Alice in Wonderland Syndrome: Micropsia, Macropsia, and Distorted Perception

Abstract

Alice in Wonderland syndrome (AIWS) is a disorienting perceptual condition in which the size, shape, distance, or speed of objects — and sometimes the body itself — is misperceived, while the eyes and the world remain objectively unchanged. A person in an episode may see a room shrink, a hand balloon, or time crawl. The distortions are transient, usually benign, and most often tied to migraine, to infectious mononucleosis in children, or to epilepsy. Named in 1955 by the psychiatrist John Todd after Lewis Carroll's heroine, AIWS is a disorder not of the eye but of perception: the sensory signal arrives intact and is then mis-scaled by the brain. This article sets out what AIWS is, its distortion types, its triggers, its mechanism, and why a syndrome of mis-sized worlds illuminates the psychology of size, distance, and bodily perception.

Keywords: metamorphopsia, micropsia, macropsia, size perception, migraine aura

A child with a fever reports that the walls of her bedroom are rushing away from her and her own hands look enormous; an hour later everything is normal and she is frightened but unharmed. A migraineur describes, in the minutes before a headache, cars on the street appearing tiny and impossibly far off, as though seen through the wrong end of a telescope. These are not failures of the eye — acuity is normal, the retina is healthy, the scene is unchanged — but failures of the brain's scaling of what the eye delivers. Alice in Wonderland syndrome is the name for this family of transient perceptual distortions, and its enduring interest is that it pulls apart two things ordinary perception fuses seamlessly: the raw sensory image, and the size, distance, and tempo the mind assigns to it.

Key Takeaways

- The eye is fine; the brain mis-scales. AIWS is a perceptual distortion of size, shape, distance, or time with no lesion of the eye — the sensory signal is intact and is then wrongly scaled centrally (Todd, 1955; Blom, 2016). - Its signature symptoms are micropsia and macropsia. Objects (or body parts) appear shrunken or enlarged; related distortions include teleopsia, pelopsia, and distorted time (Lippman, 1952; Blom, 2021). - The commonest triggers differ by age. Migraine dominates in adults; infectious mononucleosis (Epstein-Barr virus) is the leading cause in children, with epilepsy a third route (Lahat et al., 1990; Mastria et al., 2016). - It is usually benign and self-limiting. Episodes last seconds to minutes and resolve completely; management targets the underlying cause rather than the perception itself (Weissenstein et al., 2014; Farooq & Fine, 2017). - It is a window on perceptual scaling. By dissociating the retinal image from perceived size and distance, AIWS is a natural test of size-distance invariance and of the body schema (Lanska & Lanska, 2013; Mastria et al., 2023).

What Alice in Wonderland Syndrome Is

Alice in Wonderland syndrome is defined by distorted perception in the presence of an intact sensory apparatus. The person's eyes focus and resolve normally, the external world is unchanged, and yet the perceived size, shape, position, distance, or motion of objects — or of the perceiver's own body — is wrong. The distortions are typically paroxysmal: they arrive suddenly, last from a few seconds to a few minutes, and then lift completely, leaving no deficit behind (Blom, 2016). Because the eye is sound, AIWS is not an ophthalmological condition but a disorder of central perceptual processing — the brain's construction of a scaled, located world from the signals the senses deliver.

The syndrome takes its name from Lewis Carroll's Alice's Adventures in Wonderland, in which Alice repeatedly grows and shrinks, because the bodily and object-size distortions patients report echo Alice's changes of scale. The British psychiatrist John Todd coined the term in 1955, grouping a set of distortions that the migraine researcher Caro Lippman had described a few years earlier in patients who likened their experiences to Alice's (Lippman, 1952; Todd, 1955). Carroll himself suffered from migraine, and the long-standing suggestion that his own aura experiences inspired the book's transformations — though unprovable — captures the tight historical link between AIWS and migraine (Podoll & Robinson, 1999).

AIWS is best understood not as a single symptom but as an umbrella for a cluster of metamorphopsias — distortions of the form and scale of the perceptual world. MeSH files it as Alice in Wonderland Syndrome and places it among perceptual and sensation disorders as well as, by its behavioural dimension, in the behaviour-mechanisms tree. The condition is rare but not vanishingly so, and it is almost certainly under-reported, because the experiences are frightening, difficult to put into words, and easy for a patient to keep private for fear of being disbelieved (Blom, 2016; O'Toole & Modestino, 2017).

