RESUMO
Child abuse is both socially and medically troublesome and many times produces permanent consequences. A review of the literature is done from a neurosurgical standpoint, and the lesions produced at the Central Nervous System are evaluated in detail, including their physiopathology, neurological sequels and implications for rehabilitation treatment and the child's future life.
Assuntos
Maus-Tratos Infantis , Doenças do Sistema Nervoso , Criança , Maus-Tratos Infantis/reabilitação , Maus-Tratos Infantis/terapia , Humanos , Doenças do Sistema Nervoso/etiologia , Doenças do Sistema Nervoso/patologia , Doenças do Sistema Nervoso/fisiopatologia , Doenças do Sistema Nervoso/reabilitaçãoRESUMO
There is increasing evidence that physical activity is associated with a decreased stroke risk. The purpose of this study was to determine if exercise could also reduce brain damage in rats subjected to transient middle cerebral artery (MCA) occlusion, and if the reduced brain injury is associated with angiogenesis as well as cellular expression of the nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) in regions supplied by the MCA. Adult male Sprague Dawley rats (n=36) exercised 30 min each day for 3 weeks on a treadmill on which repetitive locomotor movement was required. Then, stroke was induced by a 2-h MCA occlusion using an intraluminal filament, followed by 48 h of reperfusion. In addition to the two exercised groups of animals with or without MCA occlusion, there were two other groups of animals, with or without MCA occlusion, housed for the same duration and used as non-exercised controls. Brain damage in ischemic rats was evaluated by neurologic deficits and infarct volume. Exercise preconditioned and non-exercised brains were processed for immunocytochemistry to quantify the number of microvessels or NGF- and BDNF-labeled cells. Pre-ischemic motor activity significantly (P<0.01) reduced neurologic deficits and infarct volume in the frontoparietal cortex and dorsolateral striatum. Cellular expressions of NGF and BDNF were significantly (P<0.01) increased in cortex (neuron) and striatum (glia) of rats under the exercise condition. Significant (P<0.01) increases in microvessel density were found in striatum. Physical activity reduced stroke damage. The reduced brain damage may be attributable to angiogenesis and neurotrophin overexpression in brain regions supplied by the MCA following exercise.
Assuntos
Isquemia Encefálica/fisiopatologia , Encéfalo/irrigação sanguínea , Infarto Cerebral/prevenção & controle , Neovascularização Fisiológica , Fatores de Crescimento Neural/metabolismo , Condicionamento Físico Animal/fisiologia , Animais , Encéfalo/fisiopatologia , Fator Neurotrófico Derivado do Encéfalo/metabolismo , Artérias Cerebrais/crescimento & desenvolvimento , Córtex Cerebral/irrigação sanguínea , Córtex Cerebral/metabolismo , Córtex Cerebral/patologia , Infarto Cerebral/patologia , Infarto Cerebral/fisiopatologia , Corpo Estriado/irrigação sanguínea , Corpo Estriado/metabolismo , Corpo Estriado/patologia , Modelos Animais de Doenças , Imuno-Histoquímica , Infarto da Artéria Cerebral Média/fisiopatologia , Masculino , Microcirculação/patologia , Atividade Motora/fisiologia , Fator de Crescimento Neural/metabolismo , Ratos , Ratos Sprague-Dawley , Regulação para Cima/fisiologiaRESUMO
The goal of this study was to determine if relatively complex motor training on Rota-rod involving balance and coordination plays an essential role in improving motor function in ischemic rats, as compared with simple locomotor exercise on treadmill. Adult male Sprague-Dawley rats with (n=40) or without (n=40) ischemia were trained under each of three conditions: (1) motor balance and coordination training on Rota-rod; (2) simple exercise on treadmill; and (3) non-trained controls. Motor function was evaluated by a series of tests (foot fault placing, parallel bar crossing, rope and ladder climbing) before and at 14 or 28 days after training procedures in both ischemic and normal animals. Infarct volume in ischemic animals was determined with Nissl staining. Compared with both treadmill exercised and non-trained animals, Rota-rod-trained animals with or without ischemia significantly (P<0.01) improved motor performance of all tasks except for foot fault placing after 14 days of training, with normal rats having better performance. Animals trained for up to 28 days on the treadmill did not show significantly improved function. With regard to foot fault placing task, performance on foot placing was improved in ischemic rats across the three measurements at 0, 14 and 28 days regardless of training condition, while the normal group reached their best performance at the beginning of measurement. No significant differences in infarct volume were found in rats trained either with Rota-rod (47+/-4%; mean+/-S.E.), treadmill (45+/-5%) or non-exercised control (45+/-3%). In addition, no obvious difference could be detected in the location of the damage which included the dorso-lateral portion of the neostriatum and the frontoparietal cortex, the main regions supplied by the middle cerebral artery. The data suggest that complex motor training rather than simple exercise effectively improves functional outcome.
