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People often ignore the usefulness of stroke prevention, the typical onset symptoms, and the efficacy of the new therapies. In order to attempt to correct this situation, we performed an educational campaign addressed to Rotary club associates and their relatives or friends in the Italian Rotary District 2032. The campaign consisted in three phases: (1) Compilation of a simple questionnaire on stroke, followed by a scientific relation on the disease, distribution of didactic materials, and organization of screening sessions on individual stroke risk evaluation; (2) Recompilation by participants of the same previous questionnaire; (3) Statistical evaluation of the improvement of stroke knowledge. The initial percentage of wrong answers (number of subjects 657) was 22.41% ((A) stroke general knowledge 15.45%; (B) stroke risk factors 25.65%; (C) Stroke early symptoms 22.65%). At the end of the campaign, the total percentage of wrong answers (number of subjects 296) attained the 13.18% ((A) stroke general knowledge 8.22%; (B) stroke risk factors 14.98%; (C) stroke early symptoms 13.85%). All these differences were strongly significant at the statistical analysis. We demonstrated that our educational campaign obtained an important improvement of stroke awareness in our sample. We hope that the enhanced awareness might induce a more frequent diffusion of primary prevention strategies, an increased capacity of recognizing onset stroke symptoms with shortening of patients’ presentation in the Emergency Room of the hospitals when they can undergo thrombolysis/thrombectomy.

Best medical treatments of ischemic stroke are admission to stroke unit, intravenous thrombolysis and, in selected cases, thrombectomy. Time from symptom onset to interventions is the best predictor of clinical outcome. In order to verify the effectiveness of an active education programme of awareness on the knowledge of stroke, we performed a local campaign “on the field”. We selected 101 subjects from the general population who took part in the “stroke awareness campaign” organised by the Italian Association for the fight against stroke (A.L.I.Ce). Mean age was 59 years (50% female; 50% male); 55% of the sample reported a high level of education (> 8 years: high school or university degree). After a short multiple-choice questionnaire, we administered a face-to-face standard educational protocol (15 min). The efficacy of that educational intervention was then verified after a period of 12 months, by telephone interview. There was improvement both in the definition of stroke (66% vs. 92%, p

The above article was published online with inverted given and family names The correct presentation has been corrected above The original article has been corrected

Background and aims: Several neurological complications related to SARS-CoV-2 infection have been reported. The involvement of peripheral nervous system (PNS) consists in the development of immune-mediated neuropathies such as Guillain-Barre Syndrome. In this study we aim at assessing the presence of asymptomatic abnormalities in peripheral nerves conduction during the acute phase of COVID-19 and, their correlation with blood circulating inflammatory markers. Methods: Thirty-nine patients with COVID-19 were assessed by electroneurographic study of lower limbs and blood tests within one week of hospital admission (T0) and after 30 ± 10 days (T1). Results: Electroneurographic changes were found at least on one nerve at T0 in 12 patients, consisting of axonal or demyelinating changes. Two biological markers were found to be significantly correlated with the presence of neuropathic changes: Reactive Protein C and lymphocyte count. Patients with pathological electrophysiology at T0 showed significant improvement of electrophysiological parameters at T1. The improvements in electroneurographic data were significantly correlated with the trend of laboratory parameters, in particular with fibrinogen, D-Dimer, ferritin, C Reactive protein and lymphocytes. None of the patients with neuropathic changes developed clinical evidence of a full-blown peripheral neuropathy over time. Conclusions: Our study shows that asymptomatic alterations of the PNS can be found during the acute phase of COVID-19. These alterations significantly improve after 20–40 days from the acute phase of infection and that the improvement correlates significantly with the trend of laboratory parameters. Further studies are needed to evaluate possible long-term neurological complications and the predictive value of subclinical damage of PNS in the acute phase of infection.

Several observational studies report that subjects with migraine with aura have a higher prevalence of right-to left shunt, commonly due to patent foramen ovale, and that patent foramen ovale is more prevalent in subjects with migraine with aura. Although migraine without aura has been less extensively studied, it does not seem to be associated with an increased prevalence of right-to left shunt. The mechanism that underlies the possible relationship between patent foramen ovale and migraine with aura remains speculative. The proposed mechanisms are migraine-triggering vasoactive chemicals bypassing the pulmonary filter and reaching the cerebral circulation and paradoxical microembolization. However, it is unclear, at this time, if there is a causal or comorbid association between the two conditions. In some families atrial shunts show a dominant inheritance that seems to be linked to inheritance of migraine with aura. Migraine with aura is an independent risk factor for ischemic stroke, and patent foramen ovale is present more frequently in patients with cryptogenic stroke than in controls. At this moment, there is no convincing evidence that excess stroke risk of migraine is simply mediated by patent foramen ovale through paradoxical embolism. Several non-controlled studies suggest that closure of the foramen ovale significantly reduces attack frequency in migraine patient, but the only prospective placebo-controlled trial does not support these results. Patent foramen ovale closure, at present, is not indicated as a treatment for migraine in clinical practice.

