Trait theory

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https://en.wikipedia.org/wiki/Trait_theory 

In psychology, trait theory (also called dispositional theory) is an approach to the study of human personality. Trait theorists are primarily interested in the measurement of traits, which can be defined as habitual patterns of behavior, thought, and emotion. According to this perspective, traits are aspects of personality that are relatively stable over time, differ across individuals (e.g. some people are outgoing whereas others are not), are relatively consistent over situations, and influence behavior. Traits are in contrast to states, which are more transitory dispositions. 

In some theories and systems, traits are something a person either has or does not have, but in many others traits are dimensions such as extraversion vs. introversion, with each person rating somewhere along this spectrum. 

There are two approaches to define traits: as internal causal properties or as purely descriptive summaries. The internal causal definition states that traits influence our behaviours, leading us to do things in line with that trait. On the other hand, traits as descriptive summaries are descriptions of our actions that don't try to infer causality.

History

Gordon Allport was an early pioneer in the study of traits. This early work was viewed as the beginning of the modern psychological study of personality. He also referred to traits within his work as dispositions. In his approach, "cardinal" traits are those that dominate and shape a person's behavior; their ruling passions/obsessions, such as a need for money, fame etc. By contrast, "central" traits such as honesty are characteristics found in some degree in every person - and finally "secondary" traits are those seen only in certain circumstances (such as particular likes or dislikes that a very close friend may know), which are included to provide a complete picture of human complexity.

A wide variety of alternative theories and scales were later developed, including:

• Raymond Cattell's 16PF Questionnaire
• J. P. Guilford's Structure of Intellect
• Henry Murray's System of Needs
• Timothy Leary's Interpersonal circumplex
• Myers–Briggs Type Indicator
• Gray's Biopsychological theory of personality

Currently, two general approaches are the most popular:

• Eysenck Personality Questionnaire, (EPQ) ("the three-factor model"). Using factor analysis Hans Eysenck suggested that personality is reducible to three major traits: neuroticism, extraversion, and psychoticism.
• Big Five personality traits, ("the five-factor model"). Many psychologists currently believe that five factors are sufficient: neuroticism, extraversion, openness to experience, agreeableness, and conscientiousness.

Trait theory in cross-cultural use

Cultures are widely known and accepted as being different in varying degrees. This can make the study of personality difficult as meaning and the expression of traits may be different within cultural groups. Trait theory uses a hierarchy of traits in order to separate culture from the traits, it can be said the culture is ignored in order to focus of the individual traits and how they are connected to the individual. Gordon Allport's trait theory not only served as a foundational approach within personality psychology, but also is continued to be viewed and discussed by other disciplines such as anthropology because of how he approached culture within trait theory.

Trait theory tends to focus on the individual over the situation in which they are in. This focus has relaxed within modern studies allowing for a consideration of the external factors outside of the self. As the focus becomes more relaxed (but still prominent as it is a main part of the theory) research expands. 

Comparing EPQ and Big Five

Testing methodology, and factors

Both the EPQ and Big Five approaches extensively use self-report questionnaires. The factors are intended to be orthogonal (uncorrelated), though there are often small positive correlations between factors. The five factor model in particular has been criticized for losing the orthogonal structure between factors. Hans Eysenck has argued that fewer factors are superior to a larger number of partly related ones. Although these two approaches are comparable because of the use of factor analysis to construct hierarchical taxonomies, they differ in the organization and number of factors.

Whatever the causes, psychoticism marks the two approaches apart, as the five factor model contains no such trait. Moreover, psychoticism, unlike any of the other factors in either approach, does not fit a normal distribution curve. Indeed, scores are rarely high, thus skewing a normal distribution. However, when they are high, there is considerable overlap with psychiatric conditions such as antisocial and schizoid personality disorders. Similarly, high scorers on neuroticism are more susceptible to sleep and psychosomatic disorders. Five factor approaches can also predict future mental disorders.

Lower-order factors

Similarities between lower-order factors for psychoticism and the facets of openness, agreeableness, and conscientiousness (from Matthews, Deary & Whiteman, 2003)

 

There are two higher-order factors that both taxonomies clearly share: extraversion and neuroticism. Both approaches broadly accept that extraversion is associated with sociability and positive affect, whereas neuroticism is associated with emotional instability and negative affect.

Many lower-order factors, or facets, are similar between the two taxonomies. For instance, both approaches contain factors for sociability/gregariousness, for activity levels, and for assertiveness within the higher order factor extraversion. However, there are differences too. First, the three-factor approach contains nine lower-order factors and the five-factor approach has six.

Eysenck's psychoticism factor incorporates some of the polar opposites of the lower order factors of openness, agreeableness and conscientiousness. A high scorer on tough-mindedness in psychoticism would score low on tender-mindedness in agreeableness. Most of the differences between the taxonomies stem from the three factor model's emphasis on fewer high-order factors. 

Causality

Although both major trait models are descriptive, only the three-factor model offers a detailed causal explanation. Eysenck suggests that different personality traits are caused by the properties of the brain, which themselves are the result of genetic factors. In particular, the three-factor model identifies the reticular system and the limbic system in the brain as key components that mediate cortical arousal and emotional responses respectively. Eysenck advocates that extraverts have low levels of cortical arousal and introverts have high levels, leading extraverts to seek out more stimulation from socializing and being venturesome. Moreover, Eysenck surmised that there would be an optimal level of arousal, after which inhibition would occur and that this would be different for each person.

In a similar vein, the three-factor approach theorizes that neuroticism is mediated by levels of arousal in the limbic system and that individual differences arise because of variable activation thresholds between people. Therefore, highly neurotic people when presented with minor stressors, will exceed this threshold, whereas people low in neuroticism will not exceed normal activation levels, even when presented with large stressors. By contrast, proponents of the five-factor approach assume a role of genetics and environment but offer no explicit causal explanation.

