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Background The treatment of lymphoedema requires a multi-professional and interdisciplinary approach. Despite being prescribed in the management of lymphatic disorders, the effectiveness of the phlebological insoles is still under investigation. Aim This scoping review aims to identify and analyse evidence regarding the efficacy of phlebological insoles as a conservative intervention for lower limb lymphoedema. Method The following databases were searched up to November 2022: PubMed, Cochrane Library, CINAHL Complete, PEDro and Scopus. Preventive and conservative interventions were considered. Studies considering people with lower limb oedema, of any age and type of oedema, were eligible for inclusion. No restrictions in terms of language, year of publication, study design and type of publication were applied. Additional studies were sought through grey literature. Results From 117 initial records, 3 studies met the inclusion criteria. Two quasi-experimental studies and one randomised cross-over study were included. The results of the examined studies confirmed the positive effects of insoles usage and foot and ankle mobility on the venous return. Conclusion This scoping review provided an overview of the topic. The studies analysed in this scoping review have shown that insoles seem to be beneficial in reducing the lower limb oedema in healthy individuals. However, there are still no comprehensive trials confirming this evidence on people with lymphoedema. The small number of identified articles, the selection of participants not affected by lymphoedema, the use of heterogeneous devices in terms of modifications and materials highlight the need of further investigations. Future trails should include people affected by lymphoedema, address the choice of materials in manufacturing the insoles and take in consideration the patients’ adherence to the device and concordance to the treatment.

In adult human brain, neurogenesis seems to persist throughout life and ischemic stroke was proved to stimulate this process. Using magnetic resonance spectroscopy (MRS), a 1.28-ppm peak, putative biomarker of neural progenitor cells (NPCs), was identified both in vitro and in vivo, i.e., in normal rat and healthy human brain. The aim of our study was to identify a 1.28-ppm peak in adult human ischemic brain by using 3.0 T multivoxel MRS.We studied 10 patients, six males, and four females, with a mean (± SD) age of 59.3 (± 17.3), at three different time points from ischemic stroke onset (T0: 5 days; T14: 14 ± 2 days; T30: 30 ± 2 days).In all patients except one, a 1.28-ppm peak at T14 was detected at the ischemic boundary (all p values 0.05). MRS performed on six voluntary age-matched healthy subjects did not detect any 1.28-ppm peak.The nature of this 1.28-pm peak is uncertain; however, our data support the hypothesis that it might represent a marker of NPCs in post-stroke human brain.

The risk of stroke and cerebrovascular disease complicating infection with SARS-CoV-2 has been extensively reported since the onset of the pandemic. The striking efforts of many scientists in cooperation with regulators and governments worldwide have rapidly brought the development of a large landscape of vaccines against SARS-CoV-2. The novel DNA and mRNA vaccines have offered great flexibility in terms of antigen production and led to an unprecedented rapidity in effective and safe vaccine production. However, as mass vaccination has progressed, rare but catastrophic cases of thrombosis have occurred in association with thrombocytopenia and antibodies against PF4 (platelet factor 4). This catastrophic syndrome has been named vaccine-induced immune thrombotic thrombocytopenia. Rarely, ischemic stroke can be the symptom onset of vaccine-induced immune thrombotic thrombocytopenia or can complicate the course of the disease. In this review, we provide an overview of stroke and cerebrovascular disease as a complication of the SARS-CoV-2 infection and outline the main clinical and radiological characteristics of cerebrovascular complications of vaccinations, with a focus on vaccine-induced immune thrombotic thrombocytopenia. Based on the available data from the literature and from our experience, we propose a therapeutic protocol to manage this challenging condition. Finally, we highlight the overlapping pathophysiologic mechanisms of SARS-CoV-2 infection and vaccination leading to thrombosis.

