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= Anhedonia =
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Introduction
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Anhedonia is a diverse array of deficits in hedonic function,
including reduced motivation or ability to experience pleasure. While
earlier definitions of anhedonia emphasized the inability to
experience pleasure, anhedonia is used by researchers to refer to
reduced motivation, reduced anticipatory pleasure (wanting), reduced
consummatory pleasure (liking), and deficits in reinforcement
learning. In the 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
pleasurable activities. While the ICD-10 does not explicitly mention
anhedonia, the depressive symptom analogous to anhedonia as described
in the DSM-V is a loss of interest or pleasure.
Definition
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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. 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. 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.
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.
'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. In contrast to introversion, a nonpathological
dimension of human personality, social anhedonia represents a deficit
in the ability to experience pleasure. 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. This trait is currently seen as a central
characteristic to, as well as a predictor of, schizophrenia spectrum
disorders, as it is seen as a potential evolution of most personality
disorders, if the patient is above age 24, when prodromal
schizophrenia may be excluded.
Causes
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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). 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; 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.
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".
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).
Major depressive disorder
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Anhedonia occurs in roughly 70% of people with a major depressive
disorder. 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. 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.
Schizophrenia
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Anhedonia is commonly listed as one component of negative symptoms in
schizophrenia. 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 schizophrenics, 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. 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. Schizophrenics 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.
Substance related disorders
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Anhedonia is common in people who are dependent upon a wide variety of
drugs, including alcohol, opioids, and nicotine. Although anhedonia
becomes less severe over time, it is a significant predictor of
relapse.
Post traumatic stress disorder
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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. PTSD is also associated with blunted
affect, which may be due to the high comorbidity with depression.
Parkinson's disease
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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.
Sexual anhedonia
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Sexual anhedonia in males is also known as 'ejaculatory anhedonia'.
This condition means that the man will ejaculate with no accompanying
sense of pleasure.
The condition is most frequently found in males, but women can suffer
from lack of pleasure when the body goes through the orgasm process as
well.
Sexual anhedonia may be caused by:
* Hyperprolactinaemia
* Hypoactive sexual desire disorder (HSDD), also called inhibited
sexual desire
* Low levels of the hormone testosterone
* Spinal cord injury
* Multiple sclerosis
* Use of SSRI antidepressants or having used SSRI antidepressants in
the past.
* Use (or previous use) of antidopaminergic neuroleptics
(anti-psychotics)
* Fatigue
* Physical illness
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.
Signs and symptoms
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* Decreased ability to experience interpersonal pleasure
* Social withdrawal/isolation
* Decreased need for social contact
* Lack of close friends and intimate relationships, and decreased
quality of those relationships
* Poor social adjustment
* Decreased positive affect
* Flat affect
* Depressed mood
* State-related anxiety
Background and early clinical observation
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The term 'anhedonia' is derived from the Greek 'an-', "without" and
'h�don�', "pleasure". Interest in the nature of pleasure and its
absence dates back to ancient Greek philosophers such as Epicurus. The
symptoms of anhedonia were introduced to the realm of psychopathology
in 1809 by John Haslam, who characterized a patient suffering from
schizophrenia as indifferent to �those objects and pursuits which
formerly proved sources of delight and instruction.�. 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. In particular, 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. 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.
Recent research suggests that social anhedonia may represent a
prodrome of psychotic disorders. First-degree relatives of individuals
with schizophrenia show elevated levels of social anhedonia, higher
baseline scores of social anhedonia are associated with later
development of schizophrenia. 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. Socially
anhedonic individuals perform worse on a number of neuropsychological
tests than non-anhedonic participants, and show similar physiological
abnormalities seen in patients with schizophrenia.
Comorbidity
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Anhedonia is present in several forms of psychopathology.
Depression
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Social anhedonia is observed in both depression and schizophrenia.
However, social anhedonia is a state related to the depressive episode
and the other is 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
(2001) 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. Blanchard and
colleagues (2011) found individuals with social anhedonia also had
elevated rates of lifetime mood disorders including depression and
dysthymia compared to controls.
Social anxiety
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As mentioned above, social anxiety and social anhedonia differ in
important ways. 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. It has yet to be determined what the
exact relationship between social anhedonia and social anxiety is, and
if one potentiates the other. 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. In an attempt to separate
out social anhedonia from social anxiety, the Revised Social Anhedonia
Scale didn't include items that potentially targeted social anxiety.
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.
Primary relevance in schizophrenia and schizophrenia spectrum disorders
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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. Social anhedonia is a dimension of both negative and
positive schizotypy. 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.
Not all people with schizophrenia display social anhedonia 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.
Social anhedonia may be a valid predictor of future
schizophrenia-spectrum disorders; young adults with social anhedonia
perform in a similar direction to schizophrenia patients in tests of
cognition and social behavior, showing potential predictive validity.
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.
Treatment
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There is no validated treatment for social anhedonia. 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. (2011) 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.
Gender differences
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In the general population, males score higher than females on measures
of social anhedonia. 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. 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. 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.
Assessing social anhedonia
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There are several self-report psychometric measures of schizotypy
which each contain subscales related to social anhedonia:
* Revised Social Anhedonia Scale�Chapman Psychosis Proneness Scales
* No Close Friends Subscale�Schizotypyal Personality Questionnaire
* Introverted Anhedonia Subscale�Oxford Liverpool Inventory of
Feelings & Experiences
Genetic components
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L.J. and J.P. Chapman were the first to discuss the possibility that
social anhedonia may stem from a genetic vulnerability. The Disrupted
in Schizophrenia 1 (DISC1) gene has been consistently associated with
risk for, and cause of, schizophrenia-spectrum disorders and other
mental illnesses. More recently, DISC1 has been associated with social
anhedonia within the general population. Tomppo (2009) 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. Continued study
of social anhedonia and its genetic components will help researchers
and clinicians learn more about the cause of schizophrenia-spectrum
disorders.
Neurobiological correlates
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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. 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.
Specific musical anhedonia
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Recent studies have found people who do not have any issue processing
musical tones or beat, yet receive no pleasure from listening to
music. Specific musical anhedonia is distinct from Melophobia, the
fear of music.
See also
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* Avolition
* Clinical depression
* Dysthymia
* Schizophrenia
External links
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*
[
https://web.archive.org/web/20090214230819/http://bipolardisordersymptoms.info/
bipolar-symptoms/anhedonia.htm
Anhedonia - Bipolar Disorder Symptoms]
* [
http://www.mcmanweb.com/no_pleasure.html No Pleasure, No Reward]
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=========
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Original Article:
http://en.wikipedia.org/wiki/Anhedonia
