Cognitive Complications of COVID-19 Infection.

SARS-CoV-2 is associated with a post-infectious neurocognitive syndrome characterized by fatigue and deficits in attention, memory, and executive function. As screening cognitive testing generally remains normal, the pathophysiologic basis of these symptoms remains controversial and there is no standardized treatment paradigm. We present a clinical case demonstrative of typical neurocognitive sequelae of SARS-CoV-2 infection, highlighting medical and social factors that may have contributed to the severity of symptoms. We discuss the pathophysiologic evidence for cognitive "brain fog" following COVID-19 infection as well as lifestyle changes and rehabilitation strategies that may improve recovery. As the benefits of pharmacologic therapy remain unproven, we close with a brief discussion of medication options that might be appropriate targets for future clinical trials in the context of rehabilitative treatment.

Corpus Callosum in COVID-19 Cytokinopathy

Objective: Report a COVID-19 related encephalopathy from selective white matter involvement of corpus callosum. Background: A 26-year-old African American female tested positive for SARS - COV 2 in April 2020. Her medical morbidities included uncontrolled type 1 DM (on insulin), obesity, and CKD stage III (diabetic nephropathy). She presented with fever, headache, dyspnea, myalgia, nausea, and loss of appetite. She was tachypneic, tachycardic, hypertensive, had a temperature of 39.2deg;C and saturating 98% at room air. Pertinent lab values included a glucose of 212 mg/dl, creatinine of 2.7 mg/dl, BUN of 34 mg/dl, and lipase 771 IU/L. CRP was 66.9 mg/L, with a normocytic anemia of 7.9 gm/dl, ferritin 1784 ng/ml, fibrinogen of 651 mg/dl and a peak D-dimer of 10,180 ng/ml. CXR was hypoinflated with mild bibasilar airspace opacities. A NCCT head obtained for a stroke alert, revealed a hypodense corpus collosum. She was admitted to the ICU with worsening hypoxia, kidney injury, metabolic acidosis, and alteration of consciousness. She received tocilizumab, steroids, remdesivir and convalescent plasma exchange for a severe COVID-19 infection. After extubation she developed a dysexecutive syndrome. Design/Methods: Case report Results: A contrast enhanced MR brain confirmed an expansile T2 hyperintense signal along the complete length of corpus callosum associated with restriction of diffusion, and T1 prolongation. There was no superimposed susceptibility or pathologic enhancement. No large vessel occlusions were identifiable from gradient echo (GRE), turbo spin echo (TSE), susceptibility weighted imaging (SWI) and post contrast MR sequences. A repeat MRI brain post discharge demonstrated an improving leukoencephalopathy by virtue of normalizing ADC values. Conclusions: Like prior coronaviridae, severe acute respiratory syndrome coronavirus 2 (SARSCoV-2) affects the brain over a spectrum of injury. Until we clarify direct neurotropism of SARS-CoV-2;this case is supportive of a cytokine mediated excitotoxic injury concomitant with the severity of disease.

The Combined Use of Neuropsychiatric and Neuropsychological Assessment Tools to Make a Differential Dementia Diagnosis in the Presence of "Long-Haul" COVID-19.

The longer term neurocognitive/neuropsychiatric consequences of moderate/severe COVID-19 infection have not been explored. The case herein illustrates a complex web of differential diagnosis. The onset, clinical trajectory, treatment course/response, serial neuroimaging findings, and neuropsychological test data were taken into account when assessing a patient presenting 8 months post-COVID-19 (with premorbid attention-deficit hyperactivity disorder, diabetes mellitus, mood difficulties, and a positive family history of vascular dementia). Her acute COVID-19 infection was complicated by altered mental status associated with encephalopathy and bacterial pneumonia. After recovery from COVID-19, the patient continues to experience persisting cognitive and emotive difficulties despite an ongoing psychopharmacotherapy regimen (16 + years), psychotherapy (15 + sessions), and speech-language pathology SLP; 2 × week/for 12 weeks). The purpose of her most recent and comprehensive neuropsychological evaluation was to determine the presence/absence of neurocognitive disorder. The patient is a 62-year-old Caucasian woman. Cognitive screening was completed 3 months post-acute COVID-19 as part of an SLP evaluation, and a full neuropsychological evaluation was conducted 8 months post-COVID-19 recovery on an outpatient basis (in person). The patient had serial neuroimaging. Initial neurological evaluation during acute COVID-19 included unremarkable brain computed tomography (CT)/magnetic resonance imaging. However, follow-up CT (without contrast) revealed, in part, "asymmetric perisylvian atrophy on the left." Full neuropsychological evaluation at 8 months post-COVID-19 recovery revealed a dysexecutive syndrome characterized by language dysfunction and affective theory-of-mind deficit, consistent with dementia. There is need for careful use of differential diagnosis in COVID-19 patients with multiple risk factors that make them more susceptible to long-term neurological complications post-COVID-19. Differential diagnosis should involve multidisciplinary assessment (e.g., neuropsychology, SLP, neurology, and psychiatry).

Cognitive functions and SARS-CoV-2 infection

As of January 29, 2021, in the general population, the total number of people infected with the SARS-CoV-2 virus, which we call "convalescents", was 73,961,553. In how many patients in this group will we be able to observe long-term symptoms from the cognitive sphere? This is a question that we do not know the answer to to-day. However, more and more scientific reports indicate that cognitive deficits are a frequent and serious symptom in patients with active SARS-CoV-2 infection, as well as in those who have had the disease in the past. Common symptoms include: weakening of short-term memory efficiency, weakening of the attention function and the executive functions (e.g. difficulties with inhibiting reactions, planning and problem solving). The aim of the article is to present the current state of knowledge on the possible cognitive functioning in the acute phase of infection and in the recovery period, as well as to draw attention to the need to consider possible neurocognitive symptoms of the past infection in the diagnosis process.

Neuropsychological and neurophysiological correlates of fatigue in post-acute patients with neurological manifestations of COVID-19: Insights into a challenging symptom.

More than half of patients who recover from COVID-19 experience fatigue. We studied fatigue using neuropsychological and neurophysiological investigations in post-COVID-19 patients and healthy subjects. Neuropsychological assessment included: Fatigue Severity Scale (FSS), Fatigue Rating Scale, Beck Depression Inventory, Apathy Evaluation Scale, cognitive tests, and computerized tasks. Neurophysiological examination was assessed before (PRE) and 2 min after (POST) a 1-min fatiguing isometric pinching task and included: maximum compound muscle action potential (CMAP) amplitude in first dorsal interosseous muscle (FDI) following ulnar nerve stimulation, resting motor threshold, motor evoked potential (MEP) amplitude and silent period (SP) duration in right FDI following transcranial magnetic stimulation of the left motor cortex. Maximum pinch strength was measured. Perceived exertion was assessed with the Borg-Category-Ratio scale. Patients manifested fatigue, apathy, executive deficits, impaired cognitive control, and reduction in global cognition. Perceived exertion was higher in patients. CMAP and MEP were smaller in patients both PRE and POST. CMAP did not change in either group from PRE to POST, while MEP amplitudes declined in controls POST. SP duration did not differ between groups PRE, increased in controls but decreased in patients POST. Patients' change of SP duration from PRE to POST was negatively correlated to FSS. Abnormal SP shortening and lack of MEP depression concur with a reduction in post-exhaustion corticomotor inhibition, suggesting a possible GABAB-ergic dysfunction. This impairment might be related to the neuropsychological alterations. COVID-19-associated inflammation might lead to GABAergic impairment, possibly representing the basis of fatigue and explaining apathy and executive deficits.