scholarly journals Long-term Cognitive Impairment after Critical Illness – Definition, Incidence, Pathophysiology and Hypothesis of Neurotrophic Treatment

2015 ◽  
Vol 10 (2) ◽  
pp. 195
Author(s):  
Ignacio J Previgliano ◽  
Bader Andres ◽  
Pawel J Ciesielczyk ◽  
◽  
◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Intensive Care Unit ◽  
Intensive Care ◽  
Cognitive Impairment ◽  
Brain Injury ◽  
Critical Illness ◽  
Neurovascular Unit ◽  
Public Health Problem ◽  
Brain Diseases

Cognitive impairment after critical illness (CIACI) is a frequent consequence of serious disease or injury that has been reported in as many as 66 % of patients, 3 months after an illness requiring intensive care unit hospitalisation. The condition has been recognised only within the past 15 years and its pathological mechanisms are, as yet, incompletely understood. The neurological changes and cellular and inflammatory processes of CIACI overlap with those of stroke, traumatic brain injury and neurodegenerative disorders. Patients also show brain atrophy, which worsens with the duration of intensive care unit stay. Risk factors associated with CIACI include depression, biomarkers of Alzheimer’s disease (e.g. apolipoprotein E), delirium, exposure to some drugs (e.g. fentanyl, morphine and propofol) and intubation. Current strategies to prevent or treat CIACI include treatments to reduce agitation and delirium and physical and mental rehabilitation including cognitive therapy. Many brain diseases and injuries affect the functioning of the neurovascular unit (NVU), which constitutes the key cellular building block of the blood–brain barrier (BBB). CIACI is believed to affect the integrity of the NVU and it is among the potential targets for therapy. Neurotrophic factors (NTFs), such as brain-derived neurotrophic factor (BDNF) are known to play an important role in neurogenesis, maintenance of NVU structure and neuronal repair after disease and injury. This led to the development of strategies including the NTF-preparation (Cerebrolysin®), which is effective as a post-stroke therapy and has potential in the treatment of Alzheimer’s disease and brain injury as well as CIACI. There are currently no proven treatments for CIACI; improved understanding of the condition and further evaluation of NTFs may lead to effective treatments, which are vital to tackle this increasingly serious public health problem.

scholarly journals Nutrition and cognitive impairment in the elderly

2001 ◽  
Vol 86 (3) ◽  
pp. 313-321 ◽  
Author(s):  
M. González-Gross ◽  
Ascensión Marcos ◽  
Klaus Pietrzik
Keyword(s):  
Risk Factors ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Large Scale ◽  
Public Health Problem ◽  
The Elderly ◽  
Vitamin B ◽  
Clinical Onset ◽  
Related Risk

As the number of older people is growing rapidly worldwide and the fact that elderly people are also apparently living longer, dementia, the most common cause of cognitive impairment is getting to be a greater public health problem. Nutrition plays a role in the ageing process, but there is still a lack of knowledge about nutrition-related risk factors in cognitive impairment. Research in this area has been intensive during the last decade, and results indicate that subclinical deficiency in essential nutrients (antioxidants such as vitamins C, E and β-carotene, vitamin B12, vitamin B6, folate) and nutrition-related disorders, as hypercholesterolaemia, hypertriacylglycerolaemia, hypertension, and diabetes could be some of the nutrition-related risk factors, which can be present for a long time before cognitive impairment becomes evident. Large-scale clinical trials in high-risk populations are needed to determine whether lowering blood homocysteine levels reduces the risk of cognitive impairment and may delay the clinical onset of dementia and perhaps of Alzheimer's disease. A curative treatment of cognitive impairment, especially Alzheimer's disease, is currently impossible. Actual drug therapy, if started early enough, may slow down the progression of the disease. Longitudinal studies are required in order to establish the possible link of nutrient intake – nutritional status with cognitive impairment, and if it is possible, in fact, to inhibit or delay the onset of dementia.

scholarly journals Long-Term Cognitive Impairment After Critical Illness

2018 ◽  
pp. 86-90
Keyword(s):  
Intensive Care Unit ◽  
Intensive Care ◽  
Cognitive Impairment ◽  
Critical Illness ◽  
Cognitive Outcomes ◽  
Adult Patients ◽  
Illness Experience ◽  
Icu Patients ◽  
Global Cognition

This case focuses on long-term cognitive impairment after critical illness by asking the question: What is the prevalence of long-term cognitive impairment after critical illness, and does the duration of delirium and use of sedative or analgesic medications affect cognitive outcomes? This study demonstrated that 74% of adult patients with critical illness experience delirium during their hospital course. Furthermore, patients in the intensive care unit (ICU) setting commonly experience global cognition and executive function deficits at 3 and 12 months following hospitalization. These findings highlight the importance of careful delirium surveillance in ICU patients.

