Concomitant Cognitive Impairment Research Articles

Evaluation of a multimodal diagnostic algorithm for prediction of cognitive impairment in elderly patients with dizziness

BackgroundThe current diagnostic workup for chronic dizziness in elderly patients often neglects neuropsychological assessment, thus missing a relevant proportion of patients, who perceive dizziness as a subjective chief complaint of a concomitant cognitive impairment. This study aimed to establish risk prediction models for cognitive impairment in chronic dizzy patients based on data sources routinely collected in a dizziness center.MethodsOne hundred patients (age: 74.7 ±\\documentclass[12pt]{minimal} \\usepackage{amsmath} \\usepackage{wasysym} \\usepackage{amsfonts} \\usepackage{amssymb} \\usepackage{amsbsy} \\usepackage{mathrsfs} \\usepackage{upgreek} \\setlength{\\oddsidemargin}{-69pt} \\begin{document}$$\\pm$$\\end{document} 7.1 years, 41.0% women) with chronic dizziness were prospectively characterized by (1) neuro-otological testing, (2) quantitative gait assessment, (3) graduation of focal brain atrophy and white matter lesion load, and (4) cognitive screening (MoCA). A linear regression model was trained to predict patients’ total MoCA score based on 16 clinical features derived from demographics, vestibular testing, gait analysis, and imaging scales. Additionally, we trained a binary logistic regression model on the same data sources to identify those patients with a cognitive impairment (i.e., MoCA < 25).ResultsThe linear regression model explained almost half of the variance of patients’ total MoCA score (R2 = 0.49; mean absolute error: 1.7). The most important risk-predictors of cognitive impairment were age (β = − 0.75), pathological Romberg’s sign (β = − 1.05), normal caloric test results (β = − 0.8), slower timed-up-and-go test (β = − 0.67), frontal (β = − 0.6) and temporal (β = − 0.54) brain atrophy. The binary classification yielded an area under the curve of 0.84 (95% CI 0.70–0.98) in distinguishing between cognitively normal and impaired patients.ConclusionsThe need for cognitive testing in patients with chronic dizziness can be efficiently approximated by available data sources from routine diagnostic workup in a dizziness center.

Gut dysbiosis induces the development of depression-like behavior through abnormal synapse pruning in microglia-mediated by complement C3

BackgroundRemodeling eubiosis of the gut microenvironment may contribute to preventing the occurrence and development of depression. Mounting experimental evidence has shown that complement C3 signaling is associated with the pathogenesis of depression, and disruption of the gut microbiota may be an underlying cause of complement system activation. However, the mechanism by which complement C3 participates in gut-brain crosstalk in the pathogenesis of depression remains unknown.ResultsIn the present study, we found that chronic unpredictable mild stress (CUMS)-induced mice exhibited obvious depression-like behavior as well as cognitive impairment, which was associated with significant gut dysbiosis, especially enrichment of Proteobacteria and elevation of microbiota-derived lipopolysaccharides (LPS). In addition, peripheral and central complement C3 activation and central C3/CR3-mediated aberrant synaptic pruning in microglia have also been observed. Transplantation of gut microbiota from CUMS-induced depression model mice into specific pathogen-free and germ-free mice induced depression-like behavior and concomitant cognitive impairment in the recipient mice, accompanied by increased activation of the complement C3/CR3 pathway in the prefrontal cortex and abnormalities in microglia-mediated synaptic pruning. Conversely, antidepressants and fecal microbiota transplantation from antidepressant-treated donors improved depression-like behaviors and restored gut microbiome disturbances in depressed mice. Concurrently, inhibition of the complement C3/CR3 pathway, amelioration of abnormal microglia-mediated synaptic pruning, and increased expression of the synapsin and postsynaptic density protein 95 were observed. Collectively, our results revealed that gut dysbiosis induces the development of depression-like behaviors through abnormal synapse pruning in microglia-mediated by complement C3, and the inhibition of abnormal synaptic pruning is the key to targeting microbes to treat depression.ConclusionsOur findings provide novel insights into the involvement of complement C3/CR3 signaling and aberrant synaptic pruning of chemotactic microglia in gut-brain crosstalk in the pathogenesis of depression.7Y-kpmDzT5DuysQHRM1-uuVideo

Microglial Activation: Key Players in Sepsis-Associated Encephalopathy.

