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BACKGROUND: The characteristics of plaque that ultimately lead to different subcortical infarctions remain unclear. We explored the differences in plaque characteristics between patients with small subcortical infarction (SSI) and large subcortical infarction (LSI) of the middle cerebral artery (MCA) using high-resolution magnetic resonance vessel wall imaging (HR-MRVWI). METHODS: The study group comprised 71 patients (mean age, 47.49±11.5 years; 55 male) with MCA territory ischemic stroke. Whole-brain HR-MRVWI was performed using a three-dimensional T1-weighted variable-flip-angle turbo spin echo (SPACE) sequence. Patients were divided into SSI and LSI groups based on routine MRI images. Plaque distribution was classified as the superior, inferior, ventral, or dorsal wall of the MCA. The number of quadrants with plaque formation, location of plaque, plaque burden (PB), arterial remodeling pattern (positive or negative), and degree of stenosis were analyzed and compared between groups. RESULTS: Of the 71 patients, 43 (60.6%) and 28 (39.4%) were identified as the SSI and LSI groups, respectively. The proportion of plaques involving only one quadrant was significantly higher in the SSI group, and these plaques were located in the superior or dorsal MCA vessel wall. There was no significant difference between groups in the proportion of plaques involving two or more quadrants, plaque distribution, or PB. Most plaques in both groups showed positive remodeling, and the percentage of remodeling pattern was similar. A significantly higher incidence of low-grade stenosis (

Supplemental Digital Content is available in the text., Background and Purpose: We aimed to use novel whole-brain vessel-wall magnetic resonance imaging (WB-VWI) to investigate the association between plaque distribution of middle cerebral artery (MCA) and morphological changes of the lenticulostriate arteries (LSAs) in single subcortical infarctions. Methods: Forty single subcortical infarction patients with no relevant MCA disease on magnetic resonance angiography were prospectively enrolled. Plaque location in the MCA was dichotomized as proximal (located adjacent to the LSA origin) or distal (located distal to the LSA origin) on whole-brain vessel-wall magnetic resonance imaging. The MCAs with proximal plaques were divided into the symptomatic and asymptomatic side, and asymptomatic side MCAs without proximal plaques were the control group. The morphological characteristics of the LSAs and features of proximal plaques were analyzed. Results: A total of 71 MCAs in 40 patients were analyzed (31 on the symptomatic side, 22 on the asymptomatic side, and 18 in the control group). Superior-wall plaques of MCAs were observed more frequently on the symptomatic side than the asymptomatic side (45.2% versus 9.1%, P=0.005). The wall area index, plaque burden, and remodeling index did not differ significantly between the symptomatic and asymptomatic side. The number of LSA branches was smaller (P=0.011) in the symptomatic side (5.48±1.88) compared with the control group (6.83±1.92). The symptomatic side exhibited shorter average length of the LSAs (23.23±3.44 versus 25.75±3.76 mm, P=0.025) and shorter average distance of the LSAs (16.47±3.11 versus 21.53±4.76 mm, P

Objective: Lipohyalinosis or atherosclerosis might be responsible for single subcortical infarctions (SSIs); however, ways of differentiating between the two clinically remain uncertain. We aimed to investigate whether consecutive slides on axial view or transversal diameter is more effective to differentiate mechanisms by comparing their relationships with white matter hyperintensities (WMHs). Methods: All the participants from the Standard Medical Management in Secondary Prevention of Ischemic stroke in China (SMART) cohort who had SSIs in the lenticulostriate artery territory were included and categorized according to consecutive slides on axial view (≥4 consecutive slices or not) and transversal diameter (≥15 mm or not). The associations between the severity of WMHs and the different categories were analyzed. Results: Among the 3,821 patients of the SMART study, 281 had diffusion-weighted image-proven SSIs in the lenticulostriate artery territory. When classified by consecutive slides on axial view, SSIs on ≥4 slices were significantly associated with the severity of the WMHs, both in deep WMH (DWMH) (odds ratio [OR], 0.32; 95% confidence interval [CI], 0.11-0.97; p = 0.04) and periventricular hyperintensity (PVH) (OR, 0.37; 95% CI, 0.17-0.78; p = 0.01). No such association was found on the basis of the transversal diameter (p > 0.1). Conclusion: Consecutive slides on axial view (≥4 consecutive slices) might be more effective than transversal diameter to identify the atherosclerotic mechanisms of SSIs in the lenticulostriate artery territory. Clinical Trial Registration: http://www.clinicaltrials.gov. Unique identifier: NCT00664846.