Background: Uncertainties remain about the role of common thrombophilia markers as determinants of the ischemic stroke (IS) risk. Polymorphism His1299Arg in the FV gene, named R2 haplotype (FVHR2), has been poorly investigated. The aim of the present study was to assess the prevalence of common thrombophilia markers and of FVHR2 in a cohort of IS patients compared to a nonmatched group of healthy individuals. Methods: We studied 156 consecutive patients survivors of a first ever IS and 124 healthy controls. All subjects were investigated for the gene polymorphisms factor V (FV) Leiden, prothrombin (PTH) G20210A, MTHFR C677T, and FVHR2. Protein C (PC), protein S (PS), antithrombin (ATIII), and lupus anticoagulant (LAC) activity was measured. Homocysteinemia was assessed within 48 hours and after 30 days from stroke onset. Univariate and multivariate analyses were performed. Results: Compared with controls, patients were significantly older (mean [SD] age, 50.5 [12.9] vs 37.5 [15.5] years, P < .001), less frequently females (48.1% vs 67.7%, P = .001) and had more frequently hyperhomocysteinemia (45.9% vs 11.0%) only in the acute phase (OR 6.899, CI 95% 2.993-15.899; P < .001). No differences were found in the prevalence of FV Leiden, PTH G20210A, and MTHFR C677T between patients and controls, whereas FVHR2 was present in 34/156 (22%) stroke patients and in 5/124 (4%) controls (OR 6.632, 95% CI 2.509-17.535, P < .001). In a multivariate logistic regression analysis, the FVHR2 resulted independently associated with the occurrence of IS (OR 6.071, 95% CI 1.762-20.923; P = .004). Conclusions: In our study, hyperhomocysteinemia was confirmed to be a transient consequence of the thrombotic event. FVHR2 seems to be a possible candidate prothrombotic condition related to arterial IS irrespective of age and sex in an Italian sample population.

Background and purposeAcute ischemic stroke (AIS) is a fearful complication of Coronavirus Disease-2019 (COVID-19). Aims of this study were to compare clinical/radiological characteristics, endothelial and coagulation dysfunction between acute ischemic stroke (AIS) patients with and without COVID-19 and to investigate if and how the SARS-CoV-2 spike protein (SP) was implicated in triggering platelet activation.MethodsWe enrolled AIS patients with COVID-19 within 12 h from onset and compared them with an age- and sex-matched cohort of AIS controls without COVID-19. Neuroimaging studies were performed within 24 h. Blood samples were collected in a subset of 10 patients.ResultsOf 39 AIS patients, 22 had COVID-19 and 17 did not. Admission levels of Factor VIII and von Willebrand factor antigen were significantly higher in COVID-19 patients and positively correlated with the infarct volume. In multivariate linear regression analyses, COVID-19 was an independent predictor of infarct volume (B 20.318, Beta 0.576, 95%CI 6.077–34.559; p = 0.011). SP was found in serum of 2 of the 10 examined COVID-19 patients. Platelets from healthy donors showed a similar degree of procoagulant activation induced by COVID-19 and non-COVID-19 patients' sera. The anti-SP and anti-FcγRIIA blocking antibodies had no effect in modulating platelet activity in both groups.ConclusionsSARS-CoV-2 infection seems to play a major role in endothelium activation and infarct volume extension during AIS.

Emergent reperfusion therapies have improved acute ischemic stroke prognosis, but many patients are still bound to bad clinical outcome, probably because of our incomplete knowledge of its pathophysiology. Thanks to mechanical thrombectomy, occluding material is available for histological analysis. Several studies investigated the possible relationship between thrombus composition and clinical, procedural, and radiological variables of acute ischemic stroke. The potential value of thrombus analysis as a tool for clinical practice and research is still not defined, as data from the literature are heterogeneous and sometimes conflicting. We propose a review of the existing literature regarding histological analysis of thrombi in acute ischemic stroke. We classified articles on clot composition according to the clinical variable explored in each study. We first distinguished articles about etiology, procedural, and radiological variables, and then we performed a subclassification for each group. This review could help both in the interpretation of thrombus analysis in clinical practice and in its usage for future research.

