O espessamento da íntima-média associa-se independentemente ao Acidente Vascular Cerebral Isquêmico

FUNDAMENTO: O Acidente Vascular Cerebral (AVC) constitui uma das primeiras causas de morte a nível mundial. A importância do espessamento da íntima-média na estratificação de risco cardiovascular tem sido recorrentemente estudada; contudo, essa relação gera ainda alguma controvérsia. OBJETIVOS: Determinar se o espessamento da íntima-média na Artéria Carótida Comum (ACC) pode ser utilizado como um marcador independente de alto risco para a ocorrência do AVC. MÉTODOS: A amostra compreende um grupo de 948 doentes consecutivamente estudados por Triplex Scan Cervical no período compreendido entre janeiro de 2004 e junho de 2009. Esses doentes foram agrupados em razão da presença ou ausência de AVC recente, do que resultou um grupo de doentes com AVC Isquémico (AVC I) (n = 452, 48%), outro com AVC Hemorrágico (AVC H) (n = 22, 2%) e um grupo de doentes Sem Eventos (n = 474, 50%). RESULTADOS: Na análise de regressão logística ajustada para fatores de risco cardiovascular clássicos, o espessamento da íntima-média na ACC associou-se significativamente e de forma aproximadamente linear com o AVC I (Odds Ratio = 1.808, Intervalo de Confiança: 1.291-2.534, p = 0,01), mas não com o AVC H (p = ns). Uma interação significativa com a idade foi também encontrada, demonstrando-se uma capacidade discriminativa do risco de AVC I maior em indivíduos com idade inferior a 50 anos. CONCLUSÕES: O espessamento da íntima-média na ACC revelou-se um preditor de risco independente para o AVC I, mas não para AVC H reforçando assim a utilidade da sua avaliação na prática clínica. (Arq Bras Cardiol. 2012; [online].ahead print, PP.0-0)

Análise da tendência da mortalidade por acidente vascular cerebral no Brasil no século XXI

FUNDAMENTO: Embora seja mundialmente a segunda principal causa de óbitos, o Acidente Vascular Cerebral (AVC) vem apresentando uma importante redução das taxas de mortalidade nas últimas décadas. OBJETIVO: Avaliar a tendência da taxa de mortalidade por acidente vascular cerebral no Brasil, em ambos os sexos, a partir dos 30 anos de idade, entre 2000 e 2009. MÉTODOS: Os dados populacionais foram obtidos no banco de dados do Instituto Brasileiro de Geografia e Estatística e os óbitos, por meio do Sistema de Informações sobre Mortalidade da Secretaria de Vigilância em Saúde do Ministério da Saúde, sendo incluídos os códigos I60 a I69 de acordo com a 10ª Classificação Internacional de Doenças. Foi calculada a incidência de óbitos/1.000 habitantes, as taxas de mortalidade bruta e padronizada/100.000 habitantes. A modelagem da tendência das taxas foi feita com modelos de regressão. RESULTADOS: Observou-se um aumento na incidência de óbitos até 2006, seguindo-se um declínio até 2009, quando ocorreu a incidência mínima. Comparando os anos 2000 e 2009, nota-se uma tendência de queda da taxa de mortalidade padronizada em ambos os sexos (masculino = -14,69%; feminino = -17%) e no total (-14,99%), com oscilações no período. Entre 30 e 49 anos em ambos os sexos, houve uma tendência de redução contínua e linear da taxa de mortalidade, enquanto os demais grupos etários apresentaram uma função curvilínea, culminando com uma efetiva diminuição dos valores. CONCLUSÃO: Houve uma tendência de queda na taxa de mortalidade em todas as faixas etárias e em ambos os sexos. A redução da taxa de mortalidade bruta foi mais acentuada no sexo masculino, enquanto a taxa de mortalidade padronizada mostrou uma maior redução no sexo feminino.

