Histopatologia do saco herniário da hérnia inguinal indireta e do peritônio parietal em adultos e crianças: estudo qualitativo da sua musculatura lisa

Estudo prospectivo, realizado entre abril de 1993 e julho de 1995, com o objetivo de estudar a histopatologia do saco herniário de hérnias inguinais indiretas do adulto e criança, no sentido de verificar a existência de musculatura lisa, sua incidência, apresentação morfológica e comparar com biópsias aleatórias do peritônio parietal. Os pacientes foram divididos em Grupo (1) com 123 pacientes, nos quais foram estudados os sacos herniários, e Grupo (2) constituído de 63 pacientes, nos quais foram realizadas biópsias da serosa peritoneal da cavidade abdominal. Verificou-se que fibras de músculo liso (FML) estiveram presentes em 65,4% dos 133 sacos herniários (dez pacientes com hérnia bilateral), estando presentes, também, em 19,04% dos espécimes da cavidade abdominal. Através dos testes do Qui-quadrado e t de Student, foi avaliada a associação entre a presença de FML com as variáveis categóricas (sexo, cor e lado da hérnia) e as variáveis contínuas (idade dos pacientes, comprimento e espessura do saco herniário). Os resultados mostraram que o sexo feminino apresenta uma maior incidência de FML (p=0,004) e a razão das chances (O.R.) demonstra que os pacientes desse mesmo sexo têm 5,46 vezes mais possibilidades de possuir FML nos sacos herniários. Assim, concluem que as FML são predominantes no peritônio parietal do abdome inferior e que existe, também, uma quantidade maior de FML no peritônio do saco herniário inguinal quando comparado com o peritônio parietal.

Não-fechamento dos peritônios visceral e parietal na operação cesariana

Objetivo: determinar se o não-fechamento dos folhetos peritoneais (visceral e parietal) na cesárea apresenta benefícios no intra e pós-operatório. Pacientes e Métodos: seiscentas e noventa e oito mulheres programadas para cesárea foram alocadas aleatoriamente em dois grupos: com sutura dos peritônios visceral e parietal (n = 349) e sem sutura dos peritônios (n = 349), na Maternidade da Encruzilhada (CISAM) em Recife, entre novembro de 1997 e dezembro de 1998. A análise estatística comparou as variáveis do intra-operatório e do pós-operatório entre os dois grupos. Não houve diferenças significativas entre os dois grupos em relação a idade, paridade, idade gestacional, antibiótico profilático, cefaléia pós-raquianestesia, cistite, amniorrexe prematura e indicações da cesárea. Resultados: o tempo cirúrgico, o número de fios categute simples e o uso de analgésico foram significativamente menores no grupo sem sutura do que no grupo com sutura. As incidências de febre, infecção de ferida operatória, endometrite foram similares nos dois grupos. Não houve diferenças quanto ao uso de antifisético, antiemético e óleo mineral. As médias de dias de permanência hospitalar foram similares nos dois grupos. Conclusões: o não-fechamento dos folhetos peritoneais não apresenta efeitos adversos no pós-operatório e, ao contrário, diminui o uso de analgésicos e no intra-operatório diminui o tempo e o número de fios categute simples.

Epidemiologia, sinais clínicos e distribuição das lesões encefálicas em bovinos afetados por meningoencefalite por herpesvírus bovino-5

