Expert opinion on diagnosis and management of epilepsy‐associated comorbidities

Peltola, Jukka; Surges, Rainer; Voges, Berthold; von Oertzen, Tim J.

doi:10.1002/epi4.12851

Cited by 6 publications

(1 citation statement)

References 115 publications

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“…VNS has demonstrated efficacy for seizure control in randomized controlled trials ( 1 , 2 ), long-term extension studies ( 3 , 4 ) and real-world follow-up studies ( 5 , 6 ). Recently, there has been increasing interest in the effects of VNS on cognition since cognitive impairment is a common comorbidity in both DRE ( 7 ) and depression ( 8 ). Working memory performance and executive functions are particularly impaired in patients with epilepsy ( 9 – 11 ).…”

Section: Introductionmentioning

confidence: 99%

Complex executive functions assessed by the trail making test (TMT) part B improve more than those assessed by the TMT part A or digit span backward task during vagus nerve stimulation in patients with drug-resistant epilepsy

Lähde,

Basnyat,

Raitanen

et al. 2024

Front. Psychiatry

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IntroductionThere is a paucity of clinical studies examining the long-term effects of vagus nerve stimulation (VNS) on cognition, although a recent study of patients with drug-resistant epilepsy (DRE) treated with VNS therapy demonstrated significant improvement in executive functions as measured by the EpiTrack composite score. The present study aimed to investigate performance variability in three cognitive tests assessing executive functions and working memory in a cohort of DRE patients receiving VNS therapy during a follow-up duration of up to 5 years.MethodsThe study included 46 DRE patients who were assessed with the Trail Making Test (TMT) (Parts A and B) and Digit Span Backward (DB) task prior to VNS implantation, 6 months and 12 months after implantation, and yearly thereafter as a part of the clinical VNS protocol. A linear mixed-effects (LME) model was used to analyze changes in test z scores over time, accounting for variations in follow-up duration when predicting changes over 5 years. Additionally, we conducted descriptive analyses to illustrate individual changes.ResultsOn average, TMT-A z scores improved by 0.024 units (95% confidence interval (CI): 0.006 to 0.042, p = 0.009), TMT-B z scores by 0.034 units (95% CI: 0.012 to 0.057, p = 0.003), and DB z scores by 0.019 units per month (95% CI: 0.011 to 0.028, p < 0.001). Patients with psychiatric comorbidities achieved the greatest improvements in TMT-B and DB z scores among all groups (0.0058 units/month, p = 0.036 and 0.028 units/month, p = 0.003, respectively). TMT-A z scores improved the most in patients taking 1–2 ASMs as well as in patients with psychiatric comorbidities (0.042 units/month, p = 0.002 and p = 0.003, respectively).ConclusionPerformance in all three tests improved at the group level during the follow-up period, with the most robust improvement observed in TMT-B, which requires inhibition control and set-switching in addition to the visuoperceptual processing speed that is crucial in TMT-A and working-memory performance that is essential in DB. Moreover, the improvement in TMT-B was further enhanced if the patient had psychiatric comorbidities.

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Section: Introductionmentioning

confidence: 99%

Complex executive functions assessed by the trail making test (TMT) part B improve more than those assessed by the TMT part A or digit span backward task during vagus nerve stimulation in patients with drug-resistant epilepsy

Lähde,

Basnyat,

Raitanen

et al. 2024

Front. Psychiatry

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The sphingosine‐1‐phosphate signaling pathway (sphingosine‐1‐phosphate and its receptor, sphingosine kinase) and epilepsy

Wang,

Kong,

Leng

et al. 2024

Epilepsia Open

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Epilepsy is one of the common chronic neurological diseases, affecting more than 70 million people worldwide. The brains of people with epilepsy exhibit a pathological and persistent propensity for recurrent seizures. Epilepsy often coexists with cardiovascular disease, cognitive dysfunction, depression, etc., which seriously affects the patient's quality of life. Although our understanding of epilepsy has advanced, the pathophysiological mechanisms leading to epileptogenesis, drug resistance, and associated comorbidities remain largely unknown. The use of newer antiepileptic drugs has increased, but this has not improved overall outcomes. We need to deeply study the pathogenesis of epilepsy and find drugs that can not only prevent the epileptogenesis and interfere with the process of epileptogenesis but also treat epilepsy comorbidities. Sphingosine‐1‐phosphate (S1P) is an important lipid molecule. It not only forms the basis of cell membranes but is also an important bioactive mediator. It can not only act as a second messenger in cells to activate downstream signaling pathways but can also exert biological effects by being secreted outside cells and binding to S1P receptors on the cell membrane. Fingolimod (FTY720) is the first S1P receptor modulator developed and approved for the treatment of multiple sclerosis. More and more studies have proven that the S1P signaling pathway is closely related to epilepsy, drug‐resistant epilepsy, epilepsy comorbidities, or other epilepsy‐causing diseases. However, there is much controversy over the role of certain natural molecules in the pathway and receptor modulators (such as FTY720) in epilepsy. Here, we summarize and analyze the role of the S1P signaling pathway in epilepsy, provide a basis for finding potential therapeutic targets and/or epileptogenic biomarkers, analyze the reasons for these controversies, and put forward our opinions.Plain Language SummaryThis article combines the latest research literature at home and abroad to review the sphingosine 1‐phosphate signaling pathway and epileptogenesis, drug‐resistant epilepsy, epilepsy comorbidities, other diseases that can cause epilepsy, as well as the sphingosine‐1‐phosphate signaling pathway regulators and epilepsy, with the expectation of providing a certain theoretical basis for finding potential epilepsy treatment targets and/or epileptogenic biomarkers in the sphingosine‐1‐phosphate signaling pathway.

