Unilateral temporal lobe atrophy after massive caffeine overdose

Abstract

A 24-year-old man with autism spectrum disorder (ASD) and no history of seizures was admitted to the emergency department after ingesting 800 mg/kg of caffeine in a suicide attempt. He initially presented with generalized tonic–clonic seizures that lasted at least 40 min, which progressed to status epilepticus, necessitating continuous midazolam infusion for 4 days. Thereafter, he had no further convulsive seizures. On Day 8, fluid-attenuated inversion recovery (FLAIR) magnetic resonance imaging (MRI) of the brain revealed a high-intensity signal in the left temporal lobe, suggestive of partial cerebral edema (Figure 1A–C). He resumed oral clonazepam for ASD from Day 12.

Two years after the caffeine overdose, the patient was admitted due to the recurrence of convulsive seizures. A subsequent brain MRI revealed marked atrophy of the left temporal lobe, especially the superior temporal and parahippocampal gyri, as observed on FLAIR (Figure 1D–F arrows and arrowheads). Clinically, he exhibited symptoms of depression, irritability, and dysmnesia.

In the rat hippocampal models, caffeine induced persistent neuronal bursting even after drug washout.¹ Also, caffeine deteriorated epileptiform discharges in the hippocampal and parahippocampal gyrus in a patient with temporal lobe epilepsy.² This case suggests that nonconvulsive status epilepticus, following a massive caffeine overdose, can cause unilateral temporal lobe atrophy.

The authors declare no conflicts of interest.

Approval of the research protocol: N/A.

Informed consent: Informed consent was obtained from the patient.

Registry and registration no. of the study/trial: N/A.

Animal studies: N/A.