Symptoms of Neurosis and Their Reflection in Popular Culture

Philosophical Framework

The consideration of neuroses and their reflection in popular culture inevitably fits within the traditions of critical theory and the sociology of knowledge, where media do not merely reflect reality but actively construct it. We face the question of how cultural narratives shape our understanding of mental states, influencing stigmatization or, conversely, destigmatization. This also touches on epistemological questions about the nature of knowledge: what do we consider "true" about neurosis — the clinical definition or its media image?

Introduction

Neurosis, as a functional mental disorder not associated with organic brain damage, manifests in prolonged emotional and behavioral disturbances that significantly affect an individual's quality of life. Key symptoms may range from anxiety and phobias to intrusive thoughts and actions, as well as hysterical manifestations and somatic disorders. Particular clinical attention is given to obsessive-compulsive neurosis, or obsessive-compulsive disorder (OCD), characterized by involuntary, repetitive thoughts (obsessions) and ritualistic actions (compulsions) [Najjar et al., 2013].

At the same time, popular culture, including media objects, entertainment, and trends, is a powerful tool for shaping public opinion and perception [Kidd, 2017]. It often addresses themes of mental disorders, including neuroses, but does so in its own way. Depictions of neurotic states in film, literature, television, and social networks can both contribute to destigmatization and, conversely, distort the real clinical picture by exaggerating or romanticizing symptoms. This creates a complex dynamic between medical understanding and cultural interpretation of mental states.

Literature Review

The Nature of Obsessive-Compulsive Neurosis (OCD) and Its Cognitive Mechanisms

What exactly makes obsessive-compulsive disorder (OCD) one of the most debilitating mental conditions, capable of leading to chronic unemployment and relationship breakdowns? It is not merely a set of strange habits but a complex disorder deeply rooted in cognitive distortions and physiological processes. Understanding its nature requires a multidimensional approach beyond superficial observations.

Obsessions are involuntary, repetitive thoughts, images, or urges that cause significant anxiety or distress. Compulsions are repetitive behaviors or mental acts that a person feels compelled to perform in response to an obsession to prevent some dreadful event or reduce anxiety. For example, fear of contamination (obsession) may lead to repeated hand washing (compulsion). However, these rituals provide only temporary relief and, in the long term, intensify the anxiety cycle.

Historically, OCD research has advanced significantly, deepening our understanding of its cognitive phenomenology as well as developmental and physiological correlates. This has allowed moving away from simplistic models toward a more nuanced view of the disorder. For instance, David Clark, referencing Rahman’s work, emphasizes the need to develop specialized theories and treatment methods targeting specific phenomenological characteristics and underlying processes of OCD subtypes [Clark, 2007]. This approach allows deeper insight into the unique phenomenology of specific obsessive fears, such as contamination fear.

Rahman, a leading expert in OCD, argues that a microanalytic approach to studying the disorder yields surprisingly fresh ideas about its core cognitive processes [Clark, 2007]. This means that instead of viewing OCD as a single entity, we should study its individual manifestations to understand how specific obsessions and compulsions form and are maintained. For example, contamination fear may be linked to particular beliefs about cleanliness, danger, and responsibility that require specific therapeutic intervention.

Beyond cognitive and behavioral aspects, increasing attention is paid to biological correlates of mental disorders, including OCD. Neuroinflammation, for example, is considered a potential factor in the pathogenesis of several psychiatric illnesses [Najjar et al., 2013]. Although the direct link between neuroinflammation and OCD is still actively researched, data indicate a role for autoimmune processes. For example, PANDAS syndrome (pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections) demonstrates how immune response to infection can trigger or worsen OCD symptoms in children [Najjar et al., 2013]. This underscores that mental disorders are not always exclusively "psychological" in nature but may have profound biological roots.

In the broader context of mental states such as hikikomori, we see how sociocultural factors like modernization, globalization, and internet proliferation influence youth behavioral characteristics, leading to unprecedented levels of anxiety, depression, and loneliness [Kato et al., 2019]. Although hikikomori is not OCD, this example illustrates how external conditions can shape vulnerability to various forms of mental distress, including obsessive states. Reduced opportunities for direct communication and a shift to "indirect" interaction via the internet may foster certain cognitive patterns that, in turn, may be linked to obsessive thoughts.

