Front. Psychiatry Frontiers in Psychiatry Front. Psychiatry 1664-0640 Frontiers Media S.A. 10.3389/fpsyt.2025.1643264 Original Research Painting psychosis: an empirical investigation of the self-portraits of Edvard Munch BettelheimEric C. 1 2 * Writing – review & editing Investigation Data curation Writing – original draft Conceptualization LiuJingyi 1 Writing – review & editing Methodology Software DazzanPaola 2 Supervision Writing – review & editing TurkheimerFederico 2 Funding acquisition Writing – review & editing Conceptualization Supervision Methodology Department of Neuroimaging, King’s College London, London, United Kingdom Department of Neuroimaging, King’s College London School of Neuroscience, London, United Kingdom Correspondence: Eric C. Bettelheim, eric@ericbettelheim.com 05 02 2026 2025 16 1643264 08 06 2025 17 12 2025 04 12 2025 Copyright © 2026 Bettelheim, Liu, Dazzan and Turkheimer. 2026 Bettelheim, Liu, Dazzan and Turkheimer https://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

Substantial evidence demonstrates that the brain is more interested in faces than in other subjects and that self-related material, particularly self-images, have higher saliency than non-self-referential material. Studies of self-portraits have revealed correlations between stylistic elements and artists’ states of mind. Edvard Munch, a founder of Expressionism and most famous for “The Scream”, was pre-occupied with depicting his subjective experience and a prolific painter of self-portraits. He has been posthumously diagnosed as suffering from schizophrenia, anxiety, bipolar and other disorders associated with altered perception. Munch’s painted self-portraits were empirically examined to determine if variations in stylistic elements, contrast, colour and fractal dimension, correlate with life events associated with psychopathology. His portraits were also examined as controls and to test whether images of others, related and unrelated to him, vary stylistically from his self-portraits and from each other. Productivity was examined as an independent indicator. Significant changes in contrast, colour, fractal dimension and productivity during critical periods in his life were identified in his self-portraits consistent with the conclusion that Munch is diagnostically best described as suffering from early onset psychosis. Examination of his portraits of related and unrelated people revealed differences from self-portraits and from each other consistent with comorbid social anxiety disorder.

 psychosis schizophrenia Edvard Munch painting self-portraits neuroscience of art stylistics quantitative methods NIHR Maudsley Biomedical Research Centre 10.13039/100019418 The author(s) declared that financial support was received for this work and/or its publication. NIHR Maudsley Biomedical Research Centre at South London and Maudsley NHS Foundation Trust and Institute for Human and Synthetic Minds, King’s College London. section-at-acceptance Psychological Therapy and Psychosomatics Background

The brain is more interested in faces than other subjects and in self-images more than non-self-referential material (1–3). Uniquely in art, in self-portraits the subject and object are the same. During their creation three images of the artist are involved: i) the face in the mirror or photograph, ii) the internal self-representation and iii) the image on a surface. The artist’s gaze, internal and external, never leaves the self. This constitutes a unique feedback system engaging visual perception, self-reflection and motor activity suggesting that self-portraits are more likely to reveal the artist’s state of mind than other artworks. In previous work, we have used quantitative tools for the analysis of self-portraits to infer pathophysiological traits from the production of artists with known mental health disturbances but not clear pathophysiology. Hence we have demonstrated a strong association of increased contrast in in the self-portraits of Vincent van Gogh during periods of extreme absinthe- consumption, a liquor popular with the artistic crowd in Paris in the 1860s but also a potent GABA interneuron inhibitor likely to generate psychotic episodes in subject with schizophrenic traits (4). We have also demonstrated the use of colour intensity (e.g. reds and yellows), in the self-portraits of Frida Kahlo during episodes of anger and pain (5). Others have similarly used fractal dimension (an indicator of healthy neuronal activity) in paintings to reveal reduced complexity in prominent aging artists suffering from forms of dementia (6) and increased complexity in particular periods of artist’s careers associated with behavioural change (7). More broadly, impairment in visual processing and spatial orientation in their art has been found in patients suffering from schizophrenia and obsessive compulsive disorder and in artists with psychosic experience (8, 9). Studies have revealed relationships between perceptual distortion in patients suffering from schizophrenia and artistic creativity suggestive of expression of emotional states (10).

Disturbances in the sense of self have been associated with various disorders including both depression (morbid pre-occupation) and schizophrenia (loss of boundaries) since the foundations of psychiatry (11–13). In schizophrenia these disturbances extend to self-perception (14, 15). ‘Signe du mirroir’, the inability to recognise, or a sense of strangeness when regarding, oneself in the mirror has long been recognised as characteristic (16–18). Sufferers often complain of a sense of disintegration of themselves and of their environment and of vivid, often overwhelming, sensory (19) and particularly visual, experiences (20, 21).1 The Scream’ can be understood as a depiction of such an event.2 Recent research has identified numerous morphological and functional deficiencies in the visual systems of those suffering from schizophrenia (25, 26) and its frequent comorbidities (27) of depression (28–30), and alcohol (31) and nicotine (32, 33) abuse, which provide a neurobiological foundation for such experiences (26, 34–36)‘.

Edvard Munch (1863-1944) ‘Munch’ lived in the era in which the foundations of modern psychiatry were being laid (37–40) and he and his circle were aware of these developments (41, hereafter, ‘Prideaux’). Diagnosis, while at an early stage, was recognizably in accordance with modern constructs but not contemporaneously applied to him. Munch has been retrospectively diagnosed with a variety of disorders including schizophrenia (42), bipolar disorder (BPD) (43–45), narcissistic personality disorder (46, 47), borderline personality disorder (48), anxiety of various kinds including agoraphobia (49, 49, 50) and depression (46, 51). This illustrates both the complexity of his condition and the difficulty of post-mortem diagnosis even if relatively recent and where, as here, there is voluminous documentation (52–54)3.

 Biography – critical events

Munch is regarded by many as the father of Expressionism a school of art focused on conveying the artist’s subjective experience particularly using colour and distortion (59, 60). Although Munch initially painted in a naturalistic manner this began to change with the ‘The Sick Child’ an image of his older sister dying of tuberculosis. He later referred to it as his ‘breakthrough’ (61, p. 184; hereafter, ‘Holland’). This change in style became consolidated in 1889 after the death of his father. Emerging from his grief he wrote his ‘St Cloud Manifesto’ in which he committed himself to no longer painting “interiors, people who read and women who knit” but instead, “living people who breathe and feel, suffer and love” (62, p. 60; hereafter, ‘Tøjner’).

His determination to convey his own feelings in a new style became manifest in paintings of Despair (1892), Melancholy (1892), the Scream (1893), Anxiety (1894) and Jealousy (1895). Loneliness, illness, death, and bitter erotic experience became themes which continued to preoccupy him throughout his life.4 Munch was keenly aware of the role physical and psychological illness played in his life and considered both essential to his art (63).5 This may explain why he resisted treatment, like other creative people, until he had a complete breakdown in 1908 (43). He saw his art as essentially confessional, a form of autobiography and of self-therapy (64, hereafter, ‘Ustvedt’, 57). This is reflected in the number of self-portraits he painted, 51, in addition to 20 lithographs, including his first, and over 100 other works on paper (65–67).

Munch was the second of five children born within six years to an army physician and a considerably younger tubercular mother. At the time of his December birth his parents were living in rented rooms in a rural farmhouse. In his first year the family moved to the then rapidly industrialising capital city of Kristiana (now Oslo). Although from a prominent family, Munch’s father had a modest income which declined as he established his practice in poor areas of the city causing the family to move several times as it approached poverty. This trend worsened after the death of Munch’s mother from tuberculosis when he was 5. His older sister, to whom he was deeply attached, died of the same disease when he was 14. Tuberculosis was so common in Norway at the time that it was known as the national disease (68, 69). In 1912, near its peak, 80% of children in Kristiana were infected by the time they started school (70).

At birth Munch was so ill with respiratory disease that his father made arrangements for his immediate baptism and burial (Prideaux). Munch suffered respiratory illness throughout his life on several occasions requiring hospitalisation. He was unable to attend school for extended periods due to ill health spending entire winters confined to bed and ultimately could not continue. At the time of his mother’s death and again during an episode of tubercular-like infection age 13, he experienced vivid religious hallucinations. He blamed himself for the death of his sister in the following year as she had nursed him. In addition to his mother and sister the disease was responsible for the deaths of his maternal grandmother and maternal aunt. Despite his chronic vulnerability he survived pneumonia and the Spanish Flu ultimately dying of bronchitis in old age.

There is evidence of mental illness in Munch’s family. His paternal grandfather died in an asylum.6 One of Munch’s younger sisters had symptoms of schizophrenia in adolescence and spent most of her adult life in an institution. His father, a lifetime smoker who came from a devout family, became depressed following his wife’s death and expressed increasing religious obsession and dependence on alcohol. His father’s preoccupation with divine punishment in the form of disease and death was such that Munch’s childhood hallucinations were terrifying audible and visual images of skeletons, angels, and devils there to draw him into death (Prideaux). He often woke in the middle of the night wondering whether he was in hell (Tøjner).

Munch therefore had multiple reasons for emotional distress. His respiratory disease presented a constant, life-long threat of death, embodied in the deaths of close relatives, an anxiety reinforced by his father’s religious preoccupations. It imposed repeated periods of social isolation compounded by frequent changes in household. Soon after birth his mother put him in her sister’s care. After this initial separation he then experienced the death of his mother and older sister to whom he attached himself in the aftermath. His aunt, who he suspected of wanting to marry his father and replace his mother, became the only adult on whom he could rely although she too was tubercular (58; Tøjner). Unlike his father, who strongly disapproved, she recognised and nurtured his artistic talent and supported his ambition to be an artist (71). Despite her life-long attention and affection Munch kept her at a distance even unwilling to attend her funeral (Prideaux).

Against his father’s wishes Munch left technical college to pursue an artistic career attending art school for a year and then seeking informal instruction from various local artists. He adopted a bohemian lifestyle led by local writers and political radicals. During this time his abuse of alcohol and tobacco became apparent (Prideaux; 72). His first exhibition in 1885 attracted the attention of the local art establishment which provided him with the means to study in Paris. He postponed the trip due to ill health and had his first love affair with a woman of his mother’s age, the wife of a cousin, a military physician like his father. The experience filled him with what can be reasonably seen as Oedipal guilt and shame expressed in a painting called “Ashes”.

The end of the affair precipitated a period of mental disturbance which included heavy drinking and smoking, vertigo, agoraphobia, despair and jealousy (Prideaux). By year-end he was sufficiently recovered to visit Paris then at the height of the Impressionism wave; a style he adopted for a time. On his return to Kristiana, he began work lasting over a year on ‘The Sick Child’ exhibited in 1886. To his dismay, given the importance of the subject to him and the intense effort he had made, it was heavily criticised by critics and the public. Munch was so discouraged he left Norway beginning two decades of voluntary exile first in France in 1889 and from 1892 in Germany. While in France he was virtually destitute, often going without food, drinking heavily, visiting brothels and gambling unsuccessfully (Heller. Prideaux, Stang).

In 1889 he suffered near fatal pneumonia and in 1890 received news of his father’s death. He moved away from his bohemian circle and became deeply depressed. Soon thereafter he was again hospitalised with pneumonia and suffered a nervous collapse. Still unrecognised as an artist he continued to drink heavily often painting for days without rest (Prideaux). An exhibition in Berlin in 1892 so disturbed the conservative establishment that it was immediately closed down. The resulting ‘succes de scandale’ made him famous and attracted the attention of patrons and critics. In 1893, he recalled and painted the hallucinatory experience depicted in The Scream in which the figure and the environment seem to be dissolving.

“The air turned to blood – with cutting veins of flame….That shrill, bloody red. On the road and the fence. The faces of my comrades became a garish yellow-white. I felt a huge scream welling up inside me – and I really did hear a huge scream. The colours in nature broke the lines in nature. The lines and the colours quivered with movement. These vibrations of light caused not only the oscillation of my eyes. My ears were also affected and began to vibrate. So I actually heard a scream. Then I painted The Scream” (Tøjner, p. 96).

In 1894 his younger sister was institutionalised in an asylum near the bridge depicted in The Scream (Prideaux). In 1896 his only brother died of pneumonia age 30, shortly after his marriage, confirming Munch’s fear of marriage, association of female intimacy with death and compounding his sense of loss (73; Stenersen; Tøjner). His difficulty in maintaining relationships and intense social anxiety7 led to frequent impulsive travelling both to escape intimate contact, particularly with women, and to pursue commercial opportunities (Prideaux; Stang). His sometimes intense friendships did not last long. He could not tolerate the physical presence of people for any length of time including family members with whom he maintained life-long attachments (Heller; 74, hereafter ‘Howe’; Prideaux).

During this period Munch displayed a wide variety of symptoms including panic, phobias, insomnia, somatic complaints, pressured speech, strange ideas, hallucinations, delusions and paranoia. The latter was evident on several occasions when he provoked others violently. His brawls with strangers were notorious. On at least four occasions he used a firearm. He had three love affairs but never established a stable intimate relationship relying on prostitutes, servants and models for sexual experience. Munch’s abuse of alcohol was so severe that he was the subject of concern by his contemporaries (Ustvedt). He sought respite in various sanatoria8 for a variety of somatic complaints including insomnia, gastrointestinal and cardiac distress, vertigo, limb numbness and phobias including agoraphobia and fear of beds which he associated with illness and death (Tøjner). During this time he also took various drugs including bromides, aspirin and medication for the heart, fever and rheumatism (Prideaux).

He experienced increasing paranoia, convinced that others were speaking disparagingly of and plotting against him. In 1902 a struggle with an obsessive lover involving a revolver resulted in the loss of part of a finger on his left hand. He depicted her several times as Charlotte Corday and himself as the murdered Marat encapsulating both his anxiety about women and his association of sex and death. His condition deteriorated and in 1908, experiencing vivid auditory and visual hallucinations and paranoid delusions, he was admitted to a clinic in Copenhagen where he remained for 9 months. On admission he was diagnosed as having dementia paralytica due to alcohol poisoning (Heller; Prideaux; Tøjner).

He was initially kept sedated and then received mild electric treatment, massage and scented baths but the ‘therapy’ essentially consisted of enforced abstinence, regular meals and rest. He became sober and remained largely abstinent thereafter. In a self-portrait painted just before his release he appears to be emerging from dissolution. In 1909 he returned to Norway having received a national honour and the public recognition he had long sought. He purchased rural property outside of Oslo and thereafter he lived in isolation “just like a monk” (318; Prideaux; Stang, p. 222; Stenersen). He was unable to tolerate the presence even of close family members (Prideaux). Several housekeepers and models with whom he had sexual relations were tolerated but only so long as those relations continued.

He occasionally allowed patrons who had commissioned portraits to visit, but none were allowed to stay the night (Stenersen). He worked in an eccentric fashion talking constantly which he described as, “a defence” preventing others from speaking and their words entering and taking him over. He glanced at his subjects and then painted his first impression. Sitters often moved or left as he continued to talk and paint. He famously said, ‘I paint not what I see but what I saw” (Heller p. 42; Prideaux; Tøjner). This was his modus operandi; to capture not the detail of the image but its immediate impact on him (Ustvedt).

Although awarded large state and private commissions and accumulating increasing wealth he lived an ascetic life. His style noticeably changed from his pre-treatment period and included landscapes and local people. He surrounded himself with copies of portraits he had painted which he referred to as his “guardians”, “children” and his “family”. He sometimes “punished” them by leaving them outside or banishing them to an upstairs storage room (Stenersen). When indoors he continually played a radio broadcasting in languages he did not understand, or simply white noise, to drown out other sounds and exclude intrusive invisible waves which he believed encircled the world. The house was kept illuminated as he was frightened of the dark. It was surrounded by barbed wire, the gates padlocked when he was present and he kept fierce dogs. He continued to suffer insomnia, have delusions and feelings of persecution, particularly by the tax authorities, until his death which he insisted be unattended (Stenersen; Tøjner).

During his lifetime heavy drinking, and promiscuous ‘bohemian’ behaviour was common among artists (75; Prideaux; 76) yet despite this and his myriad symptoms, Munch was a productive and innovative artist throughout his life including during periods when he sought recovery in sanitoria and clinics. While there is some evidence of cognitive impairment, he was capable of successfully pursuing his commercial self-interest in a complex and rapidly evolving art market. Beginning his career in relative poverty and heavily criticised he died wealthy and internationally recognised (65; Heller; Prideaux; Stenersen).

Somatic illness

Munch’s chronic respiratory illness brought him near to death on at least four occasions. Although never diagnosed it seems likely that he suffered from congenital tuberculosis which has non-specific presentation including respiratory distress and chronic lung disease, and it mimics a variety of conditions including pneumonia (77, 78). Transmitted by the mother it can cross the blood brain barrier and cause persistent neuroinflammation (79). Tuberculosis is a heterogenous disease often characterised by remission in untreated adults and closely associated with anxiety, depression, psychosis and somatic disorders including insomnia (80–82). Although physicians attending Munch would have been familiar with tuberculosis maternal transmission was only medically described in 1935 (83).

 Mental illness

Some observers have suggested that Munch suffered from bipolar disorder (BPD) (43, 44); others incline toward schizophrenia as a diagnosis (42). Both are plausible depending on which aspects of behaviour and which periods of Munch’s life are the focus. Others have suggested disorders which encompass symptoms which can be comorbid with both schizophrenia and BPD but do not exclude either (McElroy 47, 49). Manic depression, now BPD, was distinguished from ‘dementia praecox’, now schizophrenia, 15 years before Munch was admitted to the Copenhagen clinic (40). This was well known to the clinic’s director and to other physicians Munch consulted but he was not diagnosed with either condition. His diagnosis on admission of dementia paralytica, usually associated with late stage syphilis, caused by alcohol poisoning was to a degree correct but no underlying cause of Munch’s alcohol dependence nor other source of his psychological distress was identified (Prideaux).

