Cerebral Palsy

The major complication in dental implant surgery is loss of sensation due to damage to the inferior alveolar nerve resulting from poor characterization of the location of the mandibular canal and the traveling course of the inferior alveolar nerve, artery, and vein therein. The purposes of this study were to determine the buccolingual location of the mandibular canal and to verify the topography of the inferior alveolar nerve, artery, and vein therein by three-dimensional reconstruction of these structures. Sixty-two mandible sides were used for this study. The buccolingual location of the mandibular canal was classified into 3 types: type 1 (70%), where the canal follows the lingual cortical plate at the mandibular ramus and body; type 2 (15%), where the canal follows the middle of the ramus behind the second molar and the lingual plate passing through the second and first molars; and type 3 (15%), where the canal follows the middle or the lingual one third of the mandible from the ramus to the body. Three-dimensional reconstruction of the mandibular canal revealed that the inferior alveolar vessel traveled above the inferior alveolar nerve in 8 cases (80%), with the inferior alveolar artery being lingual to the inferior alveolar vein, and in 2 cases (20%) where the inferior alveolar vessel was buccal to the nerve.

BACKGROUND AND PURPOSE: Disruption of the corticospinal tract at various locations in the brain has been shown to predict worse spontaneous motor recovery after stroke. However, the anatomic specificity of previous findings was limited by the categorical classification of infarct locations. Here we used computational methods to more precisely determine the specific anatomic locations associated with impaired motor ability. More important, however, our study also used these techniques to evaluate whether infarct location could influence motor outcomes after Constraint-Induced Movement therapy (CI therapy), a specific and controlled form of physical therapy. METHODS: Quantitative voxel-based analyses were used to determine whether infarct location could predict either initial motor ability or clinical improvement after CI therapy in chronic stroke patients. RESULTS: Although corona radiata infarcts were associated with worse in-laboratory motor ability at pretreatment, infarct location did not predict improvement in either the laboratory or the life situation after CI therapy. CONCLUSIONS: The extent of improvement from CI therapy does not depend on the location of neurological damage, despite there being a pretreatment relationship between infarct location and in-laboratory motor ability. This dissociation could be explained by brain plasticity induced by CI therapy.

Anterior temporal lobe resection is often complicated by superior quadrantic visual field deficits (VFDs). In some cases this can be severe enough to prohibit driving, even if a patient is free of seizures. These deficits are caused by damage to Meyer’s loop of the optic radiation, which shows considerable heterogeneity in its anterior extent. This structure cannot be distinguished using clinical magnetic resonance imaging sequences. Diffusion tensor tractography is an advanced magnetic resonance imaging technique that enables the parcellation of white matter. Using seed voxels antero-lateral to the lateral geniculate nucleus, we applied this technique to 20 control subjects, and 21 postoperative patients. All patients had visual fields assessed with Goldmann perimetry at least three months after surgery. We measured the distance from the tip of Meyer’s loop to the temporal pole and horn in all subjects. In addition, we measured the size of temporal lobe resection using postoperative T(1)-weighted images, and quantified VFDs. Nine patients suffered VFDs ranging from 22% to 87% of the contralateral superior quadrant. In patients, the range of distance from the tip of Meyer’s loop to the temporal pole was 24-43 mm (mean 34 mm), and the range of distance from the tip of Meyer’s loop to the temporal horn was -15 to +9 mm (mean 0 mm). In controls the range of distance from the tip of Meyer’s loop to the temporal pole was 24-47 mm (mean 35 mm), and the range of distance from the tip of Meyer’s loop to the temporal horn was -11 to +9 mm (mean 0 mm). Both quantitative and qualitative results were in accord with recent dissections of cadaveric brains, and analysis of postoperative VFDs and resection volumes. By applying a linear regression analysis we showed that both distance from the tip of Meyer’s loop to the temporal pole and the size of resection were significant predictors of the postoperative VFDs. We conclude that there is considerable variation in the anterior extent of Meyer’s loop. In view of this, diffusion tensor tractography of the optic radiation is a potentially useful method to assess an individual patient’s risk of postoperative VFDs following anterior temporal lobe resection.

