Anatomía microquirúrgica en 3D del tracto corticoespinal y de la vía del lemnisco basada en microdisección de fibras y demostración a través de tractografía / 3D microsurgical anatomy of the corticospinal tract and the lemniscus tract based on microdissection of fibres and demonstration through tractography

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3D microsurgical anatomy of the cortico-spinal tract and lemniscal pathway based on fiber microdissection and demonstration with tractography. / Anatomía microquirúrgica en 3D del tracto corticoespinal y de la vía del lemnisco basada en microdisección de fibras y demostración a través de tractografía.

OBJECTIVE: To demonstrate tridimensionally the anatomy of the cortico-spinal tract and the medial lemniscus, based on fiber microdissection and diffusion tensor tractography (DTT). MATERIAL AND METHODS: Ten brain hemispheres and brain-stem human specimens were dissected and studied under the operating microscope with microsurgical instruments by applying the fiber microdissection technique. Brain magnetic resonance imaging was obtained from 15 healthy subjects using diffusion-weighted images, in order to reproduce the cortico-spinal tract and the lemniscal pathway on DTT images. RESULTS: The main bundles of the cortico-spinal tract and medial lemniscus were demonstrated and delineated throughout most of their trajectories, noticing their gross anatomical relation to one another and with other white matter tracts and gray matter nuclei the surround them, specially in the brain-stem; together with their corresponding representation on DTT images. CONCLUSIONS: Using the fiber microdissection technique we were able to distinguish the disposition, architecture and general topography of the cortico-spinal tract and medial lemniscus. This knowledge has provided a unique and profound anatomical perspective, supporting the correct representation and interpretation of DTT images. This information should be incorporated in the clinical scenario in order to assist surgeons in the detailed and critic analysis of lesions located inside the brain-stem, and therefore, improve the surgical indications and planning, including the preoperative selection of optimal surgical strategies and possible corridors to enter the brainstem, to achieve safer and more precise microsurgical technique.

The importance of data structure in statistical analysis of dendritic spine morphology.

BACKGROUND: Dendritic spine morphology is heterogeneous and highly dynamic. To study the changing or aberrant morphology in test setups, often spines from several neurons from a few experimental units e.g. mice or primary neuronal cultures are measured. This strategy results in a multilevel data structure, which, when not properly addressed, has a high risk of producing false positive and false negative findings. METHODS: We used mixed-effects models to deal with data with a multilevel data structure and compared this method to analyses at each level. We apply these statistical tests to a dataset of dendritic spine morphology parameters to illustrate advantages of multilevel mixed-effects model, and disadvantages of other models. RESULTS: We present an application of mixed-effects models for analyzing dendritic spine morphology datasets while correcting for the data structure. COMPARISON WITH EXISTING METHODS: We further show that analyses at spine level and aggregated levels do not adequately account for the data structure, and that they may lead to erroneous results. CONCLUSION: We highlight the importance of data structure in dendritic spine morphology analyses and highly recommend the use of mixed-effects models or other appropriate statistical methods to deal with multilevel datasets. Mixed-effects models are easy to use and superior to commonly used methods by including the data structure and the addition of other explanatory variables, for example sex, and age, etc., as well as interactions between variables or between variables and level identifiers.

Excess Manganese-Induced Apoptosis in Chicken Cerebrums and Embryonic Neurocytes.

