Utility of Magnetic Resonance Spectroscopy for the Progression of Neurological Symptoms in Lenticulostriate Artery Territory Infarction.

OBJECTIVES: The present study aimed to examine the effectiveness of proton magnetic resonance spectroscopy (1HMRS) in determining the progression of neurological symptoms resulting in acute ischemic stroke in patients with lenticulostriate artery (LSA) infarction. MATERIALS AND METHODS: 1HMRS was performed within 72 h after neurological symptom onset. Voxel of interest was placed in tissue that included the pyramidal tract and identified diffusion weighted echo planar spin-echo sequence (DWI) coronal images. Infarct volume in DWI was calculated using the ABC/2 method. 1HMRS data (tNAA, tCr, Glx, tCho, and Ins) were analyzed using LCModel. Progressive neurological symptoms were defined as an increase of 1 or more in the NIHSS score. Patients who underwent 1HMRS after progressive neurological symptoms were excluded. RESULTS: In total, 77 patients were enrolled. Of these, 19 patients had progressive neurological symptoms. The patients with progressive neurological symptoms were significantly more likely to be female and had higher tCho/tCr values, higher rates of axial slices ≥ 3 slices on DWI, higher infarct volume on DWI, higher maximum diameter of infarction of axial slice on DWI, and higher SBP on admission compared to those without. Multivariable logistic analysis revealed that higher tCho/tCr values were independently associated with progressive neurological symptoms after adjusting for age, sex, and initial DWI infarct volume (tCho/tCr per 0.01 increase, OR 1.26, 95% CI 1.03-1.52, P = 0.022). CONCLUSIONS: Increased tCho/tCr score were associated with progressive neurological symptoms in patients with LSA ischemic stroke. Quantitative evaluation of 1HMRS parameters may be useful for predicting the progression of neurological symptoms.

Childhood ischaemic stroke in the basal ganglia can lead to fine motor and anxiety disorders: a retrospective analysis and follow-up of 109 cases.

BACKGROUND: Stroke in children easily causes long-term dysfunction. Whether the prognoses of motor and anxiety disorders are related to the affected stroke area has not been reported. METHODS: One hundred nine cases of children with ischaemic stroke were reviewed and divided into three groups: lenticular nucleus lesions only (lenticular nucleus group), lenticular nucleus and caudate head lesions (caudate head group), and lenticular nucleus and thalamus lesions (thalamus group). Overall prognosis was evaluated by the mRS score. The SCAS-P was used to evaluate anxiety in children aged ≥6 years. RESULTS: mRS scores were ≤ 2 points (mean: 0.62), no significant difference among groups. 3/21 (14.2%) patients in the caudate head group changed handedness, which is significantly higher than other groups. Patients with lesions in thalamus group had significantly higher SCAS-P scores. CONCLUSIONS: The overall prognosis of children with basal ganglia ischaemic stroke is good. However, hand preference changes and anxiety disorders may develop. Patients in the caudate head groups are more likely to suffer from fine motor disorders and changes in handedness. Patients within the thalamus group are more prone to anxiety than patients in the other groups. Anxiety disorders should be noted in children with basal ganglia stroke.

Patterns of motor recovery and structural neuroplasticity after basal ganglia infarcts.

OBJECTIVE: To elucidate the timeframe and spatial patterns of cortical reorganization after different stroke-induced basal ganglia lesions, we measured cortical thickness at 5 time points over a 6-month period. We hypothesized that cortical reorganization would occur very early and that, along with motor recovery, it would vary based on the stroke lesion site. METHODS: Thirty-three patients with unilateral basal ganglia stroke and 23 healthy control participants underwent MRI scanning and behavioral testing. To further decrease heterogeneity, we split patients into 2 groups according to whether or not the lesions mainly affect the striatal motor network as defined by resting-state functional connectivity. A priori measures included cortical thickness and motor outcome, as assessed with the Fugl-Meyer scale. RESULTS: Within 14 days poststroke, cortical thickness already increased in widespread brain areas (p = 0.001), mostly in the frontal and temporal cortices rather than in the motor cortex. Critically, the 2 groups differed in the severity of motor symptoms (p = 0.03) as well as in the cerebral reorganization they exhibited over a period of 6 months (Dice overlap index = 0.16). Specifically, the frontal and temporal regions demonstrating cortical thickening showed minimal overlap between these 2 groups, indicating different patterns of reorganization. CONCLUSIONS: Our findings underline the importance of assessing patients early and of considering individual differences, as patterns of cortical reorganization differ substantially depending on the precise location of damage and occur very soon after stroke. A better understanding of the macrostructural brain changes following stroke and their relationship with recovery may inform individualized treatment strategies.

