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  • ISSN: 2334-2307
    Early Online
    Volume 5, Issue 2
    Letter to the Editor
    Hiroshi Kanno*
    Neurocutaneous syndromes include numerous diseases which develop manifestations of central and peripheral nervous system and cutaneous manifestations, and are alternatively named as neurophacomatosis.
    Research Article
    Elgison da Luz dos Santos*, Eddy Krueger, Guilherme Nunes Nogueira-Neto, and Percy Nohama
    Spasticity is a disorder commonly found in people having upper motor neuron lesion and whose involvement can happen at different levels. The Modified Ashworth Scale (MAS) is the most routinely used instrument in clinical practice to assign spasticity levels. However, due to its inherent subjectivity, inter-evaluator discrepancies arise. Therefore, there are systems that quantitatively evaluate spasticity. This study is a literature review which aims to describe technologies for quantitative assessment of spasticity and discuss their effectiveness compared to MAS. The 27 selected papers were retrieved from PubMed, CAPES Portal, SciELO, MEDLINE and IEEE Xplore databases. Most of them had clinical goals involving patients with disorders of unique etiology. Thus, 48% and 30% of the surveyed papers included only patients with spasticity caused by stroke and cerebral palsy, respectively. Only 11% of the papers involved more than one etiology in the same trial. The remaining papers (11%) did not detail spasticity etiology. The results revealed different evaluative approaches including biomechanical data based on torque, joint angle, angular speed and muscle vibration, as well as neurophysiological approaches that analyzed electromyography signals of agonist and/or antagonist muscles. The integration of both approaches was also observed. Although MAS is widely used, quantitative assessment methods are more sensitive than MAS and, therefore, they are more suitable and safe for classifying spasticity. In conclusion, MAS should be replaced by quantitative tools, but it was not possible to determine the most effective measure for its replacement.
    Sarah E Giaccari*, Barbara R Lucas, Kate E Laver, and Christopher Barr
    Background: Early Supported Discharge (ESD) programs are a proven best evidence model of care following stroke but are yet to be evaluated within the context of Australian clinical practice.
    Objective: To compare functional outcome, quality of life, carer stress and length of stay in patients admitted to an ESD program with those receiving inpatient rehabilitation after admission for an acute ischemic stroke.
    Method: Seven outcome measures were taken during the initial hospital admission for acute stroke and at six weeks post stroke admission: Functional Independence Measure (FIM), Berg Balance, National Institutes of Health Stroke Scale (NIHHS), Modified Rankin Scale (mRS), European Quality of Life-5Dimensions (EQ-5D), Carer Stress and length of stay (LOS).
    Results: A total of 37 participants (23 males), mean age 70.9years (SD 14.8), participated in the study. The ESD group (n=19) had a significantly shorter LOS by a mean of 4.6 days (p<0.001), significantly higher quality of life (mean 89.9 vs 69.5, p<0.001) with no significant impact on carer stress (p = 0.31).There was a significant effect of time for the FIM, Berg Balance, mRS and NIHSS (all p<0.001). Patients in the ESD group demonstrated end of study Berg Balance mean score of 53.7 (p=0.01) and mRS (p=0.01) relative to those receiving inpatient rehabilitation indicative of greater improvements in the ESDgroup.
    Conclusion: An ESD service can accelerate discharge to home and increase independence compared to inpatient rehabilitation in the context of Australian clinical practice.
    Mohammed Tayyab Shera, Syeda Beenish Bareeqa, Syed Ijlal Ahmed*, Asim Haider, Ahmed Toheed, and Syeda Sana Samar
    Background: Epilepsy is a recurrent paroxysmal disorder of cerebral function characterized by sudden brief attacks of altered consciousness, motor activity, sensory phenomena or inappropriate behavior caused by abnormal excessive discharge of cerebral neurons.
    Aim and objective: To access the Quality of Life in Epileptic patients aged 13-25 presenting to Mayo Hospital, Lahore.
    Material and methods: It was a case control study conducted at Mayo Hospital, Lahore from January 2016 to June 2016. A total of 100 subjects (50 cases and 50 controls) were recruited in the study. Selection was made after taking due consent from patients. Interviews were conducted through a pretested BREF-QOL Questionnaire. Simple Randomized sampling technique was used. Data was collected, compiled and analyzed through SPSS version 16.
    Results: Four different variables were used to access the quality of life in epileptic and non-epileptic patients. By using independent t-test, psychological health, social relationships and environmental health were found to be significant among two groups.
    Conclusion: It was concluded that epilepsy significantly disturbs the quality of life among effected individuals. Its essential to pay attention to quality of life along with the treatment of ailment.
    Review Article
    Sophia Delicou*
    Hemoglobinopathies are among the most common inherited diseases around the world. Neurological manifestations in hemoglobinopathies may range from mild symptoms to serious complications. Early diagnosis and proper management of the basic disease require specialised hematological experties.
    In this review we discuss the current neurological manifestations, the management and prevention.
    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.
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