https://www.psychiatrictimes.com/view/need-speed-1
Abnormalities in basal ganglia circuitry have been implicated in the pathophysiology of psychomotor slowing in schizophrenia.5 Inflammation, which is present in (some) patients with schizophrenia, may represent one pathway that contributes to psychomotor slowing in schizophrenia via alterations in neural activity and dopamine metabolism in the basal ganglia.6,7
Goldsmith and colleagues8 examined the relationship between inflammatory markers and performance on a battery of psychomotor tasks in patients with schizophrenia and controls. These tasks included pure motor tasks (eg, finger tapping test [FTT]) as well as those requiring more cognitive demand and cortical activity (eg, trail making test [TMT] and symbol coding [SC]), which may allow distinctions between psychomotor speed and psychomotor processing speed.
Patients performed significantly worse than controls on the FTT, TMT, and SC tasks, but not the RTT. Regarding effects of inflammatory markers on psychomotor task performance after correction for multiple comparisons, for the FTT, there was a significant interaction between diagnosis and: (1) The soluble interleukin-6 receptor (sIL-6R) (dominant and non-dominant), and (2) IL-10 (non-dominant). There was also a significant interaction between diagnosis and IL-10 for the TMT. For the SC tasks, there was a significant interaction between diagnosis and (1) IL-10, (2) sIL-6R, and (3) the IL-1 receptor antagonist (IL-1RA). Using principal components analysis, the authors found that the diagnosis by sIL-6R interaction was significantly associated with slower performance on a “motor factor” (comprised of the FTT for both dominant and non-dominant hands). The interactions between diagnosis and (1) tumor necrosis factor (TNF), (2) IL-10, (3) IL-1RA, and (4) the soluble TNF receptor 2 (sTNFR2) were significantly associated with slower performance on a “psychomotor factor” (comprised on the TMT and SC).