|Year : 2021 | Volume
| Issue : 2 | Page : 133-135
Marked cognitive decline following COVID-19 infection
Sandeep Grover, Aseem Mehra, Swapnajeet Sahoo, Parvaiz Alam
Department of Psychiatry, Post Graduate Institute of Medical Education and Research, Chandigarh, India
|Date of Submission||08-Jan-2022|
|Date of Decision||10-Jan-2022|
|Date of Acceptance||12-Jan-2022|
|Date of Web Publication||31-Jan-2022|
Dr. Sandeep Grover
Department of Psychiatry, Postgraduate Institute of Medical Education and Research, Chandigarh - 160 012
Source of Support: None, Conflict of Interest: None
COVID-19 pandemic has influenced humans in many ways. In terms of mental health outcomes, many studies across the globe have shown a high prevalence of anxiety and depression among persons suffering from the acute COVID infection and during the post-COVID infection phase. Additionally, studies have also shown a high prevalence of cognitive deficits as part of the long COVID. In this report, we present a 63-year-old male who developed marked cognitive impairment after COVID-19 infection.
Keywords: Cognition, cognitive impairment, COVID-19
|How to cite this article:|
Grover S, Mehra A, Sahoo S, Alam P. Marked cognitive decline following COVID-19 infection. J Geriatr Ment Health 2021;8:133-5
|How to cite this URL:|
Grover S, Mehra A, Sahoo S, Alam P. Marked cognitive decline following COVID-19 infection. J Geriatr Ment Health [serial online] 2021 [cited 2023 Jun 4];8:133-5. Available from: https://www.jgmh.org/text.asp?2021/8/2/133/336915
| Introduction|| |
The rapid emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), officially named as COVID-19 by the World Health Organization, is characterized by common symptoms of fever, dry cough, tiredness, myalgia, headache, sore throat, diarrhea, conjunctivitis, anosmia, loss of taste, dyspnea, dizziness, confusion, and epileptic seizure and in severe cases can lead to respiratory failure., The neurological manifestation of the COVID-19 has been postulated to be due to the direct impact on the central nervous system (CNS), and in severe cases of COVID-19, cerebral hypoxia is considered to be the contributory factor for manifestation of neurological symptoms.
It is a well-known fact that CNS viral infection and cerebral hypoxia have been associated with cognitive impairment, which can be transient or long lasting. Earlier epidemics of SARS and Middle East respiratory syndrome suggested an association between the viral infections with poor concentration, decline in memory, executive dysfunctions, etc., indicating cognitive impairment.
The studies done during the ongoing COVID-19 pandemic suggest that about one-third of the patients report neurological symptoms, and are associated with a negative impact on the patient's cognitive functions. However, the data are limited. To the best of our knowledge, only one study evaluated the impact of COVID-19 on neurocognitive performance. Those patients who presented with headache, anosmia, dysgeusia, diarrhea, and required oxygen therapy scored low on the domain of memory, executive functions, and attention as compared to the asymptomatic patients. The major limitation was that those with cognitive impairment scored high on the domain of anxiety and depression, which can be considered as confounding factors for cognitive functioning. However, there is a lack of literature on development of severe cognitive impairment following COVID-19 infection. In the present case report, we present a case of an elderly male who presented with the symptoms of marked cognitive decline as sequelae of COVID-19 and discussing the possible causes of cognitive decline.
| Case Report|| |
A 63-year-old married male, self-employed, studied up to 12th std., known to be suffering from hypertension (on metoprolol 20 mg/day) for the last 20 years, developed complaints of fever, myalgia, and difficulty in breathing. On investigation, he tested positive for COVID-19 infection on reverse transcriptase-polymerase chain reaction test and at the initial assessment was found to have an oxygen saturation of 86% (SPO2). He was actively working prior to being diagnosed with COVID-19, and there was no evidence of any cognitive decline.
