A cognitive profile of multi-sensory imagery, memory and dreaming in aphantasia

Abstract

For most people, visual imagery is an innate feature of many of our internal experiences, and appears to play a critical role in supporting core cognitive processes. Some individuals, however, lack the ability to voluntarily generate visual imagery altogether – a condition termed “aphantasia”. Recent research suggests that aphantasia is a condition defined by the absence of visual imagery, rather than a lack of metacognitive awareness of internal visual imagery. Here we further illustrate a cognitive “fingerprint” of aphantasia, demonstrating that compared to control participants with imagery ability, aphantasic individuals report decreased imagery in other sensory domains, although not all report a complete lack of multi-sensory imagery. They also report less vivid and phenomenologically rich autobiographical memories and imagined future scenarios, suggesting a constructive role for visual imagery in representing episodic events. Interestingly, aphantasic individuals report fewer and qualitatively impoverished dreams compared to controls. However, spatial abilities appear unaffected, and aphantasic individuals do not appear to be considerably protected against all forms of trauma symptomatology in response to stressful life events. Collectively, these data suggest that imagery may be a normative representational tool for wider cognitive processes, highlighting the large inter-individual variability that characterises our internal mental representations.

Full text

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A cognitive prole of multi-sensory
imagery, memory and dreaming in
aphantasia
Alexei J. Dawes1 ✉ , Rebecca Keogh1, Thomas Andrillon1,2 & Joel Pearson1
For most people, visual imagery is an innate feature of many of our internal experiences, and appears
to play a critical role in supporting core cognitive processes. Some individuals, however, lack the
ability to voluntarily generate visual imagery altogether – a condition termed “aphantasia”. Recent
research suggests that aphantasia is a condition dened by the absence of visual imagery, rather than
a lack of metacognitive awareness of internal visual imagery. Here we further illustrate a cognitive
“ngerprint” of aphantasia, demonstrating that compared to control participants with imagery
ability, aphantasic individuals report decreased imagery in other sensory domains, although not all
report a complete lack of multi-sensory imagery. They also report less vivid and phenomenologically
rich autobiographical memories and imagined future scenarios, suggesting a constructive role for
visual imagery in representing episodic events. Interestingly, aphantasic individuals report fewer and
qualitatively impoverished dreams compared to controls. However, spatial abilities appear unaected,
and aphantasic individuals do not appear to be considerably protected against all forms of trauma
symptomatology in response to stressful life events. Collectively, these data suggest that imagery
may be a normative representational tool for wider cognitive processes, highlighting the large inter-
individual variability that characterises our internal mental representations.
Visual imagery, or seeing with the mind’s eye, contributes to essential cognitive processes such as episodic mem-
ory1, future event prospection2, visual working memory3, and dreaming4. By allowing us to re-live the past and
simulate hypothetical futures, visual imagery enables us to exibly and adaptively interpret the events we expe-
rience in the world5, and by extension appears to be an important precursor to our ability to plan eectively
and engage in guided decision-making. Consequently, the frequency and content of maladaptive visual imagery
are oen dening features of mental illness6 and mental imagery is oen elevated in disorders characterised by
hallucinations7,8.
One of the most signicant ndings to date is that despite the prevalence of visual imagery use in the wider
population, and despite its functional utility in cognition, certain individuals lack the ability to visualise alto-
gether – a condition recently termed “aphantasia”9. Beyond self-report measures, this condition is characterised
by stark dierences between individuals who can and cannot visualise on an objective measure of imagery’s
sensory strength10. This suggests that rather than reflecting inaccurate phenomenological reports or poor
population-specic metacognition, aphantasia appears to represent a veridical absence of voluntarily generated
internal visual representations.
e potential impact of visual imagery absence on wider cognition remains unknown. No research to date
has empirically veried whether this phenomenology extends to other internal experiences and mental pro-
cesses. is presents us with a rare opportunity to extend a cognitive ngerprint of aphantasia, in order to better
clarify the role of visual imagery in wider psychological functioning and explore the impact of its absence on
the subjective lives of individuals with a “blind mind”. Here we investigated whether individuals with aphantasia
report reduced imagery in other multi-sensory domains, and assessed self-reports of episodic memory ability and
trauma symptomatology in response to stressful life events, in addition to reported mind-wandering frequency
and dreaming phenomenology.
1School of Psychology, The University of New South Wales, Sydney, New South Wales, Australia. 2School of
Psychological Sciences and Turner Institute for Brain and Mental Health, Monash University, Melbourne, Victoria,
Australia. ✉e-mail: alexei.dawes@unsw.edu.au
open
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Method
Participants. We compared a group of self-identied aphantasic individuals with two independent control
groups of individuals with self-reported intact visual imagery on a range of questionnaires. e current study
was approved by the UNSW Human Research Ethics Advisory Panel (HREAP-C) in line with National Health
and Medical Research Council (NHRMC) guidelines on ethical human research. All participants gave informed
consent before completing the study.
Given the need for more research in this area, we sought to collect data on as many aphantasic participants as
possible. With the limited number of previous studies on aphantasia using small sample sizes of N = 10–209,10, it
was dicult to estimate required sample sizes for our study based on these results alone. We nevertheless used
the limited data available to derive approximate eect sizes for group dierences in these studies in the range of
d = 1.0–3.0. Eect sizes in small sample studies are oen inated, however, and we expected weaker eects across
multiple comparisons in our study, especially in non-imagery domain comparisons. Establishing a comparatively
moderate expected eect size of d = 0.5, with 80% power and a highly conservative alpha of 0.0002 (see Statistical
Analyses in Methods), we estimated that at least 170 participants would be required in each comparison group.