Differential involvement of rubral branches in chronic capsular and pontine stroke.

BACKGROUND AND PURPOSE: Early studies have indicated that the cortico-rubro-spinal tracts play important roles in motor dysfunction after stroke. However, the differential involvement of the rubral branches in capsular and pontine stroke, and their associations with the motor impairment are still unknown. METHODS: The present study recruited 144 chronic stroke patients and 91 normal controls (NC) from three hospitals, including 102 cases with capsular stroke (CS) and 42 cases with pontine stroke (PS). The rubral branches, including bilateral corticorubral tracts (CRT), dentatorubral tracts (DRT), and rubrospinal tracts (RST), and the cortico-spinal tract (CST) were reconstructed based on the dataset of the Human Connectome Project. Group differences in diffusion scalars of each rubral branch were compared, and the associations between the diffusion measures of rubral branches and the Fugl-Meyer assessment (FMA) scores were tested. RESULTS: The bilateral CRT of the CS cases showed significantly lower factional anisotropy (FA) than in the NC. The bilateral DRT of the PS cases had lower FA than in the NC. Both CS and PS cases had significantly lower FA of the bilateral RST than the NC. Besides, the stroke patients demonstrated significantly lower FA in bilateral CSTs than the NC. Partial correlation analysis identified significantly positive correlations between the FA of the ipsilesional and CRT and the FMA scores in the CS group, and significantly positive correlations between the FA of the RST bilaterally and the FMA scores in the CS and PS groups. Furthermore, the association between RST integrity and FMA scores still survived after controlling for the effect of the CST. Finally, multiple regression modelling found that rubral tract FA explained 39.2% of the variance in FMA scores for CS patients, and 48.8% of the variance in FMA scores for PS patients. CONCLUSIONS: The bilateral rubral branches were differentially involved in the chronic capsular and pontine stroke, and the impairment severity of each rubral branch was dependent on lesion locations. The integrity of the rubral branches is related to motor impairment in both the chronic capsular and pontine stroke.

The Utility of Collaterals as a Biomarker in Pediatric Unilateral Intracranial Arteriopathy.

BACKGROUND: Intracranial arteriopathies are frequent causes of pediatric stroke and important risk factors for stroke recurrence. Without tissue diagnosis, vascular imaging is relied upon to identify the underlying etiology and prognosis. We hypothesized that children with unilateral intracranial arteriopathy with lenticulostriate collaterals would demonstrate distinct vascular outcomes compared with children without collaterals. METHODS: We retrospectively identified children with unilateral intracranial arteriopathy from two institutions. Two blinded raters from each institution reviewed magnetic resonance or digital subtraction angiography at baseline and ≥12 months. Patients were grouped according to presence or absence of lenticulostriate collaterals. Clinical features and vascular imaging outcomes were compared using univariate analysis and multivariate logistic regression. RESULTS: Forty-four children were included: 22 males, median age 8.2 years (range two to 16.9 years), and further stratified into the collateral group (n = 20) and non-collateral group (n = 24), with median follow-up of 25.5 months and 23 months, respectively. Both groups demonstrated similar rates of progression on vascular imaging at ≥12 months, 50% in the collateral group versus 37.5% in the non-collateral group (P > 0.05). The collateral group was associated with asymptomatic clinical presentation, normal brain MRI, border zone infarcts, and either vascular stabilization or new contralateral disease. The non-collateral group demonstrated either vascular improvement or discordant progression (combination of improved and progressive lesions). Using a multivariate model, collaterals continued to be an independent predictor of vascular outcome. CONCLUSIONS: This study suggests that lenticulostriate collaterals in children with unilateral intracranial arteriopathy may serve as a useful neuroimaging biomarker that helps to stratify patients with distinct clinical features and patterns of vascular evolution.