Both BPD and schizophrenia have hereditability rates above 50% (84–86) and are associated with both developmental and environmental factors (87–89) including maternal infection (90, 316), childhood trauma, and parental loss which are additive to the risk of psychosis (91–93). Loss of the mother in childhood increases the odds of psychosis by a factor of 2 (94). Loss of a sibling is comparable to the loss of a father (95). Loss of two first-degree relatives in childhood compounds the risk (96). Both BPD and schizophrenia are characterised by high rates of insomnia (97), comorbid abuse of alcohol (98, 99) and nicotine (100), and risky behaviour including gambling (101) and promiscuity (102). Munch’s life history includes all of these elements.

BPD I typically manifests in adolescence and early adulthood and diagnosis requires a manic episode not attributable to substance abuse preceded or followed by hypomanic or major depressive episodes. Mania is characterised by elated mood, persistent goal directed activity, accompanied by decreased sleep, pressured speech, racing or distracted thoughts or high risk activities. BPD 1 also must include social or occupational dysfunction, hospitalisation or psychosis. Given Munch’s hallucinations and delusions BPD II is ruled out. The absence of manic symptoms when abstinent militates against both BPD I and cyclothymic disorder (103, hereafter ‘DSM 5’) as do the childhood onset of hallucination, the persistence of delusions in adulthood as well as the experience of olfactory hallucination (104; Stenersen).

Munch’s life history reveals virtually all known risk factors and phenomenology of schizophrenia other than motor dysfunction (DSM 5; 105, 106), and all of the predicates and elements of social anxiety (107).9 In addition to the factors mentioned above, he was born in winter (110) to an older father (111) and tubercular mother (112, 113) suffering immediate physiological (81) and psychological trauma (114), moved in his first year to an industrial city (115–117), experienced childhood audio-visual hallucination (118), experienced separation from his mother at birth, on her death and then on the death of his sister (119; Prideaux) the latter accompanied by intense feelings of guilt and shame (120) and social isolation due to his chronic respiratory disease (121, 122; Prideaux). In adulthood, prior to becoming abstinent, he evidenced somatisation and conversion disorder, the presence of physical symptoms, including limb numbness, gastrointestinal and cardiovascular distress, sensory or motor dysfunction where there is no apparent neurological or physiological cause, which characterises two-thirds of schizophrenia patients (123, 124).

Disturbances in the dynamics of perception, such as hallucination, the experience of real perception where no external stimulus is present (125, 126) and delusion, fixed beliefs based on inadequate grounds, not amenable to a rational argument or evidence to the contrary, including persecutory delusions, are key elements of psychosis experienced by 70-80% of schizophrenia spectrum sufferers (127–129). Both are often comorbid with anxiety disorders (130) and may be understood as efforts to resolve perceptual incoherence and sensory misperception and to reduce anxiety (131, 132).

In delusion formation the intensity of perception is altered and inappropriately high levels of salience are attributed to sensory information which might otherwise be disregarded (39, 133). In paranoia visual information, including facial emotion and gestures, indicators of intention, are negatively biased, as is overheard speech. Threatening inferences are drawn leading to false beliefs and inappropriate behaviour (134–137) including violence and social isolation (138, 139).

The natural history of the untreated disease includes a longitudinal transition from early-stage prevalence of hallucination to chronic stage prevalence of delusion (129, 140). This appears to be related to changing dysregulation of neurotransmitters notably dopamine (141), but also involving glutamate (142), serotonin and GABA (143, 144). Childhood trauma is characterised by dopamine dysregulation, positive symptoms (145, 146) and is closely related to retinal dysfunction (34, 147) and morphological abnormalities (148).

 Visual perception

BPD is characterised by sharper, more accurate, sensory experiences including more accurate vision and hearing together with heightened states of empathy and awareness of others’ states of mind (149, 150). In schizophrenia, in contrast, there are visual deficiencies associated with functional and anatomical anomalies throughout the visual system including the occipital, temporal, parietal and prefrontal areas (25, 151–154) and throughout the ventral and dorsal pathways (26). Functionally, reduced visual acuity is widely observed; in one study approaching 70%; 60% of cases demonstrate visual disturbance of some kind. (155–158). Deficits include misperception of the size, distance (159), colour, brightness, contrast and contour of objects (160, 161), in processing spatial frequency 162), integration, binocular vision (163, 164), depth perception and re-visualisation (165) all of which are related to hallucination and delusion (156, 163, 166, 167).

Abnormality in retinal morphology and function are observed in children (168), adolescents (169, 170), young adults at high-risk (171, 172), and prodromal patients (173) and are so pervasive they may be endophenotypes of the disease (153, 174–177). Altered rod and cone electroretinogram (ERG) responses distinguish schizophrenia from other psychosis and from depression (158, 178–180). Optical coherence tomography (OCT) studies reveal reduced macular thickness and volume (181), thinning of both inner (bipolar, horizontal and amacrine cells) and outer (photoreceptor) layers (176) and reduced thickness in the retinal nerve fibre layer (RNFL) (167, 182, 183). Reductions in ganglion cell layer (GCL) and inner plexiform layer (IPL) thickness (184), enlarged optic cup volume, increased cup-to-disc ratios (185, 186) and related tissue loss are also characteristic (187–190). Inflammation and swelling of photoreceptors (191, 192) and microvascular abnormalities are also evident (167, 193) as are distinctive iris pigment dots and crypts related to altered colour vision and cognition (194). These abnormalities together with rod dysfunction appear to cause those with schizophrenia to experience colours as more vivid and are related to hallucinatory experience (148, 195).

Dysfunction at low spatial frequencies in the early stages of the disease progresses to dysfunction in higher spatial frequencies as the disease develops (174, 177, 196). Alterations in retinal morphology and visual processing appear correlated with cortical abnormalities and clinical symptoms (35, 197). Thinner retinal epithelium layer correlates with mania (189), reduced GCL and IPL volume are negatively correlated with disease severity (184), and there are non-linear associations between RNFL thickness and acute and chronic sufferers (198) and with negative and positive symptoms (199). Delusions correlate with deficits in contour integration, conceptual disorganization and perceptual instability (200).

 Contrast

Decreased contrast sensitivity and reduced contrast gain control are common in schizophrenia (160, 201–204). Deficits appear in first episodes and deteriorate as the disease progresses. (154, 205, 206). Both reduced contrast gain (207) and weaker surround suppression (208, 209) are suggestive of reduced inhibition in the visual cortex (210). Both hypo and hyper dopaminergic conditions can prevail in differing systems and at different points in disease progression (145, 211). Reduced dopamine levels in the retina lead to excessively strong coupling of horizontal and amacrine cells and to cone-amacrine cell dysfunction (212–214). This causes reduced contrast sensitivity and poorer colour vision (215–217) and loss of visual acuity (218–220). Lower contrast sensitivity at low spatial frequencies causes difficulty in discerning differing adjacent elements and the blurring of borders (221, 222). Spatial frequency processing, dependent on dopamine receptor function in the retina, is also dysregulated (223a; 224, 225).

While a large majority of studies of contrast perception in schizophrenia find an overall reduction in magnocellular function (196, 226, 227) studies of unmedicated sufferers reveal higher contrast sensitivity and hyperactivity in the pathway consistent with patient reports of vivid anomalous visual experience (228). Hypofunction may therefore be the result of antipsychotic medication (223, 229). However, medication does not explain reduced function in first degree relatives (168), prodromal (20), high risk and remitted patients (228) and in schizotypic subjects (221). Dysfunction at low spatial frequencies in the early stages of the disease progresses to dysfunction in higher spatial frequencies as the disease develops (174, 177, 196). The explanation appears to lie in the progression of the disease, characterized by retinal hyperfunction in the early stage, accompanied by hallucination and hypofunction, accompanied by delusion, as it develops (230). Moderate drinking impairs contrast sensitivity at low frequencies (231) and acute alcohol use reduces contrast sensitivity at all frequencies (232) as well as contrast gain affecting visual processing in both the magnocellular and parvocellular pathways (233, 234). This persists despite years of abstinence (235). Nicotine is associated with rod dysfunction (236).

 Colour

Colour perception dysfunction, increased intensity of, or change in perception, appears at all stages of schizophrenia (21, 36, 237–239). Elevated retinal dopamine leads to increased brightness and hyper-intense colour perception in first episode patients together with visual distortion (237, 240) consistent with reports from high risk and prodromal patients of “abnormal intensity of environmental stimuli, feelings of being flooded and inundated, and inability to focus attention to relevant details” (228, p. 183). Excess dopamine in the limbic system is associated with positive symptoms including hallucination and may be related to structural changes in the retina (189, 241). Colour vision impairment on the tritan (blue-yellow) spectrum is accompanied by retinal hypodopaminergic conditions (242). Alcohol reduces the capacity to distinguish colours increasing the recognition threshold across the colour spectrum. Impairment in perception of colour and luminance is found in young (243), chronic (244) and abstaining alcohol users (245). Reduced colour discrimination is also found in smokers consistent with cone dysfunction (32, 33, 246–249). These deficits in perception of contrast and colour are compounded in individuals on the schizophrenia spectrum who are also heavy drinkers and smokers (33, 238).

 Fractals

Mandelbrot (250) discovered that there is a random, chaotic element in the regularity of natural patterns which he called fractals. Fractals can be seen as emergent, non-linear, spatial and temporal patterns of both chaotic natural phenomena and of self-organising systems such as the brain, which can be measured empirically (251–253).10 This form of regularity can be seen to follow a log power law of fractal dimension ‘D’ varying from 1 to 2 or 2 to 3 depending on whether 2 or 3 dimensions are being measured. This variable can be seen as a measure of spatial order-disorder (number of regularities) and simplicity- complexity (number of elements). D increases as the overall structure increases in fine spatial detail reflecting the relative complexity of the object (250). The D value is essentially a ratio of filled, repeating structural detail to empty space. Fractals thus provide a statistically reliable method of quantifying visual complexity by measuring the relative amount of coarse and fine structure in any image (255–257) including art images (7, 258).

Features of the natural environment have fractal values in the mid-range of 1.3-1.5. Humans are attuned to these levels and experiments consistently demonstrate a human preference for fractal values in this range in landscapes, buildings, urban areas, artificial and biological forms as well as in art of all categories (259–261). Natural images with mid-range values are appealing (7), reduce stress (262) and stimulate calm attention (263, 264). Given its frequency in the natural world at all scales it is unsurprising that humans evolved to prefer the fractal mid-range and regard conformity with it as attractive and an element of beauty (262, 265–267). Artists unconsciously depict faces with fractal values in the mid-range (268, 269). Spatial frequencies in art significantly higher than the mid-range are associated with triggering epileptic seizure and migraine in susceptible individuals and aversion in healthy subjects (270).

Fractal analysis has illustrated changes in complexity which correspond to stylistically defined periods in artists’ careers (271). Jackson Pollack was found to have an identifiable pattern of fractal development in particular periods. Complexity in his work increased over time from a D value close to 1 to 1.72 in his ‘drip’ paintings significantly above the preferred middle range of 1.3-1.5 (7, 272, 273). This may account for early negative critical and public reactions (274). His contemporary Mondrian moved in the opposite direction from early naturalistic paintings with a fractal dimension of 1.7 to abstract paintings consisting of lines of varying thickness with fractal values approaching 1 (266, 275). Fractal analysis of the paintings of prominent artists has revealed that those suffering from neurological disorder in old age reveal declining D levels as compared with those of healthy artists which increase with age (6).

 Metrics

In summary, measuring average contrast tests rod and sensory/interneuronal function particularly depth perception. Use of colour is indicative of cone dysfunction as well as altered mood and fractal complexity reflects general cognitive organisation as each frequency reflects networks at different ranges (the faster frequencies the more local networks, the slower the distant ones).

 Hypotheses

It was hypothesised that longitudinal empirical analysis of elements of style in self-portraits would indicate the artist’s mental state and be distinct from portraits of others. In particular that contrast would decrease and that colour and fractal dimension would increase during periods of crisis and that these trends would be greater in self-portraits than in portraits. It was also hypothesised that portraits of others, related and unrelated, would vary significantly from self-portraits and from each other. It was predicted that, together with productivity, the results would be consistent with a diagnosis of schizophrenia with comorbid social anxiety.

 Material and methods Material

Munch’s extant work consists of 1789 paintings on canvas and wooden panels as well as over 7600 images on paper. He also produced approximately 260 photographs including self-portraits. Of his paintings on canvas and panel eight are known to have been lost, all of which he painted again and an additional 10 lost entirely. None of these were portraits or self-portraits. Of the total corpus of paintings 151 are executed entirely in media other than oil paint and excluded to ensure comparability. Of the remaining 1638 paintings in oil and oil mixed with other materials 51 are self-portraits; 3% of his total oeuvre. He painted self-portraits throughout his career beginning with his first exhibited painting and the last completed the year before his death (276). Included in this category are paintings in which his self-portrait is accompanied by another person; 120 self-portraits on paper are excluded (65).

Portraits examined here represent 13% of his oil paintings all of which are included except preparatory oil sketches and one for which no image is available. All of the portraits are oil on canvas, wood panel or cardboard and painted from life except four painted posthumously. The portraits include 33 images of family and friends. There are 18 images where two or more people are depicted ‘Group Portraits’ treated as single paintings two of which are included in the ‘Family and Friends’ category. Excluded are paintings of scenes in which figures may be identified as Munch, family members or friends but which lack faces or are not detailed enough to be regarded as portraits. Images of models are excluded except where included in a self-portrait. Munch often painted two versions of commissioned portraits one of which he kept for himself. In such circumstances both versions are included. The resulting study sample of 268 paintings, amounts to 16% of his total oil painted oeuvre.

There are few difficulties in authenticating Munch’s paintings. He kept most of his work which has remained in public ownership since his death. Paintings in the city of Bergen have been in public ownership since the original collector’s death. Paintings held elsewhere are well documented and their provenance is not in question. His entire extant painted oeuvre is presented in a catalogue raissone compiled by Woll (66). It is on this work that the present study relies for the paintings’ authentication and chronology.

 Methods

For present purposes the beginning of Munch’s career as an artist can be dated to 1880, the date of his first extant paintings. The following years of his life during which he was hospitalised, admitted to clinics, suffered severe privation or symptoms of physiological illness or psychological disorder which were recorded by him or others, and the years in which someone close to him died, were all identified from documentary and biographical sources and are here referred to as ‘critical years’. These were verified by review of multiple, independent source materials. All other years were deemed to be ‘non-critical’. All of Munch’s self-portraits and portraits were dated by year in which completed based on the catalogue raisonnè and categorised as being completed in a critical or ‘non-critical year’.

All of the images examined are high resolution (>300 PPI) digital images downloaded wherever possible directly from the institutions which own the original paintings. Where this was not possible high-resolution images were obtained from open sources. Most institutions provided images in Tag Image File Format (TIF or TIFF) which preserves image quality regardless of copying. Some images were provided in Portable Network Graphics (PNG) format which is equivalent to TIFF in all relevant respects. Museum TIFF and PNG image files are standardized as to colour The remaining images were obtained in high resolution non-standardised Joint Photographic Experts Group (JPEG) format. Images obtained in JPEG and PNG format were converted to TIFF using a publicly available on-line service (xconvert.com) to ensure both consistency and stability of the images during processing. Several images provided by institutions included picture frames or colour reference bars which were removed using Adobe Photoshop (adobe.com/uk). TIFF images were used to measure contrast and fractals and converted to JPEG to measure colour to meet software requirements.

The images were necessarily produced under various lighting conditions and using varying equipment which may have affected the results although there is reason to believe that this variation enhances overall reliability of results by reducing the likelihood of any one format biasing the data (277). The images had varying numbers of pixels which were not standardised as test results of all variables, contrast, colour and fractal dimension, using several resolutions, were found to be substantially the same after rounding. The images were analysed as a whole including the areas surrounding the face as no practicable and consistent method of isolating the face was found. Weighting of each variable was uniform throughout each image as differences in perception were presumed to affect the entire painting. Some portraits were deliberately weathered and others have altered due to age. Munch used only commercially produced pigments which vary consistently.

 Statistical approach

The principal empirical approach to the data is correlative. That is, to determine if changes in the variables, contrast, colour and fractal dimension, as well as productivity, correspond to critical events/periods in Munch’s life and if so in what way and if such changes are consistent with potential psychopathology. As only self-portraits (sample size 51), and portraits (sample size 268)11, as opposed to the entire oil painted oeuvre (1638), were examined the data points do not form a normal distribution nor, in the case of self-portraits, a large sample size, ruling out the use of common parametrical statistical tests such as ANOVA. The data is also dispersed and incomplete as there were years in which either no self-portraits or portraits were painted and years when multiple portraits or self-portraits were painted.

To deal with these inherent problems the principal focus was to compare the central values of each tested variable in non-critical and critical periods. In addition, non-parametrical statistical tests, Median and Mann-Whitney, were applied. The former tests whether the two medians (each variable in non-critical and critical years) are the same. Mann-Whitney tests whether the two distributions are the same. The Wilcoxon test was applied to test for changes in intervals including both non-critical and critical years.

The number of statistical tests applied may suggest the use of multiple comparisons corrections to avoid the finding of spurious results. However proper application of multiple comparisons procedures such as the Bonferroni correction becomes too conservative if the tests are correlated amongst each other both because the correlation is endogenous to the paintings (e.g. as in the case of application to different colour channels), or because it is exogenous (e.g. self-portraits and portraits are made by the same artist). Multiple comparison correction was not applied because the approach has inherently low power and measures are strongly correlated (so standard multiple comparison would overcorrect the risk of false positives). However this work can be seen as corroboratory of previous results by an author in regard to Vincent Van Gogh with similar pathophysiology (4) and therefore is strongly hypothesis driven and not exploratory, hence the much lower risk of false positives. There was no within painting normalisation in terms of edge definition, colour depth, and/or image smoothness given the absence of approaches that have been recognised as valid across the field. Appropriate normalisation of these parameters may reduce outcome variability.

