Open access peer-reviewed chapter

Psychometric Networks and Their Implications for the Treatment and Diagnosis of Psychopathologies

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Cristian Ramos-Vera, Víthor Rosa Franco, José Vallejos Saldarriaga and Antonio Serpa Barrientos

Submitted: 05 May 2022 Reviewed: 13 May 2022 Published: 26 August 2022

DOI: 10.5772/intechopen.105404

From the Edited Volume

Psychometrics - New Insights in the Diagnosis of Mental Disorders

Edited by Sandro Misciagna

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Abstract

In this chapter, we present the main methodological principles of psychological networks as a way of conceptualizing mental disorders. In the network approach, mental disorders are conceptualized as the consequence of direct interactions between symptoms, which may involve biological, psychological, and social mechanisms. If these cause-and-effect relationships are strong enough, symptoms can generate a degree of feedback to sustain them. It is discussed how such an approach contrasts with the traditional psychometric approach, known as the Latent Variable Theory, which assumes that disorders are constructs that exist but are not directly observable. Furthermore, it is also discussed how new neuropsychological hypotheses have been derived in the network approach and how such hypotheses generate direct implications for the understanding of diagnosis and treatment of psychological disorders. Finally, the recentness of the network approach in psychology and how future studies can establish its robustness are discussed.

Keywords

  • graph theory
  • network analysis
  • psychometrics
  • neuropsychology
  • clinical measurement

1. Introduction

Network psychometrics is a new approach to the study of latent variables (i.e., psychological constructs) that contrasts with the traditional psychometric approach. In the traditional approach, responses to items on a psychological instrument (e.g., responses to questions such as “Do you sleep poorly?”) are analyzed as evidence of an underlying characteristic (or psychopathology) that the researcher or clinician wishes to measure [1]. This idea is formalized in analytic methods, such as Factor Analysis, Item Response Theory, Latent Class Analysis, and Mixture Modeling, among others, which are the main ways to validate psychological and psychiatric instruments [2].

In theoretical terms, the traditional psychometric approach, known as Latent Variable Theory [3], suppose that the observed behavior (e.g., responses to items on a psychological questionnaire or scale) is the effect of a common cause (in the clinical context, usually assumed to be psychiatric disorders). This approach is used in different ways in psychology and psychiatry (see the study by Demjaha et al. [4]). Whereas in psychology metric models (i.e., those that assume that psychiatric disorders are quantitative variables) are more commonly used, in psychiatry categorical models (i.e., those that assume that a disorder is or is not present) are more common. These theoretical differences translate into differences in how to diagnose, classify, and even clinically act on psychiatric disorders [4].

Network psychometrics has the main feature in relation to the traditional psychometric approach that it does not necessarily assume that psychological constructs exist [5]. More specifically, network models of psychopathology assume that symptoms form complex cause-and-effect relationships with each other, dynamically reinforcing each other and giving rise to psychiatric disorders [6, 7, 8]. However, there are alternative network models that allow different interpretations. Some are even compatible with the Latent Variable Theory. The aim of the present study is to analyze critically the main distinctions between Latent Variables Theory and Network Psychometrics in the context of psychopathologies. As specific objectives, we will critically evaluate Latent Variable Theory in the causal perspective of Pearl [9], present the theoretical foundations of Network Psychometrics, and discuss the theoretical and practical implications for clinical study and action in the context of psychopathology.

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2. Latent variables in psychology

Latent Variable Theory, in its various implementations in statistical models, is formally indistinguishable from the so-called common cause model [9]. The models of this theory assume that when the latent variable is tested, the correlations between observable behaviors should disappear. This property is known as “local independence,” which is normatively imposed in traditional psychometric models [10]. This implication derives from the fact that correlations between effects with a common cause are suppressed whenever there is no direct causal relationship between these effects and the relationship between the two variables is controlled by the common cause [9].

Thus, the psychometric model and the causal interpretation affirm that the psychological (or psychopathological) construct naturally causes the behaviors. This relationship is certainly not a coincidence: the standard psychometric model is based on the notion that different indicators measure the same thing because they depend on the same property and no other [11]. Another consequence of Latent Variable Theory is that item response can be described in terms of a functional relationship between a single property of individuals and items [1]. Thus, in the case of unidimensional tests (i.e., based primarily on a single construct or disorder), it is assumed that all psychopathology test items are statistically interchangeable [12]. From a pragmatic point of view, Item Response Theory models, such as the Two-Parameter Logistic Model [2], can demonstrate which items are most closely related to the central construct being measured (so-called item discrimination), as well as the sensitivity of items to the magnitude of the construct (so-called item difficulty). However, it cannot be said that there are items that play a more central role in the identification of the construct, and as long as their difficulties and discriminations are adjusted, all items are equivalent. Such implication contrasts with clinical practice, where it is identified that there are more characteristic or more influential symptoms in each psychopathological disorder [4].

Regarding the development of instruments for the measurement, identification, or screening of psychopathological disorders, the common cause model provides psychometrics and psychiatry with a standard approach to test construction and analysis [13]. This approach is implemented with the following steps:

  1. create a set of items as a measure of the same construct;

  2. collect data and apply a statistical model that formalizes this common causal dependence;

  3. eliminate or modify items that do not fit the model, and

  4. repeat steps 1 through 3 until the model fits the data adequately.

Following these steps, provided we are changed from the recommended order it is possible to measure virtually any construct [1], although there is criticism as to whether such an approach actually produces a true measure [14, 15]. Such an approach will not be accurate if there is no common factor across items, which some researchers in psychopathology suggest is the case (see the study by Fried et al. [16]).

For example, in one of the most influential works in psychometric history in the clinical and psychiatric context, Krueger [17] defined the two main higher-order factors of his model in terms of two central psychopathological processes: internalizing and externalizing. These latent variables of the measurement model (i.e., the statistical factors) refer to two intrinsically significant psychological mechanisms that, in principle, could be easily observable in the expression of a picture of even heterogeneous behaviors. According to this author, internalization can lead to depression or anxiety, whereas externalization can lead to antisocial or aggressive behaviors. Although the behaviors are very different, these differences would reflect basic processes in the way psychopathology manifests itself.

In Krueger’s original approach [17], the underlying causal homogeneity is psychological in nature, but more recent studies propose that the underlying causal homogeneity is neurological or genetic. Overall, there is a growth in studies that seek to reveal the “underlying brain mechanisms” of psychopathology [18]. In essence, however, all of these approaches boil down to the same explanatory model: there is some “deeper” cause of the symptomatology (e.g., a psychological variable, a brain abnormality, a genetic mutation, among others) that explains why people show the observed symptomatology. Certainly, there are many advances in this area (see the study by Rose [19]). However, it is also known that there are a number of socioeconomic influences on the mental health of individuals, which are not considered in the identification, classification, and treatment of disorders (see the study by Silva et al. [20]).

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3. The network psychometry approach and psychopathology

The network psychometrics approach assumes that the lack of stronger evidence for the latent origins (whether psychological, neurological, genetic, or otherwise) of psychopathological disorders cannot be a matter of measurement problems or a limited understanding of genetics and the brain. The alternative proposed by the network approach is that this lack of evidence may be the result of an erroneous way of thinking about or assessing the relationship between symptoms and disorders [21]. More specifically, in the network approach to psychopathology, it is assumed that disorders emerge when, over time, specific symptoms become more strongly connected [8]. From a pragmatic point of view, psychopathology is identifiable when the probability of observing a symptom is higher than “normal” (additionally another symptom has been observed).

