Medical Case: Acute hallucinations in an “unlikely” adolescent

A teenager arrives at the ED with confusion and visual hallucinations. Negative labs and imaging complicate the search for the underlying cause.

Case presentation (03:00 AM)

During the night between Saturday and Sunday, Mark, a 17-year-old previously healthy boy, is brought to the emergency department (ED) by his parents. They had just returned from an evening at the theater and found him at home acutely agitated, confused, and speaking incoherently. They report a single episode of vomiting earlier in the night.

While they were at the theatre, Mark, an only child, stayed at home to watch a film. He did not go out because he had not been feeling well since the afternoon. The parents emphasize that Mark is a “good boy”: he does not drink, smoke, or use drugs. There is no family history of psychiatric illness, epilepsy, or relevant neurological disease.

Initial assessment (03:10)

On examination:

Initial laboratory tests (03:20)

Patient interview (03:30)

As part of routine adolescent assessment, Mark was interviewed privately, without his parents present. Despite repeated questions, he consistently denied any alcohol or drug use. His speech was at times incoherent, but his refusal remained firm.

Management (03:35)

Peripheral IV line inserted; 0.9% NaCl 500 mL IV over 60–90 minutes; ondansetron 4 mg IV. Continuous monitoring (ECG, SpO₂, NIBP). Placed in a low-stimulation environment.

Imaging (04:05)

Non-contrast head CT: normal.

Neurology consult (04:20)

Working impression: viral encephalitis (HSV high on differential) vs toxic-metabolic encephalopathy. Lumbar puncture (LP) proposed but deferred due to agitation.

Psychiatry consult (04:45)

Possible first psychotic episode; re-evaluate after organic work-up.

Targeted sedation (05:00)

Lorazepam 1 mg IV for severe agitation with good effect; no paradoxical reaction.

Clinical status (05:30)

Alternating agitation and drowsiness; mydriasis and diaphoresis persist. Intermittent myoclonus observed. No meningism; strength and reflexes preserved when cooperative. With initial labs/CT and routine toxicology negative, the ED team broadens the evaluation, prioritising urgent and treatable causes.

Extended toxicology & metabolic evaluation (05:45)

Serum and urine sent for GC–MS (synthetic cannabinoids, cathinones, tryptamines/LSD derivatives and other NPS). Acetaminophen and salicylate levels drawn. Additional metabolic tests: ammonia, TSH + free T4, morning cortisol.

Infectious work-up (06:00)

After partial sedation, an LP is performed (~8 mL clear CSF) for cell count/differential, glucose, protein, Gram/culture and PCR for HSV-1/2, VZV, enterovirus, West Nile. Blood cultures obtained. Empiric acyclovir IV 10 mg/kg every 8 h started immediately post-LP, per HSV protocols.

Neurologic investigations (06:30)

Urgent EEG requested (exclude NCSE; encephalitic patterns). Brain MRI with gadolinium scheduled (diagnostic query: early HSV changes, autoimmune limbic encephalitis, ADEM, subtle stroke).

Psychiatry revises the impression (06:45)

Given fever, tachycardia, diaphoresis, mydriasis, vomiting, myoclonus, a primary psychiatric disorder is unlikely pending organic exclusion.

Diagnosis still unknown

At this stage Mark is hydrated, partially sedated, on empiric antivirals and under close monitoring, with comprehensive toxicological, infectious and neurological investigations in progress.

What would you diagnose?

Clinical turning point

In the early hours of the morning, while Mark is still under close observation, the situation in the emergency department takes an unexpected turn. Around 07:15, another 17-year-old boy is admitted to the same unit. His name is Peter, a close friend of Mark, and his presentation is strikingly similar: repeated vomiting, confusion, alternating agitation and drowsiness, and vivid visual hallucinations.