Inborn errors of metabolism causing stroke (ischemic or haemorrhagic) or stroke-like episodes (e.g., that are also called "metabolic strokes" and include acute brain lesions not related with alterations of blood flow) cover a wide range of diseases in which acute metabolic decompensations after trigger events (e.g., fever, dehydration, sepsis etc.) may have a variable frequency. The early diagnosis of these conditions is essential because, despite their rarity, effective symptomatic treatments may be available for acute settings (e.g., arginine for Mitochondrial myopathy, Encephalopathy, Lactic Acidosis, and Stroke-like episodes- MELAS) while in other cases disease modifying therapies may be useful to prevent stroke occurrence, recurrence, or relapse (e.g., Fabry disease). The detection of a non-vascular distribution of lesions and the diffuse use of

Background. Vaccine-induced immune thrombotic thrombocytopenia (VITT) is a rare syndrome of unclear aetiology occurring after DNA-based vaccinations against COVID-19. The aim of this study was to investigate the DNA vaccine-encoded Sars-cov-2 soluble spike protein (SP). as a potential trigger of platelet activation in VITT. Methods. We studied three VITT patients and seven healthy controls (HCs) within 3 weeks from the first dose of ChAdOx1 nCoV-19, and one non vaccinated HC. Serum levels of SP and soluble angiotensin-converting enzyme 2 (sACE2), ACE2 expression in platelets and platelet response to VITT serum stimulation were studied. A thrombus retrieved during mechanical thrombectomy from one VITT patients, was analysed by immunohistochemistry for SP and ACE2. Neutrophil extracellular traps (NETs) markers and coagulation parameters were also measured. Results. We detected serum SP (up to 35 days post-vaccination) and sACE2 in all VITT patients, and respectively in two and three out of 7 vaccinated HCs. Only platelets from one non-vaccinated HC expressed ACE2. VITT sera markedly activated platelets and this activation was inhibited by both anti-SP and anti-FcγRIIA blocking antibodies. The thrombus showed positive immunohistochemical labelling of platelets using an anti-SP antibody with reduced ACE2 expression, compared to a thrombus from a pre-pandemic stroke patient. Markers of endothelial dysfunction, NETs and hypercoagulability state were present in all VITT sera. Conclusions. The present data provides first evidence that DNA vaccine-encoded Sars-cov-2 SP is detectable in VITT sera (several weeks post-vaccination) and in a platelet-rich thrombus, and that may contribute to the initial platelet stimulation in VITT patients.

Vaccine induced thrombotic thrombocytopenia is a new syndrome recently described in young adults within two weeks from the first dose of the ChAdOx1 nCoV-19 vaccine and characterized by cerebral venous thrombosis. We report two cases of malignant middle cerebral artery (MCA) infarct and thrombocytopenia within 10 days after vaccination with ChAdOx1 nCoV-19. Patient 1 was a 57-year-old woman who underwent decompressive craniectomy despite two successful mechanical thrombectomies. Patient 2 was a 55-year-old woman who developed a fatal bilateral malignant MCA infarct. Both the patients had pulmonary and portal vein thrombosis and high level of antibodies to platelet factor 4-polyanion complexes.

This review provides an updated analysis of the main aspects involving the diagnosis and the management of children with acute ischemic stroke. Acute ischemic stroke is an emergency of rare occurrence in children (rate of incidence of 1/3500 live birth in newborns and 1–2/100,000 per year during childhood with peaks of incidence during the perinatal period, under the age of 5 and in adolescence). The management of ischemic stroke in the paediatric age is often challenging because of pleomorphic age-dependent risk factors and aetiologies, high frequency of subtle or atypical clinical presentation, and lacking evidence-based data about acute recanalization therapies. Each pediatric tertiary centre should activate adequate institutional protocols for the optimization of diagnostic work-up and treatments.Conclusion: The implementation of institutional standard operating procedures, summarizing the steps for the selection of candidate for neuroimaging among the ones presenting with acute neurological symptoms, may contribute to shorten the times for thrombolysis and/or endovascular treatments and to improve the long-term outcome. What is Known:•Acute ischemic stroke has a higher incidence in newborns than in older children (1/3500 live birth versus 1–2/100,000 per year).•Randomized clinical trial assessing safety and efficacy of thrombolysis and/or endovascular treatment were never performed in children What is New:•Recent studies evidenced a low risk (2.1% of the cases) of intracranial haemorrhages in children treated with thrombolysis.•A faster access to neuroimaging and hyper-acute therapies was associated with the implementation of institutional protocols for the emergency management of pediatric stroke.