Background: The spectrum of autoimmune neurological diseases associated with voltage-gated potassium channel (VGKC)-complex antibodies (Abs) ranges from peripheral nerve disorders to limbic encephalitis. Recently, low titers of VGKC-complex Abs have also been reported in neurodegenerative disorders, but their clinical relevance is unknown. Objective: The aim of the study was to explore the prevalence of VGKC-complex Abs in slow-progression motor neuron disease (MND). Methods: We compared 11 patients affected by slow-progression MND with 9 patients presenting typical progression illness. Sera were tested for VGKC-complex Abs by radioimmunoassay. The distribution of VGKC-complex Abs was analyzed with the Mann-Whitney U test. Results: The statistical analysis showed a significant difference between the mean values in the study and control groups. A case with long-survival MND harboring VGKC-complex Abs and treated with intravenous immunoglobulins is described. Conclusion: Although VGKC-complex Abs are not likely to be pathogenic, these results could reflect the coexistence of an immunological activation in patients with slow disease progression.

Background: A 63-year-old woman with chronic atrial fibrillation treated with warfarin was admitted to emergency for coma and complete vertical gaze palsy. Investigations: Brain CT and MRI, echo-colour Doppler sonography of the supraaortic vessels, angio-CT of the intracranial vessels, EEG, transesophageal echocardiogram, biohumoral tests. Brain CT and MRI scans showed bilateral thalamic lesions with involvement of the right midbrain; EEG showed a diffuse alpha rhythm prevalent on the posterior regions; echo-colour Doppler sonography of the supraaortic vessels showed marked reduction of blood flow in the right vertebral artery; angio-CT scans showed occlusion of the right vertebral artery and a significant filling defect of the first part of the right posterior cerebral artery (P1) from which the artery of Percheron arises. A follow-up angio-CT showed a complete recanalization of P1. Diagnosis: Percheron artery syndrome. Treatment and Management: Aspirin, neurorehabilitation.

Although ultrasound-activated microbubbles (MB) accelerate clot lysis, MB activation has shown to promote blood barrier disruption and bleeding in animal models. We conducted a case-control study aimed to investigate the risk of hemorrhagic transformation (HT) after MB-enhanced sonothrombolysis in acute stroke.We evaluated a total of 296 patients with acute stroke treated with IV tissue plasminogen activator (tPA)3 hours after stroke onset. One hundred eighty-eight patients received continuous 2-hour TCD monitoring plus 3 doses of 2.5 g of MB after tPA bolus (MB group). These patients were compared with 98 historic stroke patients (control group). The presence and extent of HT on 24-hour CT were blindly assessed.Recanalization rates were higher in the MB compared with the control group at 1, 2, 6, and 12 hours (p0.05). MB administration was associated with an increased risk of hemorrhagic infarction (HI)1-HI2 (21% vs 12%, p = 0.026) and a higher degree of clinical improvement at 24 hours (54.9% vs 31.1%, p = 0.004). Parenchymal hematoma (PH)1-PH2 and symptomatic intracranial hemorrhage rates were similar in both groups. Moreover, the extent of bleeding after MB-enhanced sonothrombolysis was correlated with the time to reperfusion. Early (6 hours) recanalization independently predicted HI in the MB group (odds ratio 6.3, 95% confidence interval 2.3-56) but not in the control group. Delayed (6 hours) or no recanalization was associated with PH1-PH2 in both the MB group (p = 0.024) and the control group (p = 0.045).This hypothesis-generating study shows that microbubble administration was associated with early recanalization and a high rate of hemorrhagic transformation but does not seem to increase the risk of symptomatic intracranial hemorrhage. However, definitive conclusions cannot be made based on these data.

Several studies have reported that oral anticoagulant prophylaxis (OAC) is under-used in patients with atrial fibrillation (AF).This study investigated the attitude to prescribing OAC in patients with AF observed in an Italian Stroke Unit (SU) and the severity of ischemic stroke due to AF in comparison with that of other etiologies.We prospectively studied a continuous series of acute stroke patients admitted to our SU from January 1, 2003 to December 31, 2005. Using Multiple Logistic Regression, we analyzed factors associated with the non-use of OAC and with poor prognosis.Of 400 consecutive ischemic stroke patients, 103 (25.75 %) had AF; this group was older (mean age+/-sd= 79.74 +/- 10.15 years vs. 73.49 +/- 12.72; P = 0.0000045) and their strokes were more severe (NIHSS median value = 10 vs. 7, P0.002) in comparison with the group of patients whose strokes were due to other etiologies. Only 27.27% of patients with known AF, and without contraindications, were under OAC before the onset of stroke. The main independent factor associated with the non-use of OAC was old age. Moreover, AF proved to be a significant independent predictor of poor prognosis in our stroke population.The results of this study indicate a marked under- use of OAC prophylaxis in AF subjects in Italy. Campaigns to raise awareness and to improve the implementation of guidelines on stroke prevention strategies are strongly recommended, not least because stroke due to AF has a worse prognosis.

Silent cerebral infarcts occur in patients with chronic nonvalvular atrial fibrillation and asymptomatic or symptomatic carotid stenosis. There is not a well-defined prevalence of asymptomatic lesions in patients with transient ischemic attack or completed strokes. We attempted to determine the occurrence rate of silent brain infarction in a hospital population, including a comparison of the risk factors with those of symptomatic infarction and an evaluation of the relevance of infarction size and location.