Assuntos
Infarto da Artéria Cerebral Média/fisiopatologia , Desempenho Psicomotor/fisiologia , Recuperação de Função Fisiológica/fisiologia , Animais , Masculino , Destreza Motora/fisiologia , Ratos , Ratos Sprague-Dawley , Teste de Desempenho do Rota-Rod/métodosRESUMO
OBJECT: Image guidance provides a three-dimensional view of the lesion and allows the surgeon to plan a surgical strategy that takes the relationship of the lesion and the surrounding brain into account. We evaluated the degree of resection and the functional outcome of patients with colloid cysts from the third ventricle submitted to surgical resection using interactive image-guided approach. METHOD: Using image-guided methodology and an endoscopic approach we analyzed the functional outcome of 11 patients with diagnosis of colloid cyst of the third ventricle who were treated at our institution from August 1993 to September 2000. The mean age was 39.5 years and the mean follow-up was 36.5 months. Analyzing the clinical outcome, 54.5% of the patients developed short-term memory disturbance in the first 30 days after surgery. None of these patients persisted with this symptomatology for more than one month. In terms of late post-operative morbidity, 1 patient developed persistent post-operative seizures, which were controlled with anti-seizure medications. Complete resection of the cyst was achieved in all patients. CONCLUSIONS: The low rate of complications and high rate of total resection encourage us to continue using the multimodal technique. Longer follow-up and an increase in the number of patients are needed to assess the efficacy of this methodology.
Assuntos
Encefalopatias/cirurgia , Cistos/cirurgia , Endoscopia/métodos , Procedimentos Neurocirúrgicos/métodos , Cirurgia Assistida por Computador , Terceiro Ventrículo/cirurgia , Adolescente , Adulto , Feminino , Humanos , Masculino , Transtornos da Memória/etiologia , Pessoa de Meia-Idade , Procedimentos Neurocirúrgicos/efeitos adversos , Estudos Retrospectivos , Terceiro Ventrículo/patologia , Resultado do TratamentoRESUMO
Free fatty acid (FFA) concentrations in cerebrospinal fluid (CSF) from patients with ischemic and hemorrhagic stroke (n=25) and in contemporary controls (n=73) were examined using HPLC. Concentrations of CSF FFAs from ischemic and hemorrhagic stroke patients obtained within 48 h of the insult were significantly greater than in control patients. Higher concentrations of polyunsaturated fatty acids (PUFAs) in CSF obtained within 48 h of insult were associated with significantly lower (P<0.05) admission Glasgow Coma Scale scores and worse outcome at the time of hospital discharge, using the Glasgow Outcome Scale (P<0.01).
Assuntos
Ácidos Graxos não Esterificados/líquido cefalorraquidiano , Isquemia/líquido cefalorraquidiano , Hemorragia Subaracnóidea/líquido cefalorraquidiano , Cromatografia Líquida de Alta Pressão , Progressão da Doença , Ácidos Graxos não Esterificados/classificação , Escala de Coma de Glasgow , Humanos , Estatísticas não ParamétricasRESUMO
While the prediction of hydrodynamic properties of rigid particles is nowadays feasible using simple and efficient computer programs, the calculation of such properties and, in general, the dynamic behavior of flexible macromolecules has not reached a similar situation. Although the theories are available, usually the computational work is done using solutions specific for each problem. We intend to develop computer programs that would greatly facilitate the task of predicting solution behavior of flexible macromolecules. In this paper, we first present an overview of the two approaches that are most practical: the Monte Carlo rigid-body treatment, and the Brownian dynamics simulation technique. The Monte Carlo procedure is based on the calculation of properties for instantaneous conformations of the macromolecule that are regarded as if they were instantaneously rigid. We describe how a Monte Carlo program can be interfaced to the programs in the HYDRO suite for rigid particles, and provide an example of such calculation, for a hypothetical particle: a protein with two domains connected by a flexible linker. We also describe briefly the essentials of Brownian dynamics, and propose a general mechanical model that includes several kinds of intramolecular interactions, such as bending, internal rotation, excluded volume effects, etc. We provide an example of the application of this methodology to the dynamics of a semiflexible, wormlike DNA.
