Abstract
Anhedonia is the diminished capacity to experience pleasure or to be motivated by the prospect of reward. Coined in 1896 by Théodule Ribot and long treated as a single deficit, it has since been fractionated into dissociable components: liking (hedonic impact) versus wanting (incentive motivation), and consummatory versus anticipatory pleasure. These fractionations matter because a person may still enjoy a reward yet have no drive to pursue it, so the clinical deficit is often motivational rather than hedonic. A core symptom of depression and a negative feature of schizophrenia, anhedonia cuts across diagnoses and anchors the Positive Valence Systems of the RDoC framework. This article sets out what it is, how it is measured, and the reward circuitry underlying it, with interactive demonstrations of the liking-wanting dissociation, the reward cycle, and SHAPS scoring.
Keywords: anhedonia, reward, motivation, pleasure, liking and wanting
Of all the symptoms a clinician asks about, few are as philosophically strange as the loss of pleasure. A patient can describe a world that is intact in every detail — the food is still on the plate, the music still plays, the friends still call — and yet report that none of it lands. Anhedonia is this flattening of the hedonic surface of experience, and its study has forced psychology to ask a surprisingly hard question: what, exactly, is pleasure, such that it can be lost? The answer that has emerged over the last three decades is that pleasure is not one thing. It is a small family of separable processes — liking, wanting, and learning — and anhedonia is better understood not as a single dimmer switch but as damage to one or more of these parts, each with its own neural signature and its own measurable fingerprint.
- Anhedonia is not one deficit but several. The capacity for pleasure fractionates into liking (hedonic impact), wanting (incentive motivation), and reward learning, and anhedonia can strike any of them independently (Berridge & Robinson, 2003; Treadway & Zald, 2011). - Wanting and liking are dissociable. Animal and human work shows that the motivation to pursue a reward and the pleasure of consuming it rest on different brain systems, so a patient can want without liking or like without wanting (Berridge & Robinson, 2003). - It splits in time, too. Anticipatory anhedonia (no pleasure in prospect) and consummatory anhedonia (no pleasure in the moment) are measurably distinct, captured by instruments such as the TEPS (Gard et al., 2006). - It is transdiagnostic. Anhedonia is a core criterion of major depression and a negative symptom of schizophrenia, but also appears in Parkinson's disease, substance use, and anxiety — which is why it anchors the RDoC Positive Valence Systems (Husain & Roiser, 2018). - It can be measured and targeted. Self-report scales (SHAPS, Chapman, TEPS) and behavioural reward tasks quantify it, and treatments such as positive-affect therapy now address it directly rather than hoping it lifts with mood (Rizvi et al., 2016; Craske et al., 2016).
What Anhedonia Is
Anhedonia is defined as a markedly diminished interest or pleasure in activities that were previously rewarding or enjoyable. The word was coined by Théodule Ribot in 1896, assembled from the Greek an- (without) and hēdonē (pleasure) as the deliberate counterpart to analgesia: just as analgesia is the absence of pain, anhedonia is the absence of pleasure. For most of the twentieth century it was treated as a unitary trait — a single reduced capacity to feel good — and measured as such by the first self-report scales (Chapman et al., 1976).
The modern account is more precise, because it begins from a distinction the older view blurred. The experience of a reward involves at least three separable processes. There is the hedonic impact of the reward itself — how good it actually feels in the moment of consumption. There is the motivation to obtain it — how hard the organism will work, and how strongly it is drawn, to get it. And there is reward learning — how the value of the reward updates the expectations and choices that follow. Ordinary language collapses all three into pleasure, but they come apart in the brain, and anhedonia can selectively impair any of them (Treadway & Zald, 2011; Rømer Thomsen et al., 2015).
This is why a careful clinician no longer asks only whether the patient still enjoys things, but probes separately whether the patient still looks forward to things, still enjoys them when they happen, and still pursues them. A patient with intact consummatory pleasure but impaired anticipation and motivation will say, truthfully, that a good meal is still pleasant once it is in front of them — but that nothing seems worth the effort of getting to the table. That dissociation, invisible to a single global question, is the central insight of the modern construct.