Transcranial Doppler (TCD) is currently used in monitoring subarachnoid hemorrhage, acute stroke, and carotid endarterectomy and in diagnosing intracranial vascular disease. In this article we review other uses of TCD, in systemic conditions related to ischemic stroke. Transcranial Doppler, in fact, can identify right-to-left shunts (RLS), usually due to patent foramen ovale (PFO), a risk factor for cryptogenic stroke in the young. Recently an association between RLS and migraine with aura has been reported; migraine is a risk factor for stroke, for silent brain infarctions, and for silent white matter disease, but there are no data yet on a similar risk for the association of migraine plus PFO. TCD can also be used to stratify the risk of stroke in children with sickle cell disease, to better identify subjects to be transfused to prevent strokes.

Right-to-left shunt due to patent foramen ovale is a well-established risk factor for ischemic stroke, especially in young subjects and in patients with cryptogenic stroke. We report a detailed method for the diagnosis of a right-to-left shunt by means of transcranial Doppler as established at a recent consensus conference, and review the literature on the indications for the test.

Arginine vasopressin (AVP) may play a role in the development of ischemic brain edema and/or cerebral vasospasm. Data available on AVP plasma levels in ischemic stroke are few and discordant. In order to ascertain whether changes in AVP plasma levels occur in ischemic stroke, plasma AVP levels, plasma osmolality and mean arterial pressure were determined in 24 patients with unprecedented ischemic cerebral infarction and in 15 controls over a 24-hour period. In stroke patients, mean 24-hour plasma AVP levels (7.2 ± 0.8 ng/l) were higher (p < 0.05) than in control subjects (2.4 ± 0.3 ng/l), and correlated with the severity score of the neurologic deficit and the mean size of the lesion. In patients with a more severe neurologic deficit, the mean 24-hour plasma AVP levels (8.7 ± 1.0 ng/l) were higher than in patients with a less severe neurologic deficit (5.2 ± 0.8 ng/l). Data indicate that in ischemic stroke an increased AVP secretion occurs independently of osmotic or baroreceptorial mechanisms. The possibility that AVP may play a role in neuronal cell damage following cerebral ischemia warrants further attention.

Anderson-Fabry disease (AFD) is an X-linked recessive lysosomal disease caused by alpha-galactosidase A (alpha-gal) deficiency, causing progressive glycosphingolipid storage in various organ systems. Headache is a frequent symptom. Cerebral magnetic resonance imaging (MRI) often shows multiple white matter lesions (WML), like those seen in patients affected by migraine, in particular with aura (MA). To our knowledge, there are no reports about the prevalence of AFD in patients with MA. The objective of the study was to determine AFD prevalence, as assessed by alpha-gal activity and genetic tests, in MA patients. We evaluated 73 consecutive patients followed by the Headache Centre of our Department with a diagnosis of MA. They were screened for migraine characteristics and cerebrovascular risk factors. Gaseous contrast transcranial Doppler was used to diagnose right-to-left shunt and MRI to detect WML. All patients underwent blood test to evaluate peripheral alpha-gal activity and to identify alpha-gal gene mutations. Of 73 consecutive screened subjects (59 females, 14 males; mean age 38.3 +/- 11.8 years), the known GLA pathologic mutation p.[Asp313Tyr] was found in a 38-year-old woman, with a history of MA, deep venous thrombosis and abdominal pain. Cerebral MRI showed small WML. This is the first study reporting AFD prevalence in a cohort of MA patients. We found a relatively high prevalence (about 1.37%) among the examined patients, even if this finding needs to be confirmed in a larger sample. Despite this high prevalence, it seems not necessary to screen systematically all MA patients for AFD, but since it is a treatable genetic disorder, it is worthwhile to consider it for the subgroup of patients presenting WML and other typical AFD symptoms.

Mean blood flow velocity (MFV) of the middle cerebral arteries was monitored in 19 healthy, adult, right-handed subjects during the resting phase and the execution of a series of neuropsychological tests: two right/left discrimination tasks, two mental rotation paradigms (the Ratcliff's test and a cube comparison test) and a phonemic fluency task, which was utilised as an internal control. In the group as a whole, the Ratcliff's test was associated with a significant bilateral increase in MFV versus both the resting state (right: p.000001, left: p.000001) and right/left discrimination tasks (task 1: right: p = .003, left: p = .005; task 2: right: p = .001, left: p = .001). The cube comparison in turn produced a significant increase in MFV versus both the baseline conditions (right: p.000001, left: p.000001) and the Ratcliff's test (right: p = .01, left: p = .002). As expected, the fluency task was associated with a significant asymmetric increase in cerebral perfusion (leftright: p = .0001). Increasing task difficulty (right/left discriminationRatcliffs testcube comparison) was paralleled by a roughly proportional rise in MFV values (right: r = .424, p.01; left: r = .331, p = .01). In conclusion, we were able to demonstrate that (1) in addition to the amount of MFV variation due to right/left discrimination (when required), mental rotation per se causes a bihemispheric activation irrespective of the experimental paradigm; (2) the MFV variation is proportional to the difficulty of the tasks.

