Lenticulostriate Infarction Research Articles

Dystextia and dystypia due to phonological errors after ischemic stroke: a case report in a Japanese patient

ABSTRACT A 69-year-old Japanese male presented with acute dystextia and dystypia, defined as texting and typing impairments, respectively. His text input speed decreased due to a phonologically incorrect kana flick input on his smartphone. Additionally, dystypia occurred due to phonemic paragraphia of Romaji. Brain MRI revealed a new left lenticulostriate infarction sparing the cerebral cortex. SPECT showed reduced cerebral blood flow in the left inferior precentral frontal gyrus as well as in the infarction area. It was concluded that his abnormal phonological processes resulted from hypoperfusion in the left inferior precentral gyrus that is assumed to be an endpoint of the arcuate fasciculus.

Cerebral artery signal intensity gradient from Time-of-Flight Magnetic Resonance Angiography and clinical outcome in lenticulostriate infarction: a retrospective cohort study.

Lenticulostriate infarction requires further research of arterial hemodynamic factors, as the disease is diagnosed in the absence of major arterial stenosis or cardioembolism. In this multicenter retrospective cohort study, we included patients who were hospitalized for lenticulostriate infarction from January 2015 to March 2021 at three stroke centers in South Korea. We obtained hemodynamic information on cerebral arteries using signal intensity gradient (SIG), an in-vivo approximated wall shear stress (WSS) derived from Time-of-Flight Magnetic Resonance Angiography (TOF-MRA). A favorable outcome was defined as a modified Rankin Scale of 0 to 2 at hospital discharge. A total of 294 patients were included, of whom 146 (49.7%) had an unfavorable outcome. The unfavorable outcome group showed significantly lower SIG in both middle cerebral arteries (MCAs) than the favorable group (5.2 ± 1.2 SI/mm vs. 5.9 ± 1.2, p < 0.001), and similar findings were observed in other cerebral arteries. The SIGs in both MCAs were independently associated with favorable outcome, with an odds ratio of 1.42 (95% confidence interval, 1.11-1.80; p = 0.005) for the right MCA and 1.49 (95% CI, 1.15-1.93; p = 0.003) for the left MCA, after adjusting for potential confounders. Similar findings were observed in other cerebral artery SIGs. Cerebral artery SIG from TOF-MRA was significantly associated with short-term functional outcomes in patients with lenticulostriate infarction. Further studies are needed to investigate the temporal relationships of SIG in patients with cerebral infarction.

High resolution magnetic resonance imaging in pathogenesis diagnosis of single lenticulostriate infarction with nonstenotic middle cerebral artery, a retrospective study

BackgroundIt is usually difficult to identify stroke pathogenesis for single lenticulostriate infarction with nonstenotic middle cerebral artery (MCA). Our aim is to differentiate the two pathogeneses, non-branch atheromatous small vessel disease and branch atheromatous disease (BAD) by high-resolution magnetic resonance imaging (HR-MRI).MethodsThirty-two single lenticulostriate infarction patients with nonstenotic MCA admitted to the China-Japan Friendship Hospital from December 2014 to August 2017 were enrolled for retrospective analysis. National Institutes of Health Stroke Scale (NIHSS), modified Rankin Scale (mRS), atherosclerotic risk factors, imaging features, and the characteristic of MCA vessel wall in HR-MRI were evaluated.ResultsMCA plaques were detected in 15(46.9%) patients which implied BAD and 8 of 15 (53.3%) patients had plaques location in upper dorsal side of the vessel wall. Patients with HR-MRI identified plaques had a significantly larger infarction lesion length (1.95 ± 0.86 cm versus 1.38 ± 0.55 cm; P = 0.031) and larger lesion volume (2.95 ± 3.94 cm3 versus 0.90 ± 0.94 cm3; P = 0.027) than patients without plaques. Patients with HR-MRI identified plaques had a significant higher percentage of proximal lesions than patients without plaques (P = 0.055). However, according to the location of MCA plaques, there were no significant differences in terms of imaging features, NIHSS and mRS.ConclusionWe demonstrated high frequency of MCA atheromatous plaques visualized in single lenticulostriate infarction patients with nonstenotic MCA by using HR-MRI. Patients with HR-MRI identified plaque presented larger infarction lesions and more proximal lesions than patients without plaque, which were consistent with imaging features of BAD. HR-MRI is an important and effective tool for identifying stroke etiology in patients with nonstenotic MCA.

