Effects of high-intensity interval cycling performed after resistance training on muscle strength and hypertrophy.

Aim of the study was to investigate whether high-intensity interval cycling performed immediately after resistance training would inhibit muscle strength increase and hypertrophy expected from resistance training per se. Twenty-two young men were assigned into either resistance training (RE; N = 11) or resistance training plus high-intensity interval cycling (REC; N = 11). Lower body muscle strength and rate of force development (RFD), quadriceps cross-sectional area (CSA) and vastus lateralis muscle architecture, muscle fiber type composition and capillarization, and estimated aerobic capacity were evaluated before and after 8 weeks of training (2 times per week). Muscle strength and quadriceps CSA were significantly and similarly increased after both interventions. Fiber CSA increased significantly and similarly after both RE (type I: 13.6 ± 3.7%, type IIA: 17.6 ± 4.4%, type IIX: 23.2 ± 5.7%, P < 0.05) and REC (type I: 10.0 ± 2.7%, type IIA: 14.8 ± 4.3% type IIX: 20.8 ± 6.0%, P < 0.05). In contrast, RFD decreased and fascicle angle increased (P < 0.05) only after REC. Capillary density and estimated aerobic capacity increased (P < 0.05) only after REC. These results suggest that high-intensity interval cycling performed after heavy-resistance exercise may not inhibit resistance exercise-induced muscle strength/hypertrophy after 2 months of training, while it prompts aerobic capacity and muscle capillarization. The addition of high-intensity cycling after heavy-resistance exercise may decrease RFD partly due to muscle architectural changes.

Apolipoprotein E polymorphisms and ischaemic stroke: a two-center Greek study.

BACKGROUND AND PURPOSE: Apolipropotein E(apoE) is a plasma protein exhibiting three common isoforms (E2, E3, E4). Its involvement in lipoprotein metabolism may have an impact on stroke occurrence. As results in the literature are inconclusive further studies are needed to elucidate its role. Our objective was to study the role of apoE isoforms and the interplay with environmental risk factors in patients with first ischaemic stroke occurrence in the Greek population. METHODS: Three hundred and twenty-nine patients with first-ever ischaemic stroke were included in our study. Strokes of cardioembolic origin and patients with autoimmune or prothrombotic syndromes were excluded. A control group of 361 subjects with no stroke history were also included in our study. Risk factors (hyperlipidemia, hypertension, diabetes mellitus and smoking) were assessed. ApoE alleles were determined in all subjects participating in the study. RESULTS: Genotype ε3/ε3 was found to have a protective role against stroke occurrence compared with other genotypes (odds ratio 0.674, 95% confidence interval 0.480-0.946) especially in the female patient subgroup. In multivariate analysis after adjustment for age, body mass index (BMI), hypertension, dyslipidemia, diabetes mellitus and smoking, the role of genotype was limited and outweighed by risk factors in both genders. No association between apoE alleles and BMI, cholesterol, triglycerides or high-density lipoprotein plasma levels was noted. CONCLUSIONS: Our study was indicative of a protective role of the ε3/ε3 genotype, especially in female patients. However, risk factors such as age, BMI, hypertension, dyslipidemia, diabetes mellitus and smoking have a strong impact on stroke occurrence and outweigh the protective role of the ε3/ε3 genotype.

Etiology of first-ever ischaemic stroke in European young adults: the 15 cities young stroke study.

BACKGROUND AND PURPOSE: Risk factors for IS in young adults differ between genders and evolve with age, but data on the age- and gender-specific differences by stroke etiology are scare. These features were compared based on individual patient data from 15 European stroke centers. METHODS: Stroke etiology was reported in detail for 3331 patients aged 15-49 years with first-ever IS according to Trial of Org in Acute Stroke Treatment (TOAST) criteria: large-artery atherosclerosis (LAA), cardioembolism (CE), small-vessel occlusion (SVO), other determined etiology, or undetermined etiology. CE was categorized into low- and high-risk sources. Other determined group was divided into dissection and other non-dissection causes. Comparisons were done using logistic regression, adjusting for age, gender, and center heterogeneity. RESULTS: Etiology remained undetermined in 39.6%. Other determined etiology was found in 21.6%, CE in 17.3%, SVO in 12.2%, and LAA in 9.3%. Other determined etiology was more common in females and younger patients, with cervical artery dissection being the single most common etiology (12.8%). CE was more common in younger patients. Within CE, the most frequent high-risk sources were atrial fibrillation/flutter (15.1%) and cardiomyopathy (11.5%). LAA, high-risk sources of CE, and SVO were more common in males. LAA and SVO showed an increasing frequency with age. No significant etiologic distribution differences were found amongst southern, central, or northern Europe. CONCLUSIONS: The etiology of IS in young adults has clear gender-specific patterns that change with age. A notable portion of these patients remains without an evident stroke mechanism according to TOAST criteria.