 Contrast

To measure changes in levels of contrast an average measure of contrast was derived from each painting. In digital images the luminance of a pixel is derived from its red, green, and blue (RGB) wavelength components as 0.299R + 0.587G + 0.114B (Digital Image Processing Using MATLAB, 3rd edition). The images were analysed as a two-dimensional random process and the mean and autocorrelation function provided a value for the contrast of brightness. The autocorrelation function quantifies the average relationship between data points in a time series and their previous data points using the Wiener–Kinchin theorem (278). Matrix transformation of luminance values was conducted using the 2-D Fourier Fast Transform and the average spatial contrast was characterized by the value at origin (4). The calculations were performed using MATLAB (v. R2021a) resulting in the values on the y axis in Figures 1–3.

The plot shows the average contrast in Munch’s self-portraits in chronological order. Critical years are underscored.

Line graph showing fluctuations in data values between 1882 and 1943. Notable peaks occur at 1888 with 0.312, 1915 with 0.362, 1926 with 0.405, and 1942 with 0.350. Data points generally range from 0.040 to 0.405.

The plot shows average contrast in Munch’s portraits in chronological order. Critical years are underscored.

Line graph depicting fluctuating data points with labels on both axes. The x-axis has numeric labels from zero to one hundred. The y-axis ranges from zero point two hundred to zero point five hundred. Data points show peaks and troughs, indicating variability.

The plot shows the average contrast value in Munch’s portraits in chronological order excluding those of family and friends. Critical years are underscored.

Line chart depicting daily numerical values with fluctuations between 0.000 and 0.700 over a specified period. Each data point is labeled. Periodic peaks and troughs are visible throughout. Colour

For each painting the colour median was measured in RGB and Cyan Magenta Yellow Black (CYMK) models. RGB, often known as additive colour mixing, is a method of encoding the three cone receptor wavelengths. In concept, each colour is made up of red, green, and blue light that shines with varying intensities. Hexadecimal coding allows integers ranging from 0 to 255 to be represent wavelengths plotted on the y-axis in Figures 4–7. The CMYK colour model is a subtractive colour model used in colour printing. It subtracts or masks colours from the white backdrop of the paper as ink decreases reflected light. The RGB and CMYK average values were calculated using MATLAB (v. R2021a) which applies consistent ranges of intensity in greyscale images to identify the specified colours.12

The plot illustrates the average levels of contrast in Munch’s portraits of family and friends in chronological order. Critical years are underscored.

Line graph showing contrast values over time from 1881 to 1917. Peaks occur at 0.299 in 1882, 0.240 in 1886, and 0.375 in 1889, with a general upward trend despite fluctuations.

The plot shows the average use of red in Munch’s self-portraits in chronological order. Critical years are underscored.

Line graph showing fluctuations in a dataset from 1882 to 1943. The y-axis ranges from 0 to 200. Peaks occur around 1889, 1902, 1912, 1920, 1926, 1943, with several notable troughs in between.

The plot shows the average use of green in Munch’s self-portraits in chronological order. Critical years are underscored.

Line graph showing annual fluctuations from 1882 to 1943. Peaks occur around 1892, 1906, 1915, and 1939, with highest value exceeding 140. Values vary between 20 and 160 over time.

The plot shows the average use of blue in Munch’s self-portraits in chronological order. Critical years are underscored.

Line graph depicting annual count of lynchings in the United States from 1882 to 1943. Peaks occur in the late 1880s, mid-1890s, 1901, mid-1910s, early 1920s, and early 1930s, showing fluctuations over the period. Fractal dimension

There are two common methods of fractal analysis: one ‘2’ and one ‘3’ dimensional. Both utilise “box counting” a widely used sampling and data collection process. The fundamental approach is converting the image to greyscale and placing a sequence of grids of decreasing calibre (boxes) over a picture methodically and recording data for each subsequent calibre (counting) creating grids of progressively larger sizes. The 3-dimensional method has been selected here as considerable colour information is lost after conversion to greyscale which can affect the accuracy in roughness measurement.

Every pixel of grayscale images has only one intensity channel; pixels of colour images have multiple intensity channels made up of red, green and blue. In order to reduce potential inaccuracy, a modified differential box counting approach (280) was used to determine fractal dimension values of RGB colour images. Combining the “probabilistic algorithm” method (281) and the “box merging” method extending box counting, (282) the fractal dimension of the resulting “3D” colour images was estimated using vectors in 5-dimensions (x, y, r, g, b). A greyscale image in this format generates 256 distinct shades of colour between 0 and 255. Applying this method to the 24-bit format for colour images resulted in individual RGB components calculated based on six possible combinations ranging from Ix,y (1) to Ix,y (6) which are averaged to improve accuracy of the roughness estimate. The range of D values using this method are between 2 and 3 which were plotted with log(S) on the x-axis and log(N(s)) on the y-axis in Figures 8–11. The midpoint of 3D analysis, 2.5, is equivalent to 1.5 in 2D analysis (283).

The plot shows the average use of yellow in Munch’s self-portraits in chronological order. Critical years are underscored.

Line graph showing yearly fluctuations in data from 1882 to 1943, with peaks around 1884, 1915, and 1940, and lower values around 1886, 1904, and 1924.

The plot shows the average fractal dimension of Munch’s self- portraits in chronological order. Critical years are underscored.

Line graph showing annual data from 1882 to 1943 with values ranging between 2.016 and 3.099. The graph fluctuates, displaying peaks around 1895, 1903, 1919, 1938, and 1943, with some notable dips between these years.

The plot shows the average fractal dimension of Munch’s portraits in chronological order. Critical years are underscored.

Line chart depicting fluctuations in values along the horizontal axis. Data points with vertical lines indicate values ranging between approximately zero point nine and three point eight, showing a pattern of peaks and troughs.

The table shows the number of oil paintings completed annually by Munch in chronological order. Critical years are underscored.

Line graph depicting data from 1880 to 1943 with fluctuations in values. Notable peaks occur in 1898, 1916, and 1930, while significant low points are seen in 1887 and 1933. The vertical axis ranges from 0 to 90. Productivity

Productivity was measured by number of oil paintings completed in each year of Munch’s career as shown in Figure 11. Other works, including works in other media, works on paper and photographs were excluded due to a lack of reliable data as to dates of production.

 Results Contrast

Contrast analysis revealed a statistically significant positive correlation with age (Pearson R = 0.515. R^2 = 0.265, P<0.001). Overall lifetime average contrast declines in crisis years and more in the self-portraits than in the portraits (Figures 1, 2, Table 1). Although, the Median and Mann-Whitney tests revealed no statistically significant relationship between critical years and contrast, the mean levels of contrast are noticeably higher in the portraits (Non-Critical Mean: 0.264; Critical Mean: 0.253; Hedges’ g: 0.104) than in the self-portraits (Non-Critical Mean: 0.241; Critical Mean: 0.204; Hedges’ g: 0.574). Analysis of the self-portraits in crisis periods reveals sharp increases in average contrast from previous levels and then declines as the period progresses. One can see an example of this trend in the period leading up to and during Munch’s stay in the Copenhagen clinic (1903-1909). There are notable singularities (point-change > 3 Std) in the years 1888, 1906, 1920, 1924 and 1926 where there are initial dramatic increases in contrast followed by declines. All of these occur during periods of crisis. There is also a notable increase in 1913 a non-critical year.

The table compares contrast in Munch’s self-portraits (SP) and portraits (P) shown in Figures 1, 2 in terms of Range (R), Grand Median (GM), Non-Critical Median (NCM, Critical Median (CM), Median Test p-value (MT P), and Mann-Whitney p-value (M-W P).

R N-CM CM MT P M-W P
SP Contrast 0.056-0.405 0.251 0.205 0.115 0.199
P Contrast 0.025-0.596 0.265 0.261 0.453 0.274

Analysis of the portraits reveals a similar pattern. There is again a statistically significant positive correlation of the average contrast with age (Pearson R = 0.400, R^2 = 0.16, P<0.001) with very similar quantitative values between the two sets and an identical rate of change: 0.003 units of positive change in contrast for every year. When the portraits are disaggregated it is noteworthy that unrelated individual portraits had the highest of all mean levels: Non-Critical Mean: 0.277; Critical Mean: 0.254; Hedges’ g: 0.226 (Figure 3) and that the mean levels of those of family and friends were the lowest of all: Non-Critical Mean: 0.173. Critical Mean: 0.201; Hedges’ g: 0.268 (Figure 4).

 Colour

Munch’s use of colour in his self-portraits also reveals a pattern of surges at the beginning of critical periods (Figures 5-8). Colour analysis reveals that Munch’s use of red and yellow tended to increase in periods of crisis and his use of blue decreases. There are statistically positive significant correlations of age with colours extracted with the RGB format. There was a positive correlation with Red (Pearson R = 0.303, R^2 = 0.091, P = 0.031; Hedges’ g: 0.059), Green, (Pearson R = 0.487, R^2 = 237 P<0.001; Hedges’ g: 0.201 and Blue (Pearson R = 0.440, R^2 = 0.194, P<0.001; Hedges’ g: 0.152). These changes likely underly a general increase in colour intensity (Pearson R = 0.413, R^2 = 0.17, P<0.001) but perceptual lightness, hue and saturation did not change with age. It is noteworthy that while red increased after 1906, its value was not sustained afterwards and correlation was weaker (did not survive multiple comparisons correction) which may indicate that red perception may be associated only with the acute phase of psychotic episodes. There were no associations of elements of the CMYK palette with age.

There are also similarly statistically positive significant correlations of age with colours extracted with the RGB format in the portraits. There was a positive correlation with Red (Pearson R = 0.378, R^2 = 0.143 P<0.001), Green, (Pearson R = 0.407, R^2 = 0.166, P<0.001) and Blue (Pearson R = 0.379, R^2 = 0.144, P<0.001). These changes likely underlay a general increase in colour intensity (Pearson R = 0.440, R^2 = 0.194, P<0.001) but again perceptual lightness, hue and saturation did not change with age. The portraits seem to follow the same general course as found in the self-portraits of increases in colour during critical periods followed by decreases in the RBG spectrum. Differently from the self-portraits, in the CMYK colour model all elements except K (black) were negatively associated with age. The largest correlation was a negative Pearson R correlation (R=-0.397, R^2 = 0.158, P<0.001) for Yellow. No statistically significant corelations were revealed by the Median or Mann-Whitney tests (see Table 2).

The table summarises the results of examining average colour in Munch’s self-portraits (SP) and portraits (P) shown in Figures 5-8.

Munch SP R N-CM CM MT P M-W P
Red 34-176 116 113.5 0.872 0.697
Green 42-168 117 97.5 0.568 0.254
Blue 30-154 90 80 0.196 0.278
Cyan 0.043-0.8 0.31 0.265 0.872 0.512
Magenta 0.076-0.81 0.3 0.295 0.872 0.864
Yellow 0.073-0.81 0.3 0.325 0.686 0.917
Munch P
Red 18-229 131 132 0.944 0.96
Green 21-217 127 120 0.732 0.269
Blue 20-202 100.5 91 0.246 0.176
Cyan 0-0.94 0.4 0.36 0.195 0.991
Magenta 0.012-0.9 0.38 0.35 0.374 0.929
Yellow 0.02-0.9 0.375 0.35 0.634 0.935

Range (R), Non-Critical Median (NCM), Critical Median (CM), Median Test p-value (MT P), Mann-Whitney p-value (M-W P).

 Fractals

The median fractal value of Munch’s self-portraits rises in critical years (2.429; Hedges’ g: 0.259) (Figure 9). There are very significant results in both the Median (P<0.0001) and the Mann-Whitney tests (P<0.0001) of the portraits (Table 3) where the same pattern appears (Non-Critical Median: 2.392. Critical Median: 2.599; Hedges’ g: 0.680) (Figure 10). The Median test reveals greater increases in the self-portraits than in the portraits (Table 3) with portraits following the same pattern (Non-Critical Median: 2.295; Critical Median: 2.382) but at the lowest overall levels (Figure 10). Unrelated individual portraits, as with contrast, had the highest overall levels (Non-Critical Median: 2.42; Critical Median: 2.63, Hedges’ g: 0.690; data not shown).

The table summarises the results of examining the average fractal values in Munch’s self-portraits (SP) and portraits (P) shown in Figures 9, 10.

R N-CM CM MT P M-W P
SP Fractal 1.983-3.071 2.33 2.423 0.903 0.608
P Fractal 1.512-3.308 2.423 2.624 0.0001 0.0001

Range (R), Non-Critical Median (NCM, Critical Median (CM), Median Test p-value (MT P), Mann-Whitney p-value (M-W P).

 Productivity

Munch was productive throughout his 60-year career with an annual average of 27 paintings (Figure 11). His median productivity during non-critical years (24.8) was 8% below the median (27.4) and 29% higher in critical years (31). The Generalized Linear model revealed a highly significant relationship between critical years and productivity (p<0.001). The most dramatic increase in productivity was in the period 1896 to 1909 reaching the second highest point in his career in 1907, the year before he entered the Copenhagen clinic. There were less dramatic but discernible rises in productivity in critical periods before, (1885-1895) and after, (1924-1926, 1930) his admission. In contrast, his productivity reached its highest point in 1915–16 a period of considerable success and large commissions. The other apparent exception, a drop in productivity in a period of crisis between 1936-1941, occurred when he was well into old age and suffered an embolism in one eye and deteriorating vision in both eyes. Nevertheless, once his vision recovered his productivity began to rise and he painted several important self-portraits before his death.

 Discussion

Munch was, from birth, a sick child; physically and mentally. The indications are that he inherited a genetic predisposition to schizophrenia and alcoholism and suffered maternally transmitted infection. Physiological trauma at birth was compounded by the psychological trauma of separation from his preoccupied mother; both must have been sources of intense anxiety. He depicted the additional trauma of witnessing his mother’s illness and death on numerous occasions. After his mother’s death he shifted attachment to his older sister who then died of the same disease that killed his mother. This further traumatic separation was compounded by his guilt that he had been the cause of her death. The impact of these deaths from tubercular-type illness, which his aunt suffered, as he did, was compounded by witnessing his father’s and his younger sister’s increasing mental disorder. It is thus not hard to see why he wrote:

“I inherited two of humanity’s most dreaded enemies – consumption and mental illness. Sickness, madness and death were the black angels that surrounded my crib. My mother died prematurely – from her I inherited the seeds of consumption. My father was obsessively nervous and obsessively religious – to the point of madness. This had been the fate of his family for generations. From him I inherited the seeds of madness.” (Tøjner p. 203-4).

The evidence is that Munch was correct in his self-diagnosis. His chronic illness, given its immediate onset upon birth, was very likely congenital tuberculosis. His mother, already ill when pregnant with him, both her sisters and likely his brother, died from tuberculosis. Munch’s life-long experience of respiratory illness in various forms is consistent with maternally transmitted disease. His genetic inheritance is indicated by a first degree relative, his sister, suffering from schizophrenia (92) and another, his father, evidenced depression (284), anxiety (285) in the form of obsessive religiosity (286, 287), and alcohol (288) and nicotine dependence (289), each of which entails a significant genetic component. Further, there is a bidirectional relationship between tuberculosis and psychosis (81, 290). It is certainly conceivable that this combination of transmitted illness and inherited predisposition can account for his condition.

Environmental and experiential factors are likely to have increased the likelihood of psychosis. Given the loss of not one but two primary attachments, his ambivalent relationship with his aunt, his difficulty in establishing relationships with women and association of female intimacy with death, it is reasonable to assume an insecure/anxious/avoidant attachment style which, together with trauma, is closely associated with psychosis and schizophrenia in particular (291–293). His inherited susceptibilities and the panorama of multiple developmental and environmental risk factors made childhood onset of psychosis highly probable (294). His social isolation due to his respiratory illness and the shame of his father’s religious preoccupation and disapproval of his choice of an artistic career and bohemian lifestyle, laid firm predicates for social anxiety.

Empirical, stylistic analysis of Munch’s self-portraits and portraits is consistent with perception in, and the natural history of, schizophrenia comorbid with social anxiety. Examination of contrast shows sudden increases at the start of critical periods then declines consistent with vivid episodes and reduced visual perception of contours (edges). There are a statistically significant positive correlations of average contrast with age both in the self-portraits and in the portraits with very similar quantitative values between the two. There is also an identical rate of change in contrast for every year. indicating a progressive deterioration of Munch’s condition as he grew older. Over time, the base levels of contrast increase consistent with deterioration in his untreated condition.

Colour use surges in critical periods in both self-portraits and portraits consistent with vivid psychotic periods. There are statistically significant positive correlations of age with colours extracted with the RGB format from the self-portraits indicating a general increase in colour intensity. The exception, a negative correlation for yellow, is an indication of dysfunction on the tritan axis consistent with dopaminergic dysregulation and psychosis. Colour evidence from the portraits, with both RGB and CYMK significantly increasing as he aged, is consistent with schizophrenia.

Fractal analysis reveals lower levels of complexity in non-critical years and higher levels in critical years in both the self-portraits and portraits, with markedly greater increases in the self-portraits. Greater complexity can be associated with more intense feelings. Munch’s productivity also increased significantly in critical periods commensurate with his own recognition that painting was a means of helping him to manage his emotions.13

When portraits are disaggregated, while following the same pattern between non-critical and critical years as the self-portraits, the levels of contrast, colour and fractal dimension are all lowest in related portraits and highest in unrelated portraits. This suggests not only greater distress in critical periods generally but heightened stress when painting strangers generally, consistent with comorbid social anxiety.