There were many studies about the effect of excess manganese (Mn) on nervous system apoptosis; however, Mn-induced apoptosis in chicken cerebrums and embryonic neurocytes was unclear. The purpose of this study was to investigate the effect of excess Mn on chicken cerebrum and embryonic neurocyte apoptosis. Seven-day-old Hyline male chickens were fed either a commercial diet or three levels of manganese chloride (MnCl2)-added commercial diets containing 600-, 900-, and 1800-mg/kg-Mn diet, respectively. On the 30th, 60th, and 90th days, cerebrums were collected. Fertilized Hyline chicken eggs were hatched for 6-8 days and were selected. Embryonic neurocytes with 0, 0.5, 1, 1.5, 2, 2.5, and 3 mM Mn were collected and were cultured for 12, 24, 36, and 48 h, respectively. The following research contents were performed: superoxide dismutase (SOD) and total antioxidant capacity (T-AOC) activities; tumor protein p53 (p53), B cell lymphoma-2 (Bcl-2), B cell lymphoma extra large (Bcl-x), Bcl-2-associated X protein (Bax), Bcl-2 homologous antagonist/killer (Bak), fas, and caspase-3 messenger RNA (mRNA) expression; and morphologic observation. The results indicated that excess Mn inhibited SOD and T-AOC activities; induced p53, Bax, Bak, fas, and caspase-3 mRNA expression; and inhibited Bcl-2 and Bcl-x mRNA expression in chicken cerebrums and embryonic neurocytes. There were dose-dependent manners on all the above factors at all the time points and time-dependent manners on SOD activity of 1800-mg/kg-Mn group, T-AOC activity, and apoptosis-related gene mRNA expression in all the treatment groups in chicken cerebrums. Excess Mn induced chicken cerebrum and embryonic neurocyte apoptosis.

Acid Ceramidase Deficiency in Mice Results in a Broad Range of Central Nervous System Abnormalities.

Farber disease is a rare autosomal recessive disorder caused by acid ceramidase deficiency that usually presents as early-onset progressive visceral and neurologic disease. To understand the neurologic abnormality, we investigated behavioral, biochemical, and cellular abnormalities in the central nervous system of Asah1P361R/P361R mice, which serve as a model of Farber disease. Behaviorally, the mutant mice had reduced voluntary locomotion and exploration, increased thigmotaxis, abnormal spectra of basic behavioral activities, impaired muscle grip strength, and defects in motor coordination. A few mutant mice developed hydrocephalus. Mass spectrometry revealed elevations of ceramides, hydroxy-ceramides, dihydroceramides, sphingosine, dihexosylceramides, and monosialodihexosylganglioside in the brain. The highest accumulation was in hydroxy-ceramides. Storage compound distribution was analyzed by mass spectrometry imaging and morphologic analyses and revealed involvement of a wide range of central nervous system cell types (eg, neurons, endothelial cells, and choroid plexus cells), most notably microglia and/or macrophages. Coalescing and mostly perivascular granuloma-like accumulations of storage-laden CD68+ microglia and/or macrophages were seen as early as 3 weeks of age and located preferentially in white matter, periventricular zones, and meninges. Neurodegeneration was also evident in specific cerebral areas in late disease. Overall, our central nervous system studies in Asah1P361R/P361R mice substantially extend the understanding of human Farber disease and suggest that this model can be used to advance therapeutic approaches for this currently untreatable disorder.

Novel pathologic findings in patients with Pelizaeus-Merzbacher disease.

Pelizaeus-Merzbacher disease (PMD) is an X-linked inherited hypomyelinating disorder caused by mutations in the gene encoding proteolipid protein (PLP), the major structural protein in central nervous system (CNS) myelin. Prior to our study, whether hypomyelination in PMD was caused by demyelination, abnormally thin sheaths or failure to form myelin was unknown. In this study, we compared the microscopic pathology of myelin from brain tissue of 3 PMD patients with PLP1 duplications to that of a patient with a complete PLP1 deletion. Autopsy tissue procured from PMD patients was embedded in paraffin for immunocytochemistry and plastic for electron microscopy to obtain highresolution fiber pathology of cerebrum and corpus callosum. Through histological stains, immunocytochemistry and electron microscopy, our study illustrates unique pathologic findings between the two different types of mutations. Characteristic of the patient with a PLP1 deletion, myelin sheaths showed splitting and decompaction of myelin, confirming for the first time that myelin in PLP1 deletion patients is similar to that of rodent models with gene deletions. Myelin thickness and g-ratios of some fibers, in relation to axon diameter was abnormally thin, suggesting that oligodendrocytes remain metabolically functional and/or are attempting to make myelin. Many fibers showed swollen, progressive degenerative changes to axons in addition to the dissolution of myelin. All three duplication cases shared remarkable fiber pathology including swellings, constriction and/or transection and involution of myelin. Characteristic of PLP1 duplication patients, many axons showed segmental demyelination along their length. Still other axons had abnormally thick myelin sheaths, suggestive of continued myelination. Thus, each type of mutation exhibited unique pathology even though commonality to both mutations included involution of myelin, myelin balls and degeneration of axons. This pathology study describes findings unique to each mutation that suggests the mechanism causing fiber pathology is likewise heterogeneous.

