Article summary of The network approach to psychopathology: a review of the literature 2008-2018 and an agenda for future research by Robinaugh et al.
...........Read moreThe levels problem in psychopathology refers to the fact that psychopathological disorders are investigated in different ways (or at different levels). Most frequently, these include the psychological level and the biological level. The boundary between these two levels is blurry, and it may be difficult at times to differentiate between them. For example, autism is not only a psychological disorder but also a biological one, so from what level should it be analyzed? As will be explained in the next section, there are also multiple different ways of categorizing levels. Since these categorizations have much overlap, levels should not be taken too literally, and should instead be used for heuristic purposes. The level problem makes it more difficult for researchers and clinicians to decide the best framework for advancing psychopathology research.
Three common ways of conceptualizing different levels are the following: part-whole related levels, levels based on the scale of what is being measured, and levels based on the time range of what is being measured. Although these are not the only ways to think about levels, they are the most relevant in terms of psychopathology. To begin, part-whole levels refer to hierarchies, for example, within an organism. An organism can be broken down into tissues, cells, cell parts, molecules, and eventually atoms. The whole of an organism is at a higher level than that of its parts — thus, it is a hierarchical structure. This hierarchical system of levels, however, can vary even within the same organism, as what is considered a higher or lower level is determined by what is being measured. Additionally, the concept of part-whole levels is not always clear-cut. Ideally, there would be no overlap between levels in the hierarchy and no components that would fall between levels, but this is seldom the case in practice. There is also no agreed-upon way to decide with consistency which component belongs to which level in the part-whole system.
Levels can also be thought of in terms of scales. Essentially, this means that the size of the thing being studied is what determines its level. The example of analyzing the activity of neurons is given in the article. In functional neuroimaging, each data point consists of millions of neurons, whereas cellular neuroscience analyzes neurons individually. In this case, the scale of functional imaging is much broader. Finally, there is the temporal scale, in which the length of the process being studied determined its level. For example, the interactions between brain areas take much longer than the interactions between neurotransmitters and receptors. Importantly, the temporal scale can be applied quite easily to the concept of psychopathology, because the time that it takes for symptoms and mental states to appear, progress, and fade can be measured and compared to the time it takes for neurobiological states to change.
People that take an extreme explanatory reductionist view believe that the neurobiological mechanisms of the brain make explanations at the psychological level useless. They think that the only reason psychological-level explanations are accepted as explanations at all is because we do not know the neurobiology behind those explanations yet. Those who subscribe to a more lenient version of explanatory reductionism believe that psychological explanations are real, but will never be as important or powerful as explanations on the neurobiological level. All explanatory reductionists think that biological explanations, which are on a lower level, are more useful than psychological explanations, which are on a higher level. This is partially due to explanatory reductionists’ reasoning that all behavior is merely an outward expression of biological activity, which in “mind-body debate” terms is a monism view. In past scientific research, it has often been very helpful to study the lowest biological levels. DNA, for instance, was discovered this way. However, it is not always sensible to ignore higher levels. In physics, for example, investigating only very low levels like molecules is not sufficient for actually explaining and predicting physical laws and behavior on a higher level.
In the context of psychopathology, explanatory pluralism is more useful than explanatory reductionism. Explanatory pluralism advocates not just for exploring higher levels, but for investigating multiple levels (both higher and lower) in the context of one concept. Explanatory pluralism is most useful when the information received from each level is integrated into a more comprehensive system. Integrating all this information may mean that professionals from many fields have to compile and align concepts related to a specific psychological problem.
The field of clinical psychology relies on higher-level explanations of psychopathologies because it is exceedingly difficult to discover genes or other biological anomalies that wholly or substantially explain a specific psychiatric disorder. It is very unlikely that something as low level as a strand of DNA can ever explain something as high level and abstract as a mood disorder, for instance. On the other hand, researchers have made much progress in understanding the causes and subtypes of obsessive-compulsive disorder through analyzing the disorder's typical cognitive processes. Considering this, it would be prudent for psychopathological research to be done at multiple levels which differ in time, scale, and part-whole hierarchies.
