Your browser doesn't support javascript.
Show: 20 | 50 | 100
Results 1 - 15 de 15
Filter
1.
Lancet Respir Med ; 9(5): 533-544, 2021 05.
Article in English | MEDLINE | ID: covidwho-1537202

ABSTRACT

Cough is one of the most common presenting symptoms of COVID-19, along with fever and loss of taste and smell. Cough can persist for weeks or months after SARS-CoV-2 infection, often accompanied by chronic fatigue, cognitive impairment, dyspnoea, or pain-a collection of long-term effects referred to as the post-COVID syndrome or long COVID. We hypothesise that the pathways of neurotropism, neuroinflammation, and neuroimmunomodulation through the vagal sensory nerves, which are implicated in SARS-CoV-2 infection, lead to a cough hypersensitivity state. The post-COVID syndrome might also result from neuroinflammatory events in the brain. We highlight gaps in understanding of the mechanisms of acute and chronic COVID-19-associated cough and post-COVID syndrome, consider potential ways to reduce the effect of COVID-19 by controlling cough, and suggest future directions for research and clinical practice. Although neuromodulators such as gabapentin or opioids might be considered for acute and chronic COVID-19 cough, we discuss the possible mechanisms of COVID-19-associated cough and the promise of new anti-inflammatories or neuromodulators that might successfully target both the cough of COVID-19 and the post-COVID syndrome.


Subject(s)
COVID-19/complications , COVID-19/physiopathology , Cough/etiology , Inflammation/etiology , Nervous System Diseases/etiology , Neuroimmunomodulation , Cough/physiopathology , Humans , Inflammation/physiopathology , Nervous System Diseases/physiopathology , SARS-CoV-2 , Syndrome
2.
J Am Med Dir Assoc ; 22(7): 1352-1356.e2, 2021 07.
Article in English | MEDLINE | ID: covidwho-1240413

ABSTRACT

OBJECTIVES: We aimed to examine the association between the transition to social isolation and cognitive decline in older adults during the coronavirus disease 2019 (COVID-19) pandemic. DESIGN: Longitudinal study. SETTING AND PARTICIPANTS: The study included participants from a community in a semiurban area of Japan. We conducted a mailed questionnaire survey of 2000 noninstitutionalized older adults who were randomly sampled. Of those who completed both the baseline and follow-up surveys in March and October 2020, respectively, participants aged ≥70 years without cognitive impairment at baseline were included in the analysis. METHODS: Participants were classified into 4 groups based on their baseline and follow-up social isolation status, which were as follows: "remained nonisolated," "isolated from nonisolation," "nonisolated from isolation," and "consistent isolation." Self-reported cognitive function was assessed using the Cognitive Performance Scale, and level 2 (mild impairment) or higher (moderate to severe impairment) was defined as cognitive impairment. RESULTS: Ultimately, 955 older adults were analyzed. The mean age of the participants was 79.6 years (standard deviation = 4.7) and 54.7% were women. During the follow-up period, 54 (5.7%) participants developed cognitive impairment. Multivariable logistic regression analysis revealed that compared with the group that remained nonisolated, the isolated from nonisolation and consistent isolation groups were significantly associated with the onset of cognitive impairment [isolated from nonisolation: odds ratio (OR) = 2.74, 95% confidence interval (CI) = 1.13-6.61, P = .026; consistent isolation: OR = 2.33, 95% CI = 1.07-5.05, P = .033]. CONCLUSIONS AND IMPLICATIONS: Social isolation during the COVID-19 pandemic was associated with a decline in cognitive function among older adults. Attention to the social isolation process during the pandemic may be necessary to protect older adults' cognitive health.


