We read with interest the article by Mudabbir et al. about a 41 years old male who was diagnosed with “acute cerebellar ataxia (ACA)” starting two weeks after complete resolution of a COVID-19 infection [1]. The patient profited from steroids and recovered completely within 10 days after starting the therapy [1]. The study is appealing but raises concerns that need to be discussed. We do not agree with the notion that the patient had SARS-CoV-2 associated cerebellitis [1]. The patient had pre-existing cerebellar atrophy on imaging [1]. Therefore, it is more likely that previously asymptomatic cerebellar atrophy became symptomatic from the viral infection.

There is a discrepancy between the three-day history of “walking difficulty” and the normal gait on clinical neurologic exam [1]. This discrepancy should be solved. 

We do not agree with the statement that the most common manifestations of neuro-COVID are stroke, cerebral hypoxia, epilepsy, and critical ill neuropathy/myopathy [1]. The most common manifestations of neuro-COVID are headache, ageusia, anosmia, and Guillain-Barre syndrome (GBS) [2]. Hypoxic encephalopathy is extremely rare as patients with respiratory insufficiency are usually well monitored for their oxygen saturation and immediately supplied with oxygen or even mechanically ventilated in case of desaturations.

Missing is an explanation of the cause of cerebellar atrophy. It is not conceivable that it developed during the SARS-CoV-2 infection but was rather pre-existing. We therefore should be told if the family history was positive for ataxia or a genetic disorder manifesting with ataxia.

Missing is the determination of the cytokine and chemokine profile in the CSF. Particularly, interleukine 6 (IL-6), IL-8, IL-1b, and TNF-alpha have been shown upregulated in the CSF of patients with neuro-COVID [3]. 

Missing is the MR venography to rule out venous sinus thrombosis.

Overall, the interesting study has some limitations and inconsistencies that call the results and their interpretation into question. Clarifying these weaknesses would strengthen the conclusions and could improve the status of the study. Affection of the cerebellum in COVID-19 is rather immune-mediated than infectious.