Enlarged perivascular spaces in the centrum semiovale are associated with poststroke depression: A 3-month prospective study.

BACKGROUND: Enlarged perivascular spaces (EPVS), markers of cerebral small vessel disease, are associated with unfavorable prognosis of stroke. This study explored the relationship between EPVS and poststroke depression (PSD). METHODS: A total of 725 patients with acute ischemic stroke were recruited from the Stroke Unit of a university-affiliated hospital in Hong Kong. PSD was defined as a Geriatric Depression Scale score of ≥ 7 assessed at three months after stroke. The extent of EPVS in the basal ganglia (BG) and the centrum semiovale (CS) was assessed on axial T2 weighted magnetic resonance imaging using a validated scale. Patients' EPVS status was categorized as either mild or moderate to severe degree. The association between EPVS and PSD was examined with logistic regression. RESULTS: One hundred and fifty-three (21.1%) of the study sample had PSD three month after stroke. 55.6% of the study sample were classified as having a minor stroke. The median scores of CS- and BG-EPVS were 1 (1-2) and 1 (0-2), respectively. After adjusting for demographic, clinical and imaging characteristics in multivariate logistic regression analyses, the CS-EPVS continuous score remained an independent predictor of PSD [odds ratio (OR) = 1.27; 95% confidence interval (CI) = 1.03-1.57]. After dichotomized, moderate to severe CS-EPVS was independently associated with PSD with an OR of 1.68 (95%CI = 1.10-2.57). LIMITATIONS: The diagnosis of PSD was based on GDS score rather than a standardized clinical examination. The study favored the patients with milder stroke. CONCLUSION: CS-EPVS were associated with PSD identified at three months after mild to moderate acute ischemic stroke.

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

OBJECTIVE: The 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. METHODS: In 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. RESULTS: The 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. CONCLUSION: The 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.

Functional lateralization in cingulate cortex predicts motor recovery after basal ganglia stroke.

The basal ganglia (BG) is involved in higher order motor control such as movement planning and execution of complex motor synergies. Neuroimaging study on stroke patients specifically with BG lesions would help to clarify the consequence of BG damage on motor control. In this paper, we performed a longitudinal study in the stroke patients with lesions in BG regions across three motor recovery stages, i.e., less than 2week (Session 1), 1-3m (Session 2) and more than 3m (Session 3). The patients showed an activation shift from bilateral hemispheres during early sessions (<3m) to the ipsilesional cortex in late session (>3m), suggesting a compensation effect from the contralesional hemisphere during motor recovery. We found that the lateralization of cerebellum(CB) for affected hand task correlated with patients' concurrent Fugl-Meyer index (FMI) in Session 2. Moreover, the cingulate cortex lateralization index in Session 2 was shown to significantly correlate with subsequent FMI change between Session 3 and Session 2, which serves as a prognostic marker for motor recovery. Our findings consolidated the close interactions between BG and CB during the motor recovery after stroke. The dominance of activation in contralateral cingulate cortex was associated with a better motor recovery, suggesting the important role of ipsilesional attention modulation in the early stage after BG stroke.

Lenticulostriate infarction.

Lenticulostriate infarcts result from ischemia within the territory supplied by the deep perforating branches of the middle cerebral artery (MCA). They are too often associated with infarctions of the deep perforating branches of the internal carotid artery. Lenticulostriate arteries usually arise from the main trunk of the MCA, but can emerge from the cortical branches. The clinical aspects of lenticulostriate infarction should be properly differentiated from those of other anterior circulation infarcts. Clinical signs include motor deficit, sensory deficit and cognitive dysfunction. The principal mechanism for lenticulostriate infarction seems to be an embolism of cardiac origin. The concept of lacunar infarctions relating to lipohyalinosis is perhaps too often proposed without evidence. The prognosis is dependent primarily on the intensity of damage to the upper part of the posterior limb of the internal capsule. They are terminal arteries without anastomoses, making them more susceptible to ischemia and resulting in a greater risk of arteriolar necrosis and hemorrhagic transformation.

