**5. Aging, COVID-19, and neurocovid**

Frailty elderly are more prone to cognitive impairment and SAR-CoV-2 infection [3]. Preexisting comorbidities (i.e., cerebrovascular, and cardiovascular

#### *"Neurocovid": An Analysis of the Impact of Covid-19 on the Older Adults. Evolving Psychological… DOI: http://dx.doi.org/10.5772/intechopen.99414*

diseases, diabetes, hypertension, obesity, malignancy, and respiratory diseases) seem to be predictor of disease severity and neurological complications [40]. Moreover, elderly individuals with pre-existing neurological diseases are susceptible to more severe forms of COVID-19 infection and higher mortality rates [40, 41]. Indeed, it is now established that older people with Alzheimer's and Parkinson's diseases exhibit independent association with the rate of change in both physical frailty and cognitive impairment [42], placing these individuals at higher risk of COVID-19 disease severity [40]. Specifically, patients with Parkinson's disease are vulnerable to infection due to advanced age, bulbar symptoms, respiratory dysfunction, frailty and cognitive impairment. Similarly, patients with Alzheimer's disease and major neurocognitive disorder are at increased risk of infection and adverse events [43].

Elderly patients aged 65 years or older are known to have higher rates of neurological complications [40]. Commonly reported neurological dysfunctions include dizziness, confusion, fatigue, and headache. They may experience also atypical presentations such as falling or postural instability. Other neurological complications include cerebrovascular disease, cognitive impairment and neuropsychiatric disease [40]. Altered mental status and epilepsy have been also reported [25].

Older patients are particularly vulnerable to the psychological burden of COVID-19 [40]. Disturbed sleep, moderate to severe depression and anxiety have been reported [44]. Loneliness related to quarantine and social isolation has had a significant impact on mental health outcomes in the elderly [45], especially for those with chronic neurological diseases and neurocognitive disorder [46]. Quarantine comes to induce a rapid increase in behavioral and psychological symptoms in ~60% of patients and stress-related symptoms in two-thirds of caregivers [46]. The most common symptoms included agitation, anxiety, apathy, irritability, and sleep disturbances [46]. Similarly, a worsening of symptoms was observed in 67.5% of Parkinson's patients during the quarantine period [47].

#### **6. Implications for neurocognitive and neuropsychiatric disorders**

COVID-19 causes high levels of acute respiratory distress, hypoxia, and proinflammatory cytokines - all of which contribute to the onset of cognitive decline in the elderly [26]. It therefore seems reasonable that cardiovascular and cerebrovascular disease secondary to infection may contribute to an increased long-term risk of cognitive decline and major neurocognitive disorders in recovered individuals [26, 48, 49].

After the SARS pandemics, one in five infected individuals reported memory problems [50]. Likewise, the current pandemic situation appears to have resulted in a dysexecutive syndrome in one in three individuals who have been hospitalized [50]. Poor memory, attention and speed of information processing impairments have commonly been reported with COVID-19 [39, 51].

This could lead to a vicious circle whereby impaired cognitive abilities may cause poor occupational and functional outcomes for individuals recovered from COVID-19 that precipitate or exacerbate mental health concerns, and poor mental health may likewise contribute to cognitive dysfunction [52].

Abnormalities in the mental status (defined as a severe change in personality, behavior, cognition, or consciousness) have been reported [39, 53], in line with what happened previously with the SARS pandemic [26]. COVID-19 patients experienced a high level of post-traumatic stress symptoms and a significantly higher level of depressive symptoms [39, 54]. In the post-illness phase, the point prevalence of post-traumatic stress disorder seems to be around 32%, depression and anxiety disorder both around 15% [50]. Patients with pre-existing psychiatric disorders reported a worsening of their symptomatology [54].

