Antihistamine induced blood oxygenation level dependent response changes related to visual processes during sensori-motor performance

Abstract

The histaminergic involvement in selective processes underlying its role in human sensori-motor performance is largely unknown. Recently, selective effects of central H₁-inverse agonism on sensory visual processes were observed in electrophysiological--but not behavioral data; a discrepancy suggested to result from speeded response-choice related processes. This study attempts to establish the effects on visual processes and identify putative compensatory mechanisms related to increased visual and response-choice task demands by assessing H₁-inverse agonism induced changes in blood oxygenation level dependent (BOLD) response. Twelve participants received oral doses of dexchlorpheniramine 4 mg, lorazepam 1 mg, and placebo in a three-way crossover designed study. Brain activity was assessed for choice reaction time task performance in a 3 T magnetic resonance scanner 2 h after drug administration. Participants responded with their left or right hand and index or middle finger as indicated by the laterality of stimulus presentation and identity of the stimulus, respectively. Stimuli were intact or visually degraded and responses were compatible or incompatible with the laterality of stimulus presentation. Both dexchlorpheniramine and lorazepam affected the BOLD response in the occipital cortex indicating affected visual information processing. Dexchlorpheniramine decreased BOLD response in the dorsal precuneus and left precentral gyrus as part of a motor network, which however might not be interpreted as a compensatory mechanism, but may be the upstream consequence of impaired visual processing.

Cognitive Control Network Function in Alcohol Use Disorder Before and During Treatment With Lorazepam

“…For one, more AUD than HC in the present study had recently taken psychoactive medications. However, quetiapine, citalopram, diphenhydramine, or oxazepam, for example, would have been expected to decrease activation, if anything, and therefore was unlikely to be driving the group task-related effects (Abbott, Jaramillo, Wilcox, & Hamilton, 2013; Coull et al, 1999; McCabe, Mishor, Cowen, & Harmer, 2010; Sperling, 2002; van Ruitenbeek et al, 2013). Second, the fMRI tasks themselves were different (e.g., HC underwent a longer, more involved task than AUD).…”

“…Effects of benzodiazepines on brain networks in AUD or individuals with anxiety have not been investigated. However, benzodiazepines are associated with decreased brain activation in PFC and other brain regions during cognitive tasks in HC (Coull, Frith, & Dolan 1999; Sperling et al, 2002; van Ruitenbeek, Vermeeren, Mehta, Drexler, & Riedel, 2013). Treating anxiety in AUD with concurrent anxiety could, theoretically, either improve or worsen cognitive control, but we hypothesized that, given their anxiety, treatment with benzodiazepines in these AUD would be associated with normalization (decreased activation) in the cognitive control network.…”

Functional connectivity of cognition-related brain networks in adults with fetal alcohol syndrome

“…In four participants, no fMRI data could be acquired because of claustrophobia. After data acquisition, further participants were excluded after review of potentially biasing medication, structural brain lesions, and MRI data quality control before any FC group analyses: Two participants were excluded from the analyses due to use of potentially psychoactive anti-allergic medication unrelated to FAS, which can alter rs-fMRI measurements [ 40 ]. One subject was excluded because of a callosal hypoplasia leading to structural image misregistration.…”