In 7 people having mild/moderate coronavirus disease, a subacute cognitive syndrome was observed that was suggestive of SARS-CoV-2-elicited impairment to the cortico-subcortical associative pathways. Such dysfunctions can not be attributed solely to hypoxia and inflammation, as per the findings of a study published in Frontiers in Neurology.

This case series describes cases of outpatients (age 18 to 60 years) suffering from prior SARS-CoV-2 infection who developed subacute cognitive disturbances. Notably, people who presented with encephalopathy at least seven days following the manifestations of respiratory symptoms were examined.

Using Enzyme-Linked Immunosorbent Assay (ELISA) kit, testing of paired sera and cerebrospinal fluid for SARS-CoV-2 IgA and IgG antibodies was done. With the aid of reverse transcription-polymerase chain reaction (RT-PCR), SARS-CoV-2-specific RNA was tested. With the aid of IgG index and oligoclonal bands, evaluation of serum and intrathecal antibody dynamics was done. Examination of cognitive dysfunctioning was carried out via Clock Drawing Test (CDT), Mini-Mental State Examination (MMSE), and Montreal Cognitive Assessment (MoCA).

Following the initial coronavirus symptoms, the neurologic symptoms were first reported at a median of sixteen days. All the participants were found to have a headache and changed behaviour.

Cognitive impairment was noted majorly in phonemic verbal fluency (assessed via MoCA) with a median of 6 words/minute and modified visuospatial construction with a median of 4 points (assessed via CDT). The cerebrospinal fluid pleocytosis was not noticed. Only 1 participant was reported to be positive for coronavirus.