Ankle-brachial index long-term outcome after first-ever ischaemic stroke.

BACKGROUND AND PURPOSE: Ankle-brachial blood pressure index (ABI) is a clinical tool to identify the presence of peripheral artery disease. There is a scarcity of data associating ABI with long-term outcome in patients with IS. The association between ABI and long-term outcome in patients with first-ever acute IS was assessed. METHODS: Ankle-brachial blood pressure index was assessed in all consecutive patients with a first-ever acute IS admitted at Alexandra University hospital (Athens, Greece) between January 2005 and December 2010. ABI was considered normal when > 0.90 and ≤ 1.30. The Kaplan-Meier product limit method was used to estimate the probability of 5-year composite cardiovascular event-free (defined as recurrent stroke, myocardial infarction or cardiovascular death) and overall survival. A multivariate analysis was performed to assess whether ABI is an independent predictor of 5-year mortality and dependence. RESULTS: Amongst 653 patients, 129 (19.8%) with ABI ≤ 0.9 were identified. Five-year cumulative composite cardiovascular event-free and overall survival rates were better in normal ABI stroke patients (log-rank test: 7.22, P = 0.007 and 23.40, P < 0.001, respectively). There was no difference in 5-year risk of stroke recurrence between low and normal ABI groups (hazard ratio, HR = 1.23, 95% CI 0.68-2.23). In multivariate Cox regression analysis, independent predictors of 5-year mortality included age (HR = 2.55 per 10 years, 95% CI 1.86-3.48, P < 0.001), the National Institutes of Health Stroke Scale (per point increase HR = 1.12, 95% CI 1.08-1.16, P < 0.001), and low ABI (HR = 2.22, 95% CI 1.22-4.03, P = 0.009). Age (HR = 1.21 per 10 years, 95% CI 1.01-1.45, P = 0.04) and low ABI (HR = 1.72, 95% CI 1.11-2.67, P = 0.01) were independent predictors of the composite cardiovascular end-point. CONCLUSIONS: Low ABI in patients with acute IS is associated with increased 5-year cardiovascular event risk and mortality. However, ABI does not appear to predict long-term stroke recurrence.

Late onset glycogen storage disease type II: pitfalls in the diagnosis.

BACKGROUND/AIMS: Glycogen storage disease type II (GSD-II) is a lysosomal disorder caused by acid α glucosidase (GAA) deficiency. The infantile form is easier to recognize compared with the milder adult form that may manifest as myopathy without specific clinical characteristics. The aim of this study is to highlight frequent diagnostic errors in adult GSD-II patients. CASE REPORTS: We report four patients with confirmed GSD-II who were at first diagnosed with hypothyroid myopathy, connective tissue disorder, an underlying liver disease and muscular dystrophy, respectively. CONCLUSION: Internists but even neurologists with low suspicion may misdiagnose GSD-II. The early respiratory involvement and the characteristic laboratory abnormalities in a myopathic patient should include GAA deficiency in the differential diagnosis especially in the era of enzyme replacement therapy.

Etiology and treatment of ischaemic stroke in patients with ß-thalassemia major.

BACKGROUND AND PURPOSE: Although hypercoagulability-induced thromboembolism is generally accepted as cause of cerebral ischaemia in thalassemic patients, cardiogenic embolism has been recently suggested as another possible stroke etiology. METHODS: We present four adult ß-thalassemia major patients with manifest cardiac involvement who suffered territorial strokes. RESULTS: In the presence of siderotoxic cardiomyopathy and arrhythmia, we assumed cardiogenic embolism as etiology of stroke and initiated oral anticoagulation as preventive medication. Two of our patients were the first ß-thalassemia major patients who underwent successful thrombolysis with rtPA. CONCLUSIONS: Cardioembolism seems to be the cause of stroke in cases of ß-thalassemia major. Thrombolysis can be applied in the setting of acute brain ischaemia in such high risk patients.

