Correlation of plasma beta-2 microglobulin levels with total magnetic resonance imaging burden of cerebral small-vessel disease in elderly patients with lacunar stroke / 中华老年医学杂志

Objective:To investigate the relationship between plasma beta-2 microglobulin(β2M)levels and the total magnetic resonance imaging(MRI)burden of cerebral small-vessel disease(CSVD)in elderly patients with lacunar stroke.Methods:A total of 93 elderly patients with lacunar stroke admitted to the Department of Neurology, Changzhou Second People's Hospital form August 2018 to August 2019 were enrolled retrospectively, all with complete records of cranial magnetic resonance imaging and plasma β2M measurement.According to the total MRI CSVD burden, which ranges from an ordinal score of 0 to 4, patients were divided into 5 groups.Single-factor analysis was used to compare clinical data between the 5 groups.The association between the plasma β2M level and total MRI CSVD burden was analyzed by ordered multiple Logistic regression models.Results:Among elderly patients with lacunar infarction, 19 had a CSVD score of 0, 19 had a score of 1, 23 had a score of 2, 21 had a score of 3, and 11 had a score of 4, with statistically significant differences in age, percentage with diabetes, systolic blood pressure, diastolic blood pressure, glycosylated hemoglobin, plasma β2M, and eGFR between the 5 groups( P<0.05). Spearman correlation analysis showed that plasma β2M level was significantly positively correlated with total MRI CSVD burden( r=0.687, P<0.001). In ordered multivariate logistic regression models, after adjustment for possible confounding factors such as age, sex and hypertension, the results demonstrated that plasma β2M level( OR=5.253, 95% CI: 2.350-11.740, P<0.001)was an independent risk factor for total MRI CSVD burden. Conclusions:In elderly lacunar stroke patients, the plasma β2M level is closely related to the total MRI CSVD burden and can be used as a marker for predicting the severity of lesions.

The etiologies of post-stroke depression: Different between lacunar stroke and non-lacunar stroke

Abstract Objectives: Depression is common after both lacunar stroke and non-lacunar stroke and might be associated with lesion locations as proven by some studies. This study aimed to identify whether lesion location was critical for depression after both lacunar and non-lacunar strokes. Methods: A cohort of ischemic stroke patients was assigned to either a lacunar stroke group or a non-lacunar stroke group after a brain MRI scan. Neurological deficits and treatment response was evaluated during hospitalization. The occurrence of depression was evaluated 3 months later. Logistic regressions were used to identify the independent risk factors for depression after lacunar and non-lacunar stroke respectively. Results: 83 of 246 patients with lacunar stroke and 71 of 185 patients with non-lacunar stroke developed depression. Infarctions in the frontal cortex, severe neurological deficits, and a high degree of handicap were identified as the independent risk factors for depression after non-lacunar stroke, while lesion location was not associated with depression after lacunar stroke. Conclusion: The main determinants for depression after lacunar and non-lacunar stroke were different. Lesion location was critical only for depression after non-lacunar stroke.

Importance of the diagnosis, treatment and research of acute cerebral small vessel disease / 中华神经科杂志

Based on a comprehensive literature review with long-term experiences of clinical practice and researches, the authors propose the following concepts of the diagnosis, treatment and research of acute cerebral small vessel disease: (1) Cerebral small vessel disease could be grouped into acute and non-acute categories. Acute cerebral small vessel disease indicates an acute stroke due to small vessel disease, including ischemic (ie. acute lacunar stroke) and hemorrhagic (hypertensive arteriopathy- and cerebral amyloid angiopathy-related intracerebral hemorrhage) stroke. (2) Acute ischemic cerebral small vessel disease, defined traditionally by the infarction size (lacunar stroke), is regarded as the syndrome caused by a variety of mechanisms recently, although mainly characterized by lipohyalinosis in the small arterioles. The understanding of pathological mechanisms has experienced a history from autopsy observation, to inference based on risk factors, and then to direct observation of arteriole morphology using high-resolution magnetic resonance angiography. The advancement in imaging technology has brought new opportunities for studies on pathological mechanisms of cerebral small vessel disease. (3) Acute cerebral small vessel disease is manifested as acute stroke, which could be with or without the non-acute symptoms or imaging markers. (4) Individualized treatment based on the pathogenesis is the future direction for practice and research of cerebral small vessel disease. Reducing the incidence, recurrence and major outcomes (death, disability and dementia) is the main target of prevention and treatment.