Some researchers also note that the pathogenesis of mental illnesses cannot be explained solely by genetics [Kato et al., 2019]. Various historical, cultural, and sociological factors, especially psychosocial stress, cause brain changes, including epigenetic modifications and neuroglial correlates, which may manifest in characteristic phenotypes corresponding to the time and society in which they arise [Kato et al., 2019]. This means OCD, like other disorders, results from a complex interaction between genetic predisposition, biological processes, and the environment. The nature of OCD is far more complex than it appears at first glance. It is not just "bad habits" or "excessive anxiety" but a multifaceted disorder involving cognitive distortions, behavioral rituals, and potential biological and sociocultural factors. Understanding this complexity is critical for developing effective treatment and support strategies. However, despite all advances, the question remains open as to how exactly the uncertainty inherent in the modern world affects the formation and maintenance of these obsessive states and how this relates to general anxiety mechanisms.

The Impact of Uncertainty on Anxiety and Belief Formation

In the previous section, we discussed the cognitive mechanisms of obsessive-compulsive disorder, where intrusive thoughts and rituals serve as attempts to control internal chaos. However, upon closer examination, it becomes clear that a fundamental inability to cope with uncertainty underlies many such states. The human mind, by nature, strives for predictability and order, and when this need is unmet, anxiety arises.

Intolerance of Uncertainty (IU) is not merely discomfort with the unknown but a deep cognitive predisposition whereby uncertain situations are perceived as threatening and unbearable, regardless of their objective probability or consequences. [Freeston et al., 2020] notes that IU is a transdiagnostic factor, occurring across various mental disorders beyond a single diagnosis. This means that the inability to accept uncertainty may be a common denominator for OCD, generalized anxiety disorder, panic attacks, and even depression.

How does this intolerance manifest in everyday life? For one person, uncertainty may be a source of inspiration and new opportunities; for another, it becomes a catalyst for endless rumination and attempts to predict all possible outcomes. For example, a person with OCD may repeatedly check whether the door is locked, not because they genuinely doubt their actions, but because the mere thought of the possibility of an unlocked door causes unbearable anxiety. This anxiety, in turn, fuels compulsive rituals, creating a vicious cycle.

Uncertainty also plays a key role in belief formation, especially concerning conspiracy theories. When official explanations seem insufficient or contradictory and the future is unclear, people tend to seek simple, all-encompassing answers. [Bruder et al., 2013] showed that belief in conspiracy theories is strengthened under the influence of uncertainty and perceived morality. If the world seems chaotic and unjust, the idea of a secret conspiracy explaining everything can be psychologically appealing, as it restores an illusion of control and order, albeit through a negative narrative.

Interestingly, the phenomenon of hikikomori, described by [Kato et al., 2019] as a "syndrome related to modern society," can also be viewed through the lens of intolerance of uncertainty. Hikikomori, or social withdrawal, often arises as a reaction to stressful events and manifests in avoidant behavior. People with "modern-type depression" (MTD), which [Kato et al., 2019] consider a "gateway" to hikikomori, tend to avoid social situations and frequently complain of depressive feelings. In this context, withdrawal from the world may be an extreme attempt to eliminate uncertainty associated with social interactions, expectations, and potential failures.

Historically, as noted by [Kato et al., 2019], phenotypes of mental disorders have changed depending on the era and culture. While in late 19th and early 20th century Europe there was an "epidemic" of hysteria, in recent decades in Japan, hikikomori and MTD have come to the forefront. These changes, according to the authors, reflect the influence of lifestyle and cultural characteristics. For example, Japanese culture, with its emphasis on indirect communication and the value of haji (shame), may have contributed to the development of hikikomori as a strategy to avoid shame. In such a case, uncertainty about social approval or condemnation becomes unbearable, and isolation appears as the only way to eliminate it.