Subject(s)
COVID-19 , Cognitive Dysfunction , Aged , Cognitive Dysfunction/epidemiology , Female , Humans , Japan/epidemiology , Longitudinal Studies , Pandemics , SARS-CoV-2 , Self Report , Social Isolation
3.
Transl Neurodegener ; 10(1): 15, 2021 04 30.
Article in English | MEDLINE | ID: covidwho-1215126

ABSTRACT

Alzheimer's disease (AD) has emerged as a key comorbidity of coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). The morbidity and mortality of COVID-19 are elevated in AD due to multiple pathological changes in AD patients such as the excessive expression of viral receptor angiotensin converting enzyme 2 and pro-inflammatory molecules, various AD complications including diabetes, lifestyle alterations in AD, and drug-drug interactions. Meanwhile, COVID-19 has also been reported to cause various neurologic symptoms including cognitive impairment that may ultimately result in AD, probably through the invasion of SARS-CoV-2 into the central nervous system, COVID-19-induced inflammation, long-term hospitalization and delirium, and post-COVID-19 syndrome. In addition, the COVID-19 crisis also worsens behavioral symptoms in uninfected AD patients and poses new challenges for AD prevention. In this review, we first introduce the symptoms and pathogenesis of COVID-19 and AD. Next, we provide a comprehensive discussion on the aggravating effects of AD on COVID-19 and the underlying mechanisms from molecular to social levels. We also highlight the influence of COVID-19 on cognitive function, and propose possible routes of viral invasion into the brain and potential mechanisms underlying the COVID-19-induced cognitive impairment. Last, we summarize the negative impacts of COVID-19 pandemic on uninfected AD patients and dementia prevention.


Subject(s)
Alzheimer Disease/complications , COVID-19/complications , Pandemics , Aged , Aged, 80 and over , Alzheimer Disease/epidemiology , COVID-19/epidemiology , Comorbidity , Humans
4.
Acta Clin Belg ; : 1-8, 2021 Apr 17.
Article in English | MEDLINE | ID: covidwho-1191081

ABSTRACT

AIM: Associations of depression, dementia, and poor life quality with mortality of COVID-19have not been studied yet. We aimed to identify the risk factors for mortality and analyze the associations with patients' physiological and mental well-being, as reflected by comorbidities, life quality, depression, and cognitive impairment. METHODS: : Older patients receiving inpatient hospital care for COVID-19 were included.Demographic data, medical history, symptoms at admission, laboratory findings, and treatment outcomes were recorded. RESULTS: : There were 122 patients with a median age of 73.0 years. The mortality rate was 9.0% (n = 11 patients). Patients with mortality were significantly active smokers, obese, and having comorbidities using polypharmacy. Weight loss ≥of 10% during hospitalization was significantly associated with mortality.Poor life quality and a higher risk of depression, cognitive impairment, and falling were more frequently seen in non-survived patients. (p < 0.05). High ferritin was the only independent risk factor for mortality (OR = 15.61, 95% CI:1.08-226.09, p = 0.044). CONCLUSION: : The presence of comorbidities, depression, cognitive impairment, higher falling risk, and poor life quality were significantly associated with higher mortality rates in older adults with COVID-19. High ferritin level was an independent risk factor for mortality.

5.
Dement Geriatr Cogn Disord ; 50(1): 68-73, 2021.
Article in English | MEDLINE | ID: covidwho-1183423

ABSTRACT

BACKGROUND: Hyposmia is frequently reported as an initial symptom in coronavirus disease 2019 (COVID-19). OBJECTIVE: As hyposmia accompanies cognitive impairment in several neurological disorders, we aimed to study whether hyposmia represents a clinical biomarker for both neurological involvement and cognitive impairment in mild CO-VID-19. We aimed to study whether olfactory dysfunction (OD) represents a clinical biomarker for both neurological involvement and cognitive impairment in mild COVID-19. METHODS: Formal olfactory testing using the Sniffin'Sticks® Screening test, neuropsychological assessment using the Montreal Cognitive Assessment (MoCA), and detailed neurological examination were performed in 7 COVID-19 patients with mild disease course and no history of olfactory or cognitive impairment, and 7 controls matched for age, sex, and education. Controls were initially admitted to a dedicated COVID-19 screening ward but tested negative by real-time PCR. RESULTS: The number of correctly identified odors was significantly lower in COVID-19 than in controls (6 ± 3, vs. 10 ± 1 p = 0.028, r = 0.58). Total MoCA score was significantly lower in COVID-19 patients than in controls (20 ± 5 vs. 26 ± 3, p = 0.042, r = 0.54). Cognitive performance indicated by MoCA was associated with number of correctly identified odors in COVID-19 patients and controls (COVID-19: p = 0.018, 95% CI = 9-19; controls: p = 0.18, r = 0.63, 95% CI = 13-18.5 r = 0.64). DISCUSSION/CONCLUSION: OD is associated with cognitive impairment in controls and mild COVID-19. OD may represent a potentially useful clinical biomarker for subtle and even subclinical neurological involvement in severe acute respiratory distress syndrome coronavirus-2 infection.


