Corpus Callosum

Aim of reviewThe presence of isolated, reversible lesions in the splenium of the corpus callosum (SCC) is essential to confirm the diagnosis of mild encephalitis/encephalopathy. The lesions usually heal within a month after the onset of neurological symptoms. Magnetic resonance imaging (MRI) has increasingly been used as a diagnostic tool, which has led to the publication of an increasing number of case reports. These have highlighted some inconsistencies about encephalitis/encephalopathy. First, the condition is not always mild and may be severe. Second, reversible lesions in the SCC have been identified in various diseases and conditions other than viral encephalitis/encephalopathy. Third, lesions in SCC are not always completely reversible. On this note, this review describes the specific clinical and radiological features of encephalitis/encephalopathy.FindingsThe reversible lesion in SCC is an MRI finding observable in a wide variety of diseases and conditions. Thus, it should be considered as a secondary change rather than a peculiar feature associated with mild encephalitis/encephalopathy. If reversible lesions are present in the SCC, the symptoms and prognosis are not necessarily favorable, with manifestations of encephalitis/encephalopathy varying from absent to severe. Neuroradiological features that appear as isolated high-intensity signals on diffusion-weighted images and a decreased apparent diffusion coefficient of the lesion might indicate a diagnosis of cytotoxic edema. Findings of previous studies suggest that cytokine-mediated cytotoxic edema of the SCC may be an important pathophysiological manifestation of this condition.ConclusionThe reversible lesions in the SCC found on MRI are not exclusive to encephalitis/encephalopathy but may be secondary to other disorders.

Background and purposeThe splenium of the corpus callosum is the most posterior part of the corpus callosum. Its embryological development, anatomy, vascularization, function, imaging of pathology, possible pathophysiological mechanisms by which pathology may develop and the clinical consequences are discussed.MethodsA literature-based description is provided on development, anatomy and function. MR and CT images are used to demonstrate pathology. The majority of pathology, known to affect the splenium, and the clinical effects are described in three subsections: (A) limited to the splenium, with elaboration on pathophysiology of reversible splenial lesions, (B) pathology in the cerebral white matter extending into or deriving from the splenium, with special emphasis on tumors, and (C) splenial involvement in generalized conditions affecting the entire brain, with a hypothesis for pathophysiological mechanisms for the different diseases.ResultsThe development of the splenium is preceded by the formation of the hippocampal commissure. It is bordered by the falx and the tentorium and is perfused by the anterior and posterior circulation. It contains different caliber axonal fibers and the most compact area of callosal glial cells. These findings may explain the affinity of specific forms of pathology for this region. The fibers interconnect the temporal and occipital regions of both hemispheres reciprocally and are important in language, visuospatial information transfer and behavior. Acquired pathology may lead to changes in consciousness.ConclusionThe development, location, fiber composition and vascularization of the splenium make it vulnerable to specific pathological processes. It appears to play an important role in consciousness.

Preterm children often have language problems. This atypical language development is probably due to atypical brain development. We conducted a systematic review to provide an overview of the extensive and diverse scientific literature on the relations between language outcome and underlying brain structures in school-aged preterm-born children. Embase, Medline Ovid, Web of Science, Cochrane central and Google scholar were searched for relevant studies. Inclusion criteria were: cases are school-aged preterm children; structural MRI (T1- and T2-weighted sequences) or DTI used in combination with a neurocognitive language test; publication in an English-language peer-reviewed journal. Correlational measures between language scores and brain volume or fractional anisotropy of a brain structure were extracted. 23 studies were included. The relations between oral language, verbal fluency and/or written language and MRI/DTI measurements of white matter, gray matter, cerebellum, corpus callosum and/or the fasciculi are presented. Oral language skills and verbal fluency appear to be related to the corpus callosum. Oral language skills are also related to the uncinate fasciculus. There seems to be no clear relation between cerebellar development and verbal fluency skills. Not one single brain area is responsible for atypical language development, but several brain areas and their connections are essential. For future research it is recommended to relate brain areas to oral language skills on a microstructural level in preterm children. We also recommend to use language tests in which it is possible to distinguish between several language domains, such as perceptive and expressive language.

White matter abnormalities are consistently observed in Shank3-related autism spectrum disorders (ASD), yet the mechanisms underlying oligodendrocyte dysfunction and myelination deficits remain poorly characterized. Here, we demonstrate that Shank3 deficiency disrupts oligodendrocyte development by promoting oligodendrocyte precursor cell (OPC) proliferation while impairing functional maturation and myelination. Mechanistically, Shank3 deficiency induced hyperactivation of the Erk signalling pathway, which compromised oligodendrocyte maturation and contributes to hypomyelination. Pharmacological inhibition of the Erk pathway effectively restored oligodendrocyte maturation in vitro, rescued myelination deficits in vivo, and partially improved autism-related behaviors and motor function in Shank3-deficient mice. Transcriptomic analyses furtherly revealed dysregulation of Wnt signalling, particularly the upregulation of Wnt5a, a key ligand of the non-canonical Wnt pathway, in Shank3-deficient oligodendrocytes. Consistently, Wnt5a treatment was found to activate Erk signalling in primary oligodendrocytes and replicate the observed myelination deficits. These findings uncover the Wnt5a-Erk axis as a critical regulator of oligodendrocyte dysfunction in Shank3-related ASD and highlight its therapeutic potential for addressing associated white matter deficits.