Deep Cerebral Infarcts Research Articles

Long-Term Outcomes Following Freehand Minimally Invasive Aspiration for Deep Supratentorial Intracerebral Hemorrhage: A Multicenter Cohort Study.

The aim of this study was to compare the therapeutic effects of non-navigated freehand minimally invasive aspiration and conservative medical care in patients with deep supratentorial intracerebral hemorrhage (ICH). We analyzed data from a prospective multicenter cohort study. Propensity score matching was performed to adjust for possible confounding factors. A total of 122 patients with first-onset deep supratentorial ICH with a volume ≥ 20ml were enrolled. All patients were followed up at 30days, 90days, and 1year. The mortality rate, functional outcomes, complications, and treatment costs were compared between the two groups. After propensity score matching, 122 patients with a mean age of 56.0years were included, 77.9% of whom were male. The median ICH volumes were 45.5ml in the surgery group and 48.0ml in the conservative group. The mortality rate at 30days was significantly lower in the surgery group than in the conservative group (P = 0.0127). There were no significant differences in functional outcomes at the 90-day and 1-year follow-ups between the two groups (P > 0.05). There was no significant difference in complications, including recurrent bleeding (6.6% vs. 4.9%), pulmonary infection (57.4% vs. 41.0%), deep venous thrombosis (9.8% vs. 11.5%), heart failure (1.6% vs. 6.6%), and cerebral infarction (4.9% vs. 3.3%), between the two groups. For deep supratentorial ICH, non-navigated freehand minimally invasive aspiration was safe and reduced short-term mortality but did not effectively improve long-term functional outcomes.

Balloon pulmonary angioplasty followed by pulmonary endarterectomy: Combination treatment for high-surgical-risk patients with chronic thromboembolic pulmonary hypertension.

Our goal was to evaluate the combined effects of balloon pulmonary angioplasty (BPA) followed by pulmonary endarterectomy (PEA) to treat high-surgical-risk patients with chronic thromboembolic pulmonary hypertension (CTEPH). This study included 58 patients with CTEPH who had pulmonary vascular resistance of ≥1000 dyn·s/cm5, mean pulmonary arterial pressure (mPAP) of ≥45 mmHg or mPAP of 38-44 mmHg with comorbidities. Of these, 21 patients underwent the combined therapy of BPA followed by PEA (BPA group) and 37 underwent direct PEA (non-BPA group). Preoperative and postoperative results were compared between the 2 groups. An early postoperative composite event comprised the postoperative use of extracorporeal membrane oxygenation or intra-aortic balloon pump, in-hospital death, rescue BPA, prolonged ventilation, tracheostomy, prolonged stay in the intensive care unit, deep sternal wound infection and cerebral infarction. Before the first intervention (before BPA or direct PEA), patients in the BPA group had a higher mPAP than those in the non-BPA group. After undergoing BPA before PEA, the BPA group demonstrated significantly decreased mPAP and pulmonary vascular resistance (43 vs 52 mmHg, P < 0.001; 636 vs 965 dyn·s/cm5, P = 0.003, respectively) and significantly increased cardiac output (4.1 vs 3.5 l/min, P = 0.041). Notably, the number of patients with the early postoperative composite event was significantly lower in the BPA group than in the non-BPA group (4.8% vs 35.1%, P = 0.011). Compared with direct PEA, the combination therapy of BPA followed by PEA can be a feasible and effective risk-reduction strategy for high-surgical-risk patients with CTEPH.

The prevalence of VKORC1 alleles in the population of the Republic of Srpska, Bosnia and Herzegovina