A distensibilidade da aorta prediz o acidente vascular cerebral em pacientes hipertensos

FUNDAMENTO: A doença cardiovascular continua a ser principal causa de morte nos países desenvolvidos e não é inteiramente prevista por fatores de risco clássicos. O aumento da rigidez arterial constitui um importante determinante de morbidade e mortalidade cardiovascular. OBJETIVO: Avaliar se a velocidade da onda de pulso prediz a ocorrência de acidente vascular cerebral (AVC) em pacientes hipertensos. MÉTODOS: Estudo de coorte, observacional, prospetivo, multicêntrico, incluindo 1.133 pacientes hipertensos (586 homens), com uma média de idade de 51,05 ± 12,64 anos. Todos os pacientes foram submetidos à avaliação da VOP pelo método Complior, a uma avaliação clínica pormenorizada e à medição da pressão arterial. RESULTADOS: A incidência cumulativa de risco de AVC nos hipertensos com VOP aumentada foi de 3,25% (IC: 1,97%-5,25%), em comparação com 0,78% (IC: 0,28% - 1,87%) nos hipertensos com VOP normal (risco relativo (RR) = 4,15; IC: 1,53 - 11,26). Numa análise multivariável, ajustando o modelo aos fatores de risco cardiovasculares clássicos, a VOP foi um preditor independente de AVC, com um hazard ratio (HR) = 1,40 (IC: 1,13 - 1,73, p < 0,002), indicando um incremento de 40% no risco de AVC por cada incremento de 1 m/seg na VOP. A adição da VOP a um modelo composto pelos fatores de risco cardiovascular convencionais melhorou significativamente a sua capacidade discriminativa para o risco de AVC (C de Harrel aumentou de 0,68 para 0,71 após inclusão da VOP; p <0,01). CONCLUSÃO: A distensibilidade arterial aferida pela VOP aórtica é um fator de risco independente de AVC em pacientes hipertensos, sendo recomendável a sua integração em programas de follow-up de situações em que o risco cardiovascular é manifesto.

Hemodynamics and virtual stenting of cerebral aneurysms

Magdeburg, Univ., Fak. für Verfahrens- und Systemtechnik, Diss., 2011

Computer-aided detection of cerebral aneurysms in angiographies

Magdeburg, Univ., Fak. für Informatik, Diss., 2013

Neuronal alterations in chronic cerebral Toxoplasma gondii infection

Magdeburg, Univ., Fak. für Naturwiss., Diss., 2015

Estudos sôbre a excitação química da córtex cerebral (Ação da acetilcolina)

The author has studied the influence of acetylcholine solutions directly applied on the motor cortex of dogs, cats monkeys and rabbits. For this purpose small squares of filter paper were soaked in the acetylcholine solution and soon afterwards laid on the motor cortex. Solutions varying from 0,2 to 10 per cent have been experimented. It has been shown that local application of the solutions on the motor points, previously localized by induction coil, produced motor reactions. It has been found, in the dogs that 10 per cent acetylcholine solutions cause localized muscular twitchings (clonus) in almost all the animals experimented. Generalised epileptiform convulsions were obtained in44,4% of the dogs. Convulsions were also obtained by employing 1 per cent solution of acetylcholine. Definite response has been obtained with 0,2 per cent solution. Failure of motor action, pointed out by other authors, has been related to the use of anesthetics. Convulsions were easily produced by rapid light mechanical stimulations of the skin covering the muscles in conection with the excited motor point, and the application on the motor point of acetylcholine. The results on monkeys can be summarized as follows. Two species of monkeys were experimented: Cebus capucinus and Macaca mulata. In the monkeys C. capucinus generalised convulsive reactions were induced with actylcholine solutions in a concentration as low as 0,5 per cent. Motor reaction or convulsive seizeres were obtained in seven of the eight monkeys used. Three monkeys M. mulata were stimulated with 10 per cent acetylcholine solution but only localized muscular contraction hae been observed. Similar results has been obtained on the motor cortex of cats and rabbits. One of the three cats employed has shown epileptiform convulsions and the remaining only localized muscular contractions. In the rabbits muscular twitchings have been also induced. The sensitizing power of eserine on the action of acetylcholine has been also searched. The results indicate that a previous application of eserine solution on the motor center, potentiates the action of acetylcholine. The intensity of the muscular twitchings is greater than the obtained before the application of the eserine solution. Generalised epileptiform convulsions sometimes appeared following the use of lower concentrations of acetylcholine than those previously employed. Experiments have been carried out by injecting eserine and prostigmine by parenteral route. A dosis dufficient for induce small muscular tremors did not enhance obviously the motor effects produced by the application of the acetylcholine solutions on the motor cortex. From seven dogs experimented, all previously tested for convulsive seiruzes by application of 1 and 10 per cent acetylcholine solution with negative results, only one has shown epileptiform convulsions after the injection of prostigmine. Morphine has also been tested as facilitating substance for convulsions induced by acetylcholine. Six from the nine dogs submitted to the experiments, developed epileptiform seizures after injection of morphine and stimulation of the motor cortex with acetylcholine. (Table IV). In another series of experiments atropine and nicotine have been studied as for to their action on the motor effects of acetylcholine. Nicotine has a strong convulsant action, even when employed in very high concentration. Since a depressant effect has not appeared even by the applications of high concentrations of nicotine in the motor corteõ of dogs, unlike the classical observations for the autonomus nervous system, it was not possible to verify the action of acetylcholine on a motor center paralised by nicotine. It is important to not that the motor phenomena observed after the first aplication of acetylcholine, can desappear by the renewal of the pieces of filter paper soaked in the acetylcholine solution. Atropine, either applied on the motor point in low concentration, or injected in sufficient amount for inhibiting the “muscarinic effects” of acetylcholine on the autonomous nervous system, did not prevent the motor reactions of acetylcholine on the cerebral cortex.

