Anhedonia | |
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Melancholia, by Tadeusz Pruszkowski | |
Pronunciation | |
Specialty | Psychiatry |
Symptoms | Reduced motivation and ability to experience pleasure, particularly from previously enjoyable activities |
Anhedonia is a diverse array of deficits in hedonic function, including reduced motivation or ability to experience pleasure. [1] While earlier definitions emphasized the inability to experience pleasure, anhedonia is currently used by researchers to refer to reduced motivation, reduced anticipatory pleasure (wanting), reduced consummatory pleasure (liking), and deficits in reinforcement learning. [2] [3] [4] In the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), anhedonia is a component of depressive disorders, substance-related disorders, psychotic disorders, and personality disorders, where it is defined by either a reduced ability to experience pleasure, or a diminished interest in engaging in previously pleasurable activities. [5] [6] While the International Statistical Classification of Diseases and Related Health Problems, Tenth Revision (ICD-10) does not explicitly mention anhedonia, the depressive symptom analogous to anhedonia as described in the DSM-5 is a loss of interest or pleasure. [3]
While anhedonia was originally defined in 1896 by Théodule-Armand Ribot as the reduced ability to experience pleasure, it has been used to refer to deficits in multiple facets of reward. Re-conceptualizations of anhedonia highlight the independence of "wanting" and "liking". "Wanting" is a component of anticipatory positive affect, mediating both the motivation (i.e. incentive salience) to engage with reward, as well as the positive emotions associated with anticipating a reward. "Liking", on the other hand, is associated with the pleasure derived from consuming a reward. [2] [1] The consciousness of reward-related processes has also been used to categorize reward in the context of anhedonia, as studies comparing implicit behavior versus explicit self-reports demonstrate a dissociation of the two. [7] Learning has also been proposed as an independent facet of reward that may be impaired in conditions associated with anhedonia, but empirical evidence dissociating learning from either "liking" or "wanting" is lacking. [7]
Anhedonia has also been used to refer to "affective blunting", "restricted range of affect", "emotional numbing", and "flat affect", particularly in the context of post-traumatic stress disorders. In PTSD patients, scales measuring these symptoms correlate strongly with scales that measure more traditional aspects of anhedonia, supporting this association. [2]
Studies in clinical populations, healthy populations, and animal models have implicated a number of neurobiological substrates in anhedonia. Regions implicated in anhedonia include the prefrontal cortex as a whole, particularly the orbitofrontal cortex (OFC), the striatum, amygdala, anterior cingulate cortex (ACC), hypothalamus, and ventral tegmental area (VTA). [5] [3] Neuroimaging studies in humans have reported that deficits in consummatory aspects of reward are associated with abnormalities in the ventral striatum and medial prefrontal cortex, while deficits in anticipatory aspects of reward are related to abnormalities in hippocampal, dorsal ACC and prefrontal regions. These abnormalities are generally consistent with animal models, except for inconsistent findings with regard to the OFC. This inconsistency may be related to the difficulty in imaging the OFC due to its anatomical location, or the small number of studies performed on anhedonia; [8] a number of studies have reported reduced activity in the OFC in schizophrenia and major depression, as well as a direct relationship between reduced activity and anhedonia. [9] Researchers theorize that anhedonia may result from the breakdown in the brain's reward system, involving the neurotransmitter dopamine. Anhedonia can be characterised as "impaired ability to pursue, experience and/or learn about pleasure, which is often, but not always accessible to conscious awareness". [10]
The conditions of akinetic mutism and negative symptoms are closely related. In akinetic mutism, a stroke or other lesion to the anterior cingulate cortex causes reduction in movement (akinetic) and speech (mutism). [11]
Anhedonia occurs in roughly 70% of people with a major depressive disorder. [2] Anhedonia is a core symptom of major depressive disorder; therefore, individuals experiencing this symptom can be diagnosed with depression, even in the absence of low/depressed mood. [12] The Diagnostic and Statistical Manual of Mental Disorders (DSM) describes a "lack of interest or pleasure", but these can be difficult to discern given that people tend to become less interested in things which do not give them pleasure. The DSM criterion of weight loss is probably related, and many individuals with this symptom describe a lack of enjoyment of food. They can portray any of the non-psychotic symptoms and signs of depression. [13]