Dramatic unilateral decrease in uptake via the dopamine transporter: Imaging in a patient with hemiparkinsonism following the lacunar stroke in substantia nigra

@#Vascular parkinsonism (VaP) is typically defined as having predominant lower body involvement, postural instability, less prominent rest tremor and little or no response to treatment with levodopa. In this study, we report a patient with VaP with clear demonstration of a dramatic unilateral decrease of radiotracer uptake in a 18F-FP-CIT-PET study. A 62-year-old right-handed woman was referred to the neurology department due to rest tremor and rigidity in the right hand, which began after undergoing resection surgery for a left acoustic neuroma 7 years prior. Brain MRI, taken at 1 year after surgery showed an ischemic stroke lesion in the left medial pons and the left substantia nigra. 18F-FP-CIT-PET revealed a marked reduction of radiotracer uptake in left striatum compared to that of the right. We treated the patient with 100 mg of levodopa, 200 mg of entacarpone and 25 mg of carbidopa. There was an improvement in bradykinesia and tremor, but the symptoms persisted, and there was no deterioration during 6 months of observation. After acoustic neuroma surgery, ischemic complications are uncommon, and even a small lesion in the nigrostriatal pathway can cause a hemiparkinsonism. If a patient experience sudden onset hemiparkinsonism, they should be carefully examined for lesions in the nigrostriatal pathways. Under these conditions, the 18F-FP-CIT-PET scan can enable visualization of a unilateral decrease and is a useful tool for diagnosis and differentiation from idiopathic Parkinson’s disease

Hemorrhagic Transformation in Thalamic Infarction

No abstract available.

Diferenciación clínica del déficit cognitivo del CADASIL con respecto a otras demencias vasculares / Clinical differentiation of the cognitive deficit of CADASIL whit respect to the other vascular dementias

En el mundo hay unos 47 millones de personas que padecen demencia, y cada año se registran cerca de 10 millones de nuevos casos. La demencia es una de las principales causas de discapacidad y dependencia entre las personas mayores de 65 años. La demencia vascular constituye la segunda causa de demencia en adultos mayores y en ocasiones su diagnóstico es poco asertivo por la variedad y similitud de síntomas entre las diferentes enfermedades que originan demencia vascular, incluyendo CADASIL (acrónimo inglés de Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy); particularmente el déficit cognitivo es de los síntomas más complejos de diagnóstico, teniendo en cuenta que su manifestación clínica depende de la magnitud y localización de la lesión. La enfermedad de CADASIL, aunque se constituye como una infrecuente causa de demencia vascular de naturaleza hereditaria a nivel mundial, representa una patología de gran importancia en el ámbito nacional, dado que en familias colombianas se ha reportado mutaciones que conllevan a dicha patología. Por lo tanto, su diagnóstico y tratamiento constituyen un reto para el personal clínico, sabiendo que la identificación temprana y precisa es la mejor estrategia para evitar la progresión precoz de la enfermedad y el mejoramiento de la calidad de vida del paciente. De acuerdo con lo anterior, se realizó una revisión de la diferenciación clínica del déficit cognitivo del CADASIL con respecto a las demás demencias vasculares, con el fin de generar una herramienta que apoye la diferenciación clínica de dicha patología.

In the world, there are approximately 47 million people who have dementia, and every year they register near 10 million new cases. The dementia is one of the principal reasons for disability and dependence between people older than 65 years old. Vascular dementia constitutes the second reason of dementia in the elders, and sometimes the diagnosis is slightly assertive because of the variety and similarity of symptoms between the different diseases that originate vascular dementia, including CADASIL (Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy). Particularly, the cognitive deficit is one of the most complex symptoms of diagnosis, bearing in mind that its clinical manifestation depends on the magnitude and location of the injury. CADASIL disease, though it constituted as an infrequent reason of vascular dementia of hereditary nature worldwide, represents a pathology of great importance in the national area, because, in Colombian families, there have been reported mutations that carry to the above-mentioned pathology. Therefore, its diagnosis and treatment constitute a challenge for the clinical personnel, knowing that the early and precise identification is the best strategy to avoid the rapid progression of the disease and the improvement of the quality of life of the patient. In agreement with the previous information, there was made a review of the clinical differentiation of the cognitive deficit of CADASIL regarding other vascular dementias, to generate a tool that supports the clinical differentiation of the pathology mentioned above.

