scholarly journals Erratum to: Neural correlates of correct and failed response inhibition in heavy versus light social drinkers: an fMRI study during a go/no-go task by healthy participants

2016 ◽  
Vol 11 (6) ◽  
pp. 1932-1932
Author(s):  
Salvatore Campanella ◽  
Julie Absil ◽  
Carina Carbia Sinde ◽  
Elisa Schroder ◽  
Philippe Peigneux ◽  
...  
2016 ◽  
Vol 11 (6) ◽  
pp. 1796-1811 ◽  
Author(s):  
Salvatore Campanella ◽  
Julie Absil ◽  
Carina Carbia Sinde ◽  
Elisa Schroder ◽  
Philippe Peigneux ◽  
...  

Cephalalgia ◽  
2019 ◽  
Vol 40 (1) ◽  
pp. 79-87 ◽  
Author(s):  
Maike Möller ◽  
Jan Mehnert ◽  
Arne May

Background The role of the trigeminal autonomic reflex in headache syndromes, such as cluster headache, is undisputed but sparsely investigated. The aim of the present study was therefore, to identify neural correlates that play a role in the initiation of the trigeminal autonomic reflex. We further aimed to discriminate between components of the reflex that are involved in nociceptive compared to non-nociceptive processing. Methods Kinetic Oscillation Stimulation (KOS) in the left nostril was applied in order to provoke autonomic symptoms (e.g. lacrimation) via the trigeminal autonomic reflex in 26 healthy participants using functional magnetic resonance imaging. Unpleasantness and painfulness were assessed on a visual analog scale (VAS), in order to assess the quality of the stimulus (e.g. pain or no pain). Results During non-painful activation, specific regions involved in the trigeminal autonomic reflex became activated, including several brainstem nuclei but also cerebellar and bilateral insular regions. However, when the input leading to activation of the trigeminal autonomic reflex was perceived as painful, activation of the anterior hypothalamus, the locus coeruleus (LC), the ventral posteriomedial nucleus of the thalamus (VPM), as well as an activation of ipsilateral insular regions, was observed. Conclusion Our results suggest the anterior hypothalamus, besides the thalamus and specific brain stem regions, play a significant role in networks that mediate autonomic output (e.g. lacrimation) following trigeminal input, but only if the trigeminal system is activated by a stimulus comprising a painful component.


2006 ◽  
Author(s):  
Arthur Aron ◽  
Helen Fisher ◽  
Greg Strong ◽  
Deb Mashek ◽  
HaiFang Li ◽  
...  

2013 ◽  
Author(s):  
Antonello Pellicano ◽  
Houpand Horoufchin ◽  
Harshal Patel ◽  
Iring Koch ◽  
Ferdinand Binkofski

2004 ◽  
Vol 31 (S 1) ◽  
Author(s):  
R Ilg ◽  
K Vogeley ◽  
T Goschke ◽  
A Bolte ◽  
NJ Shah ◽  
...  

Author(s):  
Gianluca Serafini ◽  
Maurizio Pompili ◽  
Andrea Romano ◽  
Denise Erbuto ◽  
Dorian A. Lamis ◽  
...  

2021 ◽  
Vol 2021 (1) ◽  
Author(s):  
Mirko Lehmann ◽  
Claudia Neumann ◽  
Sven Wasserthal ◽  
Johannes Schultz ◽  
Achilles Delis ◽  
...  

Abstract Only little research has been conducted on the pharmacological underpinnings of metacognition. Here, we tested the modulatory effects of a single intravenous dose (100 ng/ml) of the N-methyl-D-aspartate-glutamate-receptor antagonist ketamine, a compound known to induce altered states of consciousness, on metacognition and its neural correlates. Fifty-three young, healthy adults completed two study phases of an episodic memory task involving both encoding and retrieval in a double-blind, placebo-controlled fMRI study. Trial-by-trial confidence ratings were collected during retrieval. Effects on the subjective state of consciousness were assessed using the 5D-ASC questionnaire. Confirming that the drug elicited a psychedelic state, there were effects of ketamine on all 5D-ASC scales. Acute ketamine administration during retrieval had deleterious effects on metacognitive sensitivity (meta-d′) and led to larger metacognitive bias, with retrieval performance (d′) and reaction times remaining unaffected. However, there was no ketamine effect on metacognitive efficiency (meta-d′/d′). Measures of the BOLD signal revealed that ketamine compared to placebo elicited higher activation of posterior cortical brain areas, including superior and inferior parietal lobe, calcarine gyrus, and lingual gyrus, albeit not specific to metacognitive confidence ratings. Ketamine administered during encoding did not significantly affect performance or brain activation. Overall, our findings suggest that ketamine impacts metacognition, leading to significantly larger metacognitive bias and deterioration of metacognitive sensitivity as well as unspecific activation increases in posterior hot zone areas of the neural correlates of consciousness.


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