Given this emphasis on biology in the three-factor approach, it would be expected that the third trait, psychoticism, would have a similar explanation. However, the causal properties of this state are not well defined. Eysenck has suggested that psychoticism is related to testosterone levels and is an inverse function of the serotonergic system, but he later revised this, linking it instead to the dopaminergic system.

List of personality traits

Personality traits

Openness to experience	Composed of two related but separable traits, Openness to Experience and Intellect. Behavioral aspects include having wide interests, and being imaginative and insightful, correlated with activity in the dorsolateral prefrontal cortex. Considered primarily a cognitive trait.
Conscientiousness	Scrupulous, meticulous, principled behavior guided or conforming to one's own conscience. Associated with the dorsolateral prefrontal cortex.
Extraversion	Gregarious, outgoing, sociable, projecting one's personality outward. The opposite of extraversion is introversion. Extraversion has shown to share certain genetic markers with substance abuse. Extraversion is associated with various regions of the prefrontal cortex and the amygdala.
Agreeableness	Refers to a compliant, trusting, empathic, sympathetic, friendly and cooperative nature.
Neuroticism	Identifies people who are prone to psychological distress. Individuals who are high in neuroticism tend to be anxious, depressed, self-conscious, impulsive, vulnerable and display angry hostility. "Neuroticism is the major factor of personality pathology" (Eysenck & Eysenck, 1969). Neuroticism has been linked to serotonin transporter (5-HTT) binding sites in the thalamus: as well as activity in the insular cortex. Neuroticism also predicts the occurrence of more negative life experiences.
Honesty-humility	Tendency towards sincerity, modesty, fairness, and greed avoidance. Those who score high on this trait feel little desire to manipulate others or to break the rules for personal gain.
Self-esteem (low)	A "favorable or unfavorable attitude toward the self" (Rosenberg, 1965). An individual's sense of his or her value or worth, or the extent to which a person values, approves of, appreciates, prizes, or likes him or herself" (Blascovich & Tomaka, 1991).
Harm avoidance	A tendency towards shyness, being fearful and uncertain, tendency to worry. Neonatal complications such as preterm birth have been shown to affect harm avoidance. People affected by eating disorders exhibit high levels of harm avoidance. The volume of the left amygdala in girls was correlated to levels of HA, in separate studies HA was correlated with reduced grey matter volume in the orbitofrontal, occipital and parietal regions.
Novelty seeking	Impulsive, exploratory, fickle, excitable, quick-tempered, and extravagant. Associated with addictive behavior.
Sensory processing sensitivity (SPS)	The defining trait of highly sensitive persons, characterized by the increased depth of processing of sensory input that underlies HSPs' greater proclivity to overstimulation, emotional reactivity and empathy, and sensitivity to stimuli.
Perfectionism	"I don't think needing to be perfect is in any way adaptive." (Paul Hewitt, PhD) Socially prescribed perfectionism – "believing that others will value you only if you are perfect." Self-oriented perfectionism – "an internally motivated desire to be perfect." Perfectionism is one of the traits associated with obsessional behavior and like obsessionality is also believed to be regulated by the basal ganglia.
Alexithymia	The inability to express emotions. "To have no words for one's inner experience" (Rený J. Muller PhD). In studies done with stroke patients, alexithymia was found to be more prevalent in those who developed lesions in the right hemisphere following a cerebral infarction. There is a positive association with post-traumatic stress disorder (PTSD), childhood abuse and neglect and alexithymia. Utilizing psychometric testing and fMRI, studies showed positive response in the insula, posterior cingulate cortex (PCC), and thalamus.
Rigidity	Inflexibility, difficulty making transitions, adherence to set patterns. Mental rigidity arises out of a deficit of the executive functions. Originally termed frontal lobe syndrome it is also referred to as dysexecutive syndrome and usually occurs as a result of damage to the frontal lobe. This may be due to physical damage, disease (such as Huntington's disease) or a hypoxic or anoxic insult.
Impulsivity	Risk taking, lack of planning, and making up one's mind quickly (Eysenck and Eysenck). A component of disinhibition. Abnormal patterns of impulsivity have been linked to lesions in the right inferior frontal gyrus and in studies done by Antonio Damasio author of Descartes Error, damage to the ventromedial prefrontal cortex has been shown to cause a defect in real-life decision making in individuals with otherwise normal intellect. Those who sustain this type of damage are oblivious to the future consequences of their actions and live in the here and now.
Disinhibition	Behavioral disinhibition is an inability or unwillingness to constrain impulses, it is a key component of executive functioning. Researchers have emphasized poor behavioral inhibition as the central impairment of ADHD. It may be symptomatic of orbitofrontal lobe syndrome, a subtype of frontal lobe syndrome which may be an acquired disorder as a result of traumatic brain injury, hypoxic ischemic encephalopathy (HIE), anoxic encephalopathy, degenerative diseases such as Parkinson's, bacterial or viral infections such as Lyme disease and neurosyphilis. Disinhibition has been consistently associated with substance abuse disorders, obesity, higher BMI, excessive eating, an increased rate of eating, and perceived hunger.
Psychoticism	Psychoticism is a personality pattern typified by aggressiveness and interpersonal hostility, one of four traits in Hans Eysenck's model of personality. High levels of this trait were believed by Eysenck to be linked to increased vulnerability to psychosis such as schizophrenia. He also believed that blood relatives of psychotics would show high levels of this trait, suggesting a genetic basis to the trait.
Obsessionality	Persistent, often unwelcome, and frequently disturbing ideas, thoughts, images or emotions, rumination, often inducing an anxious state. Obsessionality may result as a dysfunction of the basal ganglia.

Mania

From Wikipedia, the free encyclopedia

https://en.wikipedia.org/wiki/Mania

Mania
Other names	Manic syndrome, manic episode
Graphical representation of mania and hypomania
Specialty	Psychiatry

Mania, also known as manic syndrome, is a state of abnormally elevated arousal, affect, and energy level, or "a state of heightened overall activation with enhanced affective expression together with lability of affect." Although mania is often conceived as a "mirror image" to depression, the heightened mood can be either euphoric or irritable; indeed, as the mania intensifies, irritability can be more pronounced and result in anxiety, or violence.