Besides psychological aspects, biological correlates may influence our ability to cope with uncertainty and, consequently, anxiety levels. For instance, neuroinflammation, extensively discussed by [Najjar et al., 2013], may play a role in the pathophysiology of various mental disorders, including OCD. Studies show that COX-2 inhibitors, such as celecoxib, can significantly reduce OCD symptoms, indicating a potential link between brain inflammatory processes and the severity of obsessive states. Although the direct connection between neuroinflammation and intolerance of uncertainty is yet to be established, it can be hypothesized that chronic inflammation may affect cognitive functions, including flexible thinking and adaptation to new conditions.

Intolerance of uncertainty acts as a powerful factor that not only intensifies anxiety but also shapes specific cognitive patterns, from intrusive thoughts to conspiratorial thinking and social avoidance. It is not merely a personality trait but a deeply rooted mechanism that may be amplified by psychological and possibly biological factors. Understanding this interrelation allows a new perspective on the nature of mental disorders and their manifestations in the modern world, where uncertainty becomes increasingly pervasive. In the context of global challenges such as climate change, this inability to cope with the unknown may take new, collective forms, giving rise to phenomena like ecological anxiety.

Ecological Anxiety and Grief as a Functional Response to Climate Change

If in the previous section we discussed uncertainty as a fundamental source of anxiety, now it is worth considering how this uncertainty manifests in specific global challenges such as climate change. Ecological anxiety and grief related to climate change are not merely pathological states but rather functional responses to real and impending threats. This is not just abstract fear but a profound emotional experience caused by awareness of irreversible losses and potential collapse of the familiar world.

Indeed, Cunsolo [Cunsolo et al., 2020] argues that ecological grief and anxiety are reasonable and functional responses to climate-related losses. This does not mean such experiences do not require attention or support. On the contrary, the author emphasizes that given the expected increase in emotional distress, anxiety, and grief at the population level, urgent responses are needed from clinicians, public health specialists, families, researchers, educators, and policymakers [Cunsolo et al., 2020]. Here we see a paradox: a normal reaction requires clinical intervention. Why? Because the scale of the problem is such that individual adaptive mechanisms may be overwhelmed.

Such states, although not classical neuroses in the traditional sense, demonstrate similar mechanisms of anxiety formation and intrusive thoughts. For example, constant rumination about future catastrophes, guilt over personal consumption, or helplessness in the face of global problems may take on the character of obsessions. A person may endlessly replay scenarios of ecological apocalypse in their mind, trying to find a way out or at least prepare for the worst, which in turn intensifies anxiety.

Interestingly, in the context of global crises such as the climate crisis, we can observe phenomena reminiscent of social isolation characteristic of the Japanese hikikomori phenomenon. Kato, Kanba, and Teo [Kato et al., 2019] describe hikikomori as a state of prolonged social isolation where a person avoids contact with the outside world, often spending time at home immersed in the internet or other forms of escapism. Although the causes of hikikomori are diverse and often linked to individual psychological factors, economic difficulties, or societal pressure, a parallel can be drawn with how ecological anxiety may contribute to withdrawal from the world. If the world seems doomed, why participate in it?

Such withdrawal can be both passive and active. Passive withdrawal manifests as apathy and hopelessness, where a person stops believing in the possibility of change and simply "switches off" from active life. Active withdrawal may involve radical lifestyle changes, retreat into autonomous communities, or, conversely, aggressive denial of the problem as a defense mechanism against unbearable anxiety. Kato, Kanba, and Teo [Kato et al., 2019] note that the development of the internet has greatly facilitated the possibility of living in isolation, allowing shopping and entertainment without leaving home. This creates fertile ground for exacerbating social isolation, including for those experiencing ecological grief.

However, unlike hikikomori, where isolation is often a consequence of individual problems, ecological anxiety and grief are collective experiences that may lead to similar behavioral patterns. People may avoid news and conversations about climate to not face painful emotions, which essentially is a form of avoidant behavior. This, in turn, may exacerbate feelings of loneliness and helplessness, as the person loses the opportunity to share their experiences with others.

It is important to understand that these reactions are not signs of weakness or mental disorder in the traditional sense. On the contrary, they indicate a person's capacity for empathy, awareness of global problems, and mourning losses that have not yet occurred but seem inevitable. This is a kind of "anticipatory grief," mourning future losses — species extinction, landscape changes, loss of familiar lifestyles.

