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Cerebral Hypoxia (cerebral + hypoxia)
Selected AbstractsIn the hypoxic central nervous system, endothelial cell proliferation is followed by astrocyte activation, proliferation, and increased expression of the ,6,4 integrin and dystroglycanGLIA, Issue 10 2010Longxuan Li Abstract Cerebral hypoxia induces a profound angiogenic response in the central nervous system (CNS). Using a mouse model of chronic cerebral hypoxia, we previously demonstrated that angiogenic vessels in the hypoxic CNS show marked upregulation of the extracellular matrix (ECM) protein fibronectin, along with increased expression of its major receptor, ,5,1 integrin on brain endothelial cells (BEC). As cerebral hypoxia also leads to glial activation, the aim of the current study was to define the temporal relationship between BEC responses and glial cell activation in this model of cerebral hypoxia. This revealed that BEC fibronectin/,5,1 integrin expression and proliferation both reached maximal level after 4-day hypoxia. Interestingly, up to 4-day hypoxia, all dividing cells were BEC, but at later time-points proliferating astrocytes were also observed. GFAP staining revealed that hypoxia induced marked astrocyte activation that reached maximal level between 7- and 14-day hypoxia. As newly formed cerebral capillaries require ensheathment by astrocyte end-feet to acquire mature brain endothelium characteristics, we next examined how expression of astrocyte end-feet adhesion molecules is regulated by hypoxia. This showed that the astrocyte adhesion receptors ,6,4 integrin and dystroglycan were both markedly upregulated, with a time-course that closely resembled astrocyte activation. Taken together, this evidence shows that cerebral hypoxia promotes first an endothelial response, in which fibronectin promotes BEC proliferation. This is then followed by an astrocyte response, involving astrocyte activation, proliferation, and reorganization of astrocyte end-feet, which correlates with increased expression of astrocyte end-feet adhesion molecules. © 2010 Wiley-Liss, Inc. [source] Cerebral oximetry improves detection of sickle cell patients at risk for nocturnal cerebral hypoxia,PEDIATRIC PULMONOLOGY, Issue 11 2006Ashok B. Raj MD Abstract We previously used cerebral oximetry to identify low cerebral venous oxygen saturation in waking children with sickle cell disease (SCD). Because arterial oxyhemoglobin desaturation is common during sleep in SCD patients, this study compared both waking and sleeping systemic arterial and cerebral venous oxygenation dynamics in children with and without SCD. Seventeen African-American (AA) children with homozygous SCD [8 (4,15) years; 29% male; normal transcranial Doppler velocities] were compared with a control cohort (CON) comprised of six healthy AA children [9 (4,16) years, 33% male]. Standard all-night polysomnographic recordings were performed, including measurement of arterial oxygen saturation by pulse oximetry (SpO2). Regional cerebral oxygen saturation (rSO2) was measured non-invasively with cerebral oximetry. Intra-cohort comparisons examined the influence of sleep on SpO2 and rSO2 in the subjects. Inter-cohort comparisons of SpO2, rSO2, and the rSO2/SpO2 ratio assessed the impact of SCD on systemic and cerebral oxygenation during wakefulness and sleep. Cohort differences in SpO2 were not statistically significant in either wakefulness or sleep. However, only in the SCD cohort was the magnitude of SpO2 change statistically significant (P,=,0.002). In contrast, both waking and sleep rSO2 cohort median values did differ significantly [awake: CON 76 (67,86) vs. SCD 62 (58,71), P,=,0.01; sleep: CON 65 (60,77) vs. SCD 55 (48,61), P,=,0.01)]. The waking rSO2/SpO2 ratio was also significantly lower in the SCD group [CON 0.78 (0.68,0.88) vs. SCD of 0.66 (0.61,0.72); P,=,0.015]. During sleep, the ratio was also significantly lower in the SCD group [CON 0.71 (0.66,0.81) vs. SCD 0.59 (0.52,0.65); P,=,0.011]. Our findings suggest that SCD patients may be at increased risk of cerebral hypoxia during both wakefulness and sleep. Pediatr Pulmonol. 2006, 41:1088,1094. © 2006 Wiley-Liss, Inc. [source] A review of paroxysmal sympathetic hyperactivity after acquired brain injuryANNALS OF NEUROLOGY, Issue 2 2010Iain Perkes BMedSc Severe excessive autonomic overactivity occurs in a subgroup of people surviving acquired brain injury, the majority of whom show paroxysmal sympathetic and motor overactivity. Delayed recognition of paroxysmal sympathetic hyperactivity (PSH) after brain injury may increase morbidity and long-term disability. Despite its significant clinical impact, the scientific literature on this syndrome is confusing; there is no consensus on nomenclature, etiological information for diagnoses preceding the condition is poorly understood, and the evidence base underpinning our knowledge of the pathophysiology and management strategies is largely anecdotal. This systematic literature review identified 2 separate categories of paroxysmal autonomic overactivity, 1 characterized by relatively pure sympathetic overactivity and another group of disorders with mixed parasympathetic/sympathetic features. The PSH group comprised 349 reported cases, with 79.4% resulting from traumatic brain injury (TBI), 9.7% from hypoxia, and 5.4% from cerebrovascular accident. Although TBI is the dominant causative etiology, there was some suggestion that the true incidence of the condition is highest following cerebral hypoxia. In total, 31 different terms were identified for the condition. Although the most common term in the literature was dysautonomia, the consistency of sympathetic clinical features suggests that a more specific term should be used. The findings of this review suggest that PSH be adopted as a more clinically relevant and appropriate term. The review highlights major problems regarding conceptual definitions, diagnostic criteria, and nomenclature. Consensus on these issues is recommended as an essential basis for further research in the area. ANN NEUROL 2010;68:126,135 [source] | ||||||||||