Subject(s)
Anosmia/etiology , COVID-19/complications , Cognition , Cognitive Dysfunction , Aged , Aged, 80 and over , Anosmia/pathology , Biomarkers , COVID-19/pathology , Female , Humans , Male , Mental Status and Dementia Tests , SARS-CoV-2
6.
J Nucl Med ; 62(7): 910-915, 2021 07 01.
Article in English | MEDLINE | ID: covidwho-1167265

ABSTRACT

Cognitive impairment is a frequent complaint in coronavirus disease 2019 (COVID-19) and can be related to cortical hypometabolism on 18F-FDG PET at the subacute stage. However, it is unclear if these changes are reversible. Methods: We prospectively assessed the Montreal Cognitive Assessment scores and 18F-FDG PET scans of 8 COVID-19 patients at the subacute stage (once no longer infectious) and the chronic stage (˜6 mo after symptom onset). The expression of the previously established COVID-19-related covariance pattern was analyzed at both stages to examine the time course of post-COVID-19 cognitive impairment. For further validation, we also conducted a conventional group analysis. Results: Follow-up 18F-FDG PET revealed that there was a significant reduction in the initial frontoparietal and, to a lesser extent, temporal hypometabolism and that this reduction was accompanied by a significant improvement in cognition. The expression of the previously established COVID-19-related pattern was significantly lower at follow-up and correlated inversely with Montreal Cognitive Assessment performance. However, both 18F-FDG PET and cognitive assessment suggest a residual impairment. Conclusion: Although a significant recovery of regional neuronal function and cognition can be clearly stated, residuals are still measurable in some patients 6 mo after manifestation of COVID-19. Given the current pandemic situation and tremendous uncertainty concerning the long-term effects of COVID-19, the present study provides novel insights of the highest medical and socioeconomic relevance.


Subject(s)
COVID-19/physiopathology , Cognitive Dysfunction/complications , Neocortex/physiopathology , Recovery of Function , Adult , Aged , COVID-19/complications , COVID-19/diagnostic imaging , Chronic Disease , Cognitive Dysfunction/physiopathology , Female , Fluorodeoxyglucose F18 , Follow-Up Studies , Humans , Male , Middle Aged , Positron Emission Tomography Computed Tomography
7.
Neurol Res Pract ; 3(1): 17, 2021 Mar 12.
Article in English | MEDLINE | ID: covidwho-1133618