Background/Aim: Warfarin is one of the most common orally prescribed anticoagulant in patients with deep venous thrombosis, myocardial or cerebral infarctions. The main side effects of non-adequate dose of these drugs are prolonged peripheral or internal bleeding. VKORC1 1173C&gt;T polymorphism (rs9934438) is of particular importance, since carriers of non-wild type allele correlates with the lower dosage of warfarin therapy. Thus, the aim of the research was to determine the distribution of 1173C&gt;T polymorphism in population of the Republic of Srpska, Bosnia and Herzegovina (RS) and to compare results with frequencies in other populations. Methods: A total of 124 healthy participants of both genders were enrolled in the study, from all parts of the RS. Molecular genotyping was performed by real-time PCR, using drug metabolism assays according to the manufacturer's instructions. Results: Of the total number, 22 subjects (17.74 %) were genotyped as CC, 69 subjects (55.65 %) as CT and 33 subjects (26.61 %) as TT. The frequencies of alleles C and T were 45.18 % and 54.82 %, respectively. No statistical significance was found among allele distribution between genders (ch² = 0.236; p = 0.627). All observed genotype frequencies were in Hardy-Weinberg equilibrium. No statistical significance was observed among the frequency of minor T allele between presented findings and other European countries, besides Russia (p = 0.021). Conclusion: This was the first study analysing the distribution of rs9934438 alleles in population of the RS. These findings will be helpful in better and more precise drug prescribing in patients who require anticoagulant therapy.

Ischemic stroke in oral anticoagulated patients with atrial fibrillation.

Ischemic strokes in orally anticoagulated patients pose challenges for acute management and secondary prevention but the characteristics of these strokes are poorly understood. We examined the clinical and imaging features, the presumed underlying etiology and the subsequent antithrombotic management. We analyzed a consecutive series of patients enrolled into the EIDASAF study, a single center, observational study of ischemic stroke patients with a diagnosis atrial fibrillation (AF) prior to the index event who had been admitted to the Hyperacute Stroke Unit of Imperial College London between 2010 and 2017. We compared patients with oral anticoagulation therapy prior admission (OACprior ) with those without anticoagulation (OACnaive ). Brain imaging was analyzed centrally. 763 patients were included in the analysis. 481 (63%) were OACnaive while 282 (37%) were OACprior . Patients with OACprior were younger, more often had a previous history of stroke or transient ischemic attack (TIA), and more often suffered from hypertension and diabetes. In OACnaive, patients, large and deep middle cerebral artery infarcts occurred more often than in OACprior patients. The groups differed significantly in the distribution of competing etiologies underlying their stroke. At discharge, OACprior more frequently were (re)-anticoagulated compared to OACnaive patients. Within the OACprior group, patients with recurrent strokes did not differ from those with a first stroke regarding clinical characteristics and pattern of cerebral infarction but they were less frequently anticoagulated. Ischemic strokes on OAC represent a significant proportion of AF-related strokes. There is an unmet need to better understand the causes underlying these strokes and to optimize the medical management.

Impact of Deep Middle Cerebral Artery Infarcts on Stroke Thrombectomy Outcomes (4763)

Impact of Deep Middle Cerebral Artery Infarcts on Stroke Thrombectomy Outcomes (4763)

Histopathological Findings and Increased D-Dimer Are Predictive Factors of Systemic Thromboses in Eosinophilic Granulomatosis With Polyangiitis.

Eosinophilic granulomatosis with polyangiitis (EGPA; ie, Churg-Strauss syndrome) is one of the antineutrophil cytoplasmic antibody-associated vasculitis syndromes. Although extravascular granulomatoses are a well-known histopathological feature, the diverse histopathologic spectrum of cutaneous lesions has not been described in detail. Thus, this study sought to investigate the possible correlation between the clinical features and histopathology of cutaneous lesions in EGPA cases, focusing on systemic thrombogenic conditions, such as visceral infarction and deep vein thrombosis. Fourteen cases of EGPA diagnosed at the Department of Dermatology in Asahikawa Medical University from 1977 to 2017 were clinically and histopathologically reviewed. In 6 (43%) cases, skin lesions were the initial manifestation of EGPA. Among the cutaneous lesions, purpura and erythema were the most common. Persistent proteinuria and macrohematuria were observed in only 2 myeloperoxidase-antineutrophil cytoplasmic antibody-positive cases. Systemic thrombotic symptoms, such as cerebral infarction and deep vein thrombosis, were detected in 5 (36%) cases, and, in 3 of those cases, thromboses in dermal or subcutaneous vessels were observed histopathologically. Elevation of plasma D-dimer level (>2.5 μg/mL) was significantly correlated with concomitant systemic thrombotic symptoms (P = 0.0152, Fischer exact test). The histopathological finding of thrombotic features and increased plasma D-dimer were predictive factors of EGPA accompanied with systemic thromboses, such as deep vein thromboses and cerebral infarction.

