Disfagia no doente com AVC : prevalência e determinantes

Introdução: O acidente vascular cerebral (AVC) assume em Portugal elevadas taxas de morbilidade e reinternamento hospitalar. A disfagia surge como uma complicação frequente deste evento neurológico, com índices de morbilidade elevados pelo risco de desnutrição, desidratação e aspiração broncopulmonar. O diagnóstico e a sua monitorização no processo de reabilitação do doente são ações fundamentais na prevenção de aspirações alimentares, redução do internamento hospitalar e na eficácia da reabilitação do doente. Objetivo: Identificar e avaliar o grau de disfagia na pessoa com AVC e analisar a relação entre esta, e as variáveis socio-demográficas e clínicas no sentido de poder melhorar futuramente os cuidados de enfermagem de reabilitação. Métodos: Trata-se de um estudo não experimental, transversal, descritivo-correlacional de caráter quantitativo, que foi realizado numa amostra não probabilística por conveniência, constituída por 25 doentes com diagnóstico de AVC, internados na Rede Nacional Cuidados Continuados Integrados (RNCCI), em unidades de Convalescença e Reabilitação. O instrumento de colheita de dados integra uma seção de caracterização sócio-demográfica e clínica e duas escalas: Escala Gugging Swallowing Screen (GUSS) e Índice de Barthel, a fim de avaliar a disfagia e a funcionalidade, respetivamente. Resultados: A amostra apresenta uma média de idade de 76,8 anos, sendo 68% do sexo feminino e 32% do sexo masculino. Verificámos que 68% dos participantes apresenta mais de dois antecedentes clínicos e apenas 24% dos participantes não apresenta disfagia. Dos restantes, 12% apresenta disfagia grave, 36% moderada e 28% disfagia ligeira. A área de lesão parece influenciar a deglutição, demonstrando a Artéria Cerebral Média (ACM) e Artéria Cerebral Posterior (ACP) como áreas de maior sensibilidade. Denotou-se que quanto maior o grau de dependência, maior gravidade de disfagia. Conclusão: Doentes com AVC isquémico apresentam disfagia, com gravidade relacionada com a área vascular. A existência de vários antecedentes clínicos pode gerar perturbações na deglutição do doente. De igual modo, quanto maior for a dependência funcional do doente, maior é o grau de disfagia e o risco de aspiração pulmonar. Palavras-chave: AVC; Disfagia; Reabilitação.

Microglial Cells Prevent Hemorrhage in Neonatal Focal Arterial Stroke

Perinatal stroke leads to significant morbidity and long-term neurological and cognitive deficits. The pathophysiological mechanisms of brain damage depend on brain maturation at the time of stroke. To understand whether microglial cells limit injury after neonatal stroke by preserving neurovascular integrity, we subjected postnatal day 7 (P7) rats depleted of microglial cells, rats with inhibited microglial TGFbr2/ALK5 signaling, and corresponding controls, to transient middle cerebral artery occlusion (tMCAO). Microglial depletion by intracerebral injection of liposome-encapsulated clodronate at P5 significantly reduced vessel coverage and triggered hemorrhages in injured regions 24 h after tMCAO. Lack of microglia did not alter expression or intracellular redistribution of several tight junction proteins, did not affect degradation of collagen IV induced by the tMCAO, but altered cell types producing TGFβ1 and the phosphorylation and intracellular distribution of SMAD2/3. Selective inhibition of TGFbr2/ALK5 signaling in microglia via intracerebral liposome-encapsulated SB-431542 delivery triggered hemorrhages after tMCAO, demonstrating that TGFβ1/TGFbr2/ALK5 signaling in microglia protects from hemorrhages. Consistent with observations in neonatal rats, depletion of microglia before tMCAO in P9 Cx3cr1(GFP/+)/Ccr2(RFP/+) mice exacerbated injury and induced hemorrhages at 24 h. The effects were independent of infiltration of Ccr2(RFP/+) monocytes into injured regions. Cumulatively, in two species, we show that microglial cells protect neonatal brain from hemorrhage after acute ischemic stroke. SIGNIFICANCE STATEMENT The pathophysiological mechanisms of brain damage depend on brain maturation at the time of stroke. We assessed whether microglial cells preserve neurovascular integrity after neonatal stroke. In neonatal rats, microglial depletion or pharmacological inhibition of TGFbr2/ALK5 signaling in microglia triggered hemorrhages in injured regions. The effect was not associated with additional changes in expression or intracellular redistribution of several tight junction proteins or collagen IV degradation induced by stroke. Consistent with observations in neonatal rats, microglial depletion in neonatal mice exacerbated stroke injury and induced hemorrhages. The effects were independent of infiltration of monocytes into injured regions. Thus, microglia protect neonatal brain from ischemia-induced hemorrhages, and this effect is consistent across two species.

