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Acute inflammation and psychomotor slowing: Experimental assessment using lipopolysaccharide administration in healthy humans.

ABSTRACT: Data from clinical and cross-sectional studies suggest that inflammation contributes to psychomotor slowing and attentional deficits found in depressive disorder. However, experimental evidence is still lacking. The aim of this study was to clarify the effect of inflammation on psychomotor slowing using an experimental and acute model of inflammation, in which twenty-two healthy volunteers received an intravenous injection of lipopolysaccharide (LPS, dose: 0.8 ng/kg body weight) and of placebo, in a randomized order following a double-blind within-subject crossover design. A reaction time test and a go/no-go test were conducted 3 h after the LPS/placebo injection and interleukin (IL)-6 and tumor necrosis factor (TNF)-α concentrations were assessed. No effect of experimental inflammation on reaction times or errors for either test was found. However, inflammation was related to worse self-rated performance and lower effort put in the tasks. Exploratory analyses indicated that reaction time fluctuated more over time during acute inflammation. These data indicate that acute inflammation has only modest effects on psychomotor speed and attention in healthy subjects objectively, but alters the subjective evaluation of test performance. Increased variability in reaction time might be the first objective sign of altered psychomotor ability and would merit further investigation.

SUBMITTER: Handke A

PROVIDER: S-EPMC8474655 | biostudies-literature | 2020 Oct

REPOSITORIES: biostudies-literature

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Acute inflammation and psychomotor slowing: Experimental assessment using lipopolysaccharide administration in healthy humans.

Handke Analena A Axelsson John J Benson Sven S Boy Karoline K Weskamp Vera V Hasenberg Till T Remy Miriam M Hebebrand Johannes J Föcker Manuel M Brinkhoff Alexandra A Unteroberdörster Meike M Engler Harald H Schedlowski Manfred M Lasselin Julie J

Brain, behavior, & immunity - health 20200820

Data from clinical and cross-sectional studies suggest that inflammation contributes to psychomotor slowing and attentional deficits found in depressive disorder. However, experimental evidence is still lacking. The aim of this study was to clarify the effect of inflammation on psychomotor slowing using an experimental and acute model of inflammation, in which twenty-two healthy volunteers received an intravenous injection of lipopolysaccharide (LPS, dose: 0.8 ng/kg body weight) and of placebo, ...[more]

PMID: 34589881

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Project description:Psychomotor slowing is a key feature of depressive disorders. Despite its great clinical importance, the pathophysiology and prevalence across different diagnoses and mood states are still poorly understood. Actigraphy allows unbiased, objective, and naturalistic assessment of physical activity as a marker of psychomotor slowing. Yet, the true effect-sizes remain unclear as recent, large systematic reviews are missing. We conducted a novel meta-analysis on actigraphically measured slowing in depression with strict inclusion and exclusion criteria for diagnosis ascertainment and sample duplications. Medline/PubMed and Web-of-Science were searched with terms combining mood-keywords and actigraphy-keywords until September 2021. Original research measuring actigraphy for ⩾24 h in at least two groups of depressed, remitted, or healthy participants and applying operationalized diagnosis was included. Studies in somatically ill patients, N < 10 participants/group, and studies using consumer-devices were excluded. Activity-levels between groups were compared using random-effects models with standardized-mean-differences and several moderators were examined. In total, 34 studies (n = 1804 patients) were included. Patients had lower activity than controls [standardized mean difference (s.m.d.) = -0.78, 95% confidence interval (CI) -0.99 to -0.57]. Compared to controls, patients with unipolar and bipolar disorder had lower activity than controls whether in depressed (unipolar: s.m.d. = -0.82, 95% CI -1.07 to -0.56; bipolar: s.m.d. = -0.94, 95% CI -1.41 to -0.46), or remitted/euthymic mood (unipolar: s.m.d. = -0.28, 95% CI -0.56 to 0.0; bipolar: s.m.d. = -0.92, 95% CI -1.36 to -0.47). None of the examined moderators had any significant effect. To date, this is the largest meta-analysis on actigraphically measured slowing in mood disorders. They are associated with lower activity, even in the remitted/euthymic mood-state. Studying objective motor behavior via actigraphy holds promise for informing screening and staging of affective disorders.

Project description:Psychomotor slowing is a frequent symptom of schizophrenia. Short-interval intracortical inhibition assessed by transcranial magnetic stimulation demonstrated inhibitory dysfunction in schizophrenia. The inhibitory deficit results from additional noise during information processing in the motor system in psychosis. Here, we tested whether cortical inhibitory dysfunction was linked to psychomotor slowing and motor network alterations. In this cross-sectional study, we included 60 patients with schizophrenia and psychomotor slowing determined by the Salpêtrière Retardation Rating Scale, 23 patients without slowing and 40 healthy control participants. We acquired single and double-pulse transcranial magnetic stimulation effects from the left primary motor cortex, resting-state functional connectivity and diffusion imaging on the same day. Groups were compared on resting motor threshold, amplitude of the motor evoked potentials, as well as short-interval intracortical inhibition. Regression analyses calculated the association between motor evoked potential amplitudes or cortical inhibition with seed-based resting-state functional connectivity from the left primary motor cortex and fractional anisotropy at whole brain level and within major motor tracts. In patients with schizophrenia and psychomotor slowing, we observed lower amplitudes of motor evoked potentials, while the short-interval intracortical inhibition/motor evoked potentials amplitude ratio was higher than in healthy controls, suggesting lower cortical inhibition in these patients. Patients without slowing also had lower amplitudes of motor evoked potentials. Across the combined patient sample, cortical inhibition deficits were linked to more motor coordination impairments. In patients with schizophrenia and psychomotor slowing, lower amplitudes of motor evoked potentials were associated with lower fractional anisotropy in motor tracts. Moreover, resting-state functional connectivity between the primary motor cortex, the anterior cingulate cortex and the cerebellum increased with stronger cortical inhibition. In contrast, in healthy controls and patients without slowing, stronger cortical inhibition was linked to lower resting-state functional connectivity between the left primary motor cortex and premotor or parietal cortices. Psychomotor slowing in psychosis is linked to less cortical inhibition and aberrant functional connectivity of the primary motor cortex. Higher neural noise in the motor system may drive psychomotor slowing and thus may become a treatment target.

Dataset Information

Acute inflammation and psychomotor slowing: Experimental assessment using lipopolysaccharide administration in healthy humans.

Publications

Acute inflammation and psychomotor slowing: Experimental assessment using lipopolysaccharide administration in healthy humans.

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