Unilateral Isolated Basal Vein Thrombosis Associated with Deep Cerebral Venous Infarction

Unilateral Isolated Basal Vein Thrombosis Associated with Deep Cerebral Venous Infarction

Characteristics of paramedian pontine arteries disease and its association with hemoglobinA1c.

ObjectivesThe association of branch atherosclerotic disease (BAD) and diabetes mellitus (DM) in the territory of posterior circulation is rarely discussed. Intracranial BAD was divided into two different types: paramedian pontine arteries (PPA) disease (PPD) and lenticulostriate arteries (LSA) disease. The goal of the study was to evaluate the clinical characteristics of PPD and its association with hemoglobinA1c (HbA1c) in China.Materials and MethodsRadiologically confirmed PPD was defined as an isolated unilateral infarction extending to the ventral surface of the pons. Small deep cerebral infarctions are usually caused by two different pathological changes of arteries: BAD and lipohyalinotic degeneration (LD). We compared the vascular risk factors between BAD and LD in PPA territory. A total of 159 stroke patients were analyzed (PPD, n = 75; LD, n = 84). Patients with PPD were also categorized into two groups according to follow‐up modified Rankin Scale (FmRS) scores. Logistic regression analyses were used for the evaluation of independent risk factors of PPD and prognosis.ResultsComparison between PPD and LD revealed statistical significance in fasting glucose, HbA1c, estimated glomerular filtration rate (eGFR), and uric acid (p = .011, p = .005, p = .027, p = .018, respectively). Compared with LD, PPD was only related to HbA1c (p = .011) in logistic regression analysis. There were statistically significant differences between the two groups based on the stratification of FmRS scores in fasting glucose, HbA1c, homocysteine, eGFR, and the occurrence of DM. After multivariate analysis, only HbA1c was related with poor prognosis of PPD (p = .002).ConclusionsThe subtypes and prognosis of small deep brain infarcts are significantly influenced by elevated HbA1c level in PPA territory. DM might play an important role in the pathogenesis of PPD.

Safety and efficacy of long-term treatment of chronic/persistent ITP with eltrombopag: final results of the EXTEND study

AbstractIn phase 2/3 trials, eltrombopag treatment of 6 months or less in patients with chronic/persistent immune thrombocytopenia (ITP) increased platelet counts and reduced bleeding. The open-label EXTEND study evaluated long-term safety and efficacy of eltrombopag in adults with ITP who had completed a previous eltrombopag study. For the 302 patients enrolled, median duration of eltrombopag treatment was 2.37 years (2 days-8.76 years). Median platelet counts increased to 50 × 109/L or more by week 2 and were sustained throughout the treatment period. Overall, 259 patients (85.8%) achieved a response (platelet count ≥50 × 109/L at least once in the absence of rescue), and 133 (52%) of 257 patients achieved a continuous response of 25 weeks or longer. Responses in patients with platelet counts lower than 15 × 109/L, more previous therapies, and/or splenectomy were somewhat lower. Thirty-four (34%) of 101 patients receiving concomitant ITP medication discontinued 1 or more medication. In patients with assessments, bleeding symptoms (World Health Organization grades 1-4) decreased from 57% at baseline to 16% at 1 year. Forty-one patients (14%) withdrew because of adverse events. Hepatobiliary adverse events (n = 7), cataracts (n = 4), deep vein thrombosis (n = 3), cerebral infarction (n = 2), headache (n = 2), and myelofibrosis (n = 2) occurred in more than 1 patient; the remaining adverse events occurred only once. Rates of thromboembolic events (6%) and hepatobiliary adverse events (15%) did not increase with treatment duration past 1 year. EXTEND demonstrated that long-term use of eltrombopag was effective in maintaining platelet counts of 50 × 109/L or more and reducing bleeding in most patients with ITP of more than 6 months' duration. Important adverse events (eg, thrombosis, hepatobiliary, and bone marrow fibrosis) were infrequent. (ClinicalTrials.gov:NCT00351468).

