Association between cerebral palsy and microscopically verified placental infarction in extremely preterm infants.

INTRODUCTION: Previously, cerebral palsy has been associated with placental infarctions diagnosed macroscopically by midwifes. However, the risk of misclassification of infarctionsis is high without a histological verification. Therefore, the objective of this study was to study placental histopathology in relation to developmental outcome at 2.5 years corrected age in a population born extremely preterm. MATERIAL AND METHODS: A prospective cohort study was carried out at Karolinska University Hospital, Stockholm, Sweden on a population of 139 live born infants delivered <27 gestational weeks during 2004-2007. A senior perinatal pathologist, who was blinded to outcome data, evaluated all placental slides microscopically. Neuromotor and sensory functions of the children were evaluated. Bayley Scales of Infant and Toddler Development-III (Bayley-III) were used to assess development at corrected age 2.5 years. The outcome data were evaluated without reference to obstetrical and pathology data. The primary outcome measure was neurological and developmental status at 2.5 years of corrected age. This was measured as diagnosis of cerebral palsy, visual impairment, hearing impairment as well as performance on Bayley-III scales evaluating cognitive, language and motor functions. RESULTS: Two out of seven children with placental infarction were diagnosed with cerebral palsy compared with one child of 51 without placental infarction (p = 0.036). For developmental outcome according to Bayley-III at 2.5 years no statistically significant associations with placental pathology were found. CONCLUSION: A possible association between placental infarction, verified by microscopic examination, and cerebral palsy has been identified in this extremely preterm population.

Psychosis post corona radiata and lentiform nucleus infarction.

Complications of stroke can include neuropsychiatric symptoms. However, post-stroke psychosis is rare. We report a case where an acute presentation of psychosis, depression and fluctuating cognitive impairment in a middle-aged man turned out to be related to a silent brain infarction. The patient had a background of poorly controlled type 2 diabetes mellitus with glycated haemoglobin level of 9.0-11.0%, hypertension and ischaemic heart disease. His CT brain results showed multifocal infarct with hypodensities at bilateral lentiform nucleus and bilateral corona radiata. His strong genetic predisposition of psychosis and a history of brief psychotic disorder with complete remission 3 years prior to the current presentation might possibly contribute to his post-stroke atypical neuropsychiatric presentation, and posed diagnostic challenges. He showed marked improvement with risperidone 6 mg nocte, chlorpromazine 50 mg nocte and fluvoxamine of 200 mg nocte. The need of comprehensive treatments to modify his stroke risk factors was addressed.

Conhecimento sobre a doença e mudança de estilo de vida em pessoas pós-infarto / Knowledge on disease and lifestyle changes in patients post-infarction / Conocimiento sobre la enfermedad y cambio de estilo de vida en personas post-infarto

Pesquisa descritiva que teve como objetivo identificar conhecimento sobre a doença e as mudanças de estilo de vida em pessoas pós-infarto. Foram entrevistadas 31 pessoas acompanhadas em uma Unidade de Saúde da Família. Com relação ao conhecimento, apenas 15% das pessoas souberam definir a doença e 74% souberam referir apenas de uma a duas causas. Em relação às mudanças de estilo de vida, 58% das pessoas entrevistadas não modificaram seu estilo de vida em função do infarto. É amplo o conhecimento na literatura científica sobre os fatores de risco para o infarto, no entanto, este estudo mostra que deve ser dada atenção à população que já foi acometida pela doença, pois essa ainda possui poucas informações relativas à doença e sua prevenção, sendo um dos fatores que contribuíram para a não mudança de estilo de vida.

The objective of this descriptive study was to identify the knowledge that people acquire after suffering an infarction and the lifestyle changes they make. Interviews were conducted with 31 people followed at a Family Health Unit. Regarding their knowledge, only 15% of the subjects were able to define the disease and 74% were able to state only one or two causes. Regarding lifestyle changes, 58% of the subjects did not make any changes to their lifestyle based on the infarction. There is broad knowledge in scientific literature regarding the risk factors for infarction; however, this study shows that closer attention should be given to the population that has been affected by the disease, as they have little information on the disease and on how to prevent it, which is one of the factors that contributed to their not changing their lifestyle.

Investigación descriptiva que tuvo como objetivo identificar conocimiento sobre la enfermedad y los cambios de estilo de vida en personas post-infarto. Fueron entrevistadas 31 personas en seguimiento en una Unidad de Salud de la Familia. En relación al acontecimiento, apenas 15% de los entrevistados supieron definir la enfermedad, el 74% supo referir entre una y dos causas. En relación a los cambios de estilo de vida, el 58% de las personas no lo modificó en función del infarto. Es amplio el conocimiento en la literatura científica acerca de los factores de riesgo para el infarto; no obstante, este estudio muestra que debe prestarse atención a la población que ya padeció la enfermedad, dado que poseen aún escasas informaciones relativas a la misma y su prevención, siendo éste uno de los factores que contribuyó para que no cambien su estilo de vida.

