In recent years, the increasing number of patients with upper limb musculoskeletal disorders seeking timely, intensive, prolonged and task oriented hospital- and home- based physical rehabilitation, and the decreasing numbers of trained therapist to provide the needed care, have left a palpable gab. These have resulted in several preventable deformities with associated complications leading to social and economic burdens. Although the introduction of some robotic devices has addressed some of these concerns, the shortfalls from the use of these devices limit their effectiveness. The newly introduced hand rehabilitation board (Dominic’s Board) was prospectively evaluated in 82 patients with ULMDs of different etiologies to assess its therapeutic efficacy in rehabilitation of ULMDs. Additive, but complementary effect was observed when used along with conventional hospital-based therapy and at home, suggesting the effectiveness of this device in preventing or ameliorating the complications associated with ULMDs.

Post cardiac surgery stroke is a devastating complication with an incidence as high as 50%1. The association between intra-operative mean arterial blood pressure (MAP- better called linear blood pressure) during cardiopulmonary bypass (CPB) and the development of postoperative stroke-as diagnosed by neuroimaging- and of cognitive dysfunction (POCD) is controversial. This is due to differences in the study populations, stroke assessment tools, operation and conduction of MAPs, variations in neurocognitive testing and duration of follow up. As a result there is a gap in the knowledge on an ideal MAP as a preventive measure of post CPB stroke and POCD.

A key platform underpinning the traditional understanding of the cardiovascular system, with respect to the behavior of large arterial vessels, is Otto Frank’s Windkessel Hypothesis [1]. This hypothesis posits simply that the smooth muscle walls of large arteries do not undergo rhythmic contractions in synchrony with the heartbeat but, rather, behave as passive elastic tubes undergoing distension from pulsatile pressure waves. The Windkessel Hypothesis is elegant, well described for over a century, ingrained in the understanding of cardiovascular medicine and physiology, and simply wrong. Several groups have now shown that the arterial smooth muscle wall undergoes rhythmic activation in synchrony with the heartbeat in a variety of tissues, including human brachial artery; canine coronary, femoral, and carotid arteries; rabbit aorta; feline pulmonary artery and rodent aorta [2-8]. The phasing of these events is such that the upstroke of the contraction slightly precedes the upstroke of the pulse wave, suggesting nomenclature for the events as pulse synchronized contractions, or PSCs [3,6-8]. PSCs have been found to be of neurogenic origin, sensitive to the neural blocker tetrodotoxin [3,8]. Although the specific neural pathways regulating PSCs have not been elucidated, the alpha-adrenergic system is at least partially involved, as evidenced by reduction or blockade of PSCs by the alpha-adrenergic blocker phentolamine [8]. Further, PSCs have not been observed following vessel excision in in vitro studies, as an intact nervous system is not present. The pacemaker for the PSC resides in the right atrium, as suggested by two lines of evidence. First, pacing of the right atrial region to faster than spontaneous frequencies leads to a one-to-one correspondence of PSC frequency with the stimulation rate [3]. Additionally, excision of the right, but not the left, atrial appendage results in elimination of PSCs [3]. As the pacemaker region for PSCs and the heartbeat both lie in the right atrium, this may potentially allow for coordination between the heartbeat and pulse wave with PSCs [3,5,8]. Extensive evaluations also have been performed showing the PSC was not an artifact produced either by cardiac contractility or from the vessel distension from the pulse wave [3,5,6].

