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Background The research about the influence of triglyceride-glucose index on early prognosis in stroke is lacking. Aims In this study, we evaluated the association between triglyceride-glucose index and early neurological deterioration in patients with single subcortical infarctions. Methods Consecutive patients with single subcortical infarctions within 72 h of symptom onset between 2011 and 2015. Early neurological deterioration was defined as an increase of ≥2 in the total NIHSS score or ≥1 in the motor NIHSS score. The triglyceride-glucose index was calculated using the log scale of fasting triglyceride (mg/dL) × fasting glucose (mg/dL)/2. Results A total of 305 patients with single subcortical infarctions were evaluated. In multivariable analysis, the triglyceride-glucose index (adjusted odds ratio [aOR] = 2.94, 95% confidence interval [CI] = 1.58–5.45) and age (aOR = 1.05, 95% CI = 1.01–1.09) were associated with early neurological deterioration. In subgroup analysis according to the type of single subcortical infarctions, only patients with proximal single subcortical infarctions showed a significant association between the triglyceride-glucose index and early neurological deterioration (aOR = 2.92, 95% CI = 1.35–6.29). On the other hand, there was no statistical significance in patients with distal single subcortical infarctions. Patients with untreated diabetes also showed the close association between the triglyceride-glucose index and early neurological deterioration (aOR = 3.94, 95% CI = 1.47–10.52). Conclusions The triglyceride-glucose index was associated with early neurological deterioration in single subcortical infarctions. This association differed depending on the location of lesion and the presence of untreated diabetes.

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.

Autosomal dominant cerebral arteriopathy with subcortical infarctions and leukoencephalopathy (CADASIL), is a genetic disease caused by mutations in the Notch3 gene. More than 170 monogenic mutations leading to the development of CADASIL have been reported. We describe a case of a patient and her family with compatible symptoms of CADASIL disease, in which a variable not yet described in the Notch3 gene was detected, that generates a probably pathogenic change in the protein.

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.

Aim: We assessed the long-term prognosis of patients with large subcortical infarctions (LSCI). Methods: We defined LSCI as lesions ≥15 mm confined to deep penetrating arteries without a cardioembolic or atherothrombotic source. Patients with acute ischemic strokes were consecutively registered and followed for 751 ± 441 days. The clinical characteristics and long-term prognoses of patients with LSCI were compared to those of patients with lacunar (LACI), atherothrombotic (ATI) and cardioembolic infarctions (CEI). Results: At discharge from the hospital, the proportion of good outcomes (modified Rankin Scale ≤2) for patients with LSCI (52.1%) was similar to that for ATIs (47.2%), but worse than that for LACIs (73.2%). After a 3-year follow-up period, the mortality rates from LSCI, LACIs, ATIs and CEIs were 8.4, 8.2, 22.3 and 41.1%, respectively; the recurrence rates were 9.3, 14.1, 16.6 and 23.8%, respectively. Conclusions: The short-term prognosis of functional outcomes for LSCI was worse than that for LACIs, but similar to acute-phase ATI outcomes. The long-term prognosis after a LSCI is good, and recurrence tends to be lower than for LACIs.

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.

We have recently published an experimental method useful for causing discrete cerebral microischemic foci in rabbits. In that study it was shown that on reaching the brain, plastic beads (with an average diameter of 80 or 110 μm) give rise to foci of increased [14C]2-deoxyglucose accumulation, indicating anaerobic glycolysis. Further, it was suggested that the relatively low accumulation of [14C]2-deoxyglucose, as observed in the center of some of the ischemic foci located in areas which are thought to have a poor collateral blood supply, was an indication of glucose depletion. This work is intended to be a useful approach for the study of diffusion-limited consumption of glucose and oxygen in microischemic regions, located in endarterial regions. It is shown that a mathematical model with reasonable parameters can be fitted to a measured [14C]2-deoxyglucose profile. The results of this study are compatible with the view that the glucose concentration in the ischemic center is very low and limits the rate of energy turnover. Together with animal experiments, this mathematical model may impart new information of importance for evaluating the treatment of subcortical infarctions in humans.

This multiauthored text consists of 23 chapters written by an international group of experts in stroke. It is divided into 6 sections: the general concept of subcortical infarction; the lacunar debate; clinical and investigatory aspects of lacunar syndromes; topographically defined infarcts in the region of the basal ganglia; other aspects of subcortical infarction; and classification. Topics as diverse as the history of lacunes to the occurrence of lacunes in persons with neurotuberculosis are included. The continuing debate about lacunar strokes and lacunar syndromes is included in the monograph. Although the authors of the chapters nicely summarize the data that support their opinions about the nature of small subcortical infarctions, little new information is included that will lead to a resolution. Some of the chapters apparently were written well before publication; for example, on page 118, Caplan and Helgason cite a 1990 article as being 2 years old. The highlights of

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.

by G.A. Donnan, B. Norrving, J.M. Bamford, and J. Bogousslavsky, 281 pp., ill., Oxford, Oxford University Press, 1995, $98.00 For their small size, "lacunar" infarcts have given rise to more than their fair share of debate and controversy. The low mortality and small size of these infarcts has made them difficult to study pathologically and clinically. Before the introduction of modern imaging, what we knew about small deep ischemic lesions was based on the work of a handful of eminent researchers whose conclusions were based on relatively limited autopsy material. As a result, certain conclusions drawn from the work of Marie and of Fisher, for example, were probably overstated. Over the last 15 years, CT and MR have opened up …

Language disturbances were studied in 40 patients with well-demarcated vascular lesions of the speech-dominant hemisphere. Computerized cranial tomography was used for localization of the lesion. Special emphasis was given to the analysis of automatized speech and repetitive verbal phenomena. Subcortical infarctions with basal ganglia involvement led to transient aphasia although long-lasting abnormalities of language could be detected in these patients. Aphasia was more severe if a cortical lesion was combined with a basal ganglia lesion. Automatisms and recurring utterances occurred only with combined cortical and basal ganglia lesions. A lesion of Wernicke's area alone, without involvement of prerolandic structures or subcortical nuclei, was sufficient to produce long-lasting aphasia, whereas lesions of Broca's area alone produced only transient language disturbances. The results are compatible with a recent theory of multiple cerebral representation of function.