**1. Introduction**

Coronavirus disease 2019 (COVID-19) was initially defined as a disease that only causes respiratory system infiltration. However, in addition to major respiratory system symptoms, some systemic and neurocognitive symptoms were also detected in

the acute or subacute/chronic period [1]. In these studies, the sample size and clinical and sociodemographic characteristics of the patients were heterogeneous. Therefore, the relationship between COVID-19 disease and neurocognitive dysfunction could not be determined definitively. Recent studies confirmed this relationship. Based on these results, the disease was named "infectious disease-associated encephalopathy" or "Cognitive COVID [2]." Neurological deficits associated with COVID-19 disease were investigated in the several studies. Cognitive deficits were detected more frequently in the post-hospitalization period associated with COVID-19 disease [2–4]. In addition, severe cognitive impairment was observed in some patients with COVID-19 [5, 6].

Nonspecific encephalopathy symptoms (headache, confusion, delirium, disorientation, etc.) were detected in 25% (53/214) of hospitalized patients [7]. This rate is higher in studies reported from Europe. Neurocognitive disorders and psychosis were detected 69% in studies from France and 31% from the United Kingdom (UK) [8, 9]. In a recent study, inattention and disorientation were detected at a frequency of 33% after hospitalization in patients with COVID-19 disease [8]. Micro-structural changes and functional disorders were reported during 3-month follow-up of COVID-19 patients [10]. These results demonstrate that COVID-19 disease causes structural and functional changes in the brain over a long period.

Previous studies have emphasized that the pathogenesis of encephalopathy associated with infection is different from non-infectious encephalopathy. In the literature, there are some studies on the effects of influenza A virus subtype H1N1 (A/H1N1) virus and severe acute respiratory syndrome coronavirus (SARS-CoV) virus on the central nervous system. However, scientific data regarding the etiopathogenesis of cognitive impairment are insufficient [2, 3]. Many mechanisms were reported about the acute, subacute and chronic effects of the SARS-CoV-2 virus. The first mechanism is viral neurotropism. The second mechanism is the general systemic inflammation and secondary effects of cytokine storm. The rates of acute and chronic cognitive dysfunction are higher in patients with acute respiratory distress syndrome (ARDS) and mechanical ventilation [4]. The third mechanism is neurocognitive dysfunction associated with psychosocial isolation. Pandemic-related social isolation and increasing death rates have revealed neurocognitive and neuropsychiatric symptoms over a long period [3, 11]. Evaluating the mechanisms and results of this process is important for the disease and possible treatment strategies.

COVID-19 disease affects the central nervous system with vascular and parenchymal deficits. Many cases of encephalopathy associated with COVID-19 have been reported without cerebral lesions [12]. Patients with neurological clinical symptoms are older and have more severe respiratory symptoms [7]. It is known that SARS-CoV-2 infection directly affects the central nervous system. It also produces indirect neurotoxicity with systemic immune hyperinflammation [13]. Infections damage the endothelium in cerebral vascular structures as well as systemic vascular endothelial structures and blood-brain barrier (BBB). As a result, neurological symptoms are associated with this neuroinflammatory process [14]. Previous studies have reported a relationship between chronic infection and hippocampal atrophy [15]. These results support the relationship between infections and cognitive dysfunction.

Patients with severe respiratory symptoms should be frequently evaluated for neurocognitive dysfunction during the COVID-19 disease process. Particularly, patients with cerebrovascular disease and other neurological complications should be evaluated more frequently. Detailed cognitive evaluation including long-term neurological and psychiatric symptoms should be performed on these patients. We aim to evaluate

"Cognitive COVID" and its neuropathological process in this chapter. In addition, we aim to discuss the clinical features and etiopathogenetic process of the disease with the current literature and to present the results associated with treatment.
