Callosum Changes Research Articles

P.105 Corpus callosum changes in children affected by infantile hydrocephalus

Background: Infantile hydrocephalus is characterized by an atypical accumulation of cerebrospinal fluid in the brain, diagnosed and treated before the age of 2 years. Hydrocephalus development is linked to thinning of the corpus callosum (CC), mainly due to the expansion of lateral ventricles, causing upward elevation and compression of periventricular and subcortical white matter. Methods: This study investigates structural alterations in the CC in children diagnosed with infantile hydrocephalus. We examined both macrostructural and microstructural facets of the CC, providing insights into the nature and extent of alterations associated with this condition. 18 patients with infantile hydrocephalus (mean age = 9 years), and 18 age and sex matched typically-developing healthy children, participated in the study. Structural magnetic resonance imaging and diffusion tensor imaging were utilized to assess CC volume and microstructure, respectively. Results: Our findings reveal reductions in CC volume, particularly in posterior area, and distinct microstructural disparities, notably pronounced in these same segments. Conclusions: Investigating these structural alterations provides an understanding into the mechanisms underlying the effects of infantile hydrocephalus on CC integrity, given its role as a neural bridge. This knowledge offers a more nuanced perspective on neurological disorders and underscores the significance of investigating the CC’s health in such contexts.

Graph Theory Approach for Assessment of Long-term Corpus Callosum Changes After Traumatic Brain Injury.

Graph Theory Approach for Assessment of Long-term Corpus Callosum Changes After Traumatic Brain Injury.

Corpus Callosum Atrophy in Alcohol-Dependent Men with Memory Disorders and Visual Attention Difficulties.

The earlier research confirm the relationship between structural changes in the corpus callosum and difficulties in attention and memory in the group of patients with alcohol use disorder (AUD). Nevertheless, the image of auditory and visual memory disorders in men with gradual atrophy of the corpus callosum and different alcohol abuse duration, it has not been explained yet. The overriding objective of this study was: (1) to determine whether there are principal and interaction effects of visuospatial and auditory-verbal memory on alcohol consumption and cross-sectional corpus callosum area in men with alcohol use disorder, (2) to assess the impact of callosal changes on the memory and visual attention processes. 97 men with alcohol use disorder were examined. T1-weighted scans were used to carry out corpus callosum segmentation and volumetric measurements. The cognition profile included two domains: attention, memory (visuospatial and auditory-verbal). The results showed that participants with visuospatial memory disorder had inferior education background, and were characterized by a longer duration of alcohol abuse, more severe alcohol use disorder, and greater alcohol consumption per day. Second, alcohol-dependent men with auditory and visual memory disorders had a smaller frontal and posterior part of the corpus callosum areas. Additionally, among the alcohol-dependent men with memory disorders the smaller rostral body of corpus callosum was determined by the longer alcohol abuse duration. On the other hand, the smaller rostral body of corpus callosum was predicted by the older age only in alcohol-dependent men with normal memory. Among all examined individuals were observed a statistically significant relationships among visual attention, visuospatial memory and corpus callosum subregions including in particular genu and isthmus. The smaller corpus callosum cross-sectional area significantly affects visual attention and memory difficulties in alcohol use disorder, especially have differentiated the patients with normal and disordered memory. Longer alcohol abuse duration plays also a significant role in the corpus callosum atrophy in alcohol-dependent men with disordered memory (visuospatial in particular).

A single closed head injury in male adult mice induces chronic, progressive white matter atrophy and increased phospho-tau expressing oligodendrocytes

Traumatic brain injury (TBI) acutely damages the brain; this injury can evolve into chronic neurodegeneration. While much is known about the chronic effects arising from multiple mild TBIs, far less is known about the long-term effects of a single moderate to severe TBI. We found that a single moderate closed head injury to mice induces diffuse axonal injury within 1-day post-injury (DPI). At 14 DPI, injured animals have atrophy of ipsilesional cortex, thalamus, and corpus callosum, with bilateral atrophy of the dorsal fornix. Atrophy of the ipsilesional corpus callosum is accompanied by decreased fractional anisotropy and increased mean and radial diffusivity that remains unchanged between 14 and 180 DPI. Injured animals show an increased density of phospho-tau immunoreactive (pTau+) cells in the ipsilesional cortex and thalamus, and bilaterally in corpus callosum. Between 14 and 180 DPI, atrophy occurs in the ipsilesional ventral fornix, contralesional corpus callosum, and bilateral internal capsule. Diffusion tensor MRI parameters remain unchanged in white matter regions with delayed atrophy. Between 14 and 180 DPI, pTau+ cell density increases bilaterally in corpus callosum, but decreases in cortex and thalamus. The location of pTau+ cells within the ipsilesional corpus callosum changes between 14 and 180 DPI; density of all cells increases including pTau+ or pTau− cells. >90% of the pTau+ cells are in the oligodendrocyte lineage in both gray and white matter. Density of thioflavin-S+ cells in thalamus increases by 180 DPI. These data suggest a single closed head impact produces multiple forms of chronic neurodegeneration. Gray and white matter regions proximal to the impact site undergo early atrophy. More distal white matter regions undergo chronic, progressive white matter atrophy with an increasing density of oligodendrocytes containing pTau. These data suggest a complex chronic neurodegenerative process arising from a single moderate closed head injury.