São descritos sete surtos e um caso isolado de meningoencefalite por herpesvírus bovino-5 (BoHV-5) em bovinos no Rio Grande do Sul entre 2002 e 2004. Foram afetados bovinos de 1-18 meses, de diversas raças e ambos os sexos. A maior freqüência foi observada em bovinos recém-desmamados e submetidos a outros fatores de estresse. Nesses surtos, de uma população total sob risco de 1.359 bovinos, 54 foram afetados, quatro se recuperaram e 50 morreram espontaneamente ou foram submetidos à eutanásia quando moribundos. Os índices gerais de morbidade, mortalidade e letalidade foram, respectivamente, de 3,97%, 3,67% e 92,59%. A evolução clínica variou de 3-10 dias e os sinais eram caracterizados por depressão, corrimento nasal ou ocular, ranger de dentes, andar em círculos, cegueira, febre, nistagmo, tremores, anorexia, disfagia, sialorréia, incoordenação, pressão da cabeça contra objetos, pêlos arrepiados, taquicardia, taquipnéia, dor abdominal, melena, quedas, decúbito, opistótono, convulsões e movimentos de pedalagem. Dezenove bezerros foram necropsiados. Achados de necropsia foram caracterizados por hiperemia das leptomeninges, tumefação das porções rostrais do telencéfalo, com achatamento das circunvoluções dos lobos frontais; nessas áreas havia focos marrom-amarelados e amolecidos (malacia). Nos casos de evolução clínica mais longa era observada acentuada tumefação, amolecimento e extensas áreas de hemorragia nos lobos frontais telencefálicos. Microscopicamente, todos os bovinos afetados apresentaram meningoencefalite não-supurativa e necrosante, que variou quanto à localização e intensidade nos 19 casos examinados e nas seções de encéfalo de um mesmo caso. A intensidade dessas lesões foi mais acentuada, em ordem decrescente, no córtex telencefálico frontal, nos núcleos da base, tálamo, tronco encefálico, córtex parietal, córtex occipital e cerebelo. O infiltrado inflamatório perivascular era constituído predominantemente por linfócitos e plasmócitos e, menos freqüentemente, neutrófilos. Outros achados incluíam variados graus de gliose, edema, necrose neuronal no córtex telencefálico, caracterizada por encarquilhamento e eosinofilia do citoplasma e picnose nuclear (neurônio vermelho), corpúsculos de inclusão basofílicos intranucleares em astrócitos e neurônios (21,05% dos casos), satelitose e neuronofagia. As áreas de amolecimento do parênquima eram caracterizadas por necrose do componente neuroectodérmico e manutenção das estruturas mesenquimais (vasos e micróglia), com infiltrado de células Gitter e, em casos mais graves, áreas de hemorragia. Nos casos crônicos apenas estruturas vasculares e poucas células Gitter permaneciam, formando uma cavidade entre a substância branca e as leptomeninges (lesão residual).

Fetal alcohol spectrum disorders in Finnish children and adolescents : diagnosis, cognition, behavior, adaptation and brain metabolic alterations