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Epilepsie im Rhythmus der Nacht und im Zyklus des Schlafs

Voges

2024

Clin Epileptol

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Zusammenfassung Hintergrund Epilepsie unterliegt – unter anderem – dem Rhythmus von Tag und Nacht und dem Zyklus der verschiedenen Schlafstadien. Ausprägung und Schweregrad einer Epilepsie werden mit beeinflusst von der Schlafqualität und -kontinuität des Patienten. Zielsetzung Es wird ein Überblick über die Interaktion von Schlaf und Epilepsie und über den daraus möglichen Nutzen für Diagnostik und Therapie gegeben. Methode Die Arbeit ist eine Übersichtsarbeit. Ergebnisse und Diskussion Verschiedene Arten epileptischer und nichtepileptischer Anfälle folgen einer spezifischen circadianen bzw. Wach-Schlaf-Rhythmik, was sich differenzialdiagnostisch nutzen lässt. Schlafentzug führt zu einer verstärkten Epilepsieaktivität, nicht zuletzt durch den vermehrten, aber instabilen Schlaf am Folgetag. Im NREM-Schlaf kommt es zu einer Häufung und zu einer größeren räumlichen Ausbreitung epilepsietypischer Potenziale (ETP) und darum zu einer erhöhten Wahrscheinlichkeit von Anfällen und Anfallsgeneralisierung. Der REM-Schlaf hingegen ist infolge von EEG(Elektroenzephalogramm)-Desynchronisation und -Amplitudenminderung sowie aufgrund einer REM(„rapid eye movement“)-spezifischen funktionellen Diskonnektion v. a. des Frontallappens anfallsprotektiv, dies sogar mehr als der Wachzustand. Gelingt es trotzdem, ETP oder Anfälle im REM-Schlaf zu erfassen, so lässt sich aufgrund der im REM geringen ETP-Propagationstendenz aus diesen Daten oft eine wertvolle lokalisatorische Aussage zur Seizure-Onset-Zone ableiten. Anfälle im Schlaf und auch im Wachen, aber selbst schon das Auftreten interiktualer ETP im Schlaf verschlechtern die Schlafkontinuität, -struktur und -qualität. Dies kann die Ursache für affektive und kognitiv-mnestische Störungen im täglichen Leben der Patienten sein. Schlaffragmentierung und -mangel haben aber auch prokonvulsive Potenz und können somit zu einer weiteren Anfallsverschlechterung führen, was ihrerseits die Schlafqualität weiter beeinträchtigt. Dieser Teufelskreis wird noch befeuert durch das Bestehen von komorbiden schlafmedizinischen Erkrankungen oder schlafstörenden Nebenwirkungen der Antianfallstherapien. Werden solche Zusammenhänge erkannt und behandelt, dann bestehen mit einer Ausrichtung an seinen individuellen chronobio- und somnologischen Bedingungen gute Aussichten, einen bisher therapierefraktären Patienten zu einem „Responder“ zu transformieren.

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Expert opinion on diagnosis and management of epilepsy‐associated comorbidities

Cited by 6 publications

References 115 publications

Complex executive functions assessed by the trail making test (TMT) part B improve more than those assessed by the TMT part A or digit span backward task during vagus nerve stimulation in patients with drug-resistant epilepsy

Complex executive functions assessed by the trail making test (TMT) part B improve more than those assessed by the TMT part A or digit span backward task during vagus nerve stimulation in patients with drug-resistant epilepsy

The sphingosine‐1‐phosphate signaling pathway (sphingosine‐1‐phosphate and its receptor, sphingosine kinase) and epilepsy

Epilepsie im Rhythmus der Nacht und im Zyklus des Schlafs

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