Bioeffects of Diagnostic Dynamic 3-Dimensional (4-Dimensional) Ultrasound on Ultrastructure of Cerebral Cells of Fetal Mice in Late Pregnancy.

The aim of this study was to study the bioeffects of diagnostic dynamic 3-dimensional ultrasound (4D) on ultrastructure of cerebral cells of fetal mice in late pregnancy. Thirty pregnant mice carrying 18th embryonic day fetuses were randomly allocated into 6 groups, namely, control group, sham-exposed group, 5 minute-exposed group, 10 minute-exposed group, 20 minute-exposed group, and 30 minute-exposed groups (5 in each group). In exposure groups, mice were put under the dynamic 3D ultrasound system's probe for 5 to 30 minutes. Mice in sham-exposed group did not receive ultrasound wave. At 24th hour after birth, 10 pups of each group were randomly selected (2 in each litter) and euthanized by decapitation, and the brains were immediately removed. Right parietal lobes were taken as specimen. The specimens were firstly fixed with glutaraldehyde and secondly with osmic acid, then sections were made and observed under the transmission electron microscope. There were no obvious abnormal ultrastructure changes in control group, sham-exposed group, and 5 minute-exposed group under transmission electron microscope. Ten minute-exposed group showed some enlarged mitochondria, broken crista, vacuolated endoplasmic resticulums, and a few apoptosis cells. More abnormal organelles and apoptosis cells were observed in 20 minute-exposed and 30 minute-exposed groups (P < 0.05). Dynamic 3D (4D) ultrasound exposure for more than 10 minutes may result in abnormal neuronal ultrastructure changes and apoptosis cells in fetal mouse cerebrum.

An experimental model of partial insulin-like growth factor-1 deficiency in mice

Insulin-like growth factor-1 (IGF-1) is responsible for many systemic growth hormone (GH) functions although it has an extensive number of inherent activities (anabolic, cytoprotective, and anti-inflammatory). The potential options for IGF-1 therapy arise as a promising strategy in a wide list of human diseases. However, deeper studies are needed from a suitable animal model. All human conditions of IGF-1 deficiency consist in partially decreased IGF-1 levels since total absence of this hormone is hardly compatible with life. The aim of this work was to confirm that heterozygous Igf-1 +/− mice (Hz) may be considered as an appropriate animal model to study conditions of IGF-1 deficiency, focusing on early ages. Heterozygous Igf-1 +/− mice were compared to homozygous Igf-1+/+ by assessing gene expression by quantitative PCR, serum circulating levels by ELISA, and tissue staining. Compared to controls, Hz mice (25 days old) showed a partial but significant reduction of IGF-1 circulating levels, correlating with a reduced body weight and diminished serum IGFBP-3 levels. Hz mice presented a significant decrease of IGF-1 gene expression in related organs (liver, bone, testicles, and brain) while IGF-1 receptor showed a normal expression. However, gene expression of growth hormone receptor (GHR) was increased in the liver but reduced in the bone, testicles, and brain. In addition, a significant reduction of cortical bone thickness and histopathological alterations in the testicles were found in Hz mice when compared to controls. Finally, the lifelong evolution of IGF-1 serum levels showed significant differences throughout life until aging in mice. Results in this paper provide evidence for considering heterozygous mice as a suitable experimental model, from early stages, to get more insight into the mechanisms of the beneficial actions induced by IGF-1 replacement therapy

Enlarging the nosological spectrum of hereditary diffuse leukoencephalopathy with axonal spheroids (HDLS).