Alcohol consumption during pregnancy can potentially affect the developing fetus in devastating ways, leading to a range of physical, neurological, and behavioral alterations most accurately termed Fetal Alcohol Spectrum Disorders (FASD). Despite the fact that it is a preventable disorder, prenatal alcohol exposure today constitutes a leading cause of intellectual disability in the Western world. In Western countries where prevalence studies have been performed the rates of FASD exceed, for example, autism spectrum disorders, Down’s syndrome and cerebral palsy. In addition to the direct effects of alcohol, children and adolescents with FASD are often exposed to a double burden in life, as their neurological sequelae are accompanied by adverse living surroundings exposing them to further environmental risk. However, children with FASD today remain remarkably underdiagnosed by the health care system. This thesis forms part of a larger multinational research project, The Collaborative Initiative on Fetal Alcohol Spectrum Disorders (the CIFASD), initiated by the National Institute of Alcohol Abuse and Alcoholism (NIAAA) in the U.S.A. The general aim of the present thesis was to examine a cohort of children and adolescents growing up with fetal alcohol-related damage in Finland. The thesis consists of five studies with a broad focus on diagnosis, cognition, behavior, adaptation and brain metabolic alterations in children and adolescents with FASD. The participants consisted of four different groups: one group with histories of prenatal exposure to alcohol, the FASD group; one IQ matched contrast group mostly consisting of children with specific learning disorder (SLD); and two typically-developing control groups (CON1 and CON2). Participants were identified through medical records, random sampling from the Finnish national population registry and email alerts to students. Importantly, the participants in the present studies comprise a group of very carefully clinically characterized children with FASD as the studies were performed in close collaboration with leading experts in the field (Prof. Edward Riley and Prof. Sarah Mattson, Center for Behavioral Teratology, San Diego State University, U.S.A; Prof. Eugene Hoyme, Sanford School of Medicine, University of South Dakota, U.S.A.). In the present thesis, the revised Institute of Medicine diagnostic criteria for FASD were tested on a Finnish population and found to be a reliable tool for differentiating among the subgroups of FASD. A weighted dysmorphology scoring system proved to be a valuable additional adjunct in quantification of growth deficits and dysmorphic features in children with FASD (Study 1). The purpose of Study 2 was to clarify the relationship between alcohol-related dysmorphic features and general cognitive capacity. Results showed a significant correlation between dysmorphic features and cognitive capacity, suggesting that children with more severe growth deficiency and dysmorphic features have more cognitive limitations. This association was, however, only moderate, indicating that physical markers and cognitive capacity not always go hand in hand in individuals with FASD. Behavioral problems in the FASD group proved substantial compared to the typically developing control group. In Study 3 risk and protective factors associated with behavioral problems in the FASD group were explored further focusing on diagnostic and environmental factors. Two groups with elevated risks for behavioral problems emerged: length of time spent in residential care and a low dysmorphology score proved to be the most pervasive risk factor for behavioral problems. The results underscore the clinical importance of appropriate services and care for less visibly alcohol affected children and highlight the need to attend to children with FASD being raised in institutions. With their background of early biological and psychological impairment compounded with less opportunity for a close and continuous caregiver relationship, such children seem to run an especially great risk of adverse life outcomes. Study 4 focused on adaptive abilities such as communication, daily living skills and social skills, in other words skills that are important for gradually enabling an independent life, maintain social relationships and allow the individual to become integrated into society. The results showed that adaptive abilities of children and adolescents growing up with FASD were significantly compromised compared to both typically-developing peers and IQ-matched children with SLD. Clearly different adaptive profiles were revealed where the FASD group performed worse than the SLD group, who in turn performed worse than the CON1 group. Importantly, the SLD group outperformed the FASD group on adaptive behavior in spite of comparable cognitive levels. This is the first study to compare adaptive abilities in a group of children and adolescents with FASD relative to both a contrast group of IQ-matched children with SLD and to a group of typically-developing peers. Finally, in Study 5, through magnetic resonance spectroscopic imaging (MRS) evidence of longstanding neurochemical alterations were observed in adolescents and young adults with FASD related to alcohol exposure in utero 14-20 years earlier. Neurochemical alterations were seen in several brain areas: in frontal and parietal cortices, corpus callosum, thalamus and frontal white matter areas as well as in the cerebellar dentate nucleus. The findings are compatible with neuropsychological findings in FASD. Glial cells seemed to be more affected than neurons. In conclusion, more societal efforts and resources should be focused on recognizing and diagnosing FASD, and supporting subgroups with elevated risk of poor outcome. Without adequate intervention children and adolescents with FASD run a great risk of marginalization and social maladjustment, costly not only to society but also to the lives of the many young people with FASD.

Polioencefalomalacia em bovinos: epidemiologia, sinais clínicos e distribuição das lesões no encéfalo

Trinta e um casos de polioencefalomalacia (PEM) diagnosticados de 1999-2008 em bovinos do Sul (13 casos) e Centro-Oeste (18 casos) brasileiros foram estudados. As taxas de morbidade (0,04%-6,66 %), mortalidade (0,04%-6,66 %) e letalidade (50%-100%) foram semelhantes em ambas as regiões estudadas. Não houve uma associação clara entre os casos de PEM e a idade, sexo dos bovinos e sazonalidade. Os casos ocorreram principalmente em bovinos criados de forma extensiva em pastagem. Na Região Sul a doença afetou principalmente bovinos jovens (um ano de idade ou menos), enquanto que principalmente bovinos mais velhos (3 anos de idade ou mais) foram afetados no Centro-Oeste. Os sinais clínicos mais frequentemente observados incluíram cegueira, incoordenação, andar em círculos, opistótono, decúbito e movimentos de pedalagem. A evolução do quadro clínico variou de 12 horas a 8 dias (media 3 dias e meio). Em 11 encéfalos não foram observadas alterações macroscópicas; as principais alterações macroscópicas nos outros casos incluíam congestão com tumefação e achatamento das circunvoluções, amolecimento e amarelamento do córtex telencefálico, focos de hemorragia no tronco encefálico, cerebelo e telencéfalo e herniação cerebelar. As principais alterações histológicas ocorreram no córtex dos lobos telencefálicos occipital, parietal e frontal; no entanto, lesões menos acentuadas e menos frequentemente observadas ocorreram no hipocampo, núcleos da base, tálamo, mesencéfalo e cerebelo. O tipo de lesão microscópica cortical era consistente em todos os casos e incluía necrose neuronal (neurônio vermelho) laminar segmentar, espongiose, tumefação do núcleo das células endoteliais, astrócitos Alzheimer tipo II e infiltração por células gitter. Em 20% dos casos havia um leve infiltrado celular linfo-histiocitário e em 13% dos casos havia leve infiltrado de neutrófilos e eosinófilos. Adicionalmente, lesões necro-hemorrágicas leves ou moderadas foram observadas em 49% dos casos nos núcleos da base, em 39% dos casos no tronco encefálico e em 26% dos casos no tálamo. Lesões telencefálicas foram consistentemente observadas nas lâminas dos córtices dos lobos occipital, parietal e frontal. Nessas regiões as camadas granular externa e interna foram as mais afetadas tanto por neurônios necróticos quanto por edema em todas as regiões avaliadas. Tanto os giros quanto os sulcos foram afetados igualmente.