Longitudinal corpus callosum microstructural decline in early-stage Parkinson’s disease in association with akinetic-rigid symptom severity

Previous diffusion tensor imaging (DTI) studies of Parkinson’s disease (PD) show reduced microstructural integrity of the corpus callosum (CC) relative to controls, although the characteristics of such callosal degradation remain poorly understood. Here, we utilized a longitudinal approach to identify microstructural decline in the entire volume of the CC and its functional subdivisions over 2 years and related the callosal changes to motor symptoms in early-stage PD. The study sample included 61 PD subjects (N = 61, aged 45–82, 38 M & 23 F, H&Y ≤ 2) from the Parkinson’s Progressive Markers Initiative database (PPMI). Whole-brain voxel-wise results revealed significant fractional anisotropy (FA) and mean diffusivity (MD) changes in the CC, especially in the genu and splenium. Using individually drawn CC regions of interest (ROI), our analysis further revealed that almost all subdivisions of the CC show significant decline in FA to certain extents over the two-year timeframe. Additionally, FA seemed lower in the right hemisphere of the CC at both time-points, and callosal FA decline was associated with FA and MD decline in widespread cortical and subcortical areas. Notably, multiple regression analysis revealed that across-subject akinetic-rigid severity was negatively associated with callosal FA at baseline and 24 months follow-up, and the effect was strongest in the anterior portion of the CC. These results suggest that callosal microstructure alterations in the anterior CC may serve as a viable biomarker for akinetic-rigid symptomology and disease progression, even in early PD.

Statistical shape analyses of corpus callosum changes at preoperative and postoperative scaphocephaly patients.

Scaphocephaly is the premature closure of the sagittal suture. The treatment strategies mainly focus on correcting the shape of the head, but there are very limited studies examining changes in brain structure. This study aimed to investigate shape differences in the shape of corpus callosum regarding the pre-treatment and post-treatment term at scaphocephaly patients. Cranium shape data were collected from the two-dimensional digital images. The generalized Procrustes analysis was used to obtain mean shapes in the pre- and postoperative phases. The shape deformation of the corpus callosum from the pre- to postoperative phases was evaluated using the thin plate spline method. There is an enlargement of the splenium part of corpus callosum in the late group. In the early group, corpus callosum genu and body enlargement were observed in the postoperative period compared to the preoperative period, followed by a narrowing of the isthmus region. This study showed structural deformations in the corpus callosum in scaphocephaly patients using head shape with the landmark-based geometric morphometric method by taking into consideration the topographic distribution. An enlargement at the splenium part of corpus callosum exposes after the cranial vault expansion depending on time.

Longitudinal Evaluation of Cerebellar Signs of H-ABC Tubulinopathy in a Patient and in the taiep Model.

Hypomyelination with atrophy of the basal ganglia and cerebellum (H-ABC) is a central neurodegenerative disease due to mutations in the tubulin beta-4A (TUBB4A) gene, characterized by motor development delay, abnormal movements, ataxia, spasticity, dysarthria, and cognitive deficits. Diagnosis is made by integrating clinical data and radiological signs. Differences in MRIs have been reported in patients that carry the same mutation; however, a quantitative study has not been performed so far. Our study aimed to provide a longitudinal analysis of the changes in the cerebellum (Cb), corpus callosum (CC), ventricular system, and striatum in a patient suffering from H-ABC and in the taiep rat. We correlated the MRI signs of the patient with the results of immunofluorescence, gait analysis, segmentation of cerebellum, CC, and ventricular system, performed in the taiep rat. We found that cerebellar and callosal changes, suggesting a potential hypomyelination, worsened with age, in concomitance with the emergence of ataxic gait. We also observed a progressive lateral ventriculomegaly in both patient and taiep, possibly secondary to the atrophy of the white matter. These white matter changes are progressive and can be involved in the clinical deterioration. Hypomyelination with atrophy of the basal ganglia and cerebellum (H-ABC) gives rise to a spectrum of clinical signs whose pathophysiology still needs to be understood.

