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Neural correlates of reward processing in healthy siblings of patients with schizophrenia.

Hanssen E, van der Velde J, Gromann PM, Shergill SS, de Haan L, Bruggeman R, Krabbendam L, Aleman A, van Atteveldt N - Front Hum Neurosci (2015)

Bottom Line: Studies in patients with SZ have found less activation in the ventral striatum (VS) during anticipation of reward, but these findings do not provide information on effect of the genetic load on reward processing.Thus, in contrast to prior literature in patients with SZ, the results do not point to altered brain activity in classical RP brain areas, such as the VS.However, the weaker deactivation found outside the reward-related network in siblings could indicate reduced task-related suppression (i.e., hyperactivation) of the DMN.

View Article: PubMed Central - PubMed

Affiliation: Department of Educational Neuroscience and LEARN! Institute, VU University Amsterdam Amsterdam, Netherlands ; CSI Lab, Department of Psychosis Studies, Institute of Psychiatry, King's College London London, UK.

ABSTRACT
Deficits in motivational behavior and psychotic symptoms often observed in schizophrenia (SZ) may be driven by dysfunctional reward processing (RP). RP can be divided in two different stages; reward anticipation and reward consumption. Aberrant processing during reward anticipation seems to be related to SZ. Studies in patients with SZ have found less activation in the ventral striatum (VS) during anticipation of reward, but these findings do not provide information on effect of the genetic load on reward processing. Therefore, this study investigated RP in healthy first-degree relatives of SZ patients. The sample consisted of 94 healthy siblings of SZ patients and 57 healthy controls. Participants completed a classic RP task, the Monetary Incentive Delay task, during functional magnetic resonance imaging (fMRI). As expected, there were no behavioral differences between groups. In contrast to our expectations, we found no differences in any of the anticipatory reward related brain areas (region of interest analyses). Whole-brain analyses did reveal group differences during both reward anticipation and reward consumption; during reward anticipation siblings showed less deactivation in the insula, posterior cingulate cortex (PCC) and medial frontal gyrus (MFG) than controls. During reward consumption siblings showed less deactivation in the PCC and the right MFG compared to controls and activation in contrast to deactivation in controls in the precuneus and the left MFG. Exclusively in siblings, MFG activity correlated positively with subclinical negative symptoms. These regions are typically associated with the default mode network (DMN), which normally shows decreases in activation during task-related cognitive processes. Thus, in contrast to prior literature in patients with SZ, the results do not point to altered brain activity in classical RP brain areas, such as the VS. However, the weaker deactivation found outside the reward-related network in siblings could indicate reduced task-related suppression (i.e., hyperactivation) of the DMN. The presence of DMN hyperactivation during reward anticipation and reward consumption might indicate that siblings of patients with SZ have a higher baseline level of DMN activation and possible abnormal network functioning.

No MeSH data available.


Related in: MedlinePlus

Monetary Incentive Delay task: an example of a successful large reward trial displaying all events and durations in the trial.
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Figure 1: Monetary Incentive Delay task: an example of a successful large reward trial displaying all events and durations in the trial.

Mentions: Subjects completed a modified version of the Monetary Incentive Delay (MID) task (Knutson et al., 2001b). In the current version, three levels of reward anticipation were visually cued: large reward, small reward, or no reward (control trial). The participants' reaction time of a button press to a target determined whether the reward outcome was successful (within the target presentation time) in each trial. The two phases of interest are the anticipatory phase (during the cue presentation); and the outcome phase (trial outcome presentation). Event durations were randomly assigned to the trials in each run, but equal for each participant, and summing up to a fixed total trial duration of 18.5 s (semi-random jittered). Each trial (Figure 1) consisted of (1) reward cue (semi-random jittered duration: 2000–7750 ms): a large green arrow pointing up indicating a potential reward of € 5 (large reward), a small green arrow pointing up indicating potential reward of € 0.5 (small reward), or a small green arrow pointing up combined with a red one pointing down (control trial, no reward), (2) target: presentation of a brief “target” square (duration initially 250 ms, then adjusted by an algorithm to ensure 66% success), (3) fixation 1: a delay of 2000–7750 ms (semi-random jittered), (4) reward outcome: presentation of the outcome of the trial (semi-random jittered 2000–7750 ms), (5) fixation 2 (semi-random jittered 2000–7750 ms).