Symptoms and Types of Distortion

The distortions of AIWS fall into two broad families — those affecting the perception of external objects and those affecting the perception of the body — together with distortions of time. The two cardinal symptoms are micropsia, in which objects appear smaller than they are, and macropsia, in which they appear larger. These may apply to the whole visual field or to a single object, and they may be accompanied by distortions of distance: teleopsia, in which objects seem farther away than they are (the telescope-reversed experience), and pelopsia, in which they seem closer (Lippman, 1952; Blom, 2016).

Table 1. The principal perceptual distortions of Alice in Wonderland syndrome
Distortion	What is misperceived	Direction of the error	Domain
Micropsia	Size of external objects	Smaller than actual	Visual (object)
Macropsia	Size of external objects	Larger than actual	Visual (object)
Teleopsia	Distance of objects	Farther than actual	Visual (space)
Pelopsia	Distance of objects	Nearer than actual	Visual (space)
Metamorphopsia (shape)	Form and position of objects	Curved, tilted, or displaced	Visual (form)
Body-schema distortion	Size and shape of one's own body	A part enlarged or shrunken	Somesthetic (body)
Time distortion	Perceived duration	Sped up or slowed down	Temporal

Alongside these size-and-distance distortions sit distortions of shape and position — straight lines appearing curved, objects tilted or displaced — and, strikingly, distortions of the perceiver's own body, sometimes separated out as a somesthetic rather than visual form of the syndrome. A patient may feel a limb has grown or shrunk, that the head is enlarged, or that the body's proportions have changed — a disturbance of the body schema, the brain's internal map of bodily size and configuration. Lanska and Lanska drew the useful distinction between the predominantly visual perceptual disturbances and these somesthetic ones, noting that the two can occur together or apart (Lanska & Lanska, 2013).

A third dimension is time. Many patients report that time seems to speed up or slow down during an episode — a distortion of perceived duration that a systematic review found to be a recurrent and characteristic, if often overlooked, feature of the syndrome (Blom, 2021). Blom's foundational 2016 review, assembling 169 published cases, catalogued the full range and found that visual distortions — micropsia above all — were the most common, that episodes were brief, and that the condition spanned a wide age range while clustering in childhood (Blom, 2016).

Causes and Associations

AIWS is a symptom complex, not a stand-alone disease, and the clinically important question is always what is producing it. Three causes dominate, and their relative weight depends sharply on age (Mastria et al., 2016; Farooq & Fine, 2017).

In children, the single most common cause is infectious mononucleosis — infection with the Epstein-Barr virus — which can produce AIWS as a transient neurological manifestation, sometimes as the presenting feature before the systemic illness is recognised (Lahat et al., 1990; Weissenstein et al., 2014). Pediatric case series confirm that infection is the leading trigger in the young and that the prognosis is generally excellent, the distortions resolving as the infection clears (Liu et al., 2014).

In adults, the dominant association is migraine. AIWS is widely regarded as a form of, or close relative of, migraine aura, and in a tertiary headache clinic a measurable minority of migraineurs reported AIWS-type distortions, usually in the aura phase (Mastria et al., 2021). The historical link runs deep: Lippman's original patients were migraineurs, and the Carroll connection is a migraine story (Lippman, 1952; Podoll & Robinson, 1999). The third major route, across ages, is epilepsy, where the distortions arise as ictal or peri-ictal phenomena from occipital or temporo-parietal foci. A long tail of rarer causes — other viral and febrile illnesses, certain drugs and hallucinogens, psychiatric conditions, and focal brain lesions — completes the picture (Fine, 2013; Mastria et al., 2016).

Because AIWS can be the first sign of an underlying illness — an EBV infection in a child, a migraine disorder, or, rarely, a structural lesion — a new presentation warrants a search for the cause even though the syndrome itself is usually benign (Farooq & Fine, 2017).

Mechanisms

The eye is sound, so the distortion must arise where the brain builds perceived size, distance, and bodily scale from sensory input. The leading account locates AIWS in transient dysfunction of the higher-order visual and multisensory association cortex — chiefly the temporo-parieto-occipital junction (TPO) — where visual, vestibular, and somatosensory signals are integrated into a coherent, scaled percept of objects and the body in space (Blom, 2016; Mastria et al., 2016). A disturbance here — a wave of migrainous cortical depression, an ictal discharge, an inflammatory or infectious insult — can mis-scale the integration without touching early visual processing, producing a sharp image of the wrong size.