Assuntos
Centrifugação com Gradiente de Concentração/métodos , Coloides/química , DNA/química , Modelos Químicos , Modelos Moleculares , Movimento (Física) , Proteínas/química , Soluções/química , Simulação por Computador , DNA/análise , Difusão , Elasticidade , Substâncias Macromoleculares , Modelos Estatísticos , Conformação Molecular , Proteínas/análiseRESUMO
Elevated levels of free fatty acids (FFA) have been implicated in the pathogenesis of neuronal injury and death induced by cerebral ischemia. This study evaluated the effects of immunosuppressants agents, calcineurin inhibitors and blockade of endoplasmic reticulum (ER) calcium channels on free fatty acid formation and efflux in the ischemic/reperfused (I/R) rat brain. Changes in the extracellular levels of arachidonic, docosahexaenoic, linoleic, myristic, oleic and palmitic acids in cerebral cortical superfusates during four-vessel occlusion-elicited global cerebral ischemia were examined using a cortical cup technique. A 20-min period of ischemia elicited large increases in the efflux of all six FFAs, which were sustained during the 40 min of reperfusion. Cyclosporin A (CsA) and trifluoperazine, which reportedly inhibit the I/R elicited opening of a mitochondrial permeability transition (MPT) pore, were very effective in suppressing ischemia/reperfusion evoked release of all six FFAs. FK506, an immunosuppressant which does not directly affect the MPT, but is a calcineurin inhibitor, also suppressed the I/R-evoked efflux of FFAs, but less effectively than CsA. Rapamycin, a derivative of FK506 which does not inhibit calcineurin, did not suppress I/R-evoked FFA efflux. Gossypol, a structurally unrelated inhibitor of calcineurin, was also effective, significantly reducing the efflux of docosahexaenoic, arachidonic and oleic acids. As previous experiments had implicated elevated Ca(2+) levels in the activation of phospholipases with FFA formation, agents affecting endoplasmic reticulum stores were also evaluated. Dantrolene, which blocks the ryanodine receptor (RyR) channel of the ER, significantly inhibited I/R-evoked release of docosahexaenoic, arachidonic, linoleic and oleic acids. Ryanodine, which can either accentuate or block Ca(2+) release, significantly enhanced ischemia/reperfusion-elicited efflux of linoleic acid, with non-significant increases in the efflux of myristic, arachidonic, palmitic and oleic acids. Xestospongin C, an inhibitor of the inositol triphosphate (IP(3)R) channel, failed to affect I/R-evoked FFA efflux. Thapsigargin, an inhibitor of the Ca(2+)-ATPase ER uptake pump, elicited significant elevations in the efflux of myristic, arachidonic and linoleic acids, in the absence of ischemia. Collectively, the data suggest an involvement of both ER and mitochondrial Ca(2+) stores in the chain of events which lead to PLA(2) activation and FFA formation.
Assuntos
Calcineurina/metabolismo , Canais de Cálcio/metabolismo , Córtex Cerebral/efeitos dos fármacos , Córtex Cerebral/metabolismo , Retículo Endoplasmático/metabolismo , Ácidos Graxos não Esterificados/metabolismo , Imunossupressores/farmacologia , Traumatismo por Reperfusão/metabolismo , Animais , Inibidores de Calcineurina , Ciclosporina/farmacologia , Dantroleno/farmacologia , Inibidores Enzimáticos/farmacologia , Gossipol/farmacologia , Compostos Macrocíclicos , Masculino , Oxazóis/farmacologia , Ratos , Ratos Sprague-Dawley , Rianodina/farmacologia , Sirolimo/farmacologia , Tacrolimo/farmacologia , Tapsigargina/farmacologia , Trifluoperazina/farmacologiaRESUMO
Free fatty acid (FFA) elevation in the brain has been shown to correlate with the severity of damage in ischemic injury. The etiology of this increase in FFA remains unclear and has been hypothesized to result from phospholipase activation. This study examines the effects of specific phospholipase inhibitors on FFA efflux during ischemia-reperfusion injury. A four-vessel occlusion model of cerebral ischemia was utilized to assess the effects of PLA(2) and PLC inhibitors on FFA efflux from rat cerebral cortex. In addition, FFA efflux from non-ischemic cortices exposed to PLA(2) and PLC was measured. Concentrations of arachidonic, docosahexaenoic, linoleic, myristic, oleic, and palmitic acids in cortical superfusates were determined using high performance liquid chromatography (HPLC). Exposure to the non-selective PLA(2) inhibitor 4-bromophenylacyl bromide (BPB) significantly inhibited FFA efflux during ischemia-reperfusion injury (P<0.01 arachidonic, oleic and palmitic; P<0.05 all others); exposure to the PLC inhibitor U73122 had no observed effect. The effects of the Ca(2+)-dependent PLA(2) inhibitor arachidonyl trifluoromethyl ketone (AACOCF(3)) mirrored the effects of BPB and led to reductions in all FFA levels (P<0.01 arachidonic, oleic and palmitic; P<0.05 all others). Exposure to the secretory PLA(2) inhibitor 3-(3-acetamide-1-benzyl-2-ethyl-indolyl-5-oxy) propane sulfonic acid (LY311727) and to the Ca(2+)-independent PLA(2) inhibitor bromoenol lactone (BEL) had only minimal effects on FFA efflux. Application of both PLA(2) and PLC to non-ischemic cortices resulted in significant increases in efflux of all FFA (P<0.05). The study suggests that FFA efflux during ischemia-reperfusion injury is coupled to activation of Ca(2+)-dependent PLA(2) and provides further evidence of the potential neuroprotective benefit of Ca(2+)-dependent PLA(2) inhibitors in ischemia.
