Neuroimaging features of psilocybin-induced toxic-metabolic encephalopathy in an adolescent

Description

A previously healthy adolescent presented to the emergency department with an abrupt onset of altered mental status and abnormal behaviour, including shaking of the extremities, rocking back and forth, and non-sensical speech, after ingestion of chocolate that contained psilocybin. Neurological examination demonstrated evidence of psychosis, agitation and disorganised, tangential thought processes with no other focal findings. A comprehensive drug screen was negative. Due to persistent altered mental status without improvement, MRI was performed to rule out encephalitis as a potential cause. MRI of the brain revealed an 8 mm focus of signal abnormality representing a cytotoxic lesion of the splenium of the corpus callosum figure 1A-D, supporting a diagnosis of toxic-metabolic encephalopathy secondary to psilocybin ingestion. The patient received scheduled risperidone and as needed lorazepam with improvement of mental status over 6 days. Due to significant cognitive improvement, follow-up imaging was not performed. The patient was discharged with recommendations for close follow-up on substance use and mental health support, and monitoring for any subsequent neuropsychiatric sequelae was conducted as an outpatient.

Figure 1.

MRI features of acute psilocybin-induced encephalopathy. MRI reveals an area of reduced diffusivity on diffusion-weighted (A) and apparent diffusion coefficient sequences (B). The lesion shows hyperintensity on T2-weighted sequences (C) without evidence of enhancement on post-T1-weighted images (D).

Psilocybin is a hallucinogen actively metabolised into psilocin, a 5-hydroxytryptamine 2A receptor partial agonist and a serotonin transporter inhibitor.^{1 2} Psilocybin induces changes in synaptic transmission and metabolic processes that alter cerebral blood flow to the prefrontal cortex.^1–4 Functional MRI studies further elucidate an association between psilocybin’s subjective effects and the decreased coupling of the posterior cingulate cortex and medial prefrontal cortex.⁴ Effects of psilocybin are dose-dependent and may induce sensory perception changes, anxiety, motor incoordination, hypertension and tachycardia.^{1 5} Young age is a predictor of more challenging experiences with psilocybin and confers a higher risk of emergency medical presentations.⁶ Imaging features of cytotoxic alterations secondary to psilocybin toxicity are rarely reported. A report of an adult presenting with a similar clinical presentation after psilocybin ingestion demonstrated no significant findings on MRI.⁷ Notably, a case report of an adolescent with neurological changes after 25I-NBOMe ingestion, a synthetic hallucinogen that acts through a similar mechanism to psilocybin, demonstrated diffuse white matter changes on imaging.⁸ In our case, signal abnormalities localised to the splenium of the corpus callosum. The onset of altered mental status to the time of MRI was 5 days, suggesting a time window for detectable imaging abnormalities in psilocybin-induced toxic-metabolic encephalopathy. Common imaging patterns of neurotoxicity secondary to toxic-metabolic exposures in the paediatric population include posterior reversible encephalopathy syndrome, acute toxic leucoencephalopathy and reversible splenial lesions.⁹ Reversible splenial lesions have been reported in cases of viral infections, exposures to herbicides, antiseizure therapies, cannabis and heroin.^10–16 Studies have illustrated that after neurological recovery, reversible splenial lesions resolve on imaging within 1 week to 1 month.^{15 17} In addition, it has been demonstrated that the resolution of diffusion-weighted imaging findings depends on the extent of abnormality observed in fluid-attenuated inversion recovery findings.^{15 18}

Overall, we highlight the imaging features of a cytotoxic lesion of the corpus callosum associated with a psilocybin-induced toxic-metabolic encephalopathy not yet reported in the adolescent population.

Learning points.

• Psilocybin toxicity induces cytotoxic lesions of the splenium of the corpus callosum that may become detectable on brain MRI within 5 days of onset.

• Reversible splenial lesions usually resolve on imaging within 1 week to 1 month and depend on the extent of abnormality on initial imaging.

• A clinical presentation of altered mental status in an adolescent patient warrants a comprehensive drug screen to identify substance exposure as a cause of toxic-metabolic encephalopathy.

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