The Need for Speed


Psychomotor speed may be a relevant target in studies of the immune system and its impact on the brain in patients with schizophrenia.

There is evidence of deficits in psychomotor speed in patients with schizophrenia, which may represent an independent cognitive domain in the disorder and is associated with worse outcomes.1,2 There is evidence that abnormal psychomotor activity and processing speed may be present in both high-risk and first-episode psychosis.3,4 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.

The authors recruited 43 patients with schizophrenia or schizoaffective disorder and 29 healthy controls. All subjects were age 18-65.  Controls had no history of major psychiatric disorders, as confirmed by structured clinical interview. Subjects were excluded if they had a heart attack or heart failure within the past 6 months; hospitalization, antibiotic use, or any condition requiring steroids within the past 60 days; neurologic disease, head trauma, CNS infection, epilepsy, intellectual disability, HIV, autoimmune disorder, or clinically significant hearing or visual impairment; or active substance use in the past 3 months (confirmed by structured clinical interview and urine toxicology). Psychomotor performance was assessed by the FTT, TMT, SC, and RTT (visuomotor task consisting of the measurement of reaction time). Blood samples for the measurement of inflammatory markers were also collected. Data were analyzed using generalized linear models with gamma-log link, to investigate the effect of subject group (schizophrenia versus control), controlling for age, sex, race, smoking, and body mass index, and adjusting for multiple comparisons. 

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). 

The authors concluded that schizophrenia is associated with significant slowing on a variety of psychomotor tasks, and this slowing was associated with a number of peripheral blood inflammatory markers.  Noted strengths of the study included a hypothesis-driven approach, a broad panel of inflammatory markers, and the availability of a healthy control group.  The primary study limitation was the relatively small sample size. 

The bottom line
Psychomotor speed may be a relevant target in studies of the immune system and its impact on the brain in patients with schizophrenia.


1. Morrens M, Hulstijn W, Sabbe B. Psychomotor slowing in schizophrenia. Schizophr Bull. 2007;33:1038-1053.
2. Green M F. What are the functional consequences of neurocognitive deficits in schizophrenia?Am J Psychiatry. 1996;153:321-330.
3. Gold S, Arndt S, Nopoulos P, et al. Longitudinal study of cognitive function in first-episode and recent-onset schizophrenia. Am J Psychiatry. 1999;156:1342-1348.
4. Hou CL, Xiang YT, Wang ZL, et al. Cognitive functioning in individuals at ultra-high risk for psychosis, first-degree relatives of patients with psychosis and patients with first episode schizophrenia. Schizophr Res. 2016;174:71-76.
5. Muller JL, Roder C, Schuierer G, Klein HE. Subcortical overactivation in untreated schizophrenic patients: a functional magnetic resonance image fingertapping study. Psychiatry Clin Neurosci. 2002;56:77-84.
6. Goldsmith DR, Rapaport MH, Miller BJ. A meta-analysis of blood cytokine network alterations in psychiatric patients: comparisons between schizophrenia, bipolar disorder and depression. Mol Psychiatry. 2016;21:1696-1709.
7. Brydon L, Harrison NA, Walker C, et al. Peripheral inflammation is associated with altered substantia nigra activity and psychomotor slowing in humans. Biol Psychiatry. 2008;63:1022-1029.
8. Goldsmith DR, Massa N, Pearce B, et al. Inflammatory markers are associated with psychomotor slowing in aptients with schizophrenia compared to healthy controls. NPJ Schizophr. 2020;6:8.

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