Objectives: Cardioembolic etiology is a frequent source of ischemic stroke. Echocardiogram is the mainstay of cardioembolic source detection with regard to plan secondary stroke management, however it remains unclear how often clinically actionable findings are provided hereby. In addition, it is uncertain whether echocardiography should be performed transthoracic or transesophageal (TEE). In a monocenter study, we evaluated the frequency of pathological findings from TEE evaluation in patients with ischemic stroke with suspected cardioembolic and cryptogenic source and determined whether there was an associated adjustment in the prescribed administration of antithrombotic therapy. Materials and Methods: Over a 21-month period (2012-2013), we enrolled 143 patients in a prospective monocenter study (mean age ± standard deviation, 70 ± 12 years; females, 44.1%) who were admitted to the Department of Neurology at the University of Lübeck due to ischemic stroke and who underwent TEE due to supposed cardiac embolism. We assessed the presence of atrial fibrillation; days from admission to TEE; and TEE findings, including atrial septal aneurysm, thrombogenic aortic arch, valve failure, presence of left atrial thrombus, and patent foramen ovale. Demografic information and medical history were drawn from patient records and the hospital information system. Results: On average, TEE was performed 4 days after admission to the hospital. Left atrial thrombus was detected in 3 patients (2.1%), patent foramen ovale (PFO) in 27 (18.9%), atrial septum aneurysm in 17 (11.9%), and thrombogenic aortic arch in 29 (20.3%). Findings from TEE were commonly associated with therapeutic adjustment; antiplatelet therapy increased from 30.1% to 80.4%, oral anticoagulation therapy increased from 2.8% to 27.3%. Conclusion: Findings from TEE for the evaluation of ischemic stroke lead to frequent adjustment of prior antithrombotic therapy, antiplatelet as well as anticoagulation.

Purpose: This was a prospective study conducted at Benha University hospital and National Heart Institute on one hundred patients undwent coronary artery bypass grafting (CABG) to evaluate the effect of CABG on the right ventricular (RV) function using speckle tracking echocardiography (STE). Methods: All cases were subjected to detailed medical history, full physical examination, 12 leads electrocardiogram (ECG), routine laboratory tests including (complete blood picture, liver functions, renal functions and lipid profile) and echocardiography either conventional echocardiography or STE, all parameters obtained before and within 2 weeks after surgery. Results: By conventional echocardiography there was statistically significant decrease in peak right ventricle systolic velociy (RVS) from (12.76 ± 1.72) to (7.33 ± 1.71) and tricuspid annular plane systolic excursion (TAPSE) from (22.8 ± 3.99) to (13.77 ± 4.63) among the studied patients after CABG. While there was significant increase in right ventricle fractional area change (RVFAC) from (44.69 ± 3.25) to (49.01 ± 3.36). On the other hand, there was non-significant change in right ventricle end diastolic diameter (RVEDD) at mid-cavity from (26.37 ± 2.72) to (26.53 ± 2.72) and basal segment from (36.05 ± 2.98) to (36.29 ± 3.04), right ventricle stroke volume (RVSV) from (65.44 ± 7.02) to (65.85 ± 6.86) and right myocardial performance index (RMPI) from (0.491 ± 0.088) to (0.498 ± 0.086). By STE There was statistically significant decrease in right ventricle global longitudinal strain (RVGLS) from (-20.63 to -14.1) after CABG. There was statistically significant decrease in right ventricle free wall longitudinal strain [apical decreased from (-23.73 to -13.7), mid-cavity decreased from (-25.76 to -11.53), basal decreased from (-20.39 to -10.13) and lateral wall declined from (-23.01 to -9.13)]. There was statistically significant decrease in interventricular septum longitudinal strain [apical decreased from (-19.77 to -10.06), mid-cavity decreased from (-17.81 to -10.87) and basal decreased from (-15.89 to -11.13)]. There was statistically significant increase in RV circumferential strain of lateral free wall from (-12.04 to -16.21), while there was non-significant change in RV circumferential strain of septum from (-19.77 ± 4.86) to (-20.37 ± 5.14). Conclusion: Distorted RV geometry after CABG can lead to altered deformation parameters, in other words longitudinal functional parameters may underestimate RV function and the decrease in RVGLS was compensated by increase in circumferential strain of lateral free wall of RV without change in RVSV or RMPI. Therefor changes in deformation parameters should always be interpreted in relation to change in geometry.

Atherosclerosis is an important promoter of cardiovascular disease potentiating myocardial infarction or stroke. Current demand in biomedical imaging necessitates noninvasive characterization of arterial changes responsible for transition of stable plaque into rupture-prone vulnerable plaque. in vivo contrast enhanced magnetic resonance (MR) imaging (MRI) allows quantitative and functional monitoring of pathomorphological changes through signal differences induced by the contrast agent uptake in the diseased vessel wall, therefore it is the ideal modality toward this goal. However, studies have so far focused on the cellular targets of persisting inflammation, leaving extracellular matrix (ECM) far behind. In this review, we portray ECM remodeling during atherosclerotic plaque progression by summarizing the state of the-art in MRI and current imaging targets. Finally, we aim to discuss glycosaminoglycans (GAGs) and their functional interactions, which might offer potential toward development of novel imaging probes for in vivo contrast-enhanced MRI of atherosclerosis.

