Methamphetamine-induced encephalopathy in the absence of hyperammonemia

AbstractBackground: Methamphetamine is an addictive drug with various effects on the neurotransmitters in the central nervous system. Methamphetamine-induced encephalopathy in the absence of hyperammonemia presents a unique challenge in a clinical setting. Previously published cases of methamphetamine-induced encephalopathy suggested that methamphetamine-induced hepatotoxicity and subsequent hyperammonemia may be the cause of encephalopathy. However, the literature is limited on methamphetamine-induced encephalopathy without hyperammonemia. Case: This case presents a disoriented patient following methamphetamine use disorder with acute toxicity, unable to ambulate independently, and was poorly responsive to verbal stimuli. Discussion: This patient developed encephalopathy with normal liver function tests and ammonia levels suggesting a different pathophysiological pathway for methamphetamine-induced encephalopathy. One potential pathway is through the direct action of methamphetamine on the central nervous system through acute disruption of neurotransmitter signaling and disruption of the blood-brain barrier. Conclusion: Further research should be conducted into the prevalence and pathophysiology of methamphetamine-induced encephalopathy in the absence of hyperammonemia.