Neuroimaging has begun to put this account on firmer ground. Perfusion and functional studies in AIWS have reported altered activity in visual and visual-association areas during or around episodes, and a 2023 study of migraineurs with AIWS found neuroimaging markers distinguishing them — evidence that the syndrome has a measurable neural signature in the visual-processing network rather than being a purely subjective report (Mastria et al., 2023). The convergence of migraine, epilepsy, and infection on the same perceptual output is naturally explained if each disturbs the same final common pathway — the cortical machinery of perceptual scaling — by a different route.

Size, distance, and the invariance they break

Normally the brain ties perceived size to perceived distance: for a fixed retinal image, something seen as farther is perceived as larger (S′ ∝ α × D′). Set the two distortions independently and watch when the pairing becomes one that invariance forbids — the hallmark of an AIWS distortion.

Perceived size: ×1.00 (veridical)Perceived distance: ×1.00 (veridical)

Size tracks distance (S′ ∝ α·D′): a percept consistent with size-distance invariance — not an AIWS distortion.

AIWS can get both size and distance wrong, and in combinations the normal coupling rules out — evidence that perceived size is actively computed and can fail in parts (Lanska & Lanska, 2013).

The distortion gallery

AIWS is an umbrella for several distortions of a correctly seen scene. Select one to see what the term means against the same unchanging lamp and clock.

Veridical. The scene as it truly is: a lamp of ordinary size at an ordinary distance, clock ticking at one second per second.

In every panel the lamp and clock are physically unchanged; only the central scaling of size, distance, or time differs (Blom, 2016; Blom, 2021).

Causes by age group

AIWS is a symptom complex, and which cause dominates depends sharply on age. Toggle the age group to see the characteristic shift from infection in children to migraine in adults.

Illustrative proportions showing the qualitative age pattern, not a pooled dataset: infection leads in children, migraine in adults (Lahat et al., 1990; Mastria et al., 2021; Farooq & Fine, 2017).

Figure

Figure 1

Micropsia, Macropsia, and Teleopsia Against a Veridical Scene

Note. The same physical scene is shown as it is perceived veridically, under micropsia (shrunken), under macropsia (enlarged), and under teleopsia (small and seemingly far away). Because the eye and the external scene are unchanged across the panels, the differences illustrate that AIWS distortions are imposed by central perceptual scaling, not by any change in the sensory input.

Worked Example

The size distortions of AIWS can be made precise through the perceptual principle they violate: size-distance invariance. The visual system does not read object size off the retina directly — the same object casts a smaller retinal image as it recedes — but infers it by combining the retinal visual angle with perceived distance. To a good approximation, perceived linear size is proportional to retinal angle times perceived distance:

S′ ∝ α × D′,

where S′ is perceived size, α the retinal visual angle, and D′ perceived distance. Consider a dog 50 cm tall standing 4 m away. Its retinal visual angle is

α = 2 · arctan(0.25 / 4) ≈ 7.2°,

and normally the brain, judging the distance correctly at 4 m, recovers the true 50 cm height. Now suppose an AIWS episode imposes teleopsia, so the dog is perceived at twice its real distance, D′ = 8 m, while the retinal angle α is physically unchanged. Size-distance invariance then predicts the perceived size should double — the dog should look about 100 cm tall (macropsia), exactly as the moon looks huge when perceptual cues place it far off at the horizon.

Yet AIWS patients frequently report the opposite pairing: an object that looks both small and far away — micropsia with teleopsia. That combination is impossible under size-distance invariance, which ties a farther-seeming object to a larger perceived size for a fixed retinal angle. The violation is the diagnostic clue to mechanism: AIWS is not a simple error in judging distance (which would keep size and distance coupled) but an independent mis-scaling of size and of distance by a disturbed central integrator — the cortex can get both terms wrong, and in directions the normal coupling forbids. The MetamorphopsiaDemo lets the reader set a distortion factor for size and, separately, for distance, and watch the scene — and the coupling — break. The lesson is that AIWS dissociates the components perception normally binds, which is precisely why it is informative.

Discussion

The history of AIWS is a history of naming and then explaining a set of experiences that are easy to dismiss and hard to study. Lippman described the distortions in migraineurs; Todd gave them their memorable name and gathered them into a syndrome; the modern literature, led by Blom's systematic reviews, has turned an anecdotal curiosity into a characterised clinical entity with a catalogue of symptoms, an age-dependent profile of causes, and a candidate mechanism (Lippman, 1952; Todd, 1955; Blom, 2016). The arc mirrors that of many perceptual syndromes: first the vivid report, then the taxonomy, then the search for the neural substrate.