Ventricular assist device is a portable machine which is also called an artificial heart for the patients who have terminal heart failure. The device maintains the heart’s vital functions until the suitable donor is found for the heart transplantation. It can be applied to either ventricles or both (biventricular). Although the device provides independence for the patient, it also has life-threatening complications. Such as infection, stroke secondary to thromboembolism, hemorrhage depending on anticoagulant use, right heart failure… and most of the time it is really hard to manage those complications. We will present a case, who had ischemic stroke as a complication of VAD even though he has been using aspirin, warfarin and had effective INR value.

Objective: Plaque morphology plays an important prognostic role in the occurrence of cerebrovascular events. Echolucent and heterogeneous plaques, in particular, carry an increased risk of subsequent stroke. Depending on the quality of the plaque echogenicity based on B-mode ultrasound examination, carotid plaques divide into a soft lipid-rich plaque and a hard plaque with calcification. The aim of this study was to investigate structural changes in the basement membrane of different carotid artery plaque types. Patients and methods: Biopsies were taken from 10 male patients (average age; 75 + 1 years) and 7 females (68 + 3 years). The study population included patients suffering from a filiform stenosis of the carotid artery, 8 patients with acute cerebrovascular events and 9 with asymptomatic stenosis. Scanning electron and polarised light microscopic investigations were carried out on explanted plaques to determine the morphology of calcified areas in vascular lesions. Results: By means of scanning electron microscopy, multiple foci of local calcification were identified. The endothelial layer was partially desquamated from the basement membrane and showed island-like formations. Polarised light microscopy allows us to distinguish between soft plaques with transparent structure and hard plaques with woven bone formation. Conclusion: The major finding of our study is the presence of woven bone tissue in hard plaques of carotid arteries, which may result from pathological strains or mechanical overloading of the collagen fibers. These data suggest a certain parallel with sclerosis of human aortic valves due to their similar morphological characteristics.

Seizure is clinical manifestation of sudden disruption of the normal electrical activity of cortical neurons. The brain electrical activity is periodically disturbed, alteration in neural cell integrity, increase in firing impulses and spread to adjacent normal neurons result in temporary brain dysfunction with alterations in consciousness, behavior or motor function. It may be triggered by illness, infection, stress, stroke, brain tumor, or the underlying cause may not completely understand. Status epilepticus (SE) is a medical emergency and requires prompt diagnosis and treatment. Treatment includes general support measures, drugs to suppress epileptic activity and relieving the underlying condition. Refractory SE requires admission to an intensive care unit (ICU) to allow adequate monitoring and support of respiratory, metabolic and hemodynamic functions and cerebral electrical activity. For SE treatment, benzodiazepines are the first line antiepileptic agents, and if benzodiazepines fail to control seizures, Phenytoin is usually indicated; Phenobarbital or Valproate may also be considered. For refractory SE, Propofol and Thiopental represent first line agents after careful assessment of potential risks. In refractory SE, general anesthesia may be required. There is currently no unique consensus for definite treatment option of RSE. In this review, the management protocol of seizure, assessment, monitoring, and different alternative therapy would be discussed.

We report a case of 79-year-old man who presented to our emergency department (ED) for lipothymia. The patient developed significant bradycardia with hypotension. His EKG objectified a slow atrial fibrillation .the patient rapidly installed a coma. A non-contrast CT brain scan showed a bilateral vertebrobasilar ischemic stroke. 

Introduction: Hypertensive crisis (HC) is recognized consequence of inadequate blood pressure (BP) control. A hypertensive crisis is further divided into hypertensive emergency (HT-E) and hypertensive urgency (HT-U). Method: Using a cross-sectional hospital-based study design, patients who had been diagnosed as having HC between January and October 2017 were consecutively recruited in the study. The criteria proposed by the Seventh Joint National Committee were used for the definition of HC. Result: A total of 81 (.81%) patients newly diagnosed as having HC were enrolled in the study. Of these patients, 50 (61.7 %) patients met criteria for HT-E, while 31 (38.3%) patients had HT-U. Renal impairment (16%), stroke (30.8%), acute coronary syndrome (13.6%) and heart failure (22.2%) were predominant complications associated with HT-E. Out of 81 study subjects, 13 (16%) patients died. Although there was no significant difference in residence, history of smoking, Diabetes mellitus and history of alcohol consumption between groups, old age (P=.o22), male gender(.046), history of hypertension(.007), history of non-governmental employee(.003), poor compliance (p=.002) and high case fatality rate (p=.041) were significantly associated with hypertensive emergency (HT-E). Conclusion: This study showed that HT-E has high case fatality rate among patients admitted with hypertensive crisis at kassala teaching Hospital. Therefore early detection of hypertension and appropriate management are the main stay for reducing morbidity and mortality among patients with hypertensive crisis.

