Altered cortical gyrification patterns in panic disorder: Deficits and potential compensation

Yoon, Sujung; Jun, Chansoo; Jeong, Hyeok; Lee, Sunho; Lim, Soo Mee; Ma, Jiyoung; Ko, Eun A.; Cho, Han Byul; Yeum, Tae Sung; Lyoo, In Kyoon

doi:10.1016/j.jpsychires.2013.06.015

Cited by 14 publications

(14 citation statements)

References 81 publications

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“…In the recent years, cortical folding alterations have been identified in most major psychiatric disorders: schizophrenia and obsessive-compulsive disorder (as stated above), panic disorder [51], depression [52] and bipolar disorder [53]. In our study, we present novel evidence for cortical folding alterations of the DLPFC in anorexia nervosa.…”

Section: Cortical Folding and Anorexia Nervosasupporting

confidence: 62%

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 Nervosasupporting

confidence: 62%

Evidence for alterations of cortical folding in anorexia nervosa

Schultz

Wagner

Cruz

et al. 2015

Eur Arch Psychiatry Clin Neurosci

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“…Abnormal morphology may, therefore, represent a disruption in neurodevelopment that puts one at risk for these and other disorders. Of most relevance for the current study, investigations across clinical samples of anxiety and depression in adults have revealed gyrification abnormalities in the precuneus and posterior cingulate, another key node in the posterior DMN [ 32 – 34 ]. Additionally, there is some evidence suggesting that gyrification abnormalities are linked to dysfunction in this network.…”

Section: Introductionmentioning

confidence: 99%

Cortical Gyrification Patterns Associated with Trait Anxiety

et al. 2016

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Dispositional anxiety is a stable personality trait that is a key risk factor for internalizing disorders, and understanding the neural correlates of trait anxiety may help us better understand the development of these disorders. Abnormal cortical folding is thought to reflect differences in cortical connectivity occurring during brain development. Therefore, assessing gyrification may advance understanding of cortical development and organization associated with trait anxiety. Previous literature has revealed structural abnormalities in trait anxiety and related disorders, but no study to our knowledge has examined gyrification in trait anxiety. We utilized a relatively novel measure, the local gyrification index (LGI), to explore differences in gyrification as a function of trait anxiety. We obtained structural MRI scans using a 3T magnetic resonance scanner on 113 young adults. Results indicated a negative correlation between trait anxiety and LGI in the left superior parietal cortex, specifically the precuneus, reflecting less cortical complexity among those high on trait anxiety. Our findings suggest that aberrations in cortical gyrification in a key region of the default mode network is a correlate of trait anxiety and may reflect disrupted local parietal connectivity.

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“…One structural imaging study investigated cortical gyrification in PD and detected significant reduction in gyrification in 23 patients with PD in the lateral brain, extending from the fronto-parietal to the temporal areas compared with 33 healthy individuals[58]. …”

Section: Resultsmentioning

confidence: 99%

Functional neuroanatomy in panic disorder: Status quo of the research

Sobanski¹,

Wagner²

2017

WJP

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AIMTo provide an overview of the current research in the functional neuroanatomy of panic disorder.METHODSPanic disorder (PD) is a frequent psychiatric disease. Gorman et al (1989; 2000) proposed a comprehensive neuroanatomical model of PD, which suggested that fear- and anxiety-related responses are mediated by a so-called “fear network” which is centered in the amygdala and includes the hippocampus, thalamus, hypothalamus, periaqueductal gray region, locus coeruleus and other brainstem sites. We performed a systematic search by the electronic database PubMed. Thereby, the main focus was laid on recent neurofunctional, neurostructural, and neurochemical studies (from the period between January 2012 and April 2016). Within this frame, special attention was given to the emerging field of imaging genetics.RESULTSWe noted that many neuroimaging studies have reinforced the role of the “fear network” regions in the pathophysiology of panic disorder. However, recent functional studies suggest abnormal activation mainly in an extended fear network comprising brainstem, anterior and midcingulate cortex (ACC and MCC), insula, and lateral as well as medial parts of the prefrontal cortex. Interestingly, differences in the amygdala activation were not as consistently reported as one would predict from the hypothesis of Gorman et al (2000). Indeed, amygdala hyperactivation seems to strongly depend on stimuli and experimental paradigms, sample heterogeneity and size, as well as on limitations of neuroimaging techniques. Advanced neurochemical studies have substantiated the major role of serotonergic, noradrenergic and glutamatergic neurotransmission in the pathophysiology of PD. However, alterations of GABAergic function in PD are still a matter of debate and also their specificity remains questionable. A promising new research approach is “imaging genetics”. Imaging genetic studies are designed to evaluate the impact of genetic variations (polymorphisms) on cerebral function in regions critical for PD. Most recently, imaging genetic studies have not only confirmed the importance of serotonergic and noradrenergic transmission in the etiology of PD but also indicated the significance of neuropeptide S receptor, CRH receptor, human TransMEMbrane protein (TMEM123D), and amiloride-sensitive cation channel 2 (ACCN2) genes.CONCLUSIONIn light of these findings it is conceivable that in the near future this research will lead to the development of clinically useful tools like predictive biomarkers or novel treatment options.

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Altered cortical gyrification patterns in panic disorder: Deficits and potential compensation

Cited by 14 publications

References 81 publications

Evidence for alterations of cortical folding in anorexia nervosa

Evidence for alterations of cortical folding in anorexia nervosa

Cortical Gyrification Patterns Associated with Trait Anxiety

Functional neuroanatomy in panic disorder: Status quo of the research

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