Sepsis-associated encephalopathy (SAE) is a common brain dysfunction, which results in severe cognitive and neurological sequelae and an increased mortality rate in patients with sepsis. Depending on the stimulus, microglia (resident macrophages in the brain that are involved in SAE pathology and physiology) can adopt two polarization states (M1/M2), corresponding to altered microglial morphology, gene expression, and function. We systematically described the pathogenesis, morphology, function, and phenotype of microglial activation in SAE and demonstrated that microglia are closely related to SAE occurrence and development, and concomitant cognitive impairment. Finally, some potential therapeutic approaches that can prime microglia and neuroinflammation toward the beneficial restorative microglial phenotype in SAE were outlined.

A study to evaluate the relationship between diabetes mellitus and cognitive dysfunction

Background: Diabetes mellitus (DM) is the most common endocrine disorder. It leads to slow progressive end-organ damage (both microvascular and macrovascular). The cognitive dysfunction is a less known and less addressed complication of DM. Aims and Objectives: This study aims to evaluate the cognitive dysfunction in the patient with DM and to assess the cognitive dysfunction by Mini-Mental State Examination (MMSE) of the patients who are suffering from DM. Materials and Methods: A total of 979 diabetic patients were screened for cognitive dysfunction using MMSE score. The patients were evaluated as per the history. MMSE is a 30-point questionnaire which is mainly used to measure the cognitive impairment. Results: A total of 979 diabetic patients were included in the study out of which 44.7% of the patients were found to have cognitive dysfunction. Cognitive impairment was more prevalent in female diabetics (51%) as compared to male diabetics (39.8%). The result is significant at P&lt;0.05. Patients with longer duration of diabetes had much higher incidence of cognitive impairment (80.9%) as compare with the patients with short duration of diabetes which has lesser incidence of cognitive impairment (16.2%). P&lt;0.001 was considered statistically significant. Conclusion: Majority of the subjects suffering from DM have concomitant cognitive impairment. There is a significant cognitive impairment seen in subjects with DM. Early recognition and management of the cognitive dysfunction will help in improving quality of life.

Transcranial Brain Stimulation Improves Cognition in Older Adults With Depression and Anxiety

Older adults admitted to hospital for rehabilitation often have some degree of concomitant cognitive impairment, which may be a barrier to optimizing rehabilitation approaches. Transcranial direct current stimulation (tDCS), a type of non-invasive brain stimulation, delivers a low electrical current across the brain. The neuromodulatory effects of tDCS can be of therapeutic benefit and has been shown to augment cognitive functions in both healthy and clinical populations. This study investigated the effects of tDCS on cognition in older adult inpatients with depression or anxiety. It was hypothesized that anodal tDCS over the left dorsolateral prefrontal cortex would increase cognitive performance compared to a placebo group. Twenty adults between 65 to 86 years of age admitted to the Glenrose Rehabilitation Hospital with underlying depression or anxiety were recruited. Anodal (n=10) or sham (n=10) tDCS stimulation was administered at 1.5mA over 20 minutes, for 10-15 sessions based on participant availability. Cognitive assessments were administered before and after the tDCS protocol. Anodal tDCS stimulation resulted in significant gains on the Symbol Digit Modality Test, Trail Making Test Part A, and Forward Digit Span. This study demonstrated a tDCS-invoked cognitive enhancement in the domains of attention, information processing speed, and short-term memory processes. With the rapidly ageing population, tDCS may be a potential therapeutic option for cognitive enhancement and may be beneficial in ageing-related cognitive-disorders including mild cognitive impairment and dementia.

Proteomic identification of select protein variants of the SNARE interactome associated with cognitive reserve in a large community sample.