Liking, Wanting, and Learning
The most influential fractionation of reward comes from the distinction between liking and wanting, developed from decades of work on the neuroscience of reward. Liking is the hedonic reaction to a reward as it is consumed — the pleasure proper. Wanting, or incentive salience, is the motivational pull that makes a reward attractive and worth pursuing. Crucially, these rest on different neural systems: wanting is driven largely by the mesolimbic dopamine system, whereas liking depends on smaller, more fragile hedonic hotspots in regions such as the nucleus accumbens shell and ventral pallidum, mediated by opioid and endocannabinoid signalling rather than dopamine (Berridge & Robinson, 2003).
The dissociation is not merely theoretical. Dopamine-depleted animals still show normal liking reactions to a sweet taste yet will not work to obtain it — they like without wanting. Conversely, in addiction, cues can acquire enormous wanting (craving) while the drug's actual liking wanes — wanting without liking. Transposed to the clinic, this reframes much of what used to be called anhedonia as a deficit of wanting rather than liking: the depressed patient may retain the capacity to enjoy a reward in the moment but have lost the motivational drive to seek it out. This is the reason the field increasingly speaks of reward processing deficits rather than anhedonia alone, since the symptom is often a motivational failure masquerading as a hedonic one (Treadway & Zald, 2011; Der-Avakian & Markou, 2012).
A complementary fractionation runs along the axis of time. Anticipatory pleasure is the pleasure taken in the prospect of a future reward; consummatory pleasure is the pleasure experienced in the moment of receiving it. The two are psychometrically separable, and the Temporal Experience of Pleasure Scale (TEPS) was built precisely to measure them apart (Gard et al., 2006). The mapping between the two schemes is close but not exact: anticipatory pleasure draws heavily on wanting and on the ability to represent and value a future reward, while consummatory pleasure corresponds to liking. In schizophrenia, strikingly, consummatory pleasure is often largely intact while anticipatory pleasure is impaired — patients enjoy rewards as much as anyone when they arrive but derive little pleasure from looking forward to them, a profile that explains the motivational flattening of the negative syndrome better than a global loss of pleasure would.
To complete the picture, reward learning — the updating of value from experience, formalised in reinforcement-learning models as a prediction error — is a third component that can fail. If the brain does not register that an outcome was better than expected, rewards cannot shape future behaviour, and the result again looks like anhedonia from the outside even though hedonic capacity may be intact (Rømer Thomsen et al., 2015; Zald & Treadway, 2017).
Table 1
The dissociable components of reward and their failure in anhedonia
| Component | Psychological role | Principal neural substrate | Form anhedonia takes when it fails |
|---|---|---|---|
| Liking | Hedonic impact — how good a reward feels as it is consumed | Opioid and endocannabinoid hedonic hotspots in the nucleus accumbens shell and ventral pallidum | Consummatory anhedonia — reduced pleasure in the moment of reward |
| Wanting | Incentive motivation — the pull to pursue a reward | Mesolimbic dopamine projection from the ventral tegmental area to the nucleus accumbens | Motivational (anticipatory) anhedonia — no drive to seek reward despite intact enjoyment |
| Learning | Updating value from experience via reward prediction error | Phasic dopamine signalling and the ventral striatum | Blunted reward responsiveness — a weak response bias toward rewarded options |
Liking and wanting are two axes, not one
The pleasure of a reward (liking) and the motivation to pursue it (wanting) rest on different brain systems, so they can move independently. Set each and watch which quadrant the reward falls into.
Like without want — The reward is still enjoyed once obtained, but the drive to pursue it is gone — the motivational anhedonia seen in much of clinical depression and in schizophrenia's negative syndrome.
A reward can be wanted without being liked, or liked without being wanted — the two axes come apart (after Berridge & Robinson, 2003).