Bipolar disorder

Aspects of Munch’s life history and some of his symptoms overlap with those of BPD 1 but many do not. If one focuses on the period between his first love affair and his treatment in Copenhagen Munch may be seen as suffering from BPD I with psychosis which occurs in approximately half of cases and is easily mistaken for schizophrenia (295). He would now not be diagnosed with BPD II given his psychotic experiences. BPD 1 typically becomes manifest in late adolescence or early adulthood not in childhood (296) by which time Munch had already experienced hallucination. Hallucinations can, albeit rarely, accompany BPD but do not persist and usually abate in the early years after onset (295, 297) and do not include olfactory hallucination (104). BPD is characterised by sharper, more accurate, sensory experiences including more accurate vision together with heightened states of empathy and awareness of others’ states of mind (149, 150). Munch’s portraits, consistent with reduced magnocellular function are characterised by a lack of detail, depth, and facial emotion; he ignored his sitters.

BPD’s natural course does include childhood anxiety and insomnia, but depression continues, regardless of periods of remission accompanied by long-term cognitive decline (298, 299). There are no reports by Munch or his contemporaries of low mood except as episodically related to episodes of guilt and grief nor is there any evidence of the widespread neurocognitive deficits, typical in BPD, in executive functioning, verbal and spatial memory and psychomotor performance, which usually persist in non-symptomatic periods (298, 299). While unable to function well socially, he remained in contact with a wide circle (59; Heller) and fully capable of managing his affairs including planning carefully for his death.

His periods of increased productivity, with one exception, were accompanied by negative feelings of guilt, shame and jealousy not the positive or euphoric feelings associated with mania and BPD. Mania is characterised by short bursts of goal directed activity, measured in days or weeks, not years-long periods of increased productivity (300). His reckless behaviour, violence, impulsive travelling and episodic depression all abated with abstinence. In his 35 year period of abstinence and isolation Munch does not report nor is he reported by contemporaries as appearing either manic or depressed although they did notice delusions and antisocial behaviour. His extensive journals and correspondence reveal self-absorption, sensitivity to criticism and obsessive concerns but neither the grandiosity of mania nor the futility of depression (61; Prideaux; Tøjner). There was no medication available so the absence of BPD symptoms during this period makes a diagnosis of BPD less plausible.

 Schizophrenia

Munch manifested all but one of DSM’s positive symptom of schizophrenia, deficient psychomotor behaviour, and his life history includes almost every known risk factor for the disease, genetic, developmental and environmental. The natural history of schizophrenia includes a shift from hallucination to delusion and changes in perception, accompanied, and probably caused, by commensurate dysregulation of neurotransmitters, dopamine particularly, in the retina and visual system generally. These are closely associated with deficits in perception of contrast and colour which are exacerbated by abuse of alcohol and tobacco. In Munch’s case the transition was associated with his becoming sober and choosing social isolation. The change in his behaviour was widely noted by contemporaries and the simultaneous change in subject matter and style has long been noted by art historians (Prideaux, Woll).

Such a transition, unaccompanied by depression or persistent or cyclical low mood, is indicative of schizophrenia accompanied by persecutory delusions and comorbid social anxiety rather than BPD. The correlations of increased contrast and colour with aging, particularly evident in the portraits, and the increasing fractal values in critical periods, suggest a long-term deterioration in his condition but not one accompanied by a declines in productivity or cognitive capacity. It is also noteworthy that a disrupted sense of self like that painted and described by Munch, distinguishes schizophrenia from BPD (301). Munch’s life thus parallels the natural history of schizophrenia: childhood pre-morbid and prodromal phases, first psychotic episodes, a florid psychotic phase, followed by stable delusions accompanied by negative symptoms and social deficits (230).

Although approximately 60% of schizophrenia patients express negative symptoms of blunted affect, anhedonia, alogia, avolition and asociality (302, 317). Munch appears not to have done so. Asociality, (a reduction in social initiative due to decreased motivation to form close relationships (303) seems to appear when he retreated to the countryside but does not fully account for his behaviour. Prior to that he sought out friendships, social contacts and public approval. There is little indication of other negative symptoms. Neither he nor his contemporaries report lack of affect, his emotional range was wide even exaggerated, and expressed in his art, writings and encounters with others. He had intense love affairs and an active sexual life into old age; his periods of depression and low mood prior to treatment were episodic and abated with sobriety; he was voluble, to the point of pressured speech, and articulate in both speaking and writing; and he never stopped producing new work and experimenting with media. The only dramatic declines in his productivity occurred at the time of his breakdown in 1908, he resumed work within a few months, and in old age when he suffered visual impairment and then too his productivity rose following recovery. His motivation to work persisted throughout his career. Indeed, as he recognised, work was essential to management of his emotions.

During the second half of his life he maintained, albeit from a distance, relations with his aunt and sisters who he supported financially, with a small circle of friends, lovers and patrons. These relationships were often difficult but his persistence in creating and maintaining them does not appear indicative of decreased motivation. His intolerance of their prolonged physical presence, together with other forms of anxious behaviour, including continued refusal to attend ceremonies celebrating him, despite his lifelong wish to be recognised and accepted by the public, and his continued sensitivity to criticism despite his success, appears to go beyond asociality as a negative symptom.

 Co-morbid social anxiety

Social anxiety disorder is characterised by anxious preoccupation with being judged negatively by others and avoidance of social and/or public performance situations due to an excessive concern with being humiliated and ashamed under the scrutiny of others (130, 304). It is now recognised as comorbid with schizophrenia in approximately 25% of cases, (305, 306) albeit overlapping with negative (and positive) symptoms which contributes to under-reporting (307, 309, 310). Comorbid patients’ avoidant behaviour is ego-dystonic differing qualitatively from anhedonia, or lack of social interest, are motivated, as Munch was, to gain control of their anxiety as opposed to lacking motivation to manage it (307).

His intense social anxiety, manifested prior to entering the Copenhagen clinic by impulsive travel and flight from intimate relations, continued after treatment in the extraordinary avoidance measures he employed which also appear related to his persecutorial delusions (308). It is noteworthy that when comorbid with schizophrenia social anxiety sufferers appear to present greater difficulty in mentalisation but less severe cognitive disturbance as compared with those without social anxiety (311). This fairly characterises Munch as recorded by his contemporaries and as evidenced by his voluminous correspondence. Munch had been increasingly isolated in childhood due to his illness, unable to attend school or complete higher education. When Munch abandoned the career chosen by his father in favour of an artistic one, his father condemned him publicly and privately causing Munch intense shame, a predicate for social anxiety (71). His first love affair was one of many occasions on which Munch felt deeply ashamed as was the exhibition of the Sick Child not least as blamed himself for his sister’s death He expressed deep feelings of shame, both in writing and in multiple works. He was intensely sensitive to criticism all his life avoiding exhibitions of his work and social occasions of all kinds including those celebrating his achievement (Prideaux). He often fled from personal, social and professional contacts (Stenersen). His need to avoid people worsened over time and was unaltered by treatment and abstinence. Munch’s anxiety about being judged negatively approached and at times crossed over into paranoia (312).

Comorbid sufferers are characterised by insecure attachment, childhood trauma, increased difficulty in mentalisation, a higher sense of shame, greater negative attribution bias and suicidality (304, 313). With the exception of suicidal planning, Munch demonstrates all these elements. He had multiple childhood trauma, disorganised and fearful attachments to his mother, sister and aunt, and a father who was over-controlling and shaming all of which are indicative of the social, generalised and phobic anxiety he experienced (314, 315). Contrast, colour and fractal values are all significantly higher in portraits of unrelated others in comparison to his self-portraits and portraits of those related to him, suggestive of his discomfort in the presence of strangers. This pattern of higher values in portraits is also reflected in his use of contrast and colour as he aged. This appears to confirm the greater difficulty in painting others, as opposed to himself and those close to him, throughout his life. It is also noteworthy that negative attribution bias is greater in comorbid patients (304). Munch never painted a happy face; his portraits and self-portraits all depict neutral or sad expressions.

 Conclusion

The findings here of stylistic variations in Munch’s self-portraits and portraits are consistent with the perceptual and emotional phenomena of early onset psychosis and comorbid social anxiety. BPD is inconsistent with the coincidence of alcohol abuse with mood disorder and reckless behaviour. His symptoms appear to follow the natural course of schizophrenia, shifting from hallucination to delusion. His anxiety, particularly social anxiety, like his insomnia, never abated. His painted self-portraits and portraits, which he saw, like all his painting, as a means of expressing himself. Statistically significant results reflect empirically the transitions in his state of mind: growing brighter, more colourful, more complex, and more numerous as his symptoms became more severe. This suggests that his childhood experience of both physiological and psychological distress caused him to acquire neurological traits including lasting morphological, neurobiological, and functional changes particularly affecting perception of contrast and colour. The rise in productivity during critical periods is consistent with his own understanding that his illnesses and his efforts to manage them, are reflected in his art.

 Limitations

The most important limitation of the present study is that it encompasses only a fraction of Munch’s paintings and none of his works on paper. Analysis of those works might reveal very different results. Second, the material examined are not the original paintings but digital images. These were produced under varying conditions and using a variety of equipment if to a largely consistent standard. This, at the very least, means that analysis of colour is of limited use given the difficulties which computers have of identifying colour in anything like the subtlety of the eye. Given the software employed the absence of standardized colour calibration will have generated a range of, as opposed to precise, colour values. There was no within painting normalisation in terms of edge definition, colour depth and or image smoothness given the absence of approaches that have been recognised as valid across the field. Appropriate normalisation of these parameters may reduce outcome variability Fractal and contrast analysis are more reliable but again could vary if applied to other and original works. No definitive diagnosis is possible based on such materials.

 Data availability statement

The raw data supporting the conclusions of this article will be made available by the authors, without undue reservation.

 Author contributions

EB: Writing – review & editing, Investigation, Data curation, Writing – original draft, Conceptualization. JL: Writing – review & editing, Methodology, Software. PD: Supervision, Writing – review & editing. FT: Funding acquisition, Writing – review & editing, Conceptualization, Supervision, Methodology.

 Conflict of interest

The authors declared that this work was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

 Generative AI statement

The author(s) declared that generative AI was not used in the creation of this manuscript.