ABSTRACT

BACKGROUND: The SARS-Coronavirus-2 (SARS-CoV-2) invades the respiratory system, causing acute and sometimes severe pulmonary symptoms, but turned out to also act multisystematically with substantial impact on the brain. A growing number of studies suggests a diverse spectrum of neurological manifestations. To investigate the spectrum of symptoms, we here describe the neurological manifestations and complications of patients with proven SARS-CoV-2 infection who have been hospitalized at the RWTH University Hospital Aachen, Germany. METHODS: Between March and September 2020, we evaluated common symptoms, clinical characteristics, laboratory (including cerebrospinal fluid (CSF) analysis), radiological, and electroencephalography (EEG) data from 53 patients admitted with a positive SARS-CoV-2 polymerase chain reaction (PCR). We used the Montreal Cognitive Assessment Test (MoCA) to screen for cognitive impairment, when feasible. We compared critically ill and non-critically ill patients categorized according to the presence of Acute Respiratory Distress Syndrome (ARDS). RESULTS: Major clinical neurological features of hospitalized COVID-19 patients were coordination deficits (74%), cognitive impairment (61.5%), paresis (47%), abnormal reflex status (45%), sensory abnormalities (45%), general muscle weakness and pain (32%), hyposmia (26%), and headache (21%). Patients with ARDS were more severely affected than non-ADRS patients. 29.6% of patients with ARDS presented with subarachnoid bleedings, and 11.1% showed ischemic stroke associated with SARS-CoV-2 infection. Cognitive deficits mainly affected executive functions, attention, language, and delayed memory recall. We obtained cerebrospinal fluid (CSF) by lumbar puncture in nine of the 53 patients, none of which had a positive SARS-CoV-2 PCR. CONCLUSIONS: In line with previous findings, our results provide evidence for a range of SARS-CoV-2-associated neurological manifestations. 26% of patients reported hyposmia, emphasizing the neuro-invasive potential of SARS-CoV-2, which can enter the olfactory bulb. It can therefore be speculated that neurological manifestations may be caused by direct invasion of the virus in the CNS; however, PCR did not reveal positive intrathecal SARS-CoV-2. Therefore, we hypothesize it is more likely that the para-infectious severe pro-inflammatory impact of COVID-19 is responsible for the neurological deficits including cognitive impairment. Future studies with comprehensive longitudinal assessment of neurological deficits are required to determine potential long-term complications of COVID-19.

8.
Int J Audiol ; 61(2): 97-101, 2022 02.
Article in English | MEDLINE | ID: covidwho-1132306

ABSTRACT

OBJECTIVE: To investigate whether hearing difficulties exacerbate the damaging effects of enforced social distancing due to the COVID-19 pandemic on isolation and loneliness, and lead to accelerated mental health issues and cognitive dysfunction. DESIGN: Rapid online survey. Participants completed a series of online questionnaires regarding hearing ability, socialisation (pre- and during-pandemic), loneliness, anxiety, depression and cognitive function. STUDY SAMPLE: A total of 80 participants over the age of 70 with access to the internet. RESULTS: There was a significant reduction in socialisation levels from pre-pandemic in this population. Hearing difficulties were significantly associated with greater levels of loneliness, depression and self-perceived cognitive dysfunction after controlling for age, gender, and level of education. Additionally, compared to pre-pandemic, people with hearing difficulties had increased odds of reporting worsened anxiety, depression, and memory during the COVID-19 pandemic, although only the effect of hearing difficulties on the change in memory reached statistical significance after controlling for age, gender, and level of education. CONCLUSIONS: The worse the self-reported hearing abilities are, the greater the negative impact of enforced social distancing on depression, loneliness and cognitive function.


Subject(s)
COVID-19 , Cognitive Dysfunction , Depression/diagnosis , Depression/epidemiology , Hearing , Humans , Loneliness , Pandemics , SARS-CoV-2 , Self Report
9.
Ther Adv Neurol Disord ; 14: 1756286420985175, 2021.
Article in English | MEDLINE | ID: covidwho-1081096

ABSTRACT

Neurological complications of the newly appeared severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are increasingly recognized. Here, we report a case of a young male presenting with a clinical and neuroimaging scenario of an acute necrotizing encephalopathy related to the coronavirus disease 2019 (COVID-19). This case is notable by its distinct pattern of magnetic resonance imaging findings of an extensive involvement of the cerebellum, and emergence of cognitive and behavioral impairment.