Relationship between illness duration, corpus callosum changes, and sustained attention dysfunction in major depressive disorder.

Illness duration is the main index of cumulative illness severity during depression progression. Corpus callosum (CC) damage is among the most replicated neurobiological findings in major depressive disorder (MDD). We aimed to investigate the nature and extent of the association between illness duration and CC changes. Ninety-six MDD patients and 50 controls underwent diffusion and resting-state functional magnetic resonance imaging (fMRI). White matter micro-structure and inter-hemispheric functional connectivity were quantified by fractional anisotropy (FA) and voxel-mirrored homotopic connectivity (VMHC). The CC was reconstructed by tractography and divided into five sub-regions. The associations of illness duration with FA of each CC sub-region and voxel-wise VMHC were examined using correlation analyses. Also, we investigated the potential relationship between illness duration, CC changes, and clinical variables using mediation analyses. In MDD patients, longer illness duration was selectively associated with lower FA of CC sub-regions 2 [partial correlation coefficient (pr) =-0.269, P=0.009] and 5 (pr=-0.296, P=0.004) as well as higher VMHC in the supplementary motor areas (pr=0.378, P<0.001), precuneus (pr=0.384, P<0.001), and lingual gyrus (pr=0.373, P<0.001) connected by the affected CC sub-regions. Further subgroup analyses demonstrated pronounced FA decrease and VMHC increase in patients with illness duration over 20 years relative to healthy controls (HC) and other patient subgroups with shorter illness durations. Moreover, lower FA of CC sub-regions 2 and 5 mediated the association between longer illness duration and more severe sustained attention dysfunction. These findings provide evidence for compromised structure yet compensatory function of the CC with increasing depression illness duration, which may inform effective antidepressant treatment strategies at different disease stages.

Interhemispheric plasticity is mediated by maximal potentiation of callosal inputs

Central or peripheral injury causes reorganization of the brain's connections and functions. A striking change observed after unilateral stroke or amputation is a recruitment of bilateral cortical responses to sensation or movement of the unaffected peripheral area. The mechanisms underlying this phenomenon are described in a mouse model of unilateral whisker deprivation. Stimulation of intact whiskers yields a bilateral blood-oxygen-level-dependent fMRI response in somatosensory barrel cortex. Whole-cell electrophysiology demonstrated that the intact barrel cortex selectively strengthens callosal synapses to layer 5 neurons in the deprived cortex. These synapses have larger AMPA receptor- and NMDA receptor-mediated events. These factors contribute to a maximally potentiated callosal synapse. This potentiation occludes long-term potentiation, which could be rescued, to some extent, with prior long-term depression induction. Excitability and excitation/inhibition balance were altered in a manner consistent with cell-specific callosal changes and support a shift in the overall state of the cortex. This is a demonstration of a cell-specific, synaptic mechanism underlying interhemispheric cortical reorganization.

Balkenfehlbildungen

Agenesis of the corpus callosum is reported to have an incidence of about 1:4000 live births. In 30-45% of cases, genetic etiologies can be identified, e. g., 10% chromosomal anomalies and 20-35% genetic syndromes. Environmental factors like fetal alcohol syndrome are also known to be prone to callosal agenesis. Callosal agenesis can be complete or partial and can be isolated or associated with other central nervous system (CNS) anomalies (e. g., cortical developmental disorders, callosal lipoma, intracranial cysts) or extra-CNS anomalies (e. g., eyes, face, cardiovascular). Diagnosis is made using ultrasound, computed tomography (CT) or best with magnetic resonance imaging (MRI). Typical imaging findings in callosal agenesis are colpocephaly, high riding enlarged third ventricle, Texas Longhorn configuration of frontal horns and so-called Probst bundles parasagittal. Diffusion tensor imaging and fiber-tracking, based on diffusion-weighted techniques, can also visualize fiber/tract anomalies in the patients' brains. Clinical correlations of callosal agenesis is difficult in general because of the common association of other CNS malformations. Differential diagnosis of primary complete or partial callosal agenesis are secondary callosal changes, e. g. vascular, inflammatory or posttreatment in origin.

Is the presence of corpus callosum predictable in the first trimester?