In this context, even if ecological anxiety and grief are functional, their intensity and prevalence may lead to significant deterioration in quality of life and population mental health. This brings us to the question of how these emotional states may affect physiological processes in the body. For example, chronic stress caused by persistent anxiety can lead to neuroinflammation, which research shows is an important factor in the development of various mental disorders. Najjar et al. [Najjar et al., 2013] point out that several studies in humans and animals show that some anti-inflammatory drugs may play an important adjunctive role in treating mental disorders. This suggests that emotional reactions to global threats may have tangible biological consequences requiring a comprehensive approach to understanding and possibly treating them.

The Influence of Neuroinflammation on Mental Disorders

If in the previous section we considered ecological anxiety as a functional response to external threats, now it is worth turning attention to internal biological mechanisms that may underlie mental disorders, including neurotic states. Contemporary research increasingly points to the role of neuroinflammation in the pathogenesis of various psychiatric illnesses, offering a completely different perspective on their nature. It is not merely a "malfunction" of the brain but a complex cascade of immune reactions that may lead to dysfunction of neural networks.

Neuroinflammation essentially represents the central nervous system's immune response to various damaging factors, whether infections, injuries, or chronic stress. However, as noted by Najjar et al., activation of microglia, the brain's resident immune cells, can lead to increased oxidative stress through production of proinflammatory cytokines and nitric oxide [Najjar et al., 2013]. These molecules, in turn, promote formation of reactive oxygen species that damage neuronal membranes, disrupt monoamine receptor function, and deplete endogenous antioxidant reserves. A vicious cycle arises: increased oxidative stress stimulates further microglial activation, leading to even greater inflammation and damage [Najjar et al., 2013]. This mechanism may be key in the development of some psychiatric disorders.

Besides oxidative stress, neuroinflammation may affect mitochondrial function. Mitochondria, known as the cell's powerhouses, have dysfunction closely linked to various pathologies. Najjar et al. indicate that mitochondrial dysfunction may contribute to increased oxidative stress in major depressive disorder (MDD), bipolar disorder (BD), and schizophrenia [Najjar et al., 2013]. Postmortem studies reveal abnormalities in mitochondrial DNA in patients with these disorders, consistent with the high prevalence of psychiatric symptoms in primary mitochondrial diseases. In vitro experiments on animal models show that proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-α) can reduce mitochondrial density and impair oxidative metabolism, leading to increased reactive oxygen species production [Najjar et al., 2013]. These data suggest a possible mechanistic link between neuroinflammation, mitochondrial dysfunction, and oxidative stress as overlapping pathogenic pathways in human psychiatric disorders.

Interestingly, vulnerability of nervous tissue to oxidative damage varies depending on the specific psychiatric disorder, due to differences in neuroanatomical, neurochemical, and molecular pathways [Najjar et al., 2013]. For example, in BD there is increased superoxide radical production correlating with enhanced neutrophil apoptosis mediated by oxidation. Serum antioxidant enzyme levels, such as superoxide dismutase-1, are elevated during acute depressive episodes and normalize after treatment with selective serotonin reuptake inhibitors (SSRIs) [Najjar et al., 2013]. This may indicate a compensatory mechanism aimed at counteracting acute oxidative stress. Meanwhile, in schizophrenia, levels of soluble superoxide dismutase-1 in cerebrospinal fluid are significantly reduced in patients with early-onset disease compared to chronic forms and healthy controls, suggesting a contribution of decreased brain antioxidant enzyme levels to oxidative damage in acute schizophrenia [Najjar et al., 2013].

Another important aspect is the role of the S100B protein, produced by astroglia, oligodendroglia, and ependymal cells of the choroid plexus [Najjar et al., 2013]. At nanomolar concentrations, S100B exerts neurotrophic effects, limits stress-induced neuronal damage, and suppresses TNF-α release by microglia. However, at micromolar concentrations characteristic of activated astroglia and lymphocytes, S100B has harmful effects, leading to neuronal apoptosis, production of proinflammatory mediators, and increased TNF-α secretion [Najjar et al., 2013]. Elevated S100B levels in serum and cerebrospinal fluid correlate with severity of suicidal tendencies in various psychiatric disorders, as well as with paranoid and negativistic psychosis in schizophrenia [Najjar et al., 2013]. Reduction of S100B levels after treatment with antidepressants and antipsychotics underscores its clinical significance in the pathophysiology of mental disorders.

