Growing evidence is emerging that COVID-19 can lead to long-term neuropsychological deficits, even in its mild or moderate respiratory forms, a new study has concluded.
For years, health experts have suspected the presence of long-term neuropsychological deficits after SARS-C0V-2 infection, with studies about the two previous coronavirus outbreaks – the severe acute respiratory syndrome (SARS) and the Middle East respiratory syndrome (MERS) – demonstrating the presence of neuropsychological symptoms.
These include sleep disorders, emotional instability, impaired concentration, frequent recall of traumatic experiences, impaired memory and fatigue.
The symptoms were shown to manifest in more than 15 per cent of affected patients about one month to 3.5 years following infection.
Now, a team of researchers at the University of Geneva in Switzerland reports that SARS-CoV-2 may affect the central nervous system, particularly the limbic system responsible for behavioural and emotional responses.
The study demonstrates the presence of long-lasting neuropsychological sequelae after COVID-19, regardless of the respiratory disease’s severity.
The research team’s aim was to determine the effect of SARS-CoV-2 infection on the brain and investigate whether COVID-19 causes long-term neuropsychological deficits from 6 to 9 months and what impact this would have on a patient’s quality of life.
The team administered standardised neuropsychological, neurological, psychiatric, and olfactory tests to 45 patients.
The patients were divided into three groups, according to the severity of the respiratory disease in the acute phase: severe, moderate, or mild.
Severe cases were admitted in the intensive care unit with respiratory assistance, moderate cases were hospitalised without respiratory aid, and mild patients were not admitted to the hospital.
The researchers found a high prevalence of psychiatric symptoms, regardless of disease severity, in the illness’s acute phase.
Patients in all three groups manifested depressive symptoms, mania, anxiety, stress, apathy, post-traumatic stress disorder (PTSD), and dissociative disorders. Some patients reported insomnia, fatigue, and pathological somnolence.
With another known symptom of COVID-19, the loss of the sense of smell, 33.33 percent of the mild group, 73.33 percent of the moderate group, and 46.66 percent of the severe group experienced hyposmia or the partial loss of smell six to nine months after being infected.
Though the cognitive deficits reported in the three groups were common, some domains of cognition and mood were impacted differently, depending on the disease’s severity.
In long-term episodic memory, the severe group patients performed more poorly than the mild group. They also showed more anosognosia for memory dysfunction.
Meanwhile, the mild group was more stressed, anxious, depressed, and reported more cognitive issues. The moderate group recognized multimodal emotions less well than the mild group.
“At this stage, it is difficult to determine whether the cognitive deficits can be regarded as a marker of brain damage and/or should be linked to psychiatric variables that may themselves result directly from infection with SARS-CoV-2 or else be triggered by the stressful nature of the general pandemic and the individual experience of the disease,” the researchers say.
The team recommends that clinical guidelines and recommendations should be implemented in the management of long-term neurological impairment after SARS-CoV-2 infection.