Because our study was easily accessible online and received more participant responses than anticipated within
our data collection window, we exceeded our sample size aim (N = 170) and ceased data collection for our aphan-
tasic participant group at the sample size reported below. We then collected an equivalent number of participants
for our independent control groups. Sample sizes for the aphantasia group, control group 1 and control group 2
were approximately equal aer data cleaning and exclusions (n = 267, n = 203 and n = 197, respectively).
Aphantasia group. Aphantasic individuals in our study were recruited from online community research plat-
forms (https://www.facebook.com/sydneyaphantasiaresearch/) and participated in exchange for entry into a
gi card prize draw. 317 aphantasic participants in total completed our study, of whom 33 participants were
excluded from analysis due to missing data (not completing all questionnaires). An additional 17 participants
were excluded from our aphantasic sample due to unclear reporting (e.g. scoring at ceiling on the Vividness of
Visual Imagery Questionnaire (VVIQ; see Methods) in line with older versions of the scale that used reversed
scoring compared to the current version of the scale). Our nal sample of aphantasic individuals included for
analysis contained 267 participants (48% females; mean age = 33.97 years, SD = 12.44, range = 17–75 years).
Control group 1 (MTurk). Participants in our main control group were recruited using Amazon Mechanical
Turk (MTurk) and were remunerated to complete the study. is main control group sample comprised of 205
participants, two of whom were excluded from nal analysis due to study incompletion. Our nal sample for our
main control group thus consisted of 203 participants (35% females; mean age = 33.82 years, SD = 9.33, range
= 20–70 years) who were matched on mean age with our aphantasic sample (mean age dierence = 0.15 years,
p = 0.89, BF10 = 0.107).
Control group 2 (Undergraduates). A second control group of 193 rst-year undergraduate psychology students
were tested using the same experimental design. Participants in our second control group (73% females; mean age
= 19.33 years, SD = 3.69, range = 17–55 years) completed the study in exchange for course credit. All participants
were included in nal analysis (see section titled Control Group 2: Replication Analysis, in Results).
Aphantasia sample characteristics. Demographics. A table of sample demographics for all groups can
be found in the Supplementary Information (see TableS1). Our sample population of aphantasic participants
were recruited from online community research platforms dedicated to the topic of visual imagery ability and
aphantasia. Both participants who did and didn’t identify with a history of visual imagery absence were invited
to participate in the study. Of the 267 participants in our sample who reported aphantasia, a majority reported
English as their rst language (83%, n = 220) and identied as White/Caucasian (88%, n = 235). 31 countries of
residence were listed, with a majority of participants originating from the United States of America.
Clinical history. Of the aphantasic sample, 24% of participants reported a history of mental illness (compared to
18% in control group 1; χ21,470 = 3.644, p = 0.06), 1% reported a history of epilepsy or seizures (compared to 8%
in control group 1; χ21,470 = 14.881, p < 0.001), 4% reported a neurological condition (compared to 7% in control
group 1; χ21,470 = 1.765, p = 0.184), 9% reported having suered head injury or trauma at least once (compared to
9% in control group 1; χ21,470 = 0.019, p = 0.890), and 0.7% reported having once suered a stroke (compared to
6% in control group 1; χ21,470 = 10.634, p < 0.01).
Imagery scores. Weak visual imagery ability is typically dened by a total score of 32 or less on the Vividness of
Visual Imagery Questionnaire (VVIQ: see Imagery Questionnaires in Materials), a ve-point Likert self-report
scale which ranges from 16–809,11. A total score of 32 is equivalent to rating one’s agreement on every question-
naire item at 2 (“Vague and dim”). On average, aphantasic participants in our sample scored 17.94 on the VVIQ
(including 70% with total oor scores of 16), compared to 58.12 in control group 1 (see Imagery Results section)
and 58.79 in control group 2 (see TableS2 in Supplementary Information).
Experimental procedure. Questionnaires were administered online using the Qualtrics research platform,
and presented to each participant in random order. All participants completed a total of 206 questions in eight
questionnaires. ese questionnaires assessed self-reported multi-sensory imagery, episodic memory and future
prospection, spatial abilities, mind-wandering and dreaming propensity, and response to stressful life events, as
detailed below.
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Materials. Imagery questionnaires. e Vividness of Visual Imagery Questionnaire (VVIQ11; Marks, 1973)
is a 16-item scale which asks participants to imagine a person as well as several scenes and rate the vividness of
these mental images using a 5-point scale ranging from 1 (“No image at all, you only ‘know’ that you are thinking
of the object”) to 5 (“Perfectly clear and <as> vivid as normal vision”). A single mean score on the VVIQ was
computed for each participant. e Questionnaire upon Mental Imagery (QMI12; Sheehan, 1967) asks partici-
pants to rate the clarity and vividness of a range of imagined stimuli in seven sensory domains (visual, auditory,
tactile, kinesthetic, taste, olfactory, emotion) on a 7-point scale ranging from 1 (“I think of it, but do not have an
image before me”) to 7 (“Very vivid and as clear as reality”). ere are 35 items on the QMI in total, with ve items
corresponding to each of the seven sensory domains. e Object and Spatial Imagery Questionnaire (OSIQ13;
Blajenkova, Kozhevnikov, & Motes, 2006) is a 50-item scale which requires participants to indicate how well each
of several statements on object imagery ability (e.g. “When I imagine the face of a friend, I have a perfectly clear
and bright image”) and spatial imagery ability (e.g. “I am a good Tetris player”) applies to them on a 5-point scale
ranging from 1 (“Totally disagree”) to 5 (“Totally agree”). ere are 25 items each comprising the Object and
Spatial imagery domains of the OSIQ, averaged to form a mean score on each domain.