Viral infections of the brain may have an impact on the risk of AD or Parkinson's disease [26]. Olfactory deficits (hyposmia/anosmia) are among the sentinel symptoms of COVID-19 infection [55] and are characteristic of neurodegenerative disorders [56–58]. Indeed, anosmia is associated with high levels of interleukin-6, an inflammatory mediator causally implicated in brain disorders and which action is blocked by tocilizumab as part of COVID-19 treatment [59].

To date, the mechanisms by which neurological abnormalities result from SARS-CoV-2 infection have yet to be fully established. Nevertheless, the contribution resulting from direct effects of SARS-CoV-2 on neuronal function and survival or glial reactivity, exaggerated cytokine responses or anti-neuronal antibodies are all likely, as are sequelae of cerebrovascular accidents [26]. The data available to date suggest an increase in neuropsychiatric and neuropsychological long-term sequelae, including cognitive decline, motor impairment, and affective and psychotic disorders [26].

#### **7. Management and treatment of neurocovid in elderly patients**

Treatment of neurocovid is currently based on existing evidence-based treatment for specific neurologic conditions in conjunction with systemic treatment of COVID-19 infection (i.e., antivirals, corticosteroids, and immunomodulators) [25, 40].

The contagion is associated with neuropsychiatric symptoms [60] and it is recommended to set up a baseline mental status examination for all hospitalized COVID-19 old patients [61].

Delirium management has long been a priority in the care of older adults [25]. Every hospitalized older person should be considered at high risk for developing delirium, and prevention should be optimized [58]. Non-pharmacologic interventions include patient-centered care with adequate hydration and sleep, optimization of hearing and vision, early mobilization, frequent re-orientation, reduction of social isolation and regular visits, connecting patients with their families, and minimization of unnecessary lines, tubes, polypharmacy, and precipitating medications [61, 62]. Low-potency neuroleptics and alpha-2 adrenergic agents may be useful [60].

Neurologists, geriatricians and neuropsychologists must be involved at an early stage and be prepared to handle the peculiarities of neurocovid. It is advisable to have patients undergo neuropsychological assessment even 6–8 months after their discharge from hospital, especially if cognitive problems, slowness in processing information or poor attention persist [39].

Patients with below cut-off test scores should be evaluated for rehabilitation and cognitive enhancement interventions. This would reduce the risk of facilitating an earlier/rapid age-related cognitive decline [3, 39].

#### **8. Conclusions**

The high probability of long-term neurological and neuropsychological consequences of COVID-19 indicates the importance of continuous surveillance for neuroimmune and neurodegenerative disorders in infected individuals, especially the elderly [7]. Until an effective treatment is discovered, or the expected global population-wide vaccination coverage is achieved, clinicians need to be alert to neurocovid [25].

*"Neurocovid": An Analysis of the Impact of Covid-19 on the Older Adults. Evolving Psychological… DOI: http://dx.doi.org/10.5772/intechopen.99414*

Researchers have postulated several explanations for the severity with which COVID-19 occurs in the elderly and the increased mortality rate in this population group. Age-related epigenetic changes, inflammasome activity, covalent modifications of human and viral proteins, etc. are all possibilities currently being explored by scientists [63]. Future research will lead to a full understanding of the key factors leading to the vulnerability of the elderly population, especially about the intersection of aging, vulnerability to infection and alterations in cognitive-behavioral patterns. A neurocognitive approach could prove extremely useful for this purpose. It seems particularly appropriate to deepen our knowledge of the deleterious effects of SARS-CoV-2 and COVID-19 infection on the central and peripheral nervous system (in both structural and functional terms), and to assess through predictive medicine how these effects may contribute to the chronic burden of disease in the coming years. Notably, key questions need to be answered about the impact of the risk of cognitive decline in old age, Alzheimer's disorder, Parkinson's disorder and other neurodegenerations. In addition, a change of pace in the observation of the various conditions of elderly life can make it possible to construct complementary health and welfare interventions that have the characteristic of elasticity and immediacy to be placed alongside the traditional ones - above all in response to phenomena such as neurocovid.