Assuntos
Química Encefálica/efeitos dos fármacos , Isquemia Encefálica/tratamento farmacológico , Córtex Cerebral/efeitos dos fármacos , Inibidores Enzimáticos/farmacologia , Ácidos Graxos não Esterificados/metabolismo , Fosfolipases/antagonistas & inibidores , Traumatismo por Reperfusão/tratamento farmacológico , Animais , Química Encefálica/fisiologia , Isquemia Encefálica/enzimologia , Isquemia Encefálica/fisiopatologia , Fenômenos Fisiológicos Cardiovasculares/efeitos dos fármacos , Córtex Cerebral/enzimologia , Córtex Cerebral/fisiopatologia , Modelos Animais de Doenças , Masculino , Fosfolipases/metabolismo , Fosfolipases A/antagonistas & inibidores , Fosfolipases A/metabolismo , Ratos , Ratos Sprague-Dawley , Traumatismo por Reperfusão/enzimologia , Traumatismo por Reperfusão/fisiopatologia , Resultado do Tratamento , Fosfolipases Tipo C/antagonistas & inibidores , Fosfolipases Tipo C/metabolismoRESUMO
Poly(ADP-ribose) polymerase (PARP) can initiate an energy-consuming and inefficient repair cycle following cerebral ischemia/reperfusion by transferring ADP ribose units to nuclear proteins eventually leading to cellular dysfunction and neuronal death. 3-Aminobenzamide (3-AB) is a selective inhibitor of PARP that can significantly reduce brain damage after focal ischemia in rats and displays a low toxicity in vivo. The goals of this study were to determine if inhibiting PARP with 3-AB has a long-term neuroprotective effect and if functional outcome improves in rats following focal ischemia and treatment with 3-AB. Focal ischemia was induced by a 2-h occlusion of the middle cerebral artery (MCA), using an intraluminal filament. Motor functions were evaluated from 5 to 28 days after reperfusion in four groups of rats: stroke without treatment; stroke treated with 3-AB at doses of 15 mg/kg, stroke treated with 3-AB at doses of 55 mg/kg; and the non-ischemic control rats. Functional behaviors were tested by a series of motor function tasks (foot placing, parallel bar crossing, rope and ladder climbing), as well as a neurological examination. Infarct volume of stroke brain in the same rat was determined by Nissl staining 28 days after surgery. Comparison of the untreated stroke group (n=11) and the treated stroke groups indicates that impairment of motor function was significantly (P<0.001) reduced by administration of 3-AB at doses of 15 mg/kg (n=9) or 55 mg/kg (n=10). Neurological outcome was also improved significantly (P<0.001). Infarct volume was significantly (P<0.01) reduced in both treated groups. Long-term neuroprotection following ischemia/reperfusion injury to the brain can be obtained by administration of a PARP inhibitor. The motor tests employed in this study can be used as sensitive, objective and reproducible measurements of functional impairment in rats following an ischemic stroke.
