Do You See What I See? A Case of Alice in Wonderland Syndrome With EEG Correlate

Alice in Wonderland syndrome (AIWS), first described by the British psychiatrist John Todd in 1955, is a disorienting perceptual disorder characterized by discrete episodes of bizarre visual illusions and spatial distortions, which has been associated with numerous neurologic and psychiatric conditions. ^1,2 The syndrome, named after Lewis Carroll’s well-known protagonist in the children’s book Alice’s Adventures in Wonderland, ³ involves distorted perceptions of an individual’s body size and form or of the objects in the surrounding environment. Such distortions may include micropsia (objects appear smaller), macropsia (objects appear larger), and metamorphopsia (objects appear distorted), among many others. ¹ The duration of symptoms tends to be brief, usually minutes to several days, and resolves without sequelae. ^4,5 Patients are seldom frightened or confused by these illusions, and children in particular may relate the experience in exquisite detail without amnesia. The symptoms of Alice in Wonderland syndrome have been attributed to functional and structural aberrations of the perceptual system. ⁶ While it has historically been assumed that this syndrome is rare, epidemiologic studies in patients with migraine have reported an Alice in Wonderland syndrome prevalence rate of up to 15% among this population. ^7,8 Previously published etiologies implicated in Alice in Wonderland syndrome include viral infections (particularly Epstein-Barr virus [EBV]), migraine, epilepsy, central nervous system lesions, and hallucinogenic substances. ¹ One pediatric study of Alice in Wonderland syndrome found a family history of migraine or Alice in Wonderland syndrome in nearly 50% of patients, suggesting a possible genetic predisposition to this fascinating syndrome. ⁹ No ICD-10 or DSM-5 criteria have been established for Alice in Wonderland syndrome; thus, diagnosis is made on clinical grounds, as well as by excluding other diagnoses such as epilepsy, central nervous system lesions, and primary psychiatric disorders. ¹ Ancillary tests, including blood tests, brain magnetic resonance imaging, and electroencephalography (EEG), may be indicated when there is diagnostic uncertainty.

The authors present a case of an 8-year-old, neurodevelopmentally normal boy with a history of night terrors, who presented with transient headache and visual disturbance suspicious for Alice in Wonderland syndrome. Subsequent evaluation led to an EEG which demonstrated abnormal EEG correlate with an episode of perceptual disturbance.

Case Description

An 8-year-old, right-hand preference, neurodevelopmentally normal boy presented to the emergency department with symptoms of recurrent perceptual disturbance. His past medical history was unremarkable with the exception of infrequent night terrors. The patient had been seen initially at an outside emergency department for fever and headache. Examination was notable for posterior oropharyngeal erythema. Rapid streptococcal A throat screening test was positive, leading to a diagnosis of streptococcal pharyngitis and treatment with intramuscular penicillin. The patient was not tested for Epstein-Barr virus.

His fever and headache resolved within 12 hours. Less than 24 hours later, the patient presented to our emergency department complaining of 3 episodes of seeing objects being much smaller (micropsia) and further away (teleopsia) than usual, in addition to seeing wavy or wiggly lines (dysmorphopsia). These symptoms lasted for 5 to 15 minutes and would resolve spontaneously. During the episodes, the child did not have any impairment in consciousness, headache, focal weakness, or abnormal limb movements. The patient did not have a personal history of colic, migraine, cyclic vomiting, or motion sickness. Family history was negative for epilepsy, migraine, neurodevelopmental, or other inherited neurologic conditions. Visual acuity was 20/20 OU, with normal funduscopic examination. A complete neurologic examination was also normal. The patient’s symptoms were suspected to be related to Alice in Wonderland syndrome, and he was discharged from the emergency department with arrangements for an outpatient EEG and neurologic consultation.

To exclude an underlying epileptic condition, the patient underwent a routine awake and sleep EEG 2 days later. The EEG background during wakefulness contained symmetric 9 to 10 Hz alpha activity over the posterior head regions. During the EEG recording, the patient had a recurrence of his typical visual symptoms, characterized by blurred vision with micropsia, teleopsia, and dysmorphopsia. Electrographically, the clinical symptoms were associated with brief (<10 second) periods of 5 to 6 Hz theta activity over the bilateral posterior head regions and maximal left posterior temporo-occipital region (Figure 1). No potentially epileptogenic activity was present during the clinical symptoms or during the remainder of the awake and sleep recording. Based on the clinical symptoms, normal neurologic and ophthalmologic examinations, and EEG findings, it was felt that the patient’s perceptual disturbance was consistent with Alice in Wonderland syndrome. Neuroimaging was not obtained due to the intermittent nature of the nonspecific EEG slowing and the patient’s normal neurologic examination with clinical findings suggestive of Alice in Wonderland syndrome. Given the absence of an underlying chronic condition (such as epilepsy or migraine), the family was given reassurance that the symptoms themselves are generally benign and transient. Anticipatory guidance on the association with migraine was reviewed and migraine prophylaxis was discussed if symptoms recurred. Two years since initial presentation, the patient has not experienced further perceptual disturbances nor developed migraine headaches.

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Figure 1.

Electroencephalography (EEG) tracings (bipolar montage) in an 8-year old boy with Alice in Wonderland syndrome. The tracing on the left demonstrates symmetric 9 to 10 Hz alpha activity over the posterior head regions. The tracing on the right demonstrates a brief run of 5 to 6 Hz rhythmic theta activity bilaterally in the posterior head regions, maximal over the left posterior temporo-occipital region. This EEG change correlated with the patient’s visual symptoms of micropsia, teleopsia, and dysmorphopsia.