Hereditary diffuse leukoencephalopathy with axonal spheroids (HDLS) is an autosomal dominant disease clinically characterized by cognitive decline, personality changes, motor impairment, parkinsonism and seizures. Recently, mutations in the colony-stimulating factor-1 receptor (CSF1R) gene have been shown to be associated with HDLS. We report clinical, neuropathological and molecular genetic findings of patients from a new family with a mutation in the CSF1R gene. Disease onset was earlier and disease progression was more rapid compared with previously reported patients. Psychiatric symptoms including personality changes, alcohol abuse and severe depression were the first symptoms in male patients. In the index, female patient, the initial symptom was cognitive decline. Magnetic resonance imaging (MRI) showed bilateral, confluent white matter lesions in the cerebrum. Stereotactic biopsy revealed loss of myelin and microglial activation as well as macrophage infiltration of the parenchyma. Numerous axonal swellings and spheroids were present. Ultrastructural analysis revealed pigment-containing macrophages. Axonal swellings were detected by electron microscopy not only in the central nervous system (CNS) but also in skin nerves. We identified a heterozygous mutation (c.2330G>A, p.R777Q) in the CSF1R gene. Through this report, we aim to enlarge the nosological spectrum of HDLS, providing new clinical descriptions as well as novel neuropathological findings from the peripheral nervous system.

The protective effect of myo-inositol on hippocamal cell loss and structural alterations in neurons and synapses triggered by kainic acid-induced status epilepticus.

It is known that myo-inositol pretreatment attenuates the seizure severity and several biochemical changes provoked by experimentally induced status epilepticus. However, it remains unidentified whether such properties of myo-inositol influence the structure of epileptic brain. In the present light and electron microscopic research we elucidate if pretreatment with myo-inositol has positive effect on hippocampal cell loss, and cell and synapses damage provoked by kainic acid-induced status epilepticus. Adult male Wistar rats were treated with (i) saline, (ii) saline + kainic acid, (iii) myo-inositol + kainic acid. Assessment of cell loss at 2, 14, and 30 days after treatment demonstrate cytoprotective effect of myo-inositol in CA1 and CA3 areas. It was strongly expressed in pyramidal layer of CA1, radial and oriental layers of CA3 and in less degree-in other layers of both fields. Ultrastructural alterations were described in CA1, 14 days after treatment. The structure of neurons, synapses, and porosomes are well preserved in the rats pretreated with myo-inositol in comparing with rats treated with only kainic acid.

Organization of the procerebrum in terrestrial pulmonates (Helix, Limax) reconsidered: cell mass layer synaptology and its serotonergic input system.

The synaptology of the cell body layer of the olfactory center, procerebrum, was investigated in two prominent terrestrial pulmonate gastropod species, Helix pomatia and Limax valentianus. In addition, the analysis of the 5-HT-immunoreactive innervation, including ultrastructural level, was performed at high resolution in H. pomatia. A highly complex system of synaptic and non-synaptic connections was found in the procerebrum of both species connected to local neuropil areas of different size. The procerebral (globuli) cell perikarya were richly innervated by varicosities meanwhile the axon profiles also established contacts with each other. Synaptic configurations including convergence, divergence and presynaptic modulation were also revealed. The frequent occurrence of unspecialized but close axo-somatic and axo-axonic membrane contacts referring to the modulatory forms of transmitter release were also accompanied by membrane configurations indicative of active exocytosis. In H. pomatia, the cell mass layer was shown to receive a rich 5-HT-immunoreactive innervation, forming a dense network around the cell bodies. At ultrastructural level, 5-HT-immunoreactive varicosities contacted both cell bodies and different unlabeled axon profiles. Our results suggest that the local neuropil regions in the cell body layer are site of local circuits, which may play a decisive role in olfactory integrative processes bound to the procerebrum. The pattern and form of the 5-HT-immunoreactive innervation of extrinsic origin suggest an overall modulatory role in the cell body layer. The results may serve a basis for considering the role of local intercellular events, connected to microcircuits, within the procerebrum cell body layer involved in oscillation activities.

