Predictors of quality of life after moderate to severe traumatic brain injury / Preditores de qualidade de vida após trauma crânio-encefálico moderado a grave

ABSTRACT Objective To verify correlations between age, injury severity, length of stay (LOS), cognition, functional capacity and quality of life (QOL) six months after hospital discharge (HD) of victims of traumatic brain injury (TBI). Method 50 patients consecutively treated in a Brazilian emergency hospital were assessed at admission, HD and six months after HD. The assessment protocol consisted in Abbreviated Injury Scale, Injury Severity Score, Glasgow Coma Scale (GCS), Revised Trauma Score (RTS), Mini Mental Test, Barthel Index and World Health Organization QOL - Brief. Results Strong negative correlation was observed between LOS and GCS and LOS and RTS. An almost maximal correlation was found between RTS and GCS and functional capacity and GCS at HD. Age and LOS were considered independent predictors of QOL. Conclusion Age and LOS are independent predictors of QOL after moderate to severe TBI.

RESUMO Objetivo Verificar correlações entre idade, gravidade do trauma, tempo de hospitalização (TH), cognição, capacidade funcional e qualidade de vida (QV) seis meses após alta hospitalar (AH) de vítimas de trauma crânio-encefálico (TCE). Método 50 pacientes tratados em um hospital de emergência brasileiro foram avaliados na admissão, AH e seis meses após AH. O protocolo de avaliação consistia em Escala Abreviada de Lesões, Índice de Gravidade de Lesão, Escala de Coma de Glasgow (ECG), Escore de Trauma Revisado (RTS), teste Mini-Mental, Índice de Barthel e Questionário Breve de QV da Organização Mundial de Saúde. Resultados Forte correlação negativa foi observada entre TH e ECG e TH e RTS. Correlação quase máxima foi observada entre RTS e ECG e capacidade funcional e ECG na AH. Idade e TH foram considerados preditores independentes de QV. Conclusão Idade e TH são preditores independentes de QV após TCE moderado e grave.

Supine sleep and positional sleep apnea after acute ischemic stroke and intracerebral hemorrhage

OBJECTIVE: Obstructive sleep apnea is frequent during the acute phase of stroke, and it is associated with poorer outcomes. A well-established relationship between supine sleep and obstructive sleep apnea severity exists in non-stroke patients. This study investigated the frequency of supine sleep and positional obstructive sleep apnea in patients with ischemic or hemorrhagic stroke. METHODS: Patients who suffered their first acute stroke, either ischemic or hemorrhagic, were subjected to a full polysomnography, including the continuous monitoring of sleep positions, during the first night after symptom onset. Obstructive sleep apnea severity was measured using the apnea-hypopnea index, and the NIHSS measured stroke severity. RESULTS: We prospectively studied 66 stroke patients. The mean age was 57.6±11.5 years, and the mean body mass index was 26.5±4.9. Obstructive sleep apnea (apnea-hypopnea index >5) was present in 78.8% of patients, and the mean apnea-hypopnea index was 29.7±26.6. The majority of subjects (66.7%) spent the entire sleep time in a supine position, and positional obstructive sleep apnea was clearly present in the other 23.1% of cases. A positive correlation was observed between the NIHSS and sleep time in the supine position (r s = 0.5; p<0.001). CONCLUSIONS: Prolonged supine positioning during sleep was highly frequent after stroke, and it was related to stroke severity. Positional sleep apnea was observed in one quarter of stroke patients, which was likely underestimated during the acute phase of stroke. The adequate positioning of patients during sleep during the acute phase of stroke may decrease obstructive respiratory events, regardless of the stroke subtype.

Genes e epilepsia II: expressão gênica diferencial: [revisão] / Genes and epilepsy II: differential gene expression in epilepsy: [review]

Nesta revisão, introduzimos abordagens investigativas, assim como discutimos os principais achados de expressão gênica diferencial em tecido epiléptico humano e em modelos experimentais. As alterações observadas no cérebro de indivíduos epilépticos sugerem que eventos moleculares específicos refletem diferentes expressões do quadro fisiopatológico. É possível que diferentes combinações da expressão de genes associados à morte celular, metabolismo de radicais livres, transmissão sináptica, resposta imune e de neurotrofinas reflitam propriedades características de diferentes populações neuronais e gliais, que determinam as distintas respostas de cada área cerebral. A compreensão dessas particularidades moleculares será muito importante para o desenvolvimento de uma estratégia de intervenção visando reduzir neurotoxicidade e disfunções sinápticas que ocorrem durante a epileptogênese e a fase crônica em pacientes epilépticos.

We introduce some investigative appnacher and findings on differential gene expression in human epileptic time as well as in animal models of epilepsy. Molecular alterations observed in the epileptic brain suggest that they may disclose different psychopathological stages. It is possible that different gene expression combinations involved in cell death, reactive oxygen metabolism, synaptic transmission and immune response and of neurotrophins reflect distinct functional properties of different neuronal and glial populations, which determine specific brain region responses. Understanding the molecular patterns of gene expression following epileptogenic insults will be of great importance for the development of treatments aiming to reduce neurotoxicity and subtle synaptic dyfunctions present in the early stages as well as during the chronic phase of epilepsy.

