Autonomic, neurodevelopmental, and early adversity correlates of acquired aphantasia

Abstract

Aphantasia (the inability to voluntarily generate mental imagery) has traditionally been studied as a congenital or neurological condition. However, historical and clinical reports also implicate affective and stress-related factors in the onset of imagery loss, which are themselves associated with disrupted interoception and autonomic nervous system dysfunction. To investigate these links, we surveyed individuals with self-identified acquired aphantasia (N = 59) using structured questions and validated questionnaires assessing early adversity (Childhood Trauma Questionnaire), anxiety symptoms (GAD-7), autonomic reactivity (Body Perception Questionnaire–Short Form; Atrial Fibrillation Symptoms Questionnaire), and neurodevelopmental traits (AQ-10, ASRS-6). 62 % of participants reported psychological triggers for their aphantasia, 41 % cited neurological or physiological events, and 30 % identified pharmacological factors. Nearly half of the participants described a combination of these influences, with psychological factors frequently co-occurring with medication use or physical events, suggesting that acquired aphantasia may oftenhave multifactorial origins rather than a single isolated cause. Compared to typical imagers, individuals with acquired aphantasia reported significantly higher levels of childhood trauma and increased supra-diaphragmatic autonomic reactivity, as well as significantly elevated scores on measures of ADHD and autism. These findings suggest that acquired aphantasia may not only follow neurological injury but can also emerge in the context of affective conditions shaped by early adversity and neurodevelopmental vulnerability. Affective disturbances may contribute to imagery loss by altering the subjective experience of autonomic signals and disrupting the integration of bodily, emotional, and cognitive information required to generate vivid mental representations. In conclusion, these results support an affective-autonomic pathway to acquired aphantasia.