Cerebral Palsy

Magnetic resonance imaging of the brain is invaluable in assessing the neonate who presents with encephalopathy. Successful imaging requires adaptations to both the hardware and sequences used for adults. Knowledge of the perinatal and postnatal details are essential for the correct interpretation of the imaging findings. Perinatal lesions are at their most obvious on conventional imaging between 1 and 2weeks from delivery. Very early imaging is useful to guide management in ventilated neonates but abnormalities may be subtle on conventional sequences. Diffusion-weighted imaging (DWI) is clinically useful for the early identification of ischaemic tissue in the neonatal brain, the pattern of which can predict outcome. DWI may underestimate the final extent of injury, particularly basal ganglia and thalamic lesions. Serial imaging with quantification of both tissue damage and structure size provides invaluable insights into the effects of perinatal injury on the developing brain. Copyright © 2010. Published by Elsevier Ireland Ltd.

Rhesus macaques on a calorie restricted diet (CR) develop less age-related disease, have virtually no indication of diabetes, are protected against sarcopenia, and potentially live longer. Beneficial effects of caloric restriction likely include reductions in age-related inflammation and oxidative damage. Oligodendrocytes are particularly susceptible to inflammation and oxidative stress, therefore, we hypothesized that CR would have a beneficial effect on brain white matter and would attenuate age-related decline in this tissue. CR monkeys and controls underwent diffusion tensor imaging (DTI). A beneficial effect of CR indexed by DTI was observed in superior longitudinal fasciculus, fronto-occipital fasciculus, external capsule, and brainstem. Aging effects were observed in several regions, although CR appeared to attenuate age-related alterations in superior longitudinal fasciculus, frontal white matter, external capsule, right parahippocampal white matter, and dorsal occipital bundle. The results, however, were regionally specific and also suggested that CR is not salutary across all white matter. Further evaluation of this unique cohort of elderly primates to mortality will shed light on the ultimate benefits of an adult-onset, moderate CR diet for deferring brain aging. Published by Elsevier Inc.

The purpose of our work was to determine the effects of oxidative stress on the neurodegeneration process in the substantia nigra, and to evaluate dopamine-oxidation metabolites in the plasma using a cyclic voltammetry (CV) technique. We have also studied the correlation between the increases in oxidized dopamine-species levels with the severity of lipid peroxidation in the plasma. Sixty-four male Wistar rats were divided into four experimental groups and received air (Group I, control) or ozone (0.25ppm) daily by inhalation for 4h for 15 (Group II), 30 (Group III), and 60 (Group IV) days. The brains were processed for immunohistochemical location of dopamine and p53 in the substantia nigra. Plasma collected from these animals was assayed for oxidized dopamine products using CV and lipid peroxidation levels were measured. Our results indicate that chronic exposure to low O(3) doses causes that the number of dopaminergic neurons decreased, and p53-immunoreactive cells increases until 30 days; which was a function of the time of exposure to ozone. Oxidative stress produces a significant increase in the levels of the dopamine-quinones (DAQs) that correlated well (r=0.962) with lipid peroxides in the plasma during the study period. These results suggest that DAQ could be a reliable, peripheral oxidative indicator of nigral dopaminergic damage in the brain. Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.

An overview of the methods of fixation of the skull bones is presented,as well as discussion and characterization of different methods of fixation. A new system of fixation of the skull bones was used in osseous-plastic trepanation and reconstructive operations using nitinol craniofixators. Results of cranioplasty using craniofixators were analyzed in 62 patients with craniocerebral injuries and its consequences, vascular and oncological diseases of the brain. There were no complications in the postoperative period. Articles made of nitinol are very strong, elastic and have the effect of thermo-mechanical memory of the form.

Abstract Aging is the major risk factor for neurodegenerative diseases and oxidative stress and is involved in their pathophysiology. Oxidative stress can induce neuronal damage and modulate intracellular signaling, ultimately leading to neuronal death by apoptosis or necrosis. In this study we investigated the neuroprotective properties of the natural polyphenolic antioxidant compound, curcumin, against homocysteine (Hcy) neurotoxicity. Curcumin (5, 15, or 45 mg/kg) was injected intraperitoneally once daily for a period of 10 days beginning 5 days prior to Hcy (0.2 mumol/muL) intracerebroventricular injection in rats. Biochemical and behavioral studies, including passive avoidance learning and locomotor activity tests, were evaluated 24 hours after the last injection of curcumin or vehicle. Results indicated that Hcy induces lipid peroxidation and increases malondialdehyde (MDA) and superoxide anion (SOA) levels in whole rat brain. In addition, Hcy impaired memory retention in the passive avoidance learning test. However, curcumin treatment significantly decreased MDA and SOA levels and improved learning and memory in rats. These results suggest that Hcy may induce lipid peroxidation in rat brain and that polyphenol treatment (curcumin) improves learning and memory deficits by protecting the nervous system against oxidative stress.

Previous studies have demonstrated that electrical stimulation (ES) enhances axonal regeneration following central and peripheral nerve injury. However, the effect of ES on peripheral remyelination after nerve damage has been investigated less, and the mechanism underlying its action remains unclear. In the present study, neuron/Schwann cell (SC) co-cultures in vitro and crush-injured sciatic nerves in rats were subjected to 1 h of continuous ES (20 Hz, 100 mus, 3 V). Electron microscopy and nerve morphometry were performed to investigate the extent of regenerated nerve myelination. The expression profiles of P0,Par-3 and brain-derived neurotrophic factor (BDNF) in vitro and in vivo were examined by western blotting. We reported that 20 Hz ES increased the number of regenerated and myelinated axons at 4 and 8 weeks after injury. P0 level in the ES-treated groups, as well as myelin sheath thickness, were enhanced compared with the controls. The earlier peak Par-3 in the ES-treated groups indicated earlier initiation of SC myelination. Moreover, the similar results were achieved in the cell co-culture. Additionally, brief ES significantly elevated BDNF expression in co-cultured cells and nerve tissues. In conclusion, ES of the site of nerve injury potentiates axonal regrowth and myelin maturation during peripheral nerve regeneration. Further, the therapeutic actions of ES on myelination that is mediated via enhanced BDNF signals, which driving the promyelination effect on SCs at the onset of myelination. Copyright © 2010. Published by Elsevier Ltd.