Anhedonia is one of the negative symptoms of schizophrenia. [2] Although five domains are usually used to classify negative symptoms, factor analysis of questionnaires yield two factors, with one including deficits in pleasure and motivation. People with schizophrenia retrospectively report experiencing fewer positive emotions than healthy individuals. However, "liking" or consummatory pleasure, is intact in people with schizophrenia, as they report experiencing the same degree of positive affect when presented with rewarding stimuli. Neuroimaging studies support this behavioral observation, as most studies report intact responses in the reward system (i.e. ventral striatum, VTA) to simple rewards. However, studies on monetary rewards sometimes report reduced responsiveness. More consistent reductions are observed with regard to emotional response during reward anticipation, which is reflected in a reduced responsiveness of both cortical and subcortical components of the reward system. [14] Schizophrenia is associated with reduced positive prediction errors (a normal pattern of response to an unexpected reward), which a few studies have demonstrated to be correlated with negative symptoms. People with schizophrenia demonstrate impairment in reinforcement learnings tasks only when the task requires explicit learning, or is sufficiently complex. Implicit reinforcement learning, on the other hand, is relatively intact. These deficits may be related to dysfunction in the ACC, OFC and dlPFC leading to abnormal representation of reward and goals. [15]
Anhedonia is common in people who are dependent upon any one or more of a wide variety of drugs, including alcohol, opioids, cannabinoids, and nicotine. Although anhedonia becomes less severe over time, it is a significant predictor of relapse. [16]
While PTSD is associated with reduced motivation, part of the anticipatory "wanting", it is also associated with elevated sensation seeking, and no deficits in physiological arousal, or self reported pleasure to positive stimuli. [17] PTSD is also associated with blunted affect, which may be due to the high comorbidity with depression. [2]
Anhedonia occurs frequently in Parkinson's disease, with rates between 7%–45% being reported. Whether or not anhedonia is related to the high rates of depression in Parkinson's disease is unknown. [18]
Anhedonia is also reported to appear in people with bipolar depression. [19]
Anhedonia may be associated with ADHD. Impairments of dopaminergic and serotonergic function in the brain of those with ADHD result in dysregulation of reward processing which can lead to anhedonia. [20]
Sexual anhedonia in males is also known as 'ejaculatory anhedonia'. This condition means that a male will ejaculate with no accompanying sense of pleasure. [21]
The condition is most frequently found in males, but females can experience lack of pleasure when the body goes through the orgasm process as well.
Sexual anhedonia may be caused by:
It is very uncommon that a neurological examination and blood tests can determine the cause of a specific case of sexual anhedonia.
Patients may be prescribed sustained-release bupropion to aid in treatment, which has been shown to relieve sexual dysfunction even in patients without depression. [25]
Social anhedonia is defined as a disinterest in social contact and a lack of pleasure in social situations, and is characterized by social withdrawal. This characteristic typically manifests as an indifference to other people. [26] In contrast to introversion, a nonpathological dimension of human personality, social anhedonia represents a deficit in the ability to experience pleasure. [27] Additionally, social anhedonia differs from social anxiety in that social anhedonia is predominantly typified by diminished positive affect, while social anxiety is distinguished by both decreased positive affect and exaggerated negative affect. [28]
This trait is currently seen as a central characteristic, as well as a predictor, of schizophrenia spectrum disorders. [29] It is also widely linked to autism spectrum disorder. [30]
The term anhedonia is derived from the Greek an-, "without" and hēdonē, "pleasure". [32] Interest in the nature of pleasure and its absence dates back to ancient Greek philosophers such as Epicurus. [3] The symptoms of anhedonia were introduced to the realm of psychopathology in 1809 by John Haslam, who characterized a patient with schizophrenia as indifferent to "those objects and pursuits which formerly proved sources of delight and instruction". [33] The concept was formally coined by Théodule-Armand Ribot and later used by psychiatrists Paul Eugen Bleuler and Emil Kraepelin to describe a core symptom of schizophrenia. [3] In particular, Sandor Rado postulated that schizotypes, or individuals with the schizophrenic phenotype, have two key genetic deficits, one related to the ability to feel pleasure (anhedonia) and one related to proprioception. In 1962, Meehl furthered Rado's theory through the introduction of the concept of schizotaxia, a genetically driven neural integrative defect thought to give rise to the personality type of schizotypy. [34] Loren and Jean Chapman further distinguished between two types of anhedonia: physical anhedonia, or a deficit in the ability to experience physical pleasure, and social, or a deficit in the ability to experience interpersonal pleasure. [35]
Recent research suggests that social anhedonia may represent a prodrome of psychotic disorders. [26] [27] [36] First-degree relatives of individuals with schizophrenia show elevated levels of social anhedonia, [37] higher baseline scores of social anhedonia are associated with later development of schizophrenia. [38] These findings provide support for the conjecture that it represents a genetic risk marker for schizophrenia-spectrum disorders.
