Cortico-striatal networks and cognitive deficit structure in endogenous disorders with catatonic symptomatology: a factor-analytic study of neuropsychological profile

Background. Contemporary neuroimaging studies reveal that catatonia is associated with specific dysfunction patterns in cortico-striatal-thalamic networks, with particular involvement of fronto-striatal circuits regulating motor control and executive functions. Factor-analytic approaches to cognitive assessment can identify distinct neuropsychological profiles reflecting underlying neural network alterations in catatonic disorders.

Objective. To characterize the structure of neurocognitive deficits in endogenous disorders with catatonic symptomatology through factor analysis, identifying distinct cognitive profiles associated with cortico-striatal and temporo-parietal network dysfunction, and to evaluate the modifying effect of affective comorbidity on these patterns.

Material and Methods. The study included 139 patients: main group (n = 69) with endogenous disorders including catatonic symptomatology, divided into subgroups without (n = 35) and with pronounced depressive symptomatology (n = 34), and control group (n = 70) with similar subdivision. Catatonia was assessed using Bush-Francis Scale (BFCRS). Neurocognitive evaluation included BACS battery, MoCA and FAB scales. Factor analysis with varimax rotation was applied to identify cognitive deficit structure. Statistical analysis included MANOVA with Bonferroni correction.

Results. Factor analysis revealed distinct cognitive structures. In catatonia without affective symptomatology, three factors emerged: (1) a fronto-striatal factor (47.2 % of variance), comprising executive functions, psychomotor speed, and inhibitory control; (2) a temporo-parietal factor (26.3 % of variance), including visuospatial functions and constructive praxis; and (3) a hippocampal factor (19.8 % of variance), associated with episodic memory and delayed recall. In the presence of affective comorbidity, two factors were identified: (1) a fronto-limbic factor, accounting for 53.7% of the variance and encompassing attention, working memory, and emotional regulation; and (2) a fronto-striatal factor, accounting for 30.1 % of the variance and encompassing psychomotor speed and executive functions. MANOVA revealed significant group differences across all cognitive domains (d = 0.52–1.31, p < 0.001). Two-factor analysis showed main effect of catatonia (F = 31.2, p < 0.001, η² = 0.19), moderate effect of affectivity (F = 12.4, p < 0.01, η² = 0.08) and their interaction (F = 7.8, p < 0.01, η² = 0.05).

Conclusion. Catatonic disorders demonstrate distinct cognitive profiles on factor analysis, reflecting specific cortico-striatal and temporo-parietal network dysfunction. Affective comorbidity transforms the cognitive structure toward fronto-limbic involvement, indicating the need for differentiated rehabilitation targeting specific neural networks.

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