National training course, emergency medical technician - paramedic. Instructor's lesson plans. Module XIII: management of the emotionally disturbed.

Mode of access: Internet.

Blunted prolactin response to D-fenfluramine in post-stroke major depression

Background: This study investigated whether patients suffering from post-stroke depressive disorder had a similar disturbance in central serotonergic function to that described in non-brain injured depressed patients. Methods: Twenty-three depressed patients (nine major, 14 minor) and 38 non-depressed patients were examined 4-8 weeks post-stroke with a structured interview, rating scales and MRI brain scans. Patients were administered 30 mg D-fenfluramine orally and plasma prolactin and D-fenfluramine concentrations were measured for 6 h post-dose. Results: The prolactin response was significantly blunted in major depression compared to minor depression and non-depressed patients as measured by both delta prolactin and area under the prolactin versus time curve. There was no significant relationship between prolactin response and lesion lateralization or any of the measured clinical characteristics. Limitations: The major limitation of the study is the relatively small number in each depressive group. Conclusions: Patients suffering from major depression in the post-stroke period have a blunted prolactin response to D-fenfluramine. This indicates a serotonergic abnormality consistent with that found in major depression where neurological disease is not present. (C) 2003 Elsevier B.V. All rights reserved.

Alcoholic neurobiology: Changes in dependence and recovery

This article presents the proceedings of a symposium held at the meeting of the International Society for Biomedical Research on Alcoholism (ISBRA) in Mannheim, Germany, in October, 2004. Chronic alcoholism follows a fluctuating course, which provides a naturalistic experiment in vulnerability, resilience, and recovery of human neural systems in response to presence, absence, and history of the neurotoxic effects of alcoholism. Alcohol dependence is a progressive chronic disease that is associated with changes in neuroanatomy, neurophysiology, neural gene expression, psychology, and behavior. Specifically, alcohol dependence is characterized by a neuropsychological profile of mild to moderate impairment in executive functions, visuospatial abilities, and postural stability, together with relative sparing of declarative memory, language skills, and primary motor and perceptual abilities. Recovery from alcoholism is associated with a partial reversal of CNS deficits that occur in alcoholism. The reversal of deficits during recovery from alcoholism indicates that brain structure is capable of repair and restructuring in response to insult in adulthood. Indirect support of this repair model derives from studies of selective neuropsychological processes, structural and functional neuroimaging studies, and preclinical studies on degeneration and regeneration during the development of alcohol dependence and recovery from dependence. Genetics and brain regional specificity contribute to unique changes in neuropsychology and neuroanatomy in alcoholism and recovery. This symposium includes state-of-the-art presentations on changes that occur during active alcoholism as well as those that may occur during recovery-abstinence from alcohol dependence. Included are human neuroimaging and neuropsychological assessments, changes in human brain gene expression, allelic combinations of genes associated with alcohol dependence and preclinical studies investigating mechanisms of alcohol induced neurotoxicity, and neuroprogenetor cell expansion during recovery from alcohol dependence.