Stroke following coronary interventions is a devastating and most dreaded complication with signiβicant morbidity and mortality. Various factors have been ascribed for this complication including the technical errors [1]. A small percentage of strokes are iatrogenic, including those associated with invasive cardiac procedures. According to the literature, it is a rare complication of left heart catheterization [2]. Percutaneous coronary intervention is increasingly used to treat patients with diffuse atherosclerosis, acute coronary syndromes and even high-risk patients such as low ejection fraction [1]. The authors describe a patient who underwent percutaneous coronary intervention in the context of inferior infarction, which was complicated by ischemic stroke during cardic catheterization.

Background: In line with the so-called “embodiment concept”, human bodily experience is characterized by the immediate feeling that our body is localized in a certain position in space and that the self is localized within these body limits. Aim: To verify in a cohort of patients affected by unilateral spatial neglect (NSU) secondary to cerebrovascular damage the possible correlation between a comprehensive neuromotor/neuropsychological rehabilitative treatment and the modification of body representation. Setting: A rehabilitation institute for the treatment of neurological gait disorders and neuropsychological failures. Methods: 12 patients (7 males, 5 females; mean age 60 ± 2yy) affected by NSU secondary to cerebral stroke and recovered in the Neurological Rehabilitation Section of the Clinical Institute Città di Brescia were recruited for the aim of this study. In accordance with our inclusion criteria we recruited 4 patients affected by ischemic stroke and 8 patients affected by haemorragic stroke; 9 patients of our study group arrived from a coma state period. Recruited patients underwent at time T0 (hospitalization day) to a functional impairment evaluation (Motricity Index = MI; Trunk Control Test = TCT; Functional Ambulation Category = FAC) and to a neuropsychological evaluation (Behavioural Inattention Test = BIT; Representional drawing; Personal Neglect evaluation scale); each evaluation was repeated in the same way at time T1 (intertime between 2 and 4 months after hospitalization) and time T2 (inter time between 5 and 6 months after hospitalization). At time T0 each patient began an individualized integrated (motor and neuropsychological) rehabilitative treatment course. Results: In all patients recruited a statistical significant modification was observed for the MI LL left, the TCT and the FAC; no significant statistical modification was observed for the MI UL left, the MI UL and the MI LL right. The t-test showed a significant statistical modification of the personal neglect evaluation scale while no significant statistical modification was defined for the spontaneous human figure drawing test proceeding from time T0 to time T1. The spontaneous drawing of the human figure showed an individual different trend and modification in all patients recruited. A correlation analysis was made comparing the mean value of all motor scales (G1) with the mean value of all neuropsychological scales (G2) and no statistical significant correlation was observed between G1 (T0) and G1 (T1), G1 (T0) and G2 (T0), G1 (T0) and G2 (T1), G2 (T0) and G1 (T1), G2 (T0) and G2 (T1), G1 (T1) and G2 (T1). A second correlation analysis was made comparing all single motor scales with the neuropsychological scales, for the group made by 12 patients and the group made by 5 patients. For the group made by 12 patients, we observed the subsequently significant correlations: MI UL left (T0) correlates with MI LL left (T0); MI LL left (T0) correlates with MI LL left (T1); MI UL left (T1) correlates with MI LL left (T1); MI LL left (T1) correlates with FAC (T1); TCT (T1) correlates with FAC (T1). For the group made by 5 patients, we observed the subsequently significant correlation: TCT (T2) correlates with FAC (T2). In the group made by 12 patients, the mean amelioration of the time related normalized (T0-T1) motor scales is equal to 49% while to 63% was observed for the neuropsychological scales. The mean amelioration of the neuropsychological scale proceeding from time T0 to T1 is equal to 26% with an increase equal to 57% proceeding from time T1 to T2. The neurocognitive amelioration can be observed especially between the 5th and 6th month from the ischemic cerebral damage with a mean increase from 26% to 57%. Conclusions: It would certainly make sense to treat patients with NSU from the neuropsychological point of view in the long term and from the neuro-motor point of view in the first 3-4 months after stroke; in all this, we cannot exclude that an improvement of the visuo-spatial exploration, emphasized by the neuropsychological treatment, can positively influence also patient’s motor outcome.

