A small percentage of patients with neuromyelitis optica spectrum disorder (NMOSD) may have radiological manifestations that completely mimic MS. Accurate diagnosis in these patients requires paying attention to patients’ history and how they respond to treatment. Here, a patient with NMOSD is introduced, in the MRI scan of whom, the diagnostic criteria of Barkhof were outlined; however, since her blurred vision did not respond to treatment with corticosteroids, she was diagnosed with NMOSD.
{"title":"Neuromyelitis optica spectrum disorder with radiological manifestation of multiple sclerosis in the first brain MRI: a case report","authors":"A. Moghadasi, S. Baghbanian","doi":"10.2217/FNL-2018-0032","DOIUrl":"https://doi.org/10.2217/FNL-2018-0032","url":null,"abstract":"A small percentage of patients with neuromyelitis optica spectrum disorder (NMOSD) may have radiological manifestations that completely mimic MS. Accurate diagnosis in these patients requires paying attention to patients’ history and how they respond to treatment. Here, a patient with NMOSD is introduced, in the MRI scan of whom, the diagnostic criteria of Barkhof were outlined; however, since her blurred vision did not respond to treatment with corticosteroids, she was diagnosed with NMOSD.","PeriodicalId":12606,"journal":{"name":"Future Neurology","volume":" ","pages":""},"PeriodicalIF":