Mechanism-Transition Synthesis — 2014–2024

What the bridge is not

It is not:

CU traits → biological deficit → neurotechnology treatment

That sequence is too linear and stronger than the record supports.

What the bridge more closely resembles

A. Heterogeneity / equifinality

Similar outward conduct problems can coexist with different fear, anxiety, CU, and physiological profiles.

B. Multi-system measurement

Heart rate, skin conductance, RSA, startle, facial EMG, gaze, and neural measures are added to behavioral and informant measures.

C. Candidate mechanisms

Emotion recognition, attention allocation, fear reactivity, autonomic regulation, and prefrontal control become candidate mechanisms rather than merely correlates.

D. Subtype-specific neural/attentional testing

Amygdala, prefrontal, gaze, and emotion-processing results are tested across primary/secondary or CU/LPE-related subgroups. Findings are mixed enough to require task- and construct-specific models.

E. Experimental manipulation

cTBS of DLPFC is the clearest neural causal-manipulation gate in this period. Facial-mimicry and attention procedures provide non-neural manipulation of proximal emotional processes.

F. Transactional reintegration

Physiology continues to interact with parenting/environment rather than replacing it as an explanation.

G. Mechanism-targeted intervention

By 2024, parent-child/emotional interventions explicitly attempt to change hypothesized affective mechanisms. The evidence is strongest for proximal emotional/physiological change, not yet for a general claim of durable antisocial-behavior remission from neuroscience-informed technology.

Current bridge boundary

Measurable and manipulable does not equal clinically sufficient.

The next research pass must therefore reverse-map every 2026 intervention claim to the exact population, comparator, endpoint, follow-up, and peer-reviewed outcome paper before the atlas renders those interventions as efficacy nodes.