Clinical Significance of the Cerebral Perforating Arteries.

There is scarce data in the contemporary literature regarding the correlation of the microanatomy of the perforating arteries, their atherosclerosis, and the ischemia in their territory. In order to examine, at least partially, those parameters, the perforating arteries of 12 brains were microdissected or their vascular casts were obtained. In addition, 30 specimens of the perforators were used for a histological and immunohistochemical study. Finally, radiological images of 14 patients with deep cerebral infarcts were examined following a selection among 62 subjects. It was found out that certain groups of the perforators ranged in number between 0 to 11 (1.1-8.4 on average). In addition to the origin from the parent vessels, some of the perforators also arose from the leptomeningeal branches. Occlusion of such a branch may result in both a superficial and a deep ischemic lesion. Besides, the common stems of certain perforators supplied both right and left portions of the corresponding brain regions. Occlusion of such a common trunk leads to bilateral infarction. The atherosclerosis of the perforating vessels, which was found in one third of the specimens, is the basis for the ischemic lesions development on their territory. Among the 62 patients with ischemic lesions, 14 had a deep cerebral infarcts, most often within the thalamus, as well as on the territory of the middle cerebral and the anterior choroidal artery perforators of the hemispheres. Our study showed that a strong correlation exists between certain microanatomical features, atherosclerosis, and region of supply of the perforating arteries, on the one hand, and location of the ischemic lesions on the other hand.

Magnetic resonance imaging in neonatal citrullinemia

Citrullinemia is a rare inborn error of urea cycle metabolism causing hyperammonemia. In the classic form, a newborn presents with poor feeding, vomiting, progressive lethargy and signs of increasing intracranial pressure 3–7 d after birth, rapidly progressing to apnea, coma and death if untreated. We found only two reported cases in the literature describing magnetic resonance imaging findings of neonatal citrullinemia. We present a case of neonatal citrullinemia with more extensive and asymmetric magnetic resonance imaging abnormalities, including evidence of both superficial and deep venous cerebral infarction.

Neonatal deep white matter venous infarction and liquefaction: a pseudo-abscess lesion.

Deep white matter hemorrhagic venous infarction with subsequent cavitation due to necrosis and liquefaction has been described in neonates and may be associated with infection and meningitis. In our experience, the MRI pattern of these lesions is confused with the pattern seen with cerebral abscesses. The purpose of our study was to characterize the MRI findings of post infarction necrosis and liquefaction after hemorrhagic deep white matter venous infarction in infants and to distinguish these lesions from cerebral abscesses. An institutional review board approved a retrospective review of imaging records to identify all patients with cerebral venous infarction at a children's hospital during a 10-year period. Nine infants had deep white matter hemorrhagic venous infarction with white matter fluid signal cavitary lesions. A diagnosis of cerebral abscess was considered in all. The imaging and laboratory findings in these patients are reviewed and compared to descriptions of abscesses found in the literature. There were six female and three male infants. The mean age at presentation was 20 days (range: 0-90 days), while the corrected age at presentation was less than 30 days for all patients. Seven patients presented with seizures and signs of infection; one infant presented with lethargy and later proved to have protein C deficiency. MRI was performed 0-12 days from presentation in these eight patients. Another patient with known protein C deficiency underwent MRI at 30 days for follow-up of screening US abnormalities. There were a total of 38 deep cerebral white matter fluid signal cavitary lesions: 25 frontal, 9 parietal, 2 temporal, 2 occipital. Larger lesions had dependent debris. All lesions had associated hemorrhage and many lesions had evidence of adjacent small vessel venous thrombosis. Lesions imaged after gadolinium showed peripheral enhancement. Three lesions increased in size on follow-up imaging. Three patients, two with meningitis confirmed via microbiology and one with presumed meningitis by CSF counts, underwent surgical aspiration of a total of six lesions. All specimens were sent for pathology and culture and were negative for microorganisms. Recognizing the MR appearance of cavitary necrosis and liquefaction after deep white matter cerebral venous infarction in neonates can distinguish this entity from cerebral abscess and potentially avoid an unnecessary neurosurgical aspiration procedure.

