LSD-associated “Alice in Wonderland Syndrome”(AIWS): A Hallucinogen Persisting Perception Disorder (HPPD) Case Report

Alice in Wonderland Syndrome (AIWS), also known as Todd's syndrome, is a perceptual disorder primarily involving complex visual distortions. The syndrome is commonly described in relation to four core visual illusions: macropsia (objects perceived larger than they are), micropsia (objects perceived smaller), pelopsia (objects perceived nearer), and teleopsia (objects perceived farther away). Earlier literature has associated AIWS with a range of medical conditions including migraine and focal epilepsy, and transient AIWS-like phenomena have been reported during intoxication with hallucinogens such as LSD, but persistent AIWS after cessation of LSD—i.e. as part of Hallucinogen Persisting Perception Disorder (HPPD)—had not been documented in the professional literature prior to this report. Todd and colleagues present a clinical case intended to fill that gap: a single-patient case report of a young man who developed AIWS-type visual distortions associated with LSD use that persisted after he stopped taking the drug, consistent with HPPD as defined in DSM-5. The report aims to describe the clinical presentation, investigations, course and the authors' speculative mechanistic considerations regarding this apparently reversible phenomenon.

This paper is an individual case report. The patient, identified as Mr A, was a 26-year-old single male university student with a history of occasional recreational cannabis and alcohol use and sporadic LSD use; he also met DSM-5 criteria for tobacco use disorder. The patient provided informed consent for publication. Clinical history was obtained by interview: during LSD intoxication he experienced the four characteristic AIWS visual illusions (macropsia, micropsia, pelopsia and teleopsia) when viewing both still and moving objects, and two days after discontinuing all substances he noted recurrence of similar visual imagery. The investigators recorded specific examples reported by the patient (books appearing closer, chairs appearing further, hands larger, dog's head smaller) and documented the temporal course. Diagnostic work-up consisted of a complete physical and neurological examination, electroencephalography (EEG) and laboratory tests; the extracted text reports no abnormal findings on these assessments. No pharmacological treatment was provided because the patient declined ‘‘chemical’’ treatment; he agreed to psychiatric follow-up only. The analysis is descriptive and clinical, reporting the observed course and examination results. The extracted text does not report the clinical setting in detail (for example, outpatient clinic versus hospital) beyond the psychiatric consultation.

During an LSD ‘‘trip’’ the patient experienced the four canonical AIWS visual distortions: macropsia, micropsia, pelopsia and teleopsia. These distortions occurred for both animate and inanimate targets and for still and moving stimuli. Two days after he ceased all substance use—prompted by a longer-than-expected psychedelic experience and some anxiety—he noticed a recurrence of the visual imagery previously experienced during intoxication. Reported examples included perceiving books as slightly closer, chairs as slightly further away, his hands as larger than normal and his dog's head as smaller. He also described some still objects appearing to move slightly back and forth while being perceived as nearer or farther. On clinical evaluation there was no past or present history of neurological, ophthalmological or other medical illnesses, and no co-occurring psychiatric disorders were identified. EEG and routine laboratory investigations were normal. The persistent visual phenomena caused preoccupation, discomfort and psychological distress but did not produce major functional impairment, and the patient declined pharmacotherapy. With psychiatric follow-up alone, the visual disturbances completely resolved after approximately one year. The authors note that cannabis was not implicated as the cause of the hallucinatory experience, and they report this as, to their knowledge, the first published case of AIWS persisting as HPPD.

The investigators discuss the case in light of proposed neurophysiological mechanisms for persistent visual disturbances following hallucinogen exposure, while emphasising that comprehensive understanding remains incomplete. They focus on the lateral geniculate nucleus (LGN) in the thalamus as a plausible site of disruption, proposing that LSD-related toxic or functional effects at the LGN could transiently impair inhibitory control over visual processing and thereby allow persistent or recurring visual imagery. In this account, disinhibition of visual processors could permit visual stimuli to persist or be misrepresented, producing macropsia, micropsia, pelopsia and teleopsia. Further mechanistic speculation in the paper differentiates parvocellular and magnocellular pathways: parvocellular dysfunction might underlie distortions of form and size (macropsia, micropsia), whereas magnocellular dysfunction could affect motion and distance perception (pelopsia, teleopsia). The authors characterise the putative LGN change as short-term, limited and reversible, consistent with the patient's eventual complete remission. Limitations of the report are acknowledged: it is a single case and causality cannot be established; the extracted text notes reliance on the patient's retrospective account of the ‘‘trip’’ and current phenomena; and the neurobiological hypotheses about LSD-induced LGN changes are described as poorly understood and speculative. The researchers recommend that clinicians and investigators consider HPPD in its various manifestations among individuals with prior LSD use, but they caution against strong conclusions from this uncontrolled single case.