Long-term outcome in posterior cerebral artery stroke.

INTRODUCTION: Previous studies on posterior cerebral artery (PCA) strokes focused mainly on topography and underlying pathophysiology. However, there are no data on long-term prognosis and its association with the localization of the infarct. METHODS: All consecutive PCA strokes registered in the Athens Stroke Outcome Project between 01/1998 and 12/2009 were included in the analysis. The New England Posterior Circulation Registry criteria were applied to classify them in relation to topography: (i) pure PCA infarcts, including pure cortical-only and combined cortical/deep PCA infarcts (groups A and B respectively), and (ii) PCA-plus strokes, including cortical-only and combined cortical/deep PCA strokes with ≥1 concomitant infarcts outside PCA territory (groups C and D respectively). Patients were prospectively followed up to 10 years after stroke. RESULTS: Amongst 185 (8.1%) PCA patients that were followed up for 49.6±26.7months, 98 (53%), 24 (13%), 36 (19.5%), and 27 (14.6%) were classified in group A, B, C, and D, respectively. Infections and brain edema with mass effect were more frequently encountered in PCA-plus strokes compared to pure PCA (P<0.05 and <0.01 respectively). At 6 months, 56% of cortical-only PCA patients had no or minor disability, compared to 37%, 36%, and 26% in the other groups (P=0.015). The 10-year probability of death was 55.1% (95%CI: 42.2-68.0) for pure PCA compared to 72.5% (95%CI: 58.8-86.2) for PCA-plus (log-rank 14.2, P=0.001). Long-term mortality was associated with initial neurologic severity and underlying stroke mechanism. CONCLUSIONS: Patients with pure PCA stroke have significantly lower risk of disability and long-term mortality compared to PCA strokes with coincident infarction outside the PCA territory.

Adult Pompe disease: clinical manifestations and outcome of the first Greek patients receiving enzyme replacement therapy.

OBJECTIVE: Pompe disease is an autosomal recessive lysosomal disorder caused by α-glucosidase deficiency. A specific treatment for the disease with enzyme replacement therapy is currently available. The aim of the present study is to describe the clinical manifestations and the effect of treatment in the first Greek patients with the adult form of the disease. METHODS: Five Greek patients with adult onset Pompe disease aged between 40 and 73 years received 20 mg/kg Myozyme intravenously at two weekly intervals over a different period. Clinical and functional parameters were longitudinally registered. RESULTS: Proximal muscle weakness and respiratory insufficiency were the most common manifestations of the disease, but their severity was different even among patients with similar genotype. The effect of treatment varied with most patients experiencing some improvement in muscle strength and fatigability, while the most severely affected patient did not benefit and stopped therapy. CONCLUSION: No clear genotype-phenotype correlation emerges from our study. The different effect of treatment on our patients seems to be mainly related to their pre-treatment condition and can be reliably assessed only on a long term basis.

Body composition analysis in late-onset Pompe disease.

Pompe disease is an inherited metabolic disorder caused by α-glycosidase deficiency. The adult onset form is mainly characterized by progressive proximal muscle weakness and respiratory dysfunction. The aim of the present study is to evaluate body composition in adult patients before and after enzyme replacement therapy (ERT). Body composition was examined at baseline by means of dual x-ray absorptiometry (DXA) in nine adult patients and after different time periods in six of them who received ERT. Total BMD (bone mineral density) was initially mildly decreased in two patients, while femoral neck BMD was decreased in five patients. On the other hand fat mass was increased in the majority of patients, while body mass index (BMI) was high in four. ERT administration did not seem to induce obvious BMD changes in any patient. Conclusively, the greater femoral neck BMD involvement may be attributed to the lower mechanical load applied by the selectively weakened muscles, whereas the increased fat mass may be the result of metabolic and nutritional derangement.

Churg-Strauss syndrome complicated by neuropathy: a clinicopathological study of nine cases.