Memory questionnaires. The Episodic Memory Imagery Questionnaire (EMIQ; on request) is a custom
designed, 16-item self-report questionnaire which aims to assess the subjective vividness of episodic memory.
Items on the EMIQ were partially derived from the VVIQ11 scale (Marks, 1973) and modied for context. e
EMIQ asks participants to remember several events or scenes from their life and rate the vividness of these
scenes using a 5-point scale ranging from 1 (“No image at all, I only ‘know’ that I am recalling the memory”) to 5
(“Perfectly clear and as vivid as normal vision”). A single mean score on the EMIQ was computed for each partic-
ipant. e Survey of Autobiographical Memory (SAM14; Palombo, Williams, Abdi, & Levine, 2013) is a 26-item
scale which measures participant agreement with a number of statements related to general episodic memory
ability on a 5-point scale ranging from 1 (“Strongly disagree”) to 5 (“Strongly agree”). e scale is divided into 4
components: Event Memory (averaged across eight items, e.g. “When I remember events, in general I can recall
people, what they looked like, or what they were wearing”), Future Events (averaged across six items; e.g. “When
I imagine an event in the future, the event generates vivid mental images that are specic in time and place”),
Factual Memory (averaged across six items; e.g. “I can learn and repeat facts easily, even if I don’t remember
where I learned them”) and Spatial Memory (averaged across six items; e.g. “In general, my ability to navigate is
better than most of my family/friends”).
Dreaming and daydreaming questionnaires. Part 1 of the Imaginal Process Inventory (IPI;15,16 Giambra, 1980;
Singer & Antrobus, 1963) consists of 24 items which assess the self-reported frequency of day dreams (or
mind-wandering episodes) and night dreams on a 5-point agreement scale which diers on each question (e.g. “I
recall my night dreams vividly”, ranging from a) “Rarely or never” through to e) “Once a night”). e Subjective
Experiences Rating Scale (SERS17; Kahan & Claudatos, 2016) comprises 39 questions which assess the qualita-
tive content and subjective experience of participants’ night dreams generally (e.g. “During your dreams whilst
asleep, <to what extent> do you experience colors”) on a 5-point rating scale ranging from 0 (“None”) to 4 (“A
lot”). ere are several sub-components of the scale which measure reported structural features of participants’
dreams (e.g. how bizarre one’s actions were, or how much perceived control participants experienced, during
their dreams). e SERS is divided in our study into six dream components: Sensory, Aective, Cognitive, Spatial
Complexity, Perspective and Lucidity. ese components reect typical SERS scale divisions, with the exception
of Lucidity (in which we merge two existing components (Awareness and Control) of the previously published
SERS scale17 in order to improve the readability of Fig.2).
Trauma response questionnaire. e Post-Traumatic Stress Disorder (PTSD) Checklist for DSM-5 (PCL-518;
Weathers et al., 2013) measures self-reported responses to stressful life events. It asks participants to indicate
how much they have been bothered by a problem related to a stressful life event on a 5-point scale ranging from
1 (“Not at all”) to 5 (“Extremely”). e PCL-5 contains 20 questions which are broken into four clinically rele-
vant symptom categories: Intrusions (e.g. “Repeated, disturbing, and unwanted memories of the stressful experi-
ence”), Avoidance (e.g. “Avoiding memories, thoughts, or feelings related to the stressful experience”), Negative
Alterations in Cognitions and Mood (e.g. “Blaming yourself or someone else for the stressful experience and what
happened aer it”), and Arousal and Reactivity (e.g. “Feeling jumpy or easily startled”). PTSD diagnosis can only
be established by a professional practitioner in a structured clinical interview, and although cut-o scores on the
PCL-5 are oen used as an adjunct screening tool, the scale is not used for diagnostic purposes here.
Statistical analyses. Non-parametric Mann-Whitney U hypothesis tests were conducted in SPSS 25.0 for
Mac OS using Bonferroni adjusted alpha levels of α = 0.0002 (0.05/206 where 206 is the total number of question
items across all questionnaires) to correct for multiple comparisons. Estimates of eect sizes r were computed
using the following formula:
=r
Z
N
where Z is the Mann-Whitney standardized test statistic, N the total sample size of the combined groups, and r the
output eect size estimate (comparable with Cohen’s d eect size interpretations19). Because we adopted a highly
conservative adjusted alpha, Mann-Whitney tests were supplemented by Bayesian analyses conducted in JASP.
For all Bayesian analyses, a Cauchy prior of 0.707 was used. Bayes factors were used to help compare the weight of
evidence for between-group dierences across test comparisons, whilst Mann-Whitney tests were used to make
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overall inferences about test direction and signicance. Bayes factors were interpreted according to common
threshold guidelines20, where 1 = “No evidence”, 1–3 = “Anecdotal evidence”, 3–10 = “Moderate evidence”, 10–30
= “Strong evidence”, 30–100 = “Very strong evidence”, and >100 = “Extreme evidence”.
Data transformation. All analyses were conducted on raw data. Data visualisation for Fig.1 only, however, was
carried out on median-centered raw questionnaire data using the following transformation:
=−. +
.−.
.−.
()
yxSmin
Smax Smin
Smax Smin
2
where y is the transformed score; x the raw individual item score for scale S, and S.min and S.max the lowest and
highest possible scores on that scale, respectively. is transformation allows us to graphically compare results
across scales, with a value of −0.5 representing the lowest possible score, 0 the median score, and 0.5 the maxi-
mum possible score on each scale.
Hypotheses
We expected aphantasic individuals to report reduced visual imagery ability compared to controls, in line with
previous ndings9,10. ere is some suggestion that auditory imagery may also be reduced in individuals who
report visual imagery absence, however this evidence comes from case studies with limited sample sizes1. We
therefore had no strong hypotheses regarding group dierences in other multi-sensory imagery domains.