BACKGROUND Microalbuminuria has recently emerged as a strong, independent predictor of cardiovascular mortality in patients with essential hypertension, yet the pathophysiological mechanisms underlying this association remain to be elucidated. OBJECTIVE To study the relationship between microalbuminuria and left ventricular geometry and function and extra-cardiac vascular changes in a group of 211 untreated hypertensive patients. METHODS Albuminuria was evaluated as albumin-to-creatinine ratio in three non-consecutive first morning urine samples. Left ventricular mass index and function were assessed by M-B mode echocardiography and carotid wall thickness by high-resolution ultrasound scan. RESULTS The prevalences of microalbuminuria and left ventricular hypertrophy were 14 and 47% respectively. Patients in the top quartile of albuminuria showed a higher left ventricular mass index (57 +/- 1.8, 55 +/- 2, 47 +/- 1.4 and 48 +/- 1.6 g/m2.7, respectively; P< 0.0001) as well as a higher prevalence of left ventricular hypertrophy (72, 65, 26 and 25%, respectively; P< 0.001) and especially concentric hypertrophy (56, 47, 17 and 21%, respectively; P< 0.0001) in the four quartiles of albuminuria. Microalbuminuric patients showed depressed left ventricular performance as indicated by a reduced midwall fractional shortening (15.7 +/- 0.3, 15.9 +/- 0.3, 16.7 +/- 0.4 and 16.8 +/- 0.3%, respectively; P< 0.02). Furthermore patients in the top quartile of albuminuria showed increased carotid wall thickness as compared to normoalbuminuric patients (0.78 +/- 0.03, 0.7 +/- 0.04, 0.65 +/- 0.03 and 0.6 +/- 0.03 mm, respectively; P < 0.001). CONCLUSIONS Hypertensive patients with microalbuminuria show a higher prevalence of unfavourable left ventricular geometric patterns, depressed left ventricular function and early signs of extra-cardiac vascular damage. These findings strengthen the role of microalbuminuria as an indicator of subclinical cardiovascular disease and may account for the worse outcome that is usually associated with increased urinary albumin excretion in essential hypertension.

Reliable, simple and safe criteria are needed for the early prediction of short-term outcome in patients with acute ischemic stroke. The aim of our study was to evaluate, in terms of their individual and combined power, the prognostic value of a few widely available clinical and instrumental variables obtained during the acute phase. The study involved 351 consecutive patients who were examined within 48 hours of their first ischemic stroke. Eight variables were chosen: age, initial level of consciousness, limb paresis, arterial blood pressure, glycemia, the results of electrocardiography and electroencephalography, and the infarct size revealed by computed tomography. Mortality and disability were evaluated on Day 30, when the variables that significantly correlated with disability were the severity of limb paresis, electroencephalographic abnormalities, infarct size and (less significantly) the level of consciousness and hyperglycemia. There was no statistical correlation with blood pressure. Logistic analysis confirmed only infarct size, the severity of limb paresis and electroencephalographic abnormalities as independent variables. The variables that significantly correlated with early death were the severity of limb paresis, infarct size, electrocardiographic abnormalities, the level of consciousness, electroencephalographic abnormalities and hyperglycemia. More intriguingly, logistic analysis confirmed only the electroencephalographic and electrocardiographic abnormalities as independent variables. The predictive prognostic value of limb paresis, infarct size, the level of consciousness and hyperglycemia is well known, but we would like to stress the fact that only a few independent variables are predictive of early death (electroencephalographic and electrocardiographic abnormalities) and poor recovery (infarct size, the severity of limb paresis, electroencephalographic abnormalities). The prognostic value of electroencephalography may express the potential involvement of dynamic non-structural phenomena, such as penumbra ischemica and diaschisis.

Bilateral ophthalmoplegia may be an unusual sign of vertebrobasilar ischemia. We report the cases of two patients (75 and 73 years old), who suddenly developed drowsiness, bilateral ophthalmoplegia with bilateral ptosis and mild right hemiparesis. In both patients, MRI revealed bilateral thalamic and midbrain infarcts, ECG showed the presence of atrial fibrillation and Doppler study of the extracranial and intracranial vertebral arteries found no significant alterations. Ischemia involving the midbrain and thalamic paramedian regions may cause bilateral ophthalmoplegia and consciousness disturbances. In these two cases, the most plausible etiologic mechanism was cardiac embolism, and the prognosis for bilateral ocular palsy was poor.

Right-to-left shunt due to patent foramen ovale is a well-established risk factor for stroke in the young. The magnitude of shunt seems to be correlated to the risk of stroke in individuals. We report the cases of two 51-year-old identical twins, with similar risk factors for ischemic stroke, in which the sibling with a large and permanent shunt suffered a left hemispheric stroke and the other, with a small and latent shunt, was asymptomatic. In a three-year follow-up, the siblings were both asymptomatic, and the dimensions of shunts were unchanged. Our cases stress the importance of quantifying right-to-left shunt in order to stratify the risk of stroke in individuals, and suggest a role of heredity in patency of foramen ovale.