Assuntos
Infarto da Artéria Cerebral Média/tratamento farmacológico , Infarto da Artéria Cerebral Média/enzimologia , Atividade Motora/efeitos dos fármacos , Fármacos Neuroprotetores/farmacologia , Fármacos Neuroprotetores/uso terapêutico , Inibidores de Poli(ADP-Ribose) Polimerases , Animais , Benzamidas/farmacologia , Benzamidas/uso terapêutico , Infarto Cerebral/enzimologia , Infarto Cerebral/patologia , Infarto Cerebral/fisiopatologia , Circulação Cerebrovascular/efeitos dos fármacos , Inibidores Enzimáticos/farmacologia , Inibidores Enzimáticos/uso terapêutico , Feminino , Infarto da Artéria Cerebral Média/fisiopatologia , Ataque Isquêmico Transitório/tratamento farmacológico , Ataque Isquêmico Transitório/enzimologia , Ataque Isquêmico Transitório/fisiopatologia , Exame Neurológico , Poli(ADP-Ribose) Polimerases/biossíntese , Ratos , Ratos Sprague-DawleyRESUMO
Reversal of the Na(+)/Ca(2+) exchanger (NCX) occurs during ischemia-reperfusion injury as a result of changes in intracellular pH and sodium concentration. Inhibition of NCXs has been shown to be neuroprotective in vitro. In this study, we evaluated the effects of KB-R7943 (50 microM), a specific inhibitor of the reverse mode of NCX, applied topically onto rat cerebral cortex prior to and during ischemia. Amino acid and free fatty acid levels in cortical superfusates, withdrawn at 10-min intervals from bilateral cortical windows, were analyzed by high-performance liquid chromatography. During a 20-min period of ischemia in control animals, there were significant increases in all amino acids and in all FFAs. Following reperfusion, all FFAs remained significantly elevated. Application of KB-R7943 (50 microM) significantly inhibited effluxes of phosphoethanolamine, but had no effect on glutamate, aspartate, taurine or GABA levels. KB-R7943 also resulted in significant reductions in levels of myristic, docosahexaenoic and arachidonic acid during ischemia and in reperfusion levels of arachidonic and docosahexaenoic acids. These data indicate that inhibition of Na(+)/Ca(2+) exchange likely prevented the activation of phospholipases that usually occurs following an ischemic insult as evidenced by its attenuation of phosphoethanolamine and free fatty acid efflux. The inhibition of phospholipases may be an essential component of the neuroprotective benefits of Na(+)/Ca(2+) exchange inhibitors in ischemia-reperfusion injury and may provide a basis for their possible use in therapeutic strategies for stroke.
Assuntos
Antiarrítmicos/farmacologia , Córtex Cerebral/efeitos dos fármacos , Etanolaminas/antagonistas & inibidores , Ácidos Graxos não Esterificados/antagonistas & inibidores , Traumatismo por Reperfusão/tratamento farmacológico , Trocador de Sódio e Cálcio/antagonistas & inibidores , Tioureia/análogos & derivados , Tioureia/farmacologia , Aminoácidos/antagonistas & inibidores , Aminoácidos/metabolismo , Animais , Isquemia Encefálica/tratamento farmacológico , Isquemia Encefálica/metabolismo , Isquemia Encefálica/fisiopatologia , Córtex Cerebral/metabolismo , Córtex Cerebral/fisiopatologia , Cromatografia Líquida de Alta Pressão , Relação Dose-Resposta a Droga , Etanolaminas/metabolismo , Ácidos Graxos não Esterificados/metabolismo , Homeostase/efeitos dos fármacos , Homeostase/fisiologia , Concentração de Íons de Hidrogênio/efeitos dos fármacos , Masculino , Fármacos Neuroprotetores/farmacologia , Fosfolipases A/antagonistas & inibidores , Fosfolipases A/metabolismo , Ratos , Ratos Sprague-Dawley , Traumatismo por Reperfusão/metabolismo , Traumatismo por Reperfusão/fisiopatologia , Trocador de Sódio e Cálcio/metabolismoRESUMO
The Na(+)/H(+) exchanger (NHE) is activated during ischemia-reperfusion in an effort to restore intracellular pH to normal levels. Inhibition of NHE with non-selective amiloride derivatives has been shown to be neuroprotective and to attenuate free fatty acid efflux during ischemia-reperfusion. We evaluated the effects of SM-20220 (20 microM), a highly selective and specific NHE inhibitor, applied topically onto rat cerebral cortex prior to and during a 20-min period of ischemia. SM-20220 application significantly reduced the ischemia-evoked efflux of myristic, palmitic, and arachidonic acids during both ischemia and reperfusion with significant decreases in linoleic and docosahexaenoic levels during reperfusion. This study confirms the importance of NHEs in eliciting free fatty acid efflux, inhibition of which may be an essential component of the neuroprotective benefits of NHE inhibitors in ischemia-reperfusion injury.