Following which, the patient was admitted in the intensive care unit (ICU) and remained there for 4 weeks. During this period, he was on oxygen support for the major part of the ICU stay. As per the family members, whenever they would talk with the patient over the video call during his ICU stay, although he would be conscious, at times patient would not be able to recognize them. However, his speech would be coherent, and he would be oriented to place. As per the medical records, he had few episodes suggestive of delirium during the ICU stay.
After 4 weeks, his condition stabilized, and he was shifted to the general ward. On repeat testing, he was found to be COVID-19 negative, and the family was allowed to meet him and later discharged from the hospital in a week time. Since the time he was shifted to the general ward while interacting with the patient, family members noticed that he would have difficulty in finding suitable words for things around, for example, he would not be able to name the fruits, was not able to carry out routine activities like brushing, was not able to follow the conversation, and appeared perplexed. The patient had difficulty in recalling the recent activities and, at times, would become irritable without any appropriate reason. There was no history of fluctuation of symptoms, impaired consciousness, incoherent speech, altered sleep–wake cycle, psychotic symptoms, depressive symptoms, anxiety symptoms, or features suggestive of posttraumatic stress disorder. The cognitive impairment was so severe that he was not able to perform his day-to-day activities and required assistance in functioning. On initial evaluation, on Hindi mental state examination, he scored 9 out of 31, with dysfunction in the domains of attention, orientation, registration, recall, and executive functions. Magnetic resonance imaging of the brain revealed left temporoparietal cortical and subcortical T2 flair hyperintensities with significant restricted diffusion suggestive of hypoxic injury. Considering the clinical picture, a possibility of dementia (due to hypoxic injury) was considered, and he was started on tablet donepezil 5 mg/day along with cognitive retraining in the form of grain sorting, playing with color boxes, making things with cards, etc., were started. At 1 month follow-up, HMSE was repeated, and no improvement was seen in the level of cognitive functioning. There was no improvement in his level of performance of day-to-day activities.
| Discussion|| |
Although studies have reported a negative impact of COVID-19 on cognitive functioning, there is no data to suggest that the COVID-19 infection leads to dementia. The negative impact of the COVID-19 infection on the cognitive functioning can be attributed to a combination of the presence of risk factors for cognitive impairment (older age and hypertension) prior to the development of COVID-19 infection, development of severe and prolonged hypoxia during COVID-19 infection, development of delirium, and the direct effect of the virus on the brain. Available evidence suggests an association of cognitive impairment with oxygen therapy during hospitalization, advanced age, presence of medical comorbidities like hypertension, diabetes mellitus, obesity, and smoking.,, The association of delirium and dementia is well known, with a six times higher risk of developing dementia in elderly patients who develop delirium during the hospital stay.
As the pandemic is progressing and we are becoming more and more aware about the impact of COVID-19 on the brain tissue, people are feeling scared about the long-term consequences of the infection. Available data suggest that people with COVID-19 infection can have swelling and inflammation of the brain tissue, and disruption of the myelin tissues. In terms of neuropsychiatric symptoms, emerging data also suggest the emergence of symptoms of stroke, hemorrhage, altered mental state, confusion, prolonged unconsciousness, psychosis, and memory loss. At present, it is not clear whether the virus directly invades the brain tissue and it is suggested the impact on the brain can be due to the immune mechanism. In some of these patients with neurological symptoms, the respiratory symptoms have not been severe, and it is suggested that the brain was one of the main organs affected.
In the index case, the patient developed severe hypoxia and delirium prior to manifesting with persistent cognitive symptoms amounting to dementia. He also had severe respiratory symptoms requiring prolonged oxygen support, suggesting that an inflammatory mechanism could also have played a role in the development of marked cognitive impairment in the index case. The index case adds to the limited literature on the neuropsychiatric manifestations of COVID-19 infection. The index case suggests that persons who develop COVID-19 infection should be routinely evaluated for their cognitive functions. All the patients who are at risk of developing delirium and dementia should be provided with reorientation cues and should be asked to keep themselves cognitive active while going through the active phase of the infection and after recovering from the infection. The index case also suggests that there is a need to evaluate the long-term effects of COVID-19 on the brain in large sample size studies.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
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