Dataset Information

Brain white matter plasticity and functional reorganization underlying the central pathogenesis of trigeminal neuralgia.

ABSTRACT: Peripheral nerve damage does not fully explain the pathogenesis of trigeminal neuralgia (TN). Central nervous system changes can follow trigeminal nerve dysfunction. We hypothesized that brain white matter and functional connectivity changes in TN patients were involved in pain perception, modulation, the cognitive-affective system, and motor function; moreover, changes in functional reorganization were correlated with white matter alterations. Twenty left TN patients and twenty-two healthy controls were studied. Diffusion kurtosis imaging was analyzed to extract diffusion and kurtosis parameters, and functional connectivity density (FCD) mapping was used to explore the functional reorganization in the brain. In the patient group, we found lower axial kurtosis and higher axial diffusivity in tracts participated in sensory, cognitive-affective, and modulatory aspects of pain, such as the corticospinal tract, superior longitudinal fasciculus, anterior thalamic radiation, inferior longitudinal fasciculus, inferior fronto-occipital fasciculus, cingulated gyrus, forceps major and uncinate fasciculus. Patients exhibited complex FCD reorganization of hippocampus, striatum, thalamus, precentral gyrus, precuneus, prefrontal cortex and inferior parietal lobule in multiple modulatory networks that played crucial roles in pain perception, modulation, cognitive-affective system, and motor function. Further, the correlated structural-functional changes may be responsible for the persistence of long-term recurrent pain and sensory-related dysfunction in TN.

SUBMITTER: Tian T

PROVIDER: S-EPMC5078771 | biostudies-literature | 2016 Oct

REPOSITORIES: biostudies-literature

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Brain white matter plasticity and functional reorganization underlying the central pathogenesis of trigeminal neuralgia.

Tian Tian T Guo Linying L Xu Jing J Zhang Shun S Shi Jingjing J Liu Chengxia C Qin Yuanyuan Y Zhu Wenzhen W

Scientific reports 20161025

Peripheral nerve damage does not fully explain the pathogenesis of trigeminal neuralgia (TN). Central nervous system changes can follow trigeminal nerve dysfunction. We hypothesized that brain white matter and functional connectivity changes in TN patients were involved in pain perception, modulation, the cognitive-affective system, and motor function; moreover, changes in functional reorganization were correlated with white matter alterations. Twenty left TN patients and twenty-two healthy cont ...[more]

PMID: 27779254

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Project description:Vanishing white matter (VWM) is a leukodystrophy caused by biallelic pathogenic variants in eukaryotic translation initiation factor 2B. Neuropathology includes lack of reactive gliosis, paucity of myelin, and axonal abnormalities. Alteration in proteins involved in cellular metabolism has also been implicated in the disease. It, however, remains unclear which factors contribute to VWM pathogenesis. Here, we aimed at gaining insight into the basis of VWM pathogenesis using the 2b5ho mouse model of VWM. We first investigated the temporal proteome in the cerebellum, corpus callosum, cortex, and brainstem of 2b5ho and wild type (WT) mice. Protein changes observed in 2b5ho mice were then cross-referenced with published proteomic datasets from post mortem VWM patient brain tissue to define alterations relevant to the human disease. By comparing 2b5ho mice with their region- and age-matched WT counterparts, we identified region-specific protein changes associated with disease development and progression. We showed that the proteome in the cerebellum and cortex of 2b5ho mice was already deregulated prior to pathology development, whereas proteome changes in the corpus callosum only occurred after onset of pathology. Remarkably, protein changes in the brainstem were transient, indicating that a compensatory mechanism might occur in this region throughout the disease course. Gene ontology overrepresentation analysis revealed that proteome changes observed in 2b5ho mouse brains reflect alterations in features well-known in VWM. Side-by-side comparison of the 2b5ho mouse and VWM patient brain proteomes revealed that part of protein changes were the same as in VWM patients. These could represent relevant changes that contribute to the disease or even drive its progression in VWM patients. Taken together, we show that the proteome in the brain of 2b5ho mice is affected in a region-specific and time-dependent manner. We found that the 2b5ho mouse model partly replicates the human disease at the protein level, and provides a spatiotemporal proteome resource to study aspects of VWM pathogenesis. This resource highlights alterations presenting from early to late disease stages, and those that possibly drive disease progression.

Dataset Information

Brain white matter plasticity and functional reorganization underlying the central pathogenesis of trigeminal neuralgia.

Publications

Brain white matter plasticity and functional reorganization underlying the central pathogenesis of trigeminal neuralgia.

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