From the beginning of the SARS-CoV-2 virus pandemic, it was clear that the virus is highly neurotrophic. Neurological manifestations can range from nonspecific symptoms such as dizziness, headaches and olfactory disturbances to severe forms of neurological dysfunction. Some neurological complication can occur even after mild forms of respiratory disease. This study’s aims were to assess cerebrovascular reactivity in patients with nonspecific neurological symptoms after SARS-CoV-2 infection. A total of 25 patients, aged 33–62 years, who had nonspecific neurological symptoms after SARS-CoV-2 infection, as well as 25 healthy participants in the control group, were assessed for cerebrovascular reactivity according to transcranial color Doppler (TCCD) which we combined with a breath-holding test (BHT). In subjects after SARS-CoV-2 infection, there were statistically significantly lower flow velocities through the middle cerebral artery at rest period, lower maximum velocities at the end of the breath-holding period and lower breath holding index (BHI) in relation to the control group. Changes in cerebral artery flow rate velocities indicate poor cerebral vasoreactivity in the group after SARS-CoV-2 infection in regard to the control group and suggest vascular endothelial damage by the SARS-CoV-2 virus.

From the beginning of SARS-CoV-2 virus pandemic, it was clear that respiratory symptoms are often accompanied with neurological symptoms. Neurological manifestations can occur even after mild forms of respiratory disease, and neurological symptoms are very often associated with worsening of the patient’s condition. The aim of this study was to show abnormal brain neuroimaging findings evaluated by MRI in patients after SARS-CoV-2 infection and neurological symptoms. Methods: Sixteen patients after mild forms of SARS-CoV-2 infection, twenty-three patients after moderate forms of SARS-CoV-2 infection as well as sixteen healthy participants in the control group underwent MRI 3T brain scan. All subjects in the SARS-CoV-2 group had small, punctuate, strategically located and newly formed hyperintense lesions on T2 and FLAIR sequences. New lesions were formed more often in the bilateral frontal subcortical and bilateral periventricular, correlated with the severity of the clinical picture. These changes indicate an example of silent cerebrovascular disease related to SARS-CoV-2 and once again emphasize the neurotropism of the virus.

In addition to respiratory symptoms, COVID-19 often causes damage to many other organs, especially in severe forms of the disease. Long-term consequences after COVID-19 are common and often have neurological symptoms. Cerebral vasoreactivity may be impaired after acute COVID-19 and in our study, we wanted to show how constant and reversible are the changes in brain vasoreactivity after infection. This cross-sectional observational study included 49 patients diagnosed with COVID-19 and mild neurological symptoms 300 days after the onset of the disease. We used a transcranial color-coded Doppler (TCCD) and a breath-holding test (BHT) to examine cerebral vasoreactivity and brain endothelial function. We analyzed the parameters of the flow rate through the middle cerebral artery (MCA): peak systolic velocity (PSV), end-diastolic velocity (EDV), mean velocity (MV), resistance index (RI) and pulsatility index (PI), and we calculated the breath-holding index (BHI). Subjects after COVID-19 infection had lower measured velocity parameters through MCA at rest period and after BHT, lower relative increases of flow velocities after BHT, and lower BHI. We showed that subjects, 300 days after COVID-19, still have impaired cerebral vasoreactivity measured by TCCD and they have chronic endothelial dysfunction.

Recurrent episodes of hypersomnia, hypersexuality, compulsive eating, behavioral and cognitive disturbances, are the basic clinical features of Kleine-Levin syndrome (KLS). Our case report describes a patient who was diagnosed with KLS at the age of 20. With appropriate therapy, the disease had a satisfactory course until patient had a moderate form of SARS-CoV-2 infection, which led to a significant exacerbation of all symptoms. SARS-CoV-2 virus can cause almost any neurological disease, and relapse of KLS is another evidence of neurotropicity of the virus.