Age-related neuropathologies progressively impair cognitive abilities by damaging synaptic function. We aimed to identify key components within the presynaptic SNARE (soluble N-ethylmaleimide-sensitive factor attachment protein receptor) machinery associated with cognitive performance and estimate their potential contribution to brain reserve in old age. We used targeted SRM proteomics to quantify amounts of 60 peptides, encoded in 30 different genes, in postmortem specimens of the prefrontal cortex from 1209 participants of two aging studies, with available antemortem cognitive evaluations and postmortem neuropathologic assessments. We found that select (but not all) proteoforms are strongly associated with cognitive function and the burden of Alzheimer's disease (AD) pathology. Specifically, greater abundance of STX1A (but not other syntaxins), SYT12, full-length SNAP25, and the GABAergic STXBP1 variant were robustly associated with better cognitive performance. By contrast, greater abundance of other presynaptic proteins (e.g., STXBP5 or tomosyn, STX7, or SYN2) showed a negative influence on cognition. Regression models adjusting for demographic and pathologic variables showed that altered levels of these protein species explained 7.7% additional between-subject variance in cognition (more than any individual age-related neuropathology in the model), suggesting that these molecules constitute key elements of brain reserve. Network analyses indicated that those peptides associated with brain reserve, and closest to the SNARE fusogenic activity, showed greater centrality measures and were better connected in the network. Validation assays confirmed the selective loss of the STX1A (but not STX1B) isoform in cognitively impaired cases. In rodent and human brains, STX1A was selectively located at glutamatergic terminals. However, in AD brains, STX1A was redistributed adjacent to neuritic pathology, and markedly expressed in astrocytes. Our study provides strong evidence, indicating that select presynaptic proteins are key in maintaining brain reserve. Compromised ability to sustain expression levels of these proteins may trigger synaptic dysfunction and concomitant cognitive impairment.

344 - Study protocol for a feasibility RCT of Club Connect, a healthy brain ageing cognitive training program for older adults with depression

Background:Current treatments for Major Depression are only moderately effective. In fact, 20-30% do not achieve full recovery despite multiple interventions. Interestingly, while it is well recognised that cognitive impairment is associated with Major Depression, available treatments do not address cognitive impairment. In this regard, cognitive training (CT) represents a promising intervention, however CT is not typically offered in public health settings.Aim:To evaluate the feasibility of a blinded, randomised controlled trial of group-based CT in a hospital sample of older adults with clinically significant depressive symptoms or history of a major depressive episode within the last five years, and in doing so, to adapt and translate research findings to the clinical setting.Methods:40 older adults, aged at least 65 years, with depression or a history of depression, and without dementia were randomly allocated to Club Connect, a 10-week group-based healthy brain ageing CT program, or a waitlist, treatment-as-usual control group. Baseline assessment including review by a psychogeriatrician and a brief neuropsychological assessment was completed within a fortnight of the intervention starting, and follow-up assessment was completed within a fortnight of the intervention ceasing. Primary outcomes included feasibility of trial design, tolerability of the intervention, and acceptability of random allocation and data collection procedures (as perceived by both participants and clinicians). We also examined the most sensitive clinical outcomes and measurement tools to inform larger scale trials.Significance:The current health, social and economic costs of late-life depression, especially in those with concomitant cognitive impairment, renders the holistic treatment of depression in older adults a public health priority. CT represents an efficacious therapeutic intervention in this regard, however, there appears to be a paucity of CT programs being offered in public health settings. This trial represents the first step in addressing the ‘implementation gap’ that exists between care that is known to be effective and care that is delivered. We must recognise the need to evaluate not only health outcomes, but also to perform formative evaluations that assess the extent to which implementation is effective in order to optimise intervention benefits, to prolong sustainability, and to promote dissemination of findings.

Diabetic neuropathy in the elderly

The increase in the diabetes mellitus (DM) prevalence and incidence has taken on the features of the epidemic. Particularly often, DM occurs in the elderly and senile patients, while at least half of the cases of diabetes in this population remain undiagnosed. DM contributes to the deterioration of the quality of life, causes formation of dependence and progression of various geriatric syndromes leading to increased mortality. Elderly age is an independent risk factor for diabetic neuropathy. The main clinical forms of which are represented by chronic sensorimotor and autonomic impairments, complicated by impaired cardiovascular, gastrointestinal and urogenital functions, as well as chronic neuropathic pain syndrome. Progression of diabetic neuropathy aggravates walking and balance disorders, increases the risk of falls and loss of mobility, and significantly increases the risk of adverse diabetes outcomes. The article discusses in detail risk factors, pathogenesis, differential diagnosis and the possibilities of clinical and non-clinical evaluation of patients with suspected diabetic neuropathy. Possibilities for pain assessment in elderly people with communicative disorders or concomitant cognitive impairment are demonstrated. The article presents an algorithm for management of diabetic neuropathy in elderly ones, ways for optimization of risk and benefit balance, as well as the possibility of etiopathogenetic and symptomatic treatment of pain, autonomic disorders and prevention of late complications of diabetes with use of alpha-lipouc acid, taking into account key characteristics of discussed population.

