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  • ISSN: 2334-2307
    Early Online
    Volume 6, Issue 1
    Review Article
    Abhipradnya Bipin Wahul, Pranav Chintamani Joshi, Arvind Kumar, and Sumana Chakravarty*
    Stroke patients are at a higher risk of developing progressive cognitive impairment, often retarding patient rehabilitation. Studies have been carried out to find out the molecular mechanism associated with the stroke and its consequences on the various brain regions implicated in cognitive function. The current available therapy does not improve long- term outcome and remains a substantially unmet medical need. The review is an approach to emphasize the risk factors and diagnostic biomarkers of stroke that can be associated with post-stroke cognitive deficit, which may help in detecting patients at increased risk of cognitive deterioration and prevent or delay the occurrence of post-stroke cognitive impairments.
    Hiroshi Tenjin*
    Cerebral aneurysm, a common neurological disorder, has an abrupt onset and is often lethal by subarachnoid hemorrhage. Once a cerebral aneurysm ruptures, almost half of all patients will have a severe outcome. Neurological deficits last a long time and the patient costs are high [1,2]. On the other hand, methods of diagnosis and treatment are advancing rapidly.
    Research Article
    Golnaz Baghdadi, Farzad Towhidkhah*, and Reza Rostami
    Attention deficit hyperactivity disorder (ADHD) is one of the neurodevelopmental disorder that is common in children. Most of the studies showed the impairment of visual attention in ADHD children. Little investigations have also addressed the difference in auditory attention in children with and without ADHD.
    In the current study, we investigated the difference between normal and ADHD children based on the performance in visual and auditory attention.
    Twelve normal and eight ADHD-inattentive-subtype children participated in our study. They did an integrated visual and auditory attention test. Mean and variability of the correct reaction times and the accuracy of response were recorded during the test.
    Results showed the performance decline (i.e., increasing mean and variability of reaction time and response error) of ADHD children with respect to the normal in auditory attention.
    According to the results, more attention to the auditory stimuli in diagnosis tools is suggested.
    Golnaz Baghdadi, Farzad Towhidkhah*, and Reza Rostami
    The negative effect of distractions on the individuals' attention performance and the possible relation between the performance of the attention system and the pattern of saccadic eye movements has been investigated in different studies. It has been shown that distraction can lead to a delayed saccade toward a target and consequently the increment of the reaction time. The abnormal distractibility of subjects with attention deficit hyperactivity disorder has also been reported in previous studies. In the current study, we investigated the relationship between the saccadic eye movement to the distractions and speed of the response in children with attention deficit disorder (ADD) and normal ones.
    All children participated in a visual attention experiment. Subjects were requested to respond to a target when a target and a distraction were presented. Saccadic eye movements and RTs were recorded during the test. Paired samples t-test was used to compare the RT in trials with and without unwanted eye movements (saccade to distraction).
    Statistical analysis showed that unwanted saccades led to a significant increase of the RT in normal children (p<.01), but not in children with ADD (p>.05). It was also shown that the normal group had lower RTs than children with ADD in both trials with and without saccades to the distractions (p< 0.001).
    The outcomes of this study provided some suggestions about the difference between overt and covert attention to the distractions in normal and ADD children and new diagnostic methods have been proposed for future works.
    Case Report
    Ilyas Kamran*, Ahmad Qistas Malik, Yasir Muhammad, and Khan Nasir
    VZV angiitis is a rare manifestation of latent VZV activation. A 68-year-old immunocompetent adult who developed VZV angiitis of CNS was treated with high dose intravenous steroids in addition to the standard acyclovir treatment, this modality of treatment showed rapid improvement in symptoms. VZV angiitis of CNS being very rare has not been studied well; high dose steroids in addition to standard acyclovir treatment can give better clinical outcomes.
    Short Communication
    Kaushik Sundar*, Gigy Kuruttukulam, Jacob Chacko, Nimish Vijayakumar, Sunesh Edakkattil Radhakrishnan, and Raghavendra VijayakumarAkondi
    Background: Lacunar strokes accounts for up to 25% of all ischemic strokes. 20 to 30% of patients with lacunar strokes show deterioration within hours to days after the acute event. However, factors that predict such deterioration are poorly understood. In this study we aimed at classifying lacunar infarcts as Branch Atheromatous Disease (BAD) and Lipohyalinosis (LPH) using MRI parameters, and then evaluated whether such classification had an impact on prognosticating patients with lacunar syndromes.
    Methods: During a 1-year study period, patients with lacunar infarct admitted in a comprehensive stroke center in South India were identified. They were further classified as patients with lipohyalinosis (LPH) or branch atheromatous disease (BAD) based on MRI parameters. The clinical profile of these patients including NIHSS at presentation, comorbidities, modified Rankin scale (mRS) at presentation, at discharge and during follow up, duration of hospital stays and details of any clinical worsening were documented and analyzed. All statistical analysis was carried out using IBM SPSS statistics software.