Currently, i.v. thrombolysis with recombinant tissue plasminogen activator (r-TPA) in acute ischemic stroke is approved in Europe only for patients 80 y.o. or younger, but data from the literature do suggest that patients older than 80 might also benefit from it (Sanossian and Ovbiagele, 2009). These older patients do have a worse outcome than younger ones, a finding that seems to be due to worse baseline prognostic factors, but they are not more prone to r-TPA -induced haemorrhage than younger ones (Engelter et al., 2006; Toni et al., 2008). Based on these considerations, a randomized clinical trial of i.v. r-TPA vs. usual care in acute stroke in patients older than 80 years is currently under way in Italy.

Background and Purposes: In a case-control study in patients with acute ischemic stroke and extracranial internal carotid artery (eICA) occlusion, thrombolytic treatment was associated with increased mortality. The aim of this cohort study was to assess the efficacy and safety of thrombolysis in patients with eICA occlusion compared to those without eICA occlusion. Methods: Consecutive patients treated with intravenous tissue-type plasminogen activator within 4.5 h from symptom onset included in the Safe Implementation of Thrombolysis in Stroke – International Stroke Thrombolysis Registry (SITS-ISTR) in 20 Italian centres were analyzed. Acute carotid occlusion was diagnosed using ultrasound examination, angio-CT scan or angio-MRI. Since the SITS-ISTR database did not plan to report the site of vessel occlusion, each participating center provided the code of the patient with eICA occlusion. Patients were divided into 2 groups, those with and those without eICA occlusion. Main outcome measures were: death, disability (modified Rankin Scale, mRS, 3–6) and any intracranial bleeding at 3 months. Multiple logistic regression analysis was performed to reveal predictors for main outcomes. The following variables of interest were included in the analysis: presence of eICA occlusion, age, gender, diabetes mellitus, hyperlipidemia, atrial fibrillation, congestive heart failure, previous stroke, current smoking, antiplatelet treatment at stroke onset, baseline NIHSS score, baseline blood glucose, cholesterol and blood pressure, history of hypertension and stroke onset to treatment time. Results: A total of 1,761 patients without eICA occlusion and 137 with eICA occlusion were included in the study. At 3 months, 42 patients were lost to follow-up (3 with eICA occlusion). Death occurred in 30 (22.4%) patients with eICA occlusion and in 175 (10.2%) patients without (p < 0.0001). Death or disability at 3 months occurred in 91 of 134 patients with eICA occlusion (67.9%) compared with 654 of 1,722 patients without eICA occlusion (37.9%, p < 0.0001). No or minimal disability at 3 months (mRS 0–1) was reported in 25 (18.7%) patients with eICA occlusion and in 829 (48.2%) patients without (p < 0.0001). Any intracranial bleeding detected by CT or MRI at posttreatment imaging was seen in 16 (11.7%) patients with eICA occlusion and in 314 (17.8%) of those without (p = 0.09). The proportion of symptomatic intracerebral hemorrhage was 5.8% for patients with eICA occlusion and 8.0% for patients without (p = 0.16). At logistic regression analysis, eICA occlusion was associated with mortality (odds ratio, OR 5.7; 95% confidence interval, CI 2.9–11.1) and mortality or disability (OR 5.0; 95% CI 2.9–8.7) at 90 days. Conclusions: This cohort study in patients with acute ischemic stroke treated with thrombolysis showed an association between eICA occlusion and adverse outcome.

Carotid endarterectomy (CE) has recently been proved to be beneficial in symptomatic patients with severe (70-99%) appropriate carotid stenosis. After discussing the historical evolution of CE as a possible preventive treatment of ischemic stroke, we review the results of North American and European trials in order to give practical information for the management of cerebrovascular patients.

A long-term follow-up study was performed on patients with transient global amnesia (TGA) in order to evaluate the prognosis, the recurrence rate and the occurrence of stroke and dementia. 102 patients (57 women, 45 men; mean age 62.8 +/- 9.4 years) were prospectively included and followed up. The follow-up duration ranged between 12 and 241 months with an average value of 82.2 +/- 51.1 (mean +/- SD). The death rate showed no difference from that of sex- and age-matched subjects. TGA recurred in 19 cases (18.63%). Only 4 patients suffered subsequent stroke, and only 3 showed intellectual deterioration. TGA prognosis was shown to be better than that of RIA and lacunar patients.

Migraine with aura (MA) is associated with the persistence of patent foramen ovale (PFO) in about 50% of cases, and migraineurs tend to have larger shunts than controls, suggesting that right-to-left shunt (RILES) determined by PFO could play a role in triggering migraine attacks. Moreover, some preliminary reports have suggested that PFO closure may give relief to both migraine and aura attacks. The aim of this study was to clarify if shunt-associated migraine (SAM) has clinical features that allow a distinction from shunt-unrelated migraine (SUM), in a prospective, multicentre, observational study (SAM study). We enrolled consecutive MA patients, who underwent a structured, standardized questionnaire for family and personal history and for detailed migraine features. All were systematically screened for RILES with transcranial Doppler, and for coagulation disorders. Overall, 460 patients were included; the SUM and SAM classes comprised 58% and 42% of patients, respectively. SAM patients were significantly younger (34.1 ± 10 vs. 37.1 ± 11 years), had a more frequent family history of migraine (76% vs. 66%) and a higher frequency of sensory symptoms of aura (51% vs. 41%); by contrast, there was a lesser association of SAM with other cardiac abnormalities and with coagulation disorders. The SAM study suggests that the effect of RILES on migraine features is not relevant. The higher family history of migraine in SAM suggests a possible genetic linkage between migraine and RILES.

