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BackgroundIntracranial atherosclerotic disease tends to affect multiple arterial segments. Using whole-brain vessel wall imaging, we sought to study the differences in plaque features among various types of plaques in patients with a recent unilateral anterior circulation ischemic stroke.Methods and resultsSixty-one patients with unilateral anterior circulation ischemic stroke were referred to undergo whole-brain vessel wall imaging (before and after contrast) within 1month of symptom onset for intracranial atherosclerotic disease evaluations. Each plaque was classified as a culprit, probably culprit, or nonculprit lesion, according to its likelihood of causing the stroke. The associations between plaque features (thickening pattern, plaque-wall contrast ratio, high signal on T1-weighted images, plaque contrast enhancement ratio, enhancement grade, and enhancement pattern) and culprit lesions were estimated using mixed multivariable logistic regression after adjustment for maximum wall thickness. In 52 patients without motion corruption in whole-brain vessel wall imaging, a total of 178 intracranial plaques in the anterior circulation were identified, including 52 culprit lesions (29.2%), 51 probably culprit lesions (28.7%), and 75 nonculprit lesions (42.1%). High signal on T1-weighted images (adjusted odds ratio, 9.1; 95% confidence interval, 1.9-44.1; P=0.006), grade 2 (enhancement ratio of plaque ≥ enhancement ratio of pituitary) contrast enhancement (adjusted odds ratio, 17.4; 95% confidence interval, 1.8-164.9; P=0.013), and type 2 (≥50% cross-sectional wall involvement) enhancement pattern (adjusted odds ratio, 10.1; 95% confidence interval, 1.3-82.2; P=0.030) were independently associated with culprit lesions.ConclusionsHigh signal on T1-weighted images, grade 2 contrast enhancement, and type 2 enhancement pattern are associated with cerebrovascular ischemic events, which may provide valuable insights into risk stratification.

In this study, we aim to investigate the clinical features and Mutations of sodium channel alpha-subunit (SCN4A) genes in Chinese patients with normokalemic periodic paralysis (normoKPP).Six unrelated Chinese families with normoKPP were analyzed in clinical features. Genomic DNA was extracted from peripheral blood leukocytes and amplified with PCR. We screened all 24 exons of SCN4A gene with denaturing high performance liquid chromatography (DHPLC) technology, and then sequence analysis was performed in those who showed heteroduplex as compared with unaffected controls.The laboratory tests were within normal ranges. Electromyograms and electrocardiograms were normal. One muscle biopsy was performed with the patient in family 4 after a brief attack of normoKPP. Examination of light microscopy showed no changes, but electronic microscopy showed occasionally degenerating myofibers. The mutations of SCN4A genes were as follows: (1) Met1592Val occurred in family 1. (2) Val-781-Ile occurred with the patient and her father in family 4. (3) Both the patients had a novel mutation g2101a predicting the amino acid exchange Arg675Gln in family 5, which may be a disease-causing mutation.In addition to Val-781-Ile and Met1592Val, the mutation g2101a (Arg675Gln) may be the novel mutation of SCN4A genes in Chinese patients with normoKPP.