Genes e epilepsia I: epilepsia e alterações genéticas / Genes and epilepsy I: epilepsy and genetic alterations

INTRODUÇÃO: Epilepsia é uma desordem neurológica caracterizada por crises espontâneas e recorrentes, que afeta de 2 por cento a 3 por cento da população mundial. As crises epilépticas refletem atividade elétrica anormal e paroxística, preferencialmente em uma ou várias áreas do córtex cerebral, que podem ser causadas por inúmeras patologias estruturais ou neuroquímicas. Dentre os importantes estudos das últimas décadas no campo da epileptologia, destaca-se a identificação de genes associados a certos tipos de epilepsia. OBJETIVO: Nesta revisão, descrevemos as principais alterações genéticas associadas ao processo epileptogênico, discutindo as mais recentes descobertas e suas contribuições para a compreensão das bases genéticas das epilepsias idiopáticas monogênicas (EIM) e das epilepsias geneticamente complexas. RESULTADOS E CONCLUSÃO: Estudos de ligação e associação mostram que alterações em genes que codificam canais iônicos são as principais causas genéticas das epilepsias idiopáticas monogênicas e de predisposição nas epilepsias geneticamente complexas. Além disso, as síndromes nas quais a epilepsia é um aspecto importante do quadro clínico podem ser provocadas por genes envolvidos em diferentes vias celulares, tais como: migração neuronal, metabolismo de glicogênio e cadeia respiratória. Portanto, acredita-se que diferentes categorias de genes possam atuar na determinação do traço epiléptico. A identificação de tais famílias de genes não apenas nos ajudará a entender as vias moleculares associadas à hiperexcitabilidade neuronal e ao processo epileptogênico, mas também poderá conduzir ao desenvolvimento de novas e mais precisas estratégias de tratamento da epilepsia.

INTRODUCTION: Epilepsy is a neurological disorder characterized by spontaneous and recurrent seizures with an estimated prevalence of 2-3 percent in the world population. Epileptic seizures are the result of paroxystic and hypersynchronous electrical activity, preferentially in cortical areas, caused by panoply of structural and neurochemical dysfunctions. Recent advances in the field have focused on the molecular mechanisms involved in the epileptogenic process. OBJECTIVES: In the present review, we describe the main genetic alterations associated to the process of epileptogenesis and discuss the new findings that are shedding light on the molecular substrates of monogenic idiopathic epilepsies (MIE) and on genetically complex epilepsies (GCE). RESULTS AND CONCLUSION: Linkage and association studies have shown that mutations in ion channel genes are the main causes of MIE and of predisposition for GCE. Moreover, mutations in genes involved in neuronal migration, glycogen metabolism and respiratory chain are associated to other syndromes involving seizures. Therefore, different gene classes contribute to the epileptic trait. The identification of epilepsy-related gene families can help us understand the molecular mechanisms of neuronal hyperexcitability and recognize markers of early diagnosis as well as new treatments for these epilepsies.

Pushing behavior and hemiparesis: which is critical for functional recovery in pusher patients?: case report

We report a sequential neuroimaging study in a 48-years-old man with a history of chronic hypertension and lacunar strokes involving the ventral lateral posterior nucleus of the thalamus. The patient developed mild hemiparesis and severe contraversive pushing behavior after an acute hemorrhage affecting the right thalamus. Following standard motor physiotherapy, the pusher behavior completely resolved 3 months after the onset and, at that time, he had a Barthel Index of 85, although mild left hemiparesis was still present. This case report illustrates that pushing behavior itself may be severely incapacitating, may occur with only mild hemiparesis and affected patients may have dramatic functional improvement (Barthel Index 0 to 85) after resolution pushing behavior without recovery of hemiparesis.

Relatamos o estudo de neuroimagem seqüencial de um homem de 48 anos com história de hipertensão arterial crônica e acidentes vasculares cerebrais (AVCs) lacunares nos núcleos ventral lateral posterior do tálamo. O paciente desenvolveu hemiparesia leve e síndrome do empurrador (SE) grave após AVC hemorrágico no tálamo direito, sendo tratado com fisioterapia motora convencional. Três meses após o ictus, os sinais da síndrome haviam desaparecido e o paciente apresentava índice de Barthel 85, apesar da permanência da hemiparesia leve. Este caso demonstra que a síndrome do empurrador isolada pode ser gravemente incapacitante, pode ocorrer associada a hemiparesia leve e que os pacientes com esta síndrome podem apresentar recuperação funcional importante (índice de Barthel inicial 0 e final 85) após a resolução da SP sem alteração do grau de hemiparesia.

Quantitative aspects of brain perfusion dynamic induced by BOLD fMRI / Aspectos quantitativos da dinâmica perfusional do cérebro induzida pelo BOLD fMRI

The increase of relative cerebral blood flow (rCBF) may contribute for a change in blood oxygenation level dependent signal (BOLD). The main purpose of this study is to investigate some aspects of perfusional alterations in the human brain in response to a uniform stimulation: hypercapnia induced by breath holding. It was observed that the BOLD signal increased globally during hypercapnia and that it is correlated with the time of breath holding. This signal increase shows a clear distinction between gray and white matter, being greater in the grey matter.

O aumento relativo do fluxo cerebral sangüíneo (relative Cerebral Blood Flow - rCBF) pode contribuir para uma mudança no sinal dependente da oxigenação do sangue (Blood Oxygenation Level Dependent - BOLD). O objetivo principal deste trabalho foi estudar alguns aspectos da alteração perfusional no cérebro humano em resposta a um estímulo uniforme: hipercapnia, causada por um estado de apnéia induzida. Foi observado um aumento global no sinal BOLD durante a hipercapnia. Este aumento é correlacionado com a duração da apnéia e mostra uma clara distinção entre a substância branca e cinzenta, sendo maior na substância cinzenta.