Online journal of neurology and brain disorders最新文献

{"title":"Aseptic meningitis revealing isolated Kikuchi-Fujimoto disease","authors":"S. Bouomrani, Nesrine Regaïeg","doi":"10.32474/OJNBD.2018.02.000129","DOIUrl":"https://doi.org/10.32474/OJNBD.2018.02.000129","url":null,"abstract":"Introduction: Kikuchi-Fujimoto’s disease (KFD) or histiocytic necrotizing lymphadenitis is a rare entity that may represent a real diagnostic challenge for the clinician because of its highly polymorphous and sometimes unusual presentations. We report an original observation of KFD with aseptic meningitis as inaugural manifestation. Case report: 30-year-old woman, without pathological medical history, was hospitalized via the emergency department for exploration of a meningeal syndrome with cervical lymphadenopathies. The lumbar puncture showed aseptic meningitis: clear, normotensive cerebrospinal fluid with leukocytes at 28/mm3 (90% lymphocytes), red blood cells at 2/mm3, proteinrrhachia at 0.58 g/l, glucorrachia at 4 mmol/l for venous glycemia at 8 mmol/l, and negative direct examination and culture. Cerebromedullary MRI and cerebral angio-MR were without abnormalities. Further infectious and immunological investigations were negative. Cervical lymph node biopsy showed histological and Immunohistochemical aspects suggesting KFD. Treated with systemic corticosteroids, the evolution was favorable with no recurrence. Conclusion: KFD-associated aseptic meningitis remains rare, and the inaugural forms are exceptional and often difficult to diagnose. A better knowledge of this association avoids unnecessary investigations, recurrence, and improves the prognosis of the disease.","PeriodicalId":93346,"journal":{"name":"Online journal of neurology and brain disorders","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47662914","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rituximab-Rescue Therapy in Autoimmune Neurological Disorders","authors":"A. K. Roy, Saurabh Sadekar, R. Maloo, S. Murali","doi":"10.32474/OJNBD.2018.02.000128","DOIUrl":"https://doi.org/10.32474/OJNBD.2018.02.000128","url":null,"abstract":"","PeriodicalId":93346,"journal":{"name":"Online journal of neurology and brain disorders","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41379116","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Double-Blind Placebo-Controlled Trial of Acediprol (Valproate Sodium) For Global Severity in Child Autism Spectrum Disorders","authors":"Aliyev Na, Z. Aliyev","doi":"10.32474/OJNBD.2018.02.000127","DOIUrl":"https://doi.org/10.32474/OJNBD.2018.02.000127","url":null,"abstract":"","PeriodicalId":93346,"journal":{"name":"Online journal of neurology and brain disorders","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47100951","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Beta-Propeller Protein-Associated Neurodegeneration Syndrome","authors":"S. Asadi, Mahsa Jamali, Gholnesa Valizadeh, N. Ghafouri","doi":"10.32474/OJNBD.2018.02.000126","DOIUrl":"https://doi.org/10.32474/OJNBD.2018.02.000126","url":null,"abstract":"","PeriodicalId":93346,"journal":{"name":"Online journal of neurology and brain disorders","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46993914","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Running head: PEN-3 Model Cultural Framework for Health Intervention and Prevention","authors":"Lisa Marie Portugal","doi":"10.32474/OJNBD.2018.01.000123","DOIUrl":"https://doi.org/10.32474/OJNBD.2018.01.000123","url":null,"abstract":"The PEN-3 Model Cultural Framework can be used to design culturally specific, locally relevant health intervention and prevention programs to educate communities. This health intervention and prevention involves educating Hispanic females and males between the ages of 15 to 32. The health and wellness program design involve educating this group about the use of marijuana and its damaging effects on the body leading to mental illness, Diabetes, Cancer, lung and other organ damage, obesity, cognitive disorders, lowered IQ and EQ (emotional quotient), and various other damaging effects. Finally, a summary of the PEN-3 Model Cultural findings are discussed and analyzed to help health educators, practitioners, and advocates serve and address the needs of the target population.","PeriodicalId":93346,"journal":{"name":"Online journal of neurology and brain disorders","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47535768","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Sodium Valproate: Doctor Jekyll and Mister Hyde","authors":"J. Bossu","doi":"10.32474/OJNBD.2018.01.000122","DOIUrl":"https://doi.org/10.32474/OJNBD.2018.01.000122","url":null,"abstract":"The sodium valproate (VPA) is a very simple structural compound derived from the valeric acid produced by a plant “Valeriana officinalis†. Extract s of this this plant were used by the doctors of Ancient Greece to cure insomnia and by the Romans to treat palpitations and arrhythmia. VPA was used for the first time as an anticonvulsant in 1963 [1] and in 1974 Jevson and Clark [2] after their clinical study on 63 patients whom 40 of them had failed to respond to other anticonvulsants concluded that in 43% of patients, epilepsy stopped completely, and in 22% of patients, the attacks were reduced by 50%. An unusual side effect was temporary hair loss. Since then VPA is widely used to treat almost all types of seizures