Before blaming SARS-CoV-2 vaccines for thalamic lacunar stroke, alternative etiologies must be ruled out.

We read with interest the article by Shahali et al. [1] about a 72-year-old male who was admitted 9 days after the first dose of the AstraZeneca vaccine for headache, dizziness, gait disturbance with a tendency to fall, and right-sided hemichorea. The neurological deficits were attributed to left thalamic lacunar stroke due to vaccination-induced immune thrombotic thrombocytopenia and treatment with low molecular heparin (nadroparin), ozagrel, edaravone, prednisolone, and haloperidol was started. Two weeks after the start, the patient received warfarin [1]. The outcome after 3 weeks was described as “satisfactory” [1]. The study is excellent but raises concerns that should be discussed. We disagree with the notion that there is a causal relationship between vaccination and thalamic stroke. In addition to vaccination, several other causes of lacunar stroke have not been ruled out. The patient has not undergone echocardiography to rule out congestive heart failure, cardiomyopathy, myocardial ischemia, Takotsubo syndrome, noncompaction, endocarditis, or myocarditis. Or do the authors mean “echocardiography” when they use the term “echo-Doppler”? The results of the standard electrocardiogram or Holter recordings are not mentioned. Because a lacunar stroke can also be embolic, it is crucial to rule out all causes of cardioembolism, including atrial fibrillation or ventricular arrhythmias. There is no evidence of blood pressure monitoring at admission or during the 3-week hospital stay. Readers were not informed of hemoglobin A1c levels, pro-natriuretic peptide levels, or troponin levels. No information was given on anti-nuclear and anti-neutrophil cytoplasmic antibodies. There is also no information on the results of the carotid ultrasound. Because lacunar stroke is most commonly caused by microangiopathy, it is crucial that studies of generalized atherosclerosis have been performed. It remains unclear whether the patient was a smoker or not. We do not know if the patient had hyperlipidemia or a normal lipid profile. No evidence has been provided that the thalamic lesion shown in Fig. 1 of Shahali et al. [1] truly represents cytotoxic edema. We were to be told whether the apparent diffusion coefficient maps were hypo-, iso-, or hyperintense. Especially in a patient with no history of cardiovascular risk factors, it is important that cerebral ischemia be confirmed or ruled out by multimodal magnetic resonance imaging. The patient was admitted because of headache, but no explanation for the headache was given. The D-dimer was significantly increased [1]. Therefore, it is important that venous sinus thrombosis is adequately ruled out by magnetic resonance venography © Korean Vaccine Society. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (https://creativecommons.org/licenses/ by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. K O R E A N V A C C I N E S O C I E T Y