Association between cognitive impairment and criteria for frailty syndrome among older adults.

The association between cognitive impairment and physical frailty has been studied in older adults. The criteria degree of frailty may be keys to associated cognitive impairment. To analyze the association between cognitive impairment and the criteria for frailty. We cross-sectionally examined data from 667 older adults (≥60 years of age) from a study entitled 'Variables associated to cognition in elderly caregivers' involving patients in an urban and rural primary healthcare center. We defined cognitive impairment based on different groups of scores on the Mini Mental State Examination, and defined frailty and prefrailty using the criteria by the Cardiovascular Health Study. We performed multinomial regression models to analyze the association between levels of frailty and cognitive impairment. Similar proportions of women (54.8%) and men (45.2%) participated in the study (mean age: 71 years old). We found cognitive impairment, prefrailty and frailty in 34, 54, and 24% of the participants, respectively. Concomitant cognitive impairment and frailty was found in 13% of them. The chances of cognitive impairment increased up to 330% (Odds Ratio [OR]: 4.3; 95% confidence interval [95%CI] 2.4‒7.7; p<0.001) among frail individuals, and 70% (OR: 1.7; 95%CI 1.0‒2.8; p=0.033) among prefrail individuals compared to robust/non-frail individuals. After controlling for age, education, place of residence and functional dependence, slowness and fatigue criteria were significantly associated with cognitive impairment. Older adults with frailty have a greater likelihood of concomitant cognitive impairment than prefrail and robust older adults. The prevalence of cognitive impairment and frailty is consistent with data reported in literature. The present findings contribute to the investigation of cognitive frailty.

In silico analysis of the functional and structural consequences of SNPs in human ARX gene associated with EIEE1

Abstract Background Early infantile epileptic encephalopathy 1 (EIEE1) is a rare but devastating neurologic disorder that displays concomitant cognitive and motor impairment, and is often presented in the first months of life with severe intellectual disability. Purpose The objective of this study is to classify the most deleterious nsSNPs in ARX gene that may cause EIEE1 disease. Methods Despite the reported association of ARX gene mutations with vulnerability to several neurologic conditions. There is lack of an in silico analysis on the functional and structural impacts of pathogenic nonsynonymous single nucleotide polymorphisms (nsSNPs) of the ARX at protein level. Therefore, the nsSNPs in the human ARX gene obtained from NCBI, were analyzed for their functional and structural impact using bioinformatics tools like SIFT, Polyphen, PROVEAN, I-Mutant, and MUPro. The effects of the mutations on tertiary structure of the human ARX protein were predicted using RaptorX and visualized by UCSF Chimera, while STRING was used to investigate its protein–protein interaction. Results The results of in silico analysis revealed present of 11 mutations (L535Q, R528S, R380L, V374D, L343Q, T333N, T333S, R332H, R330H, G34R and L33P), thus significantly alter the structure of human ARX protein; that may disturb the domain which will affect the function of the protein. Conclusion In this study, the effect of the structural and functional role of nsSNPs in the ARX gene was analyzed through several in silico methods, which revealed 11 mutations that have a possible functional and structural impact. Thus, could be used as diagnostic markers for EIEE1.

Evolution of genetically determined generalized epilepsies

This article analyzes the available literature regarding the clinical manifestations, genetic determinants, prognosis and evolution of inherited generalized epilepsies. We describe the typical EEG characteristics and their correlations with negative prognostic factors. We also review studies on absence epilepsy of childhood, juvenile myoclonic epilepsy and epilepsy with generalized tonic-clonic seizures. Factors indicating a more severe course and outcome of the disease, and those indicating a more favorable development have been analyzed. Among those, age of the seizure onset, type of initial therapy, time passed before starting therapy and time before a response was seen, cognitive status, combination of seizures, abnormal discharges in EEG, and neurological deficit. The analysis shows that factors correlating with poor prognosis include the presence of more than one type of seizures, insufficient response to initial therapy, necessity of polytherapy and concomitant cognitive impairment.

Hypothesis and Theory: Circulating Alzheimer's-Related Biomarkers in Type 2 Diabetes. Insight From the Goto-Kakizaki Rat.