The symptoms of mania include elevated mood (either euphoric or irritable), flight of ideas and pressure of speech, increased energy, decreased need and desire for sleep, and hyperactivity. They are most plainly evident in fully developed hypomanic states. However, in full-blown mania, they undergo progressively severe exacerbations and become more and more obscured by other signs and symptoms, such as delusions and fragmentation of behavior.

Causes and Diagnosis

Mania is a syndrome with multiple causes. Although the vast majority of cases occur in the context of bipolar disorder, it is a key component of other psychiatric disorders (such as schizoaffective disorder, bipolar type) and may also occur secondary to various general medical conditions, such as multiple sclerosis; certain medications may perpetuate a manic state, for example prednisone; or substances prone to abuse, especially stimulants, such as caffeine and cocaine. In the current DSM-5, hypomanic episodes are separated from the more severe full manic episodes, which, in turn, are characterized as either mild, moderate, or severe, with certain diagnostic criteria (e.g. catatonia, psychosis). Mania is divided into three stages: hypomania, or stage I; acute mania, or stage II; and delirious mania (delirium), or stage III. This "staging" of a manic episode is useful from a descriptive and differential diagnostic point of view.

Mania varies in intensity, from mild mania (hypomania) to delirious mania, marked by such symptoms as disorientation, florid psychosis, incoherence, and catatonia. Standardized tools such as Altman Self-Rating Mania Scale and Young Mania Rating Scale can be used to measure severity of manic episodes. Because mania and hypomania have also long been associated with creativity and artistic talent, it is not always the case that the clearly manic/hypomanic bipolar patient needs or wants medical help; such persons often either retain sufficient self-control to function normally or are unaware that they have "gone manic" severely enough to be committed or to commit themselves. Manic persons often can be mistaken for being under the influence of drugs.

Classification

Mixed states

In a mixed affective state, the individual, though meeting the general criteria for a hypomanic (discussed below) or manic episode, experiences three or more concurrent depressive symptoms. This has caused some speculation, among clinicians, that mania and depression, rather than constituting "true" polar opposites, are, rather, two independent axes in a unipolar—bipolar spectrum.

A mixed affective state, especially with prominent manic symptoms, places the patient at a greater risk for completed suicide. Depression on its own is a risk factor but, when coupled with an increase in energy and goal-directed activity, the patient is far more likely to act with violence on suicidal impulses.

Associated disorders

A single manic episode, in the absence of secondary causes, (i.e., substance use disorders, pharmacologics, or general medical conditions) is often sufficient to diagnose bipolar I disorder. Hypomania may be indicative of bipolar II disorder. Manic episodes are often complicated by delusions and/or hallucinations; and if the psychotic features persist for a duration significantly longer than the episode of typical mania (two weeks or more), a diagnosis of schizoaffective disorder is more appropriate. Certain obsessive-compulsive spectrum disorders as well as impulse control disorders share the suffix "-mania," namely, kleptomania, pyromania, and trichotillomania. Despite the unfortunate association implied by the name, however, no connection exists between mania or bipolar disorder and these disorders. Furthermore, evidence indicates a B₁₂ deficiency can also cause symptoms characteristic of mania and psychosis.

Hyperthyroidism can produce similar symptoms to those of mania, such as agitation, elevated mood, increased energy, hyperactivity, sleep disturbances and sometimes, especially in severe cases, psychosis.

Signs and symptoms

A manic episode is defined in the American Psychiatric Association's diagnostic manual as a "distinct period of abnormally and persistently elevated, expansive, or irritable mood and abnormally and persistently increased activity or energy, lasting at least 1 week and present most of the day, nearly every day (or any duration, if hospitalization is necessary)," where the mood is not caused by drugs/medication or a non-mental medical illness (e.g., hyperthyroidism), and: (a) is causing obvious difficulties at work or in social relationships and activities, or (b) requires admission to hospital to protect the person or others, or (c) the person is suffering psychosis.

To be classified as a manic episode, while the disturbed mood and an increase in goal directed activity or energy is present, at least three (or four, if only irritability is present) of the following must have been consistently present:

1. Inflated self-esteem or grandiosity.
2. Decreased need for sleep (e.g., feels rested after 3 hours of sleep).
3. More talkative than usual, or acts pressured to keep talking.
4. Flights of ideas or subjective experience that thoughts are racing.
5. Increase in goal directed activity, or psychomotor acceleration.
6. Distractibility (too easily drawn to unimportant or irrelevant external stimuli).
7. Excessive involvement in activities with a high likelihood of painful consequences.(e.g., extravagant shopping, improbable commercial schemes, hypersexuality).

Though the activities one participates in while in a manic state are not always negative, those with the potential to have negative outcomes are far more likely.

If the person is concurrently depressed, they are said to be having a mixed episode.

The World Health Organization's classification system defines a manic episode as one where mood is higher than the person's situation warrants and may vary from relaxed high spirits to barely controllable exuberance, is accompanied by hyperactivity, a compulsion to speak, a reduced sleep requirement, difficulty sustaining attention and/or often increased distractibility. Frequently, confidence and self-esteem are excessively enlarged, and grand, extravagant ideas are expressed. Behavior that is out of character and risky, foolish or inappropriate may result from a loss of normal social restraint.

Some people also have physical symptoms, such as sweating, pacing, and weight loss. In full-blown mania, often the manic person will feel as though his or her goal(s) are of paramount importance, that there are no consequences or that negative consequences would be minimal, and that they need not exercise restraint in the pursuit of what they are after. Hypomania is different, as it may cause little or no impairment in function. The hypomanic person's connection with the external world, and its standards of interaction, remain intact, although intensity of moods is heightened. But those who suffer from prolonged unresolved hypomania do run the risk of developing full mania, and indeed may cross that "line" without even realizing they have done so.

