Brain lesion [Neurosurgery Wiki]

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====== Brain lesion ======

Brain [[lesion]]s can arise from [[traumatic brain injury]], [[infection]], and [[craniotomy]]. Although injectable[[ hydrogel]]s show promise for promoting healing of lesions and health of surrounding [[tissue]], enabling cellular ingrowth and restoring [[neural tissue]] continue to be challenging. 
Hu et al. hypothesized that these challenges arise in part from the mismatch of composition, stiffness and [[viscoelasticity]] between the hydrogel and the brain [[parenchyma]], and tested this [[hypothesis]] by developing and evaluating a self-healing hydrogel that not only mimicked the composition, but also the stiffness and viscoelasticity of native [[brain parenchyma]]. The hydrogel was crosslinked by dynamic boronate ester bonds between phenylboronic acid grafted hyaluronic acid (HA-PBA) and dopamine grafted [[gelatin]] (Gel-Dopa). This HA-PBA/Gel-Dopa hydrogel could be injected into a lesion cavity in a shear-thinning manner with rapid [[hemostasis]], high tissue adhesion and efficient self-healing. They tested this in an [[in vivo]] [[mouse model]] of brain lesions and found the multi-functional injectable hydrogel to support neural cell [[infiltration]], decrease [[astrogliosis]] and glial [[scar]]s, and close the lesions. The results suggest a role for [[extracellular matrix]]-mimicking [[viscoelasticity]] in [[brain lesion]] healing, and motivate additional [[experimentation]] in larger [[animal]]s as the technology progresses towards potential application in humans
((Hu Y, Jia Y, Wang S, Ma Y, Huang G, Ding T, Feng D, Genin GM, Wei Z, Xu F. An ECM-Mimicking, Injectable, Viscoelastic Hydrogel for Treatment of Brain Lesions. Adv Healthc Mater. 2022 Nov 18:e2201594. doi: 10.1002/adhm.202201594. Epub ahead of print. PMID: 36398536.)).
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During [[surgery]] for intrinsic brain lesions, it is important to distinguish the pathological [[gyrus]] from the surrounding normal [[sulci]] and [[gyri]]. This [[task]] is usually tedious because of the [[pia mater]]-[[arachnoid]] membranes with their [[arterial]] and [[venous]] complexes that obscure the underlying [[anatomy]]. Moreover, most [[tumor]]s grow in the [[white matter]] without initially distorting the [[cortical]] anatomy, making their direct visualization more difficult.
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[[Focal brain lesion]]s can alter the morphology and function of remote brain areas. When the damage is inflicted more slowly, the functional compensation by and structural reshaping of these areas seem to be more effective. It remains unclear, however, whether the momentum of lesion development also modulates the functional network topology of the remote brain areas. In this study, we compared resting-state functional connectivity data of patients with a slowly growing low-grade glioma (LGG) with that of patients with a faster-growing high-grade glioma (HGG). Using graph theory, we examined whether the tumour growth velocity modulated the functional network topology of remote areas, more specifically of the hemisphere contralateral to the lesion. We observed that the contralesional network topology characteristics differed between patient groups. Based only on the connectivity of the hemisphere contralateral to the lesion, patients could be classified in the correct tumour-grade group with 70% accuracy. Additionally, LGG patients showed smaller contralesional intramodular connectivity, smaller contralesional ratio between intra- and intermodular connectivity, and larger contralesional intermodular connectivity than HGG patients. These results suggest that, in the hemisphere contralateral to the lesion, there is a lower capacity for local, specialized information processing coupled to a higher capacity for distributed information processing in LGG patients. These results underline the utility of a network perspective in evaluating effects of focal brain injury
((De Baene W, Rutten GJM, Sitskoorn MM. The Temporal Pattern of a Lesion
Modulates the Functional Network Topology of Remote Brain Regions. Neural Plast. 
2017;2017:3530723. doi: 10.1155/2017/3530723. Epub 2017 Aug 3. PubMed PMID:
28845308; PubMed Central PMCID: PMC5560088.
)).