Distribuição do vírus rábico no sistema nervoso central em ruminantes naturalmente infectados

Com o objetivo de identificar a distribuição das lesões do vírus rábico no sistema nervoso central de casos espontâneos de raiva em ruminantes e comparar as técnicas de imunofluorescência direta (IFD), inoculação em camundongos (ICC) e presença de corpúsculos de Negri para o diagnóstico da doença foram analisados materiais proveniente de 48 casos de raiva, incluindo amostras de córtex frontal, temporal, parietal e occipital, hipocampo, tálamo, colículo rostral e caudal, cerebelo, ponte, medula oblonga, núcleo da base e porções da medula cervical, torácica e lombar. De 48 amostras analisadas, todas foram positivas na IFD e na ICC e em 30 (62,5%) foram encontrados corpúsculo de Negri (CN). No entanto, houve diferenças importantes no resultados dos três testes nas diferentes regiões do SNC avaliadas. Nos cortes de córtex cerebral, em 38 bovinos, a presença de corpúsculos de inclusão foi baixa (11%-37%) assim como a positividade para IFD e ICC (60-80%). Pelo contrário, todas as amostras de ponte, tálamo e medula testados foram positivas para IFD e ICC. Em outras regiões do tronco encefálico e também no cerebelo a positividade para ICC e IFD foi de 60% a 96,7%. No cerebelo foi encontrada a maior frequência (88,2%) de corpúsculos de inclusão. Em oito ovinos as provas de ICC e IFD foram positivas em todos os cortes e foram observados corpúsculos de inclusão em três animais. Foram analisados somente dois casos de caprinos encontrando-se corpúsculos de inclusão em um e ambos foram positivos para IFD e ICC. Os resultados obtidos nesse trabalho sugerem que a conduta recomendada pelo Manual Técnico de Controle da Raiva dos Herbívoros (MTCRH) permite o diagnóstico de raiva associando o estudo histológico aos testes de IFD e ICC que incluem cerebelo, tálamo e tronco encefálico que apresentam alta positividade para as provas de IFD e ICC. No entanto, a melhor conduta é a de incluir metade do encéfalo cortado longitudinalmente e amostras de medula. Isto permite examinar por IFD e ICC uma ou mais regiões onde essas provas apresentam maior positividade e, posteriormente, se essas provas fossem negativas, retornar ao material original e examinar outras regiões. Por outro lado, a coleta de amostras dos locais recomendados pela MTCRH, assim com a coleta de metade do encéfalo, podem prejudicar o diagnóstico de outras doenças para o qual é necessário o estudo de todo o encéfalo após a fixação em formaldeído, para constatar a simetria e a distribuição das lesões. Nestes casos, com base nos resultados obtidos neste trabalho, pode ser recomendado para diagnóstico laboratorial de raiva o envio exclusivo de porções da medula cervical, dorsal e lombar, já que as três porções apresentaram 100% de positividade nas provas de IFD e ICC. Além disso, o estudo histológico de todas as porções do cérebro incluídas neste trabalho permitirá complementar o diagnóstico.

