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Tuesday, 06/28/2022 2:46:54 PM

Tuesday, June 28, 2022 2:46:54 PM

Post# of 401757
I have never prescribed vigabatrin. As an internist, it is not in my wheelhouse. I am pleased that it is a drug where the clinical use seems to be expanding, as opposed to many of our older generics with very narrow and steadily decreasing indications. I was also excited to see it is in clinical trials for use in early anoxic brain injury following cardiac arrest. I recall a case as an intern at UPMC where the patient was flown in by helicopter after a cardiac arrest, and I wonder how this drug might have changed the outcome. The patient had been resuscitated in the field and eventually made it to us. She had already been to the cath lab by the time she was admitted to me. Her coronary obstruction was completely relieved by angioplasty. Her initial heart problem was fixed, but she had been down too long. The CCU was full, and so she was admitted to some weird old 4-bed overflow ICU in some strange, dark sub-basement. I just stayed there all morning because I was worried I wouldn't be able to find it again in a hurry. She got to the unit around 2:30am and proceeded to alternate between grand mal seizures and v-tach arrest. We all knew it was hopeless, but her family was driving in from rural PA or WV or somewhere. We coded her multiple times, and she continued to seize despite every known intervention. The family arrived a few hours after she did. She had teenage kids. I sat them down and told them what they were about to see, which wasn't pretty. They were able to say goodbye. One of the critical care fellows took over the case from there, and I still had a full day of post-call work to do before I could think about getting some rest.

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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