مجموعه مورفولوژی کورپوس و حجم بطن جانبی در نوجوانان با ارائه اول اختلال شخصیت مرزی
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|33113||2010||8 صفحه PDF||سفارش دهید||محاسبه نشده|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Psychiatry Research: Neuroimaging, Volume 183, Issue 1, 30 July 2010, Pages 30–37
Previous studies have demonstrated alterations to fronto-limbic circuitry and callosal structure in borderline personality disorder (BPD). We predicted that a first-presentation BPD cohort who demonstrated orbitofrontal cortex (OFC) reductions would show regional reductions in the anterior corpus callosum.
Structural and functional neuroimaging studies in adults with borderline personality disorder (BPD) have shown alterations in the prefrontal cortex, particularly the orbitofrontal cortex and adjacent ventral medial cortex (including the anterior cingulate gyrus), in addition to the hippocampus and amygdala (Rusch et al., 2003, Tebartz van Elst et al., 2003 and Weniger et al., 2009). This implicates disruptions to prefrontolimbic circuitry as a marker of biological vulnerability to BPD (Lis et al., 2007 and Schmahl and Bremner, 2006), or the sequelae of significant childhood trauma that are implicated in the genesis of BPD (Goodman et al., 2004). The characteristic affective dysregulation and impaired impulse control that occur in BPD may be related to altered connectivity between prefrontal and limbic regions (New et al., 2007 and Williams et al., 2006). This is supported by two recent studies showing impairments to the structural integrity of white matter in the inferior frontal region (Grant et al., 2007 and Rusch et al., 2007b). It is not clear if these alterations in prefrontal white and grey matter in BPD are related and, if so, whether white matter changes in the disorder occur independently of, or are secondary to, primary grey matter changes. We have previously demonstrated in a cohort of teenagers with first-presentation BPD that orbitofrontal, but not amygdala or hippocampal, grey matter reductions are present early in the course of BPD (Chanen et al., 2008), and recently these findings have been supported in a sample of female adolescents with BPD (Brunner et al., 2010). However, in our previous study, amygdala volume was related to measures of “state” psychopathology in female participants. We also showed volume reductions at the level of the left anterior cingulate cortex in females from this sample, which correlated with measures of impulsivity and parasuicidal behavior (Whittle et al., 2009). These findings suggest that prefrontal-limbic structures, particularly the OFC, are relevant to the early course of BPD in young people. Prefrontal cortical fibres from the orbitofrontal and ventral medial cortex pass between the hemispheres through the corpus callosum (CC), in the region of the genu (Pandya and Seltzer, 1986), whereas amygdala and hippocampal fibres do not. The CC, the brain's largest white matter bundle, connects functionally related interhemispheric regions of the cerebral cortex, predominantly through homotopic connections that connect a given specialized cortical area with its contralateral homolog, but also through heterotopic connections that connect non-homologous areas (Clarke and Zaidel, 1994, deLaCoste et al., 1985 and Witelson, 1989). Disorders that produce significant grey matter atrophy such as Alzheimer's disease, vascular dementia and frontotemporal dementia result in regional callosal reductions in the areas connecting atrophic cortical regions (Hallam et al., 2008, Kaufer et al., 1997 and Yamauchi et al., 2000); if white matter changes in BPD are indeed secondary to reductions in grey matter regions, subtle alterations at the level of the anterior CC may then be detectable in BPD. Disrupted interhemispheric connectivity has also been implicated in underlying the mood dysregulation characteristic of major affective disorders (Brambilla et al., 2003 and Brambilla et al., 2004), which can show symptomatic overlap and co-occurrence with BPD (Akiskal, 2004 and Paris et al., 2007). Additionally, the corpus callosum appears particularly vulnerable to the effects of childhood abuse and trauma, with children suffering abuse and neglect demonstrating abnormal callosal development and reduced callosal size compared to non-abused children (DeBellis et al., 1999, Teicher et al., 1997 and Teicher et al., 2004), which may alter the developmental trajectory of interhemispheric integration and functional cerebral laterality (Schiffer et al., 1995). The callosum develops in a non-linear way, and shows quadratic trajectories of micro- and macro-structural changes across the lifespan, particularly in adolescence and early adulthood (Hasan et al., 2008a, Hasan et al., 2008b and Hasan et al., 2009); these trajectories may be disrupted by the pathophysiology of trauma and major affective illness, which may be reflected in changes in callosal structure. Few studies have examined CC in BPD patients and no studies have examined young people early in the course of BPD. Two recent studies have examined CC structure in BPD patients compared with healthy controls (Rusch et al., 2007a and Zanetti et al., 2007). Zanetti et al. (2007) found no differences in CC structure between patients and controls. Rüsch et al. studied BPD patients with comorbid attention-deficit hyperactivity disorder (ADHD) and found a thinner isthmus of the callosum (connecting parietal and temporal cortices). In this study, BPD patients with an abuse history also demonstrated reductions in the posterior body of the CC compared with those without (Rüsch et al., 2007a). These authors considered that the CC changes identified were consistent with impaired interhemispheric connectivity between parietal and temporal cortices in BPD, but noted that similar regional CC reductions have been seen in ADHD, and could not exclude that these findings were driven by illness processes specific to ADHD rather than BPD. To investigate the possible role of structural alterations of the CC in this first-presentation BPD sample, we used a sensitive shape analysis method that has previously detected robust changes in the anterior CC in pre-psychotic and first-episode psychosis cohorts (Walterfang et al., 2008b, Walterfang et al., 2008c, Walterfang et al., 2009c and Walterfang et al., 2009ec,e), regional posterior reductions in patients with bipolar disorder (Walterfang et al., 2009a and Walterfang et al., 2009b) and putative state related expansions in the posterior CC in depressed patients (Walterfang et al., 2009d). In the first instance, we aimed to see if we could replicate the findings by Rüsch et al. (2007a) in a first-presentation BPD group. However, given the previously-demonstrated prefrontal cortical reductions present at first presentation in this cohort, we predicted a reduction in the anterior genu — the callosal region connecting the homotopic orbitofrontal cortex (Pandya and Seltzer, 1986) — in BPD patients compared with controls, and expansions in posterior regions associated with depressive and anxiety symptoms.