One of the signature symptoms of mania (and to a lesser extent, hypomania) is what many have described as racing thoughts. These are usually instances in which the manic person is excessively distracted by objectively unimportant stimuli. This experience creates an absent-mindedness where the manic individual's thoughts totally preoccupy him or her, making him or her unable to keep track of time, or be aware of anything besides the flow of thoughts. Racing thoughts also interfere with the ability to fall asleep.

Manic states are always relative to the normal state of intensity of the afflicted individual; thus, already irritable patients may find themselves losing their tempers even more quickly, and an academically gifted person may, during the hypomanic stage, adopt seemingly "genius" characteristics and an ability to perform and articulate at a level far beyond that which they would be capable of during euthymia. A very simple indicator of a manic state would be if a heretofore clinically depressed patient suddenly becomes inordinately energetic, enthusiastic, cheerful, aggressive, or "over happy". Other, often less obvious, elements of mania include delusions (generally of either grandeur or persecution, according to whether the predominant mood is euphoric or irritable), hypersensitivity, hypervigilance, hypersexuality, hyper-religiosity, hyperactivity and impulsivity, a compulsion to over explain (typically accompanied by pressure of speech), grandiose schemes and ideas, and a decreased need for sleep (for example, feeling rested after only 3 or 4 hours of sleep). In the case of the latter, the eyes of such patients may both look and seem abnormally "wide open", rarely blinking, and may contribute to some clinicians’ erroneous belief that these patients are under the influence of a stimulant drug, when the patient, in fact, is either not on any mind-altering substances or is actually on a depressant drug. Individuals may also engage in out-of-character behavior during the episode, such as questionable business transactions, wasteful expenditures of money (e.g., spending sprees), risky sexual activity, abuse of recreational substances, excessive gambling, reckless behavior (such as extreme speeding or other daredevil activity), abnormal social interaction (e.g. over familiarity and conversing with strangers), or highly vocal arguments. These behaviours may increase stress in personal relationships, lead to problems at work, and increase the risk of altercations with law enforcement. There is a high risk of impulsively taking part in activities potentially harmful to the self and others.

Although "severely elevated mood" sounds somewhat desirable and enjoyable, the experience of mania is ultimately often quite unpleasant and sometimes disturbing, if not frightening, for the person involved and for those close to them, and it may lead to impulsive behaviour that may later be regretted. It can also often be complicated by the sufferer's lack of judgment and insight regarding periods of exacerbation of characteristic states. Manic patients are frequently grandiose, obsessive, impulsive, irritable, belligerent, and frequently deny anything is wrong with them. Because mania frequently encourages high energy and decreased perception of need or ability to sleep, within a few days of a manic cycle, sleep-deprived psychosis may appear, further complicating the ability to think clearly. Racing thoughts and misperceptions lead to frustration and decreased ability to communicate with others.

Mania may also, as earlier mentioned, be divided into three “stages”. Stage I corresponds with hypomania and may feature typical hypomanic characteristics, such as gregariousness and euphoria. In stages II and III mania, however, the patient may be extraordinarily irritable, psychotic or even delirious. These latter two stages are referred to as acute and delirious (or Bell's), respectively.

Cause

Various triggers have been associated with switching from euthymic or depressed states into mania. One common trigger of mania is antidepressant therapy. Studies show that the risk of switching while on an antidepressant is between 6-69 percent. Dopaminergic drugs such as reuptake inhibitors and dopamine agonists may also increase risk of switch. Other medication possibly include glutaminergic agents and drugs that alter the HPA axis. Lifestyle triggers include irregular sleep-wake schedules and sleep deprivation, as well as extremely emotional or stressful stimuli.

Various genes that have been implicated in genetic studies of bipolar have been manipulated in preclinical animal models to produce syndromes reflecting different aspects of mania. CLOCK and DBP polymorphisms have been linked to bipolar in population studies, and behavioral changes induced by knockout are reversed by lithium treatment. Metabotropic glutamate receptor 6 has been genetically linked to bipolar, and found to be under-expressed in the cortex. Pituitary adenylate cyclase-activating peptide has been associated with bipolar in gene linkage studies, and knockout in mice produces mania like-behavior. Targets of various treatments such as GSK-3, and ERK1 have also demonstrated mania like behavior in preclinical models.

Mania may be associated with strokes, especially cerebral lesions in the right hemisphere.

Deep brain stimulation of the subthalamic nucleus in Parkinson's disease has been associated with mania, especially with electrodes placed in the ventromedial STN. A proposed mechanism involves increased excitatory input from the STN to dopaminergic nuclei.

Mania can also be caused by physical trauma or illness. When the causes are physical, it is called secondary mania.

Mechanism

The mechanism underlying mania is unknown, but the neurocognitive profile of mania is highly consistent with dysfunction in the right prefrontal cortex, a common finding in neuroimaging studies. Various lines of evidence from post-mortem studies and the putative mechanisms of anti-manic agents point to abnormalities in GSK-3, dopamine, Protein kinase C and Inositol monophosphatase.

Meta analysis of neuroimaging studies demonstrate increased thalamic activity, and bilaterally reduced inferior frontal gyrus activation. Activity in the amygdala and other subcortical structures such as the ventral striatum tend to be increased, although results are inconsistent and likely dependent upon task characteristics such as valence. Reduced functional connectivity between the ventral prefrontal cortex and amygdala along with variable findings supports a hypothesis of general dysregulation of subcortical structures by the prefrontal cortex. A bias towards positively valenced stimuli, and increased responsiveness in reward circuitry may predispose towards mania. Mania tends to be associated with right hemisphere lesions, while depression tends to be associated with left hemisphere lesions.

Post-mortem examinations of bipolar disorder demonstrate increased expression of Protein Kinase C (PKC). While limited, some studies demonstrate manipulation of PKC in animals produces behavioral changes mirroring mania, and treatment with PKC inhibitor tamoxifen (also an anti-estrogen drug) demonstrates antimanic effects. Traditional antimanic drugs also demonstrate PKC inhibiting properties, among other effects such as GSK3 inhibition.