Given the proposed importance of mental imagery for the reliving of past life events21, we predicted that
aphantasic individuals would report general alterations to episodic memory and future prospection processes, as
well as reductions in episodic memory vividness.
Clinical research has traditionally placed heavy emphasis on the symptomatic role of visual imagery in mental
health disorders including depression, social phobia, schizophrenia and post-traumatic stress disorder (PTSD),
amongst others6. We therefore hypothesised that visual imagery absence might partially protect aphantasic indi-
viduals from experiencing some trauma symptomatology (such as vivid memory intrusions) in response to stress-
ful past events.
Although neural measures suggest that dreaming is oen characterised by vivid and objectively measurable
internal visual experiences4, previous evidence on dreaming in aphantasia is somewhat inconclusive22. e over-
all impact of visual imagery absence on involuntary imagery processes (such as mind-wandering and dream-
ing whilst asleep) is therefore largely unclear, and we had no strong predictions regarding group dierences in
mind-wandering frequency, dream frequency, or dream phenomenology and content.
Lastly, we expected aphantasic self-reports of spatial imagery and spatial navigation abilities to align with
data from previous studies suggesting that despite visual imagery absence, spatial abilities (as measured by
questionnaires and performance on mental rotation and visuo-spatial tasks) appear to be largely preserved in
aphantasia10,22.
Results
e aim of the present study was to investigate the subjective impact of visual imagery absence on cognition.
To achieve this, we compared self-reports of aphantasic individuals with those of general population individ-
uals (with self-reported intact visual imagery) on several cognitive domains including multi-sensory imagery,
episodic memory, trauma response, dreaming and daydreaming, and spatial abilities. e main results sections
presented here all describe between-group tests comparing our aphantasic sample with our rst control group
of age-matched participants recruited from MTurk (see TablesS2–6 in Supplementary Information). For repli-
cation comparisons with our second control group sample of undergraduates, see section at end of Results titled
“Control Group 2: Replication Analysis”.
Control Group 1: Main Comparisons. Imagery results. We rst examined group dierences in visual
imagery vividness. As expected based on previous ndings9,10, aphantasic participants rated their visual imagery
ability on the VVIQ as being signicantly lower (17.94 ± 0.223, with many (70%) scoring at oor, i.e. 16) com-
pared to control group 1 (58.12 ± 0.888; Mann-Whitney U = 427.5, p < 0.0002, r = 0.87, BF10 = 1.41e12, 2-tailed;
see Fig.1 red section and FigureS1 in Supplementary Information; Fig.1 depicts median-centered data with
the aphantasia group denoted by red plots and control group 1 by blue plots throughout; FiguresS1–5 show raw
scale scores and distributions). is self-reported qualitative absence of visual imagery vividness was mirrored by
signicantly lower scores than controls on the object imagery component of the OSIQ (Mann-Whitney U = 372,
p < 0.0002, r = 0.85, BF10 = 446,931.23, 2-tailed; see Fig.1 red section and Fig. S1), which measures the perceived
ability to use imagery as a cognitive tool in task-relevant scenarios. Our data also showed that individuals with
aphantasia not only report being unable to visualise, but also report comparatively reduced imagery, on average,
in all other sensory modalities (measured using the QMI), including auditory (U = 6,152, BF10 = 5.01e11), tactile
(U = 4,473, BF10 = 4.90e9), kinesthetic (U = 5,151, BF10 = 1.04e11), taste (U = 3,069.5, BF10 = 4.82e26), olfactory
(U = 3,439.5, BF10 = 2.73e9) and emotion (U = 6,670.5, BF10 = 4.81e12) domains (all Mann-Whitney U-tests,
p < 0.0002, r = 0.65–.78, 2-tailed; see Fig.2a and Fig. S1). It is noteworthy, however, that despite reporting a
near total absence of visual imagery on the QMI (Mann-Whitney U = 620.5, p < 0.0002, r = 0.87, BF10 = 1.07e9,
2-tailed; see Fig.2a) and signicantly lower total QMI scores overall compared to controls (Mann-Whitney U =
1,868.5, p < 0.0002, r = 0.79, BF10 = 6.47e12, 2-tailed; see Fig.1 red section, second panel from top), only 26.22%
of aphantasic participants reported a complete lack of multi-sensory imagery altogether (rating each question
in each QMI domain as “1: No sensory experience at all”). e remainder of our aphantasic sample (73.78%)
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Visual
(VVIQ)
Multi-
sensory
(QMI)
Object
(OSIQ)
Episodic
imagery
(EMIQ)
Episodic
memory
(SAM)
Future
events
(SAM)
Factual
memory
(SAM)
Spatial
memory
(SAM)
Spatial
imagery
(OSIQ)
Night
(IPI)
Day
(IPI)
Trauma
Response
(PCL-5)
Median centred raw scale scores
-0.5
00.
5
TRAUMA DREAMSPATIAL ABILITY EPISODIC SIMULATION IMAGERY
Aphantasia Controls
Figure 1. Summary of self-reported cognition questionnaires for individuals with aphantasia (red, n = 267)
and control group 1 participants with visual imagery (blue, n = 203). Violin plots of median-centred scale
scores with median (bold line), lower and upper quartiles (thin lines) and kernel density-smoothed frequency
distribution (shaded area) coloured by group. Each pair of violin plots represents transformed raw data
(see Data Transformation, Method). Stars to the right of group plot segments indicate Mann-Whitney test
signicance at threshold p < 0.0002.
