Sir,Ketamine is an anesthetic with a good safety profile. It is highly lipid soluble and has cataleptic, amnestic, analgesic, and anesthetic actions. Literature regarding the convulsant potential of ketamine is currently unclear. Some authors mention that ketamine demonstrates anticonvulsant and neuroprotective properties.[1]We report here a case of an 8-year-old girl with ankyloglossia who was posted for an elective tongue-tie release under general anesthesia. There was no past/family history of convulsions. Her birth and development histories were unremarkable. Her physical examination and laboratory investigations were normal. Just before shifting to operation theater, she was premedicated with injections glycopyrrolate 0.2 mg and ketamine 100 mg intramuscularly since she was very unruly. On the table, an intravenous (IV) line was secured, and monitors were connected. She was afebrile. Her heart rate and blood pressure were within normal range. She was maintaining a normal airway, and her oxygen saturation was 100%. Suddenly, she developed perioral twitches followed by bilateral symmetrical jerky tonic–clonic movements, more in the upper limb with up-rolling of eyeballs for a few seconds. This resembled a focal seizure. She was oxygenated and administered IV injections midazolam 1.5 mg and phenytoin 20 mg/kg bolus followed by 5 mg/kg as an infusion. The surgery was postponed. She was closely monitored and oxygenated in the postanesthesia care unit. Blood that was drawn on the operating table soon after the seizure revealed normal sugar, electrolytes, and calcium levels. Magnetic resonance imaging of her brain revealed normal findings.No other precipitating factors for seizures such as hypoglycemia, hyperventilation, hypocalcemia were present in our closely monitored patient; yet she developed convulsions. This implies that the convulsions were drug induced-either due to ketamine/glycopyrrolate. Although adverse experiences like seizures have been mentioned from postmarketing experience with glycopyrrolate,[2] not many such central nervous system effects have been reported because glycopyrrolate does not cross the blood-brain barrier. Furthermore, following intramuscular administration, the onset of action of glycopyrrolate is noted in 15–30 min,[2] whereas in our patient, a seizure occurred within 10 min of giving glycopyrrolate. Therapeutic clinical trials to manage drooling in patients with neurodevelopmental disorders have not reported seizures in patients treated with glycopyrrolate tablets.[3] All this strongly points toward ketamine as the cause of seizures in our case.The factors responsible for both the proconvulsant and anticonvulsant properties of ketamine and almost every other anesthetic drug include biological variation in individual patient responsiveness and pharmacodynamic variability in the responsiveness of inhibitory and excitatory target tissues in the central nervous system.[4] Ketamine-induced generalized tonic–clonic seizures have been reported in a 10-year-old boy 5 min after intramuscular administration.[4] In a study, it was found that five of 22 cats anesthetized with ketamine developed tonic–clonic convulsions. Most of those five cats had prominent black/brown stripes thus indicating the susceptibility of some phenotypes to ketamine-induced seizures.[5]This leads us to believe that the possibility of ketamine acting as a convulsant/anticonvulsant in a particular individual depends on the phenotype of that individual.