2023 14th Annual NUBE Conference

Background: Methamphetamine is an addictive synthetic central nervous system stimulant abused for its euphoric and energizing effects (1). Acute methamphetamine use has been linked to acute and chronic neurotoxic effects via both dopamine depletion and excessive NMDA-receptor activity (1). Catatonia is a neuropsychiatric syndrome characterized by psychomotor abnormalities, likely mediated by similar pathways including disturbances in dopaminergic, glutamatergic, and GABA-ergic activity, (2). While catatonia has been noted to be provoked by drug exposures (3), only one case report links acute methamphetamine use to catatonia (3). Case: The patient is a 48-year-old man with a past medical history of diabetes, hypertension, and HIV on ART, without any formal past psychiatric diagnoses but with a longstanding history of methamphetamine use and one prior psychiatric ER visit with transient paranoia following methamphetamine use and a family history of schizophrenia in a first-degree relative, who presented to the ER reporting anxiety. On initial evaluation, Bush Francis Catatonia Rating Scale (BFCRS) score was 15 for mutism, staring, posturing, rigidity, automatic obedience, and negativism. After administration of IM lorazepam 2mg, symptoms showed marked improvement but returned in hours. Urine toxicology was positive for amphetamines only. The patient was admitted to medicine for rhabdomyolysis with CPK = 815, followed by consultation liaison psychiatry, and started on IV lorazepam 1mg TID. On re-evaluation the next morning, patient was again in a hypokinetic catatonic state with a BFCRS of 20, and IV lorazepam was increased to 2mg IV TID. Subsequently, patient remained significantly improved with a BFCRS of<5 with residual intermittent staring, psychomotor slowing, and prolonged speech latency. Lorazepam was transitioned from IV to PO and tapered down to 1mg PO BID. Subsequently, catatonic symptoms completely resolved with BFCRS = 0. On interview, the patient presented calm, linear, and euthymic and firmly denied all mood and psychotic symptoms on interview and prior to presentation. He was discharged to outpatient level of care. Discussion: Given patient’s euthymic presentation with lack of reported or observed psychotic, depressive, or manic symptoms following treatment with lorazepam, the most likely etiology for his acute catatonia is methamphetamine use. His family history of schizophrenia and personal history of substance-induced psychotic symptoms may contribute to a vulnerability to the neurotoxic effects of methamphetamine or may be additional markers for an underlying psychotic spectrum illness. Conclusion: While there is limited research on a connection between methamphetamine use and catatonia, the present case demonstrates a temporal association between methamphetamine use and acute catatonia responsive to lorazepam.

Learning Objectives:

1. Bring awareness to the temporal association between catatonia and methamphetamine use in the absence of a formal psychiatric diagnosis.
2. To highlight lorazepam as a successful treatment option for catatonia following methamphetamine use.
3. To encourage a conversation and further research on the topic of catatonia and methamphetamine use.