Two honest limits remain. The first is definition: because AIWS is a symptom complex rather than a disease, its boundaries are fuzzy, different authors include or exclude different distortions (purely visual versus somesthetic, with or without time distortion), and reported prevalence depends heavily on how the net is cast (Lanska & Lanska, 2013; Blom, 2021). The second is mechanism: the TPO-junction account is well-motivated and increasingly supported by imaging, but the evidence is still largely associative, drawn from small series and case-based neuroimaging rather than from large controlled studies (Mastria et al., 2016; Mastria et al., 2023). The syndrome's rarity and transience make it genuinely difficult to capture an episode in the scanner — a real methodological constraint, not a gap in effort.

Cognitive and Perceptual Implications

For cognitive psychology, AIWS is valuable precisely because it is a dissociation. Ordinary perception binds the retinal image to a perceived size and a perceived distance so tightly and automatically that the components are invisible to introspection; we simply see a dog, four metres off, fifty centimetres tall. AIWS prises those components apart, and in doing so it offers a natural test of theories that ordinary perception keeps hidden — above all size perception and the size-distance invariance that links it to depth perception. That patients can report size and distance distortions in combinations the invariance forbids is strong evidence that the brain computes a scaled percept actively, and that the computation can fail in parts (Lanska & Lanska, 2013).

The body-schema distortions carry a parallel lesson for the perception of the self. The felt size and configuration of one's own body is not read off the body directly but constructed, and AIWS shows that this construction, too, can be transiently rewritten — a limb enlarged, the head swollen — while the body is objectively unchanged. This places AIWS alongside other demonstrations that the body schema is a labile central model rather than a fixed given. More broadly, the syndrome is a reminder that visual perception and the perception of space and time are all constructive achievements of the brain: when the construction is disturbed, the world does not go dark or blurry — it stays sharp, and changes size (Blom, 2021; Mastria et al., 2023).

Current Directions

Three threads run through the recent literature. The first is better characterisation: Blom's systematic reviews, especially the dedicated treatment of time distortion, continue to widen and sharpen the catalogue of what counts as AIWS, which matters because an inconsistent definition has long muddied prevalence estimates (Blom, 2016; Blom, 2021). The second is epidemiology in migraine: structured studies in headache clinics are replacing anecdote with numbers, establishing how often AIWS actually accompanies migraine and in what form (Mastria et al., 2021). The third, and most active, is mechanism through neuroimaging: the search for reproducible neural markers of AIWS in the visual-association network is the current frontier, with the 2023 migraine-aura imaging study a notable step from case reports toward group-level evidence (Mastria et al., 2023). Running beneath all three is the steady accumulation of pediatric and infectious-cause series, which keep the clinical reality — a frightened child with a treatable infection — firmly in view (Farooq & Fine, 2017; Liu et al., 2014).

Common Misconceptions

AIWS is a problem with the eyes.: The eyes and the retina are normal. The distortion is central — the brain mis-scales a sharp, correctly focused image — which is why ophthalmological examination is unremarkable (Todd, 1955; Blom, 2016).
AIWS means hallucinating things that are not there.: It is a distortion of real objects' size, distance, or shape, not a hallucination of absent ones. The objects are really present; only their perceived scale is wrong (Lanska & Lanska, 2013).
It is a dangerous or progressive disease.: In the great majority of cases AIWS is benign and self-limiting, with episodes lasting seconds to minutes and resolving fully; the concern is to identify and treat the underlying cause, not the perception (Weissenstein et al., 2014; Farooq & Fine, 2017).
It only happens in children.: Although it clusters in childhood — where infection is the usual trigger — AIWS occurs across the lifespan, and in adults it is most often associated with migraine (Blom, 2016; Mastria et al., 2021).