Alice in Wonderland syndrome (AIWS) was first described in 1955 by the psychiatrist John Todd, and its symptoms include various distortions of sensory perception, including visual distortions, and distortions of time and self. These distortions differ from hallucinations and illusions in the sense that they are based in the real world but involve very specific alterations to sensory input. AIWS currently comprises 42 visual symptoms (called metamorphopsias) and 16 non-visual symptoms. The two most common symptoms are micropsia; seeing things as smaller than they really are, and macropsia; seeing things as larger than they really are. 58.6% of AIWS patients suffer from micropsia while 45% suffer from macropsia. A few other visual symptoms include kinetopsia, in which people see stationary objects as moving, and prosopometamorphopsia, in which eyes are seen as much larger than they are. Symptoms sometimes include feelings of levitation and alterations in the passage of time, among others. It is most common for people with AIWS to only experience one symptom, although many people experience up to four. Generally, AIWS symptoms tend to be short-lived, lasting a few minutes to a few days. Years-long or lifelong symptoms occur rarely.
There are many possible causes of AIWS, and more will likely be added as more cases are identified. The causes differ between young people and adults. For youths, the most common cause of AIWS is encephalitis (inflammation of brain tissues). Encephalitis can be caused by various infections, but the Epstein-Barr virus is the one most frequently cited in cases of encephalitis-induced AIWS. In adults, neurological disorders were cited most often as the medical cause for AIWS, with migraines being the most common among them. However, symptoms of AIWS are sometimes unassociated with any type of medical disorder or pathology. Symptoms of this syndrome are caused by functional and/or structural abnormalities in the perceptual system.
Although AIWS is thought of as a rare syndrome, some of its symptoms are seen quite regularly in the general population. In fact, singular symptoms of AIWS unrelated to another disorder or medical condition have been experienced by around 30% of all adolescents. When considering specific symptoms, it was found that 5.6% of male adolescents and 6.2% of female adolescents have experienced micropsia and/or macropsia. It was also found that 15% of patients with migraines suffer from AIWS.
Patients with AIWS often suffer from underlying medical conditions like encephalitis, migraines, or epilepsy. When this is the case, pharmacological treatment is used in an attempt to diminish or eliminate the underlying cause. Typically, medication is only necessary in medically-induced cases, and this treatment must target the medical condition rather than the symptoms themselves. Generally, these treatments include antiepileptic medication, antibiotics, antiviral medication, or migraine medication. Oftentimes in medical cases of AIWS, symptoms disappear and return in coordination with the severity of the disease at the time. In most cases of non-medically-induced AIWS, a helpful treatment can consist merely of reassurance from a clinician that the symptoms they are experiencing are benign. Chronic cases may warrant functional neuroimaging to better understand specific symptoms. Almost all cases of AIWS are considered benign and treatable, as full remission of symptoms is often achieved both in medically-induced and non-medically induced cases. This can occur either spontaneously or after treatment. However, the prognosis for patients with epilepsy or migraine-induced AIWS is poorer — these patients rarely achieve full remission due to the difficulty of treating their underlying conditions.
It is estimated that AIWS is severely underdiagnosed. This is partially due to its apparent similarities to schizophrenia spectrum disorders, as patients’ perceptual distortions may be attributed to hallucinations. The diagnosis of AIWS is also made more difficult because it is not featured in either the DSM-5 or the ICD-10. In practice, symptoms of AIWS may not be recognized because of this factor. It is suggested that AIWS should be included in the next versions of the DSM and ICD under the categorization of nervous system disorders or perceptual disorders. An international database that documents cases of AIWS and their treatments would also be extremely helpful for clinicians trying to learn about and diagnose this syndrome.
Emotional processing theory (EPT) proposes a hypothetical sequence of fear-reducing changes that is evoked by emotional engagement with the memory of a significant event (the trauma). It is based around the concept of a fear structure. The fear structure is a type of mental framework for reaction to threat that includes information about a feared stimulus (e.g. a spider), physiological and behavioral responses (e.g. sweating, rapid heartbeat), and the meaning of the stimulus and response elements (e.g. the spider will bite me and I am afraid). The fear structure can be changed by activating it and presenting information that is incompatible with its elements that through prolonged exposure is integrated into the fear structure and replaces the pathological elements.
The cognitive model of PTSD suggests that negative appraisals, disjointed trauma memories, and unhelpful coping strategies maintain PTSD.
Effective trauma-focused psychological treatment should include:
Patients visualize the traumatic event, usually with their eyes closed. They start with the first perception that something was wrong and end at a point when they were reasonably safe again. The patient describes moment by moment what is happening and what they are thinking and feeling. Imaginal reliving facilitates emotional engagement with the memory and gives access to details of the memory. The therapist supports the patient in maintaining awareness of the present surroundings.