It is important to specify that many diagnostic systems, such as the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) [22], do not make any explicit assumptions about the origins of the symptoms. No explanatory mechanisms of the disorder are presented, but only the main symptoms and clinical criteria. Traditionally in psychopathology, no direct attribution of relationships between symptoms of disorders and the common effect of a latent variable is made directly. The relationships between symptoms in their various contexts are established as criteria (see the study by Ramos Vera; Cramer et al.; Borsboom; and Spitzer et al. [23, 24, 25, 26]). For example, a person who often has panic attacks in public places (symptom 1) is likely to be afraid that the attacks will recur (symptom 2) and, consequently, will avoid public places frequently (symptom 3). In another example, a person who cannot sleep (symptom 1) will end up tired and unable to concentrate (symptoms 2 and 3), which may cause him or her to feel guilty about poor performance at school or work (symptom 4). Evidence of this type of relationship between symptoms is common and makes it clear that local independence and equivalence between symptoms are not real for several disorders and their indicators.

It should be noted that, despite not explicitly assuming causal symptom structure, diagnostic systems, such as DSM-5, include such structures at least implicitly [24]. For example, a person who sleeps poorly does not show symptoms of depression if the lack of sleep is attributed to a newborn child, just as a person who frequently washes his or her hands only shows a symptom of obsessive-compulsive disorder, hand washing occurs in response to an excessive obsession with hygiene. From this point of view, it can be argued that diagnostic systems, such as the DSM-5, are not purely empirical or theoretically neutral as is often claimed. It is clear that at least as far as hegemonic diagnostic practice in psychopathology is concerned, common cause models are rejected [25, 26]. Such conceptual positioning may be better elaborated under the network approach, especially in cases where a certain event external to symptoms may activate relationships between symptoms of some disorder for a long time, even in the subsequent absence of such an external event [25, 26].

Another advantage of the network approach is the method by which comorbidities can be identified and classified. Ideally, symptoms should be sufficient and necessary conditions for identifying a disorder. However, in the general clinical context, this is rarely the case (even for some disorders or diseases that are clearly biological in origin). It is more common to state that symptoms nominated as “characteristic” of a psychiatric disorder are simply those more frequent in one group of individuals than in others [21, 25]. The traditional psychometric approach, by favoring symptoms that would be more “characteristic” (i.e., occur together more frequently and thus would be more correlated), would not identify idiosyncrasies derived from an individual’s specific symptoms. Consequently, some authors [27] suggest that diagnostic comorbidity could be a consequence of spurious associations and, for this reason, could be reduced by retaining distinctive symptoms, but eliminating nonspecific symptoms, in psychopathological assessments.

In the network approach, symptoms are assessed in relation to their “importance” for the stability of the symptom network as a totality [25, 28]. For example, centrality measures indicate the degree of interconnectedness of a symptom with the other symptoms in the network. As there are different ways in which one symptom can connect to another, different centrality metrics can demonstrate different degrees of “importance” of the assessed symptom [29]. Thus, for the assessment of comorbidities, using an idiographic network analysis paradigm, it is possible to identify, for each individual and for groups of individuals, which symptoms appear most relevant in the set of networks and which expression of symptom interdependencies allows certain comorbidities to occur in some individuals [24, 30, 31, 32].

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4. Analytical methods for network psychometry

The models used in network psychometry are derived from the graph theory of mathematics [33]. Graphs (also called networks) are mathematical objects in which nodes represent various elements (such as other mathematical objects, e.g., sets and variables, or even real objects, e.g., individuals and organizations) and edges represent relationships between nodes. In the statistical derivation of graph theory, known as probabilistic graph models [34], nodes are used to represent variables (in the case of psychopathology networks, the variables are usually the possible symptoms) and edges are used to represent the dependency relationships between the nodes. Dependency relationships usually involve correlations or partial correlations, but may also involve nonlinear dependency measures [35]. It is also common to use clustering methods to identify which variables are most strongly connected [36, 37].

Unlike social networks, in which nodes (people) and the relationships between them can be directly observed [38], psychological networks are based on probabilistic graphs [20, 39]. There are three main types of probabilistic graphs, which are given below [34]:

  1. nondirectional graphs (in which the relationships between variables are symmetric);

  2. directional graphs (in which the relationships between variables are asymmetric); and.

  3. chain graphs (sometimes also called mixed graphs in which there are both symmetric and asymmetric relationships).

In the study of psychological networks, the use of nondirectional graphs where edges represent partial correlations is the most common [21, 27, 40, 41]. This preference is mainly because nondirectional graphs allow us to derive hypotheses about causal relationships without the need to make explicit assumptions about which variables are cause and which are effect.

Among the nondirectional graph models used in the study of psychological networks, three of them have received special attention in the literature, which are as follows:

  1. correlation networks;

  2. partial correlation networks; and.

  3. directional graphs (directed acyclic graphs, DAG).

The first of these is the correlation network [34]. This type of model uses correlations as measures of dependence between variables and is used when one wants to know if there is a direct dependence between variables. These models have two main limitations. First, these models do not allow inferences to be made about causal relationships since, according to the theory of causal calculus [9], these can only be derived from conditional dependencies. The second limitation of this type of model is that, being based on correlations, the dependencies are not affected by the other variables in the network.

The second type of network model, probably the most widely used, is the partial correlations network model (also known as concentration networks) [42]. This type of model uses partial correlations to measure the strength of the linear relationship between variables. There are two main ways to estimate partial correlation network models [41]. The first is to simply calculate the partial correlations of all the variables in the model and remove the edges of the correlations that are not significant. However, this type of practice is sensitive to false positives. For this reason, it has been more common to use regularized partial correlation networks [42]. which minimizes the probability of maintaining spurious relationships. The use of partial correlations is particularly interesting, as such measures can be interpreted as causal relationships between variables [9, 34]. However, care must be taken not to interpret them as mutualistic causal relationships (which is the case in some important references in the literature) [42]. In fact, partial correlation network models can also be referred to as “visual graphs,” which are the non-directional representations of DAGs [43]. This means that causal directions, in some cases, can be determined.

The third type of model is known as DAG [9]. Directional graphs of the DAG type imply all the expected causal relationships between the collected variables. DAGs allow one to appreciate the existence of cycles in the network. For example, it is possible that a variable A causes a variable B, which in turn causes a variable C, and that this in turn causes variable A. This condition is used to avoid breaking the basic assumptions of causality, such as localism and realism of natural phenomena, as well as the transitivity of causal relationships. However, working with longitudinal data, it is possible to identify cycles that are valid (i.e., when the transitivity of causal relationships at the same moment in time is respected) [44]. For example, inattention at a time point t = 1 can be the cause of inattention at the same time point t = 1. If this relationship is true, it is only causally valid to say that inattention is also the cause of inattention if inattention at time point t = 1 is the cause of inattention at time point t ≥ 2. DAGs have not been widely used in psychology given that they require explicit assumptions about which relationships are causal or not; however, few causal theories in psychology or psychopathology have the robustness to be used in this way [30, 42].

4.1 The use of network models in the context of psychopathology

It is important to emphasize that the use of network models not only allows us to address the complexity of the relationships between variables but is in fact a different approach to thinking about theories in psychopathology. Network analyses have been fundamental for researchers to work with more diverse data sources (e.g., genetic, neurological, physiological, behavioral, and other data) and to seek more comprehensive ways of theorizing. In this context, network analyses have been complemented by what is known as conjoint modeling [45]. Joint modeling is a statistical approach similar to structural equation modeling, but which allows the use of any alternative model as a measurement model (i.e., “for example, see [46]”). These models are used, for example, to develop psychological or psychopathological models sensitive to neurophysiological limitations.