Regression and simulation models for human and baboon brain parameters / Modelo regresivo y simulación para los parámetros cerebrales humanos y del babuino

The variations in morphometric parameter of mammalian brains may be influenced by process of functional complexity, evolution and adaptation. Comparative analysis of linear measurements of cerebrum in the human and baboon has shown morphometric differences. In the present study linear measurements from human and baboon cerebrum (n=10 each) were used to predict various values for human and baboon brain and body parameters through multiple regression models. The average brain weights were found to be 2.08 percent and 0.84 percent of the body weights for humans and baboons respectively. The elasticity of regression models revealed that unit percentage increase in Occipital-Frontal (OF) distance would increase the human brain weight by 66.19 percent, while the baboon brain weight would increase by 7.63 percent. The unit percentage increase in the Height of Temporal Lobe (HTL) would increase the human brain weight by 16.28 percent, while the baboon brain weight would increase by only 0.28 percent. Unit percentage increase in Frontal-Temporal (FT) distance would decrease the human and baboon brain weights by 14.04 percent and 0.46 percent respectively. Inter-species values were also predicted through simulation techniques by using the ratios of model parameters with application of programming language Python. The OF, FT and HTL values for human were found to be 2.01 times, 1.55 times and 1.91 times respectively to that of baboon.

Las variaciones en los parámetros morfométricos del cerebro de los mamíferos pueden estar influenciadas por el proceso de complejidad funcional de la evolución y adaptación. Análisis comparativo de las mediciones lineales del cerebro en el humano y babuino han puesto de manifiesto las diferencias morfométricas. En este estudio las mediciones lineales del cerebro humano y babuinos (n = 10 cada uno) fueron utilizados para predecir los valores distintivos para el cerebro de humanos y monos babuinos y los parámetros del cuerpo a través de modelos de regresión múltiple. El peso medio del cerebro resultó ser 2,08 por ciento y 0,84 por ciento del peso corporal de los seres humanos y los babuinos, respectivamente. La elasticidad de los modelos de regresión reveló que el aumento de una unidad porcentual en la distancia occipital-frontal (DE) aumentaría el peso del cerebro humano en 66,19 por ciento, mientras que el peso del cerebro babuino se incrementaría en 7,63 por ciento. El porcentaje de aumento en la altura de lóbulo temporal (HTL) aumentaría el peso del cerebro humano en 16,28 por ciento, mientras que el peso del cerebro babuino aumentaría en sólo el 0,28 por ciento. Si aumenta la distancia frontal-temporal (FT) se reduciría el peso del cerebro humano y babuinos en 14,04 por ciento y 0,46 por ciento, respectivamente. También se prevéen valores entre las especies a través de técnicas de simulación, mediante el uso de proporciones de los parámetros del modelo con la aplicación del lenguaje de programación Python. Los valores humanos de DE, FT y HTL resultaron ser 2,01, 1,55 y 1,91 veces, respectivamente con respecto a la de los babuinos.

The ultrastructural and biochemical evidences of the beneficial effects of chronic caffeic acid phenethyl ester and melatonin administration on brain and cerebellum of aged rats.

Nervous system is highly vulnerable to the deleterious effects of age-related oxidative stress. A large body of researches has consistently confirmed the implication of free radicals both in normal cerebral ageing and ageing-related pathologies. In the present study, in addition to the light and electron microscopic pictures of brain and cerebellum of young, old and antioxidant administered old Sprague-Dawley rats, pro-oxidant status was evaluated in terms of measurements of total glutathione, lipid peroxidation (malondialdehyde) and activities of superoxide dismutase, catalase and glutathione peroxidase. Taking the results together, we suggest that supplemental administration of caffeic acid phenethyl ester and melatonin is beneficial in delaying age-related cellular damage in nervous system.

Endoplasmic reticulum in the penumbra following middle cerebral artery occlusion in the rabbit.