Epidemiological data suggest an increased risk of developing Alzheimer's disease (AD) in individuals with type 2 diabetes (T2D). AD is anatomically associated with an early progressive accumulation of Aβ leading to a gradual Tau hyperphosphorylation, which constitute the main characteristics of damaged brain in AD. Apart from these processes, mounting evidence suggests that specific features of diabetes, namely impaired glucose metabolism and insulin signaling in the brain, play a key role in AD. Moreover, several studies report a potential role of Aβ and Tau in peripheral tissues such as pancreatic β cells. Thus, it appears that several biological pathways associated with diabetes overlap with AD. The link between peripheral insulin resistance and brain insulin resistance with concomitant cognitive impairment may also potentially be mediated by a liver/pancreatic/brain axis, through the excessive trafficking of neurotoxic molecules across the blood-brain barrier. Insulin resistance incites inflammation and pro-inflammatory cytokine activation modulates the homocysteine cycle in T2D patients. Elevated plasma homocysteine level is a risk factor for AD pathology and is also closely associated with metabolic syndrome. We previously demonstrated a strong association between homocysteine metabolism and insulin via cystathionine beta synthase (CBS) activity, the enzyme implicated in the first step of the trans-sulfuration pathway, in Goto-Kakizaki (GK) rats, a spontaneous model of T2D, with close similarities with human T2D. CBS activity is also correlated with DYRK1A, a serine/threonine kinase regulating brain-derived neurotrophic factor (BDNF) levels, and Tau phosphorylation, which are implicated in a wide range of disease such as T2D and AD. We hypothesized that DYRK1A, BDNF, and Tau, could be among molecular factors linking T2D to AD. In this focused review, we briefly examine the main mechanisms linking AD to T2D and provide the first evidence that certain circulating AD biomarkers are found in diabetic GK rats. We propose that the spontaneous model of T2D in GK rat could be a suitable model to investigate molecular mechanisms linking T2D to AD.

Dyskinesia and FAB score predict future falling in Parkinson's disease.

A growing body of research highlights the importance of cognition for prediction of falls in Parkinson's disease (PD). However, a previously proposed prediction model for future near falls and falls in PD, which includes history of near falls, tandem gait, and retropulsion, was developed without considering cognitive impairment. Therefore, by using a sample of 64 individuals with relatively mild PD and not excluding those with impaired cognition we aimed to externally validate the previously proposed model as well as to explore the value of additional predictors that also consider cognitive impairment. Since this validation study failed to support the proposed model in a PD sample including individuals with impaired global cognition, extended analyses generated a new model including dyskinesia (item 32 of Unified PD Rating Scale) and frontal lobe impairment (Frontal Assessment Battery-FAB) as significant independent predictors for future near falls and falls in PD. The discriminant ability of this new model was acceptable (AUC, 0. 80; 95% CI 0.68-0.91). Replacing the continuous FAB scores by a dichotomized version of FAB with a cut-off score ≤14 yielded slightly lower but still acceptable discriminant ability (AUC, 0. 79; 95% CI 0.68-0.91). Further studies are needed to test our new model and the proposed cut-off score of FAB in additional samples. Taken together, our observations suggest potentially important additions to the evidence base for clinical fall prediction in PD with concomitant cognitive impairment.

The feasibility of assessing speech and non-speech function of the speech apparatus in adults with cerebral palsy

ABSTRACTThis short note reports on observations concerning the feasibility of a set of speech and non-speech assessment tasks in an investigation of dysarthria in 21 adults (15 males/6 females; median 23 years) with cerebral palsy and concomitant cognitive impairment. The participants were assessed with nine tasks representing standard components of clinical dysarthria assessment (i.e. six speech and three non-speech tasks). The tasks were evaluated for their feasibility on the basis of common clinical criteria. Our results indicated that, overall, speech tasks were more feasible than non-speech tasks. Several participants showed signs of dysexecutive behaviour on some of the non-speech tasks, but not on the speech tasks. The current note provides tentative clues regarding the impact of cognitive deficits on the feasibility of assessment tasks in the diagnosis of dysarthria.