The proposal of the mental health-related symptom network model has promoted the application of different types of variables from different levels of psychobiological development to explore new systemic theories that may include cognitive, biological, and social aspects [47, 48, 49], as well as risk and protective factors for mental health [50]. This explanation is of great importance in the current context, for example, a network review study reported the first 18 months since the pandemic, symptomatological variables of fear, distress, and stress were used to a greater extent by COVID-19 [28].

These symptoms allow us to understand the etiological mechanisms of the psychological impact of a stressful event, such as the current pandemic. Protective factors, such as resilience or psychological well-being, and psychosocial measures, such as alcohol and drug abuse, were also included [28]. The studies reviewed by Ramos-Vera et al. [28] refer to the use of different clinical variables related to COVID-19, such as preventive behaviors; emergency personnel communication measures, atypical reactions to pandemic stress, anti-mask attitudes; components of COVID-19 dreams and nightmares, insomnia and work fatigue. One of the studies considered variables consequent to the pandemic, such as perceived present and future infection risk, loss of income, and financial worry [51], while another research conducted in Italy by Invito et al. [52] took into account psychological distress and viral contagion beliefs, and added epidemiological characteristics, such as COVID-19 diagnosis, sex status and number of COVID-19 infected and deaths according to the participant’s region. Symptom interaction network theory research has spurred several papers seeking to explore the interconnections of the most recurrent physical and psychological symptoms in certain chronic conditions, such as cancer [53], HIV [54], schizophrenia [55], stroke [56], chronic pain [57] chronic bowel disease [58], multiple sclerosis [59], arterial hypertension [7], obesity [60], and COVID-19 [61].

4.2 The use of psychological network models in the context of neuropsychology

Network neuropsychology can be useful in understanding cognitive adaptation and maladaptation in neurological disorders. Since cognitive functions are not isolated from each other, despite being framed in different domains they can be represented as a cognitive network system, additionally, the successful performance of most neuropsychological tasks is based on the interdependence of several cognitive domains [62, 63]. One of the properties of this network variant is the representation of several networks where measurable differences in neuropsychological profiles between distinct groups can be identified. Two previous studies report that differences are identified in the way neuropsychological tasks are associated in the network between those with neurological diagnoses (cognitive impairment and Alzheimer’s disease) relative to control groups [64, 65]. Specifically, regroupings of memory, language and semantic variables and executive or attention, working memory and processing speed variables are evidenced in the network system belonging to participants with Alzheimer’s disease relative to healthy control models. This feature allows for new explorations of the cognitive network reorganization that may occur throughout the stages of aging, as referred to in the cognitive dedifferentiation hypothesis. It is very likely that aging has an impact on network composition and there is a need to identify topological deviations that may be indicative of age-related neuropathology [66].

Cognitive impairment can be considered as a transdiagnostic dimension of psychopathology [67, 68], therefore, it is possible to consider the study and use of psychopathological symptoms and cognitive performance in network models. An Italian research in patients with a psychiatric diagnosis of schizophrenia included in the network system psychopathological symptoms of disorganization and avolition, positive and negative symptoms related to schizophrenia, in addition to the expressive deficit, akathisia, dystonia, parkinsonism and dyskinesia, and cognitive performance according to six domains: thought processing, attention/vigilance, working memory, verbal learning, visual learning, reasoning and problem solving, and social cognition, [69]. This work found a greater positive relationship of cognitive performance with social cognition and a negative with parkinsonism (this factor was more connected with psychopathological and cognitive measures) and disorganization.

Networks in neuropsychology may also aim to gain insight into changing associative patterns between cognitive constructs following brain damage [70]. For example, research by Iverson et al. [71] estimated the network structure of physical, cognitive, and emotional symptoms associated with attention deficit hyperactivity disorder following concussion. A total of 3074 student athletes were included who reported increased levels of difficulty concentrating and emotional symptoms. Most of the relationships between symptoms were positive, and the most influential symptoms in the network were dizziness and intensity of emotional symptoms. The relationships with the highest magnitude were emotional intensity and psychological distress, as well as forgetfulness and visual problems. There was a structural difference in the network according to sex, with a higher frequency of symptoms in women [71]. These findings demonstrate that similar studies should be encouraged in clinical participants given that from a systems neuroscience perspective, damage to one area of the brain is considered to affect the functioning of other areas adaptively (e.g., compensation, neuronal reserve, degeneration) or maladaptively (e.g., diaschisis, transneuronal degeneration, and dedifferentiation) [72].

Researchers can make supplementary assumptions, such as specifying hierarchical and/or directional relationships between cognitive functions or support other neuropsychological approaches, such as cognitive neuropsychology to create network models. Network theory can also be used to model relationships between tasks, which offers the advantage of conditioning (multivariate control) on all variables in the model, without making any assumptions about the underlying relationships between cognitive functions. In the following, certain studies are detailed with the aim of illustrating findings that would probably not be found using traditional methods of psychometric analysis.

One of the most important contributions to the field of neuropsychology, in the context of network analysis, is the study by Tosi et al. [65]. In this study, differences in networks of neuropsychological variables were evaluated in patients with and without clinical conditions, composed of 165 healthy elderly, 191 patients with Alzheimer’s disease (AD), and 129 patients with vascular encephalopathy (VE). These networks included neuropsychological measures in the domains of memory, language, executive functions, attention, and abstract reasoning, in addition to the covariates of age, sex, and years of schooling. Patients with VS obtained better results (greater connection of cognitive abilities) than those with AD even when controlling for covariates, also, two groups of variables focused on memory and frontal-executive functions were identified in these networks.

Another study evaluated the network configuration of neurocognitive measures in adults using four serial assessments approximately one year apart [73]. The sample consisted of two groups of 432 elderly who obtained, at baseline, a cognitive assessment at normal levels. However, after subsequent assessment steps, the first group retained the same cognitive diagnosis, whereas participants in the second group developed mild cognitive impairment or AD dementia. Differences in network structures (connectivity and centrality) were identified between the groups even before AD was diagnosed, with such differences increasing over time.

Ferguson [64] estimated three network structures in adults according to his neuropsychological assessment:

  1. cognitive normality;

  2. amnestic mild cognitive impairment; and

  3. AD (Alzheimer’s disease).

In these structures, the networks were composed of cognitive variables linked to the domains of attention, working memory, episodic memory, language, fluency, visuospatial ability, and sociodemographic variables (such as age and education). The centrality of episodic memory in the network structure of people with cognitive impairment was higher, whereas processing speed and fluency were more central in the network of people with AD. In addition, two groups of variables were identified in the three networks, the first focused on semantic memory and language, while the second was composed of attention, processing speed, and working memory.

The research by Foret et al. [74] composed of adults with no neurological or psychiatric history aimed to compare two simultaneous networks in men and women that included biomarkers of cognitive impairment risk, components of the metabolic syndrome (obesity, hypertension, dyslipidemia, and hyperglycemia), neuroimaging-based brain age minus chronological age, ratio of white matter hyperintensities to total brain volume, resting-state brain connectivity based on default mode network seed analysis, and ratios of N-acetyl aspartate, glutamate, and myo-inositol to creatine, which were measured by proton magnetic resonance spectroscopy [74]. Differences were found in the connectivity of both networks where women report lower relationships between cardiometabolic risk variables and brain functioning, furthermore, the most influential measures are shown to be apolipoprotein status and waist circumference.

