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A form of reliving in which a past event or aspect of it is experienced with a sense of occurring in the present. A bodily conditioned response alone does not identify this phenomenology.

Conditioning explains an important part of reexperiencing: a cue associated with a traumatic event can later trigger fear and involuntary recollection. It does not, by itself, fully explain the content, sensory qualities, sense of present occurrence or persistence of every intrusion. The best answer therefore separates a mechanism for triggering a response from a theory of what is represented and why the representation is retrieved in this particular form.

In a simple conditioning account, an initially neutral cue becomes associated with an aversive event. A similar cue encountered later can evoke defensive arousal even when the danger is absent. Stimulus generalisation explains reactions to reminders that only resemble the original cue, while avoidance can limit opportunities for learning that the present context is safer. Extinction is not necessarily erasure: new learning can compete with an earlier association, and a changed context or delay can allow fear to return.

This account predicts cue-dependent episodes and bodily responses. A particular sound, smell or visual pattern may precipitate a sudden experience before the person identifies its connection to the trauma. Absence of consciously recognising the reminder does not mean that no cue was present. However, a conditioned response could be autonomic arousal or an urge to escape; it need not include a vivid autobiographical image or the feeling that a past event is happening now. Those additional properties require explanation.

Anke Ehlers and colleagues investigated the content and quality of intrusive memories after different traumas. Intrusions often concerned sensory impressions just before the event or before its worst emotional moments. Their warning-signal hypothesis proposes that these impressions acquired predictive significance. This is compatible with associative learning, but also refines a simple replay account: what is reexperienced may be a cue that signalled worsening danger rather than a literal representation of the objectively most injurious moment. The descriptive observations motivate the hypothesis without experimentally proving the original association.^[ref]

The distinction matters because trauma is an extended, interpreted event. A moment can become especially threatening when its meaning changes—for example, when a previously ambiguous situation is understood as inescapable. The relevant reminder may reflect that subjective transition. A model that treats the whole event as one undifferentiated shock misses the organisation of the remembered experience. Retrospective descriptions, however, can be reconstructed, so prospective or carefully controlled analogue evidence is useful alongside clinical interviews.

Conditioning experiments provide converging but narrower evidence. Mohammed R. Milad and colleagues studied sixteen people with PTSD and fifteen trauma-exposed controls using a two-day fear-conditioning and extinction procedure in a 3-T fMRI scanner. Skin conductance indexed conditioned responding. The groups did not differ significantly in acquisition or immediate extinction, but the PTSD group showed poorer extinction recall the following day, with associated differences in relevant brain activity. This supports altered retention or retrieval of safety learning; it did not directly measure autobiographical flashbacks or establish whether the group difference preceded trauma.^[ref]

Memory theories address features left underspecified by a reflex account. Chris R. Brewin and colleagues' original dual-representation theory distinguished verbally accessible memories from memories automatically accessible through situational cues. It proposed that cue-triggered sensory representations can produce reliving without ordinary deliberate narrative retrieval. This is a theoretical architecture, not proof of two anatomically discrete stores. Its explanatory value depends on generating predictions that distinguish access, contextual organisation and response processes rather than relabelling the clinical phenomena.^[ref]

Anke Ehlers and David M. Clark's cognitive model emphasised a persistent sense of current threat arising from negative appraisals and properties of trauma memory, including difficulty integrating the event into its broader autobiographical context. Avoidance, suppression and other strategies can impede change. On this account, a reminder may retrieve an impression without sufficient information that the danger belongs to the past. Appraisals of an intrusion as evidence of permanent damage or loss of control can then increase distress and monitoring, potentially maintaining the problem beyond the initial cue association.^[ref]

Experimental work on representation also constrains an exclusively fear-response account. Emily A. Holmes and colleagues used a trauma-film analogue and randomly allocated participants, after a thirty-minute interval, to a brief visuospatial game or no task. Intrusions during the next week were reduced in the task condition, while recognition performance did not differ significantly. This suggests that involuntary imagery and deliberate memory performance can be affected differently. The analogue, comparator and limited follow-up do not establish prevention or treatment of clinical PTSD, nor prove that all recognition information was unchanged.^[ref]

Reexperiencing should also be distinguished from related events. Rumination about why something happened, a future-oriented image and deliberate recollection are not interchangeable with a sensory flashback. Shame, guilt and grief can accompany intrusions as well as fear. A broad associative model can incorporate links to these meanings and responses, but then it needs explicit representational and contextual assumptions. Saying that every retrieved mental event is a conditioned reaction risks making the account true by definition rather than experimentally informative.

A discriminating experiment could hold reminder exposure constant while varying contextual information or its interpretation, with careful ethical safeguards and an analogue suitable for research. Measure autonomic response, involuntary imagery, deliberate recognition and sense of current occurrence separately. A reduction in bodily fear without a corresponding change in involuntary images would show that the endpoints dissociate; a contextual manipulation reducing reliving at comparable arousal would support a role beyond response magnitude. Predefine manipulation checks and avoid treating absence of a reported image as proof that no memory was activated.

Clinical studies should add prospective sampling of reminders and intrusions where feasible, rather than relying entirely on retrospective questionnaires. Repeated within-person observations can test whether contexts and appraisals precede an episode, though they do not remove all confounding. Treatment effects can provide converging evidence, but improvement after a multicomponent therapy does not determine whether conditioning, appraisal or memory organisation was the necessary pathway.

Conditioning is consequently a useful account of why reminders become potent and why responses can recur after apparent safety learning. A full explanation of reexperiencing also needs the representation retrieved, its contextual accessibility, the sense that it is occurring now and the meaning assigned to the experience. Associative, cognitive and autobiographical memory processes can therefore be complementary, provided their separate predictions remain open to test.