Assuntos
Acidose/metabolismo , Amidas/farmacologia , Isquemia Encefálica/enzimologia , Córtex Cerebral/enzimologia , Ácidos Graxos não Esterificados/metabolismo , Indóis/farmacologia , Traumatismo por Reperfusão/enzimologia , Trocadores de Sódio-Hidrogênio/metabolismo , Acidose/tratamento farmacológico , Acidose/fisiopatologia , Animais , Isquemia Encefálica/tratamento farmacológico , Isquemia Encefálica/fisiopatologia , Membrana Celular/efeitos dos fármacos , Membrana Celular/enzimologia , Córtex Cerebral/efeitos dos fármacos , Córtex Cerebral/fisiopatologia , Regulação para Baixo/efeitos dos fármacos , Regulação para Baixo/fisiologia , Líquido Intracelular/efeitos dos fármacos , Líquido Intracelular/enzimologia , Transporte de Íons/efeitos dos fármacos , Transporte de Íons/fisiologia , Fármacos Neuroprotetores/farmacologia , Fosfolipases/efeitos dos fármacos , Fosfolipases/metabolismo , Ratos , Traumatismo por Reperfusão/tratamento farmacológico , Traumatismo por Reperfusão/fisiopatologia , Sódio/metabolismo , Trocadores de Sódio-Hidrogênio/efeitos dos fármacosRESUMO
The anatomical existence of the transforaminal ligaments has been studied extensively. However, there are very few studies examining how the transforaminal ligaments could be involved in the causation of nerve root compression and the low back pain syndrome. In this article, the authors review earlier studies in an attempt to find anatomical and biomechanical correspondence between the intervertebral foraminal ligaments of the lumbar spine and the low back pain syndrome.
Assuntos
Ligamentos Articulares/fisiopatologia , Dor Lombar/fisiopatologia , Vértebras Lombares/fisiopatologia , Síndromes de Compressão Nervosa/fisiopatologia , Raízes Nervosas Espinhais/fisiopatologia , Idoso , Fenômenos Biomecânicos , Feminino , Humanos , Ligamentos Articulares/patologia , Dor Lombar/patologia , Vértebras Lombares/patologia , Masculino , Pessoa de Meia-Idade , Síndromes de Compressão Nervosa/patologia , Valores de Referência , Raízes Nervosas Espinhais/patologiaRESUMO
The isolation, culturing and expansion of human neural progenitors cells has important potential clinical applications in cellular transplantation strategies as well as in developmental studies involving the central nervous system (CNS). This study describes an efficient method to culture neurons and astrocytes as primary cultures, as well as from proliferative progenitor cells derived from second trimester fetal CNS tissue. Second trimester fetal human tissue was mechanically dissociated and subjected to trypsin-dissociation and trituration. The resulting suspension was passed over a Percoll density gradient. The middle (second) fraction of cells was centrifuged to yield a homogenous population of cells with 80%-90% viability. These cells were either cultured directly on laminin coated dishes with defined medium supplemented with fetal bovine serum or in defined medium supplemented with growth factors including epidermal growth factor, basic fibroblast growth factor and leukemia inhibitory factor. The primary cell cultures yielded neurons and astrocytes after 3-5 days in vitro verified by immunostaining with MAP2ab and GFAP. Cells exposed to growth factor supplemented medium formed free-floating spheres within one week. Upon growth factor removal and plating on laminin-coated dishes, brain derived spheres gave rise to neurons, astrocytes and oligodendrocytes; spinal cord derived spheres generated only astrocytes. This protocol describes an efficient method to generate and culture neurons and astrocytes from second trimester human CNS tissue that may be useful in transplantation and developmental studies.
Assuntos
Astrócitos/citologia , Sistema Nervoso Central/citologia , Sistema Nervoso Central/embriologia , Técnicas Citológicas , Neurônios/citologia , Astrócitos/metabolismo , Células Cultivadas , Sistema Nervoso Central/metabolismo , Feminino , Proteína Glial Fibrilar Ácida/metabolismo , Humanos , Imuno-Histoquímica , Proteínas Associadas aos Microtúbulos/metabolismo , Neurônios/metabolismo , Oligodendroglia/metabolismo , Gravidez , Segundo Trimestre da Gravidez , Esferoides Celulares , Sulfoglicoesfingolipídeos/metabolismoRESUMO
There are many materials available for the reconstruction of calvarial defects. Even though their biomaterial properties are well known, the biomechanical properties as part of the calvarium have not been investigated. In this article, calvarial implants are reviewed with their historic development into modern cranioplasty. Materials for trephined skulls are classified by their category. Individual parameters to describe their mechanical properties are collected and revealed in detail. The laboratory testing methodology for cranioplasty material is introduced to understand each parameter. At last, we discuss an engineering technique to look into the implant behavior. Since there is no standard goal for the biomechanical and biomaterial point of view for cranioplasty, this article suggests the finite element method for evaluation of the implant behavior and the degree of damage upon the impact injury.