10.
Neurol Neuroimmunol Neuroinflamm ; 8(1)2021 01.
Article in English | MEDLINE | ID: covidwho-975946

ABSTRACT

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the cause of the coronavirus disease 2019 (COVID-19) pandemic. In addition to severe respiratory symptoms, there are a growing number of reports showing a wide range of CNS complications in patients with COVID-19. Here, we review the literature on these complications, ranging from nonspecific symptoms to necrotizing encephalopathies, encephalitis, myelitis, encephalomyelitis, endotheliitis, and stroke. We postulate that there are several different mechanisms involved in COVID-19-associated CNS dysfunction, particularly activation of inflammatory and thrombotic pathways and, in a few patients, a direct viral effect on the endothelium and the parenchyma. Last, critically ill patients frequently present with protracted cognitive dysfunction in the setting of septic encephalopathy likely due to multifactorial mechanisms. Further studies are needed to clarify the relative contribution of each of these mechanisms, but available data suggest that CNS complications in COVID-19 are rare and probably not directly caused by the virus.


Subject(s)
Brain/metabolism , Brain/pathology , COVID-19/complications , COVID-19/metabolism , Central Nervous System Diseases/etiology , Central Nervous System Diseases/metabolism , Brain/immunology , COVID-19/immunology , Central Nervous System Diseases/immunology , Humans , Inflammation Mediators/immunology , Inflammation Mediators/metabolism
11.
J Alzheimers Dis ; 78(4): 1367-1372, 2020.
Article in English | MEDLINE | ID: covidwho-968075

ABSTRACT

We analyzed the frequency of cognitive impairment (CI) in deceased COVID-19 patients at a tertiary hospital in Spain. Among the 477 adult cases who died after admission from March 1 to March 31, 2020, 281 had confirmed COVID-19. CI (21.1% dementia and 8.9% mild cognitive impairment) was a common comorbidity. Subjects with CI were older, tended to live in nursing homes, had shorter time from symptom onset to death, and were rarely admitted to the ICU, receiving palliative care more often. CI is a frequent comorbidity in deceased COVID-19 subjects and is associated with differences in care.


Subject(s)
COVID-19/psychology , Cognitive Dysfunction/psychology , Adolescent , Adult , Age Factors , Aged , Aged, 80 and over , COVID-19/epidemiology , COVID-19/mortality , Cognitive Dysfunction/epidemiology , Cognitive Dysfunction/etiology , Comorbidity , Female , Hospital Mortality , Hospitals , Humans , Male , Middle Aged , Palliative Care , Patient Admission/statistics & numerical data , Retrospective Studies , Spain/epidemiology , Young Adult
12.
J Korean Med Sci ; 35(42): e383, 2020 Nov 02.
Article in English | MEDLINE | ID: covidwho-902392

ABSTRACT

Multiple neurological complications have been associated with the coronavirus disease-19 (COVID-19), which is caused by severe acute respiratory syndrome coronavirus 2. This is a narrative review to gather information on all aspects of COVID-19 in elderly patients with cognitive impairment. First, the following three mechanisms have been proposed to underlie the neurological complications associated with COVID-19: 1) direct invasion, 2) immune and inflammatory reaction, and 3) hypoxic brain damage by COVID-19. Next, because the elderly dementia patient population is particularly vulnerable to COVID-19, we discussed risk factors and difficulties associated with cognitive disorders in this vulnerable population. We also reviewed the effects of the patient living environment in COVID-19 cases that required intensive care unit (ICU) care. Furthermore, we analyzed the impact of stringent social restrictions and COVID-19 pandemic-mediated policies on dementia patients and care providers. Finally, we provided the following strategies for working with elderly dementia patients: general preventive methods; dementia care at home and nursing facilities according to the activities of daily living and dementia characteristics; ICU care after COVID-19 infection; and public health care system and government response. We propose that longitudinal follow-up studies are needed to fully examine COVID-19 associated neurological complications, such as dementia, and the efficacy of telemedicine/telehealth care programs.


