• Contact Us
  • Indexing
  • Submit Manuscript
  • Open Access
  • Journals
  • Home
  • ISSN: 2334-2307
    Early Online
    Volume 4, Issue 2
    Review Article
    Brian Fazzone, Gabrielle Morris, Leigh-Ann Black, Jessica-Ashley Williams, Rodney Leacock, Shannon Sternberg, Dawn Blackhurst, Afred Nelson, and Thomas I. Nathaniel*
    Abstract:
    Background: Many of the exclusiveand inclusivecontraindications for recombinant tissue plasminogen activator (rt-PA) in the treatment of acute ischemic strokeare based on safety. While some contraindications have strongly been supported by both scientific and clinical data, including the clear benefit of rt-PA, there are several clinical controversies about others. We examined clinical characteristics related to rt-PAtreated versus non-treated patients according to specific contraindications in a stroke population.
    Methods: We utilized data from the Greenville Health System (GHS) stroke registry on rt-PA administration between January 2010 and December 2013. We evaluated patients who received rt-PA within 4.5 hours following the onset of acute ischemic stroke symptoms. Our analysis compared the clinical characteristics and demographics of eligible patients receiving rt-PA with those not receiving rt-PA.
    Results: A total of 663 ischemic stroke patients were eligible to receive rt-PA. Out of the 663, 241 received t-PA and 422 did not. A significant (P<0.05) number of patients with acute myocardial infarction in the 3 months prior to stroke,uncontrolledhypertensionwere excluded from rt-PA when compared to the few that received rt-PA. A significant (P<0.05) numberof patients with history of smoking receivedrt-PA when compared to the patient population who did not receive rt-PA. A combination of old age, and baseline NIHSS is important in making a decision about whether to administer rt-PA to patients with a combined prior history of stroke and diabetes mellitus.
    Conclusion: The study provides a basis to generate a hypothesis that could be investigated to allow more eligible patients to be considered for rt-PA for the treatment of acute ischemic stroke.
    Zhen He1*, Li Cui, Sherry A. Ferguson, and Merle G. Paule
    Abstract:
    Epidural steroid injections (ESIs) as minimally invasive procedures have been widely used for the relief of neck, arm, back, and leg pain potentially due to spinal stenosis, spondylolysis, or disc herniation. In rare instances, ESI therapy may cause clinical complications, some of which can be catastrophic. The surgical procedure itself including needle penetration the potential use of contrast media, the injected medications (i.e., conventional steroids), or a combination of these in association with the original cause of the targeted pain which may include local inflammation, may account for such adverse complications. Nevertheless, there is increasing evidence indicating that ischemia and/or hemorrhage (stroke) in the brain and/or spinal cord, following accidental intra - arterial injection of the medication is a primary contributor to the severe neurologic events. Descriptions of experimental intra - arterial injections simulating the noted catastrophic outcomes associated with ESI therapy are very limited in the literature. Identifying and describing the cause of severe ESI complications will likely rely on the establishment of new experimental models simulating intra - vertebral artery or intra-radiculomedullary artery steroid injections.
    Jun Wang*, Jian Pei, Jie Chen, Qin Hui Fu, Xiao Cui, and Yi Song
    Abstract:
    Autophagy and inflammation play a key role in the pathogenesis of ischemic stroke; the latest research shows that autophagy and inflammation are seen as a double-edged sword. Insufficient or excessive autophagy will cause nerve damage, promote cell death, while the moderately autophagy has a neuroprotective effect. After the occurrence of ischemic stroke, the inflammatory response activates anti-inflammatory mediators and proinflammatory mediators, breaking the dynamic balance between proinflammatory response and anti-inflammatory response, causing detriment to the brain, affecting brain function recovery. The main purpose of this article is to systematically summarize the recent studies on autophagy and inflammatory responses in acute ischemic stroke, a brief analysis the roles of autophagy and inflammatory responses in the pathophysiology of ischemic stroke, investigate the correlation between both. To build a foundation for research on how to make autophagy and proinflammatory and anti-inflammatory responses achieve the desired balance at different stages of the stroke, in order to provide research directions for acute ischemic stroke and to form new and effective therapeutic strategies.
