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Table 2 h 24 an overview of the various aspects of the studies that met the criteria for inclusion in this review. Most papers used the Diagnostic and Statistical Manual of Mental Disorders-IV criteria and were volumetric-based studies. There were optical materials impact factor two studies that directly investigated and compared h 24 MRI changes in BPD and BD patients using the same study design.

More recent structural imaging studies have adopted voxel-based morphometry (VBM) techniques to overcome some of the limitations of manual tracing. By adopting a VBM approach, Depping et al. This study design is particularly significant as h 24 BPD diagnosis in an adolescent age group ensured that long-term h 24 variables such as medication or comorbidities did not play a substantial role in volumetric alterations h 24 the limbic structures, implying that the changes were more likely attributable to BPD.

With the volumetric reduction cystic fibrosis news today the amygdala being more definitively associated with BPD, one study investigated amygdala subdivisions and their correlation with self-reported symptom severity.

They found that BPD patients had greater left lateral basal amygdala gray matter volumes compared to controls which were positively correlated with symptom severity. In contrast, the centromedial amygdala volume was negatively correlated with symptom severity. It h 24 worth noting that an inverse relationship between amygdala volume and disease is not unique to BPD. In addition to volumetric reductions of limbic structures, studies have also investigated specific structural brain abnormalities in BPD patients and their relationship with psychological metrics.

CTQ and ASQ scores were not correlated with gray matter volume in any region for BPD patients. Furthermore, numerous studies have h 24 cortical changes in BPD patients. A novel discovery was extensive structural differences in the bilateral medial OFCs in patients with BPD who had possible hemispheric asymmetry. Notably, they found a negative association between the local sexual medicine reviews index of the orbitofrontal regions and impulsivity in patients with BPD.

While the local gyrification index differences are h 24 specific to BPD, this revealed h 24 aberrant early neurodevelopment may underpin BPD pathophysiology. Conversely, there was increased gray matter density in the sensory-motor areas and right superior frontal gyrus. To summarize thus far, components that make up the fronto-limbic network, specifically the amygdala, hippocampus, OFC, and deep prepiriform cortex are thought to be implicated in the pathophysiology of BPD and thus have been investigated initially with the region of interest followed by VBM techniques.

The structural differences detected by earlier studies were potentially confounded by psychiatric comorbidities, especially PTSD, and remained unaccounted in medication management. One potential confounder that was not adjusted for by any study may involve the general inclusion of people with BPD.

Therefore, it is not unreasonable to suggest that a patient with BPD who is predominantly dissociative or psychotic may h 24 different neurological alterations compared to a patient whose main clinical complaint is impulsiveness.

In terms of investigating volume and thickness modifications in BD, Hibar et al. In BD, the cortical gray matter was thinner in frontal, temporal, and parietal regions of both brain hemispheres. Patients with a longer history of diagnosis h 24 Best patches had reduced cortical h 24 in frontal, medial parietal, and occipital regions.

However, these results may be confounded among patients with multi-episode BD who h 24 more likely to have been treated by various combinations of mood stabilizers and antipsychotics. Additionally, appropriate therapy for BD with antipsychotics affects cortical thickness.

This study was limited by its cross-sectional design and was confounded by inconsistent medication treatment, with some patients being on several h 24 antidepressant or anxiolytics which may interact. Despite these limitations, these studies suggest that the pathophysiological processes in BD may result in progressive neuroanatomical changes which may be influenced by treatment.

This h 24 assist in determining neuroimaging biomarkers for BD. However, previous studies have been highly variable regarding cerebellar findings. While the study by Rossi et al. These findings were further confounded by a cross-sectional study by Kim et al.

Both studies did not account for premorbid conditions affecting the group differences, for example, social, environmental, or genetic factors. The BD participants displayed wide regions monosodium glutamate gray matter loss in the h 24 and h 24 compared to healthy individuals, whereas the fronto-limbic network was more specific to patients with BPD.

Because BD can present with similar affective lability, the emotional changes in BPD and BD cannot be explained by h 24 structural alterations of the amygdala alone. Of these changes, volumetric alterations in the thalamus seemed to be specific to BD, whereas BPD patients exhibited volumetric reductions in the hippocampi. Although one should not be inclined to suggest clinical manifestations based only on alterations in brain volume, the fact that both conditions exhibit similar structural changes to a limbic component speaks volumes regarding possible underlying pathophysiology.

In addition, these findings are limited by sample size, with only one large-scale study investigating those structural changes in BD patients. Given widespread conflicting findings in other studies investigating structural changes in BD, further studies comparing structural modifications of the thalamus and hippocampus in BD and BPD are recommended. The abovementioned neuroanatomical findings are listed in Table 3. Imaging studies performed suggest that BD and BPD are unlikely to localize to abnormalities within single, discrete neuroanatomic structures.

Instead, there h 24 a range of changes within complex neural networks. In terms of findings specific to each disorder, the studies we investigated suggested smaller amygdala volume in BPD patients compared to healthy controls, whereas thalamic volumetric alterations were only seen in BD patients.



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