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 References Alzueta E Melcón M Jensen O Capilla A . The ‘Narcissus Effect’: Top-down alpha-beta band modulation of face-related brain areas during self-face processing. NeuroImage. (2020) 213. doi: 10.1016/j.neuroimage.2020.116754, PMID: 32194280 Northoff G Heinzel A de Greck M Bermpohl F Dobrowolny Panksepp J . Self-referential processing in our brain—A meta-analysis of imaging studies on the self. NeuroImage. (2006) 31:440–57. doi: 10.1016/j.neuroimage.2005.12.002, PMID: 16466680 Żochowska A Nowicka MM Wójcik MJ Nowicka A . Self-face and emotional faces—are they alike? Soc Cogn Affect Neurosci. (2021) 16:593–607. doi: 10.1093/scan/nsab020, PMID: 33595078 Turkheimer FE Fagerholm ED Vignando M Dafflon J Da Costa PF Dazzan P . A GABA interneuron deficit model of the art of vincent van gogh. Front Psychiatry. (2020) 11. doi: 10.3389/fpsyt.2020.00685, PMID: 32754073 Turkheimer FE Liu J Fagerholm ED Dazzan P Loggia ML Bettelheim E . The art of pain: A quantitative color analysis of the self-portraits of Frida Kahlo. Front Hum Neurosci. (2022) 16:1000656. doi: 10.3389/fnhum.2022.1000656, PMID: 36118965 Forsythe A Williams T Reilly RG . What paint can tell us: A fractal analysis of neurological changes in seven artists. Neuropsychology. (2017) 31:1–10. doi: 10.1037/neu0000303, PMID: 28026197 Taylor R Branka S Hagerhall C Van Donkelaar P . Perceptual and physiological responses to jackson pollock’s fractals. Front Hum Neurosci. (2011) 5:60. doi: 10.3389/fnhum.2011.00060, PMID: 21734876 Bersani G Quartini A Manuali G Pacitti F Iannitelli A . A preliminary study on similarities and dissimilarities of Neurological Soft Signs in schizophrenic and obsessive-compulsive disorders suggests a common maldevelopmental model. Riv. Psichiatr. (2023) 58:21–6. doi: 10.1708/3964.39427, PMID: 36715579 Hyatt E Blom JD . Perceptual distortions characteristic of Alice in Wonderland syndrome in contemporary figurative painting. Front Psychiatry. (2024) 15:1466666. doi: 10.3389/fpsyt.2024.1466666, PMID: 39698212 Saranya TS Raj G Kiso K Kharmih D Yepthomi K Kumar Gupta S . Art in the abyss: creativity and the schizophrenic mind. Front Psychiatry. (2025) 16:1617462. doi: 10.3389/fpsyt.2025.1617462, PMID: 40642414 Bleuler E . Dementia Praecox or the Group of Schizophrenias. (Trans. J. Zinkin); Zinkin J, editor. New York, NY: International Universities Press (1950). Freud S . Further remarks on the neuro-psychoses of defence. Stand. Ed. Compl. psychol Works. S. Freud. (1896) 3:157–85. Parnas J Henriksen MG . Disordered self in the schizophrenia spectrum: a clinical and research perspective. Harvard. Rev Psychiatry. (2014) 22:251–65. doi: 10.1097/HRP.0000000000000040, PMID: 25126763 Sandsten KE Nordgaard J Kjaer TW Gallese V Ardizzi M Ferroni F . Altered self-recognition in patients with schizophrenia. Schizophr Res. (2020) 218:116–23. doi: 10.1016/j.schres.2020.01.022, PMID: 32007345 Rossetti I Repossi M Florio V Demartini B Conca A Gambini O . Sense of body ownership and body agency in schizophrenia. Sci Rep. (2022) 12:19369. doi: 10.1038/s41598-022-23988-y, PMID: 36371507 Abely P . De signe du mriroir dans les psychoses et plus spécialement dans la demence précoce. Ann Medicopsychol. (1930) 01:28–36. Bortolon C Capdevielle D Altman R Macgregor A Attal J Raffard S . Mirror self-face perception in individuals with schizophrenia: Feelings of strangeness associated with one’s own image. Psychiatry Res. (2017) 253:205–10. doi: 10.1016/j.psychres.2017.03.055, PMID: 28390296 Caputo GB Ferrucci R Bortolomasi M Giacopuzzi M Priori A Zago S . Visual perception during mirror gazing at one’s own face in schizophrenia. Schizophr Res. (2012) 140:46–50. doi: 10.1016/j.schres.2012.06.029, PMID: 22835808 Javitt DC Freedman R . Sensory processing dysfunction in the personal experience and neuronal machinery of schizophrenia. Am J Psychiatry. (2015) 172:17–31. doi: 10.1176/appi.ajp.2014.13121691, PMID: 25553496 Cutting J Dunne F . The nature of the abnormal perceptual experiences at the onset of schizophrenia. Psychopathology. (1986) 19:347–52. doi: 10.1159/000284459, PMID: 3615790 Cutting J Dunne F . Subjective experience of schizophrenia. Schizophr Bull. (1989) 15:217–31. doi: 10.1093/schbul/15.2.217, PMID: 2749185 Pan CC Zhou AB . Altered Auditory Self-recognition in People with Schizophrenia. The Spanish J Psychol. (2020) 23:e52. doi: 10.1017/SJP.2020.53, PMID: 33213608 Waters F Woodward T Allen P Aleman A Sommer I . Self-recognition deficits in schizophrenia patients with auditory hallucinations: a meta-analysis of the literature. Schizophr Bull. (2012) 38:741–50. doi: 10.1093/schbul/sbq144, PMID: 21147895 Döges J . The famed painting the scream holds a hidden message. SA. Mind. (2021) 32:6. doi: 10.1038/scientificamericanmind0521-6 Butler PD Silverstein SM Dakin SC . Visual perception and its impairment in schizophrenia biol psychiatry. Addiction. (2008) 64:40–7. doi: 10.1016/j.30 Deng Y Liu K Cheng D Zhang J Chen H Chen B . Ventral and dorsal visual pathways exhibit abnormalities of static and dynamic connectivities, respectively, in patients with schizophrenia. Schizophr Res. (2019) 206:103–10. doi: 10.1016/j.schres.2018.12.005, PMID: 30545760 Degenhardt L Saha S Lim CCW Aguilar-Gaxiola S Al-Hamzawi A Alonso J . The associations between psychotic experiences and substance use and substance use disorders: findings from the World Health Organization World Mental Health surveys. Addict (Abingdon Engl). (2018) 113:924–34. doi: 10.1111/add.14145, PMID: 29284197 Bubl E Tebartz Van Elst L Gondan M Ebert D Greenlee MW . Vision in depressive disorder. World J Biol Psychiatry. (2009) 10:377–84. doi: 10.1080/15622970701513756, PMID: 17853291 Bubl E Kern E Ebert D Bach M Tebartz Van Elst L . Seeing gray when feeling blue? Depression can be measured in the eye of the diseased. Biol Psychiatry. (2010) 68:205–8. doi: 10.1016/j.biopsych.2010.02.009, PMID: 20359698 Li W Yang Y An FR Zhang L Ungvari GS Jackson T . Prevalence of comorbid depression in schizophrenia: A meta-analysis of observational studies. J Affect Disord. (2020) 273:524–31. doi: 10.1016/j.jad.2020.04.056, PMID: 32560949 Lew BJ Wiesman AI Rezich MT Wilson TW . Altered neural dynamics in occipital cortices serving visual-spatial processing in heavy alcohol users. J Psychopharmacol. (2020) 34:245–53. doi: 10.1177/0269881119863120, PMID: 31331222 Fernandes TMP Almeida NL Santos NAD . Effects of smoking and smoking abstinence on spatial vision in chronic heavy smokers. Sci Rep. (2017) 7:1690. doi: 10.1038/s41598-017-01877-z, PMID: 28490803 Fernandes TMP De Andrade MJO Santana JB Nogueira R. M. T. B. L. Dos Santos NA . Tobacco use decreases visual sensitivity in schizophrenia. Front Psychol. (2018) 9:288. doi: 10.3389/fpsyg.2018.00288, PMID: 29559947 Bernardin. F Schwan. R Lalanne L Ligier F Angioi-Duprez K Schwitzer T . The role of the retina in visual hallucinations: A review of the literature and implications for psychosis. Neuropsychologia. (2017) 99:128–38. doi: 10.1016/j.neuropsychologia.2017.03.002, PMID: 28263800 Bernardin F Schwitzer T Angioi-Duprez K Giersch A Ligier F Bourion-Bedes S . Retinal ganglion cell dysfunction is correlated with disturbed visual cognition in schizophrenia patients with visual hallucinations. Psychiatry Res. (2021) 298:113780. doi: 10.1016/j.psychres.2021.113780, PMID: 33567383 Kogata T Iidaka T . A review of impaired visual processing and the daily visual world in patients with schizophrenia. Nagoya. J Med Sci. (2018) 80:317–28. doi: 10.18999/nagjms.80.3.317, PMID: 30214081 Freud S . The interpretation of dreams. Stand. Ed. Compl. psychol Works. S. Freud. (1900) 4:ix–627. Janet P . The major symptoms of hysteria. London: Macmillan Publishing (1907). doi: 10.1037/10008-000 Jaspers K . Allgemeine Psychopathologie. In: Berlin: Springer; English translation of the 7th edition: General Psychopathology. Johns Hopkins University Press, Baltimore (1913/1997). Kraepelin. E . Dementia Praecox and Paraphrenia. trans Barclay RM , editor, 8th ed. Krieger Publishing, Huntington, NY (1896/1971). Prideaux S . Edvard Munch: Behind the Scream. New Haven, Conn: Yale University Press (2005), ISBN: 978-0-300-25000. Skryabin VY Skryabin AA Torrado MV GritChinab EA . Edvard Munch: the collision of art and mental disorder. Ment Health. Relig. Cult. (2020) 23:570–8. doi: 10.1080/13674676.2020.1777537 Rothenberg A . Bipolar illness, creativity, and treatment. Psychiatr Q. (2001) 72:131–47. doi: 10.1023/a:1010367525951, PMID: 11433879 Rothenberg A . Creativity and Mental Illness II: The Scream. New York, NY: Psychology Today (2015). Available online at: https://www.psychologytoday.com/gb/blog/creative-explorations/201503/creativity-and-mental-illness-ii-the-scream (Accessed June 5, 2024). Miranda C M Miranda C E Molina D M . Edvard Munch: enfermedad y genialidad en el gran artista noruego [Edvard Munch: disease and genius of the great Norwegian artist. Rev Med Chile. (2013) 141:774–9. doi: 10.4067/S0034-98872013000600012, PMID: 24121581 Wylie ML Wylie HW Jr . The creative relationship of internal and external determinants in the life of an artist. Annu Psychoanal. (1989) 17:73–128. doi: 10.4324/9780203778487-5s Wylie HW Jr . Edvard munch. Am Imago. Winter. (1980) 37:413–43., PMID: 7008567 Warick L Warick E . “ Edvard Munch: a study of loss, grief and creativity.” In: Panter BM Virshup E Carder S Carder L Warick L Warick E . (Eds.), Creativity & madness: psychological studies of art and artists. Aimed Press. (1995). pp. 177–186. Bowen AM . Munch and Agoraphobia: His Art and His Illness RACAR: revue d’art canadienne/Canadian Art Review (1988). Available online at: https://www.jstor.org/stable/42630379 (Accessed January 15, 2023). McElroy Bowen A . Munch and agoraphobia: his art and his illness. RACAR: Rev D’art Canad/Can. Art. Rev. (1988) 15:23–50. doi: 10.7202/1073431ar Warick L Warick E . Edvard munch A study of loss, grief and creativity (2014). Available online at: https://www.msu.edu/course/ha/446/panter.htm (Accessed November 23, 2022). Frigg R Howard C . Fact and Fiction in the Neuropsychology of Art in The Aesthetic Mind: Philosophy and Psychology. Schellekens E Goldie P , editors. Oxford: Oxford University Press (2011). doi: 10.1093/acprof:oso/9780199691517.003.0005 Ter Borg M Trenité DK . The cultural context of diagnosis: the case of Vincent van Gogh. Epilepsy. Behav.: E&B. (2012) 25:431–9. doi: 10.1016/j.yebeh.2012.08.010, PMID: 23040505 Voskuil P . Vincent van Gogh and his illness. A reflection on a posthumous diagnostic exercise. Epilepsy. Behav.: E&B. (2020) 111:107258. doi: 10.1016/j.yebeh.2020.107258, PMID: 32629415 År Til År F . Edvard Munch. A Year by Year Record of Edvard Munch’s Life. Oslo: Aschehoug & Co (1961). Forteller V . (1946). Edvard Munch Som Vi Kjente Ham: Vennene. 22ip il Dreyers Forlag. Stang R . Edvard munch: The Man and His Art. New York: Abbeville Press (1977), ISBN: 0-89659-025-9. trans. Culverwell, G. Stenersen R . Edvard munch – Close-up of a genius. Stockholm: Sem & Stenersen A/S (1944/1969), ISBN: 82-7046-057-5. Cernuschi C . Sex and Psyche, Nature and Nurture, The Personal and the Political: Edvard Munch and German Expressionism in Howe, J. Boston: Boston College (2001). Edvard Munch, Psyche, Symbol and Expressionism. Chilvers I . Oxford Dictionary of Art & Artists. 4th ed. Oxford: Oxford University Press (2009). Holland JG . (trans.) The Private Journals of Edvard Munch; We Are Flames Which Pour Out Of The Earth. Madison, Wisconsin: University of Wisconsin Press (2005), ISBN: 0-299-19810-3. Tøjner PE . Munch in his own words. London: Prestel, Munich (2001). 3-7913-2494-2 Lubow A . Edvard Munch: Beyond the Scream. Washington DC: Smithsonian Magazine (2006). Available online at: https://www.smithsonianmag.com/arts-culture/edvard-munch-beyond-the-scream-111810150/ (Accessed May 20, 2024). Ustvedt O . Edvard munch: an inner life. London: Thames & Hudson (2020), ISBN: 978-0-500-29576-2. Bruteig M Falck UK . Edvard Munch Works on Paper. Munch Museum: Yale University Press (2013). Woll G . Edvard munch complete paintings, catalogue raissone. London: Thames & Hudson (2008), ISBN: 9780500093450. Woll G . Edvard munch, the complete graphic works. New York: Abrams (2001), ISBN: 100810908743. Harris JC . Spring. Arch Gen Psychiatry. (2007) 64:996–7. doi: 10.1001/archpsyc.64.9.996 Wood SR . A contribution to the history of tuberculosis and leprosy in 19th century Norway. J R Soc Med. (1991) 84:428–30. doi: 10.1177/014107689108400715, PMID: 1865452 Teemu R . Tuberculosis-threatened children”: the rise and fall of a medical concept in Norway, c.1900-1960. Med Hist. (2008) 52:347–64. doi: 10.1017/s0025727300002672, PMID: 18641787 Harris JC . Anxiety (angst). Arch Gen Psychiatry. (2004) 61:15–6. doi: 10.1001/archpsyc.61.1.15, PMID: 14706939 Heller R . Munch, His Life and Work. Chicago: University of Chicago Press (1984), ISBN: 100226326438. Azeem H . The art of Edvard Munch: a window onto a mind. BJPsychAdvances. (2015) 21:51–3. doi: 10.1192/apt.bp.114.012963 Howe J ed. Edvard Munch. In: Psyche, Symbolism and Expression. McMullen Museum of Art, Boston, ISBN: 1892850-02-8. Eggum A . Edvard Munch Paintings, Sketches and Studies. London: Thames & Hudson (1984). Weir, David . Bohemians: A very short introduction. Oxford: Oxford University Press (2023), ISBN: 9780197538296. Li C Liu L Tao Y . Diagnosis and treatment of congenital tuberculosis: a systematic review of 92 cases. Orphanet. J Rare. Dis. (2019) 14:131. doi: 10.1186/s13023-019-1101-x, PMID: 31182120 Tomar R Gupta A Prasad TR Bhalla P Murthy G . Congenital tuberculosis. Med J. Armed. Forces. Ind. (2008) 64:78–80. doi: 10.1016/S0377-1237(08)80160-8, PMID: 27408090 Manjeese W Mvubu NE Steyn AJC Mpofana T . Mycobacterium tuberculosis causes a leaky blood-brain barrier and neuroinflammation in the prefrontal cortex and cerebellum regions of infected mice offspring. Int J Dev Neurosci. (2021) 81:428–37. doi: 10.1002/jdn.10116, PMID: 33932039 De Araújo GS Pereira SM Dos Santos DN Marinho JM Rodrigues LC Barreto ML . Common mental disorders associated with tuberculosis: a matched case-control study. PloS One. (2014) 9:e99551. doi: 10.1371/journal.pone.0099551, PMID: 24937319 Monistrol-Mula A Felez-Nobrega M Oh H Haro JM Koyanagi A . Association between tuberculosis and psychotic experiences: Mediating factors and implications for patient care in low- and middle-income countries. J Global Health. (2024) 14:4005. doi: 10.7189/jogh.14.04005, PMID: 38419459 Sossen B Richards AS Heinsohn T Frascella B Balzarini F Oradini-Alacreu A . The natural history of untreated pulmonary tuberculosis in adults: a systematic review and meta-analysis. Lancet Respir Med. (2023) 11:367–79. doi: 10.1016/S2213-2600(23)00097-8, PMID: 36966795 Saramba MI Zhao D . A perspective of the diagnosis and management of congenital tuberculosis. J Pathog. (2016) 2016:8. doi: 10.1155/2016/8623825, PMID: 27999684 Cardno AG Marshall EJ Coid B Macdonald AM Ribchester TR Davies NJ . Heritability estimates for psychotic disorders: the Maudsley twin psychosis series. Arch Gen Psychiatry. (1999) 56:162–8. doi: 10.1001/archpsyc.56.2.162, PMID: 10025441 Cardno AG Owen MJ . Genetic relationships between schizophrenia, bipolar disorder, and schizoaffective disorder. Schizophr Bull. (2014) 40:504–15. doi: 10.1093/schbul/sbu016, PMID: 24567502 Escamilla MA Zavala JM . Genetics of bipolar disorder. Dialog. Clin Neurosci. (2008) 10:141–52. doi: 10.31887/DCNS.2008.10.2/maescamilla, PMID: 18689285 Insel T . Rethinking schizophrenia. Nature. (2010) 468:187–93. doi: 10.1038/nature09552, PMID: 21068826 Radua J Ramella-Cravaro V Ioannidis JP Reichenberg A Phiphopthatsanee N Amir T . What causes psychosis? An umbrella review of risk and protective factors. World Psychiatry. (2018) 17:49–66. doi: 10.1002/wps.20490, PMID: 29352556 Robinson N Bergen SE . Environmental risk factors for schizophrenia and bipolar disorder and their relationship to genetic risk: current knowledge and future directions. Front Genet. (2021) 12:686666. doi: 10.3389/fgene.2021.686666, PMID: 34262598 Brown AS Schaefer CA Wyatt RJ Goetz R Begg MD Gorman JM . Maternal exposure to respiratory infections and adult schizophrenia spectrum disorders: a prospective birth cohort study. Schizophr Bull. (2000) 26:287–95. doi: 10.1093/oxfordjournals.schbul.a033453, PMID: 10885631 Pries L-K Guloksuz S Ten Have M De Graaf R Van Dorsselaer S Gunther N . Evidence that environmental and familial risks for psychosis additively impact a multidimensional subthreshold psychosis syndrome. Schizophr Bull. (2018) 44:710–9. doi: 10.1093/schbul/sby051, PMID: 29701807 St Clair D Lang B . Schizophrenia: a classic battle ground of nature versus nurture debate. Sci Bull. (2021) 66:1037–46. doi: 10.1016/j.scib.2021.01.032, PMID: 36654248 Sullivan PF Kendler KS Neale MC . Schizophrenia as a complex trait: evidence from a meta-analysis of twin studies. Arch Gen Psychiatry. (2003) 60:1187–92. doi: 10.1001/archpsyc.60.12.1187, PMID: 14662550 Misra S Gelaye B Koenen KC Williams DR Borba CPC Quattrone D . Early parental death and risk of psychosis in offspring: A six-country case-control study. J Clin Med. (2019) 8:1081. doi: 10.3390/jcm8071081, PMID: 31340495 Clarke MC Tanskanen A Huttunen MO Cannon M . Sudden death of father or sibling in early childhood increases risk for psychotic disorder. Schizophr Res. (2012) 143:363–6. doi: 10.1016/j.schres.11.024 Liang H Olsen J Yuan W Cnattingus S Vestergaard M Obel C . Early life bereavement and schizophrenia: A nationwide cohort study in Denmark and Sweden. Med (Balt). (2016) 95:e2434. doi: 10.1097/MD.0000000000002434, PMID: 26817875 Laskemoen JF Simonsen C Büchmann C Barrett EA Bjella T Lagerberg TV . Sleep disturbances in schizophrenia spectrum and bipolar disorders - a transdiagnostic perspective. Compr Psychiatry. (2019) 91:6–12. doi: 10.1016/j.comppsych.2019.02.006, PMID: 30856497 Castillo-Carniglia A Keyes KM Hasin DS Cerdá M . Psychiatric comorbidities in alcohol use disorder. Lancet Psychiatry. (2019) 6:1068–80. doi: 10.1016/S2215-0366(19)30222-6, PMID: 31630984 Frye MA Salloum IM . Bipolar disorder and comorbid alcoholism: prevalence rate and treatment considerations. Bipolar. Disord. (2006) 8:677–85. doi: 10.1111/j.1399-5618.2006.00370.x, PMID: 17156154 Dickerson F Stallings CR Origoni AE Vaughan C Khushalani S Schroeder J . Cigarette smoking among persons with schizophrenia or bipolar disorder in routine clinical settings 1999-2011. Psychiatr Serv (Wash D.C.). (2013) 64:44–50. doi: 10.1176/appi.ps.201200143, PMID: 23280457 Fortgang RG Hoff RA Potenza MN . Problem and pathological gambling in schizophrenia: exploring links with substance use and impulsivity. J Gambl. Stud. (2018) 34:673–88. doi: 10.1007/s10899-018-9757-z, PMID: 29453588 Grassi L Pavanati M Cardelli R Ferri S Peron L . HIV-risk behaviour and knowledge about HIV/AIDS among patients with schizophrenia. psychol Med. (1999) 29:171–9. doi: 10.1017/s0033291798007818, PMID: 10077305 American Psychiatric Association . Diagnostic and statistical manual of mental disorders. 5th Edition. Arlington (VA: American Psychiatric Publishing (2022). Goghari VM Harrow M . Twenty year multi-follow-up of different types of hallucinations in schizophrenia, schizoaffective disorder, bipolar disorder, and depression. Schizophr Res. (2016) 176:371–7. doi: 10.1016/j.schres.2016.06.027, PMID: 27349816 Tandon R Gaebel W Barch DM Bustillo J Gur RE Heckers S . Definition and description of schizophrenia in the DSM-5. Schizophr Res. (2013) 150(1):3–10. doi: 10.1016/j.schres.2013.05.028, PMID: 23800613 Valle R . Schizophrenia in ICD-11: comparison of ICD-10 and DSM-5. Rev Psiquiatr. Salud. Ment (Barc.). (2020) 13:95—104. doi: 10.1016/j.rpsm.2020.01.001, PMID: 32336596 American Psychiatric Association . Anxiety Disorders. In: Diagnostic and Statistical Manual of Mental Disorders. 