Lesion one phase of the pleasure cycle
Reward runs as a loop: wanting → liking → learning → wanting. Disable a phase and read which clinical profile of anhedonia it produces.
Wanting lesioned → motivational / anticipatory anhedonia
The reward is still enjoyed when it arrives, but nothing feels worth the effort of reaching it. This is the commonest clinical form — the 'like without want' profile of depression and the negative syndrome.
Different broken phases produce clinically different anhedonias from the same surface complaint (after Rømer Thomsen et al., 2015).
A Transdiagnostic Symptom
Anhedonia belongs to no single disorder. It is one of the two cardinal symptoms of a major depressive episode — the diagnostic criteria require either depressed mood or loss of interest and pleasure — and within depression its presence predicts a more severe, more chronic course and a poorer response to standard antidepressants. But it ranges far more widely than that (Pizzagalli, 2014):
- In schizophrenia, anhedonia is a defining negative symptom, though — as noted above — the deficit is primarily anticipatory and motivational rather than a loss of in-the-moment pleasure. - In Parkinson's disease and other conditions of dopamine depletion, anhedonia tracks the loss of the very mesolimbic signalling that drives wanting. - In substance use disorders, chronic exposure can blunt the reward system's response to natural rewards, leaving everyday pleasures flat beside the drug. - In anxiety disorders and post-traumatic stress disorder, reduced positive affect is an increasingly recognised and separable feature.
This spread across diagnoses is exactly why anhedonia has become a flagship case for transdiagnostic and dimensional approaches to psychopathology. The U.S. National Institute of Mental Health's Research Domain Criteria (RDoC) framework makes reward processing a core construct of its Positive Valence Systems domain, cutting across the traditional diagnostic categories and treating reward responsiveness, reward learning, and reward valuation as dimensions that vary continuously in both health and illness (Husain & Roiser, 2018). On this view anhedonia is not a symptom that happens to appear in several disorders but a window onto a reward system whose dysfunction produces features of several disorders.
Anhedonia is also closely related to, but distinct from, apathy — a loss of motivation that can occur with or without a loss of pleasure. The two overlap most clearly in the motivational (wanting) component, and disentangling them is an active line of transdiagnostic work (Husain & Roiser, 2018).
Assessing Anhedonia
Because anhedonia fractionates, no single measure captures it, and the choice of instrument encodes a theory of what is being measured (Rizvi et al., 2016). The main families are:
- The Snaith-Hamilton Pleasure Scale (SHAPS) is the most widely used clinical self-report measure of hedonic tone. Its 14 items each describe a commonplace pleasant experience (a favourite meal, the warmth of a sunny day, helping others); the respondent rates agreement, and disagreement — the failure to anticipate or endorse the pleasure — is scored as anhedonic. It is brief, state-sensitive, and designed to be relatively free of cultural and demographic bias (Snaith et al., 1995). - The Chapman Physical and Social Anhedonia Scales are longer trait measures that distinguish pleasure from physical sensations (food, touch, warmth) from pleasure in social contact. Developed to identify psychosis-proneness, they remain a standard in the schizophrenia literature (Chapman et al., 1976). - The Temporal Experience of Pleasure Scale (TEPS) separates anticipatory from consummatory pleasure, operationalising the temporal fractionation directly (Gard et al., 2006). - Behavioural reward tasks sidestep self-report entirely. The Probabilistic Reward Task measures a response bias toward a more frequently rewarded stimulus — a direct behavioural index of reward learning that is blunted in anhedonic individuals — while effort-based tasks such as the Effort-Expenditure for Rewards Task (EEfRT) measure how hard a person will work for a reward, indexing the motivational (wanting) component (Pizzagalli, 2014; Zald & Treadway, 2017).
The division between self-report and behaviour matters. Self-report scales ask the person to report their hedonic experience, which conflates the experience with the ability to recall and introspect on it; behavioural tasks measure reward function as it operates, without relying on the patient's insight. The two do not always agree, and a thorough assessment increasingly uses both (Rizvi et al., 2016).
