Generalidades de trauma cráneo encefálico en medicina legal / Generalities of traumatic brain injury in legal medicine

Resumen:El Trauma Cráneo Encefálico (TCE) tiene hoy en día una incidencia muy alta de morbilidad y mortalidad en nuestra población, por lo que es de suma importancia esclarecer los conceptos básicos de las lesiones producidas por el TCE, su cronología y el pronóstico de dichos traumas. Este artículo se basa en identificar las lesiones primarias y secundarias más frecuentes y las características más importantes de cada una de ellas, así como describir los mecanismos de trauma frecuentemente implicados.

Abstract:The Brain Trauma (TCE) has a very high incidence of morbidity and mortality in its population today, so it is very important to clarify the basic concepts of the injuries produced by the TCE, its timing and the prognosis of these traumas. This article is based on identifying the most frequent primary and secondary lesions and the most important characteristics of each, as well as describing the mechanisms of trauma frequently involved

Physiopathology of symptoms and signs in multiple sclerosis / Fisiopatologia dos sintomas e sinais na esclerose múltipla

The physiopathology of symptoms and signs in multiple sclerosis (MS) is a less divulged topic albeit its importance in the patients' management. OBJECTIVE: It was to summarize the main biophysical and biochemical mechanisms which produce the clinical manifestations in MS. RESULTS: The mechanisms underpinning neurological deficits are described in the relapsing and in the progressive phases, stressing inflammatory and neurodegenerative components, especially demyelination, axonal damage and conduction impairment. Transient worsening based in Uhthoff's phenomenon, mechanisms producing positive symptoms, as paraesthesias and Lhermitte sign due to axonal hiperexcitability and ephaptic interactions, and development of cortical symptoms will also be addressed. The variety of processes leading to neural repair and functional recovery in the remitting phase is focused, as remyelination and adaptive changes due to neural plasticity. CONCLUSION: The awareness of mechanisms producing symptoms in MS emphasises the role of symptomatic and rehabilitation therapies in the improvement of patients' well-being.

A fisiopatologia dos sintomas e sinais na esclerose múltipla (EM) é um tópico pouco divulgado apesar da sua importância na abordagem dos doentes. OBJETIVO: Foi apresentar os principais mecanismos biofísicos e bioquímicos que produzem manifestações clínicas da EM. RESULTADOS: Descrevem-se os mecanismos subjacentes aos défices neurológicos nas fases de surto e progressivas, realçando as componentes inflamatória e neurodegenerativa, especialmente desmielinização, lesão axonal e alterações da condução. Serão igualmente referidos os sintomas transitórios explicados pelo fenômeno de Uhthoff, a produção de sintomas positivos, como as parestesias e o sinal de Lhermitte por hiperexcitabilidade axonal e interações efáticas, e o desenvolvimento de sintomas corticais. Apresentam-se os diversos processos de reparação neural e de recuperação funcional nas fases de remissão, como a remielinização e as alterações adaptativas por neuroplasticidade. CONCLUSÃO: O conhecimento dos mecanismos que produzem os sintomas da EM realça o papel das terapêuticas sintomáticas e de reabilitação na melhoria do bem-estar dos doentes.

Tormenta simpática paroxística como manifestación de daño axonal difuso postraumatismo encefalocraneano / Paroxysmal sympathetic storm as a manifestation of diffuse axonal damage

Presentamos el caso de un hombre de 24 años que, secundario a un accidente de tránsito, presentó un traumatismo encefalocraneano grave con daño axonal difuso. Luego de un mes de evolución en la unidad de cuidados intensivos comenzó a presentar episodios súbitos de hipertensión, taquicardia, diaforesis, hipertermia, descerebración y dilatación pupilar, todo lo anterior con resolución espontánea en el curso de minutos. Estas crisis se repetían varias veces en el día. Se llegó al diagnóstico de un cuadro denominado Tormenta Simpática Paroxística que puede presentarse muy ocasionalmente como consecuencia de una lesión cerebral grave, especialmente el daño axonal postraumático. En este trastorno prima un desbalance simpático/parasimpático, lo que podría deberse a una pérdida del control cortical. El paciente fue tratado con opiáceos y betabloqueo con una respuesta satisfactoria, logrando disminuir significativamente sus episodios de tormentas simpáticas paroxísticas. En suma, nos parece importante comunicar esta experiencia dado la alta prevalencia de pacientes con trauma cerebral en nuestras Unidades de Pacientes Críticos. A pesar de que ni su diagnóstico ni tratamiento mejoran el pronóstico, su reconocimiento ahorra estudios innecesarios y permite iniciar una terapia sencilla que lleva al control precoz de la sintomatología.

