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MRI-Based Definition of a Stereotactic Two-Dimensional Template of the Human Insula

Objective: This study aimed to create a stereotactic two-dimensional description of the human insula based on accurate radiological morphometric studies. Methods: Seventy-five normal cerebral MRIs were selected and drawings of the insula then obtained from serial sagittal slices. These drawings were digitalized before superimposing the anterior (AC) and posterior (PC) commissures as references. This allowed us to quantify interindividual anatomical variations in a large cohort of subjects. Results: The morphometric analysis of the insula revealed a more complex shape than previously described. This structure is delimited by four peri-insular sulci (anterior, superior, posterior and inferior) instead of the three sulci classically mentioned. Males have a statistically larger surface area than females, according to a correlated index. Precise measurements of the different insular components allowed us to quantify their potential interindividual anatomical variations and to define their average shapes and stereotactic locations. Conclusion: These data create a two-dimensional template of the human insula, with regard to the classical AC-PC stereotactic reference system. They furthermore allow us to quantify the probability that a given element of this structure is located at a predefined position. This should be useful in functional neuroimaging studies and in insular surgery for diagnostic and therapeutic goals.

Definition of a stereotactic 3-dimensional magnetic resonance imaging template of the human insula.

BACKGROUND: This study proposes a 3-dimensional (3-D) template of the insula in the bicommissural reference system with posterior commissure (PC) as the center of coordinates. OBJECTIVE: Using the bicommissural anterior commissure (AC)–PC reference system, this study aimed to define a template and design a method for the 3-D reconstruction of the human insula that may be used at an individual level during stereotactic surgery. METHODS: Magnetic resonance imaging (MRI)–based morphometric analysis was performed on 100 cerebral cortices with normal insulae based on a 3-step procedure: Step 1: AC-PC reference system–based reconstruction of the insula from the 1-mm thick 3-D T1-weighted MRI slices. Step 2: Digitalization and superposition of the data obtained in the 3 spatial planes. Step 3: Representation of pixels as colors on a scale corresponding to the probability of localization of each insular anatomic component. RESULTS: The morphometric analysis of the insula confirmed our previously reported findings of a more complex shape delimited by 4 peri-insular sulci. A very significant correlation between the coordinates of the main insular structures and the length of AC-PC was demonstrated. This close correlation allowed us to develop a method that allows the 3-D reconstruction of the insula from MRI slices and only requires the localization of AC and PC. This process defines an area deemed to contain insula with 100% probability. CONCLUSION: This 3-D reconstruction of the insula should be useful to improve its localization and other cortical areas and allow the differentiation of insular cortex from opercular cortex. ABBREVIATIONS: AC, anterior commissure CI, confidence interval CIS, central insular sulcus PC, posterior commissure VPC, the perpendicular plane on AC-PC plane passes by the posterior commissural

Stimulation of the Motor Cortex for Chronic Neuropathic Pain: Anatomo- Clinical Correlations