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reported some degree of imagery in non-visual sensory modalities (albeit signicantly reduced compared to
controls; see Fig.1 red section, and Fig.2a), suggesting potential sub-categories of aphantasia.
Memory results. Aphantasic individuals described a significantly lower ability to remember specific life
events in general (Event Memory component of the SAM; Mann-Whitney U = 8,865, p < 0.0002, r = 0.58,
BF10 = 4.68e10, 2-tailed; see Fig.1 blue section) and reported almost no ability to generate visual sensory
details when actively remembering past events (memory vividness on the EMIQ; Mann-Whitney U =
2,186.5, p < 0.0002, r = 0.81, BF10 = 1.01e15, 2-tailed; see Fig.1 blue section and Fig. S2 in Supplementary
Information) compared to participants in control group 1. However, these self-reported reductions in
reliving events were not confined to the past, with aphantasics as a group also reporting a near total ina-
bility to imagine future hypothetical events in any sensory detail (Future Events component of the SAM;
Mann-Whitney U = 7,469.5, p < 0.0002, r = 0.63, BF10 = 2.97e10, 2-tailed; see Fig.1 blue section and Fig.
S2). Self-reported factual (or semantic) memory, which is traditionally thought to provide a kind of ‘scaffold’
for event memories more widely23, also appeared to be lower in individuals unable to visualise compared
to controls (Factual Memory component of the SAM; Mann-Whitney U = 18,601.5, p < 0.0002, r = 0.27,
BF10 = 156,732.50, 2-tailed; see Fig.1 blue section and Fig. S2), although this effect was of a lower magni-
tude than the memory reductions reported above (see Fig.1 blue section and TableS7 in Supplementary
Information). The fourth scale component of the SAM (Spatial Memory) is grouped with the Spatial
Imagery component of the OSIQ in results below (see Spatial Ability Results).
Trauma response results. Our data did not directly support the hypothesis that visual imagery absence
might protect aphantasic individuals from trauma symptomology in response to stressful life events, with
the aphantasia group scoring comparatively to control group 1 on the PCL-5 overall (total PCL-5 scores;
Mann-Whitney U = 27,515, p = 0.776, r = 0.01, BF10 = 0.12, 2-tailed; see Fig.1 grey section and FigureS3
in Supplementary Information). An analysis of group differences on the four sub-components of this scale
(Intrusions, Cognition and Mood, Avoidance, and Arousal) also revealed that there were no significant
differences between the groups in reports of emotional arousal and reactivity associated with remembering
stressful past events (Mann-Whitney U = 27,240, p = 0.924, r = 0.00, BF10 = 0.11, 2-tailed; see Fig.2b and
Fig. S3). Compared to participants with visual imagery, individuals with aphantasia appeared to report
fewer recurrent and involuntary memory intrusions (Mann-Whitney U = 22,739, p = 0.002, r = 0.14, BF10
= 14.85, 2-tailed; see Fig.2b and Fig. S3), lower engagement in avoidance behaviours (Mann-Whitney U =
23,164.5, p = 0.006, r = 0.13, BF10 = 2.13, 2-tailed; see Fig.2b and Fig. S3), and greater negative changes in
cognition and mood (Mann-Whitney U = 30,960, p = 0.008, r = 0.12, BF10 = 12.99, 2-tailed; see Fig.2b and
Fig. S3) in response to stressful life events, although none of these group differences survived Bonferroni
correction for multiple comparisons, and effect size estimates were small (r = 0.12–.14; see TableS7 in
Supplementary Information). Interestingly, however, Bayesian analyses indicated strong evidence in favour
of group differences on the Intrusions (BF10 = 14.85) and Cognition and Mood (BF10 = 12.99) sub-scales of
the PCL-5 reported above.
Day and night dream results. Here we found that although there was little evidence for or against (BF10 = 1.93
and BF01 = 0.518) a difference between groups in the reported frequency of day-dreaming (Mann-Whitney
U = 23,001.5, p = 0.005, r = 0.13, 2-tailed, non-significant after Bonferroni correction; see Fig.1 teal
section and FigureS4 in Supplementary Information), aphantasic individuals did report experiencing
significantly fewer night dreams than controls (Imaginal Process Inventory (IPI); Mann-Whitney U =
15,828.5, p < 0.0002, r = 0.37, BF10 = 4.24e6, 2-tailed; see Fig.1 teal section and Fig. S4). Interestingly, the
reported qualitative content of these night dreams also differed between groups as measured by the SERS.
Dream reports for aphantasic individuals reinforce a model of aphantasia as being primarily character-
ised by sensory deficits (Sensory; Mann-Whitney U = 15,087.5, p < 0.0002, 0.38, BF10 = 5.46e6, 2-tailed)
across all dream modalities (including olfactory, tactile, taste and auditory domains; see Fig.2c and Fig.
S4). Interestingly, aphantasic individuals also reported experiencing lower awareness and control during
their dreams (Lucidity; Mann Whitney U = 19,473.0, p < 0.0002, r = 0.25, BF10 = 1902.01, 2-tailed). We
found some evidence that the dreams aphantasic participants report are characterised by less vivid emo-
tions (Affective; Mann Whitney U = 23,463.0, p = 0.013, non-significant after Bonferroni correction, r
= 0.11, BF10 = 9.01, 2-tailed), and a less clear dreamer perspective (Perspective (PSP); Mann Whitney
U = 22,070.5, p = 0.0004, r = 0.16, non-significant after Bonferroni correction, BF10 = 127.28, 2-tailed)
compared to participants in control group 1. However, there were no significant differences between the
aphantasia group and control group 1 in the experience of within-dream cognition (e.g. planning or remem-
bering (Cognitive); Mann Whitney U = 24,592.0, p = 0.085, r = 0.08, BF10 = 1.05, 2-tailed) or the details
of dreams’ spatial features (Spatial Complexity (SC); Mann Whitney U = 24,697.0, p = 0.092, r = 0.08, BF10
= 0.31, 2-tailed). Interestingly, the only question on the SERS for which aphantasics scored significantly
higher than control group 1 participants was an item in the Cognitive domain (see Fig.2c) which asks how
much time participants spent thinking during their dreams (Mann-Whitney U = 34,401.5, p < 0.0002, BF10
= 3.53e3), which accords well with a reduction in the sensory qualities of dreams in aphantasia in favour of
semanticised contents.