Additionally, elevated levels of social anhedonia in patients with schizophrenia have been linked to poorer social functioning. [39] [40] Socially anhedonic individuals perform worse on a number of neuropsychological tests than non-anhedonic participants, [41] [42] and show similar physiological abnormalities seen in patients with schizophrenia. [42]
Anhedonia is present in several forms of psychopathology [43] as well as autism spectrum disorder. [30]
Social anhedonia is observed in both depression and schizophrenia. However, social anhedonia is a state related to the depressive episode and the other is a trait related to the personality construct associated with schizophrenia. These individuals both tend to score highly on self-report measures of social anhedonia. Blanchard, Horan, and Brown demonstrated that, although both the depression and the schizophrenia patient groups can look very similar in terms of social anhedonia cross-sectionally, over time as individuals with depression experience symptom remission, they show fewer signs of social anhedonia, while individuals with schizophrenia do not. [44] Blanchard and colleagues (2011) found individuals with social anhedonia also had elevated rates of lifetime mood disorders including depression and dysthymia compared to controls. [45]
As mentioned above, social anxiety and social anhedonia differ in important ways. [28] However, social anhedonia and social anxiety are also often comorbid. People with social anhedonia may display increased social anxiety and be at increased risk for social phobias and generalized anxiety disorder. [46] It has yet to be determined what the exact relationship between social anhedonia and social anxiety is, and if one potentiates the other. [47] Individuals with social anhedonia may display increased stress reactivity, meaning that they feel more overwhelmed or helpless in response to a stressful event compared to control subjects who experience the same type of stressor. This dysfunctional stress reactivity may correlate with hedonic capacity, providing a potential explanation for the increased anxiety symptoms experienced in people with social anhedonia. [48] In an attempt to separate out social anhedonia from social anxiety, the Revised Social Anhedonia Scale [49] didn't include items that potentially targeted social anxiety. [29] However, more research must be conducted on the underlying mechanisms through which social anhedonia overlaps and interacts with social anxiety. The efforts of the "social processes" RDoC initiative will be crucial in differentiating between these components of social behavior that may underlie mental illnesses such as schizophrenia.
Social anhedonia is a core characteristic of schizotypy, which is defined as a continuum of personality traits that can range from normal to disordered and contributes to risk for psychosis and schizophrenia. [50] Social anhedonia is a dimension of both negative and positive schizotypy. [51] It involves social and interpersonal deficits, but is also associated with cognitive slippage and disorganized speech, both of which fall into the category of positive schizotypy. [52] [53] [54] Not all people with schizophrenia display social anhedonia [55] and likewise, people who have social anhedonia may never be diagnosed with a schizophrenia-spectrum disorder if they do not have the positive and cognitive symptoms that are most frequently associated with most schizophrenia-spectrum disorders. [56]
Social anhedonia may be a valid predictor of future schizophrenia-spectrum disorders; [46] [56] young adults with social anhedonia perform in a similar direction to schizophrenia patients in tests of cognition and social behavior, showing potential predictive validity. [38] [52] Social anhedonia usually manifests in adolescence, possibly because of a combination of the occurrence of critical neuronal development and synaptic pruning of brain regions important for social behavior and environmental changes, when adolescents are in the process of becoming individuals and gaining more independence.
There is no validated treatment for social anhedonia. [47] Future research should focus on genetic and environmental risk factors to home in on specific brain regions and neurotransmitters that may be implicated in social anhedonia's cause and could be targeted with medication or behavioral treatments. Social support may also play a valuable role in the treatment of social anhedonia. Blanchard et al. [45] found that a greater number of social supports, as well as a greater perceived social support network, were related to fewer schizophrenia-spectrum symptoms and to better general functioning within the social anhedonia group. So far, no medicine has been developed to specifically target anhedonia.
