BACKGROUND: Critical illness neuropathy (CINP) is defined as an acute and primary axonal motor and sensory neural disease occurring in critically ill patients leading to severe limb weakness as well as difficulty in weaning. It could co-exist with myopathy hence the term critical illness polyneuropathy and myopathy (CIPNM). The clinical presentation of critical illness polyneuropathy includes flaccid quadriplegia without affecting cranial nerves. It usually complicates the clinical course of a patient on mechanical ventilation with severe sepsis and MODS. The cornerstone in the diagnosis of neuromuscular disorders in the critically ill is the electrophysiological evaluation. Until recently the only possible way to affect the incidence was to reduce the risk factors. Hyperglycemia is associated with adverse outcomes, including increased mortality and CIPNM, in acutely ill patients.

OBJECTIVES: To evaluate the relevant literature and determine the effect of intensive insulin therapy (ITT) versus conventional insulin therapy (ITT) in preventing the occurrence of critical illness polyneuropathy and myopathy among critically ill patients.

SEARCH STRATEGY: The search was performed by means of MEDLINE, PUBMED, Ovid SP, Science Direct, and Cochrane library database limited to studies written in English using the words "randomized clinical trial", "intensive insulin therapy", "intensive insulin therapy in critical illness", "critical illness", "critical illness polyneuropathy", "critical illness myopathy", and "critical illness polyneuropathy and myopathy". The title and abstract of the studies were evaluated. The references of each study selected were screened to identify studies that were not included on electronic search. Key journals and textbooks were also searched. References mentioned in the textbooks were likewise reviewed.

SELECTION CRITERIA: Studies were chosen if they met the following inclusion criteria: the study was a randomized controlled trial; the study participants were adults; a critical care setting used; the intensive insulin therapy was defined by a target blood glucose concentration of 80-110mg/dl; the conventional insulin therapy was defined by a target blood glucose concentration 210mg/dl; studies that documented critical illness polyneuropathy and myopathy (CIPNM).

DATA COLLECTION & ANALYSIS: Two reviewers independently did validity assessment. Analysis of data was done by statistical packs Revman 5.0 from the Cochrane Collaboration.

MAIN RESULTS: The search resulted in recovery of 3 trials met the inclusion criteria. A total of 1,188 patients from the 3 randomized trials were evaluated. Five hundred forty six (546) to received intensive insulin therapy (ITT) in contrast the six hundred forty two (642) who received conventional insulin therapy (CIT). The analysis using the presence of electrophysiological evidence of CIP/CIM showed that the IIT group had a lower event rate (151/546 or 28%) as compared to the CIT group (263/642 or 41%). This resulted to a total odds ratio (OR) of 0.51 with the confidence interval fixed at 95%. The relative risk (RR) was computed at 0.68 with a number needed to treat (NNT) of 7.8

REVIEWERS' CONCLUSIONS: IIT is an effective therapy that could actually decrease the incidence of critical illness polyneuropathy and myopathy among critically ill patients.

Human ; Humans ; Adult ; Critical Illness ; Odds Ratio ; Risk Factors ; Incidence ; Medline ; Insulin ; Blood Glucose ; Respiration, Artificial ; Confidence Intervals ; Quadriplegia ; Patient Selection ; Multiple Organ Failure ; Polyneuropathies ; Neuromuscular Diseases ; Muscular Diseases ; Critical Care ; Hyperglycemia ; Sepsis ; Cranial Nerves

OBJECTIVE: This paper aims to correlate the white matter changes seen in cranial Magnetic Resonance Imaging (MRI) the severity of cognitive impairment in patients diagnose Alzheimer Disease by using the conventional Cranial MRI weighted and Fluid-attenuated inversion recovery (FLAIR) images.

METHODS: All patients diagnosed with Probable Alzheimer's disease at the Memory Assessment Center in a tertiary hospital in Manila from January 2007 to September 2008 were included in the study who underwent cranial MRI (T2 weighted and FLAIR images), with ages varying from 65-87 years old using the following tests: Alzheimer's Disease Assessment Scale-Cognitive (ADASCOG), Mini-Mental Status Examination (MMSE), Boston Naming, Verbal Fluency, Word List Memory Task, Recall and Recognition, Trail making A and B and Clinical Dementia Rating (CDR). The Cranial MRI images were rated using the Age-Related White Matter Changes (ARWMC) rating scale for MRI. Analyses were done using the Statistical Package for the Social Sciences (SPSS version 14.) Correlation between continuous data was done using the Pearson correlation test while the correlation between ranked data utilized the Spearman test.

RESULT: Four patients with no white matter changes had mild AD while another two had made an AD. Among those with focal lesions, two were categorized as mild AD, another two cases as moderate and one case with severe AD. Among those with the beginning confluence of lesions, three had mild AD, two had moderate AD and one had severe AD. No case had severe age-related white matter changes. We found no significant relationship between the clinical dementia ratings (severity of AD) and the presence or absence of white matter lesions in the cranial MRI (T2 weighted and FLAIR images). 

CONCLUSION: Diffusion tensor imaging (DTI) captures neurodegenerative brain changes that traditional MRI may miss. Further studies using structural and functional imaging methodologies should be promoted to show cognitive performance and its correlation. In particular, compensatory networks in patients were shown to linearly correlate to cognitive performance. Thus, varied approaches to understanding networks could be valuable tools in developing new approaches for early diagnosis of AD and in the future, aid us in the effectivity of treatment strategies.

Human ; Diffusion Tensor Imaging ; Alzheimer Disease ; Cognitive Dysfunction ; Tertiary Care Centers ; White Matter ; Magnetic Resonance Imaging ; Brain ; Memory ; Cognition ; Early Diagnosis ; Social Sciences ; Mental Status And Dementia Tests

OBJECTIVES

The paper aims to determine the effect of acute ischemic stroke on cognition using the MMSE and other neuropsychological tests.

METHODS

All patients admitted at the University of Santo Tomas Hospital Pay Division for acute ischemic stroke from July to August 2007 were included in the study. Eligible patients underwent Mini-Mental State Examination (MMSE) and a detailed neuropsychological testing to characterize cognitive functioning in 6 domains: attention, executive functioning, language, visuospatial ability, visuomotor speed and memory. Scores were presented as mean standard deviation and frequency of cognitive impairment was determined. Chi square and logistic regression was used to examine the association between stroke and the impaired cognitive domain.

RESULTS

There were twenty-five participants eligible in the study. The mean age of the participants was 58.0 ± 13.3, the mean educational level (in years) was 11.6 ± 3.4, the mean MMSE score was 26.4 ± 3.0 and the mean NIHSS score was 4.2 ± 1.8. With a cutoff score of 23 and below, 4 (16%) patients failed the MMSE. On neuropsychological testing, however, all patients failed in at least one area of cognitive domain being tested. Among these patients, 60% failed in the test for visuospatial and executive functions while 92% failed in the test for visuomotor speed.

CONCLUSION

The prevalence of cognitive impairment after an acute ischemic stroke is 16% using the MMSE. Neuropsychological assessment revealed cognitive impairment in all these patients. The results suggest that the role of MMSE in detecting post stroke cognitive impairment in the acute setting maybe limited. More specific neuropsychological tests should be incorporated to detect subtle cognitive impairment especially instruments that test the areas of visuospatial, visuomotor speed and executive functions.

Human ; Cognitive Dysfunction