Abstract
Although the etiopathology of normal pressure hydrocephalus (NPH) is still not completely defined, several studies in recent years have highlighted the role of neuro-inflammation mediators in its development. During COVID-19, the infected host develops a multifaceted inflammatory syndrome, that may lead to an uncontrolled immune system response also localized in the host nervous system. In fact, the target of the viral Spike protein, the angiotensin-converting enzyme 2 (ACE2) receptors, is widely expressed in different areas of CNS such as the olfactory epithelium, and the choroid plexus. As for idiopathic NPH, the massive release of inflammatory mediators may result in altered CSF dynamics and consequent sudden clinical decompensation. We report the cases of two patients with a known iNPH condition, in which neurological symptoms suddenly worsened, requiring hospitalization, without any evident precipitating cause. Both patients tested positive for the COVID-19 virus shortly after the neurological impairment, which had occurred, therefore, during the incubation period of the infection. On the basis of our experience we advise, in cases of NPH patients with sudden neurological worsening, to perform a molecular COVID-19 swab at the moment of clinical impairment. We, therefore, recommend considering SARS-CoV-2 infection in the differential diagnosis of a sudden and otherwise unexplainable impairment of hydrocephalic patients. Furthermore, we believe clinicians should invite NPH patients to adopt adequate preventive measures to protect them from SARS-CoV-2 infection.