Anatomia comparativa da dura-máter de Sapajus libidinosus

O Sapajus libidinosus é um primata do novo mundo popularmente conhecido como macaco-prego, geograficamente distribuído por todo território sul-americano, possui características de inquietude e habilidade de manipulação de ferramentas para a obtenção de alimentos. Este estudo teve por objetivo descrever a morfologia dos seios da dura-máter de Sapajus libidinosus numa perspectiva comparativa. Foram utilizados um total de 3 animais adultos e machos oriundos da Universidade Federal de Goiás e fixados em solução aquosa de formaldeído 10%. No encéfalo de S. libidinosus, foi possível observar a fissura longitudinal, profunda e que divide o mesmo em dois hemisférios, esquerdo e direito. O lobo parietal e frontal apresenta-se relativamente lisoencefálico, mas com giros e sulcos bem definidos e no lobo occipital nota-se a predominância do aspecto lisencefálico. Nota-se a presença de 8 seios da dura-máter, que corresponde de modo geral às descrições para outros primatas como Pan, Papio e homem. Notamos a presença dos seios sagital dorsal, seio sagital ventral, seio transverso, seio reto, seio sigmóide, seio temporal e seio basilar, que são semelhantes a Pan, Papio e homem, a presença do seio parietal semelhante à Saimiri sciureus e a ausência do seio occipital, assim como em Macaca mullata. No macaco prego não foram observados os seios intracavernosos, seio esfenoparietal, seio petroso superior, seio petroso inferior, sendo estes descritos em Pan, Papio e Homem. Sendo assim, estes dados demonstram uma possível maior proximidade evolutiva entre Papio e Pan em relação ao homem do que o macaco Sapajus.

Involvement of the hippocampus, amygdala, entorhinal cortex and posterior parietal cortex in memory consolidation

A total of 182 young adult male Wistar rats were bilaterally implanted with cannulae into the CA1 region of the dorsal hippocampus and into the amygdaloid nucleus, the entorhinal cortex, and the posterior parietal cortex. After recovery, the animals were trained in a step-down inhibitory avoidance task. At various times after training (0, 30, 60 or 90 min) the animals received a 0.5-µl microinfusion of vehicle (saline) or 0.5 µg of muscimol dissolved in the vehicle. A retention test was carried out 24 h after training. Retention test performance was hindered by muscimol administered into both the hippocampus and amygdala at 0 but not at 30 min posttraining. The drug was amnestic when given into the entorhinal cortex 30, 60 or 90 min after training, or into the parietal cortex 60 or 90 min after training, but not before. These findings suggest a sequential entry operation, during the posttraining period, of the hippocampus and amygdala, the entorhinal cortex, and the posterior parietal cortex in memory processing

Rapid eye movement (REM) sleep deprivation reduces rat frontal cortex acetylcholinesterase (EC 3.1.1.7) activity

Rapid eye movement (REM) sleep deprivation induces several behavioral changes. Among these, a decrease in yawning behavior produced by low doses of cholinergic agonists is observed which indicates a change in brain cholinergic neurotransmission after REM sleep deprivation. Acetylcholinesterase (Achase) controls acetylcholine (Ach) availability in the synaptic cleft. Therefore, altered Achase activity may lead to a change in Ach availability at the receptor level which, in turn, may result in modification of cholinergic neurotransmission. To determine if REM sleep deprivation would change the activity of Achase, male Wistar rats, 3 months old, weighing 250-300 g, were deprived of REM sleep for 96 h by the flower-pot technique (N = 12). Two additional groups, a home-cage control (N = 6) and a large platform control (N = 6), were also used. Achase was measured in the frontal cortex using two different methods to obtain the enzyme activity. One method consisted of the obtention of total (900 g supernatant), membrane-bound (100,000 g pellet) and soluble (100,000 g supernatant) Achase, and the other method consisted of the obtention of a fraction (40,000 g pellet) enriched in synaptic membrane-bound enzyme. In both preparations, REM sleep deprivation induced a significant decrease in rat frontal cortex Achase activity when compared to both home-cage and large platform controls. REM sleep deprivation induced a significant decrease of 16% in the membrane-bound Achase activity (nmol thiocholine formed min-1 mg protein-1) in the 100,000 g pellet enzyme preparation (home-cage group 152.1 ± 5.7, large platform group 152.7 ± 24.9 and REM sleep-deprived group 127.9 ± 13.8). There was no difference in the soluble enzyme activity. REM sleep deprivation also induced a significant decrease of 20% in the enriched synaptic membrane-bound Achase activity (home-cage group 126.4 ± 21.5, large platform group 127.8 ± 20.4, REM sleep-deprived group 102.8 ± 14.2). Our results suggest that REM sleep deprivation changes Ach availability at the level of its receptors through a decrease in Achase activity

Spreading depression is facilitated in adult rats previously submitted to short episodes of malnutrition during the lactation period