Summaries per article with Clinical Psychology at Leiden University 22/23
Summaries per article with Clinical Psychology at Leiden University 21/22
Article summaries Clinical Psychology - UL - 2020-2021. Use the connected summaries below to broaden your skills on clinical psychology. The upper part of the articles is summarized in English, the lower part in Dutch. Specific attention is given to treatment and background of Schizophrenia and eating disorders
The network model to psychopathology states that mental disorders can be conceptualized and studied as causal systems of mutually reinforcing symptoms. This holds that symptoms are not passive indicators of a latent, common cause, of the disorder but agents in a causal system.
The causality hypothesis states that when causal relations among symptoms are strong, the onset of one symptom will lead to the onset of others. The connectivity hypothesis states that a strongly interconnected symptom network is vulnerable to a contagion effect of spreading activation through the network. Widespread symptom activation as a result of an external stressor can lead to symptoms persisting when the initiating stressor is removed. The centrality hypothesis states that highly central symptoms have greater potential to spread symptom activation throughout the network than do symptoms on the periphery. The comorbidity hypothesis states that symptoms can occur in multiple disorders and that some symptoms can thus bridge different disorders.
A mental disorder is characterized by both the state and the structure of the network (i.e. a mental disorder is characterized by a state of harmful equilibrium). The boundary between health and disorder will vary as a function of network structure. In weakly connected networks, activation varies dimensionally. However, in strongly connected networks, activation within the system rapidly leads to a state of psychopathology (i.e. more discrete rather than continuous).
The momentary perspective states that symptoms are aggregates of moment-to-moment experiences. According to this perspective, these experiences constitute the true building blocks of psychopathology. This highlights the importance of understanding the chronometry of experiences, symptoms and disorders.
The assumptions of the network model currently do not always align with how disorders are believed to operate.
There is a conditional positive manifold for most disorders. This states that symptoms of a positive disorder tend to be positively interconnected, even after controlling for shared variance among symptoms. This suggests meaningful clustering of symptoms in the syndromes we call mental disorders. Connectivity tends to be consistent across time and demographic groups. However, differences have been observed across countries.
Greater connectivity (i.e. network density) may confer risk for psychopathology. This is based on the fact that there appears to be greater connectivity between symptoms in people with more severe mental disorders. It is also possible that greater connectivity leads to disorder persistence. However, there is no consensus regarding these topics. There is some evidence that connectivity of negative mood state networks is associated with psychopathology but minimal evidence that broader networks of momentary experience exhibit such associations.
Node strength refers to the summed absolute strength of a node’s direct link. Non-DSM symptoms often exhibit elevated centrality (e.g. feeling disliked in depression) and some DSM-nodes are weakly connected to the network. It is not clear whether the symptoms which the DSM identifies as especially important are more central to less important DSM-symptoms. The DSM most likely has not captured all symptoms of a disorder and has not
.......read moreHeroin overdose is a pressing issue, with about 1 to 3% of heroin users dying from an overdose every year. In the United States in 2011, almost 11,000 people died from a heroin overdose. Accurate explanations are needed for why some addicts overdose so work can be done to reduce heroin-related deaths. One reason often given for these deaths is that the addict had taken other drugs in coordination with heroin. Heroin is a central nervous system depressant drug, so its combination with other depressants (like alcohol) can sometimes be fatal. However, most cases of heroin overdose are not due to drug mixing.
A second reason cited frequently as a cause for a heroin overdose is that addicts lose tolerance after abstaining from using the drug for a long period. According to this theory, when the addicts eventually use heroin again the drug will have a much stronger effect on their body, potentially resulting in overdose. Yet, there is evidence to suggest that drug tolerance in humans does not deteriorate after months or even years of abstaining from use. This can be shown using segmental hair analysis because temporal patterns of drug use can be seen by examining an individual’s hair. Based on the hair strands of recently deceased overdose victims, researchers have found that there is no link between recent abstinence and overdose.
The heroin overdose mystery refers to the fact that there is often no obvious reason for why an addict overdoses on a specific day. Post-mortem procedures for overdose victims include measuring the amount of morphine in the blood (because morphine is the metabolized version of heroin). It has been found that morphine levels in the blood of overdose victims are often — about 75% of the time — no higher than other heroin users who have not overdosed. Considering this, it is concluded that the causal factor of death by heroin overdose is not typically the actual amount of the drug in the body. In fact, in many cases, it has been noted that the overdose victim used the same amount of heroin the day before, and it was non-fatal. Simply put, many (if not the majority) of heroin “overdoses” are not true pharmacological overdoses. There is clearly another factor at play, and many theories have been suggested for what exactly that factor is; this article argues that it is due to the Pavlovian conditioning of drug users.
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