and epilepsy syndromes, and is used successfully, for patients displaying epilepsy resistant to other medications [3]. Behind its anticonvulsants effect, VPA targets also a wide range of neurological diseases including some neurodegenerative pathologies, addiction, bipolar and obsessive-compulsive disorders and migraine [4].","PeriodicalId":93346,"journal":{"name":"Online journal of neurology and brain disorders","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43562316","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neurological Diseases and Relation of TRP Channels","authors":"Y. Yazğan","doi":"10.32474/OJNBD.2018.01.000120","DOIUrl":"https://doi.org/10.32474/OJNBD.2018.01.000120","url":null,"abstract":"Is currently used as a comprehensive definition covering “brain disorders”, neurological diseases and mental disorders. While schizophrenia, depression, panic disorder, drug addiction and insomnia are referred to as “mental disorders”, Epilepsy, Alzheimer, Parkinson, Huntington’s disease (HD) and multiple sclerosis are considered as “neurological disorders”. Current therapies of these very common diseases require continuous drug use and at the same time cause many different side effects. Therefore preclinical and clinical investigations for new treatment approaches are on the rise. Especially the identification of the molecular basis of these diseases is the focus of researches. Examination of transient receptor potential (TRP) channels is at an early stage in the investigation of the molecular principle of these diseases, but clear results regarding the efficacy of substances activating or inhibiting these channels have not been obtained. Some diseases have been based on mutations of TRP channels. However, only a few TRP channelopathies, have been conclusively identified so far [1]. Investigation of TRP channels in psychiatric disorders will contribute to a better understanding of the etiology of psychiatric disorders and the development of new pharmacological treatments. Abbreviations: TRP: Transient Receptor Potential; GPCR: G Protein Coupled Receptor; TRPV1: TRP Vanilloid 1; CGRP: Calcitonin Gene Related Peptide; CNS: Central Nervous System; SOC: Store Operated Calcium Channels; BDNF: Brain Derived Neurotrophic Factor; Mwk: Moon Walker Mouse; BD-I: Bipolar Disorder Type I; ALS-G: Guamanian Amyotrophic Lateral Sclerosis ISSN: 2637-6628 DOI: 10.32474/OJNBD.2018.01.000120 On J Neur & Br Disord Copyrights@ Yener Yazğan. Citation: Yener Y, Betül Y. Neurological Diseases and Relation of TRP Channels. On J Neur & Br Disord 1(4)2018. OJNBD. MS.ID.000120. DOI: 10.32474/OJNBD.2018.01.000120. 71 TRP Channels in Brain Disorders TRPV1 and TRPA1 Significant evidence has been obtained that TRPV1 antagonists have anxiolytic activity in preclinical studies, but the antidepressant effect is not clear [6]. There is no direct evidence that TRP channels play a role in schizophrenia. However, the fact that TRPV1 channels play a role in central dopaminergic and cannabinoid mechanisms may suggests the potential role of these channels in schizophrenia [5]. CGRP release from trigeminal vasculature neuron network and neurogenic inflammatory response are currently accepted mechanisms for migraine attack pathophysiology. In particular, the TRP vanilloid 1 (TRPV1) and the TRP ankyrin 1 (TRPA1) are expressed in nociceptive neurons, which also express the sensory neuropeptides, tachykinins, and calcitonin gene-related peptide (CGRP), which mediate neurogenic inflammatory responses. This evidence suggests that these channels may be an important therapeutic goal in migraine treatment [7].","PeriodicalId":93346,"journal":{"name":"Online journal of neurology and brain disorders","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41645613","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acquired Cumulative Systemic Neurotoxic Effect: The Future of Medicine & Biopsychology","authors":"R. Richardson","doi":"10.32474/OJNBD.2018.01.000119","DOIUrl":"https://doi.org/10.32474/OJNBD.2018.01.000119","url":null,"abstract":"As a result of working extensively with dozens of patients who had repeated exposure to toxins and solvents throughout their lifetimes, I wrote the article “Acquired Cumulative Neurotoxic Encephalopathy: Look toward the Future” which was published in the Academy of Medical Psychology Newsletter in March of 2015. Since then, I have reviewed hundreds of studies, and worked with additional patients, who have the onset of systemic disorders such as autoimmune disorders, multiple chemical sensitivity, allergic reactions, histamine intolerance, leaky gut, metabolic syndrome, and various myalgia conditions. Many of them can trace the onset of symptoms back to one point where they had, after repeated exposure to solvents or toxins, gone from relatively normal function to significant dysfunction. The premise of Acquired Cumulative Neurotoxic Encephalopathy and Acquired Cumulative Systemic Neurotoxic Effect is that there is a threshold at which the body cannot tolerate additional exposure to toxins without a significant reaction. This may be related to genetic sensitivities, failure of the body to eliminate toxins from the body, and/or cumulative damage to the physiological/biochemical systems of the body. One of the first commonly known cases is those who played the crystal armonica, a leaded-crystal musical instrument, where