A 24-year-old man suffered a traumatic brain injury due to a car accident. After one month of hospitalization in intensive care unit, he experimented episodic crisis of hypertension, tachycardia, hyperhidrosis, hypertermia, extensor posturing and pupil dilatation. This events presented in average 10 times per day. We reached to the diagnosis of Paroxysmal Sympathetic Storm. This is a subtype of dysautonomy which is present occasionally after a brain traumatic injury. The main mechanism of this brain dysfunction is a disassociation between the sympathetic and parasympathetic nervous systems due to cortical control loss. The patient was treated with morphine and labetalol and he experimented an excellent response, reducing his episodes of paroxysmal sympathetic storm by 80 percent. The aim of this review is to communicate this entity because a prompt and accurate diagnosis could minimize unnecessary studies and treatments.

Effect of Hyperphosphorylated p38MAPK in Experimental Autoimmune Encephalomyelitis Axonal Damage / 中国康复理论与实践

@#Objective To explore the mechanism about the expression of the hyperphosphorylated p38MAPK in the central nervous system (CNS) of experimental autoimmune encephalomyelitis (EAE) mouse and its relationship to the axonal damage, and investigate the potential regulation of SB203580 to the damaged axons in the CNS of EAE mouse.Methods SJL/J mice were used to establish the EAE model. Brain and spinal cord of EAE mice in the model group, SB203580 group and control group were used respectively at different time points. Stained with HE and Luxol Fast Blue (LFB), also the immunohistochemical detection was conducted with parallel phosphorylation of p38MAPK antibody staining and APP staining at the same time. By image analysis system, the number of positive signals, the coverage and the average density value in the cytoplasm of neuron in white matter lesions were measured.Results The model of EAE mice induced by PLP peptide manifested significant neurological symptoms, signs and features of relapse and remitting. Demyelinating change was observed in local regional white matter region. Compared with the model group, SB203580 group changed lighter, with its behavioral observations and had a significant weight gain (P<0.01). In addition to the control group, amyloid precursor protein (APP) expression was detected in other groups at various time points. Compared to the model group, APP expression was slighter than in SB203580 group. The number of positive cells and strength was significantly lower in the SB203580 group (P<0.01); expression of p38MAPK in EAE mice was observed at the earlier 7th day after immunization. Compared to the model group, expression of SB203580 group was lighter, positive number and intensity decreased markedly (P<0.01).Conclusion p38MAPK blockers SB203580 can not only inhibit activation of the p38MAPK in EAE mice, but also effectively reduce expression of APP which is symbolic target of EAE axonal injury, it is confirmed that the p38MAPK is indeed involved in the EAE axonal injury.

Lesão da substância branca e doenças neurodegenerativas / White matter injury and neurodegenerative diseases

Objetivo: revisar a literatura científica sobre degeneração da substância branca, incluindo lesão do cilindro axonal, da bainha de mielina e oligodendrócitos, enfatizando o papel deste evento patológico na perda tecidual e deficiências funcionais subjacentes às doenças neurodegenerativas agudas e crônicas. Método: revisão de literatura através de pesquisa bibliográfica na base de dados PUBMED/MEDLINE. Considerações Finais: o comprometimento patológico da substância branca é um mecanismo importante dafisiopatologia de doenças neurodegenerativas agudas e crônicas. Pesquisas translacionais nesta área devem ser realizadas para o desenvolvimento de novas abordagens terapêuticas para essas desordens neurais. Um objetivo importante destes estudos deve ser a proteção dos tratos de substância branca do sistema nervoso central humano, os quais podem degenerar durante doenças, incluindo trauma cerebral e medular, acidente vascular encefálico e esclerose múltipla.

Objective: review the literature on the white matter pathology, including axonal damage, myelin impairment and oligodendrocyte degeneration, emphasizing the importance of this pathological event on the underlying functional deficits following neurodegenerative diseases. Method: bibliography search using PUBME/MEDLlNE databases. Final considerations: the pathological impairment of white matter is an important mechanism underlying the pathophysiology of both acute and chronic neurodegenerative disorders. Translational researches should beaccomplished for the development of new therapeutic approaches for human brain disorders. An important aim of these investigations must be the protection of the human white matter tracts, which are damaged following neural disorders, including brain and spinal cord trauma, stroke and multiple sclerosis.

Axonal damage of demyelination disease in mice / 第三军医大学学报

Objective To explore the axonal damages in demyelination disease and its time window and morphological features of damaged axons. Methods Mouse model of multiple sclerosis (MS) was prepared by immunizing C57BL/6J mice with myelin oligodendrocyte glycoprotein peptides35-55 (MOG 35-55) to induce experimental autoimmune encephalomyelitis (EAE). Inflammation, demyelination and axonal damage at different time points of EAE including preonset, onset, peak and chronic were observed by common histology and specific stainings for the central nervous system. Results Demyelination and axonal damage occurred at the early stage of EAE, and was strongly related to inflammatory cell infiltration and demyelination of the central nervous system. Damaged axons showed the typical morphological features, including axon distortion, swelling, irregular diameter, axon transection with the ends ovoid, or bulb, and even axon disappearance. Conclusion Axonal damage is an early and common event in demyelination disease, and many factors might contribute to axonal damage.