    Case Report
    Armando Sanchez-Jordan* and Carlos Gerardo Cant-Brito
    Abstract:
    Granulomatosis with polyangiitis is a systemic vasculitis with uncommon central nervous system involvement. Stroke, which is the primary manifestation in this subgroup, presents with a wide clinical spectrum depending on its location. The plus-minus lid syndrome consists of unilateral ptosis and contralateral eyelid retraction following a lesion of the midbrain affecting the third nerve fascicle. We present a patient with granulomatosis with poliangiitis who developed a pontine hemorrhagic stroke probably secondary to vasculitis activity, which extended to the midbrain affecting the third nerve fascicle with a consequent plus-minus lid syndrome. This is the first case in literature reporting both entitites.
    Ronald C. Pearlman*, and Bryan Steinberg
    Abstract:
    A 59-year-old HIV positive female presented with cardiac symptomatology. Cardiology workup included a cardiac catheterization during which a carotid angiogram was performed demonstrating a 90% stenosis of the right carotid artery. The stenosis was the result of lymphoid hyperplasia with pseudo - obstruction of the right carotid artery. Patients who have acquired human immunodeficiency virus (HIV) may have enlarged neck lymph tissue impinging on other anatomical structures causing displacement or stenosis, including the carotid artery.
    Special Issue on Parkinson's Disease
    Research Article
    Asako Yoritaka1,2*, Yasushi Shimo1, Masashi Takanashi1, Jiro Fukae1,3, Taku Hatano1, Toshiki Nakahara1, Nobukazu Miyamato1,4, Takao Urabe1,4 and Nobutaka Hattori1
    Abstract:
    Background and Purpose: We examined the prevalence of clinical symptoms and cumulative dose of anti-parkinsonian drugs in Japanese patients with Parkinson’s disease (PD).
    Methods: We retrospectively reviewed the charts of patients (n = 1453; 650 males) who had visited our outpatient neurology clinic between January and June 2010. Cumulative dose was calculated by calendar day to the day of onset of events, or the day of the examination. Prevalence and risk of events (pain, wearing-off, camptocormia, sleep attack, orthostatic hypotension, psychosis, and pneumonia) were analyzed using Kaplan–Meier survival curves, calculated odds ratios, and hazard ratios (HRs).
    Results: Most patients (1292, 88.9%) received levodopa, and the cumulative dose was 1263 (SD 1190) g. Moreover, 1182 patients (81.3%) received dopamine agonists (DAs; average cumulative dose, 827 (1466) g. The cumulative doses of trihexyphenidyl (n = 561), amantadine (n = 598), and selegiline (n = 620) were 8246.1 (11156.7) mg, 386.5 (829.2) g, and 7587.4 (11006.9) mg, respectively. The HRs were as follows: 0.998 (p < 0.001) for the cumulative dose of levodopa to the onset of pain, wearing-off, camptocormia, and psychosis; 0.997 (p < 0.001) for the cumulative dose of levodopa to the onset of orthostatic hypotension; 0.999 (p < 0.001) for the cumulative dose of DAs to the onset of camptocormia; and 0.999 (p < 0.001) and 0.999 (p < 0.05) for the cumulative doses of levodopa and DA to the onset of pneumonia. However, the HRs were close to 1.0.
    Conclusions: There was no relationship between the cumulative dose of anti-parkinsonian drugs and the prevalence of symptoms.
    Review Article
    Asako Yoritaka*
    Abstract: A common early non-motor symptom of Parkinson’s disease (PD) is sleep disturbance. Indeed, rapid eye movement (REM) sleep behavior disorder (RBD) and excessive daytime sleepiness (EDS) are predictors of PD. EDS and RBD are thought to be risk factors for the cognitive disturbances observed in PD. Some researchers have suggested that RBD can be used as a predictor of the pathological progression of PD. Thus far, sleep disturbances have not been recognized as a component in the progression of the disease, and therefore have not been routinely and adequately controlled in this patient population. In this review, we present evidence that the assessment of sleep (i. e. , the presence of fragmented sleep, insomnia, RBD, EDS, and sudden onset of sleep) should be a part of the routine evaluation of patients with PD.
    Yasushi Shimo and Nobutaka Hattori*
    Recently, much attention has been paid to not only motor symptoms but also Non-Motor Symptoms (NMS) of Parkinson’s disease [1]. NMS include sleep disorders, autonomic nervous system dysfunction, sensory impairment, and neuropsychiatric symptoms. Neuropsychiatric symptoms include depression, apathy, anxiety, anhedonia, attention deficit, hallucinations, confusion, Impulse Control Disorders (ICD), and cognitive dysfunction [1]. These symptoms are risk factors that influence a patient’s quality of life, and the prevalence of NMS increases along with disease progression [2].