Glossary

Aura.: A transient set of neurological symptoms, often visual, preceding or accompanying a migraine; AIWS distortions frequently occur in the aura phase.
Body schema.: The brain's internal model of the size, shape, and configuration of one's own body; its distortion produces the somesthetic (bodily) form of AIWS.
Epstein-Barr virus (EBV).: The herpesvirus causing infectious mononucleosis; the leading trigger of AIWS in children.
Ictal.: Pertaining to a seizure; AIWS distortions arising from epilepsy occur as ictal or peri-ictal phenomena, during or around a seizure.
Infectious mononucleosis.: A systemic illness caused by the Epstein-Barr virus; in children it is the commonest condition underlying an episode of AIWS.
Macropsia.: A distortion in which objects appear larger than they actually are.
Metamorphopsia.: A general term for the distorted perception of the form, size, or position of objects; AIWS is an umbrella for a cluster of metamorphopsias.
Micropsia.: A distortion in which objects appear smaller than they actually are; the single most common symptom of AIWS.
Pelopsia.: A distortion in which objects appear nearer than they actually are.
Size-distance invariance.: The perceptual principle that perceived size is proportional to retinal visual angle times perceived distance; AIWS can violate it, decoupling size from distance.
Somesthetic.: Pertaining to bodily sensation; the somesthetic form of AIWS distorts the felt size and shape of the body rather than of external objects.
Teleopsia.: A distortion in which objects appear farther away than they actually are — the wrong-end-of-a-telescope experience.
Temporo-parieto-occipital junction (TPO).: The cortical region where visual, vestibular, and somatosensory signals are integrated into a scaled percept; the leading candidate locus of AIWS.
Visual angle.: The angle an object subtends at the eye; the retinal measure from which, together with perceived distance, the brain infers an object's size.

Key Researchers

Jan Dirk Blom

(contemporary). Psychiatrist at Leiden University and the Parnassia Psychiatric Institute, The Hague; author of the foundational 2016 systematic review that assembled the modern AIWS case corpus and of the 2021 review of time distortion in the syndrome. ORCID - Google Scholar - Faculty

Giulio Mastria

(contemporary). Neurologist and researcher (University of Lausanne; CHUV), lead author of the 2016 clinical and pathophysiological review, the 2021 prevalence study in adult migraineurs, and the 2023 neuroimaging study of AIWS in migraine with aura. Faculty

Vittorio Di Piero

(contemporary). Professor of neurology at Sapienza University of Rome and senior author of the Mastria group's AIWS studies, working on headache and the neuroimaging of perceptual symptoms. Google Scholar

John Todd

(1914-1987). British psychiatrist at High Royds Hospital, Menston, who in 1955 coined the term Alice in Wonderland syndrome to group the size, distance, and body distortions his and Lippman's patients described, giving the condition its enduring name. Biography

Frequently Asked Questions

What is Alice in Wonderland syndrome in simple terms?

It is a condition in which the size, distance, shape, or speed of things, and sometimes one's own body, is misperceived, even though the eyes work normally and the world is unchanged. A person might see objects shrink or swell, or feel their own hand grow huge. The episodes are brief and usually harmless, and the name comes from Alice's changes in size in Lewis Carroll's story (Todd, 1955; Blom, 2016).

Is Alice in Wonderland syndrome a mental illness or an eye problem?

Neither. The eyes are healthy and it is not a psychiatric delusion. AIWS is a disorder of perception in which the brain mis-scales a correctly seen image, most often caused by migraine, a viral infection, or epilepsy rather than by any disease of the eye or mind (Blom, 2016; Mastria et al., 2016).

What are the main symptoms?

The cardinal symptoms are micropsia (objects look smaller) and macropsia (objects look larger). Others include teleopsia (things seem farther away), pelopsia (things seem nearer), distortions of shape, distortions of the felt size of one's own body, and distortions of time (Lippman, 1952; Blom, 2021).

What causes it?

The cause depends on age. In children the commonest trigger is infectious mononucleosis, caused by the Epstein-Barr virus; in adults it is migraine, of which AIWS is often considered a form of aura. Epilepsy is a third major cause, with rarer triggers including other infections, some drugs, and brain lesions (Lahat et al., 1990; Mastria et al., 2021; Fine, 2013).

Is it dangerous, and will it go away?

In most cases it is benign and self-limiting: episodes last seconds to minutes and resolve completely, and the long-term outlook is good, especially in children. The important step is to find and treat the underlying cause, since AIWS can be the first sign of a treatable illness (Weissenstein et al., 2014; Farooq & Fine, 2017).

Did Lewis Carroll have it?

Carroll suffered from migraine, and it has often been suggested that his own aura experiences inspired Alice's changes of size. The idea is plausible and historically appealing but cannot be proven; what is certain is the tight link between AIWS and migraine that the connection reflects (Podoll & Robinson, 1999).

