SwePub
Tyck till om SwePub Sök här!
Sök i SwePub databas

  Extended search

Träfflista för sökning "L773:1873 2402 srt2:(2010-2014)"

Search: L773:1873 2402 > (2010-2014)

  • Result 1-10 of 59
Sort/group result
   
EnumerationReferenceCoverFind
1.
  •  
2.
  •  
3.
  •  
4.
  •  
5.
  • Berna, Chantal, et al. (author)
  • Induction of Depressed Mood Disrupts Emotion Regulation Neurocircuitry and Enhances Pain Unpleasantness
  • 2010
  • In: Biological Psychiatry. - : ELSEVIER SCIENCE INC. - 0006-3223 .- 1873-2402. ; 67:11, s. 1083-1090
  • Journal article (peer-reviewed)abstract
    • Background: Depressed mood alters the pain experience. Yet, despite its clear clinical relevance, little is known about the cognitive and neural mechanisms underlying this phenomenon. We tested an experimental manipulation to unravel the interaction between depressed mood and pain. We hypothesized that dysregulation of the neural circuitry underlying emotion regulation is the mechanism whereby pain processing is affected during depressed mood. Methods: Using functional magnetic resonance imaging, we compared the effects of sad and neutral cognitive mood inductions on affective pain ratings, pain-specific cognitions, and central pain processing of a tonic noxious heat stimulus in 20 healthy volunteers. Results: The increase in negative pain-specific cognitions during depressed mood predicted the perceived increase in pain unpleasantness. Following depressed mood induction, brain responses to noxious thermal stimuli were characterized by increased activity in a broad network including prefrontal areas, subgenual anterior cingulate cortex, and hippocampus, as well as significantly less deactivation when compared with pain responses in a neutral mood. The participants who reported the largest increase in pain unpleasantness after the sad mood induction showed greater inferior frontal gyrus and amygdala activation, linking changes in emotion regulation mechanisms with enhancement of pain affect. Conclusions: Our results inform how depressed mood and chronic pain co-occur clinically and may serve to develop and translate effective interventions using pharmacological or psychological treatment.
  •  
6.
  •  
7.
  •  
8.
  •  
9.
  • Browning, Michael, et al. (author)
  • Lateral Prefrontal Cortex Mediates the Cognitive Modification of Attentional Bias
  • 2010
  • In: Biological Psychiatry. - : ELSEVIER SCIENCE INC. - 0006-3223 .- 1873-2402. ; 67:10, s. 919-925
  • Journal article (peer-reviewed)abstract
    • Background: A tendency to orient attention toward threatening stimuli may be involved in the etiology of anxiety disorders. In keeping with this, both psychological and pharmacological treatments of anxiety reduce this negative attentional bias. It has been hypothesized, but not proved, that psychological interventions may alter the function of prefrontal regions supervising the allocation of attentional resources. Methods: The current study examined the effects of a cognitive training regime on attention. Participants were randomly assigned to one of two training conditions: "attend-threat" training, which increases negative attentional bias, or "avoid-threat" training, which reduces it. The behavioral effects of training were assessed using a sample of 24 healthy participants. Functional magnetic resonance imaging data were collected in a further 29 healthy volunteers using a protocol that allowed the influence of both stimuli valence and attention to be discriminated. Results: Cognitive training induced the expected attentional biases in healthy volunteers. Further, the training altered lateral frontal activation to emotional stimuli, with these areas responding specifically to violations of the behavioral rules learned during training. Connectivity analysis confirmed that the identified lateral frontal regions were influencing attention as indexed by activity in visual association cortex. Conclusions: Our results indicate that frontal control over the processing of emotional stimuli may be tuned by psychological interventions in a manner predicted to regulate levels of anxiety. This directly supports the proposal that psychological interventions may influence attention via an effect on the prefrontal cortex.