Free and total catecholamines in critical illness

1988 ◽  
Vol 254 (3) ◽  
pp. E287-E291 ◽  
Author(s):  
P. D. Woolf ◽  
R. W. Hamill ◽  
L. A. Lee ◽  
J. V. McDonald
Keyword(s):  
Intensive Care Unit ◽  
Traumatic Brain Injury ◽  
Intensive Care ◽  
Brain Injury ◽  
Critical Illness ◽  
Glasgow Coma Score ◽  
Neurological Dysfunction ◽  
Surgical Patients ◽  
Range Of Values ◽  
Catecholamine Concentration

The magnitude of circulating free and total (free plus conjugated) catecholamine responses to a strong and sustained stimulus was investigated in four groups of patients: traumatic brain injury (n = 24), vascular brain injury (n = 10), polysystem trauma (n = 7) and medical/surgical patients in an intensive care unit (n = 29). Despite significant three- to sevenfold elevations in both free and total norepinephrine (NE) and epinephrine (E), the ratio of free to total NE and E remained constant over a very broad range of values. The proportion of free E was twice normal (30.1-33.5 vs. 16.2%) in all but patients with polytrauma, whereas the percentage of free NE was unchanged in all patients (43.0%). All dopamine (DA) parameters remained generally normal. In the patients with traumatic or vascular brain injury, significant inverse correlations were present between the degree of neurological dysfunction, as indicated by the concomitant Glasgow coma score, and free NE, E, and DA and total NE and DA levels. Thus, during conditions of intense and prolonged catecholamine release, the proportion of free catecholamine remains constant and the total as well as free catecholamine concentration is proportional to the Glasgow coma score.

Metformin: A Growing Journey from Glycemic Control to the Treatment of Alzheimer’s Disease and Depression

2020 ◽  
Vol 27 ◽  
Author(s):  
Mohamed El Massry ◽  
Lynn M. Alaeddine ◽  
Leen Ali ◽  
Celine Saad ◽  
Assaad A. Eid
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Brain Injury ◽  
Neurological Disorders ◽  
Wide Spectrum ◽  
Metabolic Stress ◽  
Therapeutic Benefit ◽  
Brain Diseases ◽  
Energy Status ◽  
Therapeutic Benefits

: Metabolic stress, transduced as an altered cellular redox and energy status, presents as the main culprit in many diseases including diabetes. However, its role in the pathology of neurological disorders is still not fully elucidated. Metformin, a biguanide compound, is an FDA approved antidiabetic drug generally used for the treatment of type 2 diabetes. The recently described wide spectrum of action executed by this drug suggests a potential therapeutic benefit in a panoply of disorders. Current studies imply that metformin could play a neuroprotective role by reversing hallmarks of brain injury (metabolic dysfunction, neuronal dystrophy and cellular loss), in addition to cognitive and behavioral alterations that accompany the onset of certain brain diseases such as Alzheimer’s disease (AD) and depression. However, the mechanisms by which metformin exerts its protective effect in neurodegenerative disorders is not yet fully elucidated. The aim of this review is to reexamine the mechanisms through which metformin performs its function while concentrating on its effect on reestablishing homeostasis in a metabolically disturbed milieu. We will also highlight the importance of metabolic stress, not only as a component of many neurological disorders, but also as a primary driving force for neural insult. Of interest, we will explore the involvement of metabolic stress in the pathobiology of AD and depression. The derangement in major metabolic pathways including AMPK, insulin and glucose transporters will be dissected and the potential therapeutic benefits of metformin administration on the reversal of brain injury in such metabolism dependent diseases will be exposed.

scholarly journals Traumatic Brain Injury Precipitates Cognitive Impairment and Extracellular Aβ Aggregation in Alzheimer's Disease Transgenic Mice

PLoS ONE ◽  
2013 ◽  
Vol 8 (11) ◽  
pp. e78851 ◽  
Author(s):  
Naoki Tajiri ◽  
S. Leilani Kellogg ◽  
Toru Shimizu ◽  
Gary W. Arendash ◽  
Cesar V. Borlongan
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Traumatic Brain Injury ◽  
Cognitive Impairment ◽  
Brain Injury ◽  
Transgenic Mice ◽  
Aβ Aggregation

Diagnosing Alzheimer’s disease in clinical practice

2011 ◽  
Author(s):  
Gunhild Waldemar
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Substance Abuse ◽  
Cognitive Impairment ◽  
Clinical Practice ◽  
Clinical Diagnosis ◽  
Brain Diseases ◽  
Clinical Criteria ◽  
Metabolic Conditions ◽  
Symptoms And Signs