However, despite convincing evidence of neuroinflammation's role in several psychiatric disorders, data on obsessive-compulsive disorder (OCD) remain contradictory. Najjar et al. note that results of cytokine studies in serum and cerebrospinal fluid, as well as studies of peripheral blood mononuclear cells stimulated by lipopolysaccharide in OCD, are inconsistent [Najjar et al., 2013]. This may indicate a more complex or heterogeneous nature of inflammatory processes in OCD or that neuroinflammation plays a less central role than in other disorders. Possibly, other pathogenic mechanisms predominate in OCD, or the inflammatory response manifests differently than in depression or schizophrenia.

In the context of neuroinflammation, it is also important to consider the concept of hikikomori, described by Kato and colleagues as pathological social alienation or isolation characterized by physical confinement at home [Kato et al., 2019]. Although hikikomori is not directly a neurotic disorder in the classical sense, it is often accompanied by comorbid mental illnesses such as avoidant personality disorder and major depressive disorder [Kato et al., 2019]. If neuroinflammation is a common risk factor for depression and anxiety disorders, it may potentially contribute to the development or exacerbation of conditions leading to social isolation characteristic of hikikomori. However, direct studies linking neuroinflammation with hikikomori are currently insufficient.

Neuroinflammation represents a complex and multifaceted process that may play a significant role in the pathogenesis of many psychiatric disorders, including depression, bipolar disorder, and schizophrenia. Mechanisms include oxidative stress, mitochondrial dysfunction, and dysregulation of immune mediators. However, for OCD, data are less conclusive, highlighting the need to clarify specific inflammatory profiles in various neurotic states. Understanding these biological foundations may open new avenues for therapeutic interventions complementing traditional psychotherapeutic approaches. For example, if we can modulate inflammatory processes, this may enhance the effectiveness of cognitive-behavioral therapy, discussed in the next section, especially in cases where psychiatric symptoms have a pronounced biological underpinning.

The Role of Cognitive-Behavioral Therapy (CBT) in Treating Dysmorphophobia

If in the previous section we discussed neuroinflammation as a potential mechanism underlying mental disorders, now it is worth turning to therapeutic approaches that seemingly operate on a completely different level — the level of cognition and behavior. Cognitive-behavioral therapy (CBT) is one of the most studied and widely applied methods for treating various mental conditions, including dysmorphophobia. This approach focuses on identifying and modifying dysfunctional thoughts and behavioral patterns that maintain the disorder.

Dysmorphophobia, or body dysmorphic disorder (BDD), is characterized by obsessive preoccupation with an imagined or slight defect in appearance, leading to significant distress and functional impairment. People with BDD often engage in repetitive compulsive behaviors such as excessive mirror checking, comparing their appearance with others, attempts to hide the "defect," or seeking cosmetic procedures. These behavioral rituals, although aimed at reducing anxiety, paradoxically intensify fixation on appearance and maintain the disorder cycle.

CBT for dysmorphophobia typically includes several key components. First, cognitive restructuring aimed at challenging and changing irrational beliefs about one’s appearance and its significance. Patients are taught to recognize automatic negative thoughts and replace them with more realistic and adaptive ones. Second, exposure with response prevention (ERP) involves gradual and controlled confrontation with anxiety-provoking situations and refraining from compulsive behaviors. For example, a patient may be encouraged to stop checking themselves in the mirror or deliberately go outside without attempting to conceal their "defect."

Research shows that CBT can be effective for adolescents with dysmorphophobia. It is noted: To our knowledge, this is the first randomized controlled trial testing the feasibility, acceptability, and efficacy of a CBT protocol adapted for young people with BDD. Both patients and their families found the intervention highly acceptable and helpful. This indicates that even in such a sensitive age group as adolescents, where appearance issues are especially acute, a structured CBT approach resonates and yields results.

