Trypophobia as a Psychophysiological Phenomenon: Evidence of Cortical Hyperexcitability and Contamination Disgust

Trypophobia—an intense aversion to patterns of small, clustered holes—has emerged as a condition of growing interest at the interface between neuroscience, psychology, and physiology. Although it is not formally listed in the DSM-5, its prevalence and reports of significant morbidity warrant closer scientific scrutiny. The study conducted by Le, Cole, and Wilkins (2020) provides valuable contributions to the characterization of trypophobia as a measurable neurophysiological phenomenon, beyond its appearance as a simple visual idiosyncrasy.

Using photoplethysmography (PPG) and functional near-infrared spectroscopy (NIRS), the authors demonstrated that trypophobic images are capable of inducing measurable physiological responses—specifically, increases in heart rate (HR) and heart rate variability (HRV)—but only among individuals who score high on the Trypophobia Questionnaire (TQ). This selectivity reinforces the validity of the diagnostic instrument and points to a specific emotional response triggered by such stimuli (Le, Cole & Wilkins, 2020).

It is notable that both heart rate and heart rate variability increased significantly in response to trypophobic images only in the group with high sensitivity to trypophobia. This indicates the simultaneous activation of sympathetic and parasympathetic autonomic systems, a physiological pattern typically associated with disgust due to contamination. This pattern differs from the emotional responses observed in fear or anger, in which there is typically a reduction in heart rate variability (Kreibig, 2010). Thus, the data suggest that the type of emotion underlying trypophobia is closer to disgust than to fear—an interpretation consistent with previous findings associating trypophobia with visual stimuli reminiscent of infectious diseases (Kupfer & Le, 2017).

Complementing the autonomic measures, the authors used NIRS to investigate the cortical hemodynamic response. They observed that trypophobic individuals exhibited a significantly greater response in occipital regions of the cerebral cortex when viewing trypophobic stimuli, when compared to both neutral images and the control group. This increased response in visual areas is consistent with the hypothesis of cortical hyperexcitability, a phenomenon previously implicated in conditions such as photophobia and migraine (Wilkins, 2015). The dissociation between autonomic and hemodynamic responses reinforces the notion that these dimensions are partially independent: visual discomfort and emotional arousal appear to overlap, but are not confused.

In discussing the mechanisms involved, the authors argue that trypophobia can be partially explained by the presence of visual features that activate inefficient cortical response patterns, such as the concentration of spectral energy at mid-spatial frequencies—a property shared by many stimuli considered visually uncomfortable. Neural coding models with low sparsity and excitation-inhibition imbalance simulate well the discomfort generated by such images, suggesting a computational basis for the phenomenon (Penacchio & Wilkins, 2015).

An additional relevant point concerns the influence of learning and personal history on the intensity of the aversive response. Images that mimic skin infections, such as artificially inserted holes in human faces, are particularly unpleasant. This effect may be related to traumatic memories, previous dermatological experiences, or the activation of evolutionary disease avoidance mechanisms — as demonstrated in correlational studies between dermatological history and the intensity of trypophobia (Yamada & Sasaki, 2017).

In summary, the paper by Le et al. provides robust empirical evidence that trypophobia is not merely a subjective discomfort, but a verifiable psychophysiological phenomenon with important implications for understanding the interactions between visual perception, emotion, and neurophysiology. Responses differ between individuals with and without the condition, both at the autonomic and cortical levels, and appear to be driven by complex mechanisms involving bottom-up visual processing, learned emotional aversion, and possibly evolutionary adaptations. These findings reinforce the importance of recognizing and clinically studying seemingly marginal conditions such as trypophobia, as they reveal fundamental aspects of human brain functioning.

Reference:
LE, An; COLE, Geoff G.; WILKINS, Arnold. Trypophobia: Heart rate, heart rate variability and cortical haemodynamic response. Journal of Affective Disorders, [S. l.], v. 274, p. 1147–1151, 2020. DOI: https://doi.org/10.1016/j.jad.2020.06.002. Available at: https://www.sciencedirect.com/science/article/pii/S0165032719320761. Accessed on: 17 June. 2025.

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