OBJECTIVE: The purpose of this study was to investigate the clinical, electrophysiological and pathological features of Churg Strauss syndrome (CSS) neuropathy. METHODS: Biopsies were selected from over 700 sural nerve biopsies. The diagnosis of vasculitis was based on established clinicopathological criteria. Complete laboratory, clinical, electrophysiological and pathological studies were performed in all cases. RESULTS: Nerve biopsies of 9 patients were diagnosed as Churg-Strauss syndrome. The pathological features were vasculitis with predominant axonal degeneration and a varying pattern of myelinated fiber loss. The vasculitic changes were found mainly in small epineural blood vessels. Mononeuritis multiplex and distal symmetrical and asymmetrical sensorimotor neuropathy, were equally frequent. CONCLUSION: We conclude that, Churg-Strauss syndrome complicated frequently with polyneuropathy, and as remission depends on immunosuppressive therapy, it is important to recognize it in the early stage. The diagnosis of polyneuropathy is based on clinical and electrophysiologic studies, but precise histology, immunolohistochemistry and morphometric study of the peripheral nerve biopsy may be decisive in establishing the diagnosis.

Risk factors, etiology, and outcome of first-ever ischemic stroke in young adults aged 15 to 45 - the Athens young stroke registry.

BACKGROUND AND PURPOSE: Data regarding stroke in young adults from Greece is scarce. We aimed to evaluate risk factors, etiology, and outcome in a hospital-based prospective observational study. METHODS: Data from a series of 253 first-ever ischemic stroke patients aged 15-45 were collected over 10 years. Stroke etiology was classified according to the Trial of Org 10172 in Acute Stroke Treatment criteria. Comparisons were done between groups stratified by gender and age. The probability of death or composite vascular events during follow-up was estimated by the Kaplan-Meier method. We used Multivariate Cox proportional hazard analyses to determine the effect of different factors on mortality and occurrence of composite cardiovascular events. RESULTS: Although male patients predominate in our cohort (ratio 1.3:1), females outnumber males significantly at ages under 30. Smoking (59.3%) and dyslipidemia (41.1%) were the most frequent risk factors. Small vessel disease was identified as cause of stroke in 17.4%, whereas cardioembolism caused 13.4% of all strokes. No definite etiology was found in 33.6%, whereas other causes of stroke, including dissection (6.7%), were documented in 26.5%. The probability of 10-year survival was 86.3% (95%CI: 79.1-93.6). The corresponding probability of composite vascular events was 30.4% (95%CI: 19.6-41.2). Stroke severity and heart failure were the main predictors of mortality. At the end of the follow-up period, most patients (92.7% of survivors) were independent. CONCLUSION: There are gender- and age-related differences regarding risk factors and causes of ischemic stroke in young patients. Survival and long-term outcome is generally favorable.

Incidence of rotational vertigo in supratentorial stroke: a prospective analysis of 112 consecutive patients.

BACKGROUND: Single cases with hemispheric, cortical or subcortical, ischemic lesions presenting with rotational vertigo (RV), that challenge the notion of infratentorial or peripheral generation of RV have been published, but the incidence of this symptom in a larger series is unknown. The aim of this study was to investigate whether acute hemispheric cerebrovascular lesions cause vertiginous sensations with particular emphasis on RV. METHODS: A total of 112 consecutive stroke patients were assessed in a prospective single-center study over a 22-month inclusion period. Rotational or other vertiginous sensations were assessed using a structured 5-item questionnaire and patients with vertigo were further evaluated with Yardley's Vertigo Symptom Scale. All subjects underwent standard clinical neuro-ophthalmological and neuro-otological testing and data were correlated to imaging findings. RESULTS: RV was absent among our patients. Few subjects reported non-rotational vertiginous sensations with stroke onset. These were mainly right-hemispheric strokes with concomitant subcortical leukoaraiosis. CONCLUSION: In this case series we did not find any patients with spinning sensations which is supportive of the dogma that supratenotrial lesions do not cause RV. Certain hemispheric stroke patterns, however, may be related to non-rotational dizziness.

Vertical and horizontal integrator failure in a ponto-medullary infarction: A possible role for paramedian tract neurons.

Gaze-evoked nystagmus is caused by a "leaky" neural integrator, which fails to maintain eccentric gaze positions after centrifugal eye movements. It is usually observed as the result of toxic, metabolic or paraneoplastic disorders, rather than single structural lesions. We demonstrate a case of an omnidirectional gaze-evoked nystagmus due to an ischemic paramedian ponto-medullar infarction. The most probable explanation is a damage of paramedian tract neurons, which have been recently recognized as a site of neural integration.