What is happening in the brain during an episode?

The leading view is that higher-order visual and multisensory areas, around the temporo-parieto-occipital junction, transiently malfunction, mis-scaling the integration of visual and bodily signals while leaving early visual processing intact. Neuroimaging has begun to find markers of this disturbance in the visual network (Mastria et al., 2016; Mastria et al., 2023).

Why is Alice in Wonderland syndrome interesting to cognitive psychology?

Because it separates things ordinary perception fuses: the image on the retina, the size we assign it, and the distance we place it at. Patients can report size-and-distance combinations that the normal size-distance rule forbids, which shows that perceived size is actively computed by the brain and can fail in parts (Lanska & Lanska, 2013).

References

Blom, J. D. (2016). Alice in Wonderland syndrome: A systematic review. Neurology: Clinical Practice, 6(3), 259-270. https://doi.org/10.1212/CPJ.0000000000000251

Blom, J. D., Nanuashvili, N., & Waters, F. (2021). Time distortions: A systematic review of cases characteristic of Alice in Wonderland syndrome. Frontiers in Psychiatry, 12, 668633. https://doi.org/10.3389/fpsyt.2021.668633

Farooq, O., & Fine, E. J. (2017). Alice in Wonderland syndrome: A historical and medical review. Pediatric Neurology, 77, 5-11. https://doi.org/10.1016/j.pediatrneurol.2017.08.008

Fine, E. J. (2013). The Alice in Wonderland syndrome. Progress in Brain Research, 206, 143-156. https://doi.org/10.1016/B978-0-444-63364-4.00025-9

Lahat, E., Eshel, G., & Arlazoroff, A. (1990). 'Alice in Wonderland' syndrome and infectious mononucleosis in children. Journal of Neurology, Neurosurgery & Psychiatry, 53(12), 1104. https://doi.org/10.1136/jnnp.53.12.1104

Lanska, J. R., & Lanska, D. J. (2013). Alice in Wonderland Syndrome: somesthetic vs visual perceptual disturbance. Neurology, 80(13), 1262-1264. https://doi.org/10.1212/WNL.0b013e31828970ae

Lippman, C. W. (1952). Certain hallucinations peculiar to migraine. Journal of Nervous and Mental Disease, 116(4), 346-351. PMID: 12991095.

Liu, A. M., Liu, J. G., Liu, G. W., & Liu, G. T. (2014). 'Alice in Wonderland' syndrome: Presenting and follow-up characteristics. Pediatric Neurology, 51(3), 317-320. https://doi.org/10.1016/j.pediatrneurol.2014.04.007

Mastria, G., Mancini, V., Vigano, A., & Di Piero, V. (2016). Alice in Wonderland syndrome: A clinical and pathophysiological review. BioMed Research International, 2016, 8243145. https://doi.org/10.1155/2016/8243145

Mastria, G., Mancini, V., Vigano, A., & Di Piero, V. (2021). Prevalence and characteristics of Alice in Wonderland syndrome in adult migraineurs: Perspectives from a tertiary referral headache unit. Cephalalgia, 41(5), 515-524. https://doi.org/10.1177/0333102420968245

Mastria, G., Mancini, V., Di Bonaventura, C., Puma, M., Vigano, A., & Di Piero, V. (2023). Neuroimaging markers of Alice in Wonderland syndrome in patients with migraine with aura. Frontiers in Neurology, 14, 1210811. https://doi.org/10.3389/fneur.2023.1210811

O'Toole, P., & Modestino, E. J. (2017). Alice in Wonderland Syndrome: A real life version of Lewis Carroll's novel. Brain and Development, 39(6), 470-474. https://doi.org/10.1016/j.braindev.2017.01.004

Podoll, K., & Robinson, D. (1999). Lewis Carroll's migraine experiences. The Lancet, 353(9161), 1366. https://doi.org/10.1016/S0140-6736(05)74368-3

Todd, J. (1955). The syndrome of Alice in Wonderland. Canadian Medical Association Journal, 73(9), 701-704. PMID: 13304769. PMCID: PMC1826192.

Weissenstein, A., Luchter, E., & Bittmann, M. A. S. (2014). Alice in Wonderland syndrome: A rare neurological manifestation with microscopy in a 6-year-old child. Journal of Pediatric Neurosciences, 9(3), 303-304. https://doi.org/10.4103/1817-1745.147612

Alice in Wonderland Syndrome