 20 patients. Tachycardia was observed in 24/61 (39%) and bradycardia in 3/61 (5%). The mean and median tachycardia rate was 139 and 140 beats/min (range 120-180). The longest R-R interval observed was 9 seconds. No difference was found in regard to the lateralisation of seizures and cardiac arrhytmia. One of the patients with bradycardia was fitted with a demand cardiac pacemaker, which appeared to decrease the number of his falls. In conclusion, ictal cardiac changes which may be seen in temporal lobe epilepsy (TLE) are sinus tachycardia and occasionally sinus bradycardia. Patients presenting vague complains suggestive of either TLE or cardiac dysrhythmia, simultaneous monitoring with EEG/ECG is required, and if the episodes are frequent, video-EEG should be considered. Further studies on this subject are warranted as this may shed some light on possible mechanisms for SUDEP.


2017 ◽  
Vol 72 ◽  
pp. 208-209 ◽  
Author(s):  
M. Trivisano ◽  
M. Bellusci ◽  
A. Terracciano ◽  
L. De Palma ◽  
N. Pietrafusa ◽  
...  

2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Rokia Ghchime ◽  
Halima Benjelloun ◽  
Hajar Kiai ◽  
Halima Belaidi ◽  
Fatiha Lahjouji ◽  
...  

It is well established that the temporal lobe epilepsy (TLE) is linked to the autonomic nervous system dysfunctions. Seizures alter the function of different systems such as the respiratory, cardiovascular, gastrointestinal, and urogenital systems. The aim of this work was to evaluate the possible factors which may be involved in interictal cardiovascular autonomic function in temporal lobe epilepsy with complex partial seizures, and with particular attention to hippocampal sclerosis. The study was conducted in 30 patients with intractable temporal lobe epilepsy (19 with left hippocampal sclerosis, 11 with right hippocampal sclerosis). All subjects underwent four tests of cardiac autonomic function: heart rate changes in response to deep breathing, heart rate, and blood pressure variations throughout resting activity and during hand grip, mental stress, and orthostatic tests. Our results show that the right cerebral hemisphere predominantly modulates sympathetic activity, while the left cerebral hemisphere mainly modulates parasympathetic activity, which mediated tachycardia and excessive bradycardia counterregulation, both of which might be involved as a mechanism of sudden unexpected death in epilepsy patients (SUDEP).


Circulation ◽  
2011 ◽  
Vol 123 (23) ◽  
pp. 2674-2680 ◽  
Author(s):  
Siqin Ye ◽  
Matthew Grunnert ◽  
Jens Jakob Thune ◽  
Kent M. Stephenson ◽  
Hajime Uno ◽  
...  

Author(s):  
Rady Yousif ◽  
M. Ossama Abdulghani ◽  
A. Gaber ◽  
Naglaa El Khayat ◽  
Y. A. Abo Elnaga ◽  
...  

Abstract Background Available data from witnessed and monitored sudden unexpected death in epilepsy (SUDEP) cases postulate that ictal central apnea (ICA) and ictal arrhythmias are the main causes of SUDEP. ICA is a frequent semiological feature of focal epilepsy and occasionally the only clinical manifestation of focal seizures. The aim of this study was to assess the frequency of ICA and cardiac arrhythmias in epileptic patients and to study the risk factors and predictors of their occurrence. Methods Fifty patients diagnosed with epilepsy were recruited in this study. All participants underwent prolonged surface video electroencephalography (VEEG) study using the 10-20 international electrode system with concomitant polysomnography including electrocardiography (ECG), heart rate monitoring, and peripheral capillary oxygen saturation (SpO2) using pulse oximetry. Also inductance plethysmography was used to record chest and abdominal excursions. Results Complete datasets were available in 50 patients and 112 seizures were recorded. ICA occurred exclusively in focal epilepsy (P <0.001). Temporal lobe epilepsy was associated with higher occurrence of ICA in comparison to extratemporal epilepsy (P <0.001). In addition, seizures lateralized to the left hemisphere were associated with higher occurrence of ICA (P <0.001). On the other side, tachycardia was found to be more associated with temporal lobe epilepsy and left hemispheric seizure onset (P <0.001). Conclusion ICA occurred exclusively in focal seizures and tachycardia magnitude was more with focal seizures, and both had higher percentage in temporal lobe epilepsy in comparison to other types and in seizures with left hemispheric onset.