  •  
10.
  • Browning, Michael, et al. (author)
  • Using Attentional Bias Modification as a Cognitive Vaccine Against Depression
  • 2012
  • In: Biological Psychiatry. - : ELSEVIER SCIENCE INC. - 0006-3223 .- 1873-2402. ; 72:7, s. 572-579
  • Journal article (peer-reviewed)abstract
    • Background: Negative attentional biases are thought to increase the risk of recurrence in depression, suggesting that reduction of such biases may be a plausible strategy in the secondary prevention of the illness. However, no previous study has tested whether reducing negative attentional bias causally affects risk factors for depressive recurrence. The current experimental medicine study reports the effects of a computerized attentional bias modification (ABM) procedure on intermediate measures of the risk of depressive recurrence (residual depressive symptoms and the cortisol awakening response) in patients with recurrent depression. Methods: Sixty-one patients with at least two previous episodes of depression who were currently in remission were randomized to receive either an active (positive) or placebo computer-based ABM regime. The ABM regime presented either pictures of faces or words. Residual depressive symptoms, measured using the Beck Depression Inventory and the cortisol awakening response were measured immediately before and after completion of the bias modification and then again after 4 weeks' follow-up. Results: Positive, face-based ABM reduced both measures of recurrence risk (Beck Depression Inventory and cortisol awakening response). This effect occurred during the month following completion of bias modification. Word-based modification did not influence the outcome measures. Conclusions: Positive face-based ABM was able to reduce intermediate measures of recurrence risk in previously depressed patients. These results suggest that ABM may provide a "cognitive vaccine" against depression and offer a useful strategy in the secondary prevention of the illness.
  •  
Skapa referenser, mejla, bekava och länka
  • Result 1-10 of 59
Type of publication
journal article (55)
conference paper (4)
Type of content
peer-reviewed (42)
other academic/artistic (17)
Author/Editor
Fredrikson, Mats (12)
Furmark, Tomas (12)
Frick, Andreas (10)
Engman, Jonas (8)
Gingnell, Malin (6)
Alaie, Iman (5)
show more...
Björkstrand, Johanne ... (5)
Wahlstedt, Kurt (5)
Kere, Juha (4)
Faria, Vanda (4)
Matsson, Hans (4)
Åhs, Fredrik (4)
Svenningsson, P (3)
Sullivan, PF (3)
Rietschel, M (3)
Holmes, Emily A. (3)
Wallenquist, Ulrika (3)
Peyrard-Janvid, Myri ... (3)
Blennow, Kaj, 1958 (2)
Linnman, Clas (2)
Andreassen, OA (2)
Melle, I (2)
Djurovic, S (2)
Carlbring, Per (2)
Rujescu, D (2)
Werge, T (2)
Sebat, J (2)
Larsson, Elna-Marie (2)
Cichon, S (2)
Jonsson, EG (2)
Levinson, DF (2)
Harmer, Catherine J. (2)
Uvnäs-Moberg, Kersti ... (2)
Heilig, Markus (2)
Lichtenstein, Paul (2)
Olsson, Carl-Johan (2)
Greengard, P (2)
Anckarsäter, Henrik, ... (2)
Eriksson, Elias (2)
Gustafsson, O. (2)
Andersson, Gerhard (2)
Peltonen, L (2)
Hurd, YL (2)
Jokinen, J (2)
Sigurdsson, E (2)
Asberg, M (2)
Morell, Arvid (2)
Goodwin, Guy M. (2)
Laukka, Petri (2)
Fischer, Håkan (2)
show less...
University
Karolinska Institutet (31)
Uppsala University (25)
Stockholm University (7)
University of Gothenburg (6)
Umeå University (4)
Linköping University (4)
show more...
Örebro University (2)
Södertörn University (2)
Swedish University of Agricultural Sciences (2)
Jönköping University (1)
Lund University (1)
Mid Sweden University (1)
Karlstad University (1)
show less...
Language
English (59)
Research subject (UKÄ/SCB)
Medical and Health Sciences (28)
Social Sciences (12)

Year

Kungliga biblioteket hanterar dina personuppgifter i enlighet med EU:s dataskyddsförordning (2018), GDPR. Läs mer om hur det funkar här.
Så här hanterar KB dina uppgifter vid användning av denna tjänst.

 
pil uppåt Close

Copy and save the link in order to return to this view