Explanatory Models
The pathophysiological mechanisms underlying PCS remain unclear despite numerous laboratory and imaging findings. The following processes are currently considered to be the most relevant: [3]
- Viral persistence and/or reactivation
- Autoimmune processes
- Endothelial dysfunction
- Mitochondrial dysfunction
- Alterations of the (intestinal) microbiome
- Autonomic dysregulation
Furthermore, it remains an open question to what extent these findings represent truly meaningful evidence supporting a broadly accepted scientific hypothesis of PCS, or whether they should instead be regarded merely as epiphenomena.
A carefully conducted study involving 171 patients with PCS found abnormal findings in only 1.7% of cases based on clinical neurological examination, comprehensive neurophysiological testing, cranial MRI, and cerebrospinal fluid (CSF) analysis. However, the study provided evidence of significant psychiatric comorbidity and high levels of somatization. [4]
The role of psychosomatic factors in the predisposition to, triggering of, and maintenance of PCS remains the subject of considerable debate, both within the scientific community and—perhaps even more so—among the general public. The challenging overlap between the symptomatology of PCS and that of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is discussed further below.