Purpose: Intracranial carotid artery occlusion represents an underinvestigated cause of acute ischemic stroke as well as an indication for mechanical thrombectomy. We investigated baseline and procedural characteristics, outcomes and predictors of outcome in patients with acute ischemic stroke secondary to intracranial carotid artery occlusion. Methods: A retrospective analysis of the Italian Registry of Endovascular Treatment in Acute Stroke was performed. Patients with intracranial carotid artery occlusion (infraclinoid and supraclinoid) with or without cervical artery occlusion but with patent intracranial arteries were included. The 3‑month functional independence, mortality, successful reperfusion and symptomatic intracranial hemorrhage were evaluated. Results: Intracranial carotid artery occlusion with patent intracranial arteries was diagnosed in 387 out of 4940 (7.8%) patients. The median age was 74 years and median baseline National Institute of Health Stroke Scale (NIHSS) was 18. Functional independence was achieved in 130 (34%) patients, successful reperfusion in 289 (75%) and symptomatic intracranial hemorrhage in 33 (9%), whereas mortality occurred in 111 (29%) patients. In univariate analysis functional independence was associated with lower age, lower NIHSS at presentation, higher rate of successful reperfusion and lower rate of symptomatic intracranial hemorrhage. Multivariable regression analysis found age (odds ratio, OR:1.03; P = 0.006), NIHSS at presentation (OR: 1.07; P < 0.001), diabetes (OR: 2.60; P = 0.002), successful reperfusion (OR:0.20; P < 0.001) and symptomatic intracranial hemorrhage (OR: 4.17; P < 0.001) as the best independent predictors of outcome. Conclusion: Our study showed a not negligible rate of intracranial carotid artery occlusion with patent intracranial arteries, presenting mostly as severe stroke, with an acceptable rate of 3‑month functional independence. Age, NIHSS at presentation and successful reperfusion were the best independent predictors of outcome. © 2020, Springer-Verlag GmbH Germany, part of Springer Nature.

Background The applicability of the current models for predicting functional outcome after thrombectomy in strokes with large vessel occlusion (LVO) is affected by a moderate predictive performance. Aims We aimed to develop and validate a nomogram with pre- and post-treatment factors for prediction of the probability of unfavorable outcome in patients with anterior and posterior LVO who received bridging therapy or direct thrombectomy Methods We conducted a cohort study on patients data collected prospectively in the Italian Endovascular Registry (IER). Unfavorable outcome was defined as three-month modified Rankin Scale (mRS) score 3–6. Six predictors, including NIH Stroke Scale (NIHSS) score, age, pre-stroke mRS score, bridging therapy or direct thrombectomy, grade of recanalization according to the thrombolysis in cerebral ischemia (TICI) grading system, and onset-to-end procedure time were identified a priori by three stroke experts. To generate the IER-START, the pre-established predictors were entered into a logistic regression model. The discriminative performance of the model was assessed by using the area under the receiver operating characteristic curve (AUC-ROC). Results A total of 1802 patients with complete data for generating the IER-START was randomly dichotomized into training ( n = 1219) and test ( n = 583) sets. The AUC-ROC of IER-START was 0.838 (95% confidence interval [CI]): 0.816–0.869) in the training set, and 0.820 (95% CI: 0.786–0.854) in the test set. Conclusions The IER-START nomogram is the first prognostic model developed and validated in the largest population of stroke patients currently candidates to thrombectomy which reliably calculates the probability of three-month unfavorable outcome.

Introduction: The widespread use of direct oral anticoagulants (DOACs) has been increasing the conditions in which emergency physicians are forced to rapidly reverse anticoagulation in case of life-threatening bleeding or need of urgent surgery or invasive procedures. The recent approval of Idarucizumab, a humanized monoclonal antibody fragment (Fab), offered the opportunity to rapidly and safely neutralize the anticoagulant effect of Dabigatran. However, real-world experience of its effective use in different emergency setting is now required. Lumbar Puncture (LP) is recognized as an invasive procedure at major bleeding risk and is, therefore, contraindicated in anticoagulated patients. Conclusion: We report a successful use of Idarucizumab in an emergency LP of a young woman with a possible diagnosis of encephalitis and a previous history of venous thromboembolism on long-term treatment with Dabigatran 150 mg twice a day.