Differentiation of Deep Subcortical Infarction Using High-Resolution Vessel Wall MR Imaging of Middle Cerebral Artery.

ObjectiveTo evaluate the utility of high-resolution vessel wall imaging (HR-VWI) of middle cerebral artery (MCA), and to compare HR-VWI findings between striatocapsular infarction (SC-I) and lenticulostriate infarction (LS-I).Materials and MethodsThis retrospective study was approved by the Institutional Review Board, and informed consent was waived. From July 2009 to February 2012, 145 consecutive patients with deep subcortical infarctions (SC-I, n = 81; LS-I, n = 64) who underwent HR-VWI were included in this study. The degree of MCA stenosis and the characteristics of MCA plaque (presence, eccentricity, location, extent, T2-high signal intensity [T2-HSI], and plaque enhancement) were analyzed, and compared between SC-I and LS-I, using Fisher's exact test.ResultsStenosis was more severe in SC-I than in LS-I (p = 0.040). MCA plaque was more frequent in SC-I than in LS-I (p = 0.028), having larger plaque extent (p = 0.001), more T2-HSI (p = 0.001), and more plaque enhancement (p = 0.002). The eccentricity and location of the plaque showed no significant difference between the two groups.ConclusionBoth SC-I and LS-I have similar HR-VWI findings of the MCA plaque, but SC-I had more frequent, larger plaques with greater T2-HSI and enhancement. This suggests that HR-VWI may have a promising role in assisting the differentiation of underlying pathophysiological mechanism between SC-I and LS-I.

Hyperdopaminergism in lenticulostriate stroke-related restless legs syndrome: an imaging study

ObjectiveThe pathophysiology of restless legs syndrome (RLS) involves a dopaminergic dysregulation that remains poorly understood, with controversial data from the literature. Stroke-related RLS is a rare condition that involves primarily the basal ganglia, the paramedian pons, and the thalamus. Given these elements, we studied dopaminergic metabolism in patients with RLS secondary to lenticulostriate infarction using structural and nuclear imaging in the striatum ipsilateral to the infarction area, as compared to the contralateral side. We hypothesized that dopaminergic metabolism would be impaired in the striatum ipsilateral to stroke. MethodsIn this observational case-control study, we aimed to prospectively include patients with RLS secondary to lenticulo-striate infarction, for analyses of dopamine dysfunction ipsilateral to stroke as compared to the contralateral striatum and to a control population. Four patients fulfilled inclusion criteria with either de novo RLS or major exacerbation of RLS existing prior to stroke, and all four patients were included. Structural imaging was performed using brain magnetic resonance imaging, and the stroke-induced metabolic modifications were assessed by 18F-fluorodeoxyglucose (18F-FDG) positron emission tomography (PET). Dopamine reuptake via DAT was explored using 123I-FP-CIT SPECT. PET with 18F-FDOPA was used to evaluate the functional integrity of the presynaptic dopaminergic synthesis. ResultsThe only structure damaged in all patients was the body of the caudate nucleus, right-sided for three and left-sided for one, as illustrated by magnetic resonance imaging. 18F-FDG PET showed a hypometabolism in the infarcted area, the ipsilateral thalamus, and the contralateral cerebellum. All patients displayed, in the ipsilateral putamen, increased dopaminergic tone. ConclusionThe present findings suggest that increased dopaminergic tone in the striatum may participate in the pathogenesis of RLS. These observations should encourage further research on RLS symptomatic with well-defined lesions as a promising way to further improve our understanding of its pathophysiology.