Spatial ability results. Aphantasic participants reported slightly lower spatial imagery ability on the spatial
sub-component of the OSIQ when compared to control group 1 (Mann-Whitney U = 24,462, p = 0.001, r = 0.15,
BF10 = 14.65, 2-tailed; see Fig.1 purple section and FigureS5 in Supplementary Information), although this eect
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was not signicant aer Bonferroni correction. Additionally, the scores of aphantasic individuals on the Spatial
Memory component of the SAM (which includes items measuring reported spatial navigation and naturalistic
spatial memory ability) were not signicantly dierent from controls (SAM; Mann-Whitney U = 24,720, p =
0.1, r = 0.08, BF10 = 0.23, 2-tailed; see Fig.1 purple section and Fig. S5). ese results demonstrate that overall
there were no consistent dierences in reported spatial abilities between aphantasic individuals and participants
in control group 1.
Control Group 2: Replication Analysis. Although control group 1 was age-matched, it featured a higher
ratio of males to females (see TableS1) in contrast to our aphantasic sample (which comprised of more females
than males). Some of the variables included in this study (such as spatial ability and PTSD susceptibility) are
known to be inuenced by gender. To address this potential issue, we ran a replication analysis with a second
control group of rst-year undergraduate psychology students using the same experimental design (their raw data
is depicted alongside our original control group and aphantasic sample in FiguresS1–5).
Participants in our second control group (n = 193) were recruited from a sample of undergraduate psychology
students at the University of New South Wales, and completed the study in exchange for course credit. All partic-
ipants in this second control group were included in nal analysis (with no exclusions). ese participants (mean
age = 19.33 years, SD = 3.69, range = 17–55 years) were not matched on mean age with our aphantasic sample
(mean age dierence = 14.6 years, p < 0.01, BF10 = 1.23e10), but instead featured a higher proportion of females
to males (73% females, compared to 48% females in our aphantasic sample and 35% females in control group 1
(our main control group of MTurk responders).
Comparison with this second control group revealed a similar overall pattern of group dierences to those
reported above, with few eect changes in imagery and memory related domains in particular (see FiguresS1–5
and TablesS2–6 in Supplementary Information for a comparison of test results, as well as TableS7 for a compari-
son of eect sizes). Aphantasic participants scored signicantly lower than control group 2 on all outcomes of the
imagery and episodic memory questionnaires (all p < 0.0002, al l r > 0.52, all BF10 > 1.42e8) with the exception of
the factual memory component of the SAM (which was no longer signicantly lower in aphantasics when com-
pared to control group 2 aer controlling for multiple comparisons; Mann-Whitney U = 21,496.0, p = 0.002, r =
0.14, BF10 = 3.196, 2-tailed).
Although our Bayes analysis suggested strong evidence for higher total PCL-5 scores in control group 2 com-
pared to the aphantasic group (Mann-Whitney U = 21,464.0, p = 0.002, r = 0.14, BF10 = 12.76, 2-tailed), this
eect was not signicant aer Bonferroni correction. However, the previously non-signicant reduction in mem-
ory intrusions amongst aphantasic participants (compared to control group 1) was much stronger in this second
group comparison (Mann-Whitney U = 15,134.5, p < 0.0002, r = 0.35, BF10 = 2.20e7, 2-tailed), as were lower
reports of avoidance behaviours by aphantasic individuals compared to control group 2 (Mann-Whitney U =
18,494.5, p < 0.0002, r = 0.24, BF10 = 2494.67, 2-tailed). Compared to control group 2, however, aphantasic
participants did not report signicantly higher negative cognition and mood (Mann-Whitney U = 25,827.5, p
= 0.97, r = 0.00, BF10 = 0.12, 2-tailed) or arousal (Mann-Whitney U = 25,517.0, p = 0.12, r = 0.07, BF10 = 0.34,
2-tailed) in response to stressful life events, in line with our main control group 1 comparisons.
a
Multi-Sensory Imagery (QMI)
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Figure 2. Group dierences in visual imagery ability on scale sub-components. Radar plots for (a) multi-
sensory imagery; (b) trauma response; and (c) dreaming scales (SC. = Spatial Complexity; PSP. = Perspective;
LUC. = Lucidity). Concentric dashed circles represent raw scale scores for each scale (e.g. a; 1–7 Likert-type),
with lowest possible item scores falling on innermost solidcircle and highest possible item scores falling
on outermost coloured circle; radial dashed lines denote item grouping for scale sub-components (e.g. c;
Intrusions, Avoidance, Negative Cognition and Mood, Arousal and Reactivity); central coloured lines (red
= aphantasia group, blue = control group 1) represent raw total group scores on individual scale items, with
translucent shading denoting standard-deviation.