Background and Purpose— Prognostic value of copeptin in acute ischemic stroke has been widely reported. This study aimed to evaluate copeptin temporal profile according to revascularization strategies and the development of brain edema and hemorrhagic transformation. Methods— Plasma copeptin and brain edema and hemorrhagic transformation assessed by computed tomography/magnetic resonance imaging were evaluated upon admission ( T0 ), at 24 hours ( T1 ), and between the third and fifth day of hospitalization ( T2 ) in 34 acute ischemic stroke patients. Results— Median copeptin concentration was 50.71 pmol/L at T0 , 18.31 pmol/L at T1 , and 10.92 pmol/L at T2 . Copeptin at T1 was higher in patients with medium/severe brain edema at T2 (32.25 versus 13.67 pmol/L; P =0.038) and hemorrhagic transformation at T1 (93.10 versus 13.67 pmol/L; P T2 (85.70 versus 14.45 pmol/L; P =0.024). Copeptin level drop (CopΔ T1−T0 ) was significantly steeper in patients receiving revascularization, particularly in those undergoing combined therapy (−129.34 versus −5.43 pmol/L; P =0.038). Δ T1−T0 also correlated with Thrombolysis in Cerebral Infarction score ( P Conclusions— Copeptin resulted associated with brain edema and hemorrhagic transformation in acute ischemic stroke, and its drop at 24 hours may mirror effective brain vessel recanalization.

A Peruvian woman was admitted to the Emergency Department, due to an acute flaccid paralysis (AFP) of the upper limbs that progressively involved also lower limbs and respiratory muscles. She previously suffered from non-Hodgkin's lymphoma and had to undergo hematopoietic stem cell transplantation. A magnetic resonance imaging showed a T2 hyperintensity in the anterior and central region of the cervical segment with an elective involvement of gray matter. This finding, combined with other clinical, laboratory, and electrophysiological data, led to a diagnosis of AFP. Enterovirus D68 was isolated in the patient's cerebrospinal fluid, plasma, and throat swab. To our knowledge, this is the first Italian case of AFP by Enterovirus D68 infection in an adult. The diagnostic assessment and management of AFP by Enterovirus D68 are discussed.

The expression of corticotrophin-releasing factor (CRF) receptors in cerebral arteries and arterioles suggests that CRF may modulate cerebral blood flow (CBF). In the present study, the effects of CRF, CRF-like peptides and the CRF broad spectrum antagonist DPhe-CRF on CBF have been investigated under normal physiologic conditions and in the margins of focal ischaemic insult. The experiments were carried out in anaesthetised and ventilated rats. Changes in CBF after subarachnoid microapplication of CRF and related peptides were assessed with a laser-Doppler flowmetry (LDF) probe. In the ischaemic animals, agents were injected approximately 60 minutes after permanent middle cerebral artery occlusion (MCAo). Microapplication of CRF and related peptides in normal rats into the subarachnoid space produced sustained concentration-dependent increases in CBF. This effect was attenuated by co-application with DPhe-CRF, which did not alter CBF itself. A second microapplication of CRF 30 min after the first failed to produce increases in CBF in normal animals. Microapplication of CRF in the subarachnoid space overlying the ischaemic cortex effected minor increases in CBF whereas D-Phe-CRF had no significant effect on CBF. Activation of the CRF peptidergic system increases CBF in the rat. Repeated activation of CRF receptors results in tachyphylaxis of the vasodilator response. CRF vasodilator response is still present after MCAo in the ischaemic penumbra, suggesting that the CRF peptidergic system may modulate CBF in ischaemic stroke.

Aortic dissection is an uncommon cause of stroke in young patients, and can lead to a severe prognosis, especially if not promptly diagnosed and adequately treated. Among the etiologies that can underlie an arterial dissection in the young, there are heritable connective tissue disorders (HCTDs) with increased vascular fragility [1]. Among them, the Loeys–Dietz syndrome (LDS) is a recently defined aortic aneurysm syndrome, inherited as an autosomal-dominant disease, and caused by heterozygous mutations in various proteins of the transforming growth factor beta (TGF-b) pathway [2]. We report a case of a young woman with LDS, which had been unrecognized until the patient presented to the emergency department (ED) with focal neurological symptoms due to an acute ischemic stroke secondary to aortic dissection. The diagnosis of LDS type 2, confirmed at the molecular level, offered the opportunity to describe and discuss several causes of arterial dissection in the young, and focus on the underlying diseases, particularly focusing on this recently described HCTD.