Considering sex differences in the cognitive controls of feeding

Women are disproportionately affected by obesity, and obesity increases women's risk of developing dementia more so than men. Remarkably little is known about how females make decisions about when and how much to eat. Research in animal models with males supports a framework in which previous experiences with external food cues and internal physiological energy states, and the ability to retrieve memories of the consequences of eating, determines subsequent food intake. Additional evidence indicates that consumption of a high-fat, high-sugar diet interferes with hippocampal-dependent mnemonic processes that operate to suppress eating, such as in situations of satiety. Recent findings also indicate that weakening this form of hippocampal-dependent inhibitory control may also extend to other forms of learning and memory, perpetuating a vicious cycle of increased Western diet intake, hippocampal dysfunction, and further impairments in the suppression of appetitive behavior that may ultimately disrupt other types of memorial interference resolution. How these basic learning and memory processes operate in females to guide food intake has received little attention. Ovarian hormones appear to protect females from obesity and metabolic impairments, as well as modulate learning and memory processes, but little is known about how these hormones modulate learned appetitive behavior. Even less is known about how a sex-specific environmental factor – widespread hormonal contraceptive use – affects associative learning and the regulation of food intake. Extending learned models of food intake to females will require considerably investigation at many levels (e.g., reproductive status, hormonal compound, parity). This work could yield critical insights into the etiology of obesity, and its concomitant cognitive impairment, for both sexes.

Epidemiology, Risk Factors, and Clinical Features of Intracerebral Hemorrhage: An Update.

Intracerebral hemorrhage (ICH) is the second most common subtype of stroke and a critical disease usually leading to severe disability or death. ICH is more common in Asians, advanced age, male sex, and low- and middle-income countries. The case fatality rate of ICH is high (40% at 1 month and 54% at 1 year), and only 12% to 39% of survivors can achieve long-term functional independence. Risk factors of ICH are hypertension, current smoking, excessive alcohol consumption, hypocholesterolemia, and drugs. Old age, male sex, Asian ethnicity, chronic kidney disease, cerebral amyloid angiopathy (CAA), and cerebral microbleeds (CMBs) increase the risk of ICH. Clinical presentation varies according to the size and location of hematoma, and intraventricular extension of hemorrhage. Patients with CAA-related ICH frequently have concomitant cognitive impairment. Anticoagulation related ICH is increasing recently as the elderly population who have atrial fibrillation is increasing. As non-vitamin K antagonist oral anticoagulants (NOACs) are currently replacing warfarin, management of NOAC-associated ICH has become an emerging issue.

Regional tau deposition measured by [18F]THK5317 positron emission tomography is associated to cognition via glucose metabolism in Alzheimer's disease.

BackgroundThe recent development of tau-specific positron emission tomography (PET) tracers has allowed in vivo quantification of regional tau deposition and offers the opportunity to monitor the progression of tau pathology along with cognitive impairment. In this study, we investigated the relationships of cerebral tau deposition ([18F]THK5317-PET) and metabolism ([18F]FDG-PET) with concomitant cognitive function in patients with probable Alzheimer’s disease (AD).MethodsNine patients diagnosed with AD dementia and 11 with prodromal AD (mild cognitive impairment, amyloid-positive on [11C]PiB-PET) were included in this study. All patients underwent PET scans using each tracer, as well as episodic memory and global cognition assessment. Linear models were used to investigate the association of regional [18F]THK5317 retention and [18F]FDG uptake with cognition. The possible mediating effect of local metabolism on the relationship between tau deposition and cognitive performance was investigated using mediation analyses.ResultsSignificant negative associations were found between [18F]THK5317 regional retention, mainly in temporal regions, and both episodic memory and global cognition. Significant positive associations were found between [18F]FDG regional uptake and cognition. The association of [18F]FDG with global cognition was regionally more extensive than that of [18F]THK5317, while the opposite was observed with episodic memory, suggesting that [18F]THK5317 retention might be more sensitive than [18F]FDG regional uptake to early cognitive impairment. Finally, [18F]FDG uptake had a mediating effect on the relationship between [18F]THK5317 retention in temporal regions and global cognition.ConclusionsThese findings suggest a mediating role for local glucose metabolism in the observed association between in vivo tau deposition and concomitant cognitive impairment in AD.Electronic supplementary materialThe online version of this article (doi:10.1186/s13195-016-0204-z) contains supplementary material, which is available to authorized users.

