We read with interest the case report by Della Corte et al. detailing a 12-year-old male with neuro-COVID presenting with drowsiness, memory impairment, prosopagnosia, myoclonus, and other neurological symptoms, all of which resolved following treatment with intravenous immunoglobulins (IVIG). While the case is noteworthy, we raise several concerns. The claim that this is the first pediatric case of SARS-CoV-2–associated myoclonus is questionable, as earlier reports have described similar presentations. Furthermore, the patient exhibited signs of Quadri spasticity, clonus, and a positive Babinski sign, suggesting involvement of the pyramidal tract—findings that were not fully explored in the original report. Discrepancies exist between the described clinical findings and the supplementary video data, particularly regarding limb involvement. Essential diagnostic details, such as video-EEG, spinal MRI, inflammatory markers (e.g., interleukin-6, D-dimer), and the exclusion of venous sinus thrombosis, are missing. The delayed initiation of a neurological work-up also raises concerns. While the report is significant for being the first to link prosopagnosia with pediatric neuro-COVID, other key neurological features were insufficiently addressed, limiting the strength and interpretation of the study’s conclusions.

We reviewed with interest the study by Diaz et al [1]. on three cases of Guillain-Barré Syndrome (GBS) associated with SARS-CoV-2 infection, all of whom were treated with intravenous immunoglobulins (IVIG) and showed favorable outcomes despite prolonged ICU stays. While the study contributes valuable insights, it presents several limitations. The diagnostic algorithm for GBS in sedated or ventilated patients should be expanded to include autonomic disturbances, cytokine profiles, and response to ex juvantibus IVIG. Important clinical details are missing, including the duration of intubation, timing of symptom recognition, and rationale for delayed GBS diagnosis in two patients. In one case, critical illness neuropathy and drug-induced neuropathy were not adequately ruled out. CSF analyses lacked SARS-CoV-2 PCR testing, and post-vaccination outcomes were not discussed. Autonomic dysfunction and cranial nerve involvement, especially facial diplegia, require further elaboration given their relevance in neuro-COVID. The use of the term “differential diagnoses” for infectious triggers of GBS is inappropriate and should be revised. Overall, while the study offers meaningful observations, these limitations should be addressed to strengthen its conclusions and clinical utility.

A limitation of the study is that a SARS-CoV-2 infection was not ruled out as the cause of gastro-enteritis leading to the initial admission. Because the events apparently took place after the start of the SARS-CoV-2 pandemic, it cannot be ruled out that the patient deteriorated because of an undiagnosed COVID-19 infection. Arguments for a SARS-CoV-2 infection are that the patient was institutionalized and manifested with gastro-enteritis. Institutionalized patients are at an increased risk of contracting and dying from a SARS-CoV-2 infection [2]. It is also known that SARS-CoV-2 infections can manifest itself not only in the lungs but also in extra-pulmonary sites, including the gastro-intestinal tract [3]. In patients with manifestations of COVID-19 with extra-pulmonary onset, the causative agent can be difficult to confirm. We should be told whether the patient was SARS-CoV-2 vaccinated at the time of the first deterioration. 

A limitation of the study is that a SARS-CoV-2 infection was not ruled out as the cause of gastro-enteritis leading to the initial admission. Because the events apparently took place after the start of the SARS-CoV-2 pandemic, it cannot be ruled out that the patient deteriorated because of an undiagnosed COVID-19 infection. Arguments for a SARS-CoV-2 infection are that the patient was institutionalised and manifested with gastro-enteritis. Institutionalised patients are at an increased risk of contracting and dying from a SARS-CoV-2 infection.[2] It is also known that SARS-CoV-2 infections can manifest itself not only in the lungs but also in extra-pulmonary sites, including the gastro-intestinal tract.[3] In patients with manifestations of COVID-19 with extra-pulmonary onset, the causative agent can be difficult to confirm. We should be told whether the patient was SARS-CoV-2 vaccinated at the time of the first deterioration.

Concerning cardiac compromise, we should know if Takotsubo Cardiomyopathy (TTS) was ruled out as a differential of the cardiological complaints. TTS has been repeatedly reported as a complication of SARS-CoV-2 vaccinations [2]. Arguments for TTS are that the myocardium was hypokinetic, that the ECG showed ST-depression, and that troponin and CK were elevated. TTS mimics myocardial infarction clinically, chemically, electro-physiologically, and on echocardiography but coronary angiography is normal.  Rhabdomyolysis has been repeatedly reported as a complication of SARS-CoV-2 vaccinations [3]. However, symptoms started with sensory disturbances [1]. Because the patient complained about sensory disturbances at onset and because Nerve Conduction Studies (NCSs) of the lower extremities revealed reduced amplitude of the sensory Nerve Action Potential (SNAP), sensory polyneuropathy or Small Fiber Neuropathy (SFN) need to be ruled out appropriately. Both sensory polyneuropathy and SFN have been previously reported as complications of SARS-CoV-2 vaccinations [4].