Corpus callosum agenesis (CCA) is a clinical condition accompanied by various aneuploidy and genetic syndromes. We identified the development of the corpus callosum (CC) in 278 patients before 18 weeks of gestational age by visualising the pericallosal artery (PCA) in the callosal sulcus and changes in the lengths and ratios of the midbrain (MB) and falx (F), which suggested elevation of the third ventricle and thalamus due to CCA in the first trimester. We succeeded in visualising the path of the PCA in 273 patients. As expected, we observed an increase in the lengths of the MB and F throughout the pregnancies. The MB:F ratio was 0.5–0.6, and it was independent of gestational age. In all 278 patients, the MB:F ratio was <0.6 (95th percentile = 0.79). We observed the presence of the CC during anatomical screening at gestational weeks 18–24. Visualisation of the PCA path (98% sensitivity) and calculation of the MB:F ratio <95th percentile (0.79–100% sensitivity) had very high sensitivity that indirectly confirmed the presence of the CC in the first trimester of pregnancy.Impact statementWhat is already known on this subject: After reading the articles for detecting the absence of corpus callosum (CC) at first trimester with midbrain (MB) and falx (F) measurement by Lachmann et al. (2013) and visualising pericallosal artery (PCA) as an indirect sign of CC agenesis by Pati et al. (2012), we aimed to have a look for our records visualising PCA in callosal sulcus and measure MB–F, as well as their ratios for an indirect sign of ‘presence’ of CC at first trimester.What the results of this study add: In recent literature, it is not possible to find many articles suggesting the presence of CC between 11 and 13 weeks of gestation. Díaz-Guerrero et al. (2013) and Pati et al. (2012) has researched visualising PCA path. Lachmann et al. (2013) reported an article for MB and F measurements in early suspicion of CC agenesis. Our study will be the first article in visualising PCA path and measuring MB–F lengths as well as their ratios for ‘presence’ of CC with high sensitivity rates (98% and 100%).What are the implications of these findings for clinical practice and/or further research: This study encourages clinicians visualising PCA path and measure MB–F lengths when they will try to visualise repetitive times and see how it is an easy procedure when you get used to it.

Quantitative assessment of corpus callosum morphology in periventricular nodular heterotopia

We investigated systematic differences in corpus callosum morphology in periventricular nodular heterotopia (PVNH). Differences in corpus callosum mid-sagittal area and subregional area changes were measured using an automated software-based method. Heterotopic gray matter deposits were automatically labeled and compared with corpus callosum changes. The spatial pattern of corpus callosum changes were interpreted in the context of the characteristic anterior-posterior development of the corpus callosum in healthy individuals. Individuals with periventricular nodular heterotopia were imaged at the Melbourne Brain Center or as part of the multi-site Epilepsy Phenome Genome project. Whole brain T1 weighted MRI was acquired in cases (n=48) and controls (n=663). The corpus callosum was segmented on the mid-sagittal plane using the software "yuki". Heterotopic gray matter and intracranial brain volume was measured using Freesurfer. Differences in corpus callosum area and subregional areas were assessed, as well as the relationship between corpus callosum area and heterotopic GM volume. The anterior-posterior distribution of corpus callosum changes and heterotopic GM nodules were quantified using a novel metric and compared with each other. Corpus callosum area was reduced by 14% in PVNH (p=1.59×10(-9)). The magnitude of the effect was least in the genu (7% reduction) and greatest in the isthmus and splenium (26% reduction). Individuals with higher heterotopic GM volume had a smaller corpus callosum. Heterotopic GM volume was highest in posterior brain regions, however there was no linear relationship between the anterior-posterior position of corpus callosum changes and PVNH nodules. Reduced corpus callosum area is strongly associated with PVNH, and is probably associated with abnormal brain development in this neurological disorder. The primarily posterior corpus callosum changes may inform our understanding of the etiology of PVNH. Our results suggest that interhemispheric pathways are affected in PVNH.