In the general population, males score higher than females on measures of social anhedonia. [57] This sex difference is stable throughout time (from adolescence into adulthood) and is also seen in people with schizophrenia-spectrum disorders. These results may reflect a more broad pattern of interpersonal and social deficits seen in schizophrenia-spectrum disorders. [58] On average, males with schizophrenia are diagnosed at a younger age, have more severe symptoms, worse treatment prognosis, and a decrease in overall quality of life compared to females with the disorder. [59] These results, coupled with the sex difference seen in social anhedonia, outline the necessity for research on genetic and hormonal characteristics that differ between males and females, and that may increase risk or resilience for mental illnesses such as schizophrenia. [60]
There are several self-report psychometric measures of schizotypy which each contain subscales related to social anhedonia:
L.J. and J.P. Chapman were the first to discuss the possibility that social anhedonia may stem from a genetic vulnerability. [55] The disrupted in schizophrenia 1 (DISC1) gene has been consistently associated with risk for, and cause of, schizophrenia-spectrum disorders and other mental illnesses. [63] More recently, DISC1 has been associated with social anhedonia within the general population. [64] Tomppo identified a specific DISC1 allele that is associated with an increase in characteristics of social anhedonia. They also identified a DISC1 allele associated with decreased characteristics of social anhedonia, that was found to be preferentially expressed in women. More research needs to be conducted, but social anhedonia may be an important intermediate phenotype (endophenotype) between genes associated with risk for schizophrenia and phenotype of the disorder. [65]
Researchers studying the neurobiology of social anhedonia posit that this trait may be linked to dysfunction of reward-related systems in the brain. This circuitry is critical for the sensation of pleasure, the computation of reward benefits and costs, determination of the effort required to obtain a pleasant stimulus, deciding to obtain that stimulus, and increasing motivation to obtain the stimulus. In particular, the ventral striatum and areas of the prefrontal cortex (PFC), including the orbitofrontal cortex (OFC) and dorsolateral (dl) PFC, are critically involved in the experience of pleasure and the hedonic perception of rewards. With regards to neurotransmitter systems, opioid, gamma-Aminobutyric acid and endocannabinoid systems in the nucleus accumbens, ventral pallidum, and OFC mediate the hedonic perception of rewards. [3] Activity in the PFC and ventral striatum have been found to be decreased in anhedonic individuals with major depressive disorder (MDD) and schizophrenia. However, schizophrenia may be less associated with decreased hedonic capacity and more with deficient reward appraisal. [66] [67]
Recent studies have found people who do not have any issue processing musical tones or beat, yet receive no pleasure from listening to music. [68] Specific musical anhedonia is distinct from melophobia, the fear of music.
Psychosis is a condition of the mind or psyche that results in difficulties determining what is real and what is not real. Symptoms may include delusions and hallucinations, among other features. Additional symptoms are incoherent speech and behavior that is inappropriate for a given situation. There may also be sleep problems, social withdrawal, lack of motivation, and difficulties carrying out daily activities. Psychosis can have serious adverse outcomes.
Schizoid personality disorder is a personality disorder characterized by a lack of interest in social relationships, a tendency toward a solitary or sheltered lifestyle, secretiveness, emotional coldness, detachment, and apathy. Affected individuals may be unable to form intimate attachments to others and simultaneously possess a rich and elaborate but exclusively internal fantasy world. Other associated features include stilted speech, a lack of deriving enjoyment from most activities, feeling as though one is an "observer" rather than a participant in life, an inability to tolerate emotional expectations of others, apparent indifference when praised or criticized, a degree of asexuality, and idiosyncratic moral or political beliefs.
A thought disorder (TD) is a disturbance in cognition which affects language, thought and communication. Psychiatric and psychological glossaries in 2015 and 2017 identified thought disorders as encompassing poverty of ideas, neologisms, paralogia, word salad, and delusions—all disturbances of thought content and form. Two specific terms have been suggested—content thought disorder (CTD) and formal thought disorder (FTD). CTD has been defined as a thought disturbance characterized by multiple fragmented delusions, and the term thought disorder is often used to refer to an FTD: a disruption of the form of thought. Also known as disorganized thinking, FTD results in disorganized speech and is recognized as a major feature of schizophrenia and other psychoses. Disorganized speech leads to an inference of disorganized thought. Thought disorders include derailment, pressured speech, poverty of speech, tangentiality, verbigeration, and thought blocking. One of the first known cases of thought disorders, or specifically OCD as it is known today, was in 1691. John Moore, who was a bishop, had a speech in front of Queen Mary II, about "religious melancholy."
A mood swing is an extreme or sudden change of mood. Such changes can play a positive part in promoting problem solving and in producing flexible forward planning, or be disruptive. When mood swings are severe, they may be categorized as part of a mental illness, such as bipolar disorder, where erratic and disruptive mood swings are a defining feature.
