ABSTRACT
BACKGROUND: 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 with methamphetamine use disorder in acute toxicity, unable to ambulate independently, and poorly responsive to verbal stimuli. The patient was found to have normal ammonia levels. DISCUSSION: This patient's presentation and laboratory findings, namely normal ammonia levels, suggest 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. KEY POINTS: Methamphetamine-induced encephalopathy (MIE) in the absence of hyperammonemia presents a unique challenge in a clinical setting. Previously published cases of MIE suggest that methamphetamine-induced hepatotoxicity and subsequent hyperammonemia may be the cause of encephalopathy. Further research should be conducted into the prevalence and pathophysiology of MIE in the absence of hyperammonemia.