Aquaporins in cerebrovascular disease: a target for treatment of brain edema?

In cerebrovascular disease, edema formation is frequently observed within the first 7 days and is characterized by molecular and cellular changes in the neurovascular unit. The presence of water channels, aquaporins (AQPs), within the neurovascular unit has led to intensive research in understanding the underlying roles of each of the AQPs under normal conditions and in different diseases. In this review, we summarize some of the recent knowledge on AQPs, focusing on AQP4, the most abundant AQP in the central nervous system. Several experimental models illustrate that AQPs have dual, complex regulatory roles in edema formation and resolution. To date, no specific therapeutic agents have been developed to inhibit water flux through these channels. However, experimental results strongly suggest that this is an important area for future investigation. In fact, early inhibition of water channels may have positive effects in the prevention of edema formation. At later time points during the course of disease, AQP is important for the clearance of water from the brain into blood vessels. Thus, AQPs, and in particular AQP4, have important roles in the resolution of edema after brain injury. The function of these water channel proteins makes them an excellent therapeutic target.

Severity of dilated Virchow-Robin spaces is associated with age, blood pressure, and MRI markers of small vessel disease: a population-based study.

BACKGROUND AND PURPOSE: Little is known about the risk factors of dilated Virchow-Robin spaces (dVRS) and their relation with other markers of brain small vessel disease. We investigated both issues in a large population-based sample of elderly individuals. METHODS: Severity of dVRS was semiquantitatively graded in both white matter and basal ganglia using high-resolution 3-dimensional MRI images taken from 1818 stroke- and dementia-free subjects enrolled in the Three-City Dijon MRI study. Multinomial logistic regression models were used to model the association of cardiovascular risk factors, APOE genotype, brain atrophy, and MRI markers of small vessel disease with the degree of dVRS. RESULTS: Severity of dVRS was found to be strongly associated with age in both basal ganglia (degree 4 versus 1: OR, 2.1; 95% CI, 1.4 to 3.2) and white matter (OR, 1.5; 95% CI, 1.2 to 1.9). The proportion of hypertensive subjects increased with the degrees of dVRS in both basal ganglia (P = 0.02) and white matter (P = 0.048). Men presented a higher risk of severe dVRS in basal ganglia than women, particularly degree 4 (OR, 6.0; 95% CI, 1.8 to 19.8). The degree of dVRS was associated with the volume of white matter hyperintensities and the prevalence of lacunes, but not with brain atrophy. CONCLUSIONS: In this large cohort study of elderly subjects, the degree of dVRS appears independently associated with age, hypertension, volume of white matter hyperintensities, and lacunar infarctions. dVRS should be considered as another MRI marker of cerebral small vessel disease in the elderly with regional variations in their severity.

The role of imaging in the diagnosis of vascular parkinsonism.

Parkinsonism is a syndrome that features bradykinesia (slowness of the initiation of voluntary movement) and at least 1 of the following conditions: rest tremor, muscular rigidity, or postural instability. Criteria for the clinical diagnosis of vascular parkinsonism (VP) have been proposed, which are derived from a postmortem examination study. Computed tomography and magnetic resonance imaging can support this clinical diagnosis with positive imaging findings. Dopamine transporter single-photon emission computed tomography may also be of help to distinguish VP from Parkinson disease and other parkinsonisms.

Resting cerebral blood flow: a potential biomarker of the effects of HIV in the brain.