Caspase-12 has been localized to endoplasmic reticulum (ER) and showed to involve ER stress-induced apoptosis. In the present work we investigated the temporospatial alterations of caspase-12 immunoreactivity in the penumbra following cerebral ischemia/reperfusion in rabbit. Transient cerebral ischemia was produced by intraluminal occlusion of the middle cerebral artery for 2 h followed by 1 h, 6 h, 1 day, 3 days, 7 days and 14 days of reperfusion. Caspase-12 immunohistochemistry was first increased in the penumbra 1 h after reperfusion, with a peak at day 1 to day 3, and then gradually decreased to basal level at day 14. The number of TUNEL-positive cells and ultrastructural observation of brain sections in the penumbra showed a similar change at the same time points. ER mediated by caspase-12 participated in apoptosis induced by cerebral ischemia/reperfusion injury, which may provide a new area for therapeutic intervention to ameliorate outcomes following cerebral ischemia.

Synaptic mRNAs are modulated by learning.

We have recently demonstrated that brain plastic events significantly modify synaptic protein synthesis measured by the incorporation of [(35)S]methionine in brain synaptosomal proteins. Notably, in rats learning a two-way active avoidance task, the local synthesis of two synaptic proteins was selectively enhanced. Because this effect may be attributed to transcriptional modulation, we used reverse transcriptase-polymerase chain reaction methods to determine the content of discrete synaptosomal mRNAs in rats exposed to the same training protocol. Correlative analyses between behavioral responses and synaptosomal mRNA content showed that GAT-1 mRNA (a prevalent presynaptic component) correlates with avoidances and escapes in rat cerebellum, while glial fibrillary acid protein mRNA (an astrocytic component) correlates with freezings in cerebellum and cerebral cortex. These observations support the hypothesis that synaptic protein synthesis may be transcriptionally regulated. The cellular origin of synaptic transcripts is briefly discussed, with special regard to those present at large distances from neuron somas.

Characterization of white matter microstructure in fetal alcohol spectrum disorders.

BACKGROUND: Exposure to alcohol during gestation is associated with CNS alterations, cognitive deficits, and behavior problems. This study investigated microstructural aspects of putative white matter abnormalities following prenatal alcohol exposure. METHODS: Diffusion tensor imaging was used to assess white matter microstructure in 27 youth (age range: 8 to 18 years) with (n = 15) and without (n = 12) histories of heavy prenatal alcohol exposure. Voxelwise analyses, corrected for multiple comparisons, compared fractional anisotropy (FA) and mean diffusivity (MD) between groups, throughout the cerebrum. RESULTS: Prenatal alcohol exposure was associated with low FA in multiple cerebral areas, including the body of the corpus callosum and white matter innervating bilateral medial frontal and occipital lobes. Fewer between-group differences in MD were observed. CONCLUSIONS: These data provide an account of cerebral white matter microstructural integrity in fetal alcohol spectrum disorders and support extant literature showing that white matter is a target of alcohol teratogenesis. The white matter anomalies characterized in this study may relate to the neurobehavioral sequelae associated with gestational alcohol exposure, especially in areas of executive dysfunction and visual processing deficits.

Antagonizing L-type Ca2+ channel reduces development of abnormal involuntary movement in the rat model of L-3,4-dihydroxyphenylalanine-induced dyskinesia.

BACKGROUND: Chronic L-3,4-dihydroxyphenylalanine (L-DOPA) treatment of Parkinson's disease (PD) leads to debilitating involuntary movements, termed L-DOPA-induced dyskinesia. Striatofugal medium spiny neurons (MSN) lose their dendritic spines and cortico-striatal glutamatergic synapses in PD and in experimental models of DA depletion. This loss of connectivity is triggered by a dysregulation of intraspine Cav1.3 L-type Ca2+ channels. Here we address the possible implication of DA denervation-induced spine pruning in the development of L-DOPA-induced dyskinesia. METHODS: The L-type Ca2+ antagonist, isradipine was subcutaneously delivered to rats at the doses of .05, .1, or .2 mg/kg/day, for 4 weeks, starting the day after a unilateral nigrostriatal 6-hydroxydopamine (6-OHDA) lesion. Fourteen days later, L-DOPA treatment was initiated. RESULTS: Isradipine-treated animals displayed a dose-dependent reduction in L-DOPA-induced rotational behavior and abnormal involuntary movements. Dendritic spine counting at electron microscopy level showed that isradipine (.2 mg/kg/day) prevented the 6-OHDA-induced spine loss and normalized preproenkephalin-A messenger RNA expression. Involuntary movements were not reduced when isradipine treatment was started concomitantly with L-DOPA. CONCLUSIONS: These results indicate that isradipine, at a therapeutically relevant dose, might represent a treatment option for preventing L-DOPA-induced dyskinesia in PD.

