Cognitive Dysfunction In Survivors Research Articles

Comparison of fatigue, cognitive dysfunction and psychological disorders in post-COVID patients and patients after sepsis: is there a specific constellation?

BackgroundSequelae of COVID-19 can be severe and longlasting. We compared frequencies of fatigue, depression and cognitive dysfunction in survivors of SARS-CoV-2-infection and sepsis.MethodsWe performed a prospective cohort study of 355 symptomatic post-COVID patients who visited our out-patient clinic for post-COVID-19 care. We compared them with 272 symptomatic patients from the Mid-German Sepsis Cohort, which investigates the long-term courses of sepsis survivors. Possible predictors for frequent clinical findings (fatigue, signs of depression, cognitive dysfunction) in post-COVID were investigated with multivariable logistic regression.ResultsMedian age of the post-COVID patients was 51 years (range 17–86), 60.0% were female, and 31.8% required hospitalization during acute COVID-19. In the post-COVID patients (median follow-up time: 163 days) and the post-sepsis patients (180 days), fatigue was found in 93.2% and 67.8%, signs of depression were found in 81.3% and 10.9%, and cognitive dysfunction was found in 23.5% and 21.3%, respectively. In post-COVID, we did not observe an association between fatigue or depression and the severity of acute COVID-19. In contrast, cognitive dysfunction was associated with hospitalization (out-patient versus in-patient) and more frequent in post-COVID patients treated on an ICU compared to the MSC patients.ConclusionIn post-COVID patients, fatigue and signs of depression are more common than in sepsis survivors, independent from the acute SARS-CoV-2-infection. In contrast, cognitive dysfunction is associated with hospitalization. Despite the differences in frequencies, owing to the similarity of post-COVID and post-sepsis sequelae, this knowledge may help in implementing follow-up approaches after SARS-CoV-2 infection.

Deficiency of cGAS signaling protects against sepsis-associated encephalopathy

Sepsis is a life-threatening inflammatory syndrome secondary to infection. Thanks to the advances of antibiotics and life-supporting techniques, the mortality of sepsis has been decreasing in recent decades. Nevertheless, sepsis-associated encephalopathy (SAE) is still common in septic patients, which promotes the mortality of septic patients and results in cognitive dysfunction in survivors. Full understanding and effective medicine in the treatment of SAE is currently scant. Here, we revealed a novel role of cGAS signaling in the pathogenesis of SAE. Deficiency of cGas significantly restored cognitive impairment in sepsis mice model. The restoration may attribute to the recovery of neo-neuron decline that associated with the decrease of activated microglia and astrocytes in the hippocampus of cGas-deficient mice. In addition, type I interferon (IFN) signaling, a downstream of cGAS pathway, was boosted in the hippocampus of septic mice, which was dramatically attenuated by deleting cGas. Moreover, administration of recombinant IFNβ markedly reversed the protection of ablation of cGas in the cognitive impairment in sepsis. Collectively, cGAS promotes the pathogenesis of SAE by up-regulating type I IFN signaling. Blocking cGAS may be a promising strategy for preventing encephalopathy in sepsis.

Predicting Long-term Cognitive Dysfunction in Survivors of Critical Illness with Plasma Inflammatory Markers: a Retrospective Cohort Study.

Persistent inflammation in intensive care unit (ICU) survivors is associated with higher long-term mortality and poorer mobility. However, it is unknown if inflammatory markers are associated with other dysfunctions observed in survivors of critical illness. Thus, it was investigated if plasma levels of interleukin (IL)-6 and IL-10 at hospital discharge were associated with long-term functional and cognitive performance after ICU discharge. Adult patients admitted for >48h to a 20-bed mixed ICU in a University Hospital had blood collected within 48h before hospital discharge to measure IL-6 and IL-10 levels. After a median time of 48months, cognitive status was determined by the Mini-Mental State Examination (MMSE), and functional status was determined by the Barthel Index. Patients at the higher 25th percentile of both IL-6 and IL-10 had a worse long-term cognitive performance, but not worse functional status, even when adjusted for confounders after long-term follow-up. In conclusion, elevated circulating IL-6 and IL-10 concentrations at hospital discharge were associated with long-term cognitive dysfunction in ICU survivors.

Neuropsychological and self-reporting outcomes following rehabilitation of cognitive dysfunction in survivors of breast cancer: A pilot study involving survivor-partner dyads.

Neuropsychological and self-reporting outcomes following rehabilitation of cognitive dysfunction in survivors of breast cancer: A pilot study involving survivor-partner dyads.

Does permissive hypoxaemia during extracorporeal membrane oxygenation cause long-term neurological impairment?: A study in patients with H1N1-induced severe respiratory failure.