An investigation in Scottish patients with multiple sclerosis evaluated two networks with a difference of a 12-month follow-up period where psychological aspects more prevalent in this clinical condition, such as fatigue, sleep quality, anxiety, and depression, were evaluated [59]. Measures of physical disability, upper extremity dexterity, gait speed, body mass index, and cognitive performance based on the domains of information processing speed, auditory information processing, working memory, and attention span, as well as neuroanatomical variables related to intracranial volume in the natural space were also considered. The results report that fatigue was related to most variables with the exception of brain measures and depression was the most central element in both networks, respectively [59].

The most recent study by Rotstein et al. [75] evaluated psychometric networks of cognitive impairment in more than 1000 American patients with Alzheimer’s disease assessed by the cognitive subscale of the Alzheimer’s Disease Assessment Scale composed of seven domains: temporal and spatial orientation, attention, learning, memory, abstract thinking, verbal fluency, and naming. Several network systems were represented between two groups that received treatment with donepezil and placebo at 24 weeks of follow-up, the results showed a statistically significant difference in the global strength of the network integrated by the patients who received medication, evidencing a lower cognitive deterioration in this group.

Also, other network variants that assess dimensionality have been implemented, such as Exploratory Graphical Analysis (EGA; [36]). EGA employs a network algorithm to detect Walktrap communities [76]. Therefore, EGA estimates the dimensionality of multivariate data by combining network analysis with a community detection algorithm, where a community represents a latent variable reported in a factor technique [36, 37]. Consequently, it is a method to detect dimensions in networks, and additionally reports factor loadings of network variables with their respective communities. In addition to using the EBICglasso estimator for regularized partial correlation networks, this variant of the psychometric network can also group the variables in a graphical model composed of a zero-order correlation matrix using the Maximally Filtered Triangulated Graph Method (TMFG; [77]). This method allows regularizing the relationships and selecting the most parsimonious network structure.

The use of the Bootstrap Exploratory Bootstrap Graphical Analysis (bootEGA) module is recommended, to evaluate the structural consistency of an estimated dimensional structure. Structural consistency is understood as the extent to which a dimension is interrelated (internal consistency) and homogeneous in the presence of other related dimensions [78, 79], such a measure provides an alternative but complementary approach to internal consistency measures in the factor analytic framework. In bootEGA estimation, two metrics are required for structural consistency. The first consists of investigating the solidity of the structure of the dimensionality and the second in the robustness of the location of each element within these dimensions. Three steps have been described for this purpose: (1) estimating a network using EGA, (2) then generating new replicate data from a multivariate normal distribution (with the same number of cases as the original distribution), (3) then applying EGA to the replicate data sets, continuing interactively until the desired number of samples (e.g., 500 participants; [80]) is achieved. Therefore, there are two reasons for employing the parametric bootstrap: resampling smaller samples increase the influences that outlier cases may have on the estimated sampling distribution, and (2) its higher accuracy is the detection of the correct dimensionality structure in the simulated populations [80].

Finally, the need for more studies with multilayer networks (network of networks) is highlighted since they allow better statistical accuracy of the joint use of neurophysiological and psychological data [81, 82]. This may be important in the current pandemic context, as COVID-19 can affect the central nervous system and cause neuropsychiatric disorders [83]. Naturally, this clinical condition has a complex etiology, composed of associative networks of inflammatory biomarkers that can be represented in a network system [84], together with other physical and mental health risk phenotypes [84, 85] and neuroanatomical measures [59, 81, 86]. In this sense, network assessment of variables at different psychobiological levels related to COVID-19 can add to findings reported widely in the literature [87, 88, 89, 90, 91, 92, 93].

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5. Conclusions

The main objective of this research was to critically analyze the main distinctions between Latent Variables Theory and Network Psychometrics in the context of psychopathologies. To achieve this goal, relevant implications of the common cause model have been presented which, in contrast to the discussion on Network Psychometrics, do not seem to correctly represent some of the empirical evidence. It is important to note that research in using network analysis is still being refined and specific theories are still scarce [94]. However, the observed results have been promising and consolidation of the field will show how important this new line of research can be [24, 41]. On the other hand, although the network approach is not, after all, the most suitable for the study of psychopathology and psychological constructs in general, the exemplified applications, especially those involving variables external to psychological symptoms, are important for the promotion of new hypotheses in the neuropsychological field [95, 96, 97], in the face of the inclusion of new network centrality metrics that allow the identification of different structural features following the systemic grouping of transdiagnostic variables in network models [98, 99, 100], including longitudinal data to assess how the network is organized over time [101].

In this perspective, network analysis has the potential to change the field of psychopathology, and even neuropsychology, given its tools that allow combining evidence from different contexts and backgrounds in a way that was not previously used, this is essential in the complex assessment of psychosocial and public health risk factors (e.g., addictions and suicidal behavior, see the study by Anderson et al.; Penzel et al.; Hirota et al.; Sanchez-Garcia et al.; and Calati et al. [101, 102, 103, 104, 105]). Therefore, future studies that combine data and evidence from different levels of analysis and from different sources may lead to a better understanding of transdiagnostic factors [106, 107, 108, 109], cognitive deficits [67], and especially of the integration of neural, behavioral, and symptomatic systems [110, 111, 112, 113].

Finally, it is recognized that the understanding and study of psychological variables is a complex task, involving a multitude of variables at multiple levels of analysis (biological, cognitive, and social), which are related to each other in a complex way [114]. However, network analysis may lead to a change in the current epistemological and methodological approach to psychological phenomena so that this complexity can be effectively assessed [115, 116]. Network analysis is unlikely to be one of the best innovations in the field of studying psychological phenomena and problems remain to be solved [28, 96, 117, 118, 119, 120, 121, 122], but we believe that the presented discussion highlights positive expectations for the future.

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Conflict of interest

The authors have no conflict of interest.