The Reward Circuitry of Anhedonia
The neural account of anhedonia follows its psychological fractionation. The engine of wanting is the mesolimbic dopamine pathway, projecting from the ventral tegmental area to the nucleus accumbens; it assigns incentive salience and drives the pursuit of reward. The sparser circuitry of liking — the hedonic hotspots of the accumbens shell and ventral pallidum — depends on opioid and endocannabinoid rather than dopamine signalling, which is why boosting dopamine increases how hard an animal works for a reward without necessarily increasing how much it enjoys it (Berridge & Robinson, 2003; Der-Avakian & Markou, 2012).
Layered on top is a valuation and control network. The ventral striatum signals reward prediction and prediction error; the orbitofrontal and ventromedial prefrontal cortex represent reward value and integrate it into decisions; the anterior cingulate weighs effort against expected payoff. Functional-imaging studies of depression converge on blunted ventral striatal responses to reward and reward-predicting cues, and a systematic review of this literature maps the blunting onto the specific sub-processes — anticipation, consummation, and learning — rather than a single global hypoactivation (Borsini et al., 2020; Höflich et al., 2019).
Figure 1
The reward circuitry underlying liking, wanting, and valuation
An integrative model ties the circuitry to its most reliable environmental trigger: stress. Chronic or severe stress, acting partly through its effects on dopamine, degrades reward sensitivity, and this stress-induced blunting of the reward system is proposed as a central path by which adversity produces the anhedonic, motivationally-flattened form of depression (Pizzagalli, 2014). The model is valuable precisely because it is mechanistic: it predicts which component of reward should fail, in whom, and under what conditions, rather than treating anhedonia as an undifferentiated symptom.
Worked Example
How is a patient's hedonic capacity turned into a number? The most common clinical instrument is the Snaith-Hamilton Pleasure Scale (SHAPS), 14 items each describing an ordinary pleasure (Snaith et al., 1995). In its standard dichotomous scoring, each item is scored 1 when the respondent disagrees (fails to endorse the pleasure — the anhedonic direction) and 0 when they agree. The total therefore ranges from 0 (no anhedonia; every pleasure endorsed) to 14 (complete anhedonia; none endorsed), and the conventional clinical cut-off for abnormal hedonic tone is a score of greater than 2 — that is, 3 or more.
Consider a patient who endorses (agrees with) 7 of the 14 pleasant statements and disagrees with the other 7. Their SHAPS total is the count of disagreements:
14 − 7 = 7.
To place that on the scale, express it as a proportion of the full range: 7 / 14 = 0.50, exactly the midpoint of the instrument's range. Against the clinical threshold, a score of 7 is well above the cut-off of 2, so this patient would screen positive for clinically significant anhedonia — and by a wide margin, since the cut-off (3) sits at just 3/14 ≈ 0.21 of the range while the patient is at 0.50. The distance above threshold, 7 − 2 = 5 points, is a rough index of severity: this is not a borderline positive but a substantial loss of hedonic tone. The demonstration below lets the reader toggle each of the 14 items and watch the total, the proportion of the range, and the threshold verdict update.
Score hedonic tone with the SHAPS
The Snaith-Hamilton Pleasure Scale lists 14 ordinary pleasures. Each is scored 1 when the respondent disagrees (fails to endorse the pleasure — the anhedonic direction) and 0 when they agree. Toggle each item; the clinical cut-off is a total greater than 2.
Total 7 — above the clinical cut-off of 2, by 5 points.
A score greater than 2 marks abnormal hedonic tone (after Snaith et al., 1995).
Discussion
The study of anhedonia is a case study in what happens when a vague clinical symptom is taken apart by experimental science. For decades loss of pleasure was a single tick-box, and treatments that lifted mood were assumed to restore it. The fractionation of reward into liking, wanting, and learning — and the parallel split of pleasure into anticipatory and consummatory phases — revealed that this was too coarse: the most common form of clinical anhedonia is often a failure of motivation and anticipation with hedonic capacity partly spared, which is a different target entirely (Berridge & Robinson, 2003; Treadway & Zald, 2011; Gard et al., 2006).