Assuntos
Transplante Ósseo/fisiologia , Craniotomia/métodos , Implantação de Prótese , Crânio/fisiologia , Crânio/cirurgia , Fenômenos Biomecânicos , Substitutos Ósseos/uso terapêutico , HumanosRESUMO
Neural transplantation holds promise for the treatment of traumatic brain and spinal cord injury by replacing lost cellular elements as well as repairing neural damage. Fetal human stem cells derived from central nervous system (CNS) tissue are potential transplantable sources for all cell types found in the mature human nervous system including neurons, astrocytes and oligodendroglia. Although nearly all areas of the fetal human neuraxis contain undifferentiated neural precursor cells, the phenotypic fate of the daughter cells might vary from one region to another during a specific developmental period. The purpose of this study was to compare the various cell types derived from neural precursors cultured from second trimester fetal human brain and spinal cord. To this end, brains (n = 8) and spinal cords (n = 8) of 15-24 week fetuses were dissociated and grown in culture medium supplemented with epidermal growth factor (EGF), basic fibroblast growth factor (FGF) and leukemia inhibitory factor (LIF). The proliferating precursor cells from both brain and spinal cord grew as spherical masses that were plated on laminin-coated dishes after seven days in culture. During the next 5-7 days, the cells that emerged from these spheres were fixed and processed for immunocytochemistry. Brain derived spheres gave rise to cells expressing antigens specific for neurons (MAP-2ab and neuron specific-intermediate filaments), astrocytes (GFAP) and oligodendrocytes (A007). In contrast, cells that emerged from spinal cord derived spheres were only immunoreactive for GFAP. These data suggest that neuroepithelial precursor cells from different CNS regions, although similar in their responsiveness to proliferative growth factors, might differ in their ability to generate different cell types in the adult CNS.
Assuntos
Sistema Nervoso Central/citologia , Sistema Nervoso Central/embriologia , Neurônios/citologia , Células-Tronco/citologia , Astrócitos/citologia , Linhagem da Célula , Células Cultivadas , Feminino , Feto/citologia , Proteína Glial Fibrilar Ácida/análise , Humanos , Imuno-Histoquímica , Proteínas Associadas aos Microtúbulos/análise , Proteínas de Neurofilamentos/análise , Oligodendroglia/citologia , Gravidez , Segundo Trimestre da GravidezRESUMO
Traumatic vascular lesions can occur after severe or even the most mild of head and cervical trauma. The initial evaluation of the injured patient must be thorough and the clinical suspicion of vascular injury must be highly suspected based on the mechanism of injury. Traumatic vascular injuries can be broadly classified into traumatic aneurysms, dissections and occlusions and fistulae of the carotid or vertebral arteries. The current management and treatment options of each condition are discussed.
Assuntos
Lesões Encefálicas/fisiopatologia , Lesões das Artérias Carótidas/fisiopatologia , Aneurisma Intracraniano/fisiopatologia , Lesões Encefálicas/diagnóstico por imagem , Lesões das Artérias Carótidas/diagnóstico por imagem , Angiografia Cerebral , Humanos , Aneurisma Intracraniano/diagnóstico por imagem , Artéria Vertebral/lesões , Dissecação da Artéria Vertebral/diagnóstico por imagem , Dissecação da Artéria Vertebral/fisiopatologiaRESUMO
With the rapid development of computer equipment, approximation by analytical solutions has become popular in mathematical modeling. Finite element (FE) analysis uses numerical methods to solve problems with physical phenomena, and these can be applied to various geometrically complex materials, such as brain. The FE formulation can provide such diverse domains as heat conduction, torsion of elastic material, diffusion and fluid flow, and it can view different objects of study in the neurosurgical field. In this article, the various applications of FE methods are introduced to illustrate the usefulness of the technique and the link between the external biomechanical aspect and internal phenomena in brain research.