References

  1. 1. Borsboom D, Mellenbergh GJ, Van Heerden J. The theoretical status of latent variables. Psychological Review. 2003;110(2):203-2019. DOI: 10.1037/0033-295X.110.2.203
  2. 2. Coulacoglou C, Saklofske DH. Psychometrics and Psychological Assessment: Principles and Applications. London: Academic Press; 2017
  3. 3. McDonald RP. Test Theory: A unified Treatment. New York: Psychology Press; 1999
  4. 4. Demjaha A, Morgan K, Morgan C, Landau S, Dean K, Reichenberg A, et al. Combining dimensional and categorical representation of psychosis: The way forward for DSM-V and ICD-11? Psychological Medicine. 2009;39(12):1943-1955. DOI: 10.1017/S0033291709990651
  5. 5. Epskamp S, Borsboom D, Fried EI. Estimating psychological networks and their accuracy: A tutorial paper. Behavior Research Methods. 2017;50(1):195-212. DOI: 10.3758/s13428-017-0862-1
  6. 6. Blanchard MA, Heeren A. Ongoing and future challenges of the network approach to psychopathology: From theoretical conjectures to clinical translations. In: Asmundson G, Noel M, editors. Comprehensive Clinical Psychology. 2nd ed. Amsterdam: Elsevier; 2022. Available from: https://dial.uclouvain.be/pr/boreal/object/boreal%3A237881/datastream/PDF_01/view
  7. 7. Ramos-Vera C, Baños-Chaparro J, Ogundokun R. Network structure of depressive symptoms in Peruvian adults with arterial hypertension. F1000Research. 2022;10(19):1-21. DOI: 10.12688/f1000research.27422.3
  8. 8. Robinaugh DJ, Hoekstra RH, Toner ER, Borsboom D. The network approach to psychopathology: A review of the literature 2008-2018 and an agenda for future research. Psychological Medicine. 2020;50(3):353-366. DOI: 10.1017/S0033291719003404
  9. 9. Pearl J. Causality: Models, Reasoning, and Inference. Cambridge: Cambridge University Press; 2009
  10. 10. Mellenbergh GJ. Generalized linear item response theory. Psychological Bulletin. 1994;115:300-307. DOI: 10.1037/0033-2909.115.2.300
  11. 11. Mellenbergh GJ. Measurement precision in test score and item response models. Psychological Methods. 1996;1(3):293-299. DOI: 10.1037/1082-989X.1.3.293
  12. 12. Diaconis P, Freedman D. Finite exchangeable sequences. The Annals of Probability. 1980;8(4):745-764. DOI: 10.1214/aop/1176994663
  13. 13. Furr M. Scale Construction and Psychometrics for Social and Personality Psychology. California: Sage; 2011
  14. 14. Michell J. Is psychometrics pathological science? Measurement. 2008;6(1-2):7-24. DOI: 10.1080/15366360802035489
  15. 15. Trendler G. Measurement theory, psychology and the revolution that cannot happen. Theory & Psychology. 2009;19(5):579-599. DOI: 10.1177/0959354309341926
  16. 16. Fried EI, van Borkulo CD, Cramer AO, Boschloo L, Schoevers RA, Borsboom D. Mental disorders as networks of problems: A review of recent insights. Social Psychiatry and Psychiatric Epidemiology. 2017;52(1):1-10. DOI: 10.1007/s00127-016-1319-z
  17. 17. Krueger RF. The structure of common mental disorders. Archives of General Psychiatry. 1999;56(10):921-926. DOI: 10.1001/archpsyc.56.10.921
  18. 18. Insel TR, Cuthbert B, N.: Medicine. Brain disorders? Precisely. Science. 2015;348(6234):499-500. DOI: 10.1126/science.aab2358
  19. 19. Rose N. Neuroscience and the future for mental health? Epidemiology and Psychiatric Sciences. 2016;25(2):95-100. DOI: 10.1017/S2045796015000621
  20. 20. Silva M, Loureiro A, Cardoso G. Social determinants of mental health: A review of the evidence. The European Journal of Psychiatry. 2016;30(4):259-292. Available from: https://scielo.isciii.es/scielo.php?pid=S021361632016000400004&script=sci_arttext&tlng=en
  21. 21. Borsboom D, Cramer AOJ. Network analysis: An integrative approach to the structure of psychopathology. Annual Review of Clinical Psychology. 2013;9:91-121. DOI: 10.1146/annurev-clinpsy-050212-185608
  22. 22. American psychiatric association diagnostic and statistical manual of mental disorders (DSM–5). American Psychiatric Association; 2014. Available from: https://www.eafit.edu.co/ninos/reddelaspreguntas/Documents/dsm-v-guia-consulta-manual-diagnostico-estadistico-trastornos-mentales.pdf
  23. 23. Ramos Vera C. Las redes de relación estadística en la investigación de nutrición. Nutrición Hospitalaria. 2021;38(3):671-672. DOI: 10.20960/nh.03522
  24. 24. Cramer AOJ, Waldorp LJ, van der Maas HLJ, Borsboom D. Comorbidity: A network perspective. Behavioral and Brain Sciences. 2010;33:137-150. DOI: 10.1017/S0140525X09991567
  25. 25. Borsboom D. A network theory of mental disorders. World Psychiatry. 2017;16(1):5-13. DOI: 10.1002/wps.20375
  26. 26. Spitzer RL, First MB, Wakefield JC. Saving PTSD from itself in DSM-V. Journal of Anxiety Disorders. 2007;21(2):233-241. DOI: 10.1016/j.janxdis.2006.09.006
  27. 27. Borsboom D, Deserno MK, Rhemtulla M, Epskamp S, Fried EI, McNally RJ, et al. Network analysis of multivariate data in psychological science. Nature Reviews Methods Primers. 2021;58(1). DOI: 10.1038/s43586-021-00055-w1-18
  28. 28. Ramos-Vera C, García-Ampudia L, Serpa-Barrientos A. Una alternativa de análisis de redes en la exploración de los estados de salud mental, condiciones crónicas y COVID-19. Iatreia. In Press 2022:1-22. Available from: https://revistas.udea.edu.co/index.php/iatreia/article/view/347261
  29. 29. Castro D, Ferreira F, de Castro I, Rodrigues AR, Correia M, Ribeiro J, et al. The differential role of 00central and bridge symptoms in deactivating psychopathological networks. Frontiers in Psychology. 2019;10:e2448. DOI: 10.3389/fpsyg.2019.02448
  30. 30. Bringmann LF, Elmer T, Epskamp S, Krause RW, Schoch D, Wichers M, et al. What do centrality measures measure in psychological networks? Journal of Abnormal Psychology. 2019;128(8):892-903. Available from: https://psycnet.apa.org/doi/10.1037/abn0000446
  31. 31. Bringmann LF, Albers C, Bockting C, Borsboom D, Ceulemans E, Cramer A, et al. Psychopathological networks: Theory, methods and practice. Behaviour Research and Therapy. 2022;149:e104011. DOI: 10.1016/j.brat.2021.104011
  32. 32. Fisher AJ, Reeves JW, Lawyer G, Medaglia JD, Rubel JA. Exploring the idiographic dynamics of mood and anxiety via network analysis. Journal of Abnormal Psychology. 2017;126(8):1044-1056. DOI: 10.1037/abn0000311
  33. 33. West DB. Introduction to Graph Theory. New Jersey: Prentice-Hall; 2001
  34. 34. Lauritzen SL. Graphical Models. Oxford: Clarendon Press; 1996
  35. 35. Isvoranu AM, Epskamp S, Waldorp L, Borsboom D. Network Psychometrics with R: A Guide for Behavioral and Social Scientists. New York: Routledge; 2022
  36. 36. Golino HF, Epskamp S. Exploratory graph analysis: A new approach for estimating the number of dimensions in psychological research. PLoS One. 2017;12(6):e0174035. DOI: 10.1371/journal.pone.0174035