However, despite encouraging data, CBT effectiveness is not always absolute. It is also noted: Nevertheless, results can be described as modest, as only 40% of treated patients were classified as responders according to one of the prevailing operational definitions of treatment response in BDD. This fact prompts reflection on why a significant portion of patients do not achieve full remission or show only partial improvement. Possibly, this relates to the multidimensional nature of the disorder, where beyond cognitive distortions, other factors such as social isolation or deep emotional conflicts may play a role.

For example, the phenomenon of hikikomori described by [Kato et al., 2019] demonstrates how social avoidance can become a self-sustaining state beyond a simple disorder. The authors suggest that hikikomori may be a stress reaction manifesting as a "hikikomori state" and may be separable from the presence or absence of mental illness in the narrow sense. This emphasizes that some forms of avoidant behavior characteristic also of dysmorphophobia may not be merely symptoms but complex coping strategies requiring broader understanding than the cognitive-behavioral model alone.

Perhaps modest CBT results in some cases relate to the fact that dysmorphophobia, like many other mental disorders, is not reducible solely to dysfunctional thoughts and behavior. [Damasio, 1994], in his work "Descartes' Error," convincingly demonstrates the inseparable connection between emotions, reason, and the body, arguing that rational thinking is impossible without emotional experience. If dysmorphophobia is rooted in deep emotional experiences related to self-esteem and self-acceptance, purely cognitive restructuring may be insufficient.

Moreover, it should be considered that some patients may have comorbid disorders or personality traits complicating therapy. For example, a tendency toward conspiratorial thinking, as shown by [Bruder et al., 2013], may affect a person's ability to trust the therapist and accept alternative explanations of their conditions. If a patient tends to interpret the world through the prism of hidden threats or conspiracies, it will be harder for them to accept the idea that their own thoughts are the source of their suffering.

Although CBT is the gold standard in treating dysmorphophobia and demonstrates significant efficacy, especially with early intervention, its results are not always universal. This raises the question of the need for more personalized approaches considering individual patient characteristics, deep emotional processes, and possibly even biological factors such as neuroinflammation discussed earlier [Najjar et al., 2013]. After all, if mental disorders have not only psychological but also neurobiological bases, therapy should be multidimensional, integrating various levels of intervention.

Criticism and Limitations

The depiction of neuroses in popular culture, despite its potential for destigmatization, faces several significant limitations that may distort the real understanding of these conditions. The main problem lies in simplification and exaggeration of symptoms for dramatic or comedic effect. For example, characters with OCD are often portrayed as eccentric but functional geniuses whose obsessive traits merely add charm or help in investigations, as in the case of detective Monk. This creates a false impression that OCD is something like a "superpower" or harmless quirk, ignoring the real suffering and functional impairments experienced by people with this disorder.

Another limitation is the romanticization of mental disorders, especially in adolescent culture and social networks. Images of "complex" and "deep" characters suffering from anxiety or depression can be appealing but often overlook the maladaptive aspects of these states. Such romanticization may lead young people to idealize symptoms, perceiving them as part of their identity rather than a problem requiring resolution. This is particularly dangerous in phenomena like hikikomori, where social isolation initially caused by stress may be seen as a "lifestyle" rather than a signal for help [Kato et al., 2019].

Finally, popular culture often does not account for individual differences in neurotic symptom manifestations and their etiology. As Clark noted, effective OCD treatment requires specialized theories targeting specific phenomenological characteristics and underlying processes of disorder subtypes [Clark, 2007]. Media images typically present an averaged and often stereotypical portrait that does not reflect the full complexity and diversity of clinical cases. This may hinder people with less "typical" neurosis manifestations from identifying with their condition and seeking adequate help, as their experience does not match what they see on screen or online.

Detailed Exposition

Symptoms of Neurosis and Obsessive-Compulsive Neurosis

Neurosis, as mentioned earlier, is a functional mental disorder not associated with organic brain damage but manifesting in prolonged emotional and behavioral disturbances. It is not merely "bad mood" or temporary stress but a persistent state significantly impairing a person's quality of life. Key neurosis symptoms are diverse and may include anxiety, phobias, intrusive thoughts and actions, hysterical manifestations, and somatic disorders.