対側線条体にT1 強調画像高信号および穿通枝梗塞を認めた非糖尿病性片側舞踏病の1 例

要旨：症例は糖尿病のない90 歳女性で，急性発症した右半身の舞踏運動が1 カ月の経過で増悪した．発症4 週後の頭部MRI では新規病変を認めなかったが，6 週後の頭部MRI で左放線冠に新規梗塞，隣接する左被殻後部にT1 強調画像高信号を認めた．MRA では主幹動脈に高度狭窄を認めなかった．舞踏運動はハロペリドール内服にて改善した．高血糖に線条体のT1 強調画像高信号を伴って片側舞踏病を生じる病態は糖尿病性片側舞踏病として知られているが，本症例は糖尿病非合併例で，片側舞踏運動の発現より遅れて対側被殻・放線冠のMRI信号変化が出現した．線条体のT1 強調画像高信号は外側レンズ核線条体動脈領域の不完全な虚血によって生じたと考えられ，高信号の程度とその大きさは舞踏運動の程度と密接な相関はないことが示唆された．

Response to Letter Regarding Article, “Initial Lesion Volume Is an Independent Predictor of Clinical Stroke Outcome at Day 90: An Analysis of the Virtual International Stroke Trials Archive (VISTA) Database”

Response: We thank the authors for their interest in our study and interesting suggestions that we have followed in some reanalyses. We believe, however, that the criticism regarding methodology of our article is largely unjustified. We have followed the suggestion to examine the interaction of the National Institutes of Health Stroke Scale (NIHSS) at baseline and lesion volume and indeed found an interaction ( P =0.02), but only on NIHSS at Day 90 as the end point, not for modified Rankin Scale (mRS; linear) or mortality. The interaction for the NIHSS end point suggests a mutual influence of both baseline parameters resulting in steepening of the baseline NIHSS regression at higher lesion volumes and vice versa. This comparably weak finding should however be regarded with caution at present. Considering the linear treatment of NIHSS, in biological systems, there is hardly any relationship of complex parameters that is really strictly linear; linear regression is a practical approximation that …

The course and outcome of unilateral intracranial arteriopathy in 79 children with ischaemic stroke

Arteriopathies are the commonest cause of arterial ischaemic stroke (AIS) in children. Repeated vascular imaging in children with AIS demonstrated the existence of a ‘transient cerebral arteriopathy’ (TCA), characterized by lenticulostriate infarction due to non-progressive unilateral arterial disease affecting the supraclinoid internal carotid artery and its proximal branches. To further characterize the course of childhood arteriopathies, and to differentiate TCA from progressive arterial disease, we studied the long-term evolution of unilateral anterior circulation arteriopathy, and explored predictors of stroke outcome and recurrence. From three consecutive cohorts in London, Paris and Utrecht, we reviewed radiological studies and clinical charts of 79 previously healthy children with anterior circulation AIS and unilateral intracranial arteriopathy of the internal carotid bifurcation, who underwent repeated vascular imaging. The long-term evolution of arteriopathy was classified as progressive or TCA. Clinical and imaging characteristics were compared between both groups. Logistic regression modelling was used to determine possible predictors of the course of arteriopathy, functional outcome and recurrence. After a median follow-up of 1.4 years, 5 of 79 children (6%) had progressive arteriopathy, with increasing unilateral disease or bilateral involvement. In the others (94%), the course of arteriopathy was classified as TCA. In 23% of TCA patients, follow-up vascular imaging showed complete normalization, the remaining 77% had residual arterial abnormalities, with improvement in 45% and stabilization in 32%. Stroke was preceded by chickenpox in 44% of TCA patients, and in none of the patients with progressive arteriopathies. Most infarcts were localized in the basal ganglia. In 14 (19%) of TCA patients, transient worsening of the arterial lesion was demonstrated before the arteriopathy stabilized or improved. Thirteen TCA patients (18%) had a recurrent stroke or TIA. Thirty TCA patients (41%) had a good neurological outcome, compared with none of the five patients with progressive arteriopathy. Arterial occlusion, moyamoya vessels and ACA involvement were more frequent in progressive arteriopathies. Cortical infarct localization was significantly associated with poor neurological outcome (OR 6.14, 95% CI 1.29–29.22, P = 0.02), while there was a trend for occlusive arterial disease to predict poor outcome (OR 3.00, 95% CI 0.98–9.23, P = 0.06). Progressive arteriopathy was associated with recurrence (OR 18.77, 95%CI 1.94–181.97, P = 0.01). The majority of childhood unilateral intracranial anterior circulation arteriopathies (94%) have a course that is consistent with TCA, in which transient worsening is common. Although the arterial inflammation probably causing TCA is ‘transient’, most children are left with permanent arterial abnormalities and residual neurological deficits.