Background: Incidental acute ischemic lesions distinct from the primary neurological insult are identified on diffusion weighted imaging (DWI) in a number of conditions where cerebral microvascular pathology plays a central role, like ICH or cerebral amyloid angiopathy. Another major manifestation of cerebral small vessel disease is ischemic stroke secondary to small artery occlusion, classically known as lacunar stroke and named as recent small subcortical infarction (RSSI) in the present-day nomenclature. In this study, we identified the prevalence and predictors of remote DWI lesions in patients with RSSI. Methods: Consecutive acute ischemic stroke patients with neuroimaging evidence of perforating arteriole territory ischemia were retrospectively analyzed. Patients with additional DWI lesions, apart from the ischemic lesion pertaining to clinical symptoms, were identified, and their clinical features together with imaging markers of chronic small vessel disease (lacunes, microbleeds, perivascular spaces, white matter hyperintensities) were compared to those patients with no such lesions. Results: Incidental acute ischemic lesions remote from the symptomatic subcortical infarction were identified in 9% of 367 patients included into the study. The lesions were linear or punctate in morphology, ≤20 mm in diameter, primarily located in ipsilateral or contralateral white matter (76%) and multiple in 47% of the cases. Patients with incidental DWI lesions were more likely to be active smokers, have history of hypertension and hyperlipidemia, and show evidence of chronic lacunes and microbleeds on imaging studies. Smoking (OR 2.2; 1.0-5.0), hyperlipidemia (OR 2.5; 1.1-5.3) and chronic lacunes (OR.6.0; 2.2-14.1) stood out as features significantly associated with incidental DWI lesions in multivariate analysis. Conclusions: Our study discloses that acute ischemic lesions involving other perforator arteriole territories can be incidentally detected in approximately 10% of patients suffering a stroke secondary to RSSI. This observation not only emphasizes the widespread nature of cerebral small vessel pathology, but also highlights that the course might be more active, temporally and spatially, in a distinct subgroup of patients.

Objectives Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarctions and Leukoencephalopathy (CADASIL) is a rare genetic disorder. It is caused by a mutation in the NOTCH3 gene on chromosome 19 which damages vascular smooth muscle cells resulting in impaired cerebral blood flow and a progressive vascular dementia. Onset typically occurs by the mid-30’s but varies widely. This case study describes a unique case of rapid disease progression. Methods The patient was a 58-year-old right-handed male. Initial symptom onset occurred at the age of 53, with blurred vision, severe headache, and difficulty speaking. Brain imaging (CT, MRI) showed significant white matter degeneration and cortical volume loss. Multiple sclerosis was hypothesized. Following the development of seizures and a right hemisphere stroke, the patient underwent genetic testing and was diagnosed with CADASIL. Initial neuropsychological evaluation revealed deficits in perceptual reasoning, working memory, processing speed, memory, and executive functioning. Serial evaluation included intelligence testing, academic achievement, the Meyers Neuropsychological Battery, and psychological functioning. Results Intellectual functioning and the overall neuropsychological test battery mean were one and a half to two standard deviations below his estimated premorbid functioning. Executive functioning declined from prior evaluation. Psychologically, the patient reported mild anger, irritability, and interpersonal difficulties. His wife endorsed significant increases in apathy and disinhibition and decline in executive functioning. The patient passed away approximately six months post-evaluation. Conclusion Findings were consistent with moderate-to-severe diffuse and lateralized deficits (RCH > LCH) resulting from subcortical/higher cortical vascular dementia due to CADASIL and its medical sequelae, with quite rapid symptom onset and decline.