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Individuals with aphantasia reported signicantly fewer night dreams than control group 2 (Mann-Whitney
U = 17,156.0, p < 0.0002, r = 0.74, BF10 = 21,124.12, 2-tailed). However, they also reported signicantly less fre-
quent mind-wandering compared to participants in control group 2 (Mann-Whitney U = 19,271.5, p < 0.0002,
r = 0.29, BF10 = 397.04, 2-tailed), in contrast to the results of our main analysis (which revealed no signicant
dierences in mind-wandering reports between the aphantasic group and control group 1). Also in contrast to
our initial dreaming results, aphantasic participants scored signicantly lower than control group 2 on all com-
ponents of the SERS (Sensory, Aective, Cognitive, Spatial Complexity, Perspective and Lucidity; all p < 0.0002,
all r > 0.71, all BF10 > 1.56e7), including on some domains where there were no signicant dierences between
aphantasic participants and age-matched participants in control group 1 (see Fig. S4 and TableS5). However,
these ndings may be partially explained by age-related decline in dream frequency and subjective recall24.
Lastly, there were no signicant dierences in reported spatial imagery ability on the OSIQ (Mann-Whitney
U = 22,635.5, p = 0.03, r = 0.10, BF10 = 0.88, 2-tailed) or spatial navigation ability on the SAM (Mann-Whitney
U = 23,760.5, p = 0.15, r = 0.07, BF10 = 0.23, 2-tailed) between the aphantasic group and control group 2, rein-
forcing our initial results as well as previous ndings of preserved spatial (but not object) imagery in aphantasic
participant samples10,22.
Discussion
Here we found that individuals with aphantasia report signicant reductions in sensory simulation across a range
of volitional and non-volitional mental processes, and overall appear to demonstrate a markedly distinct pattern
of cognition compared to individuals with visual imagery. Notably, aphantasic individuals reported signicantly
reduced imagery across all sensory modalities (and not just visual). However, only 26.22% of aphantasic par-
ticipants reported a total absence of multi-sensory imagery altogether, raising important questions about the
primary aetiology of aphantasia and suggesting possible sub-categories of aphantasia within a heterogeneous
group. Aphantasic individuals’ episodic memory and ability to imagine future events were also reported to be
signicantly reduced compared to the two control populations. ese ndings attest to the recently established
functional and anatomical overlap in brain networks supporting the exible, constructive simulation of episodic
events (whether they be real past events or hypothetical future events)25, and suggest that visual imagery may be
an essential and unifying representational format potentiating these processes.
Interestingly, our data aligns with that of previous studies demonstrating unaected spatial imagery abilities in
aphantasia10,22, suggesting an important distinction between object imagery (low-level perceptual features of objects
and scenes) and spatial imagery (spatial locations and relations in mental images)26. is distinction is indeed reected
at a neural level, with disparate brain pathways used for perceptual object processing and spatial locations, respec-
tively27. Strikingly, cognitive dierences in aphantasia were not limited to processes where visual imagery is typically
deliberate and volitional, with aphantasic individuals in our study reporting signicantly less frequent and less vivid
instances of spontaneous imagery such as night dreams. ese data suggest that any cognitive function (voluntary or
involuntary28) involving a sensory visual component is likely to be reduced in aphantasic individuals, and it is this gen-
eralised reduction in the sensory simulation of complex events and scenes that is most striking in aphantasia.
is work used a large-sample design to investigate reports of altered cognitive processes as a function of visual
imagery absence. However, due to the self-described nature of the phenomenon in our online sample, it is prudent to
rule out alternative explanations for the between-group dierences seen here. Some authors have appropriately high-
lighted that visual imagery absence does not always present congenitally, but may be acquired as an associated symptom
of neurological damage or psychopathology29. As a result, it is arguable that some aspects of our results may be more
parsimoniously attributed to underlying psychogenic factors. Whilst plausible, we do not believe the reports of our
sample here are best explained by this account. Only 9 out of 267 (3%) participants in our aphantasic sample reported
acquired imagery loss, with the majority of participants reporting having lacked visual imagery capacity since birth.
Additionally, there were no signicant dierences between our aphantasic sample and our main control group in the
number of participants reporting a history of mental illness, neurological condition, or head injury/trauma– in fact,
signicantly fewer aphantasic participants reported a history of stroke or history of epilepsy/seizures compared to par-
ticipants in control group 1 (see Sample Characteristics in Method, and TableS1 in Supplementary Information).
Importantly, a supplementary within-group analysis also showed that there were no signicant dierences between
aphantasic participants with or without a reported history of mental illness/psychopathology on any of our primary
imagery, memory, dreaming, or spatial ability outcome variables, aer controlling for multiple comparisons (see
TableS8 in Supplementary Information). Furthermore, the only signicant within-group dierences that were revealed
by this supplementary analysis (such as signicantly higher scores on some PCL-5 components in aphantasic individ-
uals with a mental illness history compared to those without; see TableS8) are dierences we might expect to nd as a
function of psychopathology status in any sample population, given the target variables of interest and clinical scope
of the scale. Considering these factors together, it is unlikely that our main results are best explained by acquired or
associated symptoms of psychogenic causes such as mental illness or psychopathology.
Aphantasic participants in our study were compared with two independent control groups of participants
with visual imagery on a range of self-reported cognitive outcomes. It is important to note that that neither of
these control groups were perfectly matched on demographic characteristics with our aphantasic sample. In our
main group comparison, the ratio of females to males was signicantly higher in the aphantasic group (48%) than
in control group 1 (35%), despite these groups being matched on mean age. In order to account for the poten-
tial inuence of sample characteristics (including gender) in our main control group of MTurk participants, we
conducted a replication analysis with a second control group of undergraduate students featuring a higher ratio
of females to males (73%). is second control group, however, was signicantly younger in mean age (19 years)
compared to the aphantasic sample (34 years; see TableS1 in Supplementary Information).