Subjects with migraine with aura (MA) have a high prevalence of white matter lesions (WMLs) on magnetic resonance imaging (MRI). Moreover, right-to-left shunt (RILES), mainly due to patent foramen ovale, is frequently associated with MA. The aim of this study was to clarify the relationship between RILES and WML in MA. We enrolled 87 consecutive subjects affected by MA. Patients were screened for migraine characteristics and cerebrovascular risk factors. Transcranial Doppler was used to diagnose RILES and MRI with T2-weighted and diffusion-weighted imaging (DWI) to evaluate presence, number and volume of WMLs. RILES was present in 45% of patients. We did not detect any DWI hyperintense lesion; WMLs were present in 61% of patients on T2-weighted images. Presence of WMLs did not correlate with any migraine clinical feature, whereas the presence, number and volume of WMLs increased with subjects' age. There was no significant difference in the total volume and number of WMLs in the group with and without RILES. In conclusion, RILES does not increase the likelihood of finding WMLs in migraineurs.

61 of 1,590 (3.8%) patients with cerebrovascular disease showed suprabulbar palsy of the pure form (42 patients; 2 had autopsy) and striate form (19 patients; 3 had autopsy). 25 patients with the pallidopyramidal syndrome were included since the clinical picture bordered on the striate form. The pure variety was characterized by dysarthria, dysphagia and automatic voluntary dissociation of facial movements. Half of the patients also had hemiparesis, primitive reflexes and short-step gait. In the striate form, the main signs were dysarthria, dysphagia, automatic voluntary dissociation, rigidity and hypokinesia. Brisk tendon reflexes, primitive reflexes, short-step gait and mental deterioration were also present in half of the patients. The pure variety was caused by multiple infarcts and/or lacunae (85.7%), while the striate form had vascular lesions by computed tomography in only 36.8% of the cases. Histological findings, showing lipohyalinosis of the arterial wall leading to stenosis and occlusion of the lumen and tissue rarefaction and disintegration, support the assumption that microinfarctions, sometimes found only by histopathological examination, are the leading pathogenetic factor in this form. Hypertension, cardiopathy, smoking habit, dyslipemia and diabetes are the most frequent risk factors in both forms.

Ferrero S, Pretta S, Bertoldi S, Anserini P, Remorgida V, Del Sette M, Gandolfo C, Ragni N. Increased frequency of migraine among women with endometriosis Human Reproduction 2004;19,:2927-2932. BACKGROUND: Our aim is to assess the prevalence and characteristics of headache in patients with endometriosis compared with women without this disease. METHODS: One hundred and thirty-three women with histologically proven endometriosis and 166 controls were interviewed by a neurologist experienced in headache diagnosis; the headache disorders were classified according to the 1988 International Headache Society criteria. RESULTS: The prevalence of migraine was significantly higher among women with endometriosis [n 5 51, 38.3%; 95% confidence interval (CI) 30.1-47.2%] than in controls (n 5 25, 15.1%; 95% CI 10.0-21.4%) (P < 0.001). Migraine with aura was observed in 18 women with endometriosis (13.5%) and in two controls (1.2%; P < 0.001). The age at migraine onset was significantly lower in women with endometriosis than in controls (16.4 versus 21.9 years; P 5 0.001). No significant difference was observed in pain intensity and attack frequency between the two groups; a trend for women with endometriosis to have longer unmedicated attacks was observed. No significant correlation was observed between attack frequency, unmedicated headache duration, migraine intensity and the severity of endometriosis. CONCLUSION: Migraine is more frequent in women with endometriosis than in controls, although its presence and characteristics are not related to the severity of endometriosis.

Increased urine albumin excretion is associated with an unfavourable cardiovascular risk profile and prognosis in primary hypertension, even though its pathogenesis is currently unknown. Microalbuminuria (Mi) has been proposed as an integrated marker to identify patients with subclinical organ damage, but its routine use is still too often neglected in clinical practice. The aim of our study was to evaluate the relationship between urinary albumin excretion and early signs of subclinical target organ damage (TOD), namely left ventricular hypertrophy and carotid atherosclerosis in a large group of non diabetic hypertensive patients. A group of 346 never treated patients with primary hypertension (212 men, 134 women, mean age 47 +/- 9 years) referred to our clinic were included in the study. They underwent the following procedures: (1) family and personal medical history and physical examination; (2) clinical blood pressure measurement; (3) routine blood chemistry and urine analysis including determination of urinary albumin excretion (ACR); (4) electrocardiogram; (5) ultrasound evaluation of left ventricular mass (LVMI) and carotid artery thickness (IMT). The overall prevalence of Mi, left ventricular hypertrophy, and carotid plaque was 13, 51, and 24% respectively. Mi was significantly correlated with LVMI (P < 0.0001), IMT (P < 0.0001) and several metabolic and non-metabolic risk factors (blood pressure, body mass index, serum lipids). Cluster analysis identified three subgroups of patients who differ significantly with regards to TOD and albuminuria (P < or = 0.001 for each of the examined variables). Patients with higher IMT and LVMI values also showed increased ACR levels. Furthermore, patients with microalbuminuria were more likely to have both LVH and IMT values above the median for the study population (OR 21, C.I. 4.6-99.97, P < 0.0001). Mi is an integrated marker of subclinical organ damage in patients with primary hypertension. Evaluation of urinary albumin excretion is a specific, cost-effective way to identify patients at higher risk for whom additional preventive and therapeutic measures are advisable.