The Extracorporeal Life Support Organisation accepts permissive hypoxaemia in adult patients during extracorporeal membrane oxygenation (ECMO). The neurological long-term outcome of this approach has not yet been studied. We investigated the prevalence of brain lesions and cognitive dysfunction in survivors from the Influenza A/H1N1 2009 pandemic treated with permissive hypoxaemia during ECMO for severe acute respiratory distress syndrome (ARDS). Our hypothesis was that this method is reasonable if tissue hypoxia is avoided. Long-term follow-up study after ECMO. Karolinska University Hospital, Sweden, from October 2012 to July 2013. Seven patients treated with ECMO for severe influenza A/H1N1-induced ARDS were studied 3.2 years after treatment. Blood lactate concentrations were used as a surrogate for tissue oxygenation. Neurocognitive outcome was studied with standardised cognitive tests and MRI of the brain. Cognitive functioning and hypoxic brain lesions after permissive hypoxaemia during ECMO. The observation period was the first 10 days of ECMO or the entire treatment period if shorter than 10 days. Eleven of 13 patients were still alive 3 years after ECMO. We were able to contact seven of these patients (mean age 31 years), who all agreed to participate in this study. Mean ± SD peripherally measured arterial saturation during the observation period was 79 ± 10%. Full-scale Intelligence Quotient was within one standard deviation or above from the mean of a healthy population in five patients, and was 1.5 SD below the mean in one patient. In one other patient, it could not be determined because of a lack of formal education. Memory functioning was normal in all patients. MRI showed no changes related to cerebral hypoxia. Permissive hypoxaemia during ECMO might not negatively affect long-term cognitive outcome if adequate organ perfusion is maintained. at Clinicaltrials.gov NCT01763060.

Prevalence of perceived cognitive dysfunction in survivors of a wide range of cancers: results from the 2010 LIVESTRONG survey.

With cancer survivors now numbering over 13 million in the United States, and expected to continue to increase, it is important to consider the needs of this growing population. In the literature, one of the most common complaints by cancer survivors is perceived cognitive dysfunction. Since the preponderance of the research has focused on breast cancer survivors, the purpose of the present study was to explore the prevalence and correlates of perceived cognitive dysfunction in a large sample of cancer survivors with representation across a wide range of different types of cancer. A sample of 3108 post-treatment cancer survivors completed the 2010 LIVESTRONG survey as part of a larger study of cancer survivorship. Respondents completed standardized questions regarding current and past perceived cognitive dysfunction, as well as depressive symptoms, and demographic and medical variables. Current perceived cognitive dysfunction was reported by nearly half of respondents (45.7%), across a wide range of cancer types, with the highest prevalence among survivors of central nervous system cancers. Receiving chemotherapy and current report of depressive symptoms were both strongly associated with current perceived cognitive dysfunction. These findings contribute to a growing appreciation of the high prevalence of perceived cognitive dysfunction in survivors of a wide range of cancer types and the potential interactive effect of concurrent symptoms of depression. These findings highlight a need to develop more effective means of preventing or reducing cognitive dysfunction in cancer survivors. Perceived cognitive dysfunction was reported in a wide range of cancer survivors. The potential interactive effect of symptoms of depression suggests the need to develop interventions targeting both cognitive dysfunction and depression to achieve improvements in cognitive functioning.

The Impact of High Versus Low Sedation Dosing Strategy on Cognitive Dysfunction in Survivors of Intensive Care Units: A Systematic Review and Meta-Analysis

Background: The practice of low vs. high sedation dosing strategy may impact the cognitive and mental health function in the intensive care unit (ICU). We aim to demonstrate that high sedation strategy will result in change of mental health function in ICU patients. Methods: We performed a systemic search and meta-analysis of medical databases in MEDLINE (from 1966 to March 2013) and EMBASE (from 1980 to March 2013), as well as the Cochrane Library using the MESH terms "Intensive Care Unit," and "Mental Health, for assessing the impact of sedation on posttraumatic stress disorder (PTSD) or anxiety/depression and delirium in the mix ICU setting including cardiac surgery patients. A total of 1216 patients were included in the final analysis. Results: We included 11 studies in the final analysis and concluded that high dose sedation strategy resulted in higher incidence of cognitive dysfunction with P value of 0.009. The result for subgroup of delirium showed P = 0.11 and PTSD/depression or anxiety of P = 0.001, Heterogeneity I2 was 64%. Overall analysis was statistically significant with a P value of 0.002. Conclusion: High sedation dosing strategy will negatively affect cognitive function in critically ill patients. Large randomized trials are needed to address cognitive dysfunction in subgroup of patients with delirium.

