Sirs: Tranexamic acid is widely used in a variety of hemorrhagic conditions. It is known that tranexamic acid exerts a powerful epileptogenic action when applied topically to the cerebral cortex in animal experiments [3, 5]. Little is known about the effect of tranexamic acid administered intrathecally in man. We describe a patient who received intrathecal tranexamic acid by accident during a spinal anesthesia procedure. A 68-year-old man underwent spinal anesthesia at level L4-L5 for a transurethral resection of the prostate. Instead of the anesthetic agent the patient mistakenly received 50 mg tranexamic acid intrathecally because of a misplaced ampoule in a box of anesthetics. Immediately after the procedure he developed a status epilepticus. Other causes of epilepsy were ruled out. The patient was unresponsive and showed regular jerks in both legs, which were extremely hypertonic. He was kept supine, and antiepileptic treatment with midazolam and phenytoin was started. This treatment did not improve his clinical condition. Two hours after the start of treatment electroencephalography (EEG) showed continuous spikes, sharp waves, and slow waves in the right temporal region. Treatment was started with thiopenthal with a first dose of 1400 mg intravenously in 30 min, continuing at 2 mg/kg per hour for 2 days. The serum concentration of thiopenthal was 10.9 mg/l after the first dose, 16.6 mg/l and 26.6 mg/l on each following day, and 17.5 mg/l 1 day after thiopental had been discontinued. The course was further complicated by multiorgan dysfunction and a severe “critical illness polyneuropathy.” Several EEGs during this period showed a burst-suppression pattern with spiky bursts. The multiorgan dysfunction was reversible with symptomatic treatment. When he became conscious, he showed prominent hypotonic paresis of all extremities. Electromyography showed widespread fibrillations and polyphasic motorunit activity. The EEG normalized completely after treatment. Over a period of 1 month he gradually improved. With the exception of a bilateral peroneal palsy and cognitive deficits, the findings on neurological examination were normal. He still is on antiepileptic drugs, without seizures so far. Tranexamic acid is an antifibrinolytic agent acting by competitive inhibition of the activation of plasminogen, thereby reducing conversion of plasminogen to plasmin. It also inhibits plasmin activity directly in higher doses [1, 2, 4]. Tranexamic acid may be useful in circumstances in which excessive bleeding cannot be controlled, and it can be administered intravenously or orally. Tranexamic acid is contraindicated in patients with a recent history of thromboembolism and in patients with increased risk of thrombosis. Little is known about the effects of tranexamic acid when applied directly on the central nervous system. Pellegrini et al.[3] have described generalized seizures induced by tranexamic acid applied to the cortex of 12 cats at low concentrations. Yamaura et al.[5] have shown in an animal model that intravenous or intracisternal administration of tranexamic acid induces epileptiform changes on the EEG and remarkable elevation in intracranial pressure and systemic blood pressure. Tranexamic acid has been used in the treatment of patients with subarachnoid hemorrhage. To our knowledge, there have been no reports of seizures induced by intravenously administered tranexamic acid in patients with subarachnoid hemorrhage.