Manic episodes may be triggered by dopamine receptor agonists, and this combined with tentative reports of increased VMAT2 activity, measured via PET scans of radioligand binding, suggests a role of dopamine in mania. Decreased cerebrospinal fluid levels of the serotonin metabolite 5-HIAA have been found in manic patients too, which may be explained by a failure of serotonergic regulation and dopaminergic hyperactivity.

Limited evidence suggests that mania is associated with behavioral reward hypersensitivity, as well as with neural reward hypersensitivity. Electrophysiological evidence supporting this comes from studies associating left frontal EEG activity with mania. As left frontal EEG activity is generally thought to be a reflection of behavioral activation system activity, this is thought to support a role for reward hypersensitivity in mania. Tentative evidence also comes from one study that reported an association between manic traits and feedback negativity during receipt of monetary reward or loss. Neuroimaging evidence during acute mania is sparse, but one study reported elevated orbitofrontal cortex activity to monetary reward, and another study reported elevated striatal activity to reward omission. The latter finding was interpreted in the context of either elevated baseline activity (resulting in a null finding of reward hypersensitivity), or reduced ability to discriminate between reward and punishment, still supporting reward hyperactivity in mania. Punishment hyposensitivity, as reflected in a number of neuroimaging studies as reduced lateral orbitofrontal response to punishment, has been proposed as a mechanism of reward hypersensitivity in mania.

Diagnosis

In the ICD-10 there are several disorders with the manic syndrome: organic manic disorder (F06.30), mania without psychotic symptoms (F30.1), mania with psychotic symptoms (F30.2), other manic episodes (F30.8), unspecified manic episode (F30.9), manic type of schizoaffective disorder (F25.0), bipolar affective disorder, current episode manic without psychotic symptoms (F31.1), bipolar affective disorder, current episode manic with psychotic symptoms (F31.2). 

Treatment

Before beginning treatment for mania, careful differential diagnosis must be performed to rule out secondary causes.

The acute treatment of a manic episode of bipolar disorder involves the utilization of either a mood stabilizer (valproate, lithium, lamotrigine, or carbamazepine) or an atypical antipsychotic (olanzapine, quetiapine, risperidone, or aripiprazole). Although hypomanic episodes may respond to a mood stabilizer alone, full-blown episodes are treated with an atypical antipsychotic (often in conjunction with a mood stabilizer, as these tend to produce the most rapid improvement).

When the manic behaviours have gone, long-term treatment then focuses on prophylactic treatment to try to stabilize the patient's mood, typically through a combination of pharmacotherapy and psychotherapy. The likelihood of having a relapse is very high for those who have experienced two or more episodes of mania or depression. While medication for bipolar disorder is important to manage symptoms of mania and depression, studies show relying on medications alone is not the most effective method of treatment. Medication is most effective when used in combination with other bipolar disorder treatments, including psychotherapy, self-help coping strategies, and healthy lifestyle choices.

Lithium is the classic mood stabilizer to prevent further manic and depressive episodes. A systematic review found that long term lithium treatment substantially reduces the risk of bipolar manic relapse, by 42%. Anticonvulsants such as valproate, oxcarbazepine and carbamazepine are also used for prophylaxis. More recent drug solutions include lamotrigine and topiramate, both anticonvulsants as well. 

In some cases, long-acting benzodiazepines, particularly clonazepam, are used after other options are exhausted. In more urgent circumstances, such as in emergency rooms, lorazepam has been used to promptly alleviate symptoms of agitation, aggression, and psychosis. Sometimes atypical antipsychotics are used in combination with the previous mentioned medications as well, including olanzapine which helps treat hallucinations or delusions, asenapine, aripiprazole, risperidone, ziprasidone, and clozapine which is often used for people who do not respond to lithium or anticonvulsants. 

Verapamil, a calcium-channel blocker, is useful in the treatment of hypomania and in those cases where lithium and mood stabilizers are contraindicated or ineffective. Verapamil is effective for both short-term and long-term treatment.

Antidepressant monotherapy is not recommended for the treatment of depression in patients with bipolar disorders I or II, and no benefit has been demonstrated by combining antidepressants with mood stabilizers in these patients. Some atypical antidepressants, however, such as mirtazepine and trazodone have been occasionally used after other options have failed.

Society and culture

In Electroboy: A Memoir of Mania by Andy Behrman, he describes his experience of mania as "the most perfect prescription glasses with which to see the world... life appears in front of you like an oversized movie screen". Behrman indicates early in his memoir that he sees himself not as a person suffering from an uncontrollable disabling illness, but as a director of the movie that is his vivid and emotionally alive life. There is some evidence that people in the creative industries suffer from bipolar disorder more often than those in other occupations. Winston Churchill had periods of manic symptoms that may have been both an asset and a liability.

English actor Stephen Fry, who suffers from bipolar disorder, recounts manic behaviour during his adolescence: "When I was about 17 ... going around London on two stolen credit cards, it was a sort of fantastic reinvention of myself, an attempt to. I bought ridiculous suits with stiff collars and silk ties from the 1920s, and would go to the Savoy and Ritz and drink cocktails." While he has experienced suicidal thoughts, he says the manic side of his condition has had positive contributions on his life.

Etymology

The nosology of the various stages of a manic episode has changed over the decades. The word derives from the Ancient Greek μανία (manía), "madness, frenzy" and the verb μαίνομαι (maínomai), "to be mad, to rage, to be furious".

Hypomania

From Wikipedia, the free encyclopedia

https://en.wikipedia.org/wiki/Hypomania

 

Hypomania
Graphical representation of hypomania and mania
Specialty	Psychiatry

Hypomania (literally "under mania" or "less than mania") is a mood state characterized by persistent disinhibition and mood elevation (euphoria), with behavior that is noticeably different from the person's typical behavior when in a non-depressed state. It may involve irritability, but less severely than full mania. According to DSM-5 criteria, hypomania is distinct from mania in that there is no significant functional impairment; mania, by DSM-5 definition, does include significant functional impairment and may have psychotic features.