O stress initiates mitochondrial DNA overproliferation and/or deletion of the organ and/or tissues, especially the mitochondrial energy demands, have been implicated in the pathogenesis of several diseases, including Alzheimer disease (AD), tumor growth, and metastasis. The present study has determined if an intimate, i.e. causal, relationship between oxidative stress and mitochondrial damage and/or vascular lesions occurs before the development of human AD, in animal models that mimic human neurodegenerative diseases and human colorectal carcinoid cancer or primary malignant brain cancer. In situ hybridization and ultrastructural analysis of the mitochondria (mitochondria with electron dense matrix, mitochondrial-derived lysosomes) showed that mitochondria with the abnormal structures and lipofuscin appear to be features of hippocampal damaged neurons in human AD, aged Tg (+) mice, 2 and 3 vessel occlusion model of the brain hypoperfusion, and malignant primary and metastatic cancer. The abnormal mitochondria appeared to be a permanent feature in all cellular compartments; in situ hybridization analysis with mouse and human mtDNA probes found a large amount of deleted mtDNA in human AD and in all models that mimic human AD (mice, rats etc.) hippocampus and cancer tissues compared to aged controls. The majority of these mtDNA deletions were found in mitochondrial-derived lysosomes in regions closely associated with lipofuscin and/or tumor growth regions. In situ hybridization with a chimeric cDNA probe for the 5kb common deletion indicated that the 5kb mtDNA is increased at least 3 and 4 fold respectively in AD and malignant tumor cases as compared to controls. Only hippocampal and cortical vulnerable neurons as well as malignant cancer tissues showed immunopositive staining for RNA oxidation markers visualized by using 8-OHG-staining, NOSs, and all oxidative stress markers. The mitochondrial DNA overproliferation and deletion detected by using cytological techniques suggests that successful dysregulation of the cell cycle is also the hallmark of neoplasm; early mitochondrial dependent cell-cycle pathophysiology in AD may recruit oncogenic signal transduction mechanisms and hence, can be viewed as an abortive neoplastic transformation. The common features on the mitochondrial abnormality were seen on the brain during tumorigenesis and AD indicating that mitochondrial DNA overproliferation and/or deletion are the key initiating factors for development, maturation, and progression of neurodegeneration as well as tumor growth and/or metastases.N 1 in 15 people in the US will suffer from post-traumatic stress disorder (PTSD) in their lifetime. Approximately 40% of patients fail to respond to pharmacotherapy and 30% receiving therapy continue to suffer a decade after the trauma. Targets of PTSD neurocircuitry, such as the amygdala, are directly accessible through invasive and relatively high-risk deep brain stimulation (DBS). DBS of the amygdala (BLn) produced symptomatic improvement in a rat model of PTSD, suggesting the utility of this target in humans. A proof-of-concept clinical trial of DBS of the amygdala (BLn) in humans is currently underway.Methods: 946 patients were treated: 568 (60.04%)-transcatheter cerebral revascularization (Test Group), 378 (39.96%)-conservative treatment (Control Group).482 patients aged 35-85 (average age 76) were re-examined. Of these, 286(59.34%) patients had undergone transcatheter cerebral revascularization, 196 (40.66%)-conservative treatment. The examination plan included: CDR, MMSE, IB assessment (all patients);cerebral CT, MRI, scintigraphy (SG), rheoencephalography (REG) (all patients);cerebral MUGA (72 (12.68%) Test Group patients and 34 (9.00%) (Control Group).The aim of this study was to search the relationship between the anatomical location of contactsand the eventual analgesic effect. Materials and Methods: 22 patients suffering from central and / or peripheral neuropathic pain were implanted withextradural stimulation of the precentral cortex. Implantation electrodes were performed using intraoperative: 1) Anatomical identification by Neuronavigation with 3D MRI, 2) Somestheticevoqued potentials monitoring, 3) Electricalstimulations to identify the motor responses. In order to locate postoperatively the electrodes, a 3D-CT was performed and fused with thepreoperative MRI. The clinical analgesic effects of cortical stimulation were collected on aregular basis (VAS reduction > 50%, drugs consumption). Results: Post implantation analgesic effects were obtained in 19 patients out of 22. The analgesic effectwas companied with reduction of the drugs consumption in 17 patients. The post-operative3 D CT analysis shows a correspondence between the effective contacts localization andthe motor cerebral cortex somatotopy in the patients with post-operative good analgesic effects. No correspondence was found between