• In the current clinical criteria, the diagnosis of Alzheimer’s disease (AD) is a clinical diagnosis based on characteristic symptoms and signs, and the exclusion of other causes.• AD must be differentiated from cognitive impairment due to depression, metabolic conditions, substance abuse, and other neurodegenerative or vascular brain diseases...

scholarly journals 1147 Sleep Correlates With Improved Functional Outcome In The Intensive Care Unit

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A437-A437
Author(s):  
L C Markun ◽  
A Sampat ◽  
R Dutta ◽  
G A Palchik ◽  
M Chow ◽  
...  
Keyword(s):  
Intensive Care Unit ◽  
Intensive Care ◽  
Brain Injury ◽  
Critical Illness ◽  
Functional Outcome ◽  
Critically Ill ◽  
Acute Brain Injury ◽  
Subdural Hemorrhage ◽  
Neurological Patients ◽  
Chi Square Analysis

Abstract Introduction Disruption of sleep may have significant implications in acute brain injury, functional recovery, and critical illness. Few data exist characterizing sleep architecture in patients admitted to an intensive care unit (ICU). We aim to describe sleep and clinical characteristics in patients with acute brain injury and critical illness. Methods Retrospective analysis was performed in ICU patients who underwent continuous electroencephalographic (EEG) monitoring from 2018-2019. Sleep was scored based on AASM-defined EEG criteria. Clinical variables, EEG characteristics, and modified Ranking Scale (mRS) were collected. Good outcome was defined as mRS<3. Differences were assessed using chi-square analysis and t-test. Results 205 patients were reviewed with a mean age of 57 years (range 18-91) and a majority (57%) were male. Patients carried a primary neurologic/neurosurgical (61%) or medical/surgical (39%) diagnosis. Status epilepticus, subdural hemorrhage, traumatic brain injury, encephalopathy and cardiac arrest accounted for the majority of diagnoses encountered. Only 58 patients (28%) achieved N1 sleep; of these 76.4% achieved N2, 2.8% N3, and none achieved REM. Of those achieving any sleep, 43% had good outcomes versus only 23% in those who did not (t=-7.45, p<0.001). Neurological patients were more likely to attain sleep compared to those with other primary diagnoses (χ 2 (1)=7.08, p=0.008). Centrally acting anesthetics did not account for sleep differences between neurologic and non-neurologic patients (χ² (1)=2.01, p=0.16). However, those with primary brain injury reached sleep more often in the absence of anesthetic use (χ 2 (1)=4.82, p=0.03). The overall mortality was 32% in this cohort. Conclusion Most critically ill patients do not achieve electrophysiologic sleep. Of those who do, N1/N2 stages are seen most often. Neurological patients were more likely to sleep, and achieving any sleep was associated with improved functional outcome. Further studies are needed to determine whether sleep augmentation in the critically ill impacts functional outcome. Support N/A.

scholarly journals The Effect of Traumatic Brain Injury on Alzheimer’s Disease and Cognitive Decline in Veterans and Non-Veterans

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. 305-306
Author(s):  
Igor Akushevich ◽  
Arseniy Yashkin ◽  
Stanislav Kolpakov Nikitin ◽  
Julia Kravchenko
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Traumatic Brain Injury ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Brain Injury ◽  
Cognitive Decline ◽  
Cognitive Status ◽  
Risk Scores ◽  
Post Traumatic Stress

Abstract We assess the differences in the effect of traumatic brain injury (TBI) on the decline in cognitive status and the risk of Alzheimer’s disease and related dementia (AD/ADRD) between veteran and non-veteran respondents of the Health and Retirement Study (HRS) and measure the sensitivity of these differences to the incremental introduction of controls for associated risk factors. Three groups of AD/ADRD risk-related variables were used: i) demographic/socioeconomic factors, including gender, race, marital status, education, income, and the number of limitations in activities of daily living; ii) comorbidities, including co-existing depression/post-traumatic stress syndrome (PTSD), substance (alcohol, tobacco and/or prescription drug) abuse, diabetes mellitus, stroke, and heart failure; and iii) genetic factors, including the presence of at least one pair of the APOE4 allele and a series of polygenic risk scores associated with AD hallmarks. The dynamics of changes in cognitive impairment in response to TBI, PTSD, and mild cognitive impairment were validated against respective measures estimated using the Department of Defense Alzheimer’s Disease Neuroimaging Initiative (DoD-ADNI) data. The results of the analyses showed that TBI and PTSD were strongly associated with cognitive decline and the risks of AD/ADRD in both veteran and non-veteran subpopulations in HRS data and the difference between them was not statistically significant. Effect magnitude decreased with the addition of risk-related control variables but remained associated with the increased risks. Prevalence of mild cognitive impairment was associated with TBI at baseline in DoD-ADNI data, but no cognitive decline was observed during one year of follow-up.

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