Anxiety is perhaps one of the most universal neurosis symptoms. It may manifest as generalized anxiety disorder, where a person constantly worries about many things, or as panic attacks — sudden episodes of intense fear accompanied by physiological symptoms such as rapid heartbeat, shortness of breath, and dizziness. Phobias are irrational and intense fears of specific objects or situations, for example, agoraphobia (fear of open spaces) or social phobia (fear of social interactions). These fears can be so strong that a person begins to avoid situations triggering them, leading to significant limitations in daily life.

A special place among neurotic disorders is occupied by obsessive-compulsive neurosis, or obsessive-compulsive disorder (OCD). This condition is characterized by two main components: obsessions and compulsions. Obsessions are involuntary, repetitive, and intrusive thoughts, images, or urges causing strong anxiety or distress. They are often linked to irrational fears such as contamination, harming oneself or others, or doubts about completed actions. For example, a person may constantly think they forgot to turn off the iron or that their hands are not clean enough.

Compulsions, in turn, are repetitive actions or mental rituals that a person feels compelled to perform in response to an obsession to reduce anxiety or prevent some dreadful event. These actions may include repeated checking (e.g., whether the iron is off), excessive hand washing, arranging objects in a certain order, or repeating specific phrases. It is important to note that compulsions provide only temporary relief and, in the long term, intensify the cycle of anxiety and intrusive thoughts. The person recognizes the irrationality of their actions but cannot control them, leading to feelings of helplessness and shame.

Besides anxiety and intrusive states, neuroses may manifest in hysterical symptoms such as conversion disorders (e.g., paralysis or blindness without physiological causes) or dissociative states (e.g., amnesia or fugue). Somatic disorders are also common companions of neuroses, manifesting as chronic pain, digestive problems, or cardiovascular issues without organic basis. For example, cardiac neurosis, or cardiophobia, is characterized by symptoms mimicking heart disease but without objective signs of heart pathology [Park et al., 2024].

All these symptoms, despite their diversity, share a common feature: they significantly disrupt a person's daily life, hindering work, study, relationships, and enjoyment of life. Neurosis is not just "nerves" but a serious condition requiring professional help. However, as we will see later, popular culture often distorts or simplifies these complex manifestations, which may influence public perception and stigmatization of people suffering from neurotic disorders.

Representation of Neuroses in Film and Television

Popular culture, as a powerful medium, shapes our perception of the world, including understanding of mental disorders [Kidd, 2017]. Film and television, in particular, play a significant role in creating images of people with neuroses, and these images are often far from clinical reality. Neurotic manifestations are frequently exaggerated or romanticized, which can distort their real understanding and contribute both to destigmatization and, paradoxically, to oversimplification of complex states.

Take, for example, characters with OCD in film and literature. They are often portrayed as eccentric but functional individuals whose obsessive traits become sources of humor or even help in their professional activities. Melvin Udall from the film "As Good as It Gets" (1997) is a vivid example. His avoidance of sidewalk cracks, use of disposable gloves, and obsessive striving for order are presented as part of his unique, albeit complex, character. The viewer sees his suffering but also his capacity for love and growth, which undoubtedly contributes to destigmatization. However, how well does such an image correspond to the real clinical picture, where OCD often leads to severe disability and social isolation?

Another example is detective Monk from the eponymous series (2002-2009). He suffers from numerous phobias and compulsions, but these traits help him notice the smallest details and solve crimes. His OCD becomes not so much a burden as a unique tool. This approach, on the one hand, shows that people with mental disorders can be talented and successful. On the other hand, it may create a false impression that OCD is something like a "superpower" rather than a debilitating condition requiring serious treatment.

Sheldon Cooper from "The Big Bang Theory" (2007-2019) also demonstrates traits similar to OCD, such as a strict daily routine, obsessive striving for order, and inflexibility. His rituals and behavioral peculiarities often become sources of comedic situations. In this case, neurotic traits are used to create comedic effect.