Despite these demographic discrepancies, the results of our replication analysis with control group 2 revealed
a remarkably similar pattern of between-group effects to our main analysis (see TablesS2–6 in Supplementary
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Information). Additionally, a majority of the signicant changes to our results that did occur are congruent with estab-
lished eects of age and gender on cognitive outcomes. For example, our nding that undergraduate participants
reported signicantly more frequent memory intrusions and avoidance behaviours than aphantasic participants in
response to stressful life events may be explained by the typically higher prevalence of PTSD diagnosis and symptom-
atology amongst females30 (and younger females in particular31). Similarly, our replication analysis results suggested
that aphantasic participants reported signicantly fewer mind-wandering episodes and qualitatively impoverished
dream phenomenology in additional SERS domains, but only in comparison to the comparatively younger under-
graduate control group 2 and not when compared to the age-matched control group 1 (see Fig. S4 and TableS5 in
Supplementary Information). is is a pattern of results which accords well with ndings of age-related decline in
spontaneous mind-wandering32 and subjective dream phenomenology24, respectively.
e few divergences in results between our main analysis (with control group 1) and replication analysis (with
control group 2) are therefore largely consistent with previous research on the roles of age and gender in cogni-
tion. e overall equivalence of our results across these independent control group comparisons (despite demo-
graphic discrepancies between groups) suggests that our major ndings are unlikely to be artifacts of sampling
bias. Nevertheless, the interaction between demographic characteristics, imagery and cognition is potentially
complex, and future research should overcome this limitation of our study design by implementing more precise
selection criteria for matched control samples.
It is also important to highlight that our study assessed intergroup dierences in cognition by using self-report
outcomes which might be inuenced by response biases. If aphantasic participants were motivated to respond
in line with a self-identied lack of imagery (or even with perceived generalised cognitive decits), for example,
we would expect them to indiscriminately report at oor on all self-report measures of cognition, or at least on
all scales measuring cognitive abilities typically thought to be reliant on visual imagery use. eir pattern of
responses on some scales (particularly those measuring reported spatial abilities) suggests otherwise. On the
SAM, aphantasic individuals reported no consistent reduction in spatial memory (or navigation) ability compared
to controls, despite reporting memory decits on all other components of this scale (see Fig.1 blue and purple
sections). More convincingly, aphantasic participants selectively reported decits in object imagery but not spatial
imagery on the OSIQ in our study, despite items corresponding to these two components being presented in ran-
domised order within the same scale (see Fig.1 blue and red sections). Lastly, previous research has shown that
participants with self-described aphantasia do not just score at oor on self-report imagery questionnaires, but
also exhibit lower scores than control group participants on a behavioural measure of sensory imagery strength
which bypasses the need for self reports10, suggesting that response bias is not a most parsimonious explanation
for presentations of self-described aphantasia. Demand characteristics cannot be unequivocally ruled out in the
current study (as with any study of self-reports), and our ndings should be validated with objective measures in
future experiments. However, this study provides useful population-level data in order to highlight the veridical
subjective dierences that exist in a range of cognitive domains as a function of visual imagery absence.
ere is strong theoretical impetus for future assessments of aphantasia, and our work highlights several areas of
relevance that should be prioritised by future studies. For example, it is noteworthy that whilst the PCL-5 assesses
one’s general response to stressful life events, it does not assess responses to recalling specic traumatic events18, nor
does it have good measurement sensitivity for the imagery-based re-experiencing of such events. Whilst the overall
pattern of our results suggests that aphantasic individuals do not appear to be markedly protected against all forms
of trauma symptomatology, it may remain the case that they discernibly benet from a reduced susceptibility to
re-living these events in vivid sensory detail. Similarly, the self-report nature of our study does not allow for an objec-
tive, content-driven account of episodic memory function and phenomenology in aphantasia. Whilst some of the
questions presented to participants on the EMIQ and on theSAM do ask them to report upon the visual experience
of their memories, the distinction between remembering past life events and visually representing them is one which
is not well delineated. ere is therefore considerable scope for future experimental research to tease apart these
separable component processes of episodic memory, and their relation to visual imagery absence in aphantasia.
Many other questions about aphantasia remain unanswered, including its longitudinal stability, the relative
contribution of genetic and developmental factors to its aetiology, and its exact contribution to individual cog-
nitive proles. Our research presents an extended cognitive ngerprint of aphantasia and helps to clarify the role
that visual imagery plays in wider consciousness and cognition. Visual imagery is a cognitive tool oen taken
for granted – an assumed precursor to our ability to think, learn, and simulate the world around us. is work
demonstrates that such tools are not shared by everyone, and shines light on the rich but oen invisible variations
that exist in the internal world of the mind.
Received: 28 December 2019; Accepted: 6 May 2020;
Published: xx xx xxxx
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Acknowledgements
We thank Marcus Wicken for his helpful insight on this project and ongoing collaboration. We also thank the
aphantasic participants who gave their time to participate in this study and contribute feedback on our research.
is work was supported by Australian NHMRC grants APP1046198 and APP1085404; J. Pearson’s Career
Development Fellowship APP1049596; and an ARC discovery project DP140101560. T. Andrillon is supported
by the International Brain Research Organization and the Human Frontiers Science Program (LT000362/2018-L).
A. Dawes is supported by an Australian Government Research Training Program (RTP) Scholarship.
Author contributions
All authors developed the study concept. A. Dawes built the study design and collected the data. A. Dawes, R. Keogh
and T. Andrillon performed data analysis. A. Dawes draed the rst version of the manuscript, and R. Keogh, T.
Andrillon and J. Pearson provided critical revisions. All the authors approved the nal manuscript for submission.
Competing interests
e authors declare no competing interests.
Additional information
Supplementary information is available for this paper at https://doi.org/10.1038/s41598-020-65705-7.
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