Association of Corpus Callosum Agenesis with Mental Retardation and Attention Deficit Hyperactivity Disorder

Aims: Anomalies of the corpus callosum have been associated with varied brain and somatic malformations. It has been associated with diverse genetic causes with identifiable syndromes. We aim to report a case of corpus callosal agenesis (CCA) associated with mental retardation and hyperactivity. Presentation of case:We report case of a 7 year old boy having CCA, abnormal facial morphological features, mental retardation and attention deficit hyperactivity diso rder (ADHD) , devoid of any chromosomal rearrangements or somatic malformations known to be associated with corpus callosal changes. Discussion: Symptoms in CCA are often related to concurrent migrational disorders, not to the callosal anomaly itself. Although multiple genetic etiologies have been associated, no single gene has been proved to be implied in all cases of CCA. Conclusion: This case highlights importance of recognizing mental retardation and ADHD as a presentation of isolated CCA which mayoccur without any known

Preserved Transcallosal Inhibition to Transcranial Magnetic Stimulation in Nondemented Elderly Patients with Leukoaraiosis

Structural corpus callosum (CC) changes in patients with leukoaraiosis (LA) are significantly associated with cognitive and motor impairment. The aim of this study is to investigate the transcallosal fibers functioning by means of transcranial magnetic stimulation (TMS) in elderly patients with LA. The resting motor threshold (rMT), the motor-evoked potentials (MEPs), and the controlateral (cSP) and ipsilateral silent periods (iSP) were determined using single-pulse TMS in 15 patients and 15 age-matched controls. The neuropsychological profile and the vascular burden at brain magnetic resonance imaging (MRI) were concomitantly explored. Patients reported abnormal scores at tests evaluating executive control functions. No significant difference was found in TMS measures of intra- and intercortical excitability. No CC lesion was evident at MRI. Transcallosal inhibitory mechanisms to TMS seem to be spared in LA patients, a finding which is in line with neuroimaging features and suggests a functional integrity of the CC despite the ischemic interruption of corticosubcortical loops implicated in cognition and behavior. The observed neurophysiological finding differs from that reported in degenerative dementia, even in the preclinical or early stage. In our group of patients, the pure extent of LA is more related to impairment of frontal lobe abilities rather than functional callosal changes.

Another Step Forward in Relating Facial and Brain Dysmorphologies Associated with Prenatal Alcohol Exposure

Another Step Forward in Relating Facial and Brain Dysmorphologies Associated with Prenatal Alcohol Exposure

Assessing Corpus Callosum Changes in Alzheimer's Disease: Comparison between Tract-Based Spatial Statistics and Atlas-Based Tractography

Tractography based on Diffusion Tensor Imaging (DTI) represents a valuable tool for investigating brain white matter (WM) microstructure, allowing the computation of damage-related diffusion parameters such as Fractional Anisotropy (FA) in specific WM tracts. This technique appears relevant in the study of pathologies in which brain disconnection plays a major role, such as, for instance, Alzheimer's Disease (AD). Previous DTI studies have reported inconsistent results in defining WM abnormalities in AD and in its prodromal stage (i.e., amnestic Mild Cognitive Impairment; aMCI), especially when investigating the corpus callosum (CC). A reason for these inconsistencies is the use of different processing techniques, which may strongly influence the results. The aim of the current study was to compare a novel atlas-based tractography approach, that sub-divides the CC in eight portions, with Tract-Based Spatial Statistics (TBSS) when used to detect specific patterns of CC FA in AD at different clinical stages. FA data were obtained from 76 subjects (37 with mild AD, 19 with aMCI and 20 elderly healthy controls, HC) and analyzed using both methods. Consistent results were obtained for the two methods, concerning the comparisons AD vs. HC (significantly reduced FA in the whole CC of AD patients) and AD vs. aMCI (significantly reduced FA in the frontal portions of the CC in AD patients), thus identifying a relative preservation of the frontal CC regions in aMCI patients compared to AD. Conversely, the atlas-based method but not the TBSS showed the ability to detect a selective FA change in the CC parietal, left temporal and occipital regions of aMCI patients compared to HC. This finding indicates that an analysis including a higher number of voxels (with no restriction to tract skeletons) may detect characteristic pattern of FA in the CC of patients with preclinical AD, when brain atrophy is still modest.

Progression of Corpus Callosum Atrophy in Early Stage of Alzheimer’s Disease: MRI Based Study

Magnetic resonance imaging (MRI) studies reveal that atrophy of the corpus callosum (CC) is involved in early Alzheimer's disease (AD). The aim of this study was to investigate when and how callosal changes occur in the early course of AD. The Open Access Series of Imaging Studies data sets were used in this study to investigate callosal change. High-resolution structural MRI was performed in 196 older patients. Subjects were characterized using the Clinical Dementia Rating (CDR); 98 healthy controls were not demented (CDR 0), and 98 patients had clinical diagnosis of AD in the very mild dementia stage (CDR 0.5; n = 70) and the mild dementia stage (CDR 1; n = 28). A semiautomatic segmentation method was used to extract the CC in the midsagittal plane. The total and regional areas of the CC were measured. The results indicated that callosal atrophy occurred in when subjects' CDRs were 0.5. The area of the genu and rostral body of the CC in the healthy controls (CDR 0) was significantly different from that of the subjects with very mild dementia (CDR 0.5) (P < .05). A significant difference could also be found in the area of the rostral body and midbody of the CC between subjects with very mild dementia (CDR 0.5) and those with mild dementia (CDR 1) (P < .05). Callosal atrophy can be detected in subjects with CDRs of 0.5. The change in the CC in the early stage of AD indicates an anterior-to-posterior atrophic process as the degree of dementia assessed by the CDR (from 0 to 0.5 to 1) increases.