Lactating rat dams were submitted to short episodes (1, 2 or 3 weeks) of nutritional restriction by receiving the "regional basic diet" (RBD, with 8% protein) of low-income human populations of Northeast Brazil. Their pups were then studied regarding the developmental effects on body and brain weights. When the rats reached adulthood, cortical susceptibility to the phenomenon of spreading depression (SD) was evaluated by performing electrophysiological recordings on the surface of the cerebral cortex. SD was elicited at 20-min intervals by applying 2% KCl for 1 min to a site on the frontal cortex and its occurrence was monitored at 2 sites in the parietal region by recording the electrocorticogram and the slow potential change of SD. When compared to control rats fed a commercial diet with 23% protein, early malnourished rats showed deficits in body and brain weights (10% to 60% and 3% to 15%, respectively), as well as increases in velocity of SD propagation (10% to 20%). These effects were directly related to the duration of maternal dietary restriction, with pups malnourished for 2 or 3 weeks presenting more intense weight and SD changes than those malnourished for 1 week. The effects of 1-week restrictions on SD were less evident in the pups malnourished during the second week of lactation and were more evident in pups receiving the RBD during the third week. The results indicate that short episodes of early malnutrition during the suckling period can affect body and brain development, as well as the cortical susceptibility to SD during adulthood. The data also suggest that the third week of lactation is the period during which the brain is most sensitive to malnutrition, concerning the effects on SD

Effect of inhibitory avoidance training on [3H]-glutamate binding in the hippocampus and parietal cortex of rats

Glutamate receptors have been implicated in memory formation. The aim of the present study was to determine the effect of inhibitory avoidance training on specific [3H]-glutamate binding to membranes obtained from the hippocampus or parietal cortex of rats. Adult male Wistar rats were trained (0.5-mA footshock) in a step-down inhibitory avoidance task and were sacrificed 0, 5, 15 or 60 min after training. Hippocampus and parietal cortex were dissected and membranes were prepared and incubated with 350 nM [3H]-glutamate (N = 4-6 per group). Inhibitory avoidance training induced a 29% increase in glutamate binding in hippocampal membranes obtained from rats sacrificed at 5 min (P<0.01), but not at 0, 15, or 60 min after training, and did not affect glutamate binding in membranes obtained from the parietal cortex. These results are consistent with previous evidence for the involvement of glutamatergic synaptic modification in the hippocampus in the early steps of memory formation.

Nocardia otitidiscaviarum (GAM-5) induces parkinsonian-like alterations in mouse

Parkinson's disease, a major neurodegenerative disorder in humans whose etiology is unknown, may be associated with some environmental factors. Nocardia otitidiscaviarum (GAM-5) isolated from a patient with an actinomycetoma produced signs similar to Parkinson's disease following iv injection into NMRI mice. NMRI mice were infected intravenously with a non-lethal dose of 5 x 10(6) colony forming units of N. otitidiscaviarum (GAM-5). Fourteen days after bacterial infection, most of the 60 mice injected exhibited parkinsonian features characterized by vertical head tremor, akinesia/bradykinesia, flexed posture and postural instability. There was a peak of nocardial growth in the brain during the first 24 h followed by a decrease, so that by 14 days nocardiae could no longer be cultured. At 24 h after infection, Gram staining showed nocardiae in neurons in the substantia nigra and occasionally in the brain parenchyma in the frontal and parietal cortex. At 21 days post-infection, tyrosine hydroxylase immunolabeling showed a 58% reduction of tyrosine hydroxylase in the substantia nigra, and a 35% reduction of tyrosine hydroxylase in the ventral tegmental region. Dopamine levels were reduced from 110 ± 32.5 to 58 ± 16.5 ng/mg protein (47.2% reduction) in brain from infected mice exhibiting impaired movements, whereas serotonin levels were unchanged (191 ± 44 protein in control and 175 ± 39 ng/mg protein in injected mice). At later times, intraneuronal inclusion bodies were observed in the substantia nigra. Our observations emphasize the need for further studies of the potential association between Parkinson's disease or parkinsonism-like disease and exposure to various nocardial species.