Back from the dead: reanimation following severe hypothermic cardiac arrest

background Hypothermia is clinically defined as a drop in core body temperature below 35°C in a previously healthy individual in the absence of pre-existing inherent underlying thermoregulatory pathology. Classification of hypothermia below 35°C is described as mild (32°C to 35°C) and moderate (28°C to 32°C). A temperature below 28°C is classified as severe. At 28°C cardiopulmonary function is likely to become compromised. The myocardium becomes vulnerable to arrhythmia, ventricular asystole and subsequently complete cardiovascular collapse. Concomitant cognitive impairment is most commonly associated with severe hypothermia and cold injury. These patients tend to be individuals with mental illness, homelessness, and alcohol and illicit drug use. Recreational accidents such as skiing comprise the second most common group for hypothermic injury.1 There has been much academic debate and speculation regarding the optimal approach to rewarming any patient suffering from hypothermia.2 Mild hypothermia responds well to external rewarming techniques like forced heated air blankets.3 Moderate hypothermia is more precarious from a physiological standpoint. The myocardium is exceptionally vulnerable at these temperatures. Consequently, rapid rewarming techniques are favoured. This includes warmed intravenous (IV) fluids and warm peritoneal lavage in those who have not demonstrated overt signs of cardiac instability.4 Less commonly, these modalities can be augmented with airway warming and pleural irrigation.4,5 If patients with severe hypothermia have a sustainable cardiac rhythm, they are at increased risk for cardiovascular collapse.6 The optimal modality for rewarming a patient with severe hypothermic cardiac arrest remains a highly controversial topic.7 The most recent retrospective comparative study in 68 patients demonstrated cardiopulmonary bypass (CPB) rewarming to be far superior to conventional methods of rewarming, with mortality rates of 15.8% and 53.3%, respectively. Reanimation on CPB allows for several advantages, including rapid rewarming, but most importantly oxygenation and perfusion are preserved. A retrospective study analyzed the long-term neurological outcomes of survivors who reported normal neuropsychological findings in 93.3% of cases and normal brain magnetic resonance imaging in 86.7% of cases.8

Effect Estimation of an Innovative Nursing Intervention to Improve Delirium among Home-Dwelling Older Adults: A Randomized Controlled Pilot Trial

Aims: Estimating the effect of a nursing intervention in home-dwelling older adults on the occurrence and course of delirium and concomitant cognitive and functional impairment. Methods: A randomized clinical pilot trial using a before/after design was conducted with older patients discharged from hospital who had a medical prescription to receive home care. A total of 51 patients were randomized into the experimental group (EG) and 52 patients into the control group (CG). Besides usual home care, nursing interventions were offered by a geriatric nurse specialist to the EG at 48 h, 72 h, 7 days, 14 days, and 21 days after discharge. All patients were monitored for symptoms of delirium using the Confusion Assessment Method. Cognitive and functional statuses were measured with the Mini-Mental State Examination and the Katz and Lawton Index. Results: No statistical differences with regard to symptoms of delirium (p = 0.085), cognitive impairment (p = 0.151), and functional status (p = 0.235) were found between the EG and CG at study entry and at 1 month. After adjustment, statistical differences were found in favor of the EG for symptoms of delirium (p = 0.046), cognitive impairment (p = 0.015), and functional status (p = 0.033). Conclusion: Nursing interventions to detect delirium at home are feasible and accepted. The nursing interventions produced a promising effect to improve delirium.

Systematic review on the inclusion of patients with cognitive impairment in hip fracture trials: a missed opportunity?

More than 320 000 hip fractures occur annually in North America. An estimated 30% of this population have cognitive impairment. We sought to determine the extent to which patients with cognitive impairment or dementia have been included in randomized controlled trials (RCTs) assessing hip fracture management. We conducted a systematic search of 3 electronic journal databases of articles published between January 2000 and June 2010. Studies were screened in duplicate to collect English-language RCTs assessing operative interventions for femoral head, neck or intertrochanteric fractures. We systematically collected descriptive data and used the χ(2) test for comparison between groups as appropriate. We screened 1201 abstracts, 72 of which were eligible for inclusion in our review. Femoral neck and intertrochanteric fractures were equally represented. Thirty-three (46%) studies did not report the inclusion or exclusion of patients with cognitive impairment. Nineteen (26%) studies explicitly included cognitively impaired patients, whereas 20 (28%) excluded them. Only 2 trials (3%) reported outcomes specific to cognitively impaired patients. Fourteen trials (19.4%) reported the use of a validated cognitive assessment tool. None of the trials that reported inclusion of cognitively impaired patients were from North American centres. One in 3 patients with hip fractures have concomitant cognitive impairment, yet 8 of 10 hip fracture trials excluded or ignored this population. The ambiguity or exclusion of these patients misses an opportunity to study outcomes and identify factors associated with improved prognosis.