Preferred Involvement of the Basal Ganglia After Lenticulostriate Infarction as a Possible Indicator of Different Gray and White Matter Vulnerability

Symptomatic progression is frequently observed in lacunar infarcts. The exact mechanisms of this phenomenon have not yet been clarified. We report 2 patients with lenticulostriate artery infarcts that presented with skip lesions that were restricted to gray matter. One of the patients subsequently developed symptomatic deterioration; the other experienced no further neurological events. A possible mechanism of differential vulnerability to ischemia of gray and white matter is considered. White matter may have a longer therapeutic time window for neuroprotective treatment than gray matter.

A child with HIV-associated transient cerebral arteriopathy

A child with HIV-associated transient cerebral arteriopathy

Ischemic stroke in patients with glioblastoma multiforme

Sirs: Tumor-related ischemic strokes are most unusual in patients with malignant gliomas [1–3]. We report here two adult patients with supratentorial glioblastoma who developed an ischemic stroke on the tumor side. Patient 1: In March 2000, a 60year-old man became confused. MRI revealed a right temporal tumor which was partially resected and found to be a glioblastoma. Focal radiotherapy was administered. Four months later, intravenous BCNU was started because of tumor progression. On 13 February, 2001, he developed acutely a left hemiplegia. CT showed an extensive infarct in the territory of the right middle cerebral artery (MCA) (Fig. 1). He became comatous and died on 22 February, 2001. Patient 2: In July 1994, a 41-yearold man developed intracranial hypertension. MRI disclosed a right temporal tumor which was partially resected and found to be a glioblastoma. A course of focal radiotherapy was administered. Three months later, he had a sudden left hemiplegia and MRI showed a right lenticulostriate infarct related to an occlusion of the right supraclinoid internal carotid artery (ICA) shown by angiography. The patient died on 5 April, 1995. Permission for autopsy was not granted for either patient. These two patients suffering from a right temporal glioblastoma presented an ischemic stroke in the right ICA-MCA territories. To explain these acute events three hypotheses were considered: 1) A fortuitous association between glioma and stroke in the same location. This hypothesis is unlikely since both patients had no cerebrovascular risk factors and the angiogram in patient 2 showed no atheroma in the cervical or cerebral vessels. 2) Radiation damage to the large intracranial cerebral vessels was also considered but the very short delay between the completion of RT (5 and 3 months) and the stroke makes this hypothesis unlikely. Indeed, radiation-induced damage to the large vessels always occurs many years after RT (mean 7 years [4–6]). 3) The third possibility is a primary role for the underlying gliomas in the development of stroke. Vasospasm with multifocal infarcts has been incriminated previously in one patient with leptomeningeal gliomatosis [7] but this hypothesis can be excluded, at least in our second patient who had a persistent ICA thrombosis three months after the stroke. A hypercoagulable state (procoagulant factors secreted by gliomas) is common and partly accounts for the high incidence of deep vein thromLETTER TO THE EDITORS

MR tractography for the evaluation of functional recovery from lenticulostriate infarcts