Assuntos
Análise de Elementos Finitos/estatística & dados numéricos , Fenômenos Biomecânicos , Lesões Encefálicas/cirurgia , Humanos , Neurocirurgia , Procedimentos Neurocirúrgicos , Condutividade Térmica , Anormalidade TorcionalRESUMO
OBJECTIVE: Hyperglycemic stroke results in increased neuronal damage, the exact mechanism of which is unknown. Lactic acidosis has been implicated; however, increases in the excitotoxic amino acid glutamate, which correlate with increased neuronal damage, may be the cause for the increased damage seen in hyperglycemic stroke. METHODS: Ten Sprague-Dawley rats were treated with streptozotocin (STZ; 50 mg/kg), and 12 normoglycemic rats were used as controls. Using a four-vessel occlusion model, global ischemia was assessed at 5 to 7 days after treatment in five animals (acute STZ group) or at 4 to 6 weeks after treatment in five animals (chronic STZ group). The cortical cup model was used to collect superfusates under basal, ischemic, and reperfusion conditions and analyzed for nine different amino acids using high-performance liquid chromatography. RESULTS: Plasma glucose levels were significantly higher in the acute and chronic STZ groups as compared with the control group. Plasma lactate levels were higher in the acute STZ group as compared with the control or chronic STZ groups. Extracellular cortical glutamate levels were significantly reduced during reperfusion in the acute STZ group and during ischemia/reperfusion in the chronic STZ group as compared with the controls. Levels of extracellular gamma-aminobutyric acid were significantly reduced in the acute and chronic STZ groups as compared with the controls. CONCLUSION: A chronic state of hyperglycemia results in reduction in extracellular brain glutamate levels during ischemia/reperfusion and therefore does not appear to be responsible for the increased neuronal damage seen in diabetic stroke. Chronic hyperglycemia also causes decreased extracellular gamma-aminobutyric acid levels, which, because of the loss of the inhibitory effects of this neurotransmitter, could contribute to the increased damage observed in hyperglycemic stroke.
Assuntos
Aminoácidos/metabolismo , Isquemia Encefálica/metabolismo , Córtex Cerebral/irrigação sanguínea , Córtex Cerebral/metabolismo , Diabetes Mellitus Experimental/metabolismo , Neurotoxinas/metabolismo , Doença Aguda , Animais , Glicemia/análise , Doença Crônica , Espaço Extracelular/metabolismo , Ácido Glutâmico/metabolismo , Ácido Láctico/sangue , Masculino , Ratos , Ratos Sprague-Dawley , Valores de Referência , Traumatismo por Reperfusão/metabolismo , Ácido gama-Aminobutírico/metabolismoRESUMO
Following permanent middle cerebral artery occlusion, extracellular penumbral glutamate levels, measured by a real-time glutamate electrode, increased in two different patterns. In 7/11 rats, glutamate increased from baseline levels of 19+/-4 (mean+/-SEM) to 208+/-29 microM and then declined towards baseline levels. Blood flow in the penumbral area declined to 30% of pre-ischemic levels with recovery to 60 and 70% of baseline values by 3 and 6 h, respectively. Four of 11 rats in the study also exhibited late peaks of glutamate release (120+/-40 microM ) 2 h after the onset of ischemia. There were no changes in the EEG recordings or cerebral blood flow during these late glutamate peaks.
Assuntos
Isquemia Encefálica/metabolismo , Córtex Cerebral/metabolismo , Ácido Glutâmico/metabolismo , Infarto da Artéria Cerebral Média/metabolismo , Animais , Isquemia Encefálica/patologia , Isquemia Encefálica/fisiopatologia , Córtex Cerebral/patologia , Córtex Cerebral/fisiopatologia , Circulação Cerebrovascular/fisiologia , Depressão Alastrante da Atividade Elétrica Cortical/fisiologia , Modelos Animais de Doenças , Eletrodos , Eletroencefalografia , Infarto da Artéria Cerebral Média/patologia , Infarto da Artéria Cerebral Média/fisiopatologia , Masculino , Potenciais da Membrana/fisiologia , Ratos , Ratos Sprague-Dawley , Fatores de TempoRESUMO
OBJECT: The goal of this study was to establish whether transplanted cells derived from fetal human brain can survive in an ischemic lesion. METHODS: Sixteen adult male Mongolian gerbils underwent transient bilateral common carotid artery occlusion. One week later, cell suspensions prepared from fetal human brain were injected using stereotactic guidance into the CA1 region of the hippocampus on one side. On the contralateral side injection of the cell suspension medium only was performed. One week after transplantation, the animals were perfusion fixed and their brains were processed for histological studies as well as expression of neuron and glia-specific antigens. Data from ischemic animals were compared with eight nonischemic gerbils that served as sham-operated controls. Last, the in vivo data were correlated with observations made from matching in vitro cultures of the fetal brain cell suspension. The in vivo data indicated that transplanted human fetus-derived brain cells survived in ischemic lesions of gerbil hippocampus after 1 week, provided that the host animal underwent adequate immunosuppression and the transplanted cells were not incorporated into the scar caused by the transplantation procedure. Unlike their in vivo counterparts, after 1 week, most cultured fetal brain cells expressed either neuron- or astrocyte-specific antigens. CONCLUSIONS: This work demonstrates that xenotransplanted fetal human brain cells are able to survive in an ischemic lesion in a rodent model. These data might be useful for future neural transplantation studies of treatments for cerebrovascular ischemia in humans.