Abstract T P351: Unbound Iron and Ceruloplasmin Levels in Cerebrospinal Fluid Are Associated with Development of Deep Cerebral Infarcts Following Subarachnoid Hemorrhage

Introduction: Iron-dependent formation of reactive oxygen species has been implicated in the development of vasospasm (VSP) and neuronal injury following experimental subarachnoid hemorrhage (SAH). We report the association between unbound (“free”) iron in CSF of SAH patients and the risk of angiographic vasospasm and cerebral infarcts (CI) on neuroimaging from a recently completed pilot study. Methods: Samples of cerebrospinal fluid (CSF) were obtained on days 1, 3, and 5. A fluorometric assay that relies on an oxidation sensitive probe was used to measure redox active iron (REDOX-Fe). Ceruloplasmin (Cp) concentration and levels of malondialdehyde (MDA), a marker of lipid peroxidation were also measured. We prospectively collected and recorded demographic, clinical, and radiological data. Logistic regression and Wilcoxon Rank Sum test were used. Results: Five of 12 patients developed angiographic VSP (41.6%) and eight developed CI (66.6%). Mean REDOX-Fe was higher in patients with CI (3.96 ± 0.97 Vs. 2.77 ± 0.87 mcg/dl, p 0.07), particularly in patients with deep-seated strokes (4.56 ± 0.67 Vs. 3.35 ± 0.89, p 0.03). Levels of Cp at day 3 were lower in patients with deep strokes (34,092 ± 23,780 Vs. 86,045 ± 34,752 ng/ml, p 0.03). A trend towards higher REDOX-Fe on day 3 in patients who developed VSP (4.52 ± 1.16 Vs. 2.96 ± 0.71, p 0.07), and lower Cp levels on day 5 (45,033 ± 29,079 Vs. 63,044 ± 24,821, p 0.1) was found. Levels of MDA were higher in patients who developed CI (10.36 ± 4.36 Vs. 5.9 ± 4.2 nmol, p 0.08). Conclusions: In this preliminary study we found higher concentrations of redox active iron in CSF of SAH patients who develop deep-seated CI on neuroimaging. Evidence of increased oxidative damage correlated with development of CI. A possible association between non-protein bound iron and angiographic VSP is suggested as well. Ceruloplasmin may exert a protective effect in this setting. Further studies are needed to validate these findings.

A case of antiphospholipid syndrome refractory to secondary anticoagulating prophylaxis after deep vein thrombosis-pulmonary embolism.

Antiphospholipid syndrome (APS) is an acquired systemic autoimmune disorder characterized by a combination of clinical criteria, including vascular thrombosis or pregnancy morbidity and elevated antiphospholipid antibody titers. It is one of the causes of deep vein thrombosis and pulmonary embolism that can be critical due to the mortality risk. Overall recurrence of thromboembolism is very low with adequate anticoagulation prophylaxis. The most effective treatment to prevent recurrent thrombosis is long-term anticoagulation. We report on a 17-year-old male with APS, who manifested blue toe syndrome, deep vein thrombosis, pulmonary thromboembolism, and cerebral infarction despite adequate long-term anticoagulation therapy.

943

Introduction: The optimal anticoagulation strategy for pediatric patients receiving extracorporeal membrane oxygenation (ECMO) is the subject of significant debate. Antithrombin (AT) has become an attractive adjunct therapy to traditional heparin, but its use remains quite variable amongst institutions. Methods: A retrospective, descriptive study was designed and institutional review board exemption obtained. Data were obtained from the Pediatric Health Information System (PHIS) database, an administrative database from 43 tertiary care children's hospitals in the United States for patients admitted from 2004-2011 who were 18 years of age or younger and placed on ECMO. Results: 7,083 patients were identified as having met study criteria. AT was utilized in only 5% of patients in 2004 versus 52% in 2011 (p<0.001). There was no change in the use of fresh frozen plasma or cryoprecipitate over time. The total number of patients receiving red blood cell transfusions decreased from 88.5% in 2004 to 68.4% in 2011 (p<0.001). The average adjusted cost of an ECMO course increased from $213,681 +/- $162,250 in 2004 to $351,735 +/- $361,280 in 2011 (p<0.001). Correlations were observed between the use of AT and the diagnosis of deep vein thrombosis (p<0.001), pulmonary embolism (p=0.001), cerebral infarction (p<0.001), intracerebral hemorrhage (p=0.037) and subdural hemorrhage (p=0.002). Overall patient mortality decreased from 44.46% in 2004 to 42.81% in 2011 (p=0.0084). Conclusions: Between 2004 and 2011, there was decreased mortality but increased cost of ECMO. During this time, AT use increased significantly. However, only red blood cell transfusions were decreased. Of note, there was an association between increasing use of AT and both thrombotic and hemorrhagic complications. Further investigation is warranted to better understand the role of AT in pediatric ECMO and whether or not it contributes to patient outcomes.