    Special Issue on Neuropsychiatric Disorders and Microglia
    Review Article
    Akira Monji1*, Yoshito Mizoguchi1 and Takahiro A Kato2
    Abstract: The etiology of schizophrenia remains unclear while, in many aspects, the neuropathology of schizophrenia has recently been reported to be closely associated with microglia dysfunction. Microglia, which are the major players of innate immunity in the CNS, respond rapidly to even minor pathological changes in the brain and contribute directly to neuroinflammation by producing various pro-inflammatory cytokines and free radicals. Recent human studies have revealed microglial activation in schizophrenia using postmortem brains or in vivo neuroimaging techniques. We and other researchers have recently shown the inhibitory effects of some antipsychotics on the release of inflammatory cytokines and free radicals from activated microglia, both of which have recently been known to cause the synaptic pathology, a decrease in neurogenesis, and white matter abnormalities often found in the brains of patients with schizophrenia. In addition, recent evidence strongly suggests a neurodevelopmental role of microglia in regulating synapse formation/function by their interaction with synapses and phagocytotic activity. It is not known whether microglia dysfunction and microglia-orchestrated neuroinflammation are the primary cause of schizophrenia but they are closely related to the progression and outcomes of schizophrenia. Understanding microglial pathology may shed new light on the therapeutic strategies for schizophrenia.
    Yoshinori Hayashi1, Zhou Wu1 and Hiroshi Nakanishi1,2*
    Abstract: Pío del Río Hortega first discovered microglia by histological staining with silver carbonate. He thought that microglia with highly branched fine processes in the healthy brain were quiescent and called these cells as resting microglia. After brain injury, microglia changes their morphology into activated type, which has phagocytic activity at the sites of neuronal damage and inflammation. At 90 years after the discovery of microglia, resting microglia in the healthy brain were found to be very dynamic, much more than any other cells in a live mouse brain using the two-photon scanning laser microscope. Beyond the roles as brain-resident macrophages, many lines of evidence have revealed that microglia have essential roles in the maturation and maintenance of neuronal circuits in the brain through both elimination and formation of dendritic spines through their processes. Furthermore, length and structural complexity of highly branched fine processes are regulated by microglial intrinsic molecular clock. Dysfunction of dendritic spine and disturbance of circadian clock system are widely accepted characteristic abnormalities in neuropsychiatric disorders. Therefore, the growing understanding of movement and functions of microglial processes may aid in the development of novel pharmacological interventions against neuropsychiatric disorders, which are associated with synapse loss and aberrant neuronal connectivity.
    Sadayuki Hashioka1*, Patrick L. McGeer2, Tsuyoshi Miyaoka1, Rei Wake1 and Jun Horiguchi1
    Abstract: Microglial activation is one of common pathological findings in the lesions of many neurodegenerative diseases. In the 1980’s immunohistochemical studies, using anti-major histocompatibility complex class II (MHCII) antibodies identified activated microglia in postmortem brains of neurodegenerative diseases. Microglial activation in the brains of patients with neurodegenerative diseases has been demonstrated since 2000 by positron emission tomography studies employing PK11195. Moreover, activated microglia have also recently been implicated in endogenous psychiatric disorders, such as schizophrenia and mood disorders, where common pathological findings had never before been identified. However, the exact functional states of microglial activation in neuropsychiatric diseases remain to be clarified, since an increase in expression of a microglial marker MHC II or PK11195 is not necessarily an indicator of classical inflammatory microglial activation. Accumulating evidence shows that both antidepressants and antipsychotics attenuate the classical activation of microglia, suggesting that such an action may be associated with their therapeutic effects. It is clearly desirable to establish reliable markers that would identify specific microglial activation states in neuropsychiatric diseases.
    Special Issue on Autism and its Treatment
    Research Article
    Fructuoso Ayala-Guerrero*, Graciela Mexicano and Sarahí Huicochea-Arredondo
    Abstract: Abstract: Autism Spectrum Disorder (ASD) is a heterogeneous, behaviorally defined neurodevelopmental disorder. Patients with ASD might also have co-morbid disorders such as intellectual impairment, epilepsy, and anxiety.
