2-Deoxyglucose terminates pilocarpine-induced status epilepticus in neonatal rats.
Level 5 - mechanism / opinion, no new human data
Preclinical animal model study (neonatal rats)
PubMed 32558935 · doi:10.1111/epi.16583
What was done
Neonatal Sprague Dawley rats (postnatal days 10-17) were treated with pilocarpine (300 mg/kg, intraperitoneally) to induce status epilepticus (SE), monitored by video-electroencephalography (V-EEG). After 30 minutes of SE, rats were administered 2-deoxyglucose (2-DG; doses including 50, 100, and 500 mg/kg, plus lower unspecified doses), phenobarbital (30 mg/kg), levetiracetam (100 mg/kg), or saline. V-EEG was recorded for approximately 60 additional minutes to measure time to seizure cessation, EEG scores, and power spectra.
What was found
Administration of 2-DG at 50, 100, or 500 mg/kg stopped behavioral and electrographic seizures within 10-15 minutes, whereas lower doses required 25-30 minutes. Phenobarbital (30 mg/kg) and levetiracetam (100 mg/kg) also terminated SE within 10-15 minutes. The abstract did not report exact animal numbers (n), exact values for doses below 50 mg/kg, or numerical EEG score and power spectrum statistics.
Why it matters
Because up to 50% of neonatal status epilepticus cases resist conventional antiseizure medications, this study identifies acute glycolytic inhibition as a potential alternative metabolic target for terminating refractory neonatal seizures.
Limits
Findings are limited to an acute chemically induced rodent model, which may not represent human neonatal pathophysiology. Sample sizes per group, specific lower-dose values, mortality, and long-term neurodevelopmental or metabolic toxicity were not reported in the abstract.
Cited by
- supports The glycolytic inhibitor 2-deoxyglucose exerts anti-seizure effects at approximately 25 mg/kg, but becomes cardiotoxic at higher doses.