To evaluate the anatomic and clinical relationship between the lenticulostriate artery (LSA) territory and the corticospinal tract (CST) in patients with acute infarcts in this territory using MR tractography. Thirteen consecutive patients who presented with acute infarcts in the LSA territory and who also had undergone an MRI study within 3 days after symptom onset were studied. Visualization of the CST was achieved by postprocessing the acquired diffusion tensor imaging data. To classify lesion location, the LSA territory was divided into four subsegments, the boundaries of which were drawn by axial and coronal planes crossing through the foramen of Monro. Infarct volume and extent of CST involvement were measured and compared with neurologic findings. All of the infarcts were located in the posterior segment. All of the depicted CSTs crossed the LSA territory only at the posterosuperior quadrant. The extent of CST involvement within the infarcts was correlated with the severity of the patient's motor deficit (p < 0.01) and with the clinical outcome (p < 0.05). The corticospinal tracts (CSTs) crossed the lenticulostriate artery territory exclusively at the posterosuperior quadrant, and the degree of CST involvement within the infarcts was directly related to stroke severity and functional recovery.

Predicting functional outcome and survival after acute ischemic stroke.

Disability and mortality represent the most relevant clinical outcome after acute ischemic stroke. However, validated and comprehensive prognostic models for recovery have not been developed. An accurate model including all previously suggested independent outcome predictors could improve the design and analysis of clinical trials. We therefore developed prognostic models for functional dependence and death after 100 days in a large cohort of stroke patients. From the German Stroke Database, 1754 prospectively collected records of patients with acute ischemic stroke were used for the development of prognostic models. Intubated patients and patients with low functional status before stroke were excluded. Functional independence was defined as a Barthel Index >/=95 after 100 days. Prognostic factors assessable within 72 hours after admission were identified by a systematic literature review. The final models of binary logistic regression analyses were internally validated and calibrated. The resulting cross-validated and calibrated models correctly classified more than 80 % of the patients and yielded the following prognostic factors for functional independence: Age, right and left arm paresis at admission, NIH-Stroke Scale at admission, Rankin Scale 48-72 hours later, gender, prior stroke, diabetes, fever, lenticulostriate infarction, neurological complications. The following variables were identified as prognostic factors for death: Age, NIH-Stroke Scale at admission, and fever. Our work gives an important insight into prognostic factors after acute ischemic stroke and presents predictive models with high prognostic accuracy. Together with a prospective validation study, currently underway, we hence hope to improve the prediction of functional outcome after ischemic stroke.

Topography of cerebral infarction associated with carotid artery dissection.

Because the pathogenesis of cerebral ischaemia in internal carotid artery dissection (ICAD) is controversial we studied the topography of cerebral infarction that results from ICAD according to pathophysiology of embolic and haemodynamic stroke. Sixty-four patients with 67 ICADs diagnosed by angiography, Doppler duplex sonography and magnetic resonance imaging (MRI) were studied prospectively during the past decade. According to current pathophysiological concepts, cortical territorial infarcts and large subcortical lenticulostriate infarcts revealed by CT or MRI were classified as embolic, while smaller infarcts in the subcortical junctional zone and infarcts in the cortical borderzone between the middle (MCA) and anterior cerebral artery were interpreted as haemodynamic infarcts. Of the 67 dissections 37 (55%) were associated with brain infarcts, of which territorial MCA infarcts of variable size accounted for 60%. These were combined with infarcts of the anterior and posterior cerebral artery in 5%; 8% of the patients had complete MCA infarction. Large lenticulostriate infarcts were present in 11%. Haemodynamic infarcts involved the subcortical junctional zone in 16% but never the anterior cortical borderzone. Although different abnormal Doppler findings indicated haemodynamically significant carotid obstruction in all symptomatic ICADs, only the characteristic high-resistance Doppler signal was significantly associated with the occurrence of brain infarction (in 66%, P < 0.01). The angiographic features of ICAD did not correlate with the incidence or with the topography of cerebral infarction. Patterns of infarction in ICAD indicate a predominantly embolic causation probably due to thrombus formation in the dissected carotid artery in the presence of severe haemodynamic obstruction, as demonstrated by Doppler sonography.