At the initial stages of Parkinson's disease (PD), levodopa (LD) is able to reduce most motor symptoms and to significantly improve the patient's quality of life. However, in the vast majority of patients with prolonged LD usage, some decline in efficacy occurs and motor complications eventually begin to appear. These complications consist not only of daily fluctuations in the voluntary motor performance often accompanied by involuntary movements, but also of fluctuations in cognitive, autonomic, and sensory functions. Several recent studies on LD complications in PD have led to a better understanding of their pathophysiology and of the possible therapeutic interventions, and a summary of these findings is presented in this review. Different observations now suggest that postsynaptic pharmacodynamic factors play a major role in determining fluctuations in PD. Two explanations are given: chronic intermittent dopaminergic therapy may lead to postsynaptic receptor downregulation in PD; or, receptor changes in the striatum may occur independently of treatment as a result of structural adaptation of the postsynaptic dopaminergic system to the progressive decline of the nigrostriatal pathway. The hypothesis of reversible postsynaptic changes as the main mechanism underlying a fluctuating response to LD lends itself to a possible pharmacological manipulation of the dopaminergic response to reverse, or even avoid, motor fluctuations (initial monotherapy with dopamine agonists and early combination LD/dopamine agonists). The role of peripheral pharmacokinetics factors is also critical and the use of controlled release LD formulations, of monoamine oxidase (MAO)-B and of catechol-O-methyltransferase (COMT) inhibitors may all, to a different degree, improve such phenomena. In the last decade, there has been a resurgence in surgical therapies in advanced PD, due to higher levels of accuracy and safety provided by the new surgical devices, and to a more precise localization of the target areas allowed by the neurophysiological mapping techniques. The surgical procedures currently used in advanced PD are stereotactic brain lesions (internal globus pallidus and subthalamic nucleus), chronic brain stimulation (of the same nuclei) and striatal grafting of dopamine-producing cells. All these procedures have already shown their efficacy in the management of severe fluctuations in PD, but their indications, and relative advantages and disadvantages, are still the subject of considerable debate and controversy.

The dopamine (DA) D-1 and D-2 receptors coupled to 3′, 5t'-cyclic adenosine monophosphate (cAMP) generation were studied in membrane particles of the frontal cortex in young (3-month-old), adult (12-month-old) and aged (24-month-old) male Sprague—Dawley rats. Activation of D-1 receptors with DA, apomorphine or fenoldopam enhanced accumulation of cAMP in the frontal cortex of young rats. The stimulatory effect elicited by DA on cAMP generation declined by about 20% in adult rats. No further decline in cAMP accumulation was noticeable in aged animals. The response to dopaminergic agonists was blocked by the D-1 receptor antagonist SCH 29390 in the three age groups examined. The presence of D-2 receptors, negatively coupled to cAMP generation, was demonstrated by incubatlng frontal cortex membrane particles with SCH 23390 and then with DA. This inhibitory response, was also elicited with D-2 receptor agonists quinpirole or bromocriptine in the absence of SCH 23390 in which these compounds produced a decrease in cAMP. The decrease in cAMP caused following D-2 receptor stimulation was shown to be enhanced with age. No difference was observed between the three age groups of animals in the activation of cAMP production by forskolin. The present data suggest a selective decrease in the coupling between the D-1 receptor and cAMP generation in the frontal cortex of adult and aged rats and of an age-dependent increase in the coupling between the D-2 receptor and cAMP inhibition. The functional consequences of these biochemical changes may have important implications in the aging of the rat frontal cortex.