Neuronal damage after seizure is correlated with blood-brain barrier (BBB) leakage. Adiponectin (Ad) has shown protective effects on endothelial function. In this study, we investigated the effects of Ad on cell survival and BBB integrity in the mouse hippocampus after kainic acid (KA) treatment. Twenty four hours after intracerebroventricular injection of recombinant Ad, mice were treated with KA, and then sacrificed 48 hrs later. Decreased serum Ad and increased hippocampal Ad receptor 1 in the hippocampus of KA-treated mice were prevented by Ad pretreatment. Using cresyl violet staining, TUNEL analysis, and immunostaining for caspase-3, histological evaluation revealed that the marked cell death noted in the hippocampus of KA-treated mice was not observed in KA-treated mice pretreated with Ad. Impairment of the BBB, which was demonstrated by the presence of IgG, was inhibited by Ad pretreatment. Immunohistochemical analysis indicated that KA caused up-regulation of hippocampal VEGF, eNOS, and NF-kappaB levels, all of which were reduced in animals that received Ad pretreatment. These data indicate that Ad preserves the integrity of the BBB and has neuroprotective effects in an animal model of seizures.

Abstract Neuroendocrine dysfunction following traumatic brain injury (TBI) has been described extensively. However, few studies are longitudinal and most lack subtle radiological, clinical, and repetitive endocrine assessment in the acute phase. Accordingly, we prospectively assessed neuroendocrine function in 71 patients after TBI. Injury was documented by a computed tomography (CT). During the first week, critical clinical data (Glasgow Coma Score, APACHE score), treatment variables such as duration of analgosedation for mechanical ventilation, were related to basal pituitary function. More than 2 years later, a subgroup of patients was re-evaluated using dynamic testing with ACTH and GHRH-arginine tests. The Pearson's correlation analysis and Mann-Whitney rank sum test for group differences were used for statistical analysis. None of the CT findings predicted neuroendocrine dysfunction following TBI. The adaptive response to critical illness with significantly elevated cortisol levels on admission and decreased levels thereafter in patients ventilated for more than 24 h (p < 0.05) was attenuated following severe TBI (p < 0.05). However, the coincidence of low serum cortisol and increased urinary excretion of glucocorticoid metabolites in about 80% of patients challenges the relevance of basal hormone measurements. In ventilated patients, total T3 and free T4 were decreased (p < 0.05), TSH was low on day 3 (p < 0.05), and a gonadotropic insufficiency was present (p < 0.05). The thyrotropic and gonadotropic system recovered completely within the follow-up period. With regard to the somatotropic system, neither brain injury severity nor mechanical ventilation was associated with an insufficiency during the acute phase post-injury. However, initially low GH levels predicted a persistent deficiency (r = 0.731, p < 0.001). We conclude that both severe TBI and prolonged mechanical ventilation result in hormonal disturbances early after injury, suggesting a pathophysiological response to brain injury and subsequent intensive care treatment rather than morphological damage.

The role of cholesterol in Alzheimer’s disease (AD) has been linked to the generation of toxic amyloid beta peptides (Abeta). Using genetic mouse models of cholesterol loading, we examined whether mitochondrial cholesterol regulates Abeta neurotoxicity and AD pathology. Isolated mitochondria from brain or cortical neurons of transgenic mice overexpressing SREBP-2 (sterol regulatory element binding protein 2) or NPC1 (Niemann-Pick type C1) knock-out mice exhibited mitochondrial cholesterol accumulation, mitochondrial glutathione (mGSH) depletion and increased susceptibility to Abeta1-42-induced oxidative stress and release of apoptogenic proteins. Similar findings were observed in pharmacologically GSH-restricted rat brain mitochondria, while selective mGSH depletion sensitized human neuronal and glial cell lines to Abeta1-42-mediated cell death. Intracerebroventricular human Abeta delivery colocalized with mitochondria resulting in oxidative stress, neuroinflammation and neuronal damage that were enhanced in Tg-SREBP-2 mice and prevented upon mGSH recovery by GSH ethyl ester coinfusion, with a similar protection observed by intraperitoneal administration of GSH ethyl ester. Finally, APP/PS1 (amyloid precursor protein/presenilin 1) mice, a transgenic AD mouse model, exhibited mitochondrial cholesterol loading and mGSH depletion. Thus, mitochondrial cholesterol accumulation emerges as a novel pathogenic factor in AD by modulating Abeta toxicity via mGSH regulation; strategies boosting the particular pool of mGSH may be of relevance to slow down disease progression.