The normal levels of thyroid hormones (THs; thyroxine, T4 & 3,5,3′-triiodo-L-thyronine, T3) are necessary for the normal development [1-48], particularly the fetal and neonatal cardiac growth and development [49]. The actions of THs are facilitated genomically by thyroid receptors (TRs, α and β) and non-genomically at the plasma membrane, in the cytoplasm and in cellular organelles [4,49-55], by stimulation of Na+, K+, Ca2+ and glucose transport, activation of protein kinase C (PKC), protein kinase A (PKA) and mitogen activated and protein kinase (ERK/MAPK) [4]. In addition, the transport of T4 and T3 in and out of cells is controlled by several classes of transmembrane TH-transporters (THTs) [56], including members of the organic anion transporter family (OATP), L-type amino acid transporters (LATs), Na+/Taurocholate cotransporting polypeptide (NTCP), and monocarboxylate transporters (MCTs) [4,49,57,58]. Adding additional complexity, the metabolism of T4 and T3 is regulated by 3 selenoenzyme iodothyronine deiodinases (Ds: D1, D2 and D3) [59-61]. On the other hand, the congenital hypothyroidism can cause the following [49,62-64], (1) congenital heart diseases; (2) diastolic hypertension; (3) reduced cardiac output, stroke volume and a narrow pulse pressure; (4) dilatation and overt heart failure; (5) elevation in the systemic vascular resistance [65-68]. Similarly, the chronic hyperthyroidism can cause the following [49,64]: (1) cardiac hypertrophy; (2) increase in the cardiomyocyte (CM) length rather than width; (3) noticeable diminution in systemic vascular resistance; (4) elevation in the cardiac contractility; (5) systolic hypertension; (6) increase in the cardiac output, venous volume return, blood volume and pulse pressure; and (7) reduction in the systemic vascular resistance [49,69]. T3-therapy can induce DNA synthesis and cardiomyocyte proliferation, and improve the cardiac contractility; though, this action is as still unidentified [49,70-74].

Objective: We evaluated the 30-day outcomes of early (≤ 14 days) or delayed (15 days to three months) carotid revascularization (CR) performed in patients who presented acute brain infarction secondary to internal carotid artery (ICA) stenosis. Methods: We included all patients with a recent cerebral infarction from July 2010 to June 2014 who underwent CR in our center within three months after the onset of symptoms for ICA stenosis. Data were retrospectively collected. Two groups were identifi ed: Group A included patients who underwent early CR within the first fourteen days after symptom onset, and Group B, patients who underwent delayed CR, from the fifteenth day up to the third month after symptom onset. Death, stroke and major adverse cardiac events (MACE) were analyzed. Results: Seventy-one patients underwent CR (73.2% men, with a median age of 71). Nineteen patients underwent early CR and 52 underwent delayed CR. The mean interval from initial examination to surgery was 9.5 days (range, 3-14 days) in Group A and 42 days (range, 15-92 days) in Group B. No complication occurred in Group A within the 30 postoperative days. In Group B, no MACE or death was observed and two patients presented with post-operative stroke (3.8%). Conclusion: This retrospective study confi rmed the satisfactory outcomes of early CR after acute brain infarct. Accurate clinical and radiological selection of patients prevents early neurological complications.