That refinement has had two consequences. The first is diagnostic and dimensional: anhedonia became the showcase for the RDoC programme's bet that reward processing is a transdiagnostic dimension more tractable than the disorder categories it cuts across (Husain & Roiser, 2018). The second is therapeutic: once anhedonia is understood as reward-system dysfunction rather than a mere shadow of low mood, it becomes a direct target. Positive-affect treatment, which trains the savouring, anticipation, and recall of positive experience, was designed on exactly this logic — to act on the reward deficit that standard, negative-affect-focused therapies and antidepressants often leave untouched (Craske et al., 2016).
The open problems are correspondingly sharper than they once were. Self-report and behavioural measures of anhedonia do not always converge, and it is not yet settled which best predicts outcome or treatment response (Rizvi et al., 2016). The imaging literature, though consistent in implicating blunted ventral striatal reward signalling, is still mapping which sub-process fails in which condition (Borsini et al., 2020). And the relationship between anhedonia and apathy — overlapping in their motivational core yet clearly separable — remains to be fully drawn (Husain & Roiser, 2018).
Cognitive and Psychological Implications
Anhedonia is, at root, a disorder of the valuation that guides behaviour — and that places it squarely within cognitive psychology rather than at its clinical margin. Every choice an organism makes rests on an estimate of expected value, and the reward system is the machinery that generates and updates those estimates. When it fails, the symptom is not only that rewards feel flat but that the entire apparatus of goal-directed action loses its fuel: without a signal that an outcome is worth pursuing, motivation collapses and effort is withheld. Anhedonia thus exposes the normally invisible link between feeling and doing — the fact that what we call pleasure is, functionally, the brain's way of tagging what is worth approaching.
The construct also sharpens the psychology of affect. The liking-wanting dissociation shows that positive affect is not a single dimension but at least two — the hedonic and the motivational — and that these can move independently. This has consequences for emotional regulation: a person who can still like but no longer wants cannot simply be exhorted to do things they enjoy, because the deficit is upstream of enjoyment, in the drive to engage at all. And because anhedonia appears across schizophrenia, bipolar disorder, and depression alike, it is a standing demonstration that very different disorders can converge on a shared disturbance of a single cognitive-affective system — the mirror image of psychomotor agitation, which shows the same convergence on the side of excess rather than deficit. Measured carefully, a symptom defined by absence turns out to be one of the most informative signals the reward system can send.
Current Directions
Three threads dominate the recent literature. The first is mechanistic imaging: large systematic reviews are now resolving the blunted-reward signal of depression into its component sub-processes, asking separately how anticipation, consummation, and reward learning are represented in the ventral striatum and prefrontal cortex, and where in that chain each disorder's deficit lies (Borsini et al., 2020; Höflich et al., 2019). The second is computational and neuroeconomic: reinforcement-learning and effort-based decision models are being used to specify anhedonia as a quantifiable parameter — a reduced reward sensitivity, a steeper effort-discounting function — rather than a verbal description, which makes it comparable across species and across disorders (Zald & Treadway, 2017). The third is targeted treatment: having established that reward deficits survive conventional antidepressant treatment, the field is developing and testing interventions aimed squarely at the reward system, from positive-affect therapy to pharmacological and neuromodulatory approaches that engage dopaminergic and reward circuitry directly (Craske et al., 2016; Pizzagalli, 2014). Across all three, the unifying ambition is the one the fractionation made possible: to move from the patient has lost pleasure to a specification of which reward process has failed, how much, and what will restore it.
Common Misconceptions
- Anhedonia just means sadness or depressed mood.