Toxoplasmose congênita

We had the opportunity to study 6 cases of the congenital form of toxoplasmosis, found in a series of 1200 necropsies of fetuses and newborn babies, realized at 3 different hospitals in Rio de Janeiro, Brazil. Among the 6 cases, 4 were premature babies liveborn at the 6th-8th gestational month and 2 were stillborn (1 premature and 1 at term). In all those cases, the diagnosis was based in the detection of the parasite in tissues and in one case it was even isolated the Toxoplasma from the necrotic material found in the cranial cavity. This strain of Toxoplasma, pathogenic to pigeons, to guinea pigs and to mice, is preserved by successive transfers in mice. Some facts observed in those cases present an interest not only strictly anatomic but also have certain value for the better acknowlegment of the disease. First, we want to call the attention to the presence of a sudden high fever, during or just before pregnancy in the 4 cases in which the maternal anamnesis was perfectly studied; this fever that was preceded by a normal beginning of pregnancy, had relatively rapid remission, but in 2 cases was immediately followed by uterine bleeding and premature delivery, although the puerperium had been apparently normal. It is known that are normal the subsequent children of the mothers that delivered a baby with toxoplasmosis and that several women have normal babies before the toxoplasmotic one. We believe that the fever observed in our cases could be indicative of the beginning of maternal infection and those are the reasons why we emphasize the need of careful anamnesis, specially in the cases actually diagnosed as inapparent infection. Another fact to notice is that in 5 of our cases the event premature delivery happened always between the 6th and the 8th months of pregnancy, and the only term fetus was delivered in advanced stage of maceration. The above mentioned facts could agree with the opinion of FRENKEL (1949), when he declared that "primary infection of the pregnant mother appears more likely to be the commoner mode of fetal toxoplasmic infection", but they would disagree with WEINMAN (1952) who believes that the transmission of Toxoplasma to the fetus is more frequent through a pregnant woman with chronic disease and who says "that infection contracted during pregnancy may and probably does happen from time to time"...Still in connection with the transmission of toxoplasmosis, we want to note the verification of inflammatory lesions in the placental villi and in the umbilical cord in 3 of the 4 cases in which such organs were examined at the microscope. In the case n. 1, we found several pseudocysts of Toxoplasma in the placenta, and the fibroblasts of Wharton's jelly were particularly rich in isolated forms and in colonies of Toxoplasma; the easy multiplication of the parasite in that tissue calls the attention and even suggests its utilisation for Toxoplasma's cultivation. The confirmation of Toxoplasma in human placenta was made only recently by CRISTEN et al. (1951) and by NEGHME et al. (1952), in Chile; it is not frequent in the literature, what gives some value to our present verification. Another observation was that provided by the case n. 6. This baby, a premature one of the 6th month, was 14 days old and-died with signs of respiratory disease, the causa mortis have been pneumonia. At the necropsy, we found no gross change that suggested toxoplasmosis, except the presence of some small necrotic focuses in the cerebral nervous substance around the ventricles. As a matter of fact, there was no enlargement of spleen or liver and neither leptomeningitis nor hydrocephalus. Such focuses were attributed to possible anoxia and in fact they are extremely similar to anoxial softenings, even when they are examined at the microscope; its structure composed of a central necrotic zone, surrounded by proliferated neuroglia and by a variable deposit of calcium salts, closely simulated the anoxial softenings, when the microscopical examination is based in the common histological preparations (hematoxilin-eosin, etc.). But when we examine preparations by the Giemsa or by the periodic acid-Schiff methods, we will note the presence of Toxoplasma, with its typical aspect or a little changed by degeneration. When we describe this observation, we wish to evidence the need of the search of Toxoplasma and closed parasites, in the cases of supposed pure anoxial softenings of nervous substance, in children. The frequency with which the congenital toxoplasmosis was anatomically verified should be emphasized, although the disease had not been clinically suspected, and it should be borne in mind that the second case of toxoplasmosis reported in the world was observed in Brazil by MAGARINOS TORRES; this case was the first to be described of the generalized congenital form of the infection, i. e. with myocardial lesions and parasites in skeletal muscles and skin.