  37. 37. Golino H, Shi D, Christensen AP, Garrido LE, Nieto MD, Sadana R, et al. Investigating the performance of exploratory graph analysis and traditional techniques to identify the number of latent factors: A simulation and tutorial. Psychological Methods. 2020;25(3):292-320. DOI: 10.1037/met0000255
  38. 38. Scott J, Carrington PJ. The SAGE Handbook of Social Network Analysis. Los Angeles: SAGE; 2011
  39. 39. Ramos-Vera C. Las redes de relación estadística en la investigación psiquiátrica: El caso del delirio en el contexto de COVID-19. Revista Colombiana de Psiquiatría (English Ed.). 2021;50(3):158-159 DOI:10.1016/j.rcpeng.2021.02.001
  40. 40. Fried EI, Von Stockert S, Haslbeck JMB, Lamers F, Schoevers RA, Penninx BWJH. Using network analysis to examine links between individual depressive symptoms, inflammatory markers, and covariates. Psychological Medicine. 2020;50(16):2682-2690. DOI: 10.1017/S0033291719002770
  41. 41. McNally RJ. Network analysis of psychopathology: Controversies and challenges. Annual Review of Clinical Psychology. 2021;17:31-53. DOI: 10.1146/annurev-clinpsy-081219-092850
  42. 42. Epskamp S, Fried EI. A tutorial on regularized partial correlation networks. Psychological Methods. 2018;23(4):617-634. DOI: 10.1037/met0000167
  43. 43. Andersson SA, Madigan D, Perlman MD. On the Markov equivalence of chain graphs, undirected graphs, and acyclic digraphs. Scandinavian Journal of Statistics. 1997;24(1):81-102. DOI: 10.1111/1467-9469.00050
  44. 44. Epskamp S. Psychometric network models from time-series and panel data. Psychometrika. 2020;85(1):206-231. DOI: 10.1007/s11336-020-09697-3
  45. 45. Gollini I, Murphy TB. Joint modeling of multiple network views. Journal of Computational and Graphical Statistics. 2016;25(1):246-265. DOI: 10.1080/10618600.2014.978006
  46. 46. Turner BM, Forstmann BU, Steyvers M. Joint Models of Neural and Behavioral Data. Switzerland: Springer International Publishing; 2019
  47. 47. Kappelmann N, Czamara D, Rost N, Moser S, Schmoll V, Trastulla L. CHARGE inflammation working group: Polygenic risk for immuno-metabolic markers and specific depressive symptoms: A multi-sample network analysis study. Brain, Behavior, and Immunity. 2021;95:256-268. DOI: 10.1016/j.bbi.2021.03.024
  48. 48. Moriarity DP, van Borkulo C, Alloy LB. Inflammatory phenotype of depression symptom structure: A network perspective. Brain, Behavior, and Immunity. 2021;93:35-42. DOI: 10.1016/j.bbi.2020.12.005
  49. 49. Saari T, Smith EE, Ismail Z. Network analysis of impulse dyscontrol in mild cognitive impairment and subjective cognitive decline. International Psychogeriatrics. 2021;1-10. DOI: 10.1017/s1041610220004123
  50. 50. Lunansky G, Van Borkulo CD, Haslbeck J, Van der Linden MA, Garay CJ, Etchevers MJ, et al. The mental health ecosystem: Extending symptom networks with risk and protective factors. Frontiers in Psychiatry. 2021;12:e301. DOI: 10.3389/fpsyt.2021.640658
  51. 51. Zavlis O, Butter S, Bennett K, Hartman TK, Hyland P, Mason L, et al. How does the COVID-19 pandemic impact on population mental health? A network analysis of COVID influences on depression, anxiety and traumatic stress in the UK population. Psychological Medicine. 2021;1-9. DOI: 10.1017/S0033291721000635
  52. 52. Invitto S, Romano D, Garbarini F, Bruno V, Urgesi C, Curcio G, et al. Major stress-related symptoms during the lockdown: A study by the Italian Society of Psychophysiology and Cognitive Neuroscience. Frontiers in Public Health. 2021;9:e250. DOI: 10.3389/fpubh.2021.636089
  53. 53. Papachristou N, Barnaghi P, Cooper B, Kober KM, Maguire R, Paul SM, et al. Network analysis of the multidimensional symptom experience of oncology. Scientific Reports. 2019;9(1):1-11. DOI: 10.1038/s41598-018-36973-1
  54. 54. Zhu Z, Hu Y, Xing W, Guo M, Zhao R, Han S, et al. Identifying symptom clusters among people living with HIV on antiretroviral therapy in China: A network analysis. Journal of Pain and Symptom Management. 2019;57(3):617-626. DOI: 10.1016/j.jpainsymman.2018.11.011
  55. 55. Abplanalp SJ, Green MF. Symptom structure in schizophrenia: Implications of latent variable modeling vs network analysis. Schizophrenia Bulletin. 2022;48(3):538-543. DOI: 10.1093/schbul/sbac020
  56. 56. Ashaie SA, Hung J, Funkhouser CJ, Shankman SA, Cherney LR. Depression over time in persons with stroke: A network analysis approach. Journal of Affective Disorders Reports. 2021;4:e100131. DOI: 10.1016/j.jadr.2021.100131
  57. 57. Gómez Penedo JM, Rubel JA, Blättler L, Schmidt SJ, Stewart J, Egloff N. The complex interplay of pain, depression, and anxiety symptoms in patients with chronic pain: A network approach. The Clinical Journal of Pain. 2020;36(4):249-259. DOI: 10.1097/AJP.0000000000000797
  58. 58. Nemirovsky A, Ilan K, Lerner L, Cohen-Lavi L, Schwartz D, Goren G, et al. Brain-immune axis regulation is responsive to cognitive behavioral therapy and mindfulness intervention: Observations from a randomized controlled trial in patients with Crohn's disease. Brain, Behavior, & Immunity-Health. 2022;19. DOI: 10.1016/j.bbih.2021.100407
  59. 59. Chang YT, Kearns PK, Carson A, Gillespie D, Meijboom R, Kampaite A, et al. Data-driven analysis shows robust links between fatigue and depression in early multiple sclerosis. medRxiv. 2022. DOI: 10.1101/2022.01.13.22269128
  60. 60. Ramos-Vera C. Serpa A, Vallejos-Saldarriaga J, Saintila J. Network analysis of depressive symptomatology in underweight and obese adults. Journal of Primary Care & Community Health. In Press. 2022. DOI: 10.1177/21501319221096917
  61. 61. Spechbach H, Jacquerioz F, Prendki V, Kaiser L, Smit M, Calmy A, et al. Network analysis of outpatients to identify predictive symptoms and combinations of symptoms associated with positive/negative SARS-CoV-2 nasopharyngeal swabs. Frontiers in Medicine. 2021;8. DOI: 10.3389/fmed.2021.685124
  62. 62. Hills TT, Kenett YN. Is the mind a network? Maps, vehicles, and skyhooks in cognitive network science. Topics in Cognitive Science. 2022;14(1):189-208. DOI: 10.1111/tops.12570
  63. 63. Mareva S, CALM team, & Holmes, J. Network models of learning and cognition in typical and atypical learners. Journal of Applied Research in Memory and Cognition. Advance online publication; 2021. DOI: 10.1037/h0101870
  64. 64. Ferguson C. A network psychometric approach to neurocognition in early Alzheimers's disease. Cortex. 2021;137:61-73. DOI: 10.1016/j.cortex.2021.01.002
  65. 65. Tosi G, Borsani C, Castiglioni S, Daini R, Franceschi M, Romano D. Complexity in neuropsychological assessments of cognitive impairment: A network analysis approach. Cortex. 2020;124(3):85-96. DOI: 10.1016/j.cortex.2019.11.004
  66. 66. Koen JD, Srokova S, Rugg MD. Age-related neural dedifferentiation and cognition. Current Opinion in Behavioral Sciences. 2020;32:7-14. DOI: 10.1016/j.cobeha.2020.01.006
  67. 67. Abramovitch A, Short T, Schweiger A. The c factor: Cognitive dysfunction as a transdiagnostic dimension in psychopathology. Clinical Psychology Review. 2021;81:e102007. DOI: 10.1016/j.cpr.2021.102007