    Findings from questionnaire studies have revealed the existence of several sleep problems in pediatric patients with ASD. However, few studies have analyzed the relationship between these disturbances and Polysomnographic (PSG) findings.
    On the other hand, about a third of people with autism also suffer from epilepsy. For this reason, long-duration electroencephalograms including an adequate amount of slow wave sleep should be carried out in order to detect epileptiform activity.
    The aim of this work is to describe the sleep characteristics and to detect EEG anormalities in ASD patients using polysomnographic recordings.
    Methods: Polysomnographic recordings were carried out in 12 autistic children for two consecutive nights and compared to those of the age and sex-matched controls. Sleep efficiency as well as percentages of each sleep phase were obtained from the two groups of participating children. Distribution of SWS and REM sleep throughout the night was also obtained and compared between both groups. Simultaneously, EEG characteristics were analyzed and compared.
    Results: ASD children presented low sleep efficiency, fragmented sleep and reduction in both SWS and REM sleep. Epileptifom brain activity was observed in 50% of ASD children.
    Conclusion: ASD patients presented quantitative and qualitative sleep disturbances as well as EEG abnormalities.
    Special Issue on Multiple Sclerosis
    Review Article
    Mari Yoshida*
    Abstract: We reviewed and compared the neuropathology of multiple sclerosis (MS), neuromyelitis optica (NMO), neuromyelitis optica spectrum disorders (NMOSD) and acute disseminated encephalomyelitis (ADEM) in Japan. Demyelinating lesions of MS are well circumscribed as compared with the lesions of NMO and NMOSD, which reveal variable, irregularly shaped and ill-defined borders that extend longitudinally along vessels, causing destructive changes with poor gliosis. Although the optic nerves and chiasm, spinal cord, cerebral white matter, brainstem, and cerebellum are involved in both MS and NMO/NMOSDs, the formation patterns of demyelinating lesions appear to differ between MS and NMO/NMOSD. NMO/NMOSD preferentially exhibit central lesions of the spinal cord with strongly softening features. Furthermore, the expression of myelin basic protein (MBP) is strongly diminished in the demyelinating lesions of MS, without loss of aquaporin-4 (AQP4) or GFAP expression. However, AQP4 and GFAP expression is decreased in the demyelinating lesions of NMO/NMOSD. Therefore, AQP4 and MBP immunoreactivity may distinguish NMO/NMOSD from MS neuropathologically. Serial sections of the spinal cord demonstrate longitudinally extensive lesions in NMO/NMOSD, although some cases with MS also reveal similar longitudinally extensive lesions of the spinal cord. In ADEM, demyelinating lesions form primarily in small perivenous foci that differ from the lesions of MS and NMO/NMOSD. Therefore, the shape and formation patterns of demyelinating lesions appear to be disease specific, and it might be possible to distinguish among MS, NMO and ADEM; the immunoreactivity patterns of MBP, AQP4, and GFAP may also aid diagnosis.
  • Clinical Images
  • JSciMed Central welcomes back astronaut Scott Kelly and cosmonaut Mikhail Kornienko.
    Readmore...

    Wonder Women Tech not only disrupted the traditional conference model but innovatively changed the way conferences should be held.
    Readmore...

    JSciMed Central Peer-reviewed Open Access Journals
    10120 S Eastern Ave, Henderson,
    Nevada 89052, USA
    Tel: (702)-751-7806
    Toll free number: 1-800-762-9856
    Fax: (844)-572-4633 (844-JSCIMED)
    E-mail: nds@jscimedcentral.com
    nds@j-scimedcentral.org
    1455 Frazee Road, Suite 570
    San Diego, California 92108, USA
    Tel: (619)-373-8720
    Toll free number: 1-800-762-9856
    Fax: (844)-572-4633 (844-JSCIMED)
    E-mail: nds@jscimedcentral.com
    nds@j-scimedcentral.org
    About      |      Journals      |      Open Access      |      Special Issue Proposals      |      Guidelines      |      Submit Manuscript      |      Contacts
    Copyright © 2016 JSciMed Central® All Rights Reserved
    Creative Commons Licence Open Access Publication by JSciMed Central® is licensed under a Creative Commons Attribution 4.0 International License.
    Based on a work at https://jscimedcentral.com/. Permissions beyond the scope of this license may be available at https://creativecommons.org/.