Evaluating the Role of Serotonin on Neuropsychological Function After Breast Cancer Using Acute Tryptophan Depletion

Although cognitive dysfunction is a prevalent and disruptive problem for many breast cancer survivors (BCSs), little research has examined its etiology. One potential mechanism that remains to be explored is serotonin. Serotonin has been implicated in normal and dysfunctional cognitive processes, and serotonin levels are significantly affected by estrogen withdrawal, a common side effect of breast cancer treatment. However, no study has evaluated serotonin's role on cognitive dysfunction in BCSs. The purpose of this study was to examine the role of serotonin in cognitive dysfunction in survivors by lowering central serotonin concentrations via acute tryptophan depletion (ATD). Based on previous research in noncancer populations, we hypothesized that alterations in central serotonin levels would induce cognitive dysfunction in these women controlling for confounding characteristics such as fluctuating mood and glucose levels. Secondarily, we explored whether genetic variations in serotonin genes would partly explain ATD. Participants included 20 female BCSs, posttreatment for nonmetastatic breast cancer, who received ATD or control in a double-blind, crossover design. Cognitive performance was measured at the 5-hr tryptophan/serotonin nadir on each test day using standardized neuropsychological tests. Specific impairment was noted in episodic memory (delayed recall) and motor speed during ATD versus control. ATD did not alter new learning (immediate recall), working memory, verbal fluency, or information processing speed. Findings suggest that serotonin may play a critical role in memory consolidation and motor functioning in BCSs.

Mental and physical disorders after ICU discharge

Research and studies related to the long-term consequences of intensive care are increasing. This review focuses on some of the most recent knowledge in this field. Still studies regarding the health-related quality of life (HRQOL) in survivors after intensive care are frequently published and reveal more details about the fact that HRQOL is reduced constantly in these groups. More specific studies regarding depression and anxiety have given more insight into this complication that is rather commonly found. Tests of cognitive dysfunction in survivors may be applied using PC and touch screen and will probably increase in use in the next year. Also recent findings regarding renal recovery in patients with acute renal failure and the natural course of critical illness polyneuropathy and myopathy are better described. Intervention studies during ICU stay or immediately after in the hope to decrease the long-term consequences of intensive care are still few, but positive effects of early mobilization during ICU care are now documented. Outcome research is increasing, and hopefully this research gradually will shift towards intervention studies aimed to reduce the continuous burden from intensive care in many survivors.

VERBAL MEMORY DEFICIT FOLLOWING TRAUMATIC BRAIN INJURY: ASSESSMENT USING ADVANCED MRI METHODS

Traumatic axonal injury resulting in disruption of functional networks in the brain is thought to be a major contributor to cognitive dysfunction in survivors of traumatic brain injury (TBI).1 However, the true significance of this disruption is not known as current clinical imaging modalities do not directly assess axonal injury or functional network connectivity. Modern MRI techniques such as resting-state fMRI correlation analysis may overcome this limitation.2,3 A 21-year-old right-handed woman presented to the outpatient TBI clinic because she was “having trouble in school and remembering things.” At 15, she was a passenger in a head-on motor vehicle collision. She had a severe TBI, clavicle fracture, and pulmonary contusions. Her initial Glasgow Coma Score was 4 (range: 3, deeply comatose, to 15, normal). Her initial head CT revealed a large left subdural hematoma with 1 cm left-to-right shift, bifrontal hemorrhagic contusions, subarachnoid hemorrhage, intraventricular hemorrhage, and punctate hemorrhages in the subcortical white matter, pons, and splenium of the corpus callosum. A left craniotomy was performed and the subdural hematoma was evacuated. She made a progressive neurologic recovery over 2 months. At discharge she was able to speak complete sentences and had no cranial nerve, motor, or sensory deficits. However, she has experienced persistent difficulties with memory and concentration affecting school performance and everyday life. Neuropsychological testing at age 21 revealed a moderately severe verbal memory deficit for auditory information but otherwise generally …

Prolonged Cognitive Dysfunction in Survivors of Critical Illness

Prolonged Cognitive Dysfunction in Survivors of Critical Illness

Prolonged cognitive dysfunction in survivors of critical illness

A prospective study using neuropsychological testing explored cognitive performance, and specifically executive function, in survivors of critical illness during the first year of recovery. Fifty-one patients who had survived 3 days or more in the intensive care unit were studied approximately 3 months after discharge; 45 of them were studied again 6 months later. General health was assessed using the Short-Form 36. Cognitive and executive functions were measured using Raven's Progressive Matrices, the Hayling Sentence completion test and the Six-Element Test. Three months after discharge from intensive care, all eight domains of Short-Form 36 were impaired among survivors; by 9 months, four of the eight domains showed significant improvement. At 3 months, 35% of patients scored at or below a level equivalent to the lowest performing 5% of a normal population (i.e. the fifth percentile) on two or more tests of cognitive function; by 9 months only 4% of patients were impaired to this extent. Although cognitive performance improved with time, it remained below normal.