OBJECTIVE: HIV enters the brain soon after infection causing neuronal damage and microglial/astrocyte dysfunction leading to neuropsychological impairment. We examined the impact of HIV on resting cerebral blood flow (rCBF) within the lenticular nuclei (LN) and visual cortex (VC). METHODS: This cross-sectional study used arterial spin labeling MRI (ASL-MRI) to measure rCBF within 33 HIV+ and 26 HIV- subjects. Nonparametric Wilcoxon rank sum test assessed rCBF differences due to HIV serostatus. Classification and regression tree (CART) analysis determined optimal rCBF cutoffs for differentiating HIV serostatus. The effects of neuropsychological impairment and infection duration on rCBF were evaluated. RESULTS: rCBF within the LN and VC were significantly reduced for HIV+ compared to HIV- subjects. A 2-tiered CART approach using either LN rCBF < or =50.09 mL/100 mL/min or LN rCBF >50.09 mL/100 mL/min but VC rCBF < or =37.05 mL/100 mL/min yielded an 88% (29/33) sensitivity and an 88% (23/26) specificity for differentiating by HIV serostatus. HIV+ subjects, including neuropsychologically unimpaired, had reduced rCBF within the LN (p = 0.02) and VC (p = 0.001) compared to HIV- controls. A temporal progression of brain involvement occurred with LN rCBF significantly reduced for both acute/early (<1 year of seroconversion) and chronic HIV-infected subjects, whereas rCBF in the VC was diminished for only chronic HIV-infected subjects. CONCLUSION: Resting cerebral blood flow (rCBF) using arterial spin labeling MRI has the potential to be a noninvasive neuroimaging biomarker for assessing HIV in the brain. rCBF reductions that occur soon after seroconversion possibly reflect neuronal or vascular injury among HIV+ individuals not yet expressing neuropsychological impairment.

Basal ganglionic infarction before mechanical thrombectomy predicts poor outcome.

BACKGROUND AND PURPOSE: Use of mechanical thrombectomy for acute cerebrovascular occlusions is increasing. Preintervention MRI patterns may be helpful in predicting prognosis. METHODS: We reviewed all Merci thrombectomy cases of either terminal ICA or M1 occlusions and classified them according to diffusion MRI patterns of (1) completed basal ganglia infarct (pure M1a), (2) near-completed basal ganglia infarct (incomplete M1a), and (3) relative sparing of deep MCA field (M1b). We compared the M1a and M1b patients with respect to neurological deficit on presentation, recanalization rates, hospital length of stay, and disability on discharge. We also determined whether deep MCA compromise predicted hematomal hemorrhagic transformation (HT) and whether this correlated with worse clinical outcome at discharge. RESULTS: The M1a group had worse pre-Merci NIHSS (21 versus 14, P=0.004), worse discharge NIHSS (12 versus 4, P<0.001), longer hospital length of stay (11.5 versus 6.4 days, P=0.003), and higher rates of discharge mRS > or = 3 (OR 8.4, 95% CI 2.1 to 44.7) despite equivalent recanalization rates when compared to the M1b group. The M1a group had a higher rate of parenchymal hematomal HT (OR 6.7, 95% CI 1.02 to 183.3). Patients with such hematomal HT had higher rates of death or dependency discharge (100% versus 60%, OR=infinite). CONCLUSIONS: Among patients with ICA and M1 occlusions, preintervention diffusion MRI evidence of advanced injury in the basal ganglia bodes worse dysfunction and disability at discharge, longer hospital stays, and higher rates of hemorrhage after intervention when compared to other diffusion patterns.

Progression of mild cognitive impairment to dementia: contribution of cerebrovascular disease compared with medial temporal lobe atrophy.

BACKGROUND AND PURPOSE: We sought to determine the predictive value of magnetic resonance imaging measures of vascular disease (white matter hyperintensities [WMHs], lacunes, microbleeds, and infarcts) compared with atrophy on the progression of mild cognitive impairment to dementia. METHODS: We included 152 consecutive patients with mild cognitive impairment. Baseline magnetic resonance imaging was used to determine the presence of medial temporal lobe atrophy and vascular disease (presence of lacunes, microbleeds, and infarcts was determined, and WMHs were rated on a semiquantitative scale). Patients were followed up for 2+/-1 years. RESULTS: Seventy-two (47%) patients progressed to dementia during follow-up. Of these, 56 (37%) patients were diagnosed with Alzheimer's disease, and 16 (10%) patients were diagnosed with a non-Alzheimer dementia (including vascular dementia, frontotemporal lobar degeneration, and Parkinson dementia). Converters were older and had a lower Mini-Mental State Examination score at baseline. On baseline magnetic resonance imaging, patients who progressed to a non-Alzheimer dementia showed more severe WMHs and had a higher prevalence of lacunes in the basal ganglia and microbleeds compared with nonconverters. Cox proportional-hazard models showed that, adjusted for age and sex, baseline medial temporal lobe atrophy (hazard ratio=2.9; 95% CI, 1.7 to 5.3), but not vascular disease, was associated with progression to Alzheimer's disease. By contrast, deep WMHs (hazard ratio=5.7; 95% CI, 1.2 to 26.7) and periventricular hyperintensities (hazard ratio=6.5; 95% CI, 1.4 to 29.8) predicted progression to non-Alzheimer dementia. Furthermore, microbleeds (hazard ratio=2.6; 95% CI, 0.9 to 7.5) yielded a >2-fold increased, though nonsignificant, risk of non-Alzheimer dementia. CONCLUSIONS: Medial temporal lobe atrophy and markers of cerebrovascular disease predict the development of different types of dementia in mild cognitive impairment patients.