Characteristic behaviors of persons experiencing hypomania are a notable decrease in the need for sleep, an overall increase in energy, unusual behaviors and actions, and a markedly distinctive increase in talkativeness and confidence, commonly exhibited with a flight of creative ideas. Other symptoms related to this may include feelings of grandiosity, distractibility, and hypersexuality. While hypomanic behavior often generates productivity and excitement, it can become troublesome if the subject engages in risky or otherwise inadvisable behaviors, and/or the symptoms manifest themselves in trouble with everyday life events. When manic episodes are separated into stages of a progression according to symptomatic severity and associated features, hypomania constitutes the first stage of the syndrome, wherein the cardinal features (euphoria or heightened irritability, pressure of speech and activity, increased energy, decreased need for sleep, and flight of ideas) are most plainly evident.

Signs and symptoms

Individuals in a hypomanic state have a decreased need for sleep, are extremely gregarious and competitive, and have a great deal of energy. They are, otherwise, often fully functioning (unlike individuals suffering from a full manic episode).

Distinctive markers

Specifically, hypomania is distinguished from mania by the absence of psychotic symptoms and grandiosity, and by its lesser degree of impact on functioning.

Hypomania is a feature of bipolar II disorder and cyclothymia, but can also occur in schizoaffective disorder. Hypomania is also a feature of bipolar I disorder; it arises in sequential procession as the mood disorder fluctuates between normal mood (euthymia) and mania. Some individuals with bipolar I disorder have hypomanic as well as manic episodes. Hypomania can also occur when moods progress downwards from a manic mood state to a normal mood. Hypomania is sometimes credited with increasing creativity and productive energy. Numerous people with bipolar disorder have credited hypomania with giving them an edge in their theater of work.

People who experience hyperthymia, or "chronic hypomania", encounter the same symptoms as hypomania but on a longer-term basis.

Associated disorders

Cyclothymia, a condition of continuous mood fluctuations, is characterized by oscillating experiences of hypomania and depression that fail to meet the diagnostic criteria for either manic or major depressive episodes. These periods are often interspersed with periods of relatively normal (euthymic) functioning.

When a patient presents with a history of at least one episode of both hypomania and major depression, each of which meet the diagnostic criteria, bipolar II disorder is diagnosed. In some cases, depressive episodes routinely occur during the fall or winter and hypomanic ones in the spring or summer. In such cases, one speaks of a "seasonal pattern".

If left untreated, and in those so predisposed, hypomania may transition into mania, which may be psychotic, in which case bipolar I disorder is the correct diagnosis.

Causes

Often in those who have experienced their first episode of hypomania – generally without psychotic features – there may be a long or recent history of depression or a mix of hypomania combined with depression (known as mixed-state) prior to the emergence of manic symptoms. This commonly surfaces in the mid to late teens. Because the teenage years are typically an emotionally charged time of life, it is not unusual for mood swings to be passed off as normal hormonal teen behavior and for a diagnosis of bipolar disorder to be missed until there is evidence of an obvious manic or hypomanic phase.

In cases of drug-induced hypomanic episodes in unipolar depressives, the hypomania can almost invariably be eliminated by lowering medication dosage, withdrawing the drug entirely, or changing to a different medication if discontinuation of treatment is not possible.

Hypomania can be associated with narcissistic personality disorder.

Psychopathology

Mania and hypomania are usually studied together as components of bipolar disorders, and the pathophysiology is usually assumed to be the same. Given that norepinephrine and dopaminergic drugs are capable of triggering hypomania, theories relating to monoamine hyperactivity have been proposed. A theory unifying depression and mania in bipolar individuals proposes that decreased serotonergic regulation of other monoamines can result in either depressive or manic symptoms. Lesions on the right side frontal and temporal lobes have further been associated with mania.

Diagnosis

The DSM-IV-TR defines a hypomanic episode as including, over the course of at least four days, elevated mood plus three of the following symptoms OR irritable mood plus four of the following symptoms, when the behaviors are clearly different from how the person typically acts when not depressed:

• pressured speech
• inflated self-esteem or grandiosity
• decreased need for sleep
• flight of ideas or the subjective experience that thoughts are racing
• easily distracted
• increase in goal-directed activity (e.g., social activity, at work, or hypersexuality), or psychomotor agitation
• involvement in pleasurable activities that may have a high potential for negative psycho-social or physical consequences (e.g., the person engages in unrestrained buying sprees, sexual indiscretions, reckless driving, physical and verbal conflicts, foolish business investments, quitting a job to pursue some grandiose goal, etc).

Medications

Antimanic drugs are used to control acute attacks and prevent recurring episodes of hypomania combined with a range of psychological therapies. The recommended length of treatment ranges from 2 years to 5 years. Anti-Depressants may also be required for existing treatments but are avoided in patients who have had a recent history with hypomania. Sertraline has often been debated to have side effects that can trigger hypomania.

These include:

• Aripiprazole
• Clozapine
• Haloperidol
• Olanzapine
• Quetiapine
• Risperidone

Other anti-manic drugs that are not antipsychotics include:-

• Clonazepam
• Lorazepam
• Lithium
• Valproate

Other drugs used to treat symptoms of mania/hypomania but considered less effective include:-

• Gabapentin
• Lamotrigine
• Levetiracetam
• Oxcarbazepine
• Ritanserin
• Topiramate
• Ziprasidone

Etymology

The Ancient Greek physician Hippocrates called one personality type 'hypomanic' (Greek: ὑπομαινόμενοι, hypomainómenoi). In 19th century psychiatry, when mania had a broad meaning of insanity, hypomania was equated by some to concepts of 'partial insanity' or monomania. A more specific usage was advanced by the German neuro-psychiatrist Emanuel Ernst Mendel in 1881, who wrote, "I recommend, taking into consideration the word used by Hippocrates, to name those types of mania that show a less severe phenomenological picture, 'hypomania'". Narrower operational definitions of hypomania were developed in the 1960s and 1970s.