    Results: A total of 63 patients (Males- 42 Females- 21) with lacunar infarct were included in this study. Of these 29 were classified as patients with BAD and 34 had LPH. Worsening of neurological symptoms within 5 days of onset was more often seen in patients with BAD. mRS at presentation was comparable between the two groups, however mRS at discharge and after three months was significantly better in LPH patients compared to BAD. Major arterial disease, as identified by an MR angiogram, was more often seen in patients with BAD. Hypertension was seen in both the groups; however diabetes was more commonly seen in patients with BAD. Recurrent cerebral ischemic events occurred more frequently in patients with BAD.
    Conclusions: Categorizing small infarcts as lipohyalinosis (LPH) and branch atheromatous disease (BAD) could help us portend patients with lacunar strokes.
    Review Article
    Ioannis Stamatatos*, Stavroula Ksylogiannopoulou, Fragkiskos Tzagkarakis, Konstantinos Bouboulis, Basileios Mpoumis, Maria Lykouri, Efstathios Metaxas, Dimitrios Lioumpas, Dimitrios Ksekalakis, and Ioannis Markakis
    Background: Dissection of the internal carotid and vertebral arteries is increasingly recognized as a cause of ischemic stroke in young people. Spontaneous cervical-artery dissection typically occurs in young and middle-aged persons, with a slight preponderance among women.
    Methods: PubMed, Scopus and Google Scholar databases were systematically searched according to the recommendations of the PRISMA statement for administrative dataset registries reporting outcomes after spontaneous dissection of the internal carotid and vertebral arteries.
    Results and Conclusions: Antithrombotic therapy has been the mainstay of medical treatment of cervical artery dissection. Despite the lack of level I evidence, most patients with cervical dissection are treated with systemic heparin followed by vitamin-K antagonists for 3 to 6 months.
    Asad Ali, Nouman Safdar Ali, Muhammad Ali Tariq, Waleed Iftikhar, Zara Z. Alvi, Malik Qistas Ahmad*, Atif Ameer, and Asma Ahmed
    The past 2 years have witnessed several landmark clinical trials showing better functional outcomes regarding acute stroke care. Endovascular intervention (including both the mechanical thrombectomy and intra-arterial thrombolysis) has unequivocal short term and long term clinical benefits as compared to conventional stroke management. In light of these major trials, AHA/ASA has now accredited endovascular thrombectomy as a gold standard intervention within 6 hours of stroke symptoms onset. Two recent trials DAWN and DEFUSE-3, showed positive outcome of delayed or extended window mechanical thrombectomy up to 16-24 hours after the stroke onset in selected patients. Promising results are seen regarding efficacy of PFO closure in stroke recurrence prevention. Similarly, in patients with atrial fibrillation with coexisting valvular heart disease, novel non-vitamin K antagonist oral anticoagulants' (NOACs) use for stroke prevention is justified.
    Clinical Image
    Khadija Sonda Moalla*, Olfa Hdiji, Salma Sakka, Hanen Haj Kacem, Nouha Farhat, Mariem Damak and Chokri Mhiri
    A 73-year-old man, with a one month past history of bilateral cerebellar infarct, presented with a continuous 4 Hz no-no type head tremor at rest, with increasing amplitude while maintaining posture or during voluntary movements. The tremor disappeared during sleep. The family history of tremor or dystonia was negative.
    Research Article
    Angana Saikia, Masaraf Hussain, Amit Ranjan Barua, and Sudip Paul*
    The present paper emphasizes the early detection of any neurodegenerative disorder using clinical diagnostic tools. It has become increasingly important to stop the future risk of death. Parkinson's disease (PD) is the second most common neurodegenerative disorder after Alzheimer's disease. It is a progressive neurological condition that causes motor and non motor manifestations. Treatment provides symptomatic benefit but no current treatment has been proven to slow disease progression. Research studies of PD require a means of rating the severity of disease by measurement of motor manifestations, assessment of ability to perform daily functional activities, and symptomatic response to medication. Advances in clinical recognition of early symptoms and signs, development of new neuroimaging technologies, identification of new neuropath logical markers of PD, are gradually translating into better understanding of predisposing and preclinical factors that lead to progressive Neurodegeneration. Neurodegeneration is the progressive loss of structure or function of neurons, including death of neurons. Many neurodegenerative diseases such as Alzheimer's disease and Huntington's disease are incurable, resulting in progressive degeneration and/or death of neuron cells. As research progresses, many similarities appear that relate these diseases to one another on a sub-cellular level. Neurodegeneration can be found in many different levels of neuronal circuitry ranging from molecular to systemic.
    In this study, we have used three different diagnostic scales for the analysis of various clinical parameters (Cognitive impairment, depression, and fatigue, oxygen level in brain and grip strength) for early detection of Parkinson's disease. The tools used were: Mini Mental state Examination (MMSE), Geriatric Depression Scale (GDS) and Fatigue Severity Score (FSS), SpO2 and grip strength. The Significance tests were carried out for all the parameters using one way ANOVA in Origin 8 software.
    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
    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.
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