- It is a distinct symptom — the loss of pleasure and reward, not the presence of low mood. The two are separable: a person can be sad without being anhedonic, and anhedonic without feeling conventionally sad, which is why major-depression criteria list them as two different cardinal symptoms (Pizzagalli, 2014).
- Anhedonia is a single inability to feel pleasure.
- It fractionates into dissociable components — liking versus wanting, anticipatory versus consummatory, and reward learning — any of which can fail on its own, so two people called anhedonic may have quite different deficits (Berridge & Robinson, 2003; Gard et al., 2006).
- If a patient still enjoys things in the moment, they are not anhedonic.
- Consummatory pleasure can be intact while anticipatory pleasure and motivation are lost — the typical profile in schizophrenia. The patient enjoys the reward once it arrives but has no drive to seek it, which is still anhedonia (Gard et al., 2006; Treadway & Zald, 2011).
- Treating the depression will automatically fix the anhedonia.
- Reward deficits frequently persist after standard antidepressants lift mood, which is why treatments such as positive-affect therapy were developed to target anhedonia directly (Craske et al., 2016).
Glossary
- Anhedonia.
- A markedly diminished capacity to experience pleasure or to be motivated by reward.
- Anticipatory pleasure.
- The pleasure taken in the prospect of a future reward; impaired in anticipatory anhedonia.
- Apathy.
- A loss of motivation that overlaps with the wanting component of anhedonia but can occur without any loss of pleasure.
- Consummatory pleasure.
- The pleasure experienced in the moment of receiving a reward; corresponds closely to liking.
- Hedonic hotspot.
- A small brain region (e.g. in the nucleus accumbens shell or ventral pallidum) where opioid or endocannabinoid signalling amplifies the liking reaction to a reward.
- Incentive salience.
- The motivational property (wanting) that makes a reward and its cues attractive and worth pursuing, driven by mesolimbic dopamine.
- Liking.
- The hedonic impact of a reward as it is consumed — pleasure proper, as distinct from the motivation to obtain it.
- Mesolimbic dopamine pathway.
- The projection from the ventral tegmental area to the nucleus accumbens that assigns incentive salience and drives reward-seeking.
- Pleasure.
- The positive hedonic experience whose loss defines anhedonia; functionally, the brain's tag for what is worth approaching.
- Positive Valence Systems.
- The RDoC domain covering reward responsiveness, learning, and valuation, under which anhedonia is modelled transdiagnostically.
- Probabilistic Reward Task.
- A behavioural task measuring the response bias toward a more frequently rewarded stimulus, indexing reward learning; blunted in anhedonia.
- Reward prediction error.
- The difference between an obtained and an expected reward, signalled by dopamine and used to update value; a failure of this signal can mimic anhedonia.
- Snaith-Hamilton Pleasure Scale (SHAPS).
- A 14-item self-report measure of hedonic tone, scored so that failure to endorse an ordinary pleasure counts as anhedonic.
- Temporal Experience of Pleasure Scale (TEPS).
- A self-report instrument that separately measures anticipatory and consummatory pleasure.
- Wanting.
- The incentive-motivational pull toward a reward, dissociable from liking and driven by mesolimbic dopamine.
Key Researchers
Kent C. Berridge
(contemporary). James Olds Collegiate Professor of Psychology and Neuroscience at the University of Michigan; originator, with Terry Robinson, of the liking versus wanting dissociation that reframed anhedonia as potentially a deficit of incentive motivation rather than of hedonic capacity. Wikipedia - Google Scholar - Faculty
Ann M. Kring
(contemporary). Professor of Psychology at the University of California, Berkeley; co-developer of the Temporal Experience of Pleasure Scale and a leading researcher on the anticipatory-consummatory distinction and emotion in schizophrenia. ORCID - Wikipedia - Google Scholar - Faculty
Diego A. Pizzagalli
(contemporary). Distinguished Professor of Psychiatry and of Neurobiology at the University of California, Irvine, and founding director of its institute for translational depression research, having previously led the Center for Depression, Anxiety and Stress Research at McLean Hospital; developer of the Probabilistic Reward Task and of an integrated stress-reward model of anhedonia in depression. ORCID - Wikipedia - Google Scholar - Faculty
Théodule-Armand Ribot
(1839-1916). French psychologist, a founder of scientific psychology in France, who coined the term anhedonia (anhédonie) in 1896 to name the loss of the capacity for pleasure, by deliberate analogy with analgesia. Wikipedia - Wikidata
Michael T. Treadway
(contemporary). Associate Professor of Psychology and Psychiatry at Emory University; developer of the Effort-Expenditure for Rewards Task (EEfRT) and a leading voice for the motivational, effort-based reconceptualisation of anhedonia. Google Scholar - Faculty
Frequently Asked Questions
What is anhedonia in simple terms?
