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Isr J Psychiatry Relat Sci - Vol. 52 - No 1 (2015) Arturo G.

Lerner and Shaul Lev Ran

LSD-associated Alice in Wonderland Syndrome


(AIWS): A Hallucinogen Persisting Perception
Disorder (HPPD) Case Report
Arturo G. Lerner, MD,1,2 and Shaul Lev Ran, MD,3
1

Lev Hasharon Mental Health Medical Center, Pardessya, Israel


Sackler School of Medicine, Tel Aviv University, Ramat Aviv, Israel
3
Addiction Medicine Clinic, Department of Psychiatry, Sheba Medical Center, Tel Hashomer, Israel
2

Abstract
A side effect associated with the use of LSD is the return
of perceptual disturbances which anteriorly emerged
during intoxication, despite absence of present use.
Here we present the case of a patient with a previous
history of sporadic and recreational cannabis, alcohol and
LSD consumption who reported LSD associated Alice
in Wonderland Syndrome (AIWS) or Todds syndrome.
AIWS is basically characterized by four frequent visual
illusions: macropsia, micropsia, pelopsia and teleopsia.
AIWS only appeared during LSD consumption and
continued after LSD suspension, namely, Hallucinogen
Persisting Perception Disorder (HPPD). This phenomenon
did not cause a major functional impairment but provoked
sufficient worry and concern due to its persistent
continuation. The patient refused medical treatment
and continued psychiatric follow-up. At the one year
follow-up he reported complete remission.
To the best of our knowledge this is the first reported case
of AIWS which persist after LSD interruption (HPPD) in
the professional literature. Reasons for this intriguing,
benign, reversible and apparently harmless side effect
are proposed.

Introduction
Alice in Wonderland Syndrome (AIWS) or Todds
syndrome is a condition predominately characterized
for complex perceptual disturbances (1). The name was

inspired by Lewis Carrolls book, Alices Adventures in


Wonderland (2). The famed hallucinogenic red and white
toadstool apparently ingested by Alice was Amanita
Muscaria or Fly Agaric, which possesses the psychoactive
alkaloid muscimol (3). This transient or chronic syndrome
may have multiple etiologies (4) and basically consists
of multiple visual aberrations. Four visual illusions have
been primarily described: macropsia (objects are perceived larger than their actual size), micropsia (objects
are perceived smaller than their actual size), pelopsia
(objects are perceived nearer than they actually are) and
teleopsia (objects are perceived much further away than
they actually are). These visual distortions have been
reported when looking at still or moving objects, human
and non-human beings (5). AIWS has been described
in different conditions such as (representative, yet not
exhaustive, list): migraine headaches (6), migraines aura
(7), influenza A infection (8), infectious mononucleosis
(9) and frontal lobe epilepsy (10). Although AIWS has
been reported by hallucinogen users during LSD intoxications or trips (5), it has never been reported after
LSD suspension, namely as an AIWS appearing as part
of hallucinogen persisting perception disorder (HPPD).
As defined in DSM-5, HPPD may recapitulate the prior
substance intoxication, reflecting the primary perceptual
experience, i.e., visual imagery experienced under hallucinogen intoxication should be re-experienced during
HPPD (11). Professional literature on HPPD has been
extensively reviewed (12).
We present the case of a patient with a prior history of
cannabis, alcohol and LSD sporadic recreational intake,
who sought professional consultation for the presence of
LSD-induced AIWS, after suspending all substance use.

Address for Correspondence: Arturo G. Lerner, MD, Lev Hasharon Mental Health Medical Center, POB 90.000, Netanya 42100, Israel
alerner@lev-hasharon.co.il, lerneram@internet-zahav.net

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Alice in Wonderland Syndrome


Isr J Psychiatry Relat Sci - Vol. 51 - No 4LSD-associated
(2014)