the contacts localization and the motor cerebral cortexsomatotopy in the 4 patients with no analgesic effects. In three out of these four patients,analgesic effects were obtained after a new surgery allowing a replacement of the electrodeposition over the motor cortex somatotopy corresponding to the painful area. Conclusion: This study shows the correlation between position of the contact (cathode) overthe precentral cortex and the analgesia obtained when the somatotopy of the stimulated cortexcorrespond to the painful area.I also plays a role in neuron growth, neuroplasticity, and neuro modulation. It has been hypothesized that in vivo impaired insulin functions may be involved in pathogenesis of demyelinating disease. There are limited data regarding glucose metabolism dysregulation in multiple sclerosis (MS). Present study investigates glucose and insulin metabolism in newly diagnosed MS patients in association to inflammatory markers. We examined 19 MS patients and 19 age, sex and body mass index (BMI) matched healthy controls. MS patients were newly diagnosed, untreated and with low Expanded Disability Status Scale (EDSS) score (1.1±0.7). Plasma glucose, lactate, insulin and GLP-1 were measured during oral glucose tolerance test. Fasting adipokines, lipid and inflammatory parameters were analyzed. Insulin sensitivity indices (ISI) were calculated. MS patients had comparable fasting and post-load glucose concentrations as controls. Insulin response to oral glucose load in MS was increased (p=0.022). Insulin sensitivity was lower in MS compared to controls [ISI (Matsuda) p=0.011 and ISI (Cederholm) p=0.032]. We did not find any difference in inflammatory parameters (interleukin 6, tumor necrosis factor, C-reactive protein), nor in lactate, GLP-1, total, HDL and LDL cholesterol, triglycerides, resistin, leptin, adiponectin levels between groups. We found decreased insulin sensitivity with postprandial hyperinsulinemia in MS patients, which seems not to be related to chronic inflammation or physical inactivity. The role of hyperinsulinemia in CNS function impairment and insulin sensitizing therapy for better remyelination repair should be further investigated.Objective: Patients with BP-II have a higher prevalence rate of metabolic disturbance and obesity than do the general population. Genetic variants of the methylene tetrahydrofolate reductase (MTHFR) gene have been regarded as predictors of weight gain in schizophrenia. In the present study, we investigated whether the MTHFR C677T polymorphism may predict changes in metabolic indices after 12 weeks of treatment in patients with BP-II.W art therapy can be a useful rehabilitative tool is a long standing and debated question. To this aim, we run a randomized, controlled and single-blinded study lasted 3 years, on 20 subjects affected by a moderate form of idiopathic Parkinson’s disease (PD), in stable treatment with L-dopa and L-dopa agonists, and without severe sensory deficits (Modugno et al 2010). Half of them were randomly assigned to a “rehabilitative theatre” program, while the other half underwent conventional physiotherapy. Patients of both groups were evaluated at the beginning of each year, using five clinical rating scales. We found that, by the end of the third year, theatre-patients showed greater improvements of motor and non-motor symptoms than those of the control group. Despite the positive results, the study had a number of weakness. Data were collected only on subjective scales, and the benefits appeared only after a long period of time. To overcome these limitations, we run a new project, with 24 PD patients with the same experimental design of the previous one, but i) collecting outputs not only on clinical scales, but also using neuropsychological and psychophysical tests; ii) using a new form of theatre where patients have to undergo to an ‘emotional’ training. We found that the ‘emotional’ theatre was extremely effective and allowed to improve mental well-being of patients in only one year’s time. Thus, we replicated and extended our previous results showing that theatre, coupled with conventional medical treatments, represents a valid complementary therapeutic interventions for PD treatment.Objectives: Bipolar II disorder (BP-II), characterized by recurrent dysregulation of mood, is a serious and chronic psychiatric illness. However, BP-II is commonly under-recognized, even in psychiatric settings. Because dopaminergic disturbance is thought to be involved in the development of bipolar disorder (BPD), it seems essential to investigate dopamine-related genes like the catechol-O-methyltransferase (COMT) gene, which are involved in dopamine metabolism, and the methylenete trahydrofolate reductase (MTHFR) gene, which may affect COMT methylation and COMT function. The current study examined the association and interaction of the COMT Val158Met and MTHFR C677T variants with BP-II.