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  • ISSN: 2334-2307
    Early Online
    Volume 6, Issue 3
    Case Report
    Mari Kumashiro* and Kazuyuki Samejima
    Social gestures convey one's own intentions or the other's mental state in face-to-face interactions. Kumashiro has shown that monkeys could communicate with humans through social gestures (Kumashiro et al., 2002, 2003, 2008). Eye contact has a robust role of social gestures. It directs the monkey's attention towards the human, and the monkey will start perceiving the human as a communicator. Direct eye gaze, however, occasionally generates fear or some sort of emotions. Some monkeys should avoid the human's eyes. Our hypothesis was that social touch would be effective in trying to make eye contact or maintaining social interactions. In case 1, we investigated whether social touch would bring the monkey's eye contact with a human. We gently stroked the face or arm as the body parts of petting in short or long duration. We found that the monkey reached a stage of eye contact by arm-petting, and it had effect on directing the monkey's attention toward the human's face or hand. In case 2, another monkey which already acquired eye contact, pointing, and imitation was subjected. We tested whether social touch would be effective for eating food which the monkey would not otherwise eat. Although social touch did not ameliorate the eating behavior, we found that it was effective for reducing annoying behavior, i.e., throwing food. Gentle stroking by the human's hand is the most convenient for the establishment of monkey's communication with the human partner. These findings may also have methodological implications for basic or clinical researches of social gestures.
    Perrotta F, Denittis N, Recchia A, Simeone A, and Del Gaudio A*
    Subarachnoid hemorrhage (SAH) secondary to closed head injury is rarely associated with traumatic aneurysm of the posterior circulation. We report a case of SAH and delayed re bleeding in a young patient with head trauma after a fight. The first line CT scan was negative for aneurysm. We analyzed the causes of posterior aneurysm formation and underline the necessity of a prompt angiography for the diagnosis and to exclude the source of the bleeding.
    Research Article
    Vahid Abbasi, Anahita Zakeri, and Afsaneh Enteshari-Moghaddam*
    Emotional intelligence (EI) is one of the most important factors for occupational and social success of individuals that are necessary for effective performance of all employed employess in health centers and hospitals. The aim of this study was to evaluating Emotional Intelligence (EI) in Ardabil city hospital workers. This cross-sectitional descriptive study was done on 120 staff employed employees in Ardabil city qovermental hospitals which selected randomly. Data collected by Goleman EI questionaire and analyzed by statistical methods in SPSS version 21. The mean age of samples was 38.7 6.9 and 65.8% of them were female. 97.5% of samples had university degree and 87.5% were married. The most of employees had EI score in moderate level (68%). Conducting appropriate and effective training courses on emotional intelligence can be very effective in promoting occupational and social success for having better interaction with people.
    Ahmadabadi F, Fattahzadeh Gh, Atalu A*, Badihi P
    The aim of this study was to investigate the effect of antiepileptic drugs (phenytoin, phenobarbital, Topiramate, carbamazepine and valproate) on sensory nerve conduction velocity (SNCV) in children under treatment of Seizure. 125 known patients with seizure were randomly categorized into 5 groups of 25, and each group received phenytoin, phenobarbital, Topiramate, valproate and carbamazepine. We used a group of 25 patients with febrile convulsion as a control group. We followed patients for 6 months and sensory and motor neural conduction velocity was recorded from each measured patient. Collected data analyzed by statistical methods in SPSS version 19.Anticonvulsant drugs all reduced the sensory nervous conduction velocity in patients and compared with drugs, the general drugs had a similar effect, but phenobarbital lowered the neurotransmission rate than the rest, and phenytoin had neuropathic complications more than other drugs. The changes mentioned were not related to the age and gender of the patients. Results showed that all of the anticonvulsants such as phenytoin, phenobarbital, Topiramate, and sodium valproate could be reduced the sensory neural conduction velocity in patients and the impact was similar between drugs.
    Abolfazl Atalu, Ghasem Fattahzadeh*, Vahid Abbasi, Farzad Ahmadabadi, and Somayeh Zarnesar
    Objective: The volume and number of lesions in white matter are indicators of brain health that related with disturbances and various illnesses such as cerebrovascular and cardiovascular diseases, psychiatric disorders, multiple sclerosis and systemic lupus erythematous. The present study was conducted to investigate the differential diagnosis of patients with periventricular hyper signal lesions which referred to the MRI unit of Ardabil city hospital.
    Methods: This is a descriptive-analytical study that has been done on 100 patients referred to the MRI unit of Ardabil city Hospital which hyper signal lesions around ventricle were observed in their T2-MRI (Magnetic resonance image). The necessary information were collected by study the MRI report which confirmed by a specialist.
    Results: 65% of patients were female and the rest were male. The average age of the patients was 54.14 16.58 years. The majority of white matter lesions including sub cortical and periventricular lesions with 34% and only periventricular lesions with 28%. Most of the differential diagnosis included small vessel disease with 38% and demyelization with 20%. Sub cortical and periventricularlesions were observed in patients with diagnosis small vessel disease and unidentified bright objects and periventricularlesions in patients with diagnosis of demyelization and Alzheimers dementia.
    Conclusion: This study showed that the frequency of observed white matter lesions in the MRI of patients were different by diagnosed of small vessel disease, Unidentified Bright Objects, demyelization, Alzheimers dementia and migraine that because of the small sample size it is suggested that similar studies with larger sample sizes be do nein the future.
    Short Communication
    Ghasem Fattahzadeh-Ardalani, Vahid Abbasi*, Afshan Sharghi, Abolfazl Atalu, and Reza Shirinkar
    Background and objective: Subarachnoid Hemorrhage (SAH) usually occurs due to the rupture of a cerebral artery aneurysm. About 9 million people suffer worldwide. According to the importance of SAH in the province, the aim of this study was to investigate the Frequency and clinical characteristics of patients with Subarachnoid Hemorrhage (SAH).
    Methods: This descriptive cross-sectional study was performed on 109 patients with SAH who were referred to Alavi Hospital during 2012-2017. Demographic data and clinical information were extracted from the patients hospital records and then analyzed by statistical methods in SPSS version 21.P-value less than 0.05 was considered significant.
    Abolfazl Atalu, Ghasem Fattahzadeh*, Afshan Sharghi, and Hamed Ezattiv
    Background and objective: In Cerebral venous thrombosis (CVT), blood clots create in the veins and sinuses. Detection of disease due to the wide spectrum of clinical symptoms may be delayed, the importance of timely diagnosis of this disease is that with early treatment, death can be avoided and serious and lifelong complications can be prevented in many patients. Also, recognizing the underlying causes and other factors that contribute to the onset of the disease can prevent the disease.
    Methods: This cross-sectional descriptive study has been done on 28 patients diagnosed with cerebral venous sinus thrombosis during years 2012 to 2017 that hospitalized in Ardabil city hospital. Demographic data of patients and information about laboratory tests and clinical and Para-clinical findings were entered in a checklist and then analyzed by statistical methods in SPSS version 19.
    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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