Referred pain

From Wikipedia, the free encyclopedia

https://en.wikipedia.org/wiki/Referred_pain

 

Referred pain
Conscious perception of visceral sensations map to specific regions of the body, as shown in this chart. Some sensations are felt locally, whereas others are perceived as affecting areas that are quite distant from the involved organ.
Identifiers
MeSH	D053591

Referred pain, also called reflective pain, is pain perceived at a location other than the site of the painful stimulus. An example is the case of angina pectoris brought on by a myocardial infarction (heart attack), where pain is often felt in the neck, shoulders, and back rather than in the thorax (chest), the site of the injury. The International Association for the Study of Pain has not officially defined the term; hence several authors have defined it differently.

Radiating pain is slightly different from referred pain; for example, the pain related to a myocardial infarction could either be referred or radiating pain from the chest. Referred pain is when the pain is located away from or adjacent to the organ involved; for instance, when a person has pain only in their jaw or left arm, but not in the chest. Referred pain has been described since the late 1880s. Despite an increasing amount of literature on the subject, the biological mechanism of referred pain is unknown, although there are several hypotheses.

Characteristics

• The size of referred pain is related to the intensity and duration of ongoing/evoked pain.
• Temporal summation is a potent mechanism for generation of referred muscle pain.
• Central hyperexcitability is important for the extent of referred pain.
• Patients with chronic musculoskeletal pains have enlarged referred pain areas to experimental stimuli. The proximal spread of referred muscle pain is seen in patients with chronic musculoskeletal pain and very seldom is it seen in healthy individuals.
• Modality-specific somatosensory changes occur in referred areas, which emphasize the importance of using a multimodal sensory test regime for assessment.
• Referred pain is often experienced on the same side of the body as the source, but not always.

Mechanism

There are several proposed mechanisms for referred pain. Currently there is no definitive consensus regarding which is correct. The cardiac general visceral sensory pain fibers follow the sympathetics back to the spinal cord and have their cell bodies located in thoracic dorsal root ganglia 1-4(5). As a general rule, in the thorax and abdomen, general visceral afferent (GVA) pain fibers follow sympathetic fibers back to the same spinal cord segments that gave rise to the preganglionic sympathetic fibers. The central nervous system (CNS) perceives pain from the heart as coming from the somatic portion of the body supplied by the thoracic spinal cord segments 1-4(5). Classically the pain associated with a myocardial infarction is located in the mid or left side of the chest where the heart is actually located. The pain can radiate to the left side of the jaw and into the left arm. Myocardial infarction can rarely present as referred pain and this usually occurs in people with diabetes or older age. Also, the dermatomes of this region of the body wall and upper limb have their neuronal cell bodies in the same dorsal root ganglia (T1-5) and synapse in the same second order neurons in the spinal cord segments (T1-5) as the general visceral sensory fibers from the heart. The CNS does not clearly discern whether the pain is coming from the body wall or from the viscera, but it perceives the pain as coming from somewhere on the body wall, i.e. substernal pain, left arm/hand pain, jaw pain. 

Convergent-projection

This represents one of the earliest theories on the subject of referred pain. It is based on the work of W.A. Sturge and J. Ross from 1888 and later TC Ruch in 1961. Convergent projection proposes that afferent nerve fibers from tissues converge onto the same spinal neuron, and explains why referred pain is believed to be segmented in much the same way as the spinal cord. Additionally, experimental evidence shows that when local pain (pain at the site of stimulation) is intensified the referred pain is intensified as well. 

Criticism of this model arises from its inability to explain why there is a delay between the onset of referred pain after local pain stimulation. Experimental evidence also shows that referred pain is often unidirectional. For example, stimulated local pain in the anterior tibial muscle causes referred pain in the ventral portion of the ankle; however referred pain moving in the opposite direction has not been shown experimentally. Lastly, the threshold for the local pain stimulation and the referred pain stimulation are different, but according to this model they should both be the same.

Convergence-facilitation

Convergence facilitation was conceived in 1893 by J MacKenzie based on the ideas of Sturge and Ross. He believed that the internal organs were insensitive to stimuli. Furthermore, he believed that non-nociceptive afferent inputs to the spinal cord created what he termed "an irritable focus". This focus caused some stimuli to be perceived as referred pain. However, his ideas did not gain widespread acceptance from critics due to its dismissal of visceral pain.

Recently this idea has regained some credibility under a new term, central sensitization. Central sensitization occurs when neurons in the spinal cord's dorsal horn or brainstem become more responsive after repeated stimulation by peripheral neurons, so that weaker signals can trigger them. The delay in appearance of referred pain shown in laboratory experiments can be explained due to the time required to create the central sensitization.

Axon-reflex

Axon reflex suggests that the afferent fiber is bifurcated before connecting to the dorsal horn. Bifurcated fibers do exist in muscle, skin, and intervertebral discs. Yet these particular neurons are rare and are not representative of the whole body. Axon-Reflex also does not explain the time delay before the appearance of referred pain, threshold differences for stimulating local and referred pain, and somatosensory sensibility changes in the area of referred pain.

Hyperexcitability

Hyperexcitability hypothesizes that referred pain has no central mechanism. However, it does say that there is one central characteristic that predominates. Experiments involving noxious stimuli and recordings from the dorsal horn of animals revealed that referred pain sensations began minutes after muscle stimulation. Pain was felt in a receptive field that was some distance away from the original receptive field. According to hyperexcitability, new receptive fields are created as a result of the opening of latent convergent afferent fibers in the dorsal horn. This signal could then be perceived as referred pain.