To evaluate effect of diabetes on transient ischemia-induced brain damage and autophagy activity, streptozotocin (STZ)-induced diabetic mellitus (DM) mice were subjected to transient common carotid artery occlusion (CCAO) operation. After the operation, immunohistochemistry and transmission electron microscopy (EM) were performed to investigate the astrocytes activation, amyloid-beta protein (Abeta) expression and accumulation of autophagy-like vacuoles containing electron-dense material (avd); and hallmarks of autophagy, the microtubule-associated protein light chain 3 (LC3)-II, was detected by western blot analysis. The results showed that DM amplified stroke-induced astrocytes activation and Abeta generation. Western blot analysis showed that LC3-II conjugate was drastically up-regulated at early stages post ischemia and it last for at least 72h in DM mice brain. DM mice demonstrated increased baseline level of LC3-II as comparing to normal mice; DM also amplifed stroke-induced LC3-II level. Under EM, avd was most markedly accumulated in neurons of DM mice brain after ischemia. Immunofluorescence double-staining showed that most Abeta and autophagosomes co-localized. Therefore, our results suggested that exacerbation of ischemia-induced Abeta generation by diabetes might be associated with autophagy activation in mice brain, and modulating neuronal autophagy might be a new therapeutic strategy to depress the risk of development of dementia in diabetic patients with stroke. Copyright © 2010. Published by Elsevier Ireland Ltd.

SUMMARY Background: Many current therapeutic strategies for several eye diseases, such as glaucoma, retinal ischemia, and optic neuropathy, are focused on protection of the retinal ganglion cells (RGCs). In fact, loss of visual field, including irreversible blindness, is caused by RGC damage in these diseases. However, recent evidence suggests that the RGC damage extends to visual center in brain: the visual impairment induced by these diseases may result not only from RGC loss, but also from neuronal degeneration within the visual center in brain. Objective: To protect neurons within the visual center in the brain, as well as retinal treatment, for the prevention of visual disorder in these diseases. Methods: Once considered difficult to study the visual center in brain following RGCs loss, because obtaining the human samples that are suitable for the study may be difficult. In addition, the monkey, mainly used as glaucomatous model, is relatively high cost and needs to long experiment-span. Here, we focused on mice, because of their high degree of availability, relatively low cost, and amenability to experimental and genetic manipulation. Conclusion: In this review, we describe time-dependent alterations in the visual center in brain following RGCs loss, and whether some drugs prevent the neuronal damage of the visual center in the brain.

Myeloid cells are mediators of central nervous system (CNS) damage and recovery in neuroinflammatory and neurodegenerative disorders. Besides endogenous myelomonocytic cell populations that reside in the brain already during development, newly migrated leukocytes are considered as important disease modulators in the adult brain. Thus, understanding of myeloid cell recruitment is pivotal for manipulating immune cell entry into the CNS and potentially reducing disease burden. Before myeloid cells engraft in the brain, they first tether to and roll on the activated brain endothelium, then they firmly adhere and eventually transmigrate into the damaged brain where they execute effector functions and differentiate into cells with microglia-like features. These steps are mainly regulated by adhesion molecules and by chemokines and their cognate receptors. Due to recent advances in our understanding of monocyte heterogeneity, the interest in chemokine receptors has significantly increased. Among others, the presence of the chemokine receptors CCR2 and CX(3)CR(1) is considered to be critical for both myeloid cell trafficking along inflamed vessels and subsequent accumulation in the brain. Therefore, these molecules present viable targets for therapeutic manipulations of myeloid cells destined for the CNS. Copyright © 2010 Elsevier B.V. All rights reserved.

Cerebellar contribution to non-motor functions has been supported by several animal, human and functional neuroimaging studies. Which cognitive skills and to what extent the cerebrocerebellar loops contribute remain unclear, however. Among other reasons, this may be explained by the fact that authors have studied patients with extracerebellar lesions. The goal of this study was to explore the role of the cerebellum in cognition and affect in patients with autosomal recessive cerebellar ataxia type 1 (ARCA-1), a newly described inherited cerebellar disease characterised by middle-age onset of ataxia as well as pure, severe and diffuse cerebellar atrophy. To this end, the performance of 21 ARCA-1 patients was compared to that of 21 normal controls paired for age and education on a 3-h battery of attention, executive, visuospatial and memory skills. Results indicated similar IQ, naming and declarative memory abilities between groups. ARCA-1 patients showed significant deficits in attention (attention span, speed of information processing, sustained attention), verbal working memory and visuospatial/visuoconstructional skills (3-D drawings, copy of a complex figure). Functional brain imaging in a subset of patients showed diffuse severe cerebellar hypometabolism associated with a small area of right parietal hypometabolism. None of the patients presented a significant affective syndrome. Correlational analyses suggested that cognitive deficits could not be explained by the severity of motor deficits, duration of disease or mood. Altogether, this study confirms that pure cerebellar damage as seen in ARCA-1 is associated with significant cognitive impairments but not with psychiatric comorbidity. These deficits are correlated with an overall moderate impact on patient’s autonomy. Our data favour an indirect participation of the dorsolateral prefrontal and posterior parietal cortical areas to the cerebrocerebellar circuit.