Unlike Mark, however, Peter has already provided his parents with a clearer account. When his symptoms began at home, he confessed that he and Mark had eaten mushrooms together earlier in the evening. He explained that he had picked them in the countryside, noting their “red caps with white spots,” and had brought them to Mark’s house to try “just to see what effect they would have.” According to Peter, Mark had only pretended to feel unwell during the afternoon so that his parents would not insist on him going out, as he usually does on Saturday nights.

Peter’s parents, alarmed by the disclosure, arrive at the ED carrying remnants of the mushrooms he had collected. Their appearance leaves little doubt: bright red caps with white warty patches, typical of Amanita muscaria. The regional Poison Control Center is contacted, and the suspicion of pantherina syndrome is promptly confirmed.

From this moment, the diagnostic puzzle changes radically. The broad differentials considered overnight - encephalitis, autoimmune disorders, toxic-metabolic encephalopathy, even first psychosis - fall into the background. The working diagnosis becomes acute intoxication with Amanita muscaria.

Both boys are admitted to short-stay observation. They receive intravenous fluids and careful monitoring; benzodiazepines are given in low doses when agitation flares. Activated charcoal is deemed unhelpful, given that more than three hours have passed since ingestion and both patients show fluctuating consciousness. Over the next day their condition steadily improves. By 24–36 hours after admission, hallucinations, agitation, and myoclonus have completely resolved. The laboratory follow-up shows no hepatic or renal injury.

The two teenagers are discharged in good clinical condition, accompanied by parents who are relieved but shaken, and who receive detailed counseling on the dangers of wild mushroom ingestion.

Discussion

Amanita muscaria, the “fly agaric,” is one of the most recognizable fungi in the world but also one of the most toxic. Its ingestion produces the pantherina syndrome, which typically begins within 30–180 minutes. Gastrointestinal symptoms, usually mild nausea and vomiting, are followed by a prominent neuropsychiatric picture: delirium, hallucinations, incoherent speech, fluctuating consciousness, myoclonus or seizures. Autonomic signs are equally typical: mydriasis, tachycardia, diaphoresis, hypersalivation.

The toxins responsible are ibotenic acid (a glutamatergic agonist) and muscimol (a potent GABA-A agonist). Muscarine, despite giving the mushroom its name, is present only in trace amounts and plays no role in the syndrome.

The case underlines the difficulty in distinguishing such intoxication from other urgent conditions. HSV encephalitis remains the classic “do not miss” differential in adolescents with delirium and should always prompt lumbar puncture and empiric acyclovir. Autoimmune encephalitis, particularly anti-NMDA receptor encephalitis, may mimic this presentation with psychosis, movement disorder, and dysautonomia.

A first psychotic episode is a frequent initial impression, but systemic signs such as fever, mydriasis, vomiting, and sweating are atypical. Synthetic hallucinogens may reproduce similar features, though simultaneous onset in two close contacts points instead to a shared ingestion.

Unlike Amanita phalloides, which causes potentially fatal hepatotoxicity, A. muscaria intoxication is rarely life-threatening. Treatment remains supportive: intravenous fluids, benzodiazepines for agitation or seizures, and airway protection if consciousness deteriorates. Activated charcoal is considered only in early presentations. Prognosis is generally benign, with spontaneous resolution in 24–48 hours.

This episode shows how a relatively benign intoxication can mimic life-threatening neurological or psychiatric illness, and how careful history taking or, in this case, the parallel presentation of a second patient, can dramatically reframe the clinical reasoning.

Sources
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  3. Dushkov A, Stoyanov P, Georgieva S, et al. Analysis of ibotenic acid, muscimol, and ergosterol in Amanita muscaria. Molecules. 2023;28(20):7414. doi:10.3390/molecules28207414.
  4. Leas EC, Kreslake JM, Prochaska JJ. Need for a public health response to the unregulated sales of Amanita muscaria mushrooms. Am J Prev Med. 2024;66(5):713-716. doi:10.1016/j.amepre.2024.01.011.