Revisiting motor inhibition in individuals with functional paralysis and spinal cord injury

Functional paralysis (FP), a subtype of functional neurological disorder (FND), is characterized by symptoms of paralysis without clinically evident damage to the nervous system. Previous research has reported impaired inhibitory control in FND, such as weaker inhibition and slower response latencies, yet the underlying neural correlates remain unclear. Moreover, it is unknown whether such neural correlates depend on the symptoms or are a specific trait of the disorder. To address this gap, we compared individuals with chronic FP, healthy controls (HCs) and individuals with spinal cord injury (SCI), who present a similar symptom phenotype but differ in the cause of their condition, hence provided the opportunity to disentangle disorder-specific from symptom-specific patterns of neural activity. In this observational study, 16 patients with FP (6 males/10 females; mean age = 39.4 ± 13.1 years), 24 patients with SCI (18 males/6 females; mean age = 42.4 ± 11.6 years) and 29 HC (8 males/21 females; mean age = 35.5 ± 12.6 years) underwent event-related functional MRI while performing a go/no-go task. We conducted a task-related validation analysis to isolate functional networks involved in response inhibition, and implemented a generalized psychophysiological interaction (gPPI) focusing on the associative motor network. We then compared behavioural performance and patterns of functional connectivity across groups with a general linear model. No group differences in task performance emerged, suggesting intact motor inhibition in FP. Validation analysis over the whole sample showed the recruitment of typical regions of the motor inhibition network. Compared with HC, we identified significant differences in functional connectivity (P < 0.05, family-wise error corrected) in both paralysis groups (FP and SCI), which exhibited higher functional connectivity between the right precentral gyrus and the left insula during response inhibition. Functional connectivity during response inhibition was similar between patient groups. These findings suggest a shared neural pattern associated with symptoms of paralysis, rather than a disorder-specific deficit, and may reflect an abnormal limbic drive of the motor network involved in movement initiation.