Correlation study of cerebral microbleeds with chronic renal failure in patients with acute lacunar stroke / 医学研究生学报

Objective Cerebral small vessel disease is closely related to kidney disease .Chronic kidney disease ( CKD) may increase the risk of hemorrhage stroke .However, its impact on hemorrhage-prone small vessel disease represented by cerebral microb-leeds( CMBs) remains unclear .The purpose of this study was to investigate the relationship of CKD with the presence and location of CMBs in patients with acute lacunar stroke . Method Consecutive patients with acute lacunar stroke within 7 days from onset were enrolled retrospectively from January 2014 to July 2016 and scanned by gradient-echo T2*-weighted imaging (GRE-T2*WI).Their demographic, clinical, laboratory and imaging data were collected .Estimate glomerular filtration rate (eGFR) was calculated individu-ally by the following chronic kidney disease epidemiology collaboration (CKD-EPI) equation for the Asian population .CKD was defined as the level of eGFR<60 mL/min/1.73 m2. Results Finally, 308 patients (mean age:65.79±8.67 years; median NHISS:3(2-5);42.2%Female) with lacunar ischemic stroke were enrolled in the final analysis .Among these patients, CMBs were present in 116 patients ( 37.7%) and CKD in 62 patients ( 20.1%) .Patients were divided into CKD group and normal group according to GFR level . The result of univariate analysis showed that patients with CKD had higher prevalence of diabetes ( P=0.014) and higher degrees of CMBs (P=0.001) compared with normal group.CMBs were refined by its location .The result of multivariable analysis showed that CMBs in deep brain [ OR=7.61, 95%CI 4.18-16.55, P=0.001] were sig-nificantly associated with CKD incidence , while no significant rela-tionship was found in CKD incidence and CMBs in the lobe and mixed location of brain . Conclusion The CKD incidence in patients with acute lacunar stroke is in dependent relationship with CMBs in deep brain and without significant correlation with CMBs in the lobe and mixed location of brain .

Parameters of Systemic Inflammatory Response in Patients with Passing Infringements of Brain Blood Circulation.

Aims: The paper aims at revealing the difference in the change of Systemic Inflammation (SI) parameters in blood plasma of patients with Passing Infringements of Brain Blood Circulation (PIBBC) and stroke during 10-day acute period. Study Design: Prospective cohort study. Place and Duration of Study: Department of Neurology and Neurosurgery of the Gomel State Medical University, Stroke Unit of the Gomel Regional Veterans Hospital, between May 2013 and March 2015. Methodology: This study included 108 patients (35 men, 73 women; age range is 46-90 years) and 20 volunteers over 45 years (11 men, 9 women, mean age is 54.3±1.6 years). We compared the parameters of systemic inflammation (blood plasma concentrations of interleukins (IL-6, IL-8, IL-10), tumor necrosis factor α (TNFα), C-reactive protein (CRP) and stable metabolites of nitric oxide (nitrite- and nitrate-ions, NOx) in patients with PIBBC including transient ischemic attack (TIA) and cerebral hypertensive crisis (CHC), patients with lacunar stroke (LS) on the first and tenth day of patient staying in the hospital and in volunteers of a control group. Results: On the first day, the IL-6 and CRP levels for PIBBC and LS groups was found to be significantly higher than the corresponding parameters for a control group. An increase in IL-6 level during the 10-day therapeutic period was observed only in blood plasma of the LS group persons. The TNF-α level was about zero level for all the studied groups except for the LS group on the tenth day. On the first day, for the patients with LS the IL-8 level was significantly decreased comparing to that for the control group and PIBBC groups and the NOx level was significantly lower than that for CHC group. Both parameters increased in values during the 10-day therapeutic period. No difference between the parameters (NOx and IL-8) for PIBBC and control groups was detected on the first day. Coefficient of reactivity characterizing the systemic inflammation level in patients of all the studied groups was nonzero level and it increased in the LS patients during the therapeutic period. Conclusion: The obtained data showed an important role a number of inflammation markers (NOx, IL-6, IL-8, TNF-α, CRP) in the pathogenesis of different stroke episodes. Absence of specific neuroimaging changes in TIA and CHC group and nonzero coefficient of reactivity (kR) suggests that systemic inflammation is not a result of the focal brain ischemia but its intrinsic cause. The differences in the concentration of IL-8, and NOx in the blood plasma of patients with CHC and LS on their admission to the hospital will help to identify sanogenetic reserves in the case of PIBBC

The Effect of Pulsatility Index on Infarct Volume in Acute Lacunar Stroke

PURPOSE: Lacunar stroke, in the context of small vessel disease, is a type of cerebral infarction caused by occlusion of a penetrating artery. Pulsatility index (PI) is an easily measurable parameter in Transcranial Doppler ultrasound (TCD) study. PI reflects distal cerebral vascular resistance and has been interpreted as a surrogate marker of small vessel disease. We hypothesized that an increased PI, a marker of small vessel disease, might be associated with a larger infarct volume in acute lacunar stroke. MATERIALS AND METHODS: This study included 64 patients with acute lacunar stroke who underwent TCD and brain MRI. We evaluated the association between the mean PI value of bilateral middle cerebral arteries and infarct volume on diffusion-weighted MRI using univariate and multivariate linear regression. RESULTS: The mean infarct volume and PI were 482.18±406.40 mm3 and 0.86±0.18, respectively. On univariate linear regression, there was a significant positive association between PI and infarct volume (p=0.001). In the multivariate model, a single standard deviation increase of PI (per 0.18) was associated with an increase of 139.05 mm3 in infarct volume (95% confidence interval, 21.25 to 256.85; p=0.022). CONCLUSION: We demonstrated that PI was an independent determinant of infarct volume in acute lacunar stroke. The PI value measured in acute stroke may be a surrogate marker of the extent of ischemic injury.