Late-life depression, heart failure and frontal white matter hyperintensity: a structural magnetic resonance imaging study

The relevance of the relationship between cardiac disease and depressive symptoms is well established. White matter hyperintensity, a bright signal area in the brain on T2-weighted magnetic resonance imaging scans, has been separately associated with cardiovascular risk factors, cardiac disease and late-life depression. However, no study has directly investigated the association between heart failure, major depressive symptoms and the presence of hyperintensities. Using a visual assessment scale, we have investigated the frequency and severity of white matter hyperintensities identified by magnetic resonance imaging in eight patients with late-life depression and heart failure, ten patients with heart failure without depression, and fourteen healthy elderly volunteers. Since the frontal lobe has been the proposed site for the preferential location of white matter hyperintensities in patients with late-life depression, we focused our investigation specifically on this brain region. Although there were no significant group differences in white matter hyperintensities in the frontal region, a significant direct correlation emerged between the severity of frontal periventricular white matter hyperintensity and scores on the Hamilton scale for depression in the group with heart failure and depression (P = 0.016, controlled for the confounding influence of age). There were no significant findings in any other areas of the brain. This pattern of results adds support to a relationship between cardiovascular risk factors and depressive symptoms, and provides preliminary evidence that the presence of white matter hyperintensities specifically in frontal regions may contribute to the severity of depressive symptoms in cardiac disease.

Use of magnitude-squared coherence to identify the maximum driving response band of the somatosensory evoked potential

The present study proposes to apply magnitude-squared coherence (MSC) to the somatosensory evoked potential for identifying the maximum driving response band. EEG signals, leads [Fpz'-Cz'] and [C3'-C4'], were collected from two groups of normal volunteers, stimulated at the rate of 4.91 (G1: 26 volunteers) and 5.13 Hz (G2: 18 volunteers). About 1400 stimuli were applied to the right tibial nerve at the motor threshold level. After applying the anti-aliasing filter, the signals were digitized and then further low-pass filtered (200 Hz, 6th order Butterworth and zero-phase). Based on the rejection of the null hypothesis of response absence (MSC(f) > 0.0060 with 500 epochs and the level of significance set at a = 0.05), the beta and gamma bands, 15-66 Hz, were identified as the maximum driving response band. Taking both leads together ("logical-OR detector", with a false-alarm rate of a = 0.05, and hence a = 0.0253 for each derivation), the detection exceeded 70% for all multiples of the stimulation frequency within this range. Similar performance was achieved for MSC of both leads but at 15, 25, 35, and 40 Hz. Moreover, the response was detected in [C3'-C4'] at 35.9 Hz and in [Fpz'-Cz'] at 46.2 Hz for all members of G2. Using the "logical-OR detector" procedure, the response was detected at the 7th multiple of the stimulation frequency for the series as a whole (considering both groups). Based on these findings, the MSC technique may be used for monitoring purposes.

Proton magnetic resonance spectroscopy of the frontal, cingulate and perirolandic cortices and its relationship to skin conductance in patients with schizophrenia

The aim of the present study was to determine whether specific subgroups of schizophrenic patients, grouped according to electrodermal characteristics, show differences in the N-acetylaspartate/creatine plus choline (NAA / (Cr + Cho)) ratios in the frontal, cingulate and perirolandic cortices. Skin conductance levels (SCL) and skin conductance responses to auditory stimulation were measured in 38 patients with schizophrenia and in the same number of matched healthy volunteers (control). All subjects were submitted to multivoxel proton magnetic resonance spectroscopic imaging. When compared to the control group, patients presented significantly lower NAA / (Cr + Cho) ratios in the right dorsolateral prefrontal cortex (schizophrenia = 0.95 ± 0.03; control = 1.12 ± 0.04) and in the right (schizophrenia = 0.88 ± 0.02; control = 0.94 ± 0.03) and left (schizophrenia = 0.84 ± 0.03; control = 0.94 ± 0.03) cingulates. These ratios did not differ between electrodermally responsive and non-responsive patients. When patients were divided into two groups: lower SCL (less than the mean SCL of the control group minus two standard deviations) and normal SCL (similar to the control group), the subgroup with a lower level of SCL showed a lower NAA / (Cr + Cho) ratio in the left cingulate (0.78 ± 0.05) than the controls (0.95 ± 0.02, P < 0.05) and the subgroup with normal SCL (0.88 ± 0.03, P < 0.05). There was a negative correlation between the NAA / (Cr + Cho) ratio in the left cingulate of patients with schizophrenia and the duration of the disease and years under medication. These data suggest the existence of a schizophrenic subgroup characterized by low SCL that could be a consequence of the lower neuronal viability observed in the left cingulate of these patients.