Stroke and neurodegenerative diseases including Alzheimer’s disease (AD) are responsible for a major proportion of mortalities in the elderly. We have previously investigated novel mechanism-based therapies of AEURA in cell culture models against viral infection and in glutamate excitotoxity. In our new studies, we propose that the homeopathic formula AEURA could serve as a potential therapeutic agent for stroke & for AD. In examining AEURA treatment of PC12 cells exposed to glutamate excitotoxicity, hypoxia /re-oxygenation injury and A-Beta toxicity. We demonstrated an increased survival rate in AEURA treated cells by comparison to control cells. In examining the therapeutic potential of AEURA in PC12 cells this homeopathic agent was found to be neuroprotective against either glutamate induced toxicity, hypoxia /re-oxygenation stress or cell stress resulting from viral infection (with either HSV-1 or rhinovirus). Our ongoing studies involve examining the neuroprotective potential AEURA in vivo using rodent models of stroke & AD.

Here we reported an interesting case of an 84-year-old woman with acute onset of paresis of left arm and paresthesia of left face and arm. The symptoms resolved within two hours. She also had a similar prior episode two weeks ago with only left arm paresthesia. Her MRI revealed different stages of lacunar ischemic lesions. Interestingly, the SWAN sequences showed lateralized rather than global multiple microhemorrhages over the right MCA and PCA territory, and the sulcal hyperintensity on FLAIR was also seen with no associated susceptibility effect and minimal enhancement, indicating probable cerebral amyloid angiopathy (CAA) based on Boston Criteria. It has been acknowledged that the CAA could manifest with certain localization preference. Cerebral microinfarct and white matter disease in CAA have been more often observed in the posterior circulation territory, however the restricted lateralization reported in our case has not been seen. Since CAA is often diagnosed when the characteristic MRI findings are picked up incidentally, recognizing this as a potential “TIA mimic” will be important for guiding treatment due to its higher risk of bleeding. In summary, this case highlights that the CAA could present as restricted lateralized lesions and occur as transient neurologic deficits, which to our knowledge has not be reported before. Recognition of it as a potential manifestation of CAA will be valuable in the clinical diagnosis process.

As per report of WHO [1] (World Health Organization), air pollution (ambient/outdoor and household/indoor air pollution) kills an estimated seven million people worldwide every year largely as a result of increased mortality from stroke, heart disease, chronic obstructive pulmonary disease, lung cancer and acute respiratory infections. Data of WHO shows that 9 out of 10 people breathe air containing high levels of pollutants. World Health Organization is working with countries to monitor air pollution and improve air quality. From smog hanging over cities to smoke inside the home, air pollution poses a major threat to health and climate. More than 80% of people living in urban areas and around 91% of the world’s population live in places where air quality levels exceed WHO limits, with developing and under-developed countries suffering from the highest exposures, both indoors and outdoors [1]. While outdoor air pollution comes from the motor vehicles, burning of fossil fuels and other industrialization activities, indoor air pollution is the result of tobacco smoke and burning fuel for cooking & heating. Furniture and construction materials also emit such pollutants. Both outdoor and indoor air pollution are harmful to the human health.

Hypertension and blood pressure are closely related, and hypertension is directly related with stroke. There are different type of blood pressures such as basal, diastolic, maximum, mean arterial, systolic, mean central venous. The present report examines the determinants of systolic blood pressure for two different groups of cardiac patients. One group of cardiac patients is those who underwent dobutamine stress echocardiography, and the other group is Worcester heart attack study. Many systolic blood pressure determinants, their effects, and correlations have been focused in the current report.

In this review After Observing biomedical literature (starting from some heart disease) results that some pathological phenomena are deeply involved in some metabolic endocrine condition: Kinetics and gradients in metabolism, catabolism, time related, toxic like effect, electrical cell membrane status, smooth vascular muscle cell hyper-reactivity, platelet iperactivations, central autonomic control after acute stroke, great electrolytes unbalances et other factors as pro-hypertrophic signaling and oxidative stress. Observing actual current therapy in some metabolic endocrine therapy often is used association of drugs (in example in type II diabetes). In Many other pathologies efficacy drug therapy exist, and often only 1 pharmacological molecule resolve the pathological condition. But in many disease even associating 2-3-4 drugs the % of cure not increase (efficacy, effectiveness). It mean that this drugs strategies are not the really best? Or it mean a low active level? Why for this pathological condition this association drugs in currently use not do the right works as really needed? There is the need for new really efficacy drugs strategy that show a profile of efficacy as requested in order to resolve the pathological condition? Or to be added to the actual therapy? The actual pharmacological strategies in some metabolic endocrine disorder is really the best? Or other strategies can be introduced?