ابعاد کنترل روانشناختی والدین: ارتباطات با پرخاشگری فیزیکی و رابطه پیش دبستانی در روسیه

The eating disorder anorexia nervosa (AN) is associated with high anxiety. The brain mechanisms that drive those behaviors are unknown. In this study we wanted to test whether brain white matter (WM) integrity is altered in AN, and related to heightened anxiety. Sixteen adult women with AN (mean age 24 ± 7 years) and 17 healthy control women (CW, mean age 25 ± 4 years) underwent diffusion tensor imaging (DTI) of the brain. The DTI brain images were used to calculate the fractional anisotropy (FA) of WM tracts, which is a measure for WM integrity. AN individuals compared to CW showed clusters of significantly reduced FA (p < 0.05, corrected) in the bilateral fimbria-fornix and the fronto-occipital fasciculus, as well as the posterior cingulum WM. In the AN group, Harm Avoidance was predicted by FA in the left and right fimbria-fornix. Those findings were not due to WM volume deficits in AN. This study indicates that WM integrity is abnormal in AN in limbic and association pathways, which could contribute to disturbed feeding, emotion processing and body perception in AN. The prediction of Harm Avoidance in AN by fimbria-fornix WM integrity suggests that this pathway may be mechanistically involved in high anxiety in AN.

The eating disorder (ED) anorexia nervosa (AN) is a severe psychiatric disorder associated with self-driven food refusal and emaciation, altered body perception and preoccupations with weight and shape (American Psychiatric Association, 2000). Heightened anxiety, such as high Harm Avoidance and Trait Anxiety, is common in AN, and has been associated with prolonged illness (Bulik et al., 2000 and Klump et al., 2004). The underlying pathophysiology of AN core behaviors or high anxiety is largely unknown. Brain imaging studies in the past identified grey (GM) and white matter (WM) volume abnormalities in youth and adults ill with AN (Katzman and Colangelo, 1996 and Swayze et al., 2003), and a recent study in adult AN showed specifically decreased GM in the anterior cingulate cortex, frontal operculum, temporo-parietal cortex and the precuneus (Joos et al., 2010). That study furthermore suggested that parietal cortex GM volume could be related to drive for thinness in AN. AN has also been associated with abnormal neurotransmitter availability (Kaye et al., 2009), but the relationship between neurobiology and illness behavior remains incompletely understood. While we are just beginning to identify functionally related brain structures that are important for AN, the visual presentation of anxiety-provoking food items has consistently activated multiple brain regions in AN more than in controls, including frontal, parietal, temporal and occipital cortex (Nozoe et al., 1995, Ellison et al., 1998, Naruo et al., 2000, Gordon et al., 2001, Seeger et al., 2002 and Uher et al., 2004), suggesting those regions to be a correlate for heightened vigilance and fear response. The presentation of tasks that tested the response of AN subjects to their own or schematic body images showed a more complex picture, with increased activation of frontal, parietal and occipital brain regions in one study (Wagner et al., 2003), but reduced parietal activation in AN subjects when viewing their own compared with someone else's body (Sachdev et al., 2008), and reduced brain response in the parietal cortex in response to body shape drawings. The insula, which processes taste as well as other sensory input, showed increased activation in AN subjects to “thin” stimuli, but reduced activation to “fat” valence in an emotional Stroop task, as well as reduced activation in recovered AN to sucrose solution compared to controls (Uher et al., 2005, Santel et al., 2006, Wagner et al., 2007, Wagner et al., 2008, Redgrave et al., 2008 and Sachdev et al., 2008). Altogether, there are various brain networks that are activated in AN depending on the task used. An important aspect here is that the cognitive bias in AN toward body shape and food most likely drives the brain activation patterns, and it is often complicated to disentangle underlying biological alterations from activations that are driven by cognitive-emotional features. Complex human behaviors are believed to be mediated by the interaction of functionally connected brain regions (Dehaene and Changeux, 2000). Brain WM axons physically connect cortical and subcortical brain structures and thus could have critical impact on cognitive and emotional processing. A relatively novel area of brain research that targets WM function is the magnetic resonance imaging (MRI) technique diffusion tensor imaging (DTI) (Filler, 2009). One of the DTI measures, the fractional anisotropy (FA) value, measures water diffusion along the WM tracts. Higher FA is thought to reflect better axonal coherence, density and myelination (Le Bihan, 2003 and Cohen et al., 2009). Another measure, the apparent diffusion coefficient (ADC), provides information about the average diffusion-freedom water molecules have in each voxel, and correlates with local cell breakdown (Jiang et al., 2006). While DTI has been previously applied in other psychiatric disorders (White et al., 2008), it has not been used in AN research. Importantly, one DTI study found that WM pathway integrity is inversely related to Trait Anxiety (Kim and Whalen, 2009), a potentially important finding for AN research, in light of the high anxiety associated with AN. Thus, pathological anxiety in AN could be directly related to altered brain structure and function (Dehaene and Changeux, 2000), and WM functionality could help identify networks of associated brain structures that drive AN-related behaviors. We hypothesized that WM integrity would be reduced in AN, suggesting a disruption of brain connectivity in AN compared to matched controls. We further wanted to test whether such altered WM function would be directly related to Harm Avoidance and Trait Anxiety in AN (Kim and Whalen, 2009), providing a possible mechanism for abnormal anxiety in this disorder.