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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

Correlation (Spearman's rank) between fMRI response strength and subclinical negative symptoms in siblings (N = 88) in the medial frontal gyrus (MFG) during the anticipation phase (large reward).
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Figure 5: Correlation (Spearman's rank) between fMRI response strength and subclinical negative symptoms in siblings (N = 88) in the medial frontal gyrus (MFG) during the anticipation phase (large reward).

Mentions: In the regions that showed an effect of group in the whole-brain analyses (see Figures 3, 4), we calculated the correlation between the fMRI response strength (beta estimates) and the CAPE scores (Figure 5). We eliminated extreme outliers (mean ± 2 sd) in beta values to ensure that possible correlations were not driven by outliers. Due to non-normal distribution of the subclinical symptom scales, we performed Spearman's rank correlations. To correct for multiple comparisons in the whole-brain areas, correlations were corrected at alpha levels of 0.00625 per test (0.05/8, Bonferroni corrected). In siblings, there was a positive correlation between MFG activation (large reward trials), where a group effect of reward anticipation was found, and negative symptoms (r = 0.368, p < 0.001).


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)

Correlation (Spearman's rank) between fMRI response strength and subclinical negative symptoms in siblings (N = 88) in the medial frontal gyrus (MFG) during the anticipation phase (large reward).
© Copyright Policy
Related In: Results  -  Collection

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

Figure 5: Correlation (Spearman's rank) between fMRI response strength and subclinical negative symptoms in siblings (N = 88) in the medial frontal gyrus (MFG) during the anticipation phase (large reward).
Mentions: In the regions that showed an effect of group in the whole-brain analyses (see Figures 3, 4), we calculated the correlation between the fMRI response strength (beta estimates) and the CAPE scores (Figure 5). We eliminated extreme outliers (mean ± 2 sd) in beta values to ensure that possible correlations were not driven by outliers. Due to non-normal distribution of the subclinical symptom scales, we performed Spearman's rank correlations. To correct for multiple comparisons in the whole-brain areas, correlations were corrected at alpha levels of 0.00625 per test (0.05/8, Bonferroni corrected). In siblings, there was a positive correlation between MFG activation (large reward trials), where a group effect of reward anticipation was found, and negative symptoms (r = 0.368, p < 0.001).

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