Brain Injury review

From Ding et al

We propose an improved version of regional competition algorithm in this paper, and apply it to the automatic segmentation of medical image series, particularly in the segmentation and recognition of brain tumor. The traditional regional competition is enhanced by combining the attractive aspects of fuzzy segmentation, and thus it provides an efficient approach to segment the fuzzy and heterogeneous medical images. In order to perform regional competition on medical image series, we utilize the segmentation result of a slice to initiate the next segmented slice, while the first slice is initialized using regional growing algorithm. Moreover, we develop an algorithm to recognize the tumors automatically, taking into account its characters. Experimental results show that our algorithm performs well on the segmentation of magnetic resonance imaging (MRI) image series with high speed and precision.

The purpose of this investigation was to describe the causes, clinical pattern, and treatment of cerebral salt wasting syndrome in children with acute central nervous system injury. This retrospective study focused on patients 120 mEq/L), and volume depletion. Fourteen patients were identified with cerebral salt wasting syndrome, 12 after a neurosurgical procedure (8 brain tumor, 4 hydrocephalus) and 2 after severe brain trauma. In 11 patients the cerebral salt wasting syndrome was diagnosed during the first 48 hours of admission. Prevalence of cerebral salt wasting syndrome in neurosurgical children was 11.3/1000 surgical procedures. The minimum sodium was 122 +/- 7 mEq/L, the maximum urine osmolarity 644 +/- 59 mOsm/kgH(2)O. The maximum sodium supply was 1 mEq/kg/h (range, 0.1-2.4). The mean duration of cerebral salt wasting syndrome was 6 +/- 5 days (range 1-9). In conclusion, cerebral salt wasting syndrome can complicate the postoperative course of children with brain injury; it is frequently present after surgery for brain tumors and hydrocephalus and in patients with severe head trauma. Close monitoring of salt and fluid balance is essential to prevent severe neurologic and hemodynamic complications.

Pub med ID is 16996399

Neural stem cells reside in defined areas of the adult mammalian brain, including the dentate gyrus of the hippocampus. Rat neural stem/progenitor cells (NSPCs) isolated from this region retain their multipotency in vitro and in vivo after grafting into the adult brain. Recent studies have shown that endogenous or grafted neural stem/progenitor cellss are activated after an injury and migrate toward lesioned areas. In these areas, reactive astrocytes are present and secrete numerous molecules and growth factors; however, it is not currently known whether reactive astrocytes can influence the lineage selection of neural stem/progenitor cells. We investigated whether reactive astrocytes could affect the differentiation, proliferation, and survival of adult neural stem/progenitor cells by modelling astrogliosis in vitro, using mechanical lesion of primary astrocytes. Initially, it was found that conditioned medium from lesioned astrocytes induced astrocytic differentiation of NSPCs without affecting neuronal or oligodendrocytic differentiation. In addition, NSPCs in coculture with lesioned astrocytes also displayed increased astrocytic differentiation and some of these NSPC-derived astrocytes participated in glial scar formation in vitro. When proliferation and survival of neural stem/progenitor cells were analyzed, no differential effects were observed between lesioned and nonlesioned astrocytes. To investigate the molecular mechanisms of the astrocyte-inducing activity, the expression of two potent inducers of astroglial differentiation, ciliary neurotrophic factor and leukemia inhibitory factor, was analyzed by Western blot and shown to be up-regulated in conditioned medium from lesioned astrocytes. These results demonstrate that lesioned astrocytes can induce astroglial differentiation of neural stem/progenitor cells and provide a mechanism for astroglial differentiation of these cells following brain injury.

From Pubmed 16998910