5th ed. Washington, DC: Psychiatric Association (2022) p. 215–31. Aderka IM Hofmann SG Nickerson A Hermesh H Gilboa-Schechtman E Marom S . Functional impairment in social anxiety disorder. J Anxiety Disord. (2012) 26:393–400. doi: 10.1016/j.janxdis.2012.01.003, PMID: 22306132 Schneier FR Johnson J Hornig CD Liebowitz MR Weissman MM . Social phobia: comorbidity and morbidity in an epidemiological sample. Arch Gen Psychiatry. (1992) 55:322–31. doi: 10.1001/archpsyc.1992.01820040034004, PMID: 1558462 Davies G Welham J Chant D Torrey EF McGrath J . A systematic review and meta-analysis of northern hemisphere season of birth studies in schizophrenia. Schizophr Bull. (2003) 29:587–93. doi: 10.1093/oxfordjournals.schbul.a007030, PMID: 14609251 Miller B Messias E Miettunen J Alaräisänen A Järvelin MR Koponen H . Meta-analysis of paternal age and schizophrenia risk in male versus female offspring. Schizophr Bull. (2011) 37:1039–47. doi: 10.1093/schbul/sbq011, PMID: 20185538 Brown AS . Exposure to prenatal infection and risk of schizophrenia. Front Psychiatry. (2011) 2:63. doi: 10.3389/fpsyt.2011.00063, PMID: 22131978 Brown AS Derkits EJ . Prenatal infection and schizophrenia: a review of epidemiologic and translational studies. Am J Psychiatry. (2010) 167:261–80. doi: 10.1176/appi.ajp.2009.09030361, PMID: 20123911 Barrigón ML Diaz FJ Gurpegui. M Ferrin. M Salcedo MD Moreno-Granados J . Childhood trauma as a risk factor for psychosis: A sib-pair study. J Psychiatr Res. (2015) 70:130–6. doi: 10.1016/j.jpsychires.2015.08.017, PMID: 26424432 Antonsen S Mok PLH Webb RT Mortensen PB McGrath JJ Agerbo E . Exposure to air pollution during childhood and risk of developing schizophrenia: a national cohort study. Lancet Planet. Health. (2020) 4:e64–73. doi: 10.1016/S2542-5196(20)30004-8, PMID: 32112749 Cantor-Graae E Selten J-P . Schizophrenia and migration: A meta-analysis and review. Am J Psychiatry. (2005) 162:12–24. doi: 10.1176/appi.ajp.162.1.12, PMID: 15625195 Margolis AE Lee SH Liu R Goolsby L Champagne F Herbstman J . Associations between prenatal exposure to second hand smoke and infant self-regulation in a New York city longitudinal prospective birth cohort. Environ Res. (2023) 227:115652. doi: 10.1016/j.envres.2023.115652, PMID: 36894114 David CN Greenstein D Clasen L Gochman P Miller R Tossell JW . Childhood onset schizophrenia: high rate of visual hallucinations. J Am Acad Child Adolesc Psychiatry. (2011) 50:681–686.e3. doi: 10.1016/j.jaac.2011.03.020, PMID: 21703495 Lavin R Bucci S Varese F Berry K . The relationship between insecure attachment and paranoia in psychosis: A systematic literature review. Br J Clin Psychol. (2020) 59:39–65. doi: 10.1111/bjc.12231, PMID: 31390076 Swee MB Hudson CC Heimberg RG . Examining the relationship between shame and social anxiety disorder: A systematic review. Clin Psychol Rev. (2021) 90:102088. doi: 10.1016/j.cpr.2021.102088, PMID: 34598054 Stein MB . An epidemiologic perspective on social anxiety disorder. J Clin Psychiatry. (2006) 67:3–8. doi: 10.4088/jcp.v67n1212, PMID: 17092189 Stein MB Stein DJ . Social anxiety disorder. Lancet. (2008) 371:1115–25. doi: 10.1016/S0140-6736(08)60488-2, PMID: 18374843 Varsamis J Adamson JD . Somatic symptoms in schizophrenia. Can Psychiatr Assoc J. (1976) 21:1–6. doi: 10.1177/070674377602100101, PMID: 1268796 Ting JH Zainal N Kanagasundram S Mohamed S . Conversion symptoms in schizophrenia: A case report. Malays. J Of. Psychiatry. (2010) 18:18. Lim A Hoek HW Deen ML Blom JD Bruggeman R Cahn W . Prevalence and classification of hallucinations in multiple sensory modalities in schizophrenia spectrum disorders. Schizophr Res. (2016) 176:493–9. doi: 10.1016/j.schres.2016.06.010, PMID: 27349814 Waters F Collerton D Ffytche DH Jardri R Pins D Dudley R . Visual hallucinations in the psychosis spectrum and comparative information from neurodegenerative disorders and eye disease. Schizophr Bull. (2014) 40:S233–45. doi: 10.1093/schbul/sbu036, PMID: 24936084 Adams RA Stephan KE Brown HR Frith CD Friston KJ . The computational anatomy of psychosis. Front Psychiatry. (2013) 4:47. doi: 10.3389/fpsyt.2013.00047, PMID: 23750138 Andreasen NC Flaum M . Schizophrenia: the characteristic symptoms. Schizophr Bull. (1991) 17:27–49. doi: 10.1093/schbul/17.1.27, PMID: 2047788 Sterzer P Adams RA Fletcher P Frith C Lawrie SM Muckli L . The predictive coding account of psychosis. Biol Psychiatry. (2018) 84:634–43. doi: 10.1016/j.biopsych.2018.05.015, PMID: 30007575 Tibbo P Swainson J Chue P LeMelledo J-M . Prevalence and relationship to delusions and hallucinations of anxiety disorders in schizophrenia. Depress. Anxiety. (2003) 17:65–72. doi: 10.1002/da.10083, PMID: 12621594 Postmes L Sno HN Goedhart S Van Der Stel J Heering HD de Haan L . Schizophrenia as a self-disorder due to perceptual incoherence. Schizophr Res. (2014) 152:41–50. doi: 10.1016/j.schres.2013.07.027, PMID: 23973319 Turetsky BI Kohler CG Indersmitten T Bhati MT Charbonnier D Gur RC . Facial emotion recognition in schizophrenia: when and why does it go awry? Schizophr Res. (2007) 94:253–63. doi: 10.1016/j.schres.2007.05.001, PMID: 17583481 Kapur S . Psychosis as a state of aberrant salience: a framework linking biology, phenomenology, and pharmacology in schizophrenia. Am J Psychiatry. (2003) 160:13–23. doi: 10.1176/appi.ajp.160.1.13, PMID: 12505794 Bucci S Startup M Wynn P Heathcote A Baker A Lewin TJ . Referential delusions of communication and reality discrimination deficits in psychosis. Br J Clin Psychol. (2008) 47:323–34. doi: 10.1348/014466508X280952, PMID: 18248692 Mitrovic M Ristic M Dimitrijevic B Hadzi Pesic M . Facial emotion recognition and persecutory ideation in paranoid schizophrenia. psychol Rep. (2020) 123:1099–116. doi: 10.1177/0033294119849016, PMID: 31092137 Pawełczyk A Kotlicka-Antczak M Łojek E Ruszpel A Pawełczyk T . Schizophrenia patients have higher-order language and extralinguistic impairments. Schizophr Res. (2018) 192:274–80. doi: 10.1016/j.schres.2017.04.030, PMID: 28438437 Trotta A Kang J Stahl D Yiend J . Interpretation bias in paranoia: A systematic review and meta-analysis. Clin psychol Sci. (2021) 9:3–23. doi: 10.1177/2167702620951552 Coid JW Ullrich S Kallis C Keers R Barker D Cowden F . The relationship between delusions and violence: findings from the East London first episode psychosis study. JAMA Psychiatry. (2013) 70:465–71. doi: 10.1001/jamapsychiatry.2013.12, PMID: 23467760 Fett AJ Hanssen E Eemers M Peters E Shergill SS . Social isolation and psychosis: an investigation of social interactions and paranoia in daily life. Eur Arch Psychiatry Clin Neurosci. (2022) 272:119–27. doi: 10.1007/s00406-021-01278-4, PMID: 34129115 Powers AR Kelley M Corlett PR . Hallucinations as top-down effects on perception. Biol Psychiatry Cogn Neurosci Neuroimaging. (2016) 1:393–400. doi: 10.1016/j.bpsc.2016.04.003, PMID: 28626813 Howes OD McCutcheon R Owen MJ Murray RM . The role of genes, stress, and dopamine in the development of schizophrenia. Biol Psychiatry. (2017) 81:9–20. doi: 10.1016/j.biopsych.2016.07.014, PMID: 27720198 Merritt K Egerton A Kempton MJ Taylor MJ McGuire PK . Nature of glutamate alterations in schizophrenia: A meta-analysis of proton magnetic resonance spectroscopy studies. JAMA Psychiatry. (2016) 73:665–74. doi: 10.1001/jamapsychiatry.2016.0442, PMID: 27304221 Stahl S . Beyond the dopamine hypothesis of schizophrenia to three neural networks of psychosis: Dopamine, serotonin, and glutamate. CNS Spectr. (2018) 23:187–91. doi: 10.1017/S1092852918001013, PMID: 29954475 Swanton T . The dopamine, glutamate, and GABA hypotheses of schizophrenia: Glutamate may be the key. ANU. Undergrad. Res J. (2020) 10:88–96. Available online at: https://studentjournals.anu.edu.au/index.php/aurj/article/view/251 (Accessed December 20, 2022). Brisch R Saniotis A Wolf R Bielau H Bernstein HG Steiner J . The role of dopamine in schizophrenia from a neurobiological and evolutionary perspective: old fashioned, but still in vogue. Front Psychiatry. (2014) 5:47. doi: 10.3389/fpsyt.2014.00047, PMID: 24904434 Cancel A Dallel S Zine A El-Hage W Fakra E . Understanding the link between childhood trauma and schizophrenia: A systematic review of neuroimaging studies. Neurosci Biobehav Rev. (2019) 107:492–504. doi: 10.1016/j.neubiorev.2019.05.024, PMID: 31163206 Ricard J Berthelot N Fortin-Fabbro É Boisvert M-C Garon-Bissonnette J Arsenault E . Childhood trauma and altered response of retinal neurons as an early risk endophenotype of schizophrenia and mood disorder. Biomarkers Neuropsychiatr. (2024) 10(5). doi: 10.1016/j.bionps.2024.100095 Silverstein SM Lai A . The phenomenology and neurobiology of visual distortions and hallucinations in schizophrenia: an update. Front Psychiatry. (2021) 12:684720. doi: 10.3389/fpsyt.2021.684720, PMID: 34177665 Parker G . The suprasensory world of bipolar II disorder. Am J Psychiatry. (2014) 171:614–5. doi: 10.1176/appi.ajp.2014.13121570, PMID: 24880508 Parker G Paterson A Romano M Graham R . Altered sensory phenomena experienced in bipolar disorder. Am J Psychiatry. (2017) 174:1146–50. doi: 10.1176/appi.ajp.2017.16121379, PMID: 29191030 Butler PD Zemon V Schechter I Saperstein AM Hoptman MJ Lim KO . Early-stage visual processing and cortical amplification deficits in schizophrenia. Arch Gen Psychiatry. (2005) 62(5):495–504. doi: 10.1001/archpsyc.62.5.495, PMID: 15867102 Dima D Dietrich DE Dillo W Emrich HM . Impaired top-down processes in schizophrenia: a DCM study of ERPs. NeuroImage. (2010) 52:824–32. doi: 10.1016/j.neuroimage.2009.12.086, PMID: 20056155 Gagné AM Hébert M Maziade M . Revisiting visual dysfunctions in schizophrenia from the retina to the cortical cells: A manifestation of defective neurodevelopment. Prog Neuropsychopharmacol Biol Psychiatry. (2015) 62:29–34. doi: 10.1016/j.pnpbp.2015.04.007, PMID: 25934388 Silverstein SM Keane BP . Perceptual organization impairment in schizophrenia and associated brain mechanisms: review of research from 2005 to 2010. Schizophr Bull. (2011) 37:690–9. doi: 10.1093/schbul/sbr052, PMID: 21700589 Shoham N Eskinazi M Hayes JF Lewis G Theodorsson M Cooper C . Associations between psychosis and visual acuity impairment: A systematic review and meta-analysis. Acta Psychiatr. Scand. (2021) 144:6–27. doi: 10.1111/acps.13330, PMID: 34028803 Silverstein SM Rosen R . Schizophrenia and the eye. Schizophr Res Cogn. (2015) 2:46–55. doi: 10.1016/j.scog.2015.03.004, PMID: 26345525 Smith D Pantelis C McGrath J Tangas C Copolov D . Ocular abnormalities in chronic schizophrenia: clinical implications. Aust New Z J Psychiatry. (1997) 31:252–6. doi: 10.3109/00048679709073828, PMID: 9140633 Viertiö S Laitinen A Perälä J Saarni SI Koskinen S Lönnqvist J . Visual impairment in persons with psychotic disorder. Soc Psychiatry Psychiatr Epidemiol. (2007) 42:902–8. doi: 10.1007/s00127-007-0252-6, PMID: 17846698 Kéri S Antal A Szekeres G Benedek G Janka Z . Spatiotemporal visual processing in schizophrenia. J Neuropsychiatr. Clin Neurosci. (2002) 14:190–6. doi: 10.1176/jnp.14.2.190, PMID: 11983794 Slaghuis WL . Contrast sensitivity for stationary and drifting spatial frequency gratings in positive- and negative-symptom schizophrenia. J Abnormal Psychol. (1998) 107:49–62. doi: 10.1037//0021-843x.107.1.49, PMID: 9505038 Chen Y Levy DL Sheremata S Nakayama K Matthysse S Holzman PS . Effects of typical, atypical, and no antipsychotic drugs on visual contrast detection in schizophrenia. Am J Psychiatry. (2003) 160:1795–801. doi: 10.1176/appi.ajp.160.10.1795, PMID: 14514493 Chen Y Norton D Ongur D . Altered center-surround motion inhibition in schizophrenia. Biol Psychiatry. (2008) 17:17. doi: 10.1016/j.biopsych.2007.11.017, PMID: 18206855 Silverstein SM Kovács I Corry R Valone C . Perceptual organization, the disorganization syndrome, and context processing in chronic schizophrenia. Schizophr Res. (2000) 43:11–20. doi: 10.1016/s0920-9964(99)00180-2, PMID: 10828411 Wang Z Yu Z Pan Z Zhao K Zhao Q Zhou D . Impaired binocular depth perception in first-episode drug-naive patients with schizophrenia. Front Psychol. (2018) 9:850. doi: 10.3389/fpsyg.2018.00850, PMID: 29904365 Schechter I Butler PD Jalbrzikowski M Pasternak R Saperstein AM Javitt DC . A new dimension of sensory dysfunction: stereopsis deficits in schizophrenia. Biol Psychiatry. (2006) 60:1282–4. doi: 10.1016/j.biopsych.2006.03.064, PMID: 16945346 Chen Y Bidwell LC Norton D . Trait vs. State Markers for Schizophrenia: Identification and Characterization through Visual Processes. Curr Psychiatry Rev. (2006) 2:431–8. doi: 10.2174/157340006778699729, PMID: 17487285 Silverstein SM Lai A Green KM Crosta C Fradkin SI Ramchandran RS . Retinal microvasculature in schizophrenia. Eye. Brain. (2021) 13:205–17. doi: 10.2147/EB.S317186, PMID: 34335068 Schubert EW Henriksson KM McNeil TF . A prospective study of offspring of women with psychosis: visual dysfunction in early childhood predicts schizophrenia-spectrum disorders in adulthood. Acta Psychiatr. Scand. (2005) 112:385–93. doi: 10.1111/j.1600-0447.2005.00584.x, PMID: 16223427 Maziade M Bureau A Jomphe V Gagné AM . Retinal function and preclinical risk traits in children and adolescents at genetic risk of schizophrenia and bipolar disorder. Prog Neuropsychopharmacol Biol Psychiatry. (2022) 112:110432. doi: 10.1016/j.pnpbp.2021.110432, PMID: 34454992 Revheim N Corcoran CM Dias E Hellmann E Martinez A Butler PD . Reading deficits in schizophrenia and individuals at high clinical risk: relationship to sensory function, course of illness, and psychosocial outcome. Am J Psychiatry. (2014) 171:949–59. doi: 10.1176/appi.ajp.2014.13091196, PMID: 25178752 Mittal VA Gupta T Keane BP Silverstein SM . Visual context processing dysfunctions in youth at high risk for psychosis: Resistance to the Ebbinghaus illusion and its symptom and social and role functioning correlates. J Abnormal Psychol. (2015) 124:953–60. doi: 10.1037/abn0000082, PMID: 26237183 Hébert M Gagné AM Paradis ME Jomphe V Roy MA Mérette C . Retinal response to light in young nonaffected offspring at high genetic risk of neuropsychiatric brain disorders. Biol Psychiatry. (2010) 67:270–4. doi: 10.1016/j.biopsych.2009.08.016, PMID: 19833322 Koethe D Kranaster L Hoyer C Gross S Neatby MA Schultze-Lutter F . Binocular depth inversion as a paradigm of reduced visual information processing in prodromal state, antipsychotic-naïve and treated schizophrenia. Eur Arch Psychiatry Clin Neurosci. (2009) 259:195–202. doi: 10.1007/s00406-008-0851-6, PMID: 19165523 Adámek P Langová V Horáček J . Early-stage visual perception impairment in schizophrenia, bottom-up and back again. Schizophr. (2022) 8:27. doi: 10.1038/s41537-022-00237-9, PMID: 35314712 Maziade M Silverstein SM . The place of the retina in psychiatry: Uniting neurobiological and neurodevelopmental research with clinical research in psychiatric disorders. Schizophr Res. (2020) 219:1–4. doi: 10.1016/j.schres.2020.03.028, PMID: 32249123 Samani NN Proudlock FA Siram V Suraweera C Hutchinson C Nelson CP . Retinal layer abnormalities as biomarkers of schizophrenia. Schizophr Bull. (2018) 44:876–85. doi: 10.1093/schbul/sbx130, PMID: 29272501 Silverstein SM . Visual perception disturbances in schizophrenia: A unified model. In: Li M Spaulding WD , editors. The neuropsychopathology of schizophrenia: Molecules, brain systems, motivation, and cognition. Cham, Switzerland: Springer International Publishing AG (2016). p. 77–132., PMID: 27627825 Demmin DL Davis Q Roché M Silverstein SM . Electroretinographic anomalies in schizophrenia. J Abnormal Psychol. (2018) 127:417–28. doi: 10.1037/abn0000347, PMID: 29745706 Demmin DL Netser R Roché MW Thompson JL Silverstein SM . People with current major depression resemble healthy controls on flash Electroretinogram indices associated with impairment in people with stabilized schizophrenia. Schizophr Res. (2020) 219:69–76. doi: 10.1016/j.schres.2019.07.024, PMID: 31375317 Hébert M Mérette C Gagné AM Paccalet T Moreau I Lavoie J . The electroretinogram may differentiate schizophrenia from bipolar disorder. Biol Psychiatry. (2020) 87:263–70. doi: 10.1016/j.biopsych.2019.06.014, PMID: 31443935 Komatsu H Onoguchi G Jerotic S Kanahara N Kakuto Y Ono T . Retinal layers and associated clinical factors in schizophrenia spectrum disorders: a systematic review and meta-analysis. Mol Psychiatry. (2022) 27:3592–616. doi: 10.1038/s41380-022-01591-x, PMID: 35501407 Adams SA Nasrallah HA . Multiple retinal anomalies in schizophrenia. Schizophr Res. (2018) 195:3–12. doi: 10.1016/j.schres.2017.07.018, PMID: 28755877 Pan J Zhou Y Xiang Y Yu J . Retinal nerve fiber layer thickness changes in Schizophrenia: A meta-analysis of case-control studies. Psychiatry Res. (2018) 270:786–91. doi: 10.1016/j.psychres.2018.10.075, PMID: 30551326 Celik M Kalenderoglu A Sevgi Karadag A Bekir Egilmez O Han-Almis B Şimşek A . Decreases in ganglion cell layer and inner plexiform layer volumes correlate better with disease severity in schizophrenia patients than retinal nerve fiber layer thickness: Findings from spectral optic coherence tomography. Eur Psychiatry. (2016) 32:9–15. doi: 10.1016/j.eurpsy.2015.10.006, PMID: 26800301 Lizano P Lutz O Ling G Lee AM Eum S Bishop JR . Association of choroid plexus enlargement with cognitive, inflammatory, and structural phenotypes across the psychosis spectrum. Am J Psychiatry. (2019) 176:564–72. doi: 10.1176/appi.ajp.2019.18070825, PMID: 31164007 Lizano P Bannai D Lutz O Kim LA Miller J Keshavan MA . Meta-analysis of retinal cytoarchitectural abnormalities in schizophrenia and bipolar disorder. Schizophr Bull. (2020) 46:43–53. doi: 10.1093/schbul/sbz029, PMID: 31112601 Jerotic S Ristic I Pejovic S Mihaljevic M Pavlovic Z Britvic D . Retinal structural abnormalities in young adults with psychosis spectrum disorders. Prog Neuropsychopharmacol Biol Psychiatry. (2020) 98:109825. doi: 10.1016/j.pnpbp.2019.109825, PMID: 31759084 Kazakos CT Karageorgiou V . Retinal changes in schizophrenia: A systematic review and meta-analysis based on individual participant data. Schizophr Bull. (2020) 46:27–42. doi: 10.1093/schbul/sbz106, PMID: 31626695 Schönfeldt-Lecuona C Kregel T Schmidt A Kassubek J Dreyhaupt J Freudenmann RW . Retinal single-layer analysis with optical coherence tomography (OCT) in schizophrenia spectrum disorder. Schizophr Res. (2020) 219:5–12. doi: 10.1016/j.schres.2019.03.022, PMID: 30981598 Schönfeldt-Lecuona C Kregel T Schmidt A Pinkhardt EH Lauda F Kassubek J . From imaging the brain to imaging the retina: Optical Coherence Tomography (OCT) in schizophrenia. Schizophr Bull. (2016) 42:9–14. doi: 10.1093/schbul/sbv073, PMID: 26048298 Appaji A Nagendra B Chako DM Padmanabha A Jacob A Hiremath CV . Relation between retinal vascular abnormalities and working memory impairment in patients with schizophrenia and bipolar disorder. Asian J Psychiatr. (2020) 49:101942. doi: 10.1016/j.ajp.2020.101942, PMID: 32070935 Jurišić D Ćavar I Sesar A Sesar I Vukojević J Ćurković M . New Insights into Schizophrenia: a Look at the Eye and Related Structures. Psychiatr. Danub. (2020) 32:60–9. doi: 10.24869/psyd.2020.60, PMID: 32303031 Appaji A Nagendra B Chako DM Padmanabha A Hiremath CV Jacob A . Retinal vascular abnormalities in schizophrenia and bipolar disorder: a window to the brain. Bipolar. Disord. (2019) 21(7):634–41. doi: 10.1111/bdi.12779, PMID: 31009139 Duan L Tian C Fu C He J Dai J Shao X . Analysis of color vision and cognitive function in first-episode schizophrenia before and after antipsychotic treatment. J Psychiatr Res. (2022) 152:278–88. doi: 10.1016/j.jpsychires.2022.06.012, PMID: 35759980 Bernardin F Schwitzer T Angioi-Duprez K Giersch A Jansen C Schwan R . Retinal ganglion cells dysfunctions in schizophrenia patients with or without visual hallucinations. Schizophr Res. (2020) 219:47–55. doi: 10.1016/j.schres.2019.07.007, PMID: 31353068 Chieffi S . Dysfunction of magnocellular/dorsal processing stream in schizophrenia. Curr Psychiatry Res Rev. (2019) 15:26–36. doi: 10.2174/1573400515666190119163522 Silverstein SM Thompson JL . A vision science perspective on schizophrenia. Schizophr Res Cogn. (2015) 2:39–41. doi: 10.1016/j.scog.2015.05.003, PMID: 26345386 Bannai D Lizano P Kasetty M Lutz O Zeng V Sarvode S . Retinal layer abnormalities and their association with clinical and brain measures in psychotic disorders: A preliminary study. Psychiatry Res Neuroimaging. (2020) 299:111061. doi: 10.1016/j.pscychresns.2020.111061, PMID: 32145500 Alizadeh M Delborde Y Ahmadpanah M Seifrabiee MA Jahangard L Bazzazi N . Non-linear associations between retinal nerve fibre layer (RNFL) and positive and negative symptoms among men with acute and chronic schizophrenia spectrum disorder. J Psychiatr Res. (2021) 141:81–91. doi: 10.1016/j.jpsychires.2021.06.007, PMID: 34182380 Javitt DC . Meeting overview: Sensory perception and schizophrenia, Lausanne, Switzerland June 31-July 1, 2014. Schizophr Res Cogn. (2015) 2:42–5. doi: 10.1016/j.scog.2015.04.003, PMID: 29114453 Butler PD Javitt DC . Early-stage visual processing deficits in schizophrenia. Curr Opin Psychiatry. (2005) 18:151–7. doi: 10.1097/00001504-200503000-00008, PMID: 16639168 Kent BW Weinstein ZA Passarelli V Chen Y Siever LJ . Deficient visual sensitivity in schizotypal personality disorder. Schizophr Res. (2011) 127:144–50. doi: 10.1016/j.schres.2010.05.013, PMID: 20541911 O’Donnell BF Bismark A Hetrick WP Bodkins M Vohs JL Shekhar A . Early stage vision in schizophrenia and schizotypal personality disorder. Schizophr Res. (2006) 86:89–98. doi: 10.1016/j.schres.2006.05.016, PMID: 16829048 Skottun BC Skoyles JR . Contrast sensitivity and magnocellular functioning in schizophrenia. Vision Res. (2007) 47:2923–33. doi: 10.1016/j.visres.2007.07.016, PMID: 17825350 Feigenson KA Keane BP Roché MW Silverstein SM . Contour integration impairment in schizophrenia and first episode psychosis: state or trait? Schizophr Res. (2014) 159:515–20. doi: 10.1016/j.schres.2014.09.028, PMID: 25306205 Uhlhaas PJ Silverstein SM . Perceptual organization in schizophrenia spectrum disorders: empirical research and theoretical implications. psychol Bull. (2005) 131:618–32. doi: 10.1037/0033-2909.131.4.618, PMID: 16060805 Tadin D Kim J Doop ML Gibson C Lappin JS Blake R . Weakened center-surround interactions in visual motion processing in schizophrenia. J Neurosci. (2006) 26:11403–12. doi: 10.1523/JNEUROSCI.2592-06.2006, PMID: 17079669 Tibber MS Anderson EJ Bobin T Antonova E Seabright A Wright B . Visual surround suppression in schizophrenia. Front Psychol. (2013) 4:88. doi: 10.3389/fpsyg.2013.00088, PMID: 23450069 Serrano-Pedraza I Romero-Ferreiro V Read JC Diéguez-Risco T Bagney A Caballero-González M . Reduced visual surround suppression in schizophrenia shown by measuring contrast detection thresholds. Front Psychol. (2014) 5:1431. doi: 10.3389/fpsyg.2014.01431, PMID: 25540631 Yoon JH Maddock RJ Rokem A Silver MA Minzenberg MJ Ragland JD . GABA concentration is reduced in visual cortex in schizophrenia and correlates with orientation-specific surround suppression. J Neurosci. (2010) 30:3777–81. doi: 10.1523/JNEUROSCI.6158-09.2010, PMID: 20220012 Vitay J Hamker FH . On the role of dopamine in cognitive vision. In: Paletta L Rome E , editors. Attention in cognitive systems. Theories and systems from an interdisciplinary viewpoint. LNAI, vol. 4840 . Springer, Berlin, Heidelberg (2007). p. 352–66. Bernardin F Schwitzer T Schwan R Angioi-Duprez K Ligier F Bourion-Bedes S . Altered central vision and amacrine cells dysfunction as marker of hypodopaminergic activity in treated patients with schizophrenia. Schizophr Res. (2022) 239:134–41. doi: 10.1016/j.schres.2021.11.049, PMID: 34891077 Dumitrescu ON Pucci FG Wong KY Berson DM . Ectopic retinal ON bipolar cell synapses in the OFF inner plexiform layer: contacts with dopaminergic amacrine cells and melanopsin ganglion cells. J Comp Neurol. (2009) 517:226–44. doi: 10.1002/cne.22158, PMID: 19731338 Kolb H . Neurotransmitters in the Retina. Kolb H Fernandez E Nelson R , editors. Webvision: The Organization of the Retina and Visual System. University of Utah Health Sciences Center (2005/2009). Available online at: https://www.ncbi.nlm.nih.gov/books/NBK11546/. Haug BA Kolle RU Trenkwalder C Oertel WH Paulus W . Predominant affection of the blue cone pathway in Parkinson’s disease. Brain.: A. J Neurol. (1995) 118:771–8. doi: 10.1093/brain/118.3.771, PMID: 7600093 Price MJ Feldman RG Adelberg D Kayne H . Abnormalities in color vision and contrast sensitivity in Parkinson’s disease. Neurology. (1992) 42:887–90. doi: 10.1212/wnl.42.4.887, PMID: 1565248 Zemon V Herrera S Gordon J Revheim N Silipo G Butler PD . Contrast sensitivity deficits in schizophrenia: A psychophysical investigation. Eur J Neurosci. (2021) 53:1155–70. doi: 10.1111/ejn.15026, PMID: 33118212 Bodis-Wollner I . Visual deficits related to dopamine deficiency in experimental animals and Parkinson’s disease patients. Trends Neurosci. (1990) 13:296–302. doi: 10.1016/0166-2236(90)90113-o, PMID: 1695407 Djamgoz MB Hankins MW Hirano J Archer SN . Neurobiology of retinal dopamine in relation to degenerative states of the tissue. Vision Res. (1997) 37:3509–29. doi: 10.1016/S0042-6989(97)00129-6, PMID: 9425527 Jackson CR Ruan GX Aseem F Abey J Gamble K Stanwood G . Retinal dopamine mediates multiple dimensions of light-adapted vision. J Neurosci. (2012) 32:9359–68. doi: 10.1523/JNEUROSCI.0711-12.2012, PMID: 22764243 Harper L Spencer E Davidson C Hutchinson CV . Selectively reduced contrast sensitivity in high schizotypy. Exp Brain Res. (2020) 238:51–62. doi: 10.1007/s00221-019-05695-9, PMID: 31781821 Schallmo M-P Sponheim SR Olman CA . Reduced contextual effects on visual contrast perception in schizophrenia and bipolar affective disorder. Psychol Med. (2015) 45:3527–37. doi: 10.1017/S0033291715001439, PMID: 26315020 Chen Y Nakayama K Levy D Matthysse S Holzman P . Processing of global, but not local, motion direction is deficient in schizophrenia. Schizophr Res. (2003) 61:215–27. doi: 10.1016/s0920-9964(02)00222-0, PMID: 12729873 Hwang CK Chaurasia SS Jackson CR Chan GC Storm DR Iuvone PM . Circadian rhythm of contrast sensitivity is regulated by a dopamine-neuronal PAS-domain protein 2-adenylyl cyclase 1 signaling pathway in retinal ganglion cells. J Neurosci. (2013) 33:14989–97. doi: 10.1523/JNEUROSCI.2039-13.2013, PMID: 24048828 Tagliati M Bodis-Wollner I Kovanecz I Stanzione P . Spatial frequency tuning of the monkey pattern ERG depends on D2 receptor-linked action of dopamine. Vision Res. (1994) 34:2051–7. doi: 10.1016/0042-6989(94)90316-6, PMID: 7941404 Cadenhead KS Dobkins K McGovern J Shafer K . Schizophrenia spectrum participants have reduced visual contrast sensitivity to chromatic (red/green) and luminance (light/dark) stimuli: new insights into information processing, visual channel function, and antipsychotic effects. Front Psychol. (2013) 4:535. doi: 10.3389/fpsyg.2013.00535, PMID: 23970874 Núñez D Rauch J Herwig K Rupp A Andermann M Weisbrod M . Evidence for a magnocellular disadvantage in early-onset schizophrenic patients: a source analysis of the N80 visual-evoked component. Schizophr Res. (2013) 144:16–23. doi: 10.1016/j.schres.2012.12.007, PMID: 23305611 Kéri S Benedek G . Visual contrast sensitivity alterations in inferred magnocellular pathways and anomalous perceptual experiences in people at high-risk for psychosis. Visual Neurosci. (2007) 24:183–9. doi: 10.1017/S0952523807070253, PMID: 17640409 Kiss I Fábián A Benedek G Kéri S . When doors of perception open: visual contrast sensitivity in never-medicated, first-episode schizophrenia. J Abnormal Psychol. (2010) 119:586–93. doi: 10.1037/a0019610, PMID: 20677847 Tandon R Nasrallah HA Keshavan MS . Schizophrenia, “just the facts” 4. Clinical features and conceptualization. Schizophr Res. (2009) 110:1–23. doi: 10.1016/j.schres.2009.03.005, PMID: 19328655 Galdino MK Mendes LC Vieira JG Simas ML Santos NA . Visual perception of radial sine-wave grating after the alcohol consumption. Psicol. Usp. (2011) 22:99–115. doi: 10.1590/S0103-65642011005000001 Casares-López M Castro-Torres JJ Martino F Ortiz-Peregrina S Ortiz C Anera RG . Contrast sensitivity and retinal straylight after alcohol consumption: effects on driving performance. Sci Rep. (2020) 10:13599. doi: 10.1038/s41598-020-70645-3, PMID: 32788613 Roquelaure Y Le Gargasson JF Kupper S Girre C Hispard E Dally S . Alcohol consumption and visual contrast sensitivity. Alcohol Alcohol. (Oxford Oxon). (1995) 30:681–5. doi: 10.1093/oxfordjournals.alcalc.a045781 Zhuang X King A McNamara P Pokorny J Cao D . Differential effects of alcohol on contrast processing mediated by the magnocellular and parvocellular pathways. J Vision. (2012) 12:16. doi: 10.1167/12.11.16, PMID: 23090614 Da Cruz É.D.N. De Andrade MJO Cavalcanti-Gaudino MK Toscano RM Nogueira BL dos Santos NA . Effects of chronic alcoholism in the sensitivity to luminance contrast in vertical sinusoidal gratings. Psicol. Refl. Crít. (2016) 29:14. doi: 10.1186/s41155-016-0023-y Varghese SB Reid JC Hartmann EE Keyser KT . The effects of nicotine on the human electroretinogram. Invest Ophthalmol Visual Sci. (2011) 52:9445–51. doi: 10.1167/iovs.11-7874, PMID: 22064991 Chapman J . The Early symptoms of schizophrenia. Br J Psychiatry. (1966) 112:225–51. doi: 10.1192/bjp.112.484.225, PMID: 4957283 Fernandes TMP Silverstein SM Butler PD Kéri S Santos LG Nogueira RL . Color vision impairments in schizophrenia and the role of antipsychotic medication type. Schizophr Res. (2019) 204:162–70. doi: 10.1016/j.schres.2018.09.002, PMID: 30201549 Shuwairi SM Cronin-Golomb A McCarley RW O’Donnell BF . Color discrimination in schizophrenia. Schizophr Res. (2002) 55:197–204. doi: 10.1016/s0920-9964(01)00180-3, PMID: 11955979 Klosterkötter J Hellmich M Steinmeyer EM Schultze-Lutter F . Diagnosing schizophrenia in the initial prodromal phase. Arch Gen Psychiatry. (2001) 58:158–64. doi: 10.1001/archpsyc.58.2.158, PMID: 11177117 Brandies R Yehuda S . The possible role of retinal dopaminergic system in visual performance. Neurosci Biobehav Rev. (2008) 32:611–56. doi: 10.1016/j.neubiorev.2007.09.004, PMID: 18061262 Vollmer-Larsen A Handest P Parnas J . Reliability of measuring anomalous experience: the Bonn Scale for the Assessment of Basic Symptoms. Psychopathology. (2007) 40:345–8. doi: 10.1159/000106311, PMID: 17657133 Brasil A Castro AJ Martins IC Lacerda EM Souza GS Herculano AM . Colour vision impairment in young alcohol consumers. PloS One. (2015) 10:e0140169. doi: 10.1371/journal.pone.0140169, PMID: 26465148 Castro AJ d. O Rodrigues AR Côrtes MIT Silveira LCDL . Impairment of color spatial vision in chronic alcoholism measured by psychophysical methods. Psychol Neurosci. (2009) 2:179–87. doi: 10.3922/j.psns.2009.2.009 Martins I. C. V. D. S. Souza GDS Brasil A Herculano AM Lacerda E. M. D. C. B. Rodrigues AR . Psychophysical evaluation of visual functions of ex-alcoholic subjects after prolonged abstinence. Front Neurosci. (2019) 13:179. doi: 10.3389/fnins.2019.00179, PMID: 30894798 Fernandes TP Silverstein SM Almeida NL Santos NA . Visual impairments in tobacco use disorder. Psychiatry Res. (2019) 271:60–7. doi: 10.1016/j.psychres.2018.11.024, PMID: 30469090 Fernandes TMP Silverstein SM Almeida NL Santos NAD . Psychophysical evaluation of contrast sensitivity using Gabor patches in tobacco addiction. J Clin Neurosci. (2018) 57:68–73. doi: 10.1016/j.jocn.2018.08.034, PMID: 30195990 Gundogan FC Durukan AH Mumcuoglu T Sobaci G Bayraktar MZ . Acute effects of cigarette smoking on pattern electroretinogram. Documenta ophthalmologica. Adv Ophthalmol. (2006) 113:115–21. doi: 10.1007/s10633-006-9021-1, PMID: 16972083 Gundogan FC Erdurman C Durukan AH Sobaci G Bayraktar MZ . Acute effects of cigarette smoking on multifocal electroretinogram. Clin Exp Ophthalmol. (2007) 35:32–7. doi: 10.1111/j.1442-9071.2006.01384.x, PMID: 17300568 Mandelbrot BB . The Fractal Geometry of Nature W.H. New York: Freeman & Co (1977/83), ISBN: 100716711869. Grosu GF Hopp AV Moca VV Bârzan H Ciuparu A Ercsey-Ravasz M . The fractal brain: scale-invariance in structure and dynamics. Cereb Cortex. (2023) 33:4574–605. doi: 10.1093/cercor/bhac363, PMID: 36156074 Di leva A . The Fractal Geometry of the Brain. New York: Springer-Verlag New York Inc (2016), ISBN: 9781493981489. doi: 10.1007/978-1-4939-3995-4 Turkheimer FE Leech R Expert P Lord LD Vernon AC . The brain’s code and its canonical computational motifs. From sensory cortex to the default mode network: A multi-scale model of brain function in health and disease. Neurosci Biobehav Rev. (2015) 55:211–22. doi: 10.1016/j.neubiorev.2015.04.014, PMID: 25956253 Pincus D Cadsky O Berardi V Asuncion CM Wann K . Fractal self-structure and psychological resilience. Nonlinear Dyn. Psychol. Life Sci. (2019) 23:57–78. doi: 10.1007/s11031-019-09772-y, PMID: 30557136 Cutting JE Garvin JJ . Fractal curves and complexity. Percept Psychophys. (1987) 42:365–370 370. doi: 10.3758/BF03203093, PMID: 3684493 Pentland A . Fractal-based description of natural scenes. IEEE Trans Pattern Anal Mach Intell. (1984) 6:661–74. doi: 10.1109/TPAMI.1984.4767591, PMID: 22499648 Spehar B Walker N Taylor RP . Taxonomy of Individual Variations in Aesthetic Responses to Fractal Patterns. Front Hum Neurosci. (2016) 10:350. doi: 10.3389/fnhum.2016.00350, PMID: 27458365 Forsythe A Nadal M Sheehy N Cela-Conde CJ Sawey M . Predicting beauty: fractal dimension and visual complexity in art. Br J Psychol (London Engl: 1953). (2011) 102:49–70. doi: 10.1348/000712610X498958, PMID: 21241285 Hagerhall CM Purcell T Taylor R . Fractal dimension of landscape silhouette outlines as a predictor of landscape preference. J Environ Psychol. (2004) 24:247–55. doi: 10.1016/j.jenvp.2003.12.004 Heerwagen JH Orians GH . Humans, habitats, and aesthetics. In: Kellert SR Wilson EO , editors. The biophilia hypothesis. Island Press, Covelo, CA (1993), ISBN: 9781559631471. p. 138–72. Taylor RP Sprott JC . Biophilic fractals and the visual journey of organic screen-savers. Nonlinear Dyn. Psychol. Life Sci. (2008) 12:117–29. doi: 10.1038/s41598-021-81421-2, PMID: 18157930 Taylor RP . Reduction of physiological stress using fractal art and architecture. Leonardo. (2006) 39:245–51. doi: 10.1162/leon.2006.39.3.245 Hagerhall CM Laike T Taylor RP Küller M Küller R Martin TP . Investigations of human EEG response to viewing fractal patterns. Perception. (2008) 37:1488–94. doi: 10.1068/p5918, PMID: 19065853 Ulrich RS . View through a window may influence recovery from surgery. Sci (New York N.Y.). (1984) 224:420–1. doi: 10.1126/science.6143402, PMID: 6143402 Spehar B Clifford CWG Newell BR Taylor RP . Universal aesthetic of fractals. Comput Graphics. (2003) 27:813–20. doi: 10.1016/S0097-8493(03)00154-7 Taylor R Newell B Spehar B . “ Fractals: A resonance between art and nature,” In: Emmer M , editor. Mathematics and Culture II. Springer, Berlin (2005). 53–63. doi: 10.1007/b137592 Viengkham C Spehar B . Preference for fractal-scaling properties across synthetic noise images and artworks. Front Psychol. (2018) 9:1439. doi: 10.3389/fpsyg.2018.01439, PMID: 30210380 Redies C Hänisch J Blickhan M Denzler J . Artists portray human faces with the Fourier statistics of complex natural scenes. Netw. (Bristol Engl). (2007) 18:235–48. doi: 10.1080/09548980701574496, PMID: 17852751 Redies C Hasenstein J Denzler J . Fractal-like image statistics in visual art: similarity to natural scenes. Spat. Vision. (2007) 21:137–48. doi: 10.1163/156856807782753921, PMID: 18073055 Fernandez D Wilkins AJ . Uncomfortable images in art and nature. Perception. (2008) 37:1098–113. doi: 10.1068/p5814, PMID: 18773732 Lopes AM Tenreiro MaChado JA . Complexity analysis of escher’s art. Entropy. (2019) 21:553. doi: 10.3390/e21060553, PMID: 33267267 De La Calleja EM Cervantes F De La Calleja J . Order-fractal transitions in abstract paintings. Ann Phys. (2016) 371:313–22. doi: 10.1016/j.aop.2016.04.007 Taylor RP Micolich AP Jonas D . Fractal analysis of Pollock’s drip paintings. Nature. (1999) 399:422–2. doi: 10.1038/20833 McElroy S . If It’s So Easy, Why Don’t You Try It. New York, NY: New York Times (2010). Available online at: https://www.nytimes.com/2010/12/05/nyregion/05spotli.html (Accessed May 15, 2024). Bountis T Fokas AS Psarakis EZ . Fractal analysis of tree paintings by Piet Mondrian, (1872-1944). Int J Arts. Technol. (2017) 10:27–42. doi: 10.1504/IJART.2017.083902 Müller-Westermann . Munch by Himself. London: Royal Academy of Arts (2005), ISBN: 1-903973-64-3. Shamir L Tarakhovsky JA . Computer analysis of art. ACM J Comput. Cult. Herit. (2012) 5:1–7. doi: 10.1145/2307723.2307726 Chatfield C Xing H . The Analysis of Time Series: An Introduction with R. 7th edn. New York: Chapman and Hall/CRC (2019). doi: 10.1201/9781351259446 Duth PS Deepa M . Color detection in RGB-modeled images using MAT LAB. Int J Eng Technol. (2018) 7:29. doi: 10.14419/ijet.v7i2.31.13391 Nayak SR Mishra J . An improved method to estimate the fractal dimension of colour images. Perspect Sci. (2016) 8:412–6. doi: 10.1016/j.pisc.2016.04.092 Ivanovici M Richard N . Fractal dimension of color fractal images. IEEE Trans Image Process. (2011) 20:227–35. doi: 10.1109/TIP.2010.2059032, PMID: 20643608 Nikolaidis NS Nikolaidis IN Tsouros CC . A variation of the box-counting algorithm applied to colour images. ArXiv. (2011). doi: 10.48550/arXiv1107.2336 Wang JH Ogawa S . Fractal analysis of colors and shapes for natural and urbanscapes URBANSCAPES. ISPRS - international archives of the photogrammetry. Remote Sens Spat. Inf Sci. (2015) XL-7/W3:1431–8. doi: 10.5194/isprsarchives-XL-7-W3-1431-2015 Kendall KM Van Assche E Andlauer TFM Choi KW Luykx JJ Schulte EC . The genetic basis of major depression. psychol Med. (2021) 51:2217–30. doi: 10.1017/S0033291721000441, PMID: 33682643 Meier SM Deckert J . Genetics of anxiety disorders. Curr Psychiatry Rep. (2019) 21:16. doi: 10.1007/s11920-019-1002-7, PMID: 30826936 Purty A Nestadt G Samuels JF Viswanath B . Genetics of obsessive-compulsive disorder. Indian J Psychiatry. (2019) 61:S37–42. doi: 10.4103/psychiatry.IndianJPsychiatry_518_18, PMID: 30745675 Rakesh K Arvind S Dutt BP Mamta B Bhavneesh S Kavita M . The role of religiosity and guilt in symptomatology and outcome of obsessive compulsive disorder. Psychopharmacol Bull. (2021) 51:38–49. doi: 10.64719/pb.4408, PMID: 34421143 Enoch MA . Genetic and environmental influences on the development of alcoholism: resilience vs. risk. Ann New York Acad Sci. (2006) 1094:193–201. doi: 10.1196/annals.1376.019, PMID: 17347351 True WR Xian H Scherrer JF Madden PA Bucholz KK Heath AC . Common genetic vulnerability for nicotine and alcohol dependence in men. Arch Gen Psychiatry. (1999) 56:655–61. doi: 10.1001/archpsyc.56.7.655, PMID: 10401514 Kuo SC Chen YT Li SY Lee YT Yang AC Chen TL . Incidence and outcome of newly-diagnosed tuberculosis in schizophrenics: a 12-year, nationwide, retrospective longitudinal study. BMC Infect Dis. (2013) 13:351. doi: 10.1186/1471-2334-13-351, PMID: 23895638 Rossi R Ciocca G Socci V Jannini TB Gorea F Pacitti F . Psychopathological mediators between insecure attachment and psychotic features in a non-clinical sample: the role of depression and interpersonal sensitivity. Riv. Di. Psichiatr. (2023) 58:160–6. doi: 10.1708/4064.40478, PMID: 37409433 Sheinbaum T Bedoya E Ros-Morente A Kwapil TR Barrantes-Vidal N . Association between attachment prototypes and schizotypy dimensions in two independent non-clinical samples of Spanish and American young adults. Psychiatry Res. (2013) 210:408–13. doi: 10.1016/j.psychres.2013.07.020, PMID: 24011849 Velikonja T Fisher HL Mason O Johnson S . Childhood trauma and schizotypy: a systematic literature review. psychol Med. (2015) 45:947–63. doi: 10.1017/S0033291714002086, PMID: 25273151 Stanton KJ Denietolis B Goodwin BJ Dvir Y . Childhood Trauma and psychosis: an updated review. Child Adolesc Psychiatr Clinics North America. (2020) 29:115–29. doi: 10.1016/j.chc.2019.08.004, PMID: 31708041 Chakrabarti S Singh N . Psychotic symptoms in bipolar disorder and their impact on the illness: A systematic review. World J Psychiatry. (2022) 12:1204–32. doi: 10.5498/wjp.v12.i9.1204, PMID: 36186500 Bolton S Warner J Harriss E Geddes J Saunders KEA . Bipolar disorder: Trimodal age-at-onset distribution. Bipolar. Disord. (2021) 23:341–56. doi: 10.1111/bdi.13016, PMID: 33030292 Goghari VM Harrow M Grossman LS Rosen C . A 20-year multi-follow-up of hallucinations in schizophrenia, other psychotic, and mood disorders. psychol Med. (2013) 43:1151–60. doi: 10.1017/S0033291712002206, PMID: 23034091 Bauer M Gitlin M . Natural Course of Bipolar Disorder and Implications for Treatment. In: The Essential Guide to Lithium Treatment. Springer, Cham (2016). doi: 10.1007/978-3-319-31214-9_2 Tsitsipa E Fountoulakis KN . The neurocognitive functioning in bipolar disorder: a systematic review of data. Ann Gen Psychiatry. (2015) 14:42. doi: 10.1186/s12991-015-0081-z, PMID: 26628905 Johnson SL Murray G Fredrickson B Youngstrom EA Hinshaw S Bass JM . Creativity and bipolar disorder: touched by fire or burning with questions? Clin Psychol Rev. (2012) 32:1–12. doi: 10.1016/j.cpr.2011.10.001, PMID: 22088366 Moe AM Docherty NM . Schizophrenia and the sense of self. Schizophr Bull. (2014) 40:161–8. doi: 10.1093/schbul/sbt121, PMID: 23970556 Correll CU Schooler NR . Negative symptoms in schizophrenia: A review and clinical guide for recognition, assessment, and treatment. Neuropsychiatr Dis Treat. (2020) 16:519–34. doi: 10.2147/NDT.S225643, PMID: 32110026 Marder SR Galderisi S . The current conceptualization of negative symptoms in schizophrenia. World Psychiatry. (2017) 16:14–24. doi: 10.1002/wps.20385, PMID: 28127915 Roy MA Demers MF Achim AM . Social anxiety disorder in schizophrenia: a neglected, yet potentially important comorbidity. J Psychiatry Neurosci. (2018) 43:287–8. doi: 10.1503/jpn.180081, PMID: 29947611 Gorun A Cieslak K Harkavy-Friedman J Deptula A Goetz D Goetz R . Frequent Comorbidity and Predictors of Social Anxiety in Persons With Schizophrenia: A Retrospective Cohort Study. In: The primary care companion for CNS disorders, vol. 17. (2015). doi: 10.4088/PCC.15m01799, PMID: 26835173 Penn DL Hope DA Spaulding W Kucera J . Social anxiety in schizophrenia. Schizophr Res. (1994) 11:277–84. doi: 10.1016/0920-9964(94)90022-1, PMID: 8193064 Lowengrub KM Stryjer R Birger M Iancu I . Social anxiety disorder comorbid with schizophrenia: the importance of screening for this under recognized and under treated condition. Isr J Psychiatry Relat Sci. (2015) 52:40–5., PMID: 25841109 Schneider K . Clinical Psychopathology. 5th ed.: Grune and Stratton. (Hamilton, M.W., Trans.) ISBN: 9780808904175.E. (1959). Available online at: https://photoshop.adobe.com/. McEnery C Lim MH Tremain H Knowles A Alvarez-Jimenez M . Prevalence rate of social anxiety disorder in individuals with a psychotic disorder: A systematic review and meta-analysis. Schizophr Res. (2019) 208:25–33. doi: 10.1016/j.schres.2019.01.045, PMID: 30722947 Pallanti S Quercioli L Hollander E . Social anxiety in outpatients with schizophrenia: A relevant cause of disability. Am J Psychiatry. (2004) 161:53–8. doi: 10.1176/appi.ajp.161.1.53, PMID: 14702250 Achim AM Ouellet R Lavoie MA Vallières C Jackson PL Roy MA . Impact of social anxiety on social cognition and functioning in patients with recent-onset schizophrenia spectrum disorders. Schizophr Res. (2013) 145:75–81. doi: 10.1016/j.schres.2013.01.012, PMID: 23415473 Michail M Birchwood M . Social anxiety disorder in first-episode psychosis: incidence, phenomenology and relationship with paranoia. Br J Psychiatry. (2009) 195:234–41. doi: 10.1192/bjp.bp.108.053124, PMID: 19721113 Achim AM Sutliff S Samson C Montreuil TC Lecomte T . Attribution bias and social anxiety in schizophrenia. Schizophr Res Cognit. (2016) 4:1–3. doi: 10.1016/j.scog.2016.01.001, PMID: 28740807 Faravelli C Lo Sauro C Godini L Lelli L Benni L Pietrini F . Childhood stressful events, HPA axis and anxiety disorders. World J Psychiatry. (2012) 2:13–25. doi: 10.5498/wjp.v2.i1.13, PMID: 24175164 Murphy F Nasa A Cullinane D Raajakesary K Gazzaz A Sooknarine V . Childhood trauma, the HPA axis and psychiatric illnesses: A targeted literature synthesis. Front Psychiatry. (2022) 13:748372. doi: 10.3389/fpsyt.2022.748372, PMID: 35599780 Lee YH Cherkerzian S Seidman LJ Papandonatos GD Savitz DA Tsuang MT . Maternal bacterial infection during pregnancy and offspring risk of psychotic disorders: variation by severity of infection and offspring sex. Am J Psychiatry. (2020) 177:66–75. doi: 10.1176/appi.ajp.2019.18101206, PMID: 31581799 Strauss GP Bartolomeo LA Harvey PD . Avolition as the core negative symptom in schizophrenia: relevance to pharmacological treatment development. NPJ Schizophr. (2021) 7:16. doi: 10.1038/s41537-021-00145-4, PMID: 33637748 Muller-Westermann . Munch by Himself. London: Royal Academy of Arts. (2005).

