scholarly journals The ups and downs of alkyl‐carbamates in epilepsy therapy: How does cenobamate differ?

Epilepsia ◽  
2021 ◽  
Author(s):  
Wolfgang Löscher ◽  
Graeme J. Sills ◽  
H. Steve White
Keyword(s):  
Epilepsia ◽  
2002 ◽  
Vol 43 (4) ◽  
pp. 365-385 ◽  
Author(s):  
Philip N. Patsalos ◽  
Walter Fröscher ◽  
Francesco Pisani ◽  
Clementina M. Van Rijn

2019 ◽  
Vol 20 (3) ◽  
pp. 577 ◽  
Author(s):  
Helmut Kubista ◽  
Stefan Boehm ◽  
Matej Hotka

Paroxysmal depolarization shifts (PDS) have been described by epileptologists for the first time several decades ago, but controversy still exists to date regarding their role in epilepsy. In addition to the initial view of a lack of such a role, seemingly opposing hypotheses on epileptogenic and anti-ictogenic effects of PDS have emerged. Hence, PDS may provide novel targets for epilepsy therapy. Evidence for the roles of PDS has often been obtained from investigations of the multi-unit correlate of PDS, an electrographic spike termed “interictal” because of its occurrence during seizure-free periods of epilepsy patients. Meanwhile, interictal spikes have been found to be associated with neuronal diseases other than epilepsy, e.g., Alzheimer’s disease, which may indicate a broader implication of PDS in neuropathologies. In this article, we give an introduction to PDS and review evidence that links PDS to pro- as well as anti-epileptic mechanisms, and to other types of neuronal dysfunction. The perturbation of neuronal membrane voltage and of intracellular Ca2+ that comes with PDS offers many conceivable pathomechanisms of neuronal dysfunction. Out of these, the operation of L-type voltage-gated calcium channels, which play a major role in coupling excitation to long-lasting neuronal changes, is addressed in detail.


2011 ◽  
Vol 51 (11) ◽  
pp. 997-999
Author(s):  
Hiroshi Shigeto
Keyword(s):  

2015 ◽  
Vol 10 (2) ◽  
pp. 164
Author(s):  
Mar Carreño ◽  
Eugen Trinka ◽  
Martin Holtkamp ◽  
◽  
◽  
...  

There is now an extensive range of anti-epileptic drugs (AEDs) available including older established treatments and a newer generation of medications. The choice of drugs and what constitutes optimal therapy, however, is unclear due to limitations in the data supporting their use, particularly among the newer treatments. In clinical trials of monotherapy, a treatment is required to show only non-inferiority to another benchmark treatment. In trials of polytherapy, comparisons are limited to placebo. It is therefore necessary to look beyond the study data and consider other parameters to ascertain the most suitable treatment for the individual patient. Available evidence suggests that efficacy is similar among most AEDs, but this does not mean they are all the same. Some show efficacy in early and refractory epilepsy and some improve depression and quality of life (QOL) in epilepsy. AEDs are associated with a range of adverse events (AEs) that can limit their usefulness. AE classifications include type A (augmented and dose related) including tiredness, fatigue, insomnia, dizziness, vertigo, imbalance, ataxia, tremor and cognitive impairment; type B (bizarre and idiosyncratic) including various hypersensitivity reactions; type C (chronic long-term toxicity) including hirsutism, alopecia, weight gain and obesity; and type D (teratogenesis and carcinogenesis). The newer AEDs have been more thoroughly assessed for AEs than older drugs and risks are better understood. In AED safety, it is not better to follow a policy of ‘better the devil you know’ but rather to carefully monitor AE incidence and be prepared to switch drugs to improve tolerability and avoid non-compliance and treatment failure.


2014 ◽  
Vol 34 ◽  
pp. 25-28
Author(s):  
Octavian V. Lie ◽  
Jose E. Cavazos
Keyword(s):  

2015 ◽  
Vol 264 ◽  
pp. 150-162 ◽  
Author(s):  
Clifford L. Eastman ◽  
Jason S. Fender ◽  
Nancy R. Temkin ◽  
Raimondo D'Ambrosio

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