Bradykinin in blood and cerebrospinal fluid after acute cerebral lesions: correlations with cerebral edema and intracranial pressure.

Abstract Bradykinin (BK) was shown to stimulate the production of physiologically active metabolites, blood-brain barrier disruption, and brain edema. The aim of this prospective study was to measure BK concentrations in blood and cerebrospinal fluid (CSF) of patients with traumatic brain injury (TBI), subarachnoid hemorrhage (SAH), intracerebral hemorrhage (ICH), and ischemic stroke and to correlate BK levels with the extent of cerebral edema and intracranial pressure (ICP). Blood and CSF samples of 29 patients suffering from acute cerebral lesions (TBI, 7; SAH,: 10; ICH, 8; ischemic stroke, 4) were collected for up to 8 days after insult. Seven patients with lumbar drainage were used as controls. Edema (5-point scale), ICP, and the GCS (Glasgow Coma Score) at the time of sample withdrawal were correlated with BK concentrations. Though all plasma-BK samples were not significantly elevated, CSF-BK levels of all patients were significantly elevated in overall (n=73) and early (≤72 h) measurements (n=55; 4.3±6.9 and 5.6±8.9 fmol/mL), compared to 1.2±0.7 fmol/mL of controls (p=0.05 and 0.006). Within 72 h after ictus, patients suffering from TBI (p=0.01), ICH (p=0.001), and ischemic stroke (p=0.02) showed significant increases. CSF-BK concentrations correlated with extent of edema formation (r=0.53; p<0.001) and with ICP (r=0.49; p<0.001). Our results demonstrate that acute cerebral lesions are associated with increased CSF-BK levels. Especially after TBI, subarachnoid and intracerebral hemorrhage CSF-BK levels correlate with extent of edema evolution and ICP. BK-blocking agents may turn out to be effective remedies in brain injuries.

Intraoperative cerebral perfusion and postoperative cognitive dysfunction in geriatric patients

Background: Inadequate intraoperative cerebral perfusion has been suggested as a possible cause of postoperative cognitive dysfunction (POCD). Methods: We investigated 35 patients aged 65 or older undergoing elective major non-cardiac surgery under standardized general anaesthesia (thiopental, sevoflurane, fentanyl, atracurium). Intraoperative cerebral perfusion was monitored with transcranial Doppler, and near-infrared spectroscopy (NIRS). Arterial blood pressure was monitored continuously with a Finapres device. Mx, an index allowing continuous monitoring of cerebrovascular autoregulation based on the changes in mean arterial blood pressure (MAP) and cerebral blood flow velocity was calculated. Mx >0.5 was defined as disturbed cerebrovascular autoregulation. Cognitive function was measured preoperatively and 7 days postoperatively using the CERAD-NAB Plus test battery. A postoperative decline >1 z-score in at least two of the tested domains was defined as POCD. Data are shown as mean } SD. Results: Mean age was 75 } 7 yrs. Sixteen patients (46%) developed POCD. These patients were older (77 } 8 vs 73 } 7 yrs), had lower MAP (77 } 12 vs 81 } 11 mm Hg), lower cerebral tissue oxygenation indices measured by NIRS (66.8 } 6.0 vs 68.6 } 4.3%) and less efficient cerebrovascular autoregulation (Mx 0.54 } 0.17 and 0.44 } 0.22) than patients without POCD. Disturbed intraoperative cerebrovascular autoregulation was found more often (56 vs 37%) in patients with POCD. However, none of these differences reached statistical significance. Conclusions: Our data show a trend towards subtle changes in intraoperative cerebral perfusion in elderly patients who develop POCD. However, a cause effect relationship must not be assumed and a greater number of patients needs to be investigated patients. However, more patients need to be investigated to confirm and characterize these differences.