Genes and gene expression in the brains of human alcoholics

Chronic alcohol misuse by human subjects leads to neuronal loss in regions such as the superior frontal cortex (SFC). Propensity to alcoholism is associated with several genes. γ-Aminobutyric acid (GABA)A receptor expression differs between alcoholics and controls, whereas glutamate receptor differences are muted. We determined whether genotype differentiated the regional presentation of GABAA and glutamate-NMDA (N-methyl-d-aspartate) receptors in SFC. Autopsy tissue was obtained from alcoholics without comorbid disease, alcoholics with liver cirrhosis, and matched controls. ADH1C, DRD2B, EAAT2, and APOE genotypes modulated GABAA-β subunit protein expression in SFC toward a less-effective form of the receptor. Most genotypes did not divide alcoholics and controls on glutamate-NMDA receptor pharmacology, although gender and cirrhosis did. Genotype may affect amino acid transmission locally to influence neuronal vulnerability.

Progressive supranuclear palsy (PSP): general pathology and visual signs and symptoms

Progressive supranuclear palsy (PSP) is a rare, degenerative disorder of the brain believed to affect between 1.39 and 6.6 individuals per 100,000 of the population. The disorder is likely to be more common than suggested by these data due to difficulties in diagnosis and especially in distinguishing PSP from other conditions with similar symptoms such as multiple system atrophy (MSA), corticobasal degeneration (CBD), and Parkinson’s disease (PD). PSP was first described in 1964 by Steele, Richardson and Olszewski and originally called Steele-Richardson-Olszewski syndrome. The disorder is the second commonest syndrome in which the patient exhibits ‘parkinsonism’, viz., a range of problems involving movement most typically manifest in PD itself but also seen in PSP, MSA and CBD. Although primarily a brain disorder, patients with PSP exhibit a range of visual clinical signs and symptoms that may be useful in differential diagnosis. Hence, the present article describes the general clinical and pathological features of PSP, its specific visual signs and symptoms, discusses the usefulness of these signs in differential diagnosis, and considers the various treatment options.

Axis-based grouping reduces visual extinction

We examined the effects on extinction of grouping by collinearity of edges and grouping by alignment of internal axes of shapes, in a patient (GK) with simultanagnosia following bilateral parietal brain damage. GK’s visual extinction was reduced when items (equilateral triangles and angles) could be grouped by base alignment (i.e., collinearity) or by axis alignment, relative to a condition in which items were ungrouped. These grouping effects disappeared when inter-item spacing was increased, though factors such as display symmetry remained constant. Overall, the results suggest that, under some conditions, grouping by alignment of axes of symmetry can have an equal beneficial effect on visual extinction as edge-based grouping; thus, in the extinguished field, there is derivation of axis-based representations from the contours present.

A psychological investigation into the relationship between hemispheric functioning and specific written language difficulties (dyslexia), using pharmaceutical intervention techniques

This thesis attempts a psychological investigation of hemispheric functioning in developmental dyslexia. Previous work using neuropsychological methods with developmental dyslexics is reviewed ,and original work is presented both of a conventional psychometric nature and also utilising a new means of intervention. At the inception of inquiry into dyslexia, comparisons were drawn between developmental dyslexia and acquired alexia, promoting a model of brain damage as the common cause. Subsequent investigators found developmental dyslexics to be neurologically intact, and so an alternative hypothesis was offered, namely that language is abnormally localized (not in the left hemisphere). Research in the last decade, using the advanced techniques of modern neuropsychology, has indicated that developmental dyslexics are probably left hemisphere dominant for language. The development of a new type of pharmaceutical prep~ration (that appears to have a left hemisphere effect) offers an oppertunity to test the experimental hypothesis. This hypothesis propounds that most dyslexics are left hemisphere language dominant, but some of these language related operations are dysfunctioning. The methods utilised are those of psychological assessment of cognitive function, both in a traditional psychometric situation, and with a new form of intervention (Piracetam). The information resulting from intervention will be judged on its therapeutic validity and contribution to the understanding of hemispheric functioning in dyslexics. The experimental studies using conventional psychometric evaluation revealed a dyslexic profile of poor sequencing and name coding ability, with adequate spatial and verbal reasoning skills. Neuropsychological information would tend to suggest that this profile was indicative of adequate right hemsiphere abilities and deficits in some left hemsiphere abilities. When an intervention agent (Piracetam) was used with young adult dyslexics there were improvements in both the rate of acquisition and conservation of verbal learning. An experimental study with dyslexic children revealed that Piracetam appeared to improve reading, writing and sequencing, but did not influence spatial abilities. This would seem to concord with other recent findings, that deve~mental dyslexics may have left hemisphere language localisation, although some of these language related abilities are dysfunctioning.

