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Tuesday, June 28, 2022 2:46:54 PM
Maybe now there is more we can do:
https://clinicaltrials.gov/ct2/show/NCT04772547?cond=VIGABATRIN&draw=2&rank=1
Detailed Description:
This pilot trial aims to demonstrate the feasibility of enteral administration of a single load of vigabatrin within targeted 48 hours of post-anoxic status epilepticus onset in unconscious survivors of cardiac arrest undergoing targeted temperature management. The load of VGB is in addition to the load of a commonly used intravenous second-line therapy given at the discretion of the treating neurologist. Serial blood tests will be obtained, including vigabatrin levels, taurine levels, neuron specific enolase, light chain neurofilament, and glial fibrillary acidic protein. In survivors that regain consciousness and survive to follow up, 6 months visual field perimetry will be obtained.
Study Type : Interventional (Clinical Trial)
Estimated Enrollment : 12 participants
Official Title: VIGABatrin in Post-anoxic STATus Epilepticus - Phase IIa
Actual Study Start Date : September 22, 2021
Estimated Primary Completion Date : May 31, 2022
Estimated Study Completion Date : December 31, 2022
https://neurolrespract.biomedcentral.com/articles/10.1186/s42466-022-00168-x
During the course of status epilepticus, there is marked alteration of gamma-aminobutyric acid (GABA) metabolism; the rate of GABA synthesis decreases GABA turnover time increases up to 3-fold [7], and cell surface GABA receptors migrate to the intracellular space [8]. Conventional first-line therapy acts by enhancing the GABAA receptor to increase its inhibitory tone. Vigabatrin, 4-amino-5-hexenoic acid or gamma-vinyl GABA, is a structural analog of GABA and irreversibly inhibits GABA-transaminase—the enzyme responsible for GABA catabolism, thereby increasing brain levels of GABA (Fig. 1) [9]. Vigabatrin may also stimulate GABA release [10]. The net effect is a significant elevation in GABA levels in nerve terminals, which facilitates GABA-mediated synaptic transmissions and leads to a marked and sustained antiseizure effect. The efficacy of vigabatrin as an adjunctive therapy for intractable focal epilepsy is well-established in the literature [11]. Vigabatrin may also potentiate the therapeutic effects of GABA-ergic anesthetics and other antiseizure medications [12] that are commonly used in the post-cardiac arrest period for either sedation, seizure control or symptomatic control of myoclonus (e.g., propofol, midazolam, and valproate). In addition to its antiseizure effect, vigabatrin may also mitigate ischemic-reperfusion injury by restoring the balance between GABA and glutamate transmissions [13].
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