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Metacognitive monitoring and metacognitive control applied to memory encoding, memory retention and memory retrieval. Different judgments predict different outcomes; a prediction of future recall need not agree with confidence in an answer currently retrieved.

Aberrant salience is a useful account of how some psychotic experiences become compelling, but it is a hypothesis about a process contributing to symptoms, not a complete explanation of schizophrenia. Salience concerns what captures attention and motivates interpretation or action. It is distinct from whether a stimulus is physically intense, pleasurable or objectively informative.

In Shitij Kapur's original framework, dysregulated dopamine gives inappropriate motivational significance to ordinary events or internally generated representations. A coincidental glance can consequently feel urgent and personally directed. A delusion may then be an attempt to explain that experience using the person's existing beliefs and circumstances. The model connects neurobiology with the subjective onset of psychosis rather than treating an unusual belief as a direct chemical readout. It also predicts that dampening salience can reduce the compelling quality of experiences before their interpretation has been revised. This is a theoretical synthesis, not an experiment proving the entire causal chain.^[ref]

The framework makes two separable predictions: inappropriate significance should attach to uninformative cues, and relevant cues may fail to gain appropriate significance. They should be measured independently. In the Salience Attribution Test used by Jonathan P. Roiser and colleagues, visual cues varied along colour and form dimensions, with only one dimension predicting monetary reinforcement. Reaction-time speeding and explicit probability ratings indexed responding to relevant versus irrelevant features. Patients showed reduced adaptive salience; importantly, the diagnostic groups did not differ overall in aberrant salience. Greater explicit aberrant salience occurred in patients with delusions relative to patients without them. The small, predominantly medicated sample, subgroup analysis and multiple comparisons prevent presenting this as a universal schizophrenia deficit.^[ref]

A useful measurement caution follows directly. If equally uninformative features receive noisy ratings $R_1,R_2$, the absolute difference $|R_1-R_2|$ is generally positive even when both estimates are unbiased. For independent normal errors of variance ${\sigma }^2$, its expectation is $2\sigma /\sqrt{\pi }$. A high score can therefore reflect rating noise or poor probability discrimination as well as genuinely assigned significance. Repeated trials, reliability assessment, explicit task comprehension and measurements of adaptive learning are needed to interpret the score.

Biological evidence is compatible with, but does not uniquely identify, the hypothesis. Oliver D. Howes and colleagues used fluorodopa PET to compare people with prodromal symptoms, patients with schizophrenia and controls. Elevated synthesis-related uptake in the associative striatum in the prodromal group links dopamine dysfunction to a stage before established psychotic illness. This was a case-control study; uptake is not a recording of cue-specific phasic dopamine, and a high-risk group does not establish that every individual will develop schizophrenia. It supplies an upstream biological constraint, not a demonstration that a particular neutral cue caused a delusion.^[ref]

Several explanatory steps remain. An account must specify why significance is assigned to this event, how a persistent interpretation is selected, and why contradictory evidence fails to revise it. Attention, memory retrieval, prior beliefs and the social environment can supply those constraints. Dopamine dysfunction need not explain all negative symptoms or cognitive difficulties. Antipsychotic effects cannot alone establish the original cause: altering a downstream component can improve symptoms arising through several pathways. Nor should a medication-associated decrease in ordinary motivation automatically be taken as recovery of selective salience.

A similar perspective is particularly productive for substance use disorder. Incentive salience distinguishes cue-triggered wanting from pleasure. Cindy L. Wyvell and colleagues separately trained a sucrose-seeking response and a reward-predictive cue. Accumbens amphetamine enhanced cue-triggered responding in a test without reward reinforcement, without enhancing sucrose liking measured by taste reactivity. A later sensitization experiment found amplified cue-triggered seeking in a drug-free test after prior exposure. The experiments distinguish motivation from hedonic impact; they do not themselves demonstrate every feature of human addiction.^[ref][ref]

This suggests how drug cues can capture behaviour even when enjoyment has declined or the person intends abstinence. Unlike psychosis, however, these cues were genuinely associated with reward. The shared issue is excessive or poorly regulated motivational control, not necessarily significance attached to statistically irrelevant events.

Anxiety disorders offer a second, more limited analogy: threat-related cues can monopolise attention, avoidance can maintain their significance, and safe cues may be treated as dangerous. In panic disorder, catastrophic interpretation can make ordinary bodily sensations feel threatening. Such accounts concern threat appraisal and discrimination and do not justify assuming identical dopamine abnormalities across diagnoses. Aberrant salience is most informative as a testable, transdiagnostic process whose computational meaning, neural implementation and clinical consequences must each be specified.

A common computational target is plausible: retrospective confidence evaluates whether an already selected answer is correct. In a Bayesian inference model this can be written $P(\text{selected answer correct}\mid \text{available evidence, action})$. The evidence might be a sensory signal in perception or retrieved information in memory retrieval. A shared target does not require the same evidence representation, parameters or neural implementation in both domains.

A basic signal detection theory account illustrates the common structure. Two alternatives generate different distributions of internal evidence, the decision selects an alternative, and confidence reflects evidence relative to the decision boundary. With equal prior probabilities and two alternatives, let $L$ be the log-likelihood ratio for the observed evidence. For the alternative with the larger posterior probability, confidence as posterior correctness probability givesThis is a normative consequence of the assumed model, rather than a universal empirical law. The same algebra can describe old/new recognition or a perceptual discrimination only when their assumed likelihoods, priors and decision rule justify it. An old/new discrimination also has a different response structure from comparing two simultaneously presented objects.

A different common account is self-consistency theory of confidence: confidence tracks how consistently a choice is supported across sampled representations. Asher Koriat found predictions of this account, previously applied to knowledge judgments, also held in perceptual judgments.^[ref] Its distinctive implication is that confidently repeated errors are possible when misleading evidence consistently favours the wrong choice. Reliable internal agreement need not entail external correctness. This differs from simply identifying subjective confidence with an objectively calibrated posterior.

Important limitations remain. Recognition can be supported by familiarity and recollection, while a perceptual choice may depend on a currently visible stimulus. The content and timing of evidence differ. Confidence can incorporate an additional retrieval attempt, response fluency, or evidence acquired after the initial decision. A common computation can therefore give different levels of metacognitive efficiency across tasks without requiring a wholly different function for confidence. Conversely, similar average rating curves do not prove a single mechanism: quite different latent processes can produce them.

Second-order inference about decisions makes the relation explicit by distinguishing the information supporting the decision from the partially correlated information supporting its evaluation.^[ref] A model in which confidence has exactly the same evidence as the choice is a stronger hypothesis than a model with a shared inferential goal and separate noisy samples. Error detection and later changes of mind are useful tests because they constrain what further information confidence can use.

Strong evidence for a common mechanism would include quantitative predictions across domains, transfer to a new domain after controlled training, and common effects of selective interventions after matching first-order performance. A shared brain region or a cross-task correlation alone is insufficient: task demands and measurement reliability can produce either apparent commonality or apparent dissociation. The most defensible common basis is a family of evidence-based evaluations of correctness, while the claim of one identical process for memory and perception remains substantially stronger.