  68. 68. Haywood D, Baughman F, Mullan B, Heslop K. What accounts for the factors of psychopathology? An investigation of the neurocognitive correlates of internalising, externalising, and the P-factor. PsyArXiv. 2022. Available from: https://psyarxiv.com/h97gw/download/?format=pdf
  69. 69. Monteleone P, Cascino G, Monteleone AM, Rocca P, Rossi A, Bertolino A, et al. Prevalence of antipsychotic-induced extrapyramidal symptoms and their association with neurocognition and social cognition in outpatients with schizophrenia in the “real-life”. Progress in Neuro-Psychopharmacology and Biological Psychiatry. 2021;109:e110250. DOI: 10.1016/j.pnpbp.2021.110250
  70. 70. Iverson GL. Network analysis and precision rehabilitation for the post-concussion syndrome. Frontiers in Neurology. 2019;10:e489. DOI: 10.3389/fneur.2019.00489
  71. 71. Iverson GL, Jones PJ, Karr JE, Maxwell B, Zafonte R, Berkner PD, et al. Network structure of physical, cognitive, and emotional symptoms at preseason baseline in student athletes with attention-deficit/hyperactivity disorder. Archives of Clinical Neuropsychology. 2020;35(7):1109-1122. DOI: 10.1093/arclin/acaa030
  72. 72. Fornito A, Zalesky A, Breakspear M. The connectomics of brain disorders. Nature Reviews Neuroscience. 2015;16(3):159-172. DOI: 10.1038/nrn3901
  73. 73. Baily AR. Network analysis of cognitive symptom domains in alzheimer's disease (AD) [thesis doctoral]. The Vegas: University of Nevada; 2020. Available from: https://digitalscholarship.unlv.edu/thesesdissertations/3986
  74. 74. Foret JT, Dekhtyar M, Cole JH, Gourley DD, Caillaud M, Tanaka H, et al. Network modeling sex differences in brain integrity and metabolic health. Frontiers in Aging Neuroscience. 2021;13:e329. DOI: 10.3389/fnagi.2021.691691
  75. 75. Rotstein A, Levine SZ, Samara M, Yoshida K, Goldberg Y, Cipriani A, et al. Cognitive impairment networks in Alzheimer's disease: Analysis of three double-blind randomized, placebo-controlled, clinical trials of donepezil. European Neuropsychopharmacology. 2022;57:50-58. DOI: 10.1016/j.euroneuro.2022.01.001
  76. 76. Pons P, Latapy M. Computing communities in large networks using random walks. Journal of Graph Algorithms and Applications. 2006;10:191-218. DOI: 10.7155/jgaa.00185
  77. 77. Massara GP, Di Matteo T, Aste T. Network filtering for big data: Triangulated maximally filtered graph. Journal of Complex Networks. 2017;5(2):161-178. DOI: 10.1093/comnet/cnw015
  78. 78. Christensen AP, Golino H, Silvia PJ. A psychometric network perspective on the validity and validation of personality trait questionnaires. European Journal of Personality. 2020;34(6):1095-1108. DOI: 10.1002/per.2265
  79. 79. Golino H, Moulder R, Shi D, Christensen AP, Garrido LE, Nieto MD, et al. Entropy fit indices: New fit measures for assessing the structure and dimensionality of multiple latent variables. Multivariate Behavioral Research. 2021;56(6):874-902. DOI: 10.1080/00273171.2020.1779642
  80. 80. Christensen AP, Golino H. Estimating the stability of psychological dimensions via bootstrap exploratory graph analysis: A Monte Carlo simulation and tutorial. Psych. 2021;3(3):479-500. DOI: 10.3390/psych3030032
  81. 81. Blanken TF, Bathelt J, Deserno MK, Voge L, Borsboom D, Douw L. Connecting brain and behavior in clinical neuroscience: A network approach. Neuroscience & Biobehavioral Reviews. 2021;130:81-90. DOI: 10.1016/j.neubiorev.2021.07.027
  82. 82. Simpson-Kent IL, Fried EI, Akarca D, Mareva S, Bullmore ET, Team CALM, et al. Bridging brain and cognition: A multilayer network analysis of brain structural covariance and general intelligence in a developmental sample of struggling learners. Journal of. Intelligence. 2021;9(2):e32. DOI: 10.3390/jintelligence9020032
  83. 83. Troyer EA, Kohn JN, Hong S. Are we facing a crashing wave of neuropsychiatric sequelae of COVID-19? Neuropsychiatric symptoms and potential immunologic mechanisms. Brain, Behavior, and Immunity. 2020;87:34-39. DOI: 10.1016/j.bbi.2020.04.027
  84. 84. Cathomas F, Klaus F, Guetter K, Chung HK, Beharelle AR, Spiller TR, et al. Increased random exploration in schizophrenia is associated with inflammation. Schizophrenia. 2021;7(1):1-9. DOI: 10.1038/s41537-020-00133-0
  85. 85. Ramos-Vera C. Las redes de correlación en la investigación de la hipertensión arterial y riesgo vascular. Hipertensión y Riesgo Vascular. 2021;38(3):156-157. DOI: 10.1016/j.hipert.2021.02.001
  86. 86. Hilland E, Landrø NI, Kraft B, Tamnes CK, Fried EI, Maglanoc LA, et al. Exploring the links between specific depression symptoms and brain structure: A network study. Psychiatry and Clinical Neurosciences. 2019;74(3):220-221. DOI: 10.1111/pcn.12969
  87. 87. Chambon M, Dalege J, Elberse JE, van Harreveld F. A: Psychological network approach to attitudes and preventive behaviors during pandemics: A COVID-19 study in the United Kingdom and the Netherlands. Social Psychological and Personality Science. 2021:1-13. DOI: 10.1177/19485506211002420
  88. 88. Gibson-Miller J, Zavlis O, Hartman TK, Bennett KM, Butter S, Levita L, et al. A network approach to understanding social distancing behaviour during the first UK lockdown of the COVID-19 pandemic. Psychology & Health. 2022:1-19. DOI: 10.1080/08870446.2022.2057497
  89. 89. Houston J, Thorson E, Kim E, Mantrala MK. COVID-19 communication ecology: Visualizing communication resource connections during a public health emergency using network analysis. American Behavioral Scientist. 2021:1-21. DOI: 10.1177/0002764221992811
  90. 90. Ramos-Vera C. The dynamic network relationships of obsession and death from COVID-19 anxiety among Peruvian university students during the second quarantine. Revista Colombiana de Psiquiatria (English Ed.). 2021;50(3):160-163. DOI: 10.1016/j.rcpeng.2021.08.002
  91. 91. Ryu S, Park IH, Kim M, Lee YR, Lee J, Kim H, et al. Network study of responses to unusualness and psychological stress during the COVID-19 outbreak in Korea. PLoS One. 2021;16(2):e0246894. DOI: 10.1371/journal.pone.0246894
  92. 92. Taylor S, Asmundson GJ. Negative attitudes about facemasks during the COVID-19 pandemic: The dual importance of perceived ineffectiveness and psychological reactance. PLoS One. 2021;16(2):e0246317. DOI: 10.1371/journal.pone.0246317
  93. 93. Taylor S, Paluszek MM, Rachor GS, McKay D, Asmundson GJ. Substance use and abuse, COVID-19-related distress, and disregard for social distancing: A network analysis. Addictive Behaviors. 2021;114:e106754. DOI: 10.1016/j.addbeh.2020.106754
  94. 94. Van Der Maas HLJ, Dolan CV, Grasman RPPP, Wicherts JM, Huizenga HM, Raijmakers MEJ. A dynamical model of general intelligence: The positive manifold of intelligence by mutualism. Psychological Review. 2006;113(4):842-861. DOI: 10.1037/0033-295X.113.4.842