The dopamine (DA) D(1) and D(2) receptors coupled to the 3',5'-cyclic adenosine monophosphate (cAMP)-generating system were studied in membrane particles of the dorsal hippocampus in 3 (considered to be young), 12 (considered to be adult) and 24 (considered to be old) month male Sprague-Dawley rats. Activation of D(1) receptors with DA, apomorphine or SKF 82526 enhanced accumulation of cAMP in the hippocampus of rats of the three age groups examined. This stimulatory effect was significantly reduced in adult rats. No further changes were noticeable in old animals. D(2) receptors negatively coupled to cAMP generation were demonstrated by incubating hippocampus membrane particles with SCH 23390 plus DA or with D(2) receptor agonists quinpirole or bromocriptine. The D(2) inhibitory effect on cAMP generation was unchanged in the three age groups. No difference was detectable between young, adult and old rats in the activation of cAMP production by forskolin.

The increasing prevalence of cerebrovascular diseases has made urgent the need to develop timely and effective treatment strategies to tackle this health problem. Stroke units (SUs) appear to be the ideal setting where the management of acute stroke patients, including specific treatments as thrombolysis, may be optimized. Which model of SU gives the best results is still an unsettled issue. The more intensive and timely multidisciplinary approach to the acute phase of stroke, the management of medical complications, and the earlier and more focused rehabilitation, are likely the most qualifying aspects of our Neurovascular treatment unit.

Galanin (Gal) is a neuropeptide with supposed neurotrophic-like action. In the present study, expression of Gal has been investigated in the core and peri-infarct zone at 1, 4, 24 and 72 h after middle cerebral artery occlusion (MCAo) in the rat. Three days after MCAo a small but consistent number of morphological intact Gal-positive neuronal cells were observed in the peri-infarct zone. Gal-positive cells were barely detectable in the infarct and peri-infarct zone at 24 h. No Gal immunopositive cells were detected in brain subjected to 1 and 4 h of ischemia. Gal immunoreactivity was also detected in myelinated fibers 4 and 24 h after focal ischemia. Gal may be a peptide with neurotrophic and plasticity functions under stress conditions.

Background and Purpose Ischemic stroke patients whose initial clinical presentation suggests an involvement of the anterior circulation (AC) are sometimes found to have a posterior circulation (PC) infarct, a fact that may generate erroneous decisions in clinical management. We investigated the prevalence of this misdiagnosis in the first few hours after stroke onset. Methods We performed a cohort study of 158 patients hospitalized within 5 hours of onset of a presumed AC ischemic stroke, as diagnosed on clinical grounds. Results Final CT or pathology diagnosis was AC infarct in 128 patients (81%), a repeatedly negative CT in 14 (9%), PC infarct (5 pons, 1 midbrain and cerebellum, 6 supratentorial territory of the posterior cerebral artery) in 12 (8%), and other or undiagnosed lesions in 4 (3%). AC and PC stroke patients did not differ in terms of age, vascular risk factors, and initial severity, but the latter were more frequently men (83% versus 53%; P =.04), were hospitalized later (mean±SD, 168±86 versus 109±55 minutes; P =.001), and presented a pure motor hemiparesis or a sensorimotor stroke (50% versus 33%) more often than their counterparts. At baseline CT, PC stroke patients never exhibited an early parenchymal hypodensity in the carotid territory or a hyperdense middle cerebral artery, which were instead found in 59% ( P =.0003) and 31% ( P =.02) of AC stroke patients, respectively. Early neurological deterioration, 1 month case-fatality rate, and disablement in survivors were comparable in the two groups. Conclusions Shortly after onset the clinical discrimination between AC and nontypical PC infarcts is not reliable, which explains the frequent occurrence of this misdiagnosis. Emergency CT scan helps in the differential diagnosis only when it demonstrates an early focal hypodensity within the carotid territory.

