Reduced prefrontal gyrification in obsessive–compulsive disorder

Wobrock, Thomas; Gruber, Oliver; McIntosh, Andrew M.; Kraft, Susanne; Klinghardt, Anne; Scherk, Harald; Reith, Wolfgang; Schneider‐Axmann, Thomas; Lawrie, Stephen M.; Falkai, Peter; Moorhead, T. William J.

doi:10.1007/s00406-009-0096-z

Cited by 38 publications

(45 citation statements)

References 43 publications

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“…However, the full relevance also regarding the relationship with other neurobiological features and the exact pathophysiological origin of cortical folding alterations is not clear and matter of an ongoing debate [26,27,46]. Cortical folding alterations have also been found in obsessive-compulsive disorder [47,48]. Again, both hypo-and hypergyria have been identified.…”

Section: Cortical Folding and Anorexia Nervosamentioning

confidence: 97%

Evidence for alterations of cortical folding in anorexia nervosa

Schultz

Wagner

Cruz

et al. 2015

Eur Arch Psychiatry Clin Neurosci

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Anorexia nervosa (AN) is highly heritable, and the perspective on the etiology of AN has changed from a behavioral to a neurobiological and neurodevelopmental view. However, cortical folding as an important marker for deviations in brain development has yet rarely been explored in AN. Hence, in order to determine potential cortical folding alterations, we investigated fine-grained cortical folding in a cohort of 26 patients with AN, of whom 6 patients were recovered regarding their weight at the time point of MRI measurement. MRI-derived cortical folding was computed and compared between patients and healthy controls at about 150,000 points per hemisphere using a surface-based technique (FreeSurfer). Patients with AN exhibited highly significant increased cortical folding in a right dorsolateral prefrontal cortex region (DLPFC). Furthermore, a statistical trend in the same direction was found in the right visual cortex. We did not find a correlation of local cortical folding and current symptoms of the disease. In conclusion, our analyses provide first evidence that altered DLPFC cortical folding plays a role in the etiology of AN. The absence of correlations with clinical parameters implicates a relatively independence of cortical folding alterations from the current symptomatology and might thus be regarded as a trait characteristic of the disease potentially related to other neurobiological features of AN.

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Section: Cortical Folding and Anorexia Nervosamentioning

confidence: 97%

Evidence for alterations of cortical folding in anorexia nervosa

Schultz

Wagner

Cruz

et al. 2015

Eur Arch Psychiatry Clin Neurosci

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“…Thicker and thinner cortical regions co-exist in 22q11.2 deletion syndrome (Bearden et al 2007, 2009; Schaer et al 2009), autism spectrum disorder (Hyde et al 2010; Jiao et al 2010), and Turner syndrome (Raznahan et al 2010). Regions of higher gyrification have been reported in 22q11.2 deletion syndrome (Bearden et al 2009), autism spectrum disorder (Awate et al 2008), children born preterm (Kesler et al 2006), and Williams syndrome (Thompson et al 2005; Gaser et al 2006); regions of lower gyrification in ADHD (Wolosin et al 2009), dyslexia (Casanova et al 2004), intellectual disability (Zhang et al 2010), obsessive-compulsive disorder (Wobrock et al 2010), and Turner syndrome (Raznahan et al 2010). Regions of both higher and lower gyrification have been reported in schizophrenia (White and Hilgetag 2011), and temporal lobe epilepsy (Lin et al 2007; Voets et al 2011).…”

Section: Many Childhood Disorders Involve Plasticity-homeostasis Dmentioning

confidence: 99%

Age, plasticity, and homeostasis in childhood brain disorders

Dennis¹,

Spiegler²,

Juranek³

et al. 2013

Neuroscience & Biobehavioral Reviews

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It has been widely accepted that the younger the age and/or immaturity of the organism, the greater the brain plasticity, the young age plasticity privilege. This paper examines the relation of a young age to plasticity, reviewing human pediatric brain disorders, as well as selected animal models, human developmental and adult brain disorder studies. As well, we review developmental and childhood acquired disorders that involve a failure of regulatory homeostasis. Our core arguments are: Plasticity is neutral with respect to outcome. Although the effects of plasticity are often beneficial, the outcome of plasticity may be adaptive or maladaptive.The young age plasticity privilege has been overstated.Plastic change operates in concert with homeostatic mechanisms regulating change at every point in the lifespan.The same mechanisms that propel developmental change expose the immature brain to adverse events, making it more difficult for the immature than for the mature brain to sustain equilibrium between plasticity and homeostasis.Poor outcome in many neurodevelopmental disorders and childhood acquired brain insults is related to disequilibrium between plasticity and homeostasis.

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“…Very recently, Nakame et al have reported significantly reduced cortical thickness I the left superior temporal gyrus and posterior insular cortex in OCD patients; in addition, there was a significant negative correlation between cortical thickness in the left postcentral and right superior parietal gyri and "cleaning" dimension scores (Nakamae et al, 2012). Till date, the only study examining cortical folding pattern in medicated OCD patients has revealed prefrontal hypogyrification (Wobrock et al, 2010). Cortical surface area profile in OCD is yet to be explored.…”

Section: Introductionmentioning

confidence: 97%