Several characteristics are in line with this mechanism of referred pain, such as dependency on stimulus and the time delay in the appearance of referred pain as compared to local pain. However, the appearance of new receptive fields, which is interpreted to be referred pain, conflicts with the majority of experimental evidence from studies including studies of healthy individuals. Furthermore, referred pain generally appears within seconds in humans as opposed to minutes in animal models. Some scientists attribute this to a mechanism or influence downstream in the supraspinal pathways. Neuroimaging techniques such as PET scans or fMRI may visualize the underlying neural processing pathways responsible in future testing.

Thalamic-convergence

Thalamic convergence suggests that referred pain is perceived as such due to the summation of neural inputs in the brain, as opposed to the spinal cord, from the injured area and the referred area. Experimental evidence on thalamic convergence is lacking. However, pain studies performed on monkeys revealed convergence of several pathways upon separate cortical and subcortical neurons. 

Examples

Location	Description
Upper chest/left limb	Myocardial ischaemia (the loss of blood flow to a part of the heart muscle tissue) is possibly the best known example of referred pain; the sensation can occur in the upper chest as a restricted feeling, or as an ache in the left shoulder, arm or even hand.
Head	"Ice-cream headache" or "brain freeze" is another example of referred pain, in which the vagus nerve or the trigeminal nerve in the throat and the palate, respectively, transmit pain signals, because of the rapid cooling and rewarming of the capillaries in the sinuses.[4]
General	Phantom limb pain, a type of referred pain, is the sensation of pain from a limb that has been lost or from which a person no longer receives physical signals. It is an experience almost universally reported by amputees and quadriplegics.
Right tip of scapula	Liver, gallbladder[citation needed]
Left shoulder	Thoracic diaphragm, Spleen (Kehr's sign), lung
Back	Pancreas
Palm of Hand	Palmaris longus A problem originating in the forearm might be felt in the palm, and not in the forearm.

Laboratory testing methods

Pain is studied in a laboratory setting due to the greater amount of control that can be exerted. For example, the modality, intensity, and timing of painful stimuli can be controlled with much more precision. Within this setting there are two main ways that referred pain is studied. 

Algogenic substances

In recent years several different chemicals have been used to induce referred pain including bradykinin, substance P, capsaicin, and serotonin. However, before any of these substances became widespread in their use a solution of hypertonic saline was used instead. Through various experiments it was determined that there were multiple factors that correlated with saline administration such as infusion rate, saline concentration, pressure, and amount of saline used. The mechanism by which the saline induces a local and referred pain pair is unknown. Some researchers have commented that it could be due to osmotic differences, however that is not verified.

Using electrical stimulation

Intramuscular electrical stimulation (IMES) of muscle tissue has been used in various experimental and clinical settings. The advantage to using an IMES system over a standard such as hypertonic saline is that IMES can be turned on and off. This allows the researcher to exert a much higher degree of control and precision in terms of the stimulus and the measurement of the response. The method is easier to carry out than the injection method as it does not require special training in how it should be used. The frequency of the electrical pulse can also be controlled. For most studies a frequency of about 10 Hz is needed to stimulate both local and referred pain.

Using this method it has been observed that significantly higher stimulus strength is needed to obtain referred pain relative to the local pain. There is also a strong correlation between the stimulus intensity and the intensity of referred and local pain. It is also believed that this method causes a larger recruitment of nociceptor units resulting in a spatial summation. This spatial summation results in a much larger barrage of signals to the dorsal horn and brainstem neurons.

Use in clinical diagnosis and treatments

Referred pain can be indicative of nerve damage. A case study done on a 63-year-old man with an injury sustained during his childhood developed referred pain symptoms after his face or back was touched. After even a light touch, there was a shooting pain in his arm. The study concluded that his pain was possibly due to a neural reorganization which sensitized regions of his face and back after the nerve damage occurred. It is mentioned that this case is very similar to what phantom limb syndrome patients suffer. This conclusion was based on experimental evidence gathered by V. Ramachandran in 1993, with the difference being that the arm that is in pain is still attached to the body.

Orthopedic diagnosis

From the above examples one can see why understanding of referred pain can lead to better diagnoses of various conditions and diseases. In 1981 physiotherapist Robin McKenzie described what he termed centralization. He concluded that centralization occurs when referred pain moves from a distal to a more proximal location. Observations in support of this idea were seen when patients would bend backward and forward during an examination.

Studies have reported that the majority of patients that experienced centralization were able to avoid spinal surgery through isolating the area of local pain. However, the patients who did not experience centralization had to undergo surgery to diagnose and correct the problems. As a result of this study there has been a further research into the elimination of referred pain through certain body movements. 

One example of this is referred pain in the calf. McKenzie showed that the referred pain would move closer to the spine when the patient bent backwards in full extension a few times. More importantly, the referred pain would dissipate even after the movements were stopped.

General diagnosis

As with myocardial ischaemia referred pain in a certain portion of the body can lead to a diagnosis of the correct local center. Somatic mapping of referred pain and the corresponding local centers has led to various topographic maps being produced to aid in pinpointing the location of pain based on the referred areas. For example, local pain stimulated in the esophagus is capable of producing referred pain in the upper abdomen, the oblique muscles, and the throat. Local pain in the prostate can radiate referred pain to the abdomen, lower back, and calf muscles. Kidney stones can cause visceral pain in the ureter as the stone is slowly passed into the excretory system. This can cause immense referred pain in the lower abdominal wall.

Further, recent research has found that ketamine, a sedative, is capable of blocking referred pain. The study was conducted on patients suffering from fibromyalgia, a disease characterized by joint and muscle pain and fatigue. These patients were looked at specifically due to their increased sensitivity to nociceptive stimuli. Furthermore, referred pain appears in a different pattern in fibromyalgic patients than non-fibromyalgic patients. Often this difference manifests as a difference in terms of the area that the referred pain is found (distal vs. proximal) as compared to the local pain. The area is also much more exaggerated owing to the increased sensitivity.