Preventing subclinical organ damage is currently a major issue in the management of patients with essential hypertension. Antihypertensive drugs which act through different pathophysiological mechanisms might confer specific target organ protection beyond what is already provided by their blood pressure lowering effect.Thirty-one patients with essential hypertension were randomized to receive long-term treatment with either a calcium channel blocker (nifedipine GITS, 90 mg/day) or an ACE-inhibitor (lisinopril, 20 mg/day). Blood pressure, left ventricular mass, carotid wall thickness and timed urinary albumin excretion were measured at baseline and over the course of 24 months of treatment.Both regimens significantly lowered mean blood pressure over the 24 months (from 124+/-2 to 103+/-2 mmHg in the lisinopril group and from 122+/-2 to 104+/-1 in the nifedipine group). Overall, end-organ damage improved with persistent blood pressure control. However, the two treatments had different specific effects. Lisinopril induced a more pronounced reduction of the left ventricular mass index (from 56+/-3 to 52+/-2 g/m2.7, P0.05) and urinary albumin excretion (from 34+/-15 to 9+/-2 microg/min, P0.01), while nifedipine achieved a greater reduction of carotid intima plus media thickness (from 0.8+/-0.06 to 0.6+/-0.06 mm, P0.01).Blood pressure control does help reduce the severity of organ damage in patients with essential hypertension. Different antihypertensive treatments may confer additional specific cardiorenal and vascular protection regardless of blood pressure control. These data could be useful when devising individualized therapeutic strategies in high-risk hypertensive patients.

Endothelin-1 (ET-1) is a potent and long-acting vasoconstrictor peptide, which may play a role in the pathophysiology of a number of diseases. Controversial data exist on its role in human ischemic stroke. In order to ascertain whether changes in ET-1 plasma levels occur in ischemic stroke, plasma ET-1 levels and mean arterial pressure were determined in 15 patients at their first ischemic cerebral infarction and in 15 control subjects, over a 24-hour period. In stroke patients, mean 24-hour plasma ET-1 levels (4.9+/-0.5 ng/L) were higher (P< 0.05) than in control subjects (3.2+/-0.3 ng/L), and correlated with the mean size of the lesion, but not with the severity score of the neurological deficit. These results support the hypothesis that ET-1 levels reflect an indicator function for the amount of damaged cerebral tissue rather than a pathophysiological role.

Cerebral vasomotor reserve (VMR) is the capability of cerebral arterioles to change their diameter in response to various stimuli, such hypercapnia. tDCS effects on cerebral haemodynamic have been poorly studied. Twenty-five healthy subjects (6M and 19F; 21–50 years; mean ± 26,43) underwent anodal/cathodal and sham tDCS on right primary motor area. Before and after tDCS, we assessed VMR by Transcranial Doppler measuring Breath Holding Index (BHI: percentage increase in flow velocity (PIV) weighted by the time the breath is held-30 s-). We also assessed Heart Rate Variability (HRV), the dynamic changes of the interval between consecutive heart beats, in particular after Valsalva manouver, such a sympathetic nervous system (SNS) activation index. A-tDCS decreased both VMR, BHI and HRV ( p p p > 0.05). tDCS modify both VMR and HRV. HRV changes suggest that VMR modulation could be mediated by SNS. Shame stimulation without any changes of the parameters would confirm our hypothesis. Further studies are needed to confirm these hypothesis, in order to modulate VMR.

Temporal hyperostosis is the major limitation of transtemporal insonation of the basal cerebral arteries in transcranial Doppler sonography. New contrast agents capable of traversing the pulmonary bed offer new prospects for overcoming this limitation. Echocontrast agents improve the diagnostic potentiality of ultrasound techniques, increasing the diagnostic accuracy of these methods in cerebrovascular diseases, vascular malformations, venous pathologies and tumors, and may contribute to reducing the need for more invasive and expensive examinations.