The SOP model family specifies testable principles of stimulus processing and association, but it does not yet have a uniquely established neural implementation. Its behavioural breadth should be distinguished from evidence identifying the biological counterparts of its states, transition rules and separate response systems. The strongest neurobiology concerns processes that the models require—priming, associative retrieval and differentiated response pathways—rather than a one-to-one mapping of every symbol onto a brain structure.

Ivan Pavlov’s classical conditioning tradition made stimulus history and the measured conditioned response objects of controlled experiment. The SOP model introduced by Allan R. Wagner represents stimuli as elements distributed among inactivity $I$, primary activation $A_1$ and secondary activation $A_2$. External presentation promotes inactive elements into $A_1$; activity then passes through $A_2$ before returning to inactivity. A learned associate can activate an expected event directly into $A_2$. Recently or associatively activated elements are less available for renewed primary processing, distinguishing self-generated priming from retrieval-generated priming. A contemporary quantitative analysis shows how these dynamics can generate several habituation regularities; these are simulations, not measurements of neuronal states.^[ref]

The association rules make the account more specific than a generic fading trace. In the original formulation, concurrent $A_{1,CS}$ and $A_{1,US}$ activity promotes excitation, whereas $A_{1,CS}$ with $A_{2,US}$ promotes inhibition. The Modified SOP model additionally permits learning involving a cue activated into $A_2$: matched-state combinations can strengthen excitation and mismatched-state combinations inhibition. This allows an absent cue’s association to change through retrieval, addressing retrospective revaluation. The model is therefore not simply equivalent to a reward-error equation or to synaptic fatigue.

Human causal-judgment experiments motivated an important constraint. Participants learned relations among compound cues and an outcome, then received information about a companion cue without the target. Retrospective changes in judgments depended on the consistency of earlier within-compound pairings. This supports a role for learned cue–cue relations in revaluation, but the behavioural result does not identify synapses implementing the modified state-pair rules. Other retrieval or inference models can also use knowledge of those relations.^[ref]

Neural adaptation alone is insufficient to explain retrieval-generated effects. A transient reduction in response to a repeated physical stimulus could result from receptor adaptation, local synaptic dynamics or wider circuit changes, whereas context-specific long-term priming requires an account of the context’s learned relation to the event. A biological test must distinguish an unfamiliar stimulus from an unexpected combination of familiar stimuli and control attention, orienting and stimulus exposure. Reduced firing cannot simply be labelled $A_2$: the theory permits secondary activity to be behaviourally silent or have a response-system-dependent effect.

Hippocampal lesion experiments provide evidence at that process level. Rats learned audiovisual sequences in which particular sounds preceded particular lights. Switching the familiar sound–light combinations renewed visual orienting in controls but not in hippocampal-lesioned animals, despite relatively preserved habituation to visual stimuli and evidence of sequence associations. This implicates the hippocampus in associative mismatch rather than novelty alone. It is compatible with a contribution to expectation or retrieval, but does not uniquely show that the hippocampus is $A_2$, nor that every SOP model process is hippocampal.^[ref]

Receptor perturbation further separates short- and long-term components. Mice lacking the GluA1 AMPA-receptor subunit showed impaired short-term spatial novelty performance but enhanced long-term performance under the tested interval conditions. Manipulating exposure and test intervals helped distinguish rapid recency-dependent effects from longer-lasting learning. This is consistent with separable processes of the kind emphasized by the SOP model, rather than an undifferentiated stronger-versus-weaker memory. Nevertheless, a lifelong mutation can alter development and network function, and task dependence prevents identifying GluA1 with a single abstract transition parameter.^[ref]

Associative access to an absent outcome has additional circuit support. In rat sensory preconditioning, orbitofrontal inactivation impaired behaviour guided by an indirectly inferred outcome while sparing behaviour supported by the directly reward-paired cue. The manipulation also altered learning when inferred value normally acted as a blocker. This shows that retrieved associative structure can influence both performance and new learning. It is relevant to the demands of Modified SOP model, but does not demonstrate that the neural representation is in exactly $A_2$ or that its plasticity has the model’s stipulated sign.^[ref]

The Affective extension of SOP, developed by Allan R. Wagner and Susan E. Brandon, distinguishes sensory-specific and emotive components with different processing time courses and response consequences. Behavioural experiments in rabbits showed modulation of a discrete conditioned eyeblink by another putatively emotive conditioned stimulus. Such dissociations motivate separate response components. They do not locate a complete emotive representation in one nucleus. Basic conditioned-eyelid experiments independently implicated cerebellar nuclear circuitry through lesions, recordings and stimulation, illustrating why a motor conditioned response cannot simply be assigned to the same mechanism as every autonomic or emotional effect.^[ref][ref]

The remaining challenge is discriminative implementation. A candidate neural model should specify what an element is, how direct and retrieved activity differ, how relevant overlap controls plasticity, and how sensory and affective components affect separate outputs. Manipulating receptor function or recording reactivation is not enough unless alternative mechanisms make different predictions. Neuromodulators could regulate transition rates, representation selection or plasticity, but there is no justified general identity such as “dopamine is $A_1$” or “serotonin is $A_2$.” Multiple biological mechanisms could realize the same functional state description.

The SOP model family is therefore a valuable framework connecting stimulus history, expectation and response organization. Primary lesion, receptor and inactivation evidence supports several component processes. Its comprehensive behavioural ambitions exceed what is currently established about its precise neurobiology; the next useful experiments distinguish direct activation from retrieved activation and test the associated plasticity rules, rather than merely find a neural correlate of one familiar behavioural effect.

Recovery of a conditioned response when the context differs from the context of extinction. It shows that performance after extinction can depend on retrieval conditions.