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• W4385667480 abstract "The article by Durrleman et al. is excellent but has limitations. The first limitation is the definition of stroke-like episode (StLE). StLEs have been defined as both a clinical and a radiological phenomenon. Although both aspects are closely related, they should be strictly separated from each other for didactic, diagnostic and scientific reasons. The term StLE refers to the clinical presentation and its imaging correlate is termed a stroke-like lesion (SLL). Both terms were coined by the pioneers of mitochondrial medicine. The classic syndromic mitochondrial disorder (MID) in which StLEs/SLLs occur is mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes (MELAS). Another limitation is the definition of the imaging aspect of StLEs as “structural cerebral magnetic resonance imaging (MRI) lesion not confined to a vascular territory” [1]. The characterization of SLLs in MIDs is much more complex. Not only do they not correspond to any vascular territory, they also follow a specific dynamic. They initially enlarge and then usually recede. They eventually resolve without a remaining structural lesion or end up as laminar cortical necrosis, white matter lesion, cyst, focal atrophy or toenail sign [2]. In the expanding stage, SLLs in MIDs are hyperintense on T2/fluid attenuated inversion recovery, diffusion-weighted imaging and perfusion-weighted imaging, but hypointense on oxygen extraction fraction MRI [2]. Magnetic resonance angiography is normal, but magnetic resonance spectroscopy usually shows a lactate peak within the SLL. On fluorodeoxyglucose positron emission tomography, SLLs show up as hypometabolism [3]. The apparent diffusion coefficient shows only inconstant results [2]. A third limitation is the retrospective design. Disadvantages of the retrospective design are that differential diagnoses can no longer be ruled out, that missing data can no longer be recorded and that MRI technology might have changed over time. Differential diagnoses of SLLs not confined to a vascular territory include post-ictal hyperintensities, posterior reversible encephalopathy syndrome, acute disseminated encephalomyelitis, myelin oligodendrocyte glycoprotein antibody disease, neuromyelitis optica spectrum disorder, multiple sclerosis, extra-pontine myelinolysis and Wernicke encephalopathy. Another limitation is that the latency between recent seizures and cerebral MRI in patients with epilepsy was not recorded. Since seizures are one of the differentials of SLLs, it is imperative to rule out seizures as a cause of SLLs. In particular, from the 28 MRIs performed within 48 h of the onset of the clinical presentation, we should know how many of these patients had seizures. In addition, 95% of group 2 had epilepsy [1]. It is therefore conceivable that SLLs found in these patients were in fact a post-ictal phenomenon, well known to epileptologists [4]. Since patients with a genetic defect can also suffer from encephalitis and StLEs can be associated with headache, seizures, weakness and photophobia, it is crucial that encephalitis due to infectious or immunological causes has been ruled out. In particular, in the 16 patients with unknown cause of StLE, encephalitis should be ruled out by cerebrospinal fluid tests including tests of antibodies associated with autoimmune encephalitis. A shortcoming of the study is that only five of 16 patients in group 3 underwent whole exome sequencing (WES). Identifying the underlying cause of StLE is more likely when WES is performed. Overall, StLEs should be distinguished from SLLs as they describe two different aspects of the same phenomenon. SLLs in non-mitochondrial patients may have a different appearance and pathophysiology compared to those in MIDs. Josef Finsterer: conceptualization; validation; formal analysis; writing—review and editing; supervision. Sounira Mehri: conceptualization; validation; supervision. Financial disclosures for the previous 12 months: the authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The authors confirm that the approval of an institutional review board or patient consent was not required for this work. We confirm that we have read the journal's position on issues involved in ethical publication and affirm that this work is consistent with those guidelines. This article is based on previously conducted studies and does not contain any new studies with human participants or animals performed by any of the authors. The data that support the findings of this study are available from the corresponding author upon reasonable request." @default.
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• W4385667480 date "2023-08-17" @default.
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• W4385667480 title "Stroke‐like episodes and stroke‐like lesions: Two aspects of the same phenomenon" @default.
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• W4385667480 doi "https://doi.org/10.1111/ene.16033" @default.
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