Multimodal MRI Analysis of the Corpus Callosum Reveals White Matter Differences in Presymptomatic and Early Huntington's Disease

Recent magnetic resonance imaging (MRI) studies suggest that abnormalities in Huntington's disease (HD) extend to white matter (WM) tracts in early HD and even in presymptomatic stages. Thus, changes of the corpus callosum (CC) may reflect various aspects of HD pathogenesis. We recruited 17 HD patients, 17 pre-HD subjects, and 34 healthy age-matched controls. Three-dimensional anatomical MRI and diffusion tensor images of the brain were acquired on a 3T scanner. Combining region-of-interest analyses, voxel-based morphometry, and tract-based spatial statistics, we investigated callosal thickness, WM density, fractional anisotropy, and radial and axial diffusivities. Compared with controls, pre-HD subjects showed reductions of the isthmus, likely due to myelin damage. Compared with pre-HD subjects, HD patients showed reductions of isthmus and body, with axonal damage confined to the body. Compared with controls, HD patients had significantly decreased callosal measures in extended regions across almost the entire CC. At this disease stage, both myelin and axonal damage are detectable. Supplementary multiple regression analyses revealed that WM reduction density in the isthmus as well as Disease Burden scores allowed to predict the "HD development" index. While callosal changes seem to proceed in a posterior-to-anterior direction as the diseases progresses, this observation requires validation in future longitudinal investigations.

Brain abnormalities in a Neuroligin3 R451C knockin mouse model associated with autism

Magnetic resonance imaging (MRI) has been used quite extensively for examining morphological changes in human and animal brains. One of the many advantages to examining mouse models of human autism is that we are able to examine single gene targets, like that of Neuroligin3 R451C knockin (NL3 KI), which has been directly implicated in human autism. The NL3 KI mouse model has marked volume differences in many different structures in the brain: gray matter structures, such as the hippocampus, the striatum, and the thalamus, were all found to be smaller in the NL3 KI. Further, many white matter structures were found to be significantly smaller, such as the cerebral peduncle, corpus callosum, fornix/fimbria, and internal capsule. Fractional anisotropy measurements in these structures were also measured, and no differences were found. The volume changes in the white matter regions, therefore, are not due to a general breakdown in the microstructure of the tissue and seem to be caused by fewer axons or less mature axons. A larger radial diffusivity was also found in localized regions of the corpus callosum and cerebellum. The corpus callosal changes are particularly interesting as the thinning (or reduced volume) of the corpus callosum is a consistent finding in autism. This suggests that the NL3 KI model may be useful for examining white matter changes associated with autism.

The Development of the Corpus Callosum in the Healthy Human Brain

The corpus callosum changes structurally throughout life, but most dramatically during childhood and adolescence. Even so, existing studies of callosal development tend to use parcellation schemes that may not capture the complex spatial profile of anatomical changes. Thus, more detailed mapping of callosal growth processes is desirable to create a normative reference. This will help to relate and interpret other structural, functional, and behavioral measurements, both from healthy subjects and pediatric patients. We applied computational surface-based mesh-modeling methods to analyze callosal morphology at extremely high spatial resolution. We mapped callosal development and explored sex differences in a large and well matched sample of healthy children and adolescents (n = 190) aged 5-18 years. Except for the rostrum in females, callosal thickness increased across the whole surface, with sex- and region-specific rates of growth, and at times shrinkage. The temporally distinct changes in callosal thickness are likely to be a consequence of varying degrees of axonal myelination, redirection, and pruning. Alternating phases of callosal growth and shrinkage may reflect a permanent adjustment and fine-tuning of fibers connecting homologous cortical areas during childhood and adolescence. Our findings emphasize the importance of taking into account sex differences in future studies, as existing developmental effects might remain disguised (or biased toward the effect of the dominant sex in unbalanced statistical designs) when pooling male and female samples.