the musician would build up lead in their system over time to the point of risks lead poisoning.","PeriodicalId":93346,"journal":{"name":"Online journal of neurology and brain disorders","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46082403","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Confrontation Naming Errors of Alzheimer’s Disease Patients","authors":"Stephen Enwefa","doi":"10.32474/OJNBD.2018.01.000117","DOIUrl":"https://doi.org/10.32474/OJNBD.2018.01.000117","url":null,"abstract":"This study investigated confrontation naming errors of Alzheimer’s disease patients. Clinicians lack a validated test battery for differentiating the communication disorders of patients with AD from either normal elderly or patients with aphasia [1,3]. The communication of AD patients is often assessed with one of the standardized test batteries for aphasia. This was done because of the marked discrepancy between language and other cognitive functions. A linguistic measure involving errors in confrontation naming was used to establish the extent of linguistic impairment of AD patients. A total of ten photographs were shown to twenty AD patients, (ten mild and ten moderate) and ten normal elderly. The results showed that naming errors increased as the disease progressed. The study concluded that the number of naming errors of AD patients increased as the severity of the disease progressed. ISSN: 2637-6628 DOI: 10.32474/OJNBD.2018.01.000117 On J Neur & Br Disord Copyrights@ Stephen C Enwefa, et al. Citation: Stephen C E, Regina E. Confrontation Naming Errors of Alzheimer’s Disease Patients. On J Neur & Br Disord 1(4)2018. OJNBD. MS.ID.000117. DOI: 10.32474/OJNBD.2018.01.000117. 62 defined as a form of dementia characterized by a gradual loss of several important mental functions that interrupts the normal flow of life. It is perhaps, the most common cause of dementia in older Americans, and goes beyond just normal forgetfulness, such as losing your car keys or forgetting where you parked. Signs of Alzheimer’s disease include language deficits, memory loss that is much more severe and more serious, such as forgetting the names of your children or perhaps where you’ve lived for the last decade or two, and remembering when you had your last meal. Numerous studies have investigated naming errors in AD by classifying errors as visual, semantic or lexical in nature [4-6]. A common finding is that AD patients produce many semantic and/or thematic naming errors (i.e. shark for dolphin). The criteria by which errors are divided can potentially overlook interactions among perceptual and lexical-semantic processes.AD can be considered a multifocal disorder; one must consider the possibility that visual perception and naming are two unrelated areas of concomitant decline. However, there is evidence of a possible link between the two processes in visual perception tasks that require discrimination of real objects according to Tippett and Blackwood [7]. Studies have found that when healthy individuals underwent fMRI while performing a visual discrimination task between line drawings, they recruited relatively more anterior regions of the fusiform gyrus when the two drawings had high structural similarity and relatively more posterior regions of the fusiform gyrus and inferior occipital cortex when the drawings were lower in structural similarity. Together these findings pose that fMRI signal in mid-anterior areas are related to processing of detailed object stru","PeriodicalId":93346,"journal":{"name":"Online journal of neurology and brain disorders","volume":"31 23","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41249286","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rett Syndrome","authors":"Rodriguez Rivera Sofia Lucila","doi":"10.32474/ojnbd.2018.01.000116","DOIUrl":"https://doi.org/10.32474/ojnbd.2018.01.000116","url":null,"abstract":"There is no specific treatment that can reverse or stop the course of the disease. The rapeutic management revolves around the restoration of synaptic function and maturation, since it has been shown that the deficitis at the level of micro circuits that involve synaptic transmission. The management is symptomatic and individualized. A multidisciplinary and dynamic approach is essential. The knowledge of the genetic causes allows a diagnostic confirmation, a family genetic counseling, an evolutionary prognosis and the application of a therapy to the disease in the very near future [7,8] (Figure 1). Abstract Rett sindrome is a severe neuro developmental disorder that is a leading cause of mental retardation in females, characterized by an apparently normal psycho motor development through the first 6 months of life, followed by stagnation and growth regression in different are as like motor, language and social skills; patients often exhibitautistic behaviors in the early stages. Other symptoms include seizures, breathing problems when awake such as hyper ventilation, apnea, and swallowing air; ataxia and stereotypich and movements. It is caused by mutations in the X-linked gene encodingmethyl-CpG-binding protein 2 (MECP2) [1,2]. One case is presented with positive molecular study.","PeriodicalId":93346,"journal":{"name":"Online journal of neurology and brain disorders","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49350157","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}