RESUMEN
BACKGROUND: Intimacy is a key psychological problem in anorexia nervosa (AN). Empirical evidence, including neurobiological underpinnings, is however, scarce. OBJECTIVE: In this study, we evaluated various emotional stimuli including intimate stimuli experienced in patients with AN and non-patients, as well as their cerebral response. METHODS: Functional magnetic resonance imaging was conducted using stimuli with positive, neutral, negative and intimate content. Participants (14 AN patients and 14 non-patients) alternated between passive viewing and explicit emotion regulation. RESULTS: Intimate stimuli were experienced less positively in AN patients compared to non-patients. AN patients showed decreased cerebral responses in superior parietal cortices in response to positive and intimate stimuli. Intimate stimuli led to stronger activation of the orbitofrontal cortex, and lower activation of the bilateral precuneus in AN patients. Orbitofrontal responses decreased in AN patients during explicit emotion regulation. CONCLUSIONS: These results show that intimate stimuli are of particular importance in AN patients, who show experiential differences compared to non-patients and altered activation of orbitofrontal and parietal brain structures. This supports that AN patients have difficulties with intimacy, attachment, self-referential processing and body perception. LEVEL OF EVIDENCE: Level III, case-control study.
Asunto(s)
Anorexia Nerviosa/diagnóstico por imagen , Regulación Emocional , Lóbulo Frontal/diagnóstico por imagen , Relaciones Interpersonales , Lóbulo Parietal/diagnóstico por imagen , Anorexia Nerviosa/fisiopatología , Anorexia Nerviosa/psicología , Estudios de Casos y Controles , Emociones , Femenino , Lóbulo Frontal/fisiopatología , Neuroimagen Funcional , Humanos , Imagen por Resonancia Magnética , Lóbulo Parietal/fisiopatología , Adulto JovenRESUMEN
OBJECTIVE: The aim of this functional magnetic resonance imaging (fMRI) study was to investigate reward-related brain activity in satiated overweight and healthy-weight participants in response to high-calorie palatable food pictures, when viewing the pictures without prior instructions (called unbiased viewing) versus imagining the taste of the shown pictures (called taste imagination). We predicted that neural activation in brain reward regions would be greater in overweight participants than in healthy-weight ones and that this difference between groups would be strongest during unbiased viewing. METHOD: Neural activation was measured using fMRI in 14 overweight (mean body mass index (BMI): 29.8 kg m(-2)) and 15 healthy-weight (mean BMI: 21.1 kg m(-2)) participants who were satiated, in response to palatable and unpalatable high-calorie and low-calorie food pictures, presented in an event-related design during two conditions: unbiased viewing (no prior instructions) versus taste imagination. RESULTS: A group × condition interaction was found in 14 brain regions involved in food reward processing during the presentation of high-calorie palatable food stimuli. During the taste imagination condition, neural activation in these regions was greater in the overweight participants than in the healthy-weight ones. Contrary to our expectations, the opposite pattern was observed during unbiased viewing: activation in reward regions in the overweight participants was reduced compared with the healthy-weight ones. In all brain reward regions except for the left amygdala, the group × condition interaction was specific to high-calorie palatable food stimuli. CONCLUSION: Greater reward activity in the overweight participants compared with the control group when imagining taste may represent an increased reward response induced by high-calorie palatable food. During unbiased viewing, reduced reward activation in the overweight participants compared with those with a healthy weight may reflect avoidance of high-calorie palatable food stimuli. Taken together, this pattern of activation may reflect ambivalence in the overweight group between desire for (in the taste imagination condition) and avoidance of (in the unbiased viewing condition) high-calorie palatable food stimuli.
Asunto(s)
Mapeo Encefálico , Imagen por Resonancia Magnética/métodos , Obesidad/fisiopatología , Corteza Prefrontal/fisiopatología , Saciedad , Adulto , Señales (Psicología) , Femenino , Alimentos , Humanos , Obesidad/psicología , Estimulación Luminosa , Periodo Posprandial , RecompensaRESUMEN
Stress-induced changes in functional brain connectivity have been linked to the etiology of stress-related disorders. Resting state functional connectivity (rsFC) is especially informative in characterizing the temporal trajectory of glucocorticoids during stress adaptation. Using the imaging Maastricht Acute Stress Test (iMAST), we induced acute stress in 39 healthy volunteers and monitored the neuroendocrine stress levels during three runs of resting state functional magnetic resonance imaging (rs-fMRI): before (run 1), immediately following (run 2), and 30 min after acute stress (run 3). The iMAST resulted in strong increases in cortisol levels. Whole-brain analysis revealed that acute stress (run 2 - 1) was characterized by changes in connectivity of the amygdala with the ventrolateral prefrontal cortex (vlPFC), ventral posterior cingulate cortex (PCC), cuneus, parahippocampal gyrus, and culmen. Additionally, cortisol responders were characterized by enhanced amygdala - medial prefrontal cortex (mPFC) connectivity. Stress recovery (run 3 - 2) was characterized by altered amygdala connectivity with the dorsolateral prefrontal cortex (dlPFC), ventral and dorsal anterior cingulate cortex (ACC), anterior hippocampal complex, cuneus, and presupplementary motor area (preSMA). Opposite to non-responders, cortisol responders were characterized by enhanced amygdala connectivity with the anterior hippocampal complex and parahippocampal gyrus, and reduced connectivity with left dlPFC, dACC, and culmen during early recovery. Acute stress responding and recovery are thus associated with changes in the functional connectivity of the amygdala network. Our findings show that these changes may be regulated via stress-induced neuroendocrine levels. Defining stress-induced neuronal network changes is pertinent to developing treatments that target abnormal neuronal activity.