Schizotypal personality disorder, also known as schizotypal disorder, is a cluster A personality disorder. The Diagnostic and Statistical Manual of Mental Disorders (DSM) classification describes the disorder specifically as a personality disorder characterized by thought disorder, paranoia, a characteristic form of social anxiety, derealization, transient psychosis, and unconventional beliefs. People with this disorder feel pronounced discomfort in forming and maintaining social connections with other people, primarily due to the belief that other people harbor negative thoughts and views about them. Peculiar speech mannerisms and socially unexpected modes of dress are also characteristic. Schizotypal people may react oddly in conversations, not respond, or talk to themselves. They frequently interpret situations as being strange or having unusual meanings for them; paranormal and superstitious beliefs are common. Schizotypal people usually disagree with the suggestion that their thoughts and behaviors are a 'disorder' and seek medical attention for depression or anxiety instead. Schizotypal personality disorder occurs in approximately 3% of the general population and is more commonly diagnosed in males.
In psychology, schizotypy is a theoretical concept that posits a continuum of personality characteristics and experiences, ranging from normal dissociative, imaginative states to extreme states of mind related to psychosis, especially schizophrenia. The continuum of personality proposed in schizotypy is in contrast to a categorical view of psychosis, wherein psychosis is considered a particular state of mind, which the person either has or does not have.
Reduced affect display, sometimes referred to as emotional blunting or emotional numbing, is a condition of reduced emotional reactivity in an individual. It manifests as a failure to express feelings either verbally or nonverbally, especially when talking about issues that would normally be expected to engage emotions. In this condition, expressive gestures are rare and there is little animation in facial expression or vocal inflection. Additionally, reduced affect can be symptomatic of autism, schizophrenia, depression, post-traumatic stress disorder, depersonalization derealization disorder, schizoid personality disorder or brain damage. It may also be a side effect of certain medications.
In psychology, emotional detachment, also known as emotional blunting, is a condition or state in which a person lacks emotional connectivity to others, whether due to an unwanted circumstance or as a positive means to cope with anxiety. Such a coping strategy, also known as emotion-focused coping, is used when avoiding certain situations that might trigger anxiety. It refers to the evasion of emotional connections. Emotional detachment may be a temporary reaction to a stressful situation, or a chronic condition such as depersonalization-derealization disorder. It may also be caused by certain antidepressants. Emotional blunting, also known as reduced affect display, is one of the negative symptoms of schizophrenia.
Cognitive slippage is considered a milder and sub-clinical presentation of formal thought disorder observed via unusual use of language. It is often identified when a person attempts to make tangential connections between concepts that are not immediately understandable to listeners. When observed repeatedly, this is taken as evidence for unusual, maladaptive or illogical thinking patterns.
A spectrum disorder is a disorder that includes a range of linked conditions, sometimes also extending to include singular symptoms and traits. The different elements of a spectrum either have a similar appearance or are thought to be caused by the same underlying mechanism. In either case, a spectrum approach is taken because there appears to be "not a unitary disorder but rather a syndrome composed of subgroups". The spectrum may represent a range of severity, comprising relatively "severe" mental disorders through to relatively "mild and nonclinical deficits".
The reward system is a group of neural structures responsible for incentive salience, associative learning, and positively-valenced emotions, particularly ones involving pleasure as a core component. Reward is the attractive and motivational property of a stimulus that induces appetitive behavior, also known as approach behavior, and consummatory behavior. A rewarding stimulus has been described as "any stimulus, object, event, activity, or situation that has the potential to make us approach and consume it is by definition a reward". In operant conditioning, rewarding stimuli function as positive reinforcers; however, the converse statement also holds true: positive reinforcers are rewarding.The reward system motivates animals to approach stimuli or engage in behaviour that increases fitness. Survival for most animal species depends upon maximizing contact with beneficial stimuli and minimizing contact with harmful stimuli. Reward cognition serves to increase the likelihood of survival and reproduction by causing associative learning, eliciting approach and consummatory behavior, and triggering positively-valenced emotions. Thus, reward is a mechanism that evolved to help increase the adaptive fitness of animals. In drug addiction, certain substances over-activate the reward circuit, leading to compulsive substance-seeking behavior resulting from synaptic plasticity in the circuit.