Role of associated cortical lesions in motor partial seizures and lenticulostriate infarcts.

In a population-based study, we evaluated seizures occurring in the first 15 days after strokes among 1,640 consecutive patients who had ischemic (814 infarcts with atheroma and 126 with cardiogenic embolism, 273 lacunar infarcts, 259 transient ischemic attacks) or hemorrhagic stroke (129 supratentorial hematomas and 24 subarachnoïd hemorrhage) on computed tomography (CT) scan. Ninety patients had an epileptic seizure in the first 15 days after stroke onset. Thirteen of the 90 had a lenticulostriate infarct, diagnosed on CT scan, without an apparent ipsilateral cortical ischemic lesion. No lenticulostriate hematoma was observed with seizures. To determine the possible existence of an ipsilateral cortical lesion, magnetic resonance imaging (MRI) with gadolinium perfusion, and HMPAO single photon emission CT (SPECT) were performed in the 13 patients with seizures. MRI showed an associated ipsilateral posterofrontal or anterotemporal cortical ischemic lesion in 11 cases, and SPECT showed decreased blood flow in the ipsilateral frontal area in all cases (superficial sylvian territory). Overall, 56 patients had a lenticulostriate infarct and clinical, CT, and MRI data from the 13 with seizures was compared with those of the 43 without seizures. Two criteria differentiated the two groups: the size of the lenticulostriate infarct was larger (8.3 vs. 3.9 cm3) and ipsilateral cortical ischemic lesions were more frequent in the group with seizures (84 vs. 9%).

Neuropsychological changes related to unilateral lenticulostriate infarcts.

According to previous studies, focal capsulostriatal lesions may produce aphasia, hemineglect, gestural apraxia, frontal lobe dysfunction, and memory impairment. A few reports of capsulostriate infarcts secondary to involvement of lenticulostriate arteries have confirmed that aphasia and hemineglect may occur whereas gestural apraxia, anosognosia and frontal-lobe symptoms are rare. Most studies used CT scan assessment and did not exclude possible associated lesions. Neuropsychological changes in 11 patients with lenticulostriate infarcts diagnosed by CT scan were prospectively investigated. MRI in five of the 11 patients showed an associated cortical lesion not seen on CT scan. Patients with pure lenticulostriate infarcts on MRI may exhibit aphasia of mild severity whereas Broca's aphasia, hemineglect, gestural apraxia, and anosognosia were only seen in the subgroup with associated cortical lesions. Aphasia in patients with pure lenticulostriate infarcts was characterised by prominent expressive and lexicosemantic task impairments. The results strongly suggest that cortical involvement is critical to the extent and severity of neuropsychological changes in patients with lenticulostriate infarcts.

Frontal lobe dysfunction in unilateral lenticulostriate infarcts. Prominent role of cortical lesions.

Most studies on frontal lobe dysfunction (FLD) in patients with striatal lesions did not consider possible associated cortical lesions not seen on computed tomographic scans. To determine the possible role of such cortical lesions, we assessed FLD in 10 patients with unilateral lenticulostriate infarct on computed tomographic scans. Magnetic resonance imaging revealed an associated cortical infarct not seen on computed tomographic scans in four patients. Using a battery of neuropsychological tests sensitive to FLD, we found that (1) the crossed tapping test was the only FLD test significantly disturbed in patients with pure unilateral lenticulostriate infarcts, (2) FLD was only present in patients with associated cortical infarct, and (3) caudate lesions only account for the number of echopraxic errors in the crossed tapping test. We conclude that unilateral isolated lenticulostriate infarcts might not lead to FLD, even though they may disturb the development of strategies involved in motor procedural learning.