Age effect in generating mental images of buildings but not common objects

Imagining a familiar environment is different from imagining an environmental map and clinical evidence demonstrated the existence of double dissociations in brain-damaged patients due to the contents of mental images. Here, we assessed a large sample of young and old participants by considering their ability to generate different kinds of mental images, namely, buildings or common objects. As buildings are environmental stimuli that have an important role in human navigation, we expected that elderly participants would have greater difficulty in generating images of buildings than common objects. We found that young and older participants differed in generating both buildings and common objects. For young participants there were no differences between buildings and common objects, but older participants found easier to generate common objects than buildings. Buildings are a special type of visual stimuli because in urban environments they are commonly used as landmarks for navigational purposes. Considering that topographical orientation is one of the abilities mostly affected in normal and pathological aging, the present data throw some light on the impaired processes underlying human navigation.

Mothers of Sparta

Mothers of Sparta is a collection of thirteen personal essays that examine place—knowing one’s place, and finding one’s place in the world. The narrative arc chronicles the narrator’s childhood, young adulthood, marriage and child rearing years, ultimately encompassing the difficulties of raising a child who, due to brain damage, faces an uncertain future. As the narrator grows older, place shifts from a concrete knowledge of the physical world around her, to learning her place within gendered and regional social constructs, and defining her place through roles such as wife, mother, student and writer. These essays are diverse in style. Woven throughout is a theme of violence, weighted with visceral language: the violence of accident and death, the violence that occurs in nature and in domestic spaces, and the violence that often goes unnoticed because we live in a violent world.

Rutiner i omvårdnad på intensivvårdavdelning av hjärnskadade patienter : Intervjustudie

Bakgrund: Traumatisk hjärnskada (THS) orsakas av våld mot huvud i samband med fallolyckor eller trafikolyckor. Varje år söker 20 000 personer vård på grund av skallskador. Vården för traumatiskt hjärnskadade patienter i Sverige skiljer sig åt, mycket beroende på avstånden som finns till specialistsjukhus, tiden och rätta åtgärder är avgörande faktorer för denna patientgrupp. Syfte: Att undersöka vikten och intensivvårdssjuksköterskors behov av rutiner i samband med vård av patienter med hjärnskador på allmänintensivvårdsavdelningar och på neurointensivvårdavdelningar. Metod: Kvalitativ studie med fokusgruppsintervjuer av tio intensivvårdsjuksköterskor som arbetar på en allmänintensivvårdsavdelning (IVA) och specialistneurointensivvårdavdelningen (NIVA). Resultat: På NIVA finns väl inarbetade rutiner och tydliga riktlinjer nedskrivna. Sjuksköterskornas upplevelse var att det fanns tillräckligt med rutiner, men några rutiner kunde utvecklas. På IVA fanns det inga nedskrivna riktlinjer och inga tydliga rutiner för att vårda denna patientgrupp. Vården och kontrollerna ordinerades av läkare som är i tjänst. Slutsats: Vården kring hjärnskadade patienter är ytterst viktigt då man ständigt måste förebygga sekundära skador/insulter. Rutiner är väl inarbetade på specialistsjukhuset, men vården börjar först på hemsjukhuset på IVA där tydliga rutiner och riktlinjer saknas.