COVID-19 and Neurocognitive Disorders

Elizabeta B. Mukaetova-Ladinska; Golo Kronenberg; Ruma Raha-Chowdhury


Curr Opin Psychiatry. 2021;34(2):149-156. 

In This Article

DSM-5 Criteria for Neurocognitive Disorder

As the observed mental health symptoms are a result of a prolonged and repetitive stress situation (COVID-19 pandemic), affecting multiple domains of social and personal life, many of them are, thus, trauma inflicted. However, they fall short of the 'Trauma- and Stressor-Related Disorders' diagnosis as per the DSM-5 criteria that includes traumatic events as exposure to actual or threatened death/serious injury/sexual violence and experiencing repeated or extreme exposure to aversive details of the traumatic event.[4] Namely, the DSM-5 clearly states that vicarious trauma cannot be the result of repeated exposure via electronic or print media. It is understandable that the unexpected and emotionally traumatic experiences (caused by social and self-isolation, closure of schools, working from home, families kept apart and so on) and the scale we have and still continue to be witnessing could not have been predicted and considered at the time. However, the protracted repetitive psychological insults, either as result of the infection per sé or by proxy have already resulted in long-term mental health constructs within the long-COVID terminology or affecting the cognitive domains.

Neurocognitive disorders (NCDs) are one of these consequences. The latest DSM-5 classification introduced levels of impairment, mild and major. The latter new category encompasses the set of existing cognitive disorders contained in the DSM-IV,[5] including dementia and amnestic disorder. The introduction of mild NCDs, as per the DSM-5, aimed to facilitate both clinical diagnostic and therapeutic advances [i.e. early detection and treatment of cognitive decline prior it becoming more pronounced and progress to dementia (major neurocognitive)] and researchers to advance diagnostic and therapeutic opportunities. Most importantly, the latest NCD criteria enable the stratification of NCD categories not only in terms of the known dementia subtypes, that is Alzheimer's disease, vascular dementia, Lewy Body diseases (dementia with Lewy bodies and Parkinson's disease dementia), but also NCD due to (another) medical condition and multiple causes, apart from the substance/medication-induced NCD and unspecified NCD that are also included as diagnoses. The NCD now can also be used for the more subtle cognitive problems including subclinical, and even transient disorders of cognition, or their exacerbation as a result of the psychological response to the pandemic, irrespective of the age at onset (reviewed in[6]). This is of utmost importance to prevent further cognitive deterioration.

Among the number of modifiable dementia risk factors, depression, social isolation, physical inactivity, smoking and diabetes count for 16% of the total of 40% identified modifiable dementia risk factors.[7] Posttraumatic stress disorder (PTSD) is, similarly, a strong and potentially modifiable risk factor for all-cause dementia. The latest meta-analysis based on nine electronic databases, found PTSD hazard ratio to be 1.61 (n = 905 896; five studies) in veterans, and 2.11 (n = 787 782; three studies) in the general population.[8] Obsessive compulsive disorder (OCD) has been described to segregate in families with dementia[9] and late-onset OCD has been reported as a precursor for several neurodegenerative conditions characterized by neuropathological involvement of neocortical and/or basal ganglia areas, including Alzheimer's disease,[10] Lewy body dementia,[11] fronto-temporal lobe dementia, amyotrophic lateral sclerosis[12] and supranuclear palsy.[13] Furthermore, disruptions in the corticostriatal activity as present in amyotrophic lateral sclerosis, fronto-temporal dementia and supranuclear palsy, also underlie the development of Parkinson's disease.[14]

Although the mental health disorders per sé are not linked directly to Parkinsonian syndromes, the latest single case reports indicate that the COVID-19 infection alone may present with reduced nigrostriatal dopamine function, and result in acute transient Parkinson's disease in younger people (reviewed in[15]) and may suggest a particular susceptibility of the basal ganglia to both stress and nootropism of the SARS-CoV-2 virus. In support of this is the latest study based on a mathematical model demonstrating that the neuroanatomical distribution of small neurological symptoms due to COVID-19 infection, as seen on neuroradiological (MRI) brain scans, spreads outward from the basal ganglia to other cortical (i.e. temporo-occipital cortices) and spinal areas,[16] thus placing the subcortex as one of the main brain areas that are susceptible to SARS-CoV-2 infection.