Fixing Hearts and Protecting Minds

Ischemic heart disease is a significant cause of mortality and morbidity in Western populations. Consistent with this, coronary artery bypass graft (CABG) surgery remains one of the most frequently performed major surgeries. Improved survival rates mean that our research focus now extends beyond surgical technique to include quality of postoperative outcome. Postoperative cognitive dysfunction (POCD) has emerged as one of the most challenging and hotly debated issues, with increasing impetus to answer the unresolved question: does fixing the heart come at a cost to the brain? CABG surgery is associated with neurological events including stroke in 1.6%1 and delirium in 5.8%2 of patients. Beyond these severe and marked alterations to neurological function, there has been a widely held belief that CABG surgery is associated with POCD, which may presage a decline toward dementia. Research has been influenced by the 1995 Consensus Statement3 into the study of POCD in patients undergoing CABG surgery. Although the methods of investigation set forth by the Consensus Statement achieved widespread acknowledgment, its specific recommendations have not always been followed.4 Despite significant methodological issues, it seems that the balance of interpretation has historically been in favor of CABG surgery as a cause of significant POCD. More recently, however, a review of a series of publications from a well-controlled longitudinal cohort study conducted at Johns Hopkins5 and a meta-analysis6 suggested that cognition is in fact stable or may even show some improvement after CABG surgery in the majority of patients, at least within the first year (Figures 1 and 2). There is little doubt that POCD affects some patients in the short term, but the pathophysiological mechanisms underlying this and the influence on longer-term cognitive function remain uncertain. For research to progress, we require a paradigmatic shift in our focus from …

Gene Expression Suggests Spontaneously Hypertensive Rats May Have Altered Metabolism and Reduced Hypoxic Tolerance

Cerebral small vessel disease (SVD) is an important cause of stroke, cognitive decline and vascular dementia (VaD). It is associated with diffuse white matter abnormalities and small deep cerebral ischemic infarcts. The molecular mechanisms involved in the development and progression of SVD are unclear. As hypertension is a major risk factor for developing SVD, Spontaneously Hypertensive Rats (SHR) are considered an appropriate experimental model for SVD. Prior work suggested an imbalance between the number of blood microvessels and astrocytes at the level of the neurovascular unit in 2-month-old SHR, leading to neuronal hypoxia in the brain of 9-month-old animals. To identify genes and pathways involved in the development of SVD, we compared the gene expression profile in the cortex of 2 and 9-month-old of SHR with age-matched normotensive Wistar Kyoto (WKY) rats using microarray-based technology. The results revealed significant differences in expression of genes involved in energy and lipid metabolisms, mitochondrial functions, oxidative stress and ischemic responses between both groups. These results strongly suggest that SHR suffer from chronic hypoxia, and therefore are unable to tolerate ischemia-like conditions, and are more vulnerable to high-energy needs than WKY. This molecular analysis gives new insights about pathways accounting for the development of SVD.