Edited by: Virginio Salvi, Asst Hospital of Crema, Italy

Reviewed by: Francesca Pacitti, University of L’Aquila, Italy

Cagdas Eker, Ege University, Türkiye

This strangeness also extends to auditory self-perception (22, 23).

Munch seems to have understood this. He wrote on the canvas: “Kan kun være malet af en gal Mand!” (“Can only have been painted by a madman!”) (24).

Munch left several thousand pages of journals, correspondence, poetry, and fiction. His exhibitions are well documented, there are numerous contemporary reviews of his art and a significant number of his contemporaries wrote memoires of him (for translated materials see: https://www.emunch.no/english.xhtml; for memoires see: 55, 56, Stang (57) and Stenersen, 1944 (hereafter, ‘Stenersen’ (58)).

For images of his work in chronological order:https://en.wikipedia.org/wiki/List_of_paintings_by_Edvard_Munch.

“My fear of life is necessary to me, as is my illness. Without anxiety and illness, I am a ship without a rudder. My art is grounded in reflections over being different from others. My sufferings are part of myself and my art. They are indistinguishable from me, and their destruction would destroy my art. I want to keep those sufferings.” (41, p.251; 62).

Although a consequence of spinal tuberculosis, it was a source of Munch’s belief in his hereditary madness (Prideaux; Tøjner).

“I can’t attend parties. Nobody understands. If I go to a party it has such a strong effect on me I simply cannot cope” (Prideaux, 295); “I feel like a prisoner when I attend parties and I don’t want to be anyone’s prisoner – my nerves can’t take it” (Stenersen,117).

Kornhaug 1899, Como 1901, Knock-su-Mer 1901, Eldursburdg 1904, Ilmenau 1905, Kosen 1906 (twice), Ilmenau 1906.

Social anxiety is the persistent fear of social situations threatening embarrassment or humiliation, which causes functional impairment in relationships with family and friends and in forming and maintaining romantic relationships (108; APA 2022b, 109).

The self can also be seen as fractal in structure (254).

Of the total portraits 33 are of ‘family and friends’ consisting of known relations and people, including some patrons, with whom he maintained relationships over several years.

For a detailed explanation of colour extraction using MatLab (see: 279).

“When I paint sickness and suffering it is…a healthy release. It is a healthy reaction from which one can learn and carry on living” (Tøjner, p.134).