Among subcortical infarctions, internal borderzone infarcts (IBI) are considered to be separate entities from perforating artery infarcts (PAI). The purpose of the present study is to examine the relationship between the presence of IBI and the degree of angiographically defined internal carotid artery (ICA) stenosis in symptomatic patients.A review of 1253 brain CTs from patients recruited by the North American Symptomatic Carotid Endarterectomy Trial was performed, using templates for the identification of subcortical and cortical vascular territories.A total of 413 patients had visible ischemic lesions on the side ipsilateral to their symptomatic ICA. Of these, 138 had PAI, 108 had IBI, 122 had cortical infarcts, and 45 had a combination of different lesions. Mean (+/-SD) lesion diameter was larger for IBI (11.0+/-5.9 mm) than for PAI (7.1+/-4.7 mm) (P0.001 for comparing 2 means). IBI was associated with higher degrees of ICA stenosis (P0. 001). Sixty-three percent of the patients with IBI had severe (70% to 99%) ICA stenosis compared with 42% of patients with PAI; 18% of the IBI patients had stenosis of 90% or more compared with 8% of the patients with PAI. Multiple logistic regression did not identify any patient characteristics as confounders.Among subcortical infarctions, IBI are associated with higher degrees of ICA stenosis in symptomatic patients. Differentiating between internal borderzone and perforating artery infarcts is important, because each may arise from different mechanisms, namely, carotid disease and small-vessel disease, respectively.

Transcranial Doppler detection of microembolic signals has been described in several clinical conditions such as carotid stenosis, prosthetic heart valves, acute stroke, and carotid surgery. The importance of these events for clinical decision-making is still a matter of debate. The authors review the literature and report their personal experience on the clinical significance of microemboli detection.

Microalbuminuria (Mi) is thought to reflect diffuse vascular damage and to predict cardiovascular morbidity and mortality in essential hypertension, although its pathogenesis remains to be fully elucidated. The relationship between microalbuminuria and several cardiovascular risk factors and target organ damage was evaluated in a large cohort of untreated essential hypertensive patients. Albuminuria was measured as the albumin to creatinine ratio in three non consecutive first morning urine samples. Cardiac damage was evaluated by ECG and retinal vascular changes by direct ophtalmoscopy. In a subgroup of 23 patients with Mi and in a control group of 22 normoalbuminurics, selected from the entire cohort of patients and carefully matched for age, gender, body mass index (BMI) and duration of disease, we also measured left ventricular mass index by M-B mode echocardiography, common carotid wall thickness by high resolution US-scan, and renal vascular resistances by US-doppler of interlobar arteries. K-means cluster analysis performed on the entire cohort of patients showed that microalbuminuria is associated with the presence of an unfavorable risk profile and target organ damage. Furthermore, microalbuminuric hypertensive patients have a larger left ventricular mass index, increased intima media thickness of carotid arteries and higher intrarenal vascular resistances as compared to a well matched group of normoalbuminuric patients. We conclude that in essential hypertension increased urinary albumin excretion can be useful to identify patients for whom more aggressive preventive strategies and/or additional treatment measures are advisable.

Microembolic signals (MES) have been described in patients with different types of prosthetic valves. The aim of our study was to compare prevalence of MES in patients with mono-leaflet and bi-leaflet valves, and to correlate them with different clinical and echocardiographic parameters. We evaluated 42 patients, 15 with mono-leaflet and 27 with bi-leaflet valves, with 30-minute bilateral simultaneous transcranial Doppler monitoring for the identification of MES. All patients performed blood testing for international normalized ratio (INR), color-coded duplex of supra-aortic vessels, and echocardiography. Eighteen patients (43%) showed MES; 61% of MES were detected bilaterally, 17% only on the left and 22% only on the right middle cerebral artery (MCA), with no interhemispheric difference. MES did not correlate with patient's age, echocardiographic parameters, INR, presence of atrial fibrillation, or site of valve replacement. One (7%) of the 15 patients with mono-leaflet valves had MES, as opposed to 17 (63%) of the 27 with bi-leaflet valves (p=0.0003). Patients with bileaflet valves and MES had valves of older implantation and, only for aortic valves, larger valve size.

Abnormalities of hypothalamo-pituitary-adrenocortical axis function have been observed frequently in stroke patients. The aim of this study was to investigate plasma beta-endorphin and cortisol 24-hour secretory patterns in patients early after stroke and in the convalescent period to evaluate a possible influence of brain damage on hormonal circadian pattern. Patients (n = 15; age, 46 to 75 years) were evaluated in the first 24 hours and 10 days after hospital admission for ischemic cerebral stroke and compared with 15 age- and sex-matched normal subjects. Blood samples for beta-endorphin and cortisol determination were drawn every 4 hours from 8 AM to 8 PM and every 2 hours from midnight to 6 AM. Mean 24-hour beta-endorphin and cortisol levels, recorded in the acute phase, were significantly (P < .05) higher than those recorded in normal subjects; circadian rhythm was not demonstrable for either hormone. In the convalescent period, plasma cortisol 24-hour mean values and circadian rhythm returned to the normal range, whereas the plasma beta-endorphin 24-hour mean values and circadian rhythm did not. Cerebral stroke induces abnormalities of beta-endorphin and cortisol circadian secretion. Whereas cortisol abnormalities are transient, those of beta-endorphin last longer. The dissociation between beta-endorphin and cortisol 24-hour secretory patterns might potentially serve as a marker of psychoneurological abnormalities occurring after stroke.