Background and Purpose— The size variation of single subcortical infarcts (SSIs) may be because of differences in stroke mechanisms or branching patterns of perforators. We aim to investigate this issue using high-resolution MRI. Methods— Patients with high-resolution MRI–identified SSI without significant (≥50%) middle cerebral artery stenosis were enrolled. Perforator stems were defined as perforators originating from the middle cerebral artery and perforator branches as linear structures inside the infarcted area, traceable from >2 adjacent slices. The branching index was calculated as the number of perforator branches divided by the number of perforator stems. Clinical and imaging characteristics were compared between large (≥20 mm in diameter) and small SSI groups. Results— Forty-one patients (10 large and 31 small SSIs) were enrolled. Larger SSIs were more closely associated with diabetes mellitus and severe neurological dysfunction but not with the presence of middle cerebral artery plaque. Although there was no difference in the number of perforator stems, the number of perforator branches (4.8±2.2 versus 2.3±1.4; P =0.005) and branching index (2.9±1.0 versus 1.2±0.8; P r =0.630; P r =0.750; P Conclusions— SSI diameter seems to be associated with anatomic branching variation rather than the mechanism of stroke. Definition of small vessel disease with lesion diameter criteria may not be appropriate.

To determine the clinical presentation and aetiology of small subcortical infarctions as found on diffusion weighted magnetic resonance imaging (DWI). DWI is both sensitive and specific in the early detection of acute ischaemic brain lesions irrespective of pre-existing vascular damage.Ninety three patients were identified showing subcortical or brainstem DWI lesions1.5 cm in diameter within a maximum of 7 days from the onset of stroke symptoms. The patients' clinical status on admission was reviewed according to the Oxfordshire Community Stroke Project (OCSP). The results of procedures searching for cerebrovascular risk factors, large artery disease, and potential sources of cardiac embolism were included to determine stroke aetiology. Magnetic resonance imaging scans were also reviewed for concomitant changes that could support the aetiologic classification.Only 41 (44.1%) patients presented clinically with a lacunar syndrome according to OCSP criteria. The nine (9.7%) patients who showed two or more DWI lesions in different vascular territories were also significantly more likely to have potential sources of cardiac embolism (5/9, 55.6% v 20/84, 23.8%). Hypertension was significantly more prevalent in the group of patients who showed a microangiopathy related imaging pattern, but this pattern did not exclude the presence of large artery disease or a possible cardioembolic source of stroke.Identification of small subcortical infarctions as the cause of stroke appears quite uncertain based on clinical characteristics only. DWI adds significant aetiologic information but does not obviate the search for other potentially causative mechanisms.

Objective: To seek evidence of potential embolic sources or other stroke mechanisms in patients who, on chance observation, had several apparently recent small subcortical infarcts on diffusion weighted magnetic resonance imaging (DWI). Methods: Patients presenting with stroke and multiple hyperintense subcortical infarcts visible on DWI were identified prospectively. Detailed clinical and radiological assessments were done independently and blinded to each other. Results: Of 10 patients with multiple hyperintense subcortical infarcts on DWI, a definite embolic source was identified in only one. Most patients were hypertensive and smoked. The DWI appearance suggested that the subcortical lesions had occurred within several weeks rather than at exactly the same time. Most patients also had significant white matter hyperintensities and four had microhaemorrhages. Conclusions: Embolic sources were not identified in most patients but they did have systemic vascular risk factors and brain imaging features of "small vessel disease." A more generalised intrinsic process affecting many small cerebral vessels contemporaneously could explain multiple acute small subcortical infarcts. White matter hyperintensities, microhaemorrhages, and multiple small subcortical infarcts may share a common pathophysiological mechanism such as a diffuse cerebral microvascular abnormality which requires further exploration.