Asociality refers to the lack of motivation to engage in social interaction, or a preference for solitary activities. Asociality may be associated with avolition, but it can, moreover, be a manifestation of limited opportunities for social relationships. Developmental psychologists use the synonyms nonsocial, unsocial, and social uninterest. Asociality is distinct from, but not mutually exclusive to, anti-social behavior. A degree of asociality is routinely observed in introverts, while extreme asociality is observed in people with a variety of clinical conditions.
Childhood schizophrenia is similar in characteristics of schizophrenia that develops at a later age, but has an onset before the age of 13 years, and is more difficult to diagnose. Schizophrenia is characterized by positive symptoms that can include hallucinations, delusions, and disorganized speech; negative symptoms, such as blunted affect and avolition and apathy, and a number of cognitive impairments. Differential diagnosis is problematic since several other neurodevelopmental disorders, including autism spectrum disorder, language disorder, and attention deficit hyperactivity disorder, also have signs and symptoms similar to childhood-onset schizophrenia.
The diagnosis of schizophrenia, a psychotic disorder, is based on criteria in either the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders, or the World Health Organization's International Classification of Diseases (ICD). Clinical assessment of schizophrenia is carried out by a mental health professional based on observed behavior, reported experiences, and reports of others familiar with the person. Diagnosis is usually made by a psychiatrist. Associated symptoms occur along a continuum in the population and must reach a certain severity and level of impairment before a diagnosis is made. Schizophrenia has a prevalence rate of 0.3-0.7% in the United States.
The imprinted brain hypothesis is an unsubstantiated hypothesis in evolutionary psychology regarding the causes of autism spectrum and schizophrenia spectrum disorders, first presented by Bernard Crespi and Christopher Badcock in 2008. It claims that certain autistic and schizotypal traits are opposites, and that this implies the etiology of the two conditions must be at odds.
The evolution of schizophrenia refers to the theory of natural selection working in favor of selecting traits that are characteristic of the disorder. Positive symptoms are features that are not present in healthy individuals but appear as a result of the disease process. These include visual and/or auditory hallucinations, delusions, paranoia, and major thought disorders. Negative symptoms refer to features that are normally present but are reduced or absent as a result of the disease process, including social withdrawal, apathy, anhedonia, alogia, and behavioral perseveration. Cognitive symptoms of schizophrenia involve disturbances in executive functions, working memory impairment, and inability to sustain attention.
Emotion perception refers to the capacities and abilities of recognizing and identifying emotions in others, in addition to biological and physiological processes involved. Emotions are typically viewed as having three components: subjective experience, physical changes, and cognitive appraisal; emotion perception is the ability to make accurate decisions about another's subjective experience by interpreting their physical changes through sensory systems responsible for converting these observed changes into mental representations. The ability to perceive emotion is believed to be both innate and subject to environmental influence and is also a critical component in social interactions. How emotion is experienced and interpreted depends on how it is perceived. Likewise, how emotion is perceived is dependent on past experiences and interpretations. Emotion can be accurately perceived in humans. Emotions can be perceived visually, audibly, through smell and also through bodily sensations and this process is believed to be different from the perception of non-emotional material.
Social problem-solving, in its most basic form, is defined as problem solving as it occurs in the natural environment. More specifically it refers to the cognitive-behavioral process in which one works to find adaptive ways of coping with everyday situations that are considered problematic. This process in self-directed, conscious, effortful, cogent, and focused. Adaptive social problem-solving skills are known to be effective coping skills in an array of stressful situations. Social problem-solving consists of two major processes. One of these processes is known as problem orientation. Problem orientation is defined as the schemas one holds about problems in everyday life and ones assessment of their ability to solve said problems.
A self-disorder, also called ipseity disturbance, is a psychological phenomenon of disruption or diminishing of a person's minimal self – the fundamental sense that one's experiences are truly one's own. People with self-disorder feel that their internal experiences are actually external; for example, they may experience their own thoughts as coming from outside themselves, whether in the form of true auditory hallucinations or merely as a vague sense that their thoughts do not belong to them.
Watson and Clark (1991) proposed the Tripartite Model of Anxiety and Depression to help explain the comorbidity between anxious and depressive symptoms and disorders. This model divides the symptoms of anxiety and depression into three groups: negative affect, positive affect and physiological hyperarousal. These three sets of symptoms help explain common and distinct aspects of depression and anxiety.
However, there are two components to the positive affect experienced in rewarding situations - anticipatory positive affect (APA) and cunsummatory positive affect (CPA)...Berridge and Robinson [2] describe these constructs as 'wanting' and 'liking', respectively.