Aphantasia is a condition in which the ability to visualize images in the mind is absent or significantly reduced. It is often described as “seeing nothing when I close my eyes” or “only a black screen.”
The term “aphantasia” was coined by Adam Zeman and colleagues in 2015. It derives from the Greek word “phantasia” (imagination). Individual differences in visual imagery ability were first systematically studied by Francis Galton in 1880 through his “breakfast table survey.”
Mental visualization ability exists on a spectrum from hyperphantasia (extremely vivid) to aphantasia (absent).
Several studies have reported on the prevalence, with estimates as follows1).
No sex differences have been observed. There is no consensus on the effect of age. Patients with a family history have been reported, suggesting a possible genetic factor, but recent genome-wide association studies have not found significant genetic associations1).
It is estimated to occur in about 2–4% of the general population. A meta-analysis reports 4.8% (Monzel et al. 2023), and a Japanese survey reports 3.6% in the VVIQ 17–32 range (Takahashi et al. 2023)1). Complete absence of imagery (VVIQ=16) is rarer, at 0.07–0.7%.
In congenital cases, many individuals are unaware of their condition until adolescence or early adulthood.
Deficits in non-visual imagery may also coexist. 54.2% report deficits across all sensory modalities, including auditory, olfactory, gustatory, tactile, and motor imagery1).
There are two subtypes: “visual aphantasia,” where only visual imagery is absent, and “multisensory aphantasia,” where imagery is absent across all sensory modalities1). Among those with reduced visualization ability, 54.2% report a lack of imagery in all senses.
There are no associated organic abnormalities in ophthalmology. External ophthalmic examinations are normal.
In acquired cases, the timeline of onset can be traced. In a case report, the VVIQ score dropped to 16 (lowest value) after stem cell transplantation, with mild improvement to 23 after 6 months2).
Reported changes in emotional response include reduced reaction to fear stimuli and decreased emotional engagement with narratives1).
Congenital
Onset: Congenital lack of imagery. Most notice it after puberty.
Organic abnormalities: No associated ophthalmological or neurological findings.
Course: Stable condition throughout life. No improvement observed.
Awareness: Many consider their condition as “normal.”
Acquired
Onset pattern: Acute onset triggered by head trauma, stroke, or post-transplant.
VVIQ score: May show a minimum value (16 points) immediately after onset.
Course: May show mild improvement, but complete recovery is rare.
Etiology: Hypoxic brain injury and neurotoxicity may be involved2).
The etiology is unknown. Some patients report a family history, suggesting a possible genetic pattern, but genome-wide association studies have not found significant genetic associations1).
Neurogenic
Traumatic brain injury (TBI): The most common cause.
Stroke: Bilateral or left posterior cerebral artery (PCA) stroke has been reported2).
Dementia: Decreased visualization ability is seen in all subtypes.
After stem cell transplantation: Hypoxic brain injury and drug neurotoxicity may be involved2).
Post-COVID-19: Cases of onset after infection have been reported.
Psychogenic
Depression: An association with onset has been reported, but some studies find no difference in visualization ability compared to healthy individuals.
Anxiety disorders: A similar association has been suggested but not established.
Dissociative disorders: An association with depersonalization/derealization disorder has been noted.
Case reports of acquired aphantasia are shown below.
Bumgardner et al. (2021) reported acquired aphantasia in a 62-year-old male after autologous stem cell transplantation (ASCT) for multiple myeloma 2). After administration of melphalan 200 mg/m², aphantasia appeared on day 9 simultaneously with the onset of spontaneous pneumothorax. The VVIQ score was 16 (lowest possible). It mildly improved to 23 after 6 months. Hypoxic brain injury due to shunt physiological hypoxemia from pneumothorax and sepsis was considered the most likely etiology.
Some patients report a family history, suggesting a possible genetic pattern, but recent genome-wide association studies have not found significant genetic associations 1). Currently, there is insufficient evidence to confirm heritability.
There are no official diagnostic criteria. It is primarily assessed based on self-report.
The following are representative examination methods.
| Examination method | Overview | Features |
|---|---|---|
| VVIQ | 16-item, 5-point self-assessment | Minimum 16 to maximum 80 points |
| Binocular rivalry task | Measures priming effect after image instruction | Allows objective assessment |
| Pupillary light response | Checks for pupillary light response to imagery | Absent in aphantasia |
Generally, many studies define aphantasia as a VVIQ score of 16-32, but there is no unified cutoff value 1). Scores of 33 or higher have also been reported in individuals who self-identify as having aphantasia, indicating limitations in diagnosis based solely on scores.
Currently, there is no approved treatment for either congenital or acquired aphantasia.
An fMRI study (2017) showed that individuals with low visualization ability had more activity in the anterior cingulate cortex and frontal regions, while those with high ability showed activity in the fusiform gyrus, parahippocampal gyrus, and posterior cingulate cortex 1).
The characteristics of the two pathways in visual processing are described below.
| Pathway | Function | Relationship with aphantasia |
|---|---|---|
| Ventral pathway (“what” pathway) | Object image processing | May be impaired |
| Dorsal pathway (“where” pathway) | Processing of spatial information images | May be preserved |
Object images are processed by the ventral pathway, while spatial images are processed by the dorsal pathway. In aphantasia, impairment of the ventral pathway is suggested, while the dorsal pathway may be preserved1).
In cases of acquired aphantasia after stem cell transplantation, the following mechanisms have been considered2).
In aphantasia, functional connectivity between the fusiform face area (FFA) and frontoparietal regions is reduced 1). Additionally, activation of the ventral pathway (fusiform gyrus, parahippocampal gyrus) involved in visual imagery is poor, and occipital and parietal lobe activation during recall is also absent. Lesion studies have confirmed that damage to the left fusiform gyrus and right lingual gyrus can eliminate imagery ability.
Aphantasia is not currently included in any clinical diagnostic system (DSM or ICD)1). Some views position it as a form of individual difference rather than a disease.
It has been suggested that progressive aphantasia may be a prodromal symptom of dementia1).
A systematic review by Jin et al. (2024) reported the following associations1).
- PTSD: Individuals with aphantasia have fewer intrusive memories after trauma and less avoidance behavior. They tend to have reduced predictors of PTSD.
- Autism Spectrum Disorder (ASD): They tend to have higher AQ (Autism Quotient) scores and are more frequently classified as having ASD.
- Prosopagnosia: 5.9% of the spatial aphantasia group had prosopagnosia, and about 20% of patients with developmental prosopagnosia report comorbid aphantasia.