Utilidad de la sonografía del parénquima cerebral en la enfermedad de Parkinson: estudio comparativo con 123I-FP-CIT SPECT / Usefulness of transcranial sonography in Parkinson’s disease. A comparative study using 123I-FP-CIT SPECT

FUNDAMENTO Y OBJETIVO: La ultrasonografía del parénquima cerebral (USPC) es una técnica novedosa,no invasiva, que permite obtener imágenes bidimensionales del parénquima cerebral ydetectar cambios en la ecogenicidad de diversas estructuras. Los objetivos del presente estudiohan sido: evaluar la presencia de hiperecogenicidad de la sustancia negra, mediante USPC, enafectados de enfermedad de Parkinson y en un grupo control; establecer un punto de corte quepermita diferenciar entre ambos grupos, e intentar correlacionar la hiperecogenicidad con determinadosparámetros clínicos y de neuroimagen funcional obtenidos mediante tomografía poremisión de fotón único (SPECT) utilizando el 123I-FP-CIT (ioflupano).PACIENTES Y MÉTODO: Se realizaron una exploración sonográfica del parénquima cerebral y unaSPECT con ioflupano a 42 sujetos incluidos de forma consecutiva en el estudio.RESULTADOS: Aproximadamente el 90% de los pacientes mostró un incremento distintivo de laecogenicidad de la sustancia negra mayor de 0,18 cm2 (punto de corte que mejor permitió diferenciarentre ambos grupos), mientras que dicho parámetro sonográfico sólo se detectó en un11% de los controles. La mayoría de los pacientes (86%) con ecogenicidad de la sustancia negramayor de 0,18 cm2 presentó una alteración de la vía nigroestriada, determinada medianteSPECT con ioflupano.CONCLUSIONES: La USPC es una herramienta útil y de fácil aplicación en el diagnóstico de la enfermedadde Parkinson. Asimismo se obtuvo una buena concordancia con la SPECT, ya que lamayoría de los casos que presentaban un área de ecogenicidad superior a 0,18 cm2 mostró unadisminución, en grado variable, de los transportadores presinápticos de la dopamina; aun asíno parece mejorar la precisión diagnóstica obtenida con esta última. Sin embargo, podría serun complemento potencial como «marcador» de vulnerabilidad de la sustancia negra

BACKGROUND AND OBJECTIVE: An increased echogenicity of the substantia nigra in patients withParkinson’s disease has been demonstrated by brain parenchyma sonography (BPS). BPS is anew and non-invasive technique that allows imaging of the brain in 2-dimensional axial slices.Changes in echogenicity can be displayed using ultrasounds. The aim of this study is to evaluatesubstantia nigra echogenicity in a group of Parkinson’s disease patients and controls andcompare with disease and functional neuroimaging parameters using ioflupane-single photonemission computed tomography (SPECT).PATIENTS AND METHOD: Fourty-two subjects were recruited consecutively. BPS and ioflupane-SPECT were performed in all.RESULTS: Around 90% of Parkinson’s disease patients showed a distinctive increase of echogenicityof substantia nigra above or equal 0.18 cm2, whereas this echo feature was detected in11% of controls. Most of patients (86%) with an area of substantia nigra echogenicity above orequal 0.18 cm2 showed a nigro-striatal impairment, that is, a decreased ioflupane uptake measuredby SPECT.CONCLUSIONS: BPS is a useful tool in the diagnosis of Parkinson’s disease. A good agreementbetween both techniques was achieved. The diagnosis accuracy obtained using BPS does notseem superior to ioflupane-SPECT. Nevertheless, hyperechogenicity could be considered as avulnerability «marker» of the substantia nigra