Subject(s)
Coronavirus Infections/epidemiology , Coronavirus Infections/prevention & control , Dementia/epidemiology , Health Services for the Aged , Pandemics/prevention & control , Pneumonia, Viral/epidemiology , Pneumonia, Viral/prevention & control , Activities of Daily Living , Aged , Betacoronavirus , Brain/physiopathology , COVID-19 , Caregivers , Cognitive Dysfunction/complications , Cognitive Dysfunction/epidemiology , Coronavirus Infections/complications , Critical Care , Dementia/complications , Humans , Hypoxia , Immune System , Inflammation , Nursing Homes , Pneumonia, Viral/complications , Preventive Medicine , Public Health , Risk Factors , SARS-CoV-2 , Social Isolation , Telemedicine
14.
Australas J Ageing ; 39(3): 283-286, 2020 Sep.
Article in English | MEDLINE | ID: covidwho-868008

ABSTRACT

OBJECTIVE: We developed interim guidance for the care of patients with cognitive impairment in hospital during the COVID-19 pandemic. METHODS: A Guidance Committee and Readers Group were recruited. The content was identified by the Committee and content-specific subgroups, resulting in a draft document, which was sent to the Readers for review. People with dementia and care partners were involved in all aspects of the process. RESULTS: Infection control measures can lead to an escalation of distress. In an environment where visiting bans are applied to care partners/advocates, hospitals need to ensure care partners can continue to provide decision-making support. Health-care professionals can proactively engage care partners using videoconferencing technologies. Developing models of care that proactively support best practice can minimise the risk of delirium, mitigate escalating symptoms and guide the use of non-pharmacological, pharmacological (start low, go slow) or physical restraint in managing behavioural and psychological symptoms.


Subject(s)
Betacoronavirus , Cognitive Dysfunction/psychology , Cognitive Dysfunction/therapy , Coronavirus Infections/epidemiology , Coronavirus Infections/prevention & control , Infection Control/organization & administration , Pandemics/prevention & control , Pneumonia, Viral/epidemiology , Pneumonia, Viral/prevention & control , Adult , Australia , COVID-19 , Coronavirus Infections/transmission , Hospitalization , Humans , Pneumonia, Viral/transmission , SARS-CoV-2
15.
J Psychiatr Res ; 129: 98-102, 2020 10.
Article in English | MEDLINE | ID: covidwho-625731

ABSTRACT

This study aims to evaluate the impacts of COVID-19 on cognitive functions in recovered patients and its relationship with inflammatory profiles. Twenty-nine patients recovered from COVID-19 as confirmed by negative nucleic tests for two consecutive times were recruited. A total of 29 age-, gender- and education-matched healthy controls were also recruited. The cognitive functions of all subjects were evaluated by the iPad-based online neuropsychological tests, including the Trail Making Test (TMT), Sign Coding Test (SCT), Continuous Performance Test (CPT), and Digital Span Test (DST). Blood samples from all patients were collected for examining inflammatory profiles, including interleukin-2 (IL-2), IL-4, IL-6, IL-10, tumor necrosis factor-α (TNF-α), interferon-γ (IFN-γ), and C-reactive protein (CRP). The relationship between cognitive functions and inflammatory profiles were analyzed by Pearson correlation. In results, although no significant differences were found in TMT, SCT, and DST between the two groups, patients with COVID-19 scored lower in the correct number of the second and third parts of CPT, they also scored higher in the missing number of the third part of CPT (all P < 0.05). In patients with COVID-19, there was a trend of significant difference for lower reaction time in the first and second parts of CPT (P = 0.050, and 0.051, respectively), as well as the lower correct number of the second part of CPT (P = 0.050). Correlation analysis showed that the reaction time for the first and second parts of CPT was positively correlated with the CRP levels (r = 0.557 and 0.410, P < 0.05). In conclusion, our findings indicated that cognitive impairments exist even in patients recovered from COVID-19, and might be possibly linked to the underlying inflammatory processes.


Subject(s)
Betacoronavirus , Cognitive Dysfunction/complications , Coronavirus Infections/complications , Inflammation/complications , Pneumonia, Viral/complications , Survivors/statistics & numerical data , Adult , COVID-19 , Cognitive Dysfunction/diagnosis , Coronavirus Infections/psychology , Female , Humans , Male , Middle Aged , Neuropsychological Tests/statistics & numerical data , Pandemics , Pneumonia, Viral/psychology , SARS-CoV-2
SELECTION OF CITATIONS
SEARCH DETAIL