Neural correlates of reward processing in healthy siblings of patients with schizophrenia.

Hanssen E, van der Velde J, Gromann PM, Shergill SS, de Haan L, Bruggeman R, Krabbendam L, Aleman A, van Atteveldt N - Front Hum Neurosci (2015)

Monetary Incentive Delay task: an example of a successful large reward trial displaying all events and durations in the trial.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4585217&req=5

Figure 1: Monetary Incentive Delay task: an example of a successful large reward trial displaying all events and durations in the trial.
Mentions: Subjects completed a modified version of the Monetary Incentive Delay (MID) task (Knutson et al., 2001b). In the current version, three levels of reward anticipation were visually cued: large reward, small reward, or no reward (control trial). The participants' reaction time of a button press to a target determined whether the reward outcome was successful (within the target presentation time) in each trial. The two phases of interest are the anticipatory phase (during the cue presentation); and the outcome phase (trial outcome presentation). Event durations were randomly assigned to the trials in each run, but equal for each participant, and summing up to a fixed total trial duration of 18.5 s (semi-random jittered). Each trial (Figure 1) consisted of (1) reward cue (semi-random jittered duration: 2000–7750 ms): a large green arrow pointing up indicating a potential reward of € 5 (large reward), a small green arrow pointing up indicating potential reward of € 0.5 (small reward), or a small green arrow pointing up combined with a red one pointing down (control trial, no reward), (2) target: presentation of a brief “target” square (duration initially 250 ms, then adjusted by an algorithm to ensure 66% success), (3) fixation 1: a delay of 2000–7750 ms (semi-random jittered), (4) reward outcome: presentation of the outcome of the trial (semi-random jittered 2000–7750 ms), (5) fixation 2 (semi-random jittered 2000–7750 ms).

Bottom Line: Studies in patients with SZ have found less activation in the ventral striatum (VS) during anticipation of reward, but these findings do not provide information on effect of the genetic load on reward processing.Thus, in contrast to prior literature in patients with SZ, the results do not point to altered brain activity in classical RP brain areas, such as the VS.However, the weaker deactivation found outside the reward-related network in siblings could indicate reduced task-related suppression (i.e., hyperactivation) of the DMN.

View Article: PubMed Central - PubMed

Affiliation: Department of Educational Neuroscience and LEARN! Institute, VU University Amsterdam Amsterdam, Netherlands ; CSI Lab, Department of Psychosis Studies, Institute of Psychiatry, King's College London London, UK.

ABSTRACT
Deficits in motivational behavior and psychotic symptoms often observed in schizophrenia (SZ) may be driven by dysfunctional reward processing (RP). RP can be divided in two different stages; reward anticipation and reward consumption. Aberrant processing during reward anticipation seems to be related to SZ. Studies in patients with SZ have found less activation in the ventral striatum (VS) during anticipation of reward, but these findings do not provide information on effect of the genetic load on reward processing. Therefore, this study investigated RP in healthy first-degree relatives of SZ patients. The sample consisted of 94 healthy siblings of SZ patients and 57 healthy controls. Participants completed a classic RP task, the Monetary Incentive Delay task, during functional magnetic resonance imaging (fMRI). As expected, there were no behavioral differences between groups. In contrast to our expectations, we found no differences in any of the anticipatory reward related brain areas (region of interest analyses). Whole-brain analyses did reveal group differences during both reward anticipation and reward consumption; during reward anticipation siblings showed less deactivation in the insula, posterior cingulate cortex (PCC) and medial frontal gyrus (MFG) than controls. During reward consumption siblings showed less deactivation in the PCC and the right MFG compared to controls and activation in contrast to deactivation in controls in the precuneus and the left MFG. Exclusively in siblings, MFG activity correlated positively with subclinical negative symptoms. These regions are typically associated with the default mode network (DMN), which normally shows decreases in activation during task-related cognitive processes. Thus, in contrast to prior literature in patients with SZ, the results do not point to altered brain activity in classical RP brain areas, such as the VS. However, the weaker deactivation found outside the reward-related network in siblings could indicate reduced task-related suppression (i.e., hyperactivation) of the DMN. The presence of DMN hyperactivation during reward anticipation and reward consumption might indicate that siblings of patients with SZ have a higher baseline level of DMN activation and possible abnormal network functioning.

No MeSH data available.


Related in: MedlinePlus