Banco de tejidos neurológicos de Sant Joan de Déu-Serveis de Salut Mental para la investigación de las enfermedades mentales. La importancia de un programa de donación en vida / The Sant Joan de Déu Brain Bank for research into mental diseases. The importance of a premortem donation program

Los bancos de tejidos neurológicos son colecciones de muestras de cerebros y otros tejidos neurológicos de donantes sanos o afectos de alguna enfermedad neurológica o mental. Los bancos de cerebros son útiles en análisis genómico y proteómico de enfermedades neuropsiquiátricas. El Banco de Tejidos Neurológicos de Sant Joan de Déu fue creado en 2004 y es un archivo de muestras de tejidos de donantes afectos de enfermedad mental. El número de donantes actualmente es de 100. Han fallecido 24, de los que se han obtenido muestras de cerebro congeladas. Los donantes, o sus representantes legales, han firmado el consentimiento informado, y sus familias han sido informadas. Se ha realizado una completa exploración física y psiquiátrica a todos los donantes. El diagnóstico se ha confirmado con la Entrevista Clínica Estructurada del DSM IV (SCID), y se ha valorado la severidad de los síntomas y las funciones neuropsicológicas. En todos los casos hay diagnóstico primario de trastorno psicótico. En las primeras muestras hemos encontrado una elevada prevalencia de enfermedades neurodegenerativas y vasculares, hecho no infrecuente en los bancos de cerebros de nueva creación. Este banco de cerebros abre la oportunidad de realizar investigaciones en pacientes psiquiátricos sobre comorbilidad entre enfermedades mentales y neurológicas y el posible papel de los tratamientos en su estilo de vida y en las enfermedades cardiovasculares. Hemos iniciado contacto con los centros, las organizaciones y los profesionales para aumentar el número de donantes, de manera que el número de muestras que se puede ofrecer a la comunidad científica para futuros estudios psiquiátricos sea mayor

Central Nervous System Tissue Banks (CNSTB, Brain Banks) contain collections of samples of brains and other neurological tissues from donors who are either healthy or affected by some sort of neurological or mental illness. Brain banks are useful for genomic and proteomic analyses of neuropsychiatric diseases. The Sant Joan de Déu Brain Bank (SJDBB) was created in 2004 and is an archive of tissue samples from donors with mental illnesses. The number of donors currently stands at 100. Of the donors, 24 have died, providing 24 frozen samples of cerebral sections. All donors, or their legal representatives, provided informed consent and their relatives were also informed. A complete psychiatric and physical examination was carried out with all donors. Diagnoses were confirmed by means of the Structured Clinical Interview (SCID) for DSM-IV, and both symptom severity and neuropsychological functioning were assessed. Although all donors had a primary diagnosis of psychotic disorder, the first few donors showed a high prevalence of neurodegenerative and vascular diseases, which is not infrequent in newly created brain banks. This brain bank opens the possibility of conducting research in psychiatric patients, as well as of investigating comorbidity between mental and neurological disorders and the possible role of treatment in lifestyle and cardiovascular disease. Contact is currently being made with centers, organizations and health professionals to increase the number of donors; thus, the number of samples that could be offered to the scientific community for future psychiatric studies would also increase

Localization of bcl-2 in the mouse brain: An anatomical study by immunohistochemistry

The presence of bcl-2 has been demonstratedin neurons of the developing adult brain ofdifferent species, including humans, the monkey,rat, rabbit and mice. Although bcl-2 expression in mouse embryo and its distribution in the central nervous system during development have been described in the cerebellar cortex and hippocampus, its distributionin the entire adult mouse brain has not yet been described. In the present work we describe bcl-2 expression in the mouse brain by immunohistochemistry and we compare it with other species showing similar patterns. We found that limbic areas have the highestbcl-2 density, suggesting a protective role ofthis protein in these regions (AU)

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