The Alice in Wonderland Syndrome

Peculiar symptoms such as those in those in the Alice in Wonderland Syndrome are hypothesized to arise from phenomenology such as cortical spreading depression.  EEG may be the most promising way to understand their relationship to brain physiology.

Neurology is rife with case studies of bizarre sets of symptoms.  In 1952 neurologist Caro Lippman published a paper titled Certain Hallucinations Peculiar to Migraine published in the Journal of Nervous and Mental Disease. The peculiar hallucinations that he reported were an unusual distortion of body image – a sensation of parts or all of their body growing or shrinking in size or being smaller or bigger than usual.

Those patients who had these symptoms worried that they were on the road to insanity, Lippman says, and therefore rarely confessed them to a doctor.  It was only because he had taken to directly asking that he found so many migraine sufferers admit to them.  And it was not just migraine sufferers who reported them.  These symptoms are also associated with Epilepsy, Epstein Barr Infection and a host of other things.

In one case study a woman reported that she periodically felt that her stature had been altered. In her words ‘the ground comes up and I go down or vice versa such that sometimes I feel myself to be six inches tall and sometimes twelve feet’.  In addition, ‘Quite suddenly everything seems strange, and people’s voices become very faint. I feel that my head is dividing in two and my second head seems to flow off my normal head and take up a position a little behind and to the right of it.’

The Alice in Wonderland connection

In 1955, J Todd who had held the position of Assistant Psychiatrist at Littlemore Hospital in Oxford England (and whose first name can no longer be easily traced on the Internet), named this set of symptoms as Alice in Wonderland syndrome (AIWS).

For those who don’t know the book (do read it), Alice’s Adventures in Wonderland is a popular children’s fantasy novel published in 1865 by the English author Lewis Carroll about a young girl named Alice who follows a white rabbit down a rabbit hole and into a fantasy world where she grows and shrinks in size among a bizarre set of anthropomorphic animals.

“I can’t explain myself, I’m afraid, sir,” said Alice, “because I’m not myself, you see.”

“I don’t see,” said the Caterpillar.

“I’m afraid I can’t put it more clearly,” Alice replied very politely, “for I can’t understand it myself to begin with; and being so many different sizes in a day is very confusing.”

“It isn’t,” said the Caterpillar.

 Alice, in addition to feeling like she was growing big and small at different times also sometimes addressed herself as two people and questioned her identity.  In technical terms, Todd says, the symptoms she described were hyperschematia, hyposchematia, derealization, depersonalization and somatopsychic duality.  All these symptoms often co-occurred.

Lewis Carroll himself suffered from Migraine Todd points out.  Perhaps Alice’s Adventures were a description of his migraine related experiences.

A connection to Cortical Spreading Depression?

What causes these altered perceptions of oneself and reality that come and go? Clearly it must involve periods of significantly altered activity in the brain.  Unfortunately, these symptoms have rarely been studied from the perspective of brain physiology.  It is also particularly difficult to do so because symptoms occur intermittently followed by periods of wellness. Unless there are easy to use home measurements, it is unlikely that data will readily available.  We are therefore left to speculate on phenomenology that might explain it.

Cortical Spreading Depression (CSD) is one such candidate. CSD is a phenomenon represented by a spreading depolarization in cerebral cortex at a characteristic velocity. It is associated with massive disturbance of ion homeostasis with a large change of the slow electrical potential and silencing of brain electrical activity.  One could imagine that it creates such sensations as it spreads through the somatosensory cortex.   Epilepsy is similarly characterized by periods of synchrony that have some parallels to CSD.  Yet it remains pure hypothesis.

EEG as a tool for understanding

EEG is perhaps one of the most promising technologies to help test hypotheses relating to various symptoms and syndromes.  With the increasing push towards portable ambulatory devices that can be worn in the home there is the potential to capture physiological signatures of these symptoms when they arise – a first step in understanding the etiology of symptoms.

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