French, JA;
Koepp, M;
Naegelin, Y;
Vigevano, F;
Auvin, S;
Rho, JM;
Rosenberg, E;
... Dichter, MA; + view all
(2017)
Clinical studies and anti-inflammatory mechanisms of treatments.
Epilepsia
, 58
pp. 69-82.
10.1111/epi.13779.
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Abstract
In this exciting era, we are coming closer and closer to bringing an anti‐inflammatory therapy to the clinic for the purpose of seizure prevention, modification, and/or suppression. At present, it is unclear what this approach might entail, and what form it will take. Irrespective of the therapy that ultimately reaches the clinic, there will be some commonalities with regard to clinical trials. A number of animal models have now been used to identify inflammation as a major underlying mechanism of both chronic seizures and the epileptogenic process. These models have demonstrated that specific anti‐inflammatory treatments can be effective at both suppressing chronic seizures and interfering with the process of epileptogenesis. Some of these have already been evaluated in early phase clinical trials. It can be expected that there will soon be more clinical trials of both “conventional, broad spectrum” anti‐inflammatory agents and novel new approaches to utilizing specific anti‐inflammatory therapies with drugs or other therapeutic interventions. A summary of some of those approaches appears below, as well as a discussion of the issues facing clinical trials in this new domain.
Type: | Article |
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Title: | Clinical studies and anti-inflammatory mechanisms of treatments |
Open access status: | An open access version is available from UCL Discovery |
DOI: | 10.1111/epi.13779 |
Publisher version: | https://doi.org/10.1111/epi.13779 |
Language: | English |
Additional information: | This version is the author accepted manuscript. For information on re-use, please refer to the publisher’s terms and conditions. |
Keywords: | Science & Technology, Life Sciences & Biomedicine, Clinical Neurology, Neurosciences & Neurology, Antiepileptogenesis, Ketogenic diet, Fingolimod, Endocannabinoid system, Vagus nerve stimulation., GLUTAMIC-ACID DECARBOXYLASE, NMDA RECEPTOR ENCEPHALITIS, TEMPORAL-LOBE EPILEPSY, FACIOBRACHIAL DYSTONIC SEIZURES, CHANNEL COMPLEX ANTIBODIES, CENTRAL-NERVOUS-SYSTEM, LIMBIC ENCEPHALITIS, AUTOIMMUNE ENCEPHALITIS, STATUS EPILEPTICUS, CASE SERIES |
UCL classification: | UCL UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences > UCL Queen Square Institute of Neurology UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Brain Sciences > UCL Queen Square Institute of Neurology > Clinical and Experimental Epilepsy |
URI: | https://discovery.ucl.ac.uk/id/eprint/10055848 |
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