Heminegligência / Hemineglect

A heminegligência, um fenômeno em que uma disfunção leva a uma desatenção da metade do campo visual e da percepção corporal, geralmente decorre de lesões do hemisfério parietal e está associado a um pior prognóstico quando acompanhada de anosognosia. O objetivo deste estudo é apresentar o caso de um paciente do sexo masculino, 73 anos, que desenvolveu heminegligência espacial associada à anosognosia e hemianopsia à esquerda decorrentes de um acidente vascular encefálico isquêmico (AU)

Hemineglect, a phenomenon in which a dysfunction leads to inattention of half the visual fi eld and body perception, usually results from damage to the parietal hemisphere and is associated with a worse prognosis when accompanied by anosognosia. The objective of this study is to present the case of a male patient, 73, who developed spatial hemineglect and anosognosia associated with left hemianopia resulting from an ischemic stroke (AU)

The Relationship of Matrix Metalloproteinase-9 and Microbleeds on T2*-Weighted Gradient-Echo MRI in Acute Lacunar Infarction

BACKGROUND: Hypointense cerebral lesions on T2*-weighted gradient-echo MRI (GRE) have been known to be related with microbleeds or advanced microangiopathy with potential for further bleeding. It has also been suggested that matrix metalloproteinases (MMPs) may play a role in blood brain barrier disruption, edema formation and hemorrhagic transformation. In this study, we investigated the relationship between microbleeds detected by GRE, MMPs and neurological worsening in acute lacunar infarctions. METHODS: Eighty-eight patients with acute lacunar infarctions, defined by TOAST classification, were included. GRE (1.5T, TR 500 ms TE 15 ms) was performed within 48 hours after stroke symptom onset. MMPs were measured by standard quantitative sandwich enzyme-linked immunosorbent assays (ELISA). Clinical characteristics, neurologic scale and MMP-9 levels were compared between groups with or without hypointense lesions in GRE (microbleeds). Neurological worsening was defined as deterioration from baseline in the score on the NIHSS by one or more points 14 days after the onset of a lacunar infarction. RESULTS: Eleven of 88 patients (12.5%) undergoing GRE demonstrated evidence of microbleeds in the ischemic region. In the groups with microbleeds, the ESR level (p=0.048) and MMP-9 activity (p=0.001) were significantly increased, and neurological worsening was more prominent (p=0.018). CONCLUSIONS: This study suggests that microbleeds detected by GRE are related with elevated MMP-9 and neurological worsening. Therefore, the finding of microbleeds in GRE, increased MMP-9 activity and elevated ESR level might be useful factors for predicting the progression of acute lacunar infarctions.

Studies on the sensory changes and somatosensory evoked potential in thalamic stroke

BACKGROUND: The thalamus is a subcortical gray-matter composed of several groups of nuclei. Though there are some characteristic clinical findings in thalamic stroke syndrome, it is not easy to identify their own function in each nuclei. We demonstrated this study to figure out the relationships between anatomic nucleus, sensory symptoms, and electrophysiologic findings in thalamic stroke. METHODS: Sixteen thalamic stroke patients were studied. Fifteen cases showed thalamic lacunar infarction by magnetic resonance imaging and one case showed thalamic hemorrhage by computed tomography. We compared their sensory symptoms and signs, somatosensory evoked potentials(SSEP), the size of lesions, and the location of lesions on imaging studies. RESULTS: There were 12 cases of a lesion on ventroposterolateral(VPL) nucleus(Group I) and 4 cases of a lesion on the other nuclei(Group II). All 8 cases which had a sensory deficit in Group I, and 2 cases - one with sensory deficit and the other without in Group II, showed abnormal SSEP findings. There were 9 cases in Group I and 3 cases in Group II with thalamic pain and there was no relationship between SSEP and thalamic pain. Five were pure sensory strokes in 6 patients with a small lesion(less than 0.5 cm), and pure sensory strokes were only 3 in 10 patients with relatively a large lesion (between 0.5 and 1.5 cm). CONCLUSION: There was significant relationship between sensory deficit and SSEP. SSEP can be used as a objective method in estimating the sensory deficit of thalamic stroke. We could ascertain the fact that other nuclei as well as VPL nucleus were associated with the development of pain in thalamic stroke, and there was significant relationship between the size of lesion and the clinical feature of stroke.