Frontal lobe white matter hyperintensities and neurofibrillary pathology in the oldest old

Current studies suggest an interaction between vascular mechanisms and neurodegenerative processes that leads to late-onset Alzheimer disease (AD). We tested whether AD pathology was associated with white matter hyperintensities (WMH) or cerebral infarcts in the oldest old individuals. Brains from 132 subjects over 85 years old, who came to autopsy from the Vantaa 85+ population-based cohort, were scanned by postmortem MRI and examined for neuropathologic changes. Coronal images were analyzed to determine the degree of frontal and parietal periventricular WMH (PVWMH) and deep WMH (DWMH) and cerebral infarcts. Neuropathologic variables included Consortium to Establish a Registry for Alzheimer's Disease scores for neuritic plaques and Braak staging among subjects in 5 groups: normal aging (NA), borderline with insufficient AD pathology, AD, AD plus other pathology, and other primary degenerative diseases. Frontal DWMH were detected in >50% of the sample. Both frontal PVWMH and DWMH were significantly more extensive in the AD group compared to the NA group or the NA and borderline groups combined. Frontal PVWMH and DWMH were also associated with increased Braak staging (p = 0.03) and the neuritic plaque load (p = 0.01). Further analysis revealed there were a greater number of cerebral infarcts associated with frontal DWMH (p = 0.03) but not with frontal PVWMH. Our study showed an association between neurofibrillary pathology and frontal PVWMH and DWMH (rather than parietal), as a surrogate of small vessel disease, particularly in very old community-dwelling individuals.

Clinical predictors of lacunar syndrome not due to lacunar infarction

BackgroundLacunar syndrome not due to lacunar infarct is poorly characterised. This single centre, retrospective study was conducted to describe the clinical characteristics of patients with lacunar syndrome not due to lacunar infarct and to identify clinical predictors of this variant of lacunar stroke.MethodsA total of 146 patients with lacunar syndrome not due to lacunar infarction were included in the "Sagrat Cor Hospital of Barcelona Stroke Registry" during a period of 19 years (1986-2004). Data from stroke patients are entered in the stroke registry following a standardized protocol with 161 items regarding demographics, risk factors, clinical features, laboratory and neuroimaging data, complications and outcome. The characteristics of these 146 patients with lacunar syndrome not due to lacunar infarct were compared with those of the 733 patients with lacunar infarction.ResultsLacunar syndrome not due to lacunar infarct accounted for 16.6% (146/879) of all cases of lacunar stroke. Subtypes of lacunar syndromes included pure motor stroke in 63 patients, sensorimotor stroke in 51, pure sensory stroke in 14, atypical lacunar syndrome in 9, ataxic hemiparesis in 5 and dysarthria-clumsy hand in 4. Valvular heart disease, atrial fibrillation, sudden onset, limb weakness and sensory symptoms were significantly more frequent among patients with lacunar syndrome not due to lacunar infarct than in those with lacunar infarction, whereas diabetes was less frequent. In the multivariate analysis, atrial fibrillation (OR = 4.62), sensorimotor stroke (OR = 4.05), limb weakness (OR = 2.09), sudden onset (OR = 2.06) and age (OR = 0.96) were independent predictors of lacunar syndrome not due to lacunar infarct.ConclusionsAlthough lacunar syndromes are highly suggestive of small deep cerebral infarctions, lacunar syndromes not due to lacunar infarcts are found in 16.6% of cases. The presence of sensorimotor stroke, limb weakness and sudden onset in a patient with atrial fibrillation should alert the clinician to the possibility of a lacunar syndrome not due to a lacunar infarct.

Clinical observation on treatment of 105 cases of cerebral apoplexy with head acupuncture and body acu-puncture

Objective To observe the therapeutic effect of treatment of cerebral apoplexy with head acupunc-ture and body acupuncture. Methods 203 cases with cerebral apoplexy were randomly divided into head acupuncture with body acupuncture group(105 cases) and body acupuncture control group(98 cases). Symptom and sign were gra-ded and comprehensive therapeutic effects were assessed. Results There were significant differences of the cure rates and the observed indices between the head acupuncture with body acupuncture group and body acupuncture control group. Conclusion The head acupuncture with body acupuncture can obviously improve the cerebral ischemia and anoxia, and increase limb motor function and ability of daily living in the patients of deep cerebral infarction. Key words: Cerebral apoplexy/acupuncture therapy; Cerebrovascular circulation/acupuncture effect; Nee-dling methods