Neural circuits localisation MEQ (psychosis and frontal change)

(i) Dopamine map. Positive symptoms are framed via mesolimbic VTA→nucleus accumbens dysregulation and aberrant salience (Howes–Kapur version III: DA as final common pathway onto which risks including stimulants converge).[1] Other pathways: mesocortical (VTA→PFC) — cognition/negative-symptom models; nigrostriatal — EPS with D2 blockade; tuberoinfundibular — hyperprolactinaemia with D2 blockade.[1]

(ii) Frontal syndromes. Progressive tactlessness after OFC TBI fits orbitofrontal disinhibited syndrome. Contrast: DLPFC → dysexecutive (planning, working memory, set-shifting failure); medial/ACC → abulia/apathy/reduced initiation.[2]

(iii) Triple network. Menon: disordered interactions among DMN (self-referential), salience network (insula/dACC switch), and CEN (goal-directed control). Psychosis can be discussed as salience misassignment and failed SN-mediated switching plus broader dysconnection of predictive self-monitoring networks.[3][4][5]

(iv) Investigations despite elegant circuitry. Stimulant screen/collateral, metabolic panel, infection as indicated, MRI brain (prior TBI anatomy, rule out new structural disease), consider EEG if seizures/fluctuation, autoimmune work-up if atypical/subacute progressive, full MSE and risk assessment. Circuit language never cancels organic exclusion in first episode.[1][4]

(v) Pitfalls. (1) Phrenology — one lesion or one fMRI map ≠ whole diagnosis. (2) Confusing group research imaging with individual diagnostic tests; also confusing EPS (nigrostriatal) with primary negative symptoms (mesocortical models).[3][1]