Transcranial sonography in movement disorders.

Over the past 15 years the use of transcranial B-mode sonography to assess brainstem and subcortical brain structures has become an important tool for the diagnosis and differential diagnosis of various movement disorders. The most widely recognised finding for movement disorders has been an increase in echogenicity of the substantia nigra, an area of the midbrain that is affected in idiopathic Parkinson's disease (PD). This finding has enabled the reliable diagnosis of PD with high predictive values. Other sonographic features, such as hypoechogenicity of the brainstem midline and hyperechogenicity of the lentiform nucleus, might help the differential diagnosis of PD and other movement disorders. This Review provides detailed information about the advantages and limitations of this novel neuroimaging method, including guidelines for the scanning procedure and considerations on the origin of ultrasound abnormalities. We discuss the use of transcranial sonography for early and preclinical diagnosis and for differential diagnosis of PD and other movement disorders, and we compare this method with other functional neuroimaging strategies. Transcranial B-mode sonography is a reliable, non-invasive, commonly available, easily applicable, and inexpensive method, which provides new information about the morphology of the brain to help the diagnosis of various movement disorders. Thus, this neuroimaging method could be recommended for general application in the diagnosis and differential diagnosis of PD.

Prediction of progressive motor deficits in patients with deep subcortical infarction.

BACKGROUND AND PURPOSE: Early motor deterioration (EMD) in deep subcortical infarction is usually associated with long-term functional disability. In this study, we investigated the clinical characteristics, biochemical markers and MRI variables in patients with deep subcortical infarction to identify the predictors of progressive motor deficits. METHODS: A total of 167 consecutive patients with deep subcortical infarction in the anterior circulation were included. All of the patients must have motor deficit as one of the presented symptoms. EMD was defined as a modified National Institutes of Health Stroke Scale (mNIHSS) motor score of >or=1 during the first week of symptom onset. The patients were assessed with clinical findings such as stroke risk factors, blood pressure on admission, laboratory variables and radiological findings; lesion characteristics on MRI, stenosis or occlusion in the relevant parental artery on MRA and diffusion/perfusion mismatch. RESULTS: Twenty-three (13.8%) of the 167 patients revealed EMD. The independent factors related to the EMD in multiple regression analysis were initial high systolic blood pressure (OR = 1.035, 95% CI = 1.007-1.063; p = 0.013) and lesion involvement in the posterolateral striatum (OR = 15.98; 95% CI = 1.842-138.534; p = 0.012); however, the other clinical and radiological factors were not related. CONCLUSIONS: The involvement of the posterolateral striatum appears to be an important predictor for EMD. It can be explained by (1) the lateral lenticulostriate artery (LSA), which supplies the posterolateral striatum vulnerable to ischemic damage due to the lack of collateral vessels, and (2) the posterolateral division of the striatum may be susceptible to progressive motor deficit because of anatomic proximity to the corticospinal tract in the same LSA territory. Further research should include precise anatomical and functional study to determine the relationship between the posterolateral striatum and corticospinal tract in predicting progressive motor deficit.

Emotional facial palsy following striato-capsular infarction.

Emotional facial palsy (EFP) is a rare condition in which facial paresis is only apparent during reflex movements of the hemiface, such as smiling and laughter. We report the case of a 32-year-old man presenting with EFP as the main symptom of a small striatocapsular infarction. Our case strongly suggests that the anterior arm of the internal capsule is part of the corticonuclear tract that is involved in emotional facial motility.