Anhedonia is the reduced ability to feel pleasure, or to be motivated by the things that used to be enjoyable. Someone with anhedonia might find that food, music, hobbies, or time with friends no longer feel rewarding, even though nothing about those things has changed. It is a symptom, not a disease in itself, and it appears in several different conditions (Pizzagalli, 2014).
Is anhedonia the same as depression?
No. Anhedonia is one of the two core symptoms of a major depressive episode, but it is distinct from depressed mood, and a person can have one without the other. Anhedonia is specifically about the loss of pleasure and reward, whereas depressed mood is about sadness and low spirits. Anhedonia also occurs outside depression, in schizophrenia, Parkinson's disease, and substance use (Husain & Roiser, 2018).
What is the difference between 'liking' and 'wanting'?
'Liking' is the pleasure a person actually feels on receiving a reward; 'wanting' is the motivation that drives them to seek it out. Research shows these rest on different brain systems, so they can come apart: a person can still enjoy something in the moment yet have no drive to pursue it. Much clinical anhedonia turns out to be a loss of wanting more than of liking (Berridge & Robinson, 2003).
Can someone be anhedonic but still enjoy things sometimes?
Yes. A common pattern, especially in schizophrenia, is intact consummatory pleasure (enjoying a reward once it arrives) alongside impaired anticipatory pleasure (looking forward to it) and reduced motivation. The person enjoys the moment but is not drawn to pursue it, so the anhedonia is real even though some pleasure remains (Gard et al., 2006; Treadway & Zald, 2011).
How is anhedonia measured?
With self-report scales and behavioural tasks. The Snaith-Hamilton Pleasure Scale (SHAPS) and the Chapman scales ask people to rate ordinary pleasures; the Temporal Experience of Pleasure Scale separates anticipatory from consummatory pleasure; and behavioural tasks such as the Probabilistic Reward Task and effort-based tasks measure reward learning and motivation directly, without relying on self-report (Snaith et al., 1995; Rizvi et al., 2016).
What part of the brain is involved in anhedonia?
Chiefly the brain's reward system. The mesolimbic dopamine pathway, running from the ventral tegmental area to the nucleus accumbens, drives 'wanting', while small 'hedonic hotspots' using opioid signalling mediate 'liking'. The ventral striatum and prefrontal cortex handle reward prediction and valuation. Depression is associated with a blunted reward response in the ventral striatum (Der-Avakian & Markou, 2012; Borsini et al., 2020).
Why is anhedonia important across different disorders?
Because it is transdiagnostic: the same reward-system dysfunction appears in depression, schizophrenia, Parkinson's disease, substance use, and anxiety. This is why the RDoC framework treats reward processing as a dimension that cuts across diagnoses, making anhedonia a model case for studying mental illness by mechanism rather than by diagnostic label (Husain & Roiser, 2018).
Can anhedonia be treated?
Yes, and increasingly it is targeted directly. Because reward deficits often persist after standard antidepressants lift mood, treatments such as positive-affect therapy were designed specifically to rebuild the capacity to anticipate, savour, and recall positive experiences, and pharmacological and neuromodulatory approaches aim at the reward circuitry itself (Craske et al., 2016; Pizzagalli, 2014).
References
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