The patient gave informed consent for the publication


of his case. To the best of our knowledge this is the first
report in the professional literature.
Case report
Mr. A is a 26-year-old single male university student who
completed compulsory military service and did not have
any previous police or criminal records. He had a fiveyear past history of occasional social cannabis and alcohol use during weekends and holidays. He also reported
recreational use of LSD. He fulfilled DSM-5 full criteria
for tobacco use disorder (11). During LSD intoxication
he reported the presence of four frequent visual illusions
namely, macropsia, micropsia, pelopsia and teleopsia. These
visual distortions were reported when looking at still or
moving objects, human and non-human beings. When
interviewed Mr. A unhesitatingly and precisely attributed
psychedelic experience solely to LSD intake. Two days after
completely stopping all substance use due to a longer than
expected hallucinogenic experience associated with slight
anxiety, he surprisingly noticed the returning of some visual
imagery previously experienced. For example, books were
seen slightly closer, chairs were seen slightly further away,
his hands were seen larger than they actually were, his dogs
head was seen smaller (13). Interestingly some still objects
were observed slightly moving back and forth and perceived
closer, i.e., pelopsia, and further away, i.e., teleopsia (14). He
clearly did not expect the return of this visual imagery. As the
condition persisted, Mr. A started expressing preoccupation
and discomfort. He felt intimidated and disheartened and
sought a psychiatric consultation. On examination there was
no prior or present history of acute or chronic neurological,
ophthalmological or other co-morbid medical illnesses or
co-occurring psychiatric disorders. A complete physical,
neurological (including EEG) and laboratory examinations
showed no abnormal findings.
Mr. A was not interested in chemical pharmacological treatment and agreed to psychiatric follow-up.
After approximately one year these visual disturbances
completely disappeared.
Discussion
The suggested mechanism underlying recapitulation
and reproduction of visual disturbances originally experienced during LSD intoxication has been extensively
discussed (15-17). Comprehensive understanding of
this clinical syndrome remains unanswered.
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The unique clinical aspect of this case is the absence


of almost all the recurrent common visual disturbances
described in the professional literature (11, 12, 15-20).
Moreover, the striking resemblance to former description
of AIWS in other pathological contexts is remarkable. As
the main perceptual disturbance is visual, much of the
research pertaining to potential mechanisms underlying
these disorders focus on the Lateral Geniculate Nucleus
(LGN). The LGN, which is located in the thalamus, has
been associated to visual perception pathways and may be
affected by LSD toxic effects (21, 22). These toxic effects
might result in temporary impairment at LGN which
might lead to benign disinhibition of visual processors
and the genesis of recurrent visual disturbances (23).
Transient absence, deficiency or insufficient inhibitory
activity of the visual pathway may permit and enable
visual stimulus to persist. This proposal may explicate
reported visual disturbances, in this case macropsia,
micropsia, pelopsia and teleopsia, which may reflect
the failure of each respective responsible visual function
(15, 23-25). Macropsia and micropsia may arise from
magnification or miniaturization of perceived images
on the grounds of abnormal cortical processing (24, 25)
related to LSD induced damage at cortical levels (17). It
could be additionally speculated that LSD intake might
produce short-term limited and reversible damage of the
LGN leading to dysfunction of the parvocellular cells
which may modulate the perception of forms and shapes,
namely, macropsia and micropsia, and magnocellulars
cells which may modulate the perception of movement
of still objects, namely, pelopsia and teleopsia (17, 23-25).
A single clinical case report has obvious limitations. It
should be stressed that cannabis use was not reported as
the cause of any hallucinogenic experience. The primary
assumption is that the patient is capable of remembering
the experienced trip and adequately describe the current phenomena. Possible LSD-inflicted transient and
permanent damage at LGN and other nuclei is poorly
and insufficiently understood. The specific development
of AIWS after LSD consumption in the specific patient
remains largely unexplainable. research may increment
our knowledge regarding the mechanism of action of LSD
and related clinical phenomena.
To our knowledge this is the first case of HPPDassociated AIWS, which may contribute to clinical
knowledge. Exploring the possibility of HPPD, in its
many forms, among individuals with prior LSD use is recommended. However, conclusions from an uncontrolled
case report should be drawn with appropriate caution.

Arturo G. Lerner and Shaul Lev Ran

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