Berberine, an isoquinoline alkaloid extracted from medicinal herbs, has been used as antipyretic, antidiarrheal, bactericide and anti-inflammatory agent. In this study, berberine effects on neuronal damage have been examined. The right carotid artery of seven-day-old rat pups was ligated (ischemic insult), then berberine solution (0.2, 0.5, 1 or 2 mg/kg) was injected intra-peritoneally, and 30 minutes later pups were passed through hypoxic condition with breathing in air containing 10% oxygen and 90% nitrogen(hypoxic insult). The day after that the brains of pups were enucleated for pathologic assessment. Pathologic review of the samples obtained from rats treated with different doses of berberine in comparison with samples from pups treated by normal saline showed that there was a significant reduction of brain injury and edema in the rats treated with berberine. Our study also demonstrates that berberine reduces brain ischemic-hypoxic injury dose-dependently. Therefore, beberine may be considered as useful anti-stroke agent.

Interlukin-17 (IL-17) is active in a variety of brain injuries, including ischemia. The objective of this study was to test the hypothesis that IL-17 potentiates neuronal injury after stroke. Increased expression of IL-17 and IL-17 receptor (IL-17R) in serum and cortex was evaluated by ELISA, RT-PCR and immunohistochemistry. In the in vitro model of oxygen-glucose deprivation (OGD), IL-17 showed a dose-dependent effect in promoting neuronal injury through IL-17-IL-17R combination which can be blocked by IL-17R/Fc chimera. Our results demonstrated the up-regulation of IL-17 and IL-17R following permanent middle cerebral artery occlusion and suggested that they contributed to stroke outcome.

Introduction Alcohol abuse has many harmful effects on human body. This study aimed to investigate the role of water extracts of thyme (Thymus vulgaris) and ginger (Zingiber officinale Roscoe) as natural product extracts to detoxify the injuries of alcohol abuse on liver and brain of mice. Materials and methods Alcohol at a dose of 1.25ml/50ml water was orally administered at the first day of treatment with continuously increase of 1.25 ml per day to the end of experiment (14 days, 0.1 ml/45 g /d). Mice also were orally administered with alcohol and water extracts of thyme and ginger in concentration of 500m g /kg body weight for 2 weeks. Results The results showed very highly significant increase in nitric oxide and malondialdehyde level in liver and brain and a very highly significant decrease in the total antioxidant capacity and glutathione peroxidase activity in alcoholic group. In addition, the liver function enzymes such as l-gamma-glutamyl transpeptidase and butyryl cholinesterase activities showed very highly significant increase in alcoholic group. In contrast, the water extracts of thyme and ginger showed significant amelioration on these changes both in liver and brain tissues. Conclusion The water extracts of thyme and ginger has detoxifying and antioxidant effects. Therefore, it is recommended to use them to avoid alcohol toxicity.

Pesticide exposure has been suggested as a risk factor in developing Parkinson’s disease (PD). While the molecular mechanism underlying this association is not clear, several studies have demonstrated a role for mitochondrial dysfunction and oxidative damage in PD. Although data on specific pesticides associated with PD are often lacking, several lines of evidence point to the potential involvement of the organochlorine class of pesticides. Previously, we have found that the organochlorine pesticide methoxychlor (mxc) causes mitochondrial dysfunction and oxidative stress in isolated mitochondria. Here, we sought to determine whether mxc-induced mitochondrial dysfunction results in oxidative damage and dysfunction of the dopamine system. Adult female CD1 mice were dosed with either vehicle (sesame oil) or mxc (16, 32, or 64 mg/kg/day) for 20 consecutive days. Following treatment, we observed a dose-related increase in protein carbonyl levels in non-synaptic mitochondria, indicating oxidative modification of mitochondrial proteins which may lead to mitochondrial dysfunction. Mxc exposure also caused a dose-related decrease in striatal levels of dopamine (16-31%), which were accompanied by decreased levels of the dopamine transporter (DAT; 35-48%) and the vesicular monoamine transporter 2 (VMAT2; 21-44%). Because mitochondrial dysfunction, oxidative damage, and decreased levels of DAT and VMAT2 are found in PD patients, our data suggest that mxc should be investigated as a possible candidate involved in the association of pesticides with increased risk for PD, particularly in highly exposed populations.