COVID-19 is frequently associated with a wide spectrum of neurological dysfunction that can persist long after the acute infection. Remsik et al. analysed cerebrospinal fluid from patients with cancer who had neurological manifestations after SARS-CoV-2 infection. They found an increase in intracranial inflammatory mediators such as IL-6, IL-8, IFNγ and MMP10, in the absence of viral neuroinvasion. IFNγ and its downstream effectors CXCL9, CXCL10 and CXCL11 were still elevated nearly 2 months after the infection and intracranial levels of MMP10 correlated with the degree of neurological dysfunction. These findings support the investigation of anti-inflammatory drugs to treat neurological symptoms following COVID-19.