  95. 95. Korem N, Cohen LD, Rubinsten O. The link between math anxiety and performance does not depend on working memory: A network analysis study. Consciousness and Cognition. 2022;100:e103298. DOI: 10.1016/j.concog.2022.103298
  96. 96. Ferguson CE. Network neuropsychology: The map and the territory. Neuroscience & Biobehavioral Reviews. 2022;132:638-647. DOI: 10.1016/j.neubiorev.2021.11.024
  97. 97. Burns GL, Preszler J, Ahnach A, Servera M, Becker SP. Multisource network and latent variable models of sluggish cognitive tempo, ADHD-Inattentive, and depressive symptoms with spanish children: Equivalent findings and recommendations. Research on Child and Adolescent Psychopathology. 2022:1-14. DOI: 10.1007/s10802-021-00890-1
  98. 98. Castro D, Ferreira F, Ferreira TB. Modularity of the personality network. European Journal of Psychological Assessment. 2021;36(6):998-1008. DOI: 10.1027/1015-5759/a000613
  99. 99. Ferreira F, Castro D, Ferreira TB. The modular structure of posttraumatic stress disorder in adolescents. Current Psychology. 2022:1-13. DOI: 10.1007/s12144-021-02538-1
  100. 100. Jimeno N, Gomez-Pilar J, Poza J, Hornero R, Vogeley K, Meisenzahl E, et al. (Attenuated) hallucinations join basic symptoms in a transdiagnostic network cluster analysis. Schizophrenia Research. 2022;243:43-54. DOI: 10.1016/j.schres.2022.02.018
  101. 101. Anderson AR, Kurz AS, Szabo YZ, McGuire AP, Frankfurt SB. Exploring the longitudinal clustering of lifestyle behaviors, social determinants of health, and depression. Journal of Health Psychology. Advance online publication; 2022:e13591053211072685. DOI: 10.1177/ 13591053211072685
  102. 102. Penzel N, Antonucci LA, Betz LT, Sanfelici R, Weiske J, Pogarell O, et al. Association between age of cannabis initiation and gray matter covariance networks in recent onset psychosis. Neuropsychopharmacology. 2021;46(8):1484-1493. DOI: 10.1038/s41386-021-00977-9
  103. 103. Hirota T, McElroy E, So R. Network analysis of internet addiction symptoms among a clinical sample of Japanese adolescents with autism spectrum disorder. Journal of Autism and Developmental Disorders. 2021;51(8):2764-2772. DOI: 10.1007/s10803-020-04714-x
  104. 104. Sanchez-Garcia M, de la Rosa-Cáceres A, Díaz-Batanero C, Fernández-Calderón F, Lozano OM. Cocaine use disorder criteria in a clinical sample: An analysis using item response theory, factor and network analysis. The American Journal of Drug and Alcohol Abuse. 2022;1-9. DOI: 10.1080/00952990.2021.2012185
  105. 105. Calati R, Romano D, Magliocca S, Madeddu F, Zeppegno P, Gramaglia C. The interpersonal-psychological theory of suicide and the role of psychological pain during the COVID-19 pandemic: A network analysis: Suicide and psychological pain. Journal of Affective Disorders. 2022;302:435-439. DOI: 10.1016/j.jad.2022.01.078
  106. 106. Smith AR, Hunt RA, Grunewald W, Jeon ME, Stanley IH, Levinson CA, et al. Identifying central symptoms and bridge pathways between autism spectrum disorder traits and suicidality within an active duty sample. Archives of Suicide Research. 2021:1-16. DOI: 10.1080/13811118.2021.1993398
  107. 107. Eadeh HM, Markon KE, Nigg JT, Nikolas MA. Evaluating the viability of neurocognition as a transdiagnostic construct using both latent variable models and network analysis. Research on Child and Adolescent Psychopathology. 2021:1-14. DOI: 10.1007/s10802-021-00770-8
  108. 108. Chattrattrai T, Blanken TF, Lobbezoo F, Su N, Aarab G, Van Someren EJ. A network analysis of self-reported sleep bruxism in the Netherlands Sleep Registry: Its associations with insomnia and several demographic, psychological, and life-style factors. Sleep Medicine. 2022;93:63-70. DOI: 10.1016/j.sleep.2022.03.018
  109. 109. Pappa E, Peters E, Bell V. Insight-related beliefs and controllability appraisals contribute little to hallucinated voices: A transdiagnostic network analysis study. European Archives of Psychiatry and Clinical Neuroscience. 2020:1-11 DOI:10.1007/s00406-020-01166-3
  110. 110. Guineau M, Ikani N, Rinck M, Collard R, Van Eijndhoven P, Tendolkar I, et al. Anhedonia as a transdiagnostic symptom across psychological disorders: A network approach. Psychological Medicine. 2022:1-12. DOI: 10.1017/S0033291722000575
  111. 111. Isvoranu AM, Abdin E, Chong SA, Vaingankar J, Borsboom D, Subramaniam M. Extended network analysis: From psychopathology to chronic illness. BMC Psychiatry. 2021;21(1):1-9. DOI: 10.1186/s12888-021-03128-y
  112. 112. Letina S, Blanken TF, Deserno MK, Borsboom D. Expanding network analysis tools in psychological networks: Minimal spanning trees, participation coefficients, and motif analysis applied to a network of 26 psychological attributes. Complexity. 2019. DOI: 10.1155/2019/9424605
  113. 113. Kraft B, Bø R, Heeren A, Ulset V, Stiles T, Landrø NI. Depression-related impairment in executive functioning is primarily associated with fatigue and anhedonia. PsyArXiv. 2022. DOI: 10.31234/osf.io/qh47y
  114. 114. Michelini G, Palumbo IM, DeYoung CG, Latzman RD, Kotov R. Linking RDoC and HiTOP: A new interface for advancing psychiatric nosology and neuroscience. Clinical Psychology Review. 2021;86:e102025. DOI: 10.1016/j.cpr.2021.102025
  115. 115. Brooks D, Hulst HE, de Bruin L, Glas G, Geurts JJ, Douw L. The multilayer network approach in the study of personality neuroscience. Brain Sciences. 2020;10(12):915. DOI: 10.3390/brainsci10120915
  116. 116. Zainal NH, Newman MG. Elevated anxiety relates to future executive dysfunction: A cross-lagged panel network analysis of psychopathology and cognitive functioning components. PsyArXiv. 2021. DOI: 10.31234/osf.io/hrfqa
  117. 117. Hoffart A, Johnson SU. Latent trait, latent-trait state, and a network approach to mental problems and their mechanisms of change. Clinical Psychological Science. 2020;8(4):595-613. DOI: 10.1177/2167702620901744
  118. 118. Morvan Y, Fried EI, Chevance A. Network modeling in psychopathology: Hopes and challenges. L'Encéphale. 2020;46(1):1-2. DOI: 10.1016/j.encep.2020.01.001
  119. 119. Borsboom D. Possible futures for network psychometrics. Psychometrika. 2022;87:253-265. DOI: 10.1007/s11336-022-09851-z
  120. 120. Bringmann LF, Eronen MI. Don’t blame the model: Reconsidering the network approach to psychopathology. Psychological Review. 2018;125(4):606-615. DOI: 10.1037/rev0000108
  121. 121. Krendl AC, Betzel RF. Social cognitive network neuroscience. Social Cognitive and Affective Neuroscience. 2022:nsac020. DOI: 10.1093/scan/nsac020
  122. 122. Xie S, McDonnell E, Wang Y. Conditional Gaussian graphical model for estimating personalized disease symptom networks. Statistics in Medicine. 2022;41(3):543-553. DOI: 10.1002/sim.9274

Written By

Cristian Ramos-Vera, Víthor Rosa Franco, José Vallejos Saldarriaga and Antonio Serpa Barrientos

Submitted: 05 May 2022 Reviewed: 13 May 2022 Published: 26 August 2022