We investigated the effects of hyperglycaemia on infarct size of 82 acute ischaemic stroke patients with angiographically diagnosed intracranial occlusion in middle cerebral artery territory. There were 9 diabetics, 40 non-diabetic hyperglycaemics and 33 non-diabetic normoglycaemics (mean age 67 +/- 8 SD years, male/female ratio 1:1). For each patient the infarct at CT was compared to that predicted from the location of the arterial occlusion. The extent of the infarct was then classified as equal to, smaller than and larger than estimated, taking a standard anatomical template of arterial territories as reference. The results were analysed separately according to the presence or absence of a collateral blood supply (CBS) at angiography. The clinical outcome at 30 days was also evaluated. The 35 patients lacking CBS had a high frequency of equal to estimated lesions (75%), without substantial differences among the three subgroups (72% of hyperglycaemics, 82% of normoglycaemics and 67% of diabetics; Fisher's exact test not significant for any of the pairwise comparisons). On the contrary, the 47 patients with CBS exhibited an overall predominance of smaller than estimated lesions (66%) but with a very uneven distribution among hyperglycaemics, normoglycaemics and diabetics (82%, 64% and 0%, respectively; p < 0.05 at Fisher's exact test for diabetics vs hyperglycaemics). Finally, the clinical outcome was bad (death and neurological impairment) in 89% of diabetics, 72% of hyperglycaemics and 54% of normoglycaemics (p < 0.05). These results suggest that in patients with intracranial arterial occlusion associated with CBS the effects of hyperglycaemia might be beneficial in non-diabetics and harmful in diabetics.(ABSTRACT TRUNCATED AT 250 WORDS)

Age-related changes of the sympathetic (noradrenergic) innervation of the kidney were studied in young (3 months) and old (25 months) female Wistar rats by means' of high-pressure liquid chromatography (HPLC) with electrochemical detection and catecholamine histofluorescence techniques. Body and kidney weights were significantly increased in old rats. Renal noradrenaline levels were slightly but not significantly decreased in aged animals. The density of fluorescent catecholaminergic nerve fibres was significantly decreased in old rats, primarily within branches of renal artery (at the hilum) and within interlobular and cortical radial arteries. However, in old rats the number of axonal varicosities corresponding to the site of neurotransmitter release was slightly increased in interlobular and cortical radial arteries but not in hilar branches of the renal artery. The number of cortical tubules supplied with a catecholaminergic innervation remarkably decreased with age. These findings are indicative of age-dependent changes of the intrarenal noradrenergic innervation in Wistar rats. The lack of correspondence between the results obtained using HPLC and catecholamine histofluorescence techniques underscore the importance of evaluating the age-related changes of autonomic innervation using more than one methodology.

Background and Purpose Pure motor hemiparesis and sensorimotor stroke syndromes are not accurate predictors of lacunar infarct when described in the first 12 hours of stroke onset. We evaluate here whether this inaccuracy of clinical diagnosis might have influenced the planning of patient management either in routine practice or in therapeutic trials. Methods A consecutive hospital series of 517 first-ever ischemic hemispheric stroke patients presented lacunar or nonlacunar syndromes at the first examination within 12 hours of the event. A distinction was subsequently made, by means of a CT scan or autopsy performed within 15±2 days of stroke, between patients affected by lacunar or nonlacunar infarcts. We compared stroke risk factors, considered to be indicative of potential pathogenetic mechanisms, and the clinical outcome of lacunar infarct versus nonlacunar infarct patients and those of lacunar syndrome versus nonlacunar syndrome patients. Results Two hundred nineteen patients (42%) presented a lacunar syndrome and 298 (58%) a nonlacunar syndrome, while 170 (33%) had lacunar infarcts and 347 (67%) nonlacunar infarcts. Lacunar infarct patients were more frequently associated with hypertension and a previous transient ischemic attack and less frequently with atrial fibrillation when compared with their nonlacunar infarct counterparts, whereas no differences were apparent between lacunar syndrome and nonlacunar syndrome patients. Logistic regression analysis showed that hypertension and a previous transient ischemic attack on the one hand and atrial fibrillation on the other were strongly correlated with the diagnosis of lacunar infarct and nonlacunar infarct, respectively, while no risk factor was correlated with the diagnosis of lacunar syndrome. Twenty-two percent of lacunar infarct patients and 68% of nonlacunar infarct subjects had a poor outcome (death plus disability of survivors) as opposed to 40% of lacunar syndrome and 63% of nonlacunar syndrome patients. Logistic regression selected age, severity of neurological deficit at entry, cardiopathies, diabetes, and lacunar infarct, but not lacunar syndrome, as predictors of outcome. Conclusions The inaccurate clinical diagnosis of lacunar infarct made in the first 12 hours of stroke might lead to no distinction being made between stroke subgroups with potentially different pathogenetic mechanisms and prognostic estimates, thus negatively influencing the planning of patient management.