How Well Do Neurochecks Perform After Stroke?

BACKGROUND: In the certification of stroke centers, the performance of serial nursing neurological assessments and reassessments, commonly known as neurochecks, is often cited as one of the most problematic standards. The role of neurochecks is to readily detect neurological change, but it is surprising that this practice has undergone relatively little scientific study. Their effectiveness in detecting worsening in acute ischemic stroke patients has not been well studied. Our objective was to investigate the sensitivity of neurochecks to detect neurological deterioration after acute ischemic stroke. We performed a retrospective chart review of patients with acute ischemic stroke who were admitted to a comprehensive stroke center over a 2-year period and who received intravenous thrombolysis. The incidence, reasons, and detection rates for neurological deterioration by neurochecks were collected during the first 72 hours of admission. RESULTS: A total of 231 patient records were reviewed. Over the first 72 hours of admission, each patient had a mean of 63±15 neurochecks. Neurological worsening as determined by a stroke neurologist was found in 62 (27%) patients. This deterioration was first detected by a scheduled neurocheck in 28 (45%) patients and was discovered by the nurse outside of a scheduled neurocheck in 16 (26%) patients. In 18 out of 62 (29%) patients, the worsening was not detected. CONCLUSIONS: Although neurochecks detected neurological deterioration in almost half of patients with acute stroke, a significant proportion of deteriorations were found outside scheduled assessments or remained undetected. This suggests that novel monitoring strategies are needed to readily identify worsening neurological status in acute stroke.

Perspectivas en el abordaje farmacológico de la Epilepsia: una revisión extensa de la farmacoterapia / Perspectives on the pharmacologic management of epilepsy: A comprehensive review

Resumen Antecedentes: La epilepsia constituye la tercera causa más común de trastorno neurológico que se reporta, secundario tan solo a eventos cerebrovasculares y enfermedad de Alzheimer. Se ha determinado que aproximadamente entre el 70% al 80% de los cuadros convulsivos son controlados exitosamente con monoterapia, aproximadamente el 10-15% con terapia combinada mientras que cerca del 10% no son controlados con terapia farmacológica solamente. Objetivo: El presente documento constituye una revisión bibliográfica que pretende exponer las alternativas en el abordaje actual de cuadros de epilepsia. No pretende hacer de guía terapéutica senso estricto, sino dotar al médico tratante de herramientas que simplifiquen la selección del fármaco apropiado de acorde a su criterio, circunstancias y realidad clínica. Metodología: Se recurrió a motores de búsqueda médicos, artículos y resúmenes, al igual que a guías publicadas por la ILAE con el objetivo de recolectar datos pertinentes e interpretar estos hallazgos. Conclusión: Mediante esta revisión se logró exponer criterios clásicos e innovadores abarcando la extensión del conocimiento actual respecto al abordaje farmacológico de la epilepsia.

Abstract Background: Epilepsy represents the third most common reported neurologic disorder, surpassed only by cerebrovascular accidents and Alzheimer's disease. Iyt is believed that around 70% to 80% of all convulsive disorders can be successfully controlled with monotherapy alone and an additional 10% to 15% with combination therapy. Around 10% of cases never achieve remission through pharmacological therapy alone. Objectives: Through this comprehensive review of the literature describing the current available pharmacologic therapies for the management of epilepsy and their recognized indications, the authors intend to provide an educational tool that could assist the general practitioner to make decisions when selecting a suitable treatment strategy according to a specific clinical scenario (and as guided by their own professional judgment, circumstances and clinical reality)-. Methods: We used a wide variety of medical search engines, articles and abstracts for the purpose of data collection and interpretation. Conclusions: Through this review the authors managed to present all current and innovative approaches regarding the pharmacologic management of epilepsy encompassing the scope of current knowledge.

Neuroimaging of Cerebral Small Vessel Disease and Age-Related Cognitive Changes.

Subclinical cerebrovascular disease is frequently identified in neuroimaging studies and is thought to play a role in the pathogenesis of cognitive disorders. Identifying the etiologies of different types of lesions may help investigators differentiate between age-related and pathological cerebrovascular damage in cognitive aging. In this review article, we aim to describe the epidemiology and etiology of various brain magnetic resonance imaging (MRI) measures of vascular damage in cognitively normal, older adult populations. We focus here on population-based prospective cohort studies of cognitively unimpaired older adults, as well as discuss the heterogeneity of MRI findings and their relationships with cognition. This review article emphasizes the need for a better understanding of subclinical cerebrovascular disease in cognitively normal populations, in order to more effectively identify and prevent cognitive decline in our rapidly aging population.

Neurogranin as a predictor of memory and executive function decline in MCI patients.

OBJECTIVE: To determine whether high CSF levels of neurogranin (Ng) predict longitudinal decline in memory and executive function during early-stage Alzheimer disease (AD). METHODS: Baseline levels of CSF Ng were studied in relation to cross-sectional and longitudinal cognitive performance over 8 years. Data were obtained from the Alzheimer's Disease Neuroimaging Initiative database, and participants with normal cognition (n = 111) and mild cognitive impairment (MCI) (n = 193) were included. RESULTS: High levels of CSF Ng were associated with poor baseline memory scores (ß = -0.21, p < 0.0001). CSF Ng predicted both memory and executive function decline over time (ß = -0.0313, p = 0.0068 and ß = -0.0346, p = 0.0169, respectively) independently of age, sex, education, and APOE ε4 status. When the rate of decline by tertiles was examined, CSF Ng was a level-dependent predictor of memory function, whereby the group with highest levels of Ng showed the fastest rates of decline in both memory and executive function. When examined separately, elevated Ng was associated with cognitive decline in participants with MCI but not in those with normal cognition. The levels of CSF Ng were not associated with cognitive measures when tau and amyloid 42 (Aß42) were controlled for in these analyses. CONCLUSIONS: High CSF Ng associates with poor memory scores in participants with MCI cross-sectionally and with poor memory and executive function longitudinally. The association of Ng with cognitive measures disappears when tau and Aß42 are included in the statistical models. Our findings suggest that CSF Ng may serve as a biomarker of cognition. Synaptic dysfunction contributes to cognitive impairment in early-stage AD.