El corazón delator: algunas reflexiones desde el psicoanálisis a propósito de los infartos cardiovasculares y la época actua / The tell-tale heart: some reflections from psychoanalysis on cardiovascular infarcts and the current epoch

Este artículo presenta algunas conjeturas derivadas del análisis de entrevistas realizadas con sujeto que han padecido enfermedades cardiovasculares, específicamente infarto. Se ponen aquí en evidencia algunas modalidades en las respuestas del sujeto ante la angustia y el encuentro con lo que Freud denominó sentimiento inconsciente de culpa, particularmente por la vía del masoquismo moral.

This article presents some conjectures derived from the analysis of interviews conducted with subjects who have suffered from cardiovascular diseases, specifically heart attack. Some modalities in the responses of the subject to anxiety and the encounter with what Freud called the unconscious feeling of guilt are brought out here, particularly by way of moral masochism.

[Cognitive disturbances in cerebellum infarctions]. / Kognitivnye narusheniia pri infarktakh mozzhechka.

The influence of the cerebellum on cognitive functions (CF) is poorly known and understudied so far. Neurological, neuropsychological and neuroimaging non-randomized study was carried out in 25 patients (14 women, 11 men, mean age 51.8 +/- 18.0 years) with isolated cerebellum infarctions. Cognitive disturbances (CD) were detected in 22 (88%) patients. They included impairment of attention, planning, control, abstract reasoning, memory; speech (naming, fluency, agrammatism, dysprosodia), special visual, quasi-spatial and counting disorders that indicated dysfunction of the anterior and posterior associative areas of the brain cortex. The expression of CD was different: being clinically obvious in 6 patients (24%), they were found only by neuropsychological methods in 16 patients (64%). Clinically significant CD developed in the lesions of certain areas (posterior-lower- lateral and posterior-medial) of the cerebellum hemisphere related to the dominant brain hemisphere. The presence of these CD did not depend on infarctions size: in expressed CD it was smaller (mean 5.65 cm3) than in other cases (mean 12.8 cm3). Typical appearances of cerebellum infarction (ataxia, vertigo, vomiting) were observed in all the patients with clinically non-significant CD and only in 2 out of 6 with clinically significant CD. The study demonstrated a role of the cerebellum in CF modulation. The expression of CD in cerebellum infarctions depends on their localization. Topic localization of the cerebellum areas, controlling CD and movement, is different.

Autobiographical amnesia resulting from bilateral paramedian thalamic infarction. A case study in cognitive neurobiology.

A patient with a chronic amnesic state resulting from bilateral paramedian thalamic infarction showed a pattern of retrograde amnesia not previously reported. Personally relevant autobiographical memory was profoundly impaired, whereas knowledge of famous people and public events was relatively spared. Furthermore, knowledge of famous people, including the ability to make accurate temporal judgements, was less affected than knowledge of public events. In addition, we have documented a severe and systematic distortion of personal memory. These findings are not compatible with current accounts of retrograde amnesia based either upon the type of information stored (e.g. episodic versus semantic memory), or upon simple storage versus access models. We propose an explanation based upon an interactive cognitive model in which the patient shows a disorder at the 'thematic retrieval framework' level of memory organization due to a disconnection of frontal and medial temporal memory systems.

Left tuberothalamic artery territory infarction: neuropsychological and MRI features.

We examined a 29-year-old woman who had language disturbances and memory impairment after a left thalamic infarction. MRI showed injury that was limited to the tuberothalamic artery territory. Beside reduced voice volume and verbal memory trouble, she presented with aspontaneity, loss of psychic self-activation and affective drive. Considering thalamic lesions, this loss of psychic self-activation or 'athymhormie' was found in a left thalamic infarct and could not be considered as an exclusive characteristic of bithalamic infarctions. The disappearance of the neurobehavioral disturbances within 15 days after the onset of the troubles was associated with the decreasing of the mass lesion found by MRI.

Frontal lobe dysfunction in unilateral lenticulostriate infarcts. Prominent role of cortical lesions.

Most studies on frontal lobe dysfunction (FLD) in patients with striatal lesions did not consider possible associated cortical lesions not seen on computed tomographic scans. To determine the possible role of such cortical lesions, we assessed FLD in 10 patients with unilateral lenticulostriate infarct on computed tomographic scans. Magnetic resonance imaging revealed an associated cortical infarct not seen on computed tomographic scans in four patients. Using a battery of neuropsychological tests sensitive to FLD, we found that (1) the crossed tapping test was the only FLD test significantly disturbed in patients with pure unilateral lenticulostriate infarcts, (2) FLD was only present in patients with associated cortical infarct, and (3) caudate lesions only account for the number of echopraxic errors in the crossed tapping test. We conclude that unilateral isolated lenticulostriate infarcts might not lead to FLD, even though they may disturb the development of strategies involved in motor procedural learning.

Brain energy metabolism in bilateral paramedian thalamic infarcts. A positron emission tomography study.

Positron emission tomography (PET) studies of the cerebral metabolic rate of oxygen (CMRO2) were performed in seven consecutive patients with bilateral paramedian thalamic infarcts (BPTI), selected on neuroradiological and clinical criteria. The latter consisted of sudden onset of coma or confusion followed by a persistent amnesia of varying severity, with or without language impairment and frontal lobe signs. There was a highly significant decrease of CMRO2 for the whole cortex as well as for all the regions analysed: medial-frontal, latero-frontal, temporal, sensorimotor and posterior associative cortex. The mean regional metabolic ratios (region/whole cortex CMRO2) were not significantly different from controls, indicating an essentially uniform effect in the cortex, except the sensorimotor ratio which was significantly increased. Diffuse cortical hypometabolism most likely reflects thalamo-cortical deafferentation secondary to damage to the 'non-specific' thalamic nuclei, while sparing of the latero-ventral thalamus presumably explains the relative preservation of the sensorimotor cortex metabolism. Although no clear-cut individual relationship was found between magnitude of cortical hypometabolism and the severity and pattern of neuropsychological impairment, the data suggest that the former underlies and/or reflects the latter. Further studies with higher resolution PET devices might shed more light on the relationships between distinct cognitive patterns and specific topography of cortical hypometabolism in BPTI patients.

Further analysis of the psychometric properties of the Levine Denial of Illness Scale.

This study contributes cross-validational data with regard to the Levine Denial of Illness Scale from a sample of 152 hospitalized myocardial infarction patients. A factor analysis and subsequent examination of the data yielded four usable factors of denial termed: Cognitive Denial of Illness, Denial of Impact on Future, Denial of Need for Care, and Affective Denial. In an analysis of subscale correlations, these four factor-based scales were related, but distinguishable, thus supporting the idea of the multidimensionality of denial. Furthermore, these factors were not related to demographic variables. Correlating these four scales with standardized measures of affect indicated that it can be useful in research to distinguish between several types of denial of illness in myocardial infarction patients.

Photochemically induced graded spinal cord infarction. Behavioral, electrophysiological, and morphological correlates.

Neurological and morphological outcome was evaluated in a rat model of graded spinal cord infarction initiated by a photochemical reaction. In this model, light-dye interactions induce primary microvascular stasis, resulting in consistent patterns of tissue necrosis. Four groups of rats underwent photoinduction times ranging from 30 seconds to 10 minutes. Neurological and electrophysiological functions were assessed starting 1 week after irradiation and continuing for 8 weeks. A functional neurological score was obtained by combining results from sensory and motor tasks, and electrophysiological function was evaluated from the somatosensory evoked potential recordings. In rats irradiated for short periods (30 seconds and 1 minute) mild behavioral deficits were documented. In contrast, electrical conduction was suppressed acutely in both groups; this recovered by 8 weeks to baseline or near baseline in the 30-second group but not in the 1-minute group. In rats irradiated for longer periods (5 and 10 minutes), severe behavioral and conduction abnormalities were detected at both the subacute and chronic testing periods. Although no significant difference in behavior was documented between the 5- and 10-minute groups acutely, the rats with 5-minute photoinduction time demonstrated a significant improvement in behavior over time whereas the group with 10-minute photoinduction time showed no improvement. A severe conduction block was present in both animal groups during the course of the study. Histopathological examination combined with morphometric measurements of the lesion area in cross section revealed four different degrees of spinal cord necrosis which correlated significantly with photoinduction times and neurological scores at 8 weeks. Reproducible degrees of ischemic damage to spinal cord parenchyma following primary microvascular occlusion result in a predictable sequence of behavioral and functional abnormalities, which in some cases recover with time.

The syndrome of bilateral paramedian thalamic infarction.

Bilateral anterior paramedian thalamic infarction resulting from occlusion of a bilaterally distributed thalamosubthalamic paramedian artery was demonstrated on CT in two patients. Patient 1 presented with a transient coma followed by asterixis, hypersomnia, vertical gaze disturbances, profound Korsakoff amnesic syndrome, and a subcortical dementia. Patient 2, with a predominantly right-sided thalamic infarct, showed good recovery from amnesia and vertical gaze disturbances. However, patient 1 remained with severe amnesia and mild subcortical dementia at follow-up 1 year later. These and similar reported cases constitute a lacunar syndrome with characteristic clinical and CT features.