2018 ◽  
Vol 10 (3) ◽  
pp. 63-70
Author(s):  
E. D. Belousova ◽  
M. A. Shkolnikova

It is well known that sudden unexpected death in epilepsy (SUDEP) is one of the most significant factors of mortality in epileptic patients. There is an increased risk of SUDEP in genetic epileptic encephalopathies (EE), partly because those syndromes are associated with mutations in the “neurocardiac” genes, which have been implicated in both epilepsy and cardiac arrhythmias. In these clinical conditions, functions of ion selective channels (sodium, potassium and etc.) are affected; for example, in children with Dravet syndrome, the risk of SUDEP is 40 times higher than that in children with common epilepsy syndromes. In a murine model of SCN1A epilepsy, a prolongation of QT interval coincided with a seizure; in addition, an excessive excitability of cultured cardiomyocytes was demonstrated. A high risk of SUDEP is characteristic for EE caused by mutation in the SCN8A gene. Other prognostic biomarkers of SUDEP may include mutations in sodium channel genes, such as SCN4A, SCN10A, and SCN11A. Our knowledge about SUDEP associated with potassium channel dysfunctions is still very limited. There are likely some mutations in other genes, that can modify (increase or decrease) the risk of SUDEP in EE. If patients with genetic EE are indeed at a high risk for SUDEP, they must be followed up by cardiologists alongside with neurologists. Provided this hypothesis is proved, any newly diagnosed arrhythmia should be carefully monitored and treated (with medications and/or interventions), in order to improve the survival rate in genetic EE.


2021 ◽  
Vol 9 ◽  
Author(s):  
Floortje Kanits ◽  
Monique P. L'Hoir ◽  
Magda M. Boere-Boonekamp ◽  
Adèle C. Engelberts ◽  
Edith J. M. Feskens

Background: The incidence of Sudden Unexpected Death in Infancy (SUDI) is low in the Netherlands, with an incidence rate of 0.18 per 1,000 live births. Therefore, prevention advice may receive less attention, potentially leading to increasing incidence rates. It is currently unknown whether the risks for SUDI changed in the Netherlands, and if other risk factors might be present. The aim of this study was to examine the current risks and preventive factors for SUDI in Dutch infants, in order to determine if it is necessary to adapt the prevention advice toward the current needs.Methods: A case-control study was conducted comparing SUDI cases aged &lt;12 months from 2014–2020 in the Netherlands (n = 47), to a Dutch national survey control group from 2017 including infants &lt;12 months of age (n = 1,192).Results: Elevated risks for several well-known factors were observed, namely: duvet use (aOR = 8.6), mother smoked during pregnancy (aOR = 9.7), or after pregnancy (aOR = 5.4) and the prone sleeping position (aOR = 4.6). Reduced risks were observed for the well-known factors: room-sharing (aOR = 0.3), sleep sack use (aOR = 0.3), breastfeeding (aOR = 0.3), and the use of a pacifier (aOR = 0.4). For infants &lt;4 months, the risk for SUDI was higher when bed-sharing (aOR = 3.3), and lower when room-sharing (aOR = 0.2) compared to older infants. For older infants, the sleep sack was found to be more protective (aOR = 0.2). A high risk for SUDI when bed-sharing was found when mother smoked, smoked during pregnancy, or if the infant did not receive any breastfeeding (respectively aOR = 17.7, aOR = 10.8, aOR = 9.2).Conclusions: Internationally known factors related to the sudden unexpected death of infants were also found in this study. Relatively new findings are related to specific groups of infants, in which the strengths of these risk factors differed. In a low-incidence country like the Netherlands, renewed attention to the current prevention advice is needed. Furthermore, additional attention for prevention measures in low educated groups, and additional advice specifically targeting high-risk groups is recommended.


2020 ◽  
Author(s):  
Dominique F. Leitner ◽  
James D. Mills ◽  
Geoffrey Pires ◽  
Arline Faustin ◽  
Eleanor Drummond ◽  
...  

AbstractSudden unexpected death in epilepsy (SUDEP) is the leading type of epilepsy-related death. Severely depressed brain activity in these cases may impair respiration, arousal, and protective reflexes, occurring as a prolonged postictal generalized EEG suppression (PGES) and resulting in a high-risk for SUDEP. In autopsy hippocampus and cortex, we observed no proteomic differences between SUDEP and epilepsy cases, contrasting our previously reported robust differences between epilepsy and controls. Transcriptomics in hippocampus and cortex from surgical epilepsy cases segregated by PGES identified 55 differentially expressed genes (37 protein-coding, 15 lncRNAs, three pending) in hippocampus. Overall, the SUDEP proteome and high-risk SUDEP transcriptome largely reflected other epilepsy cases in the brain regions analyzed, consistent with diverse epilepsy syndromes and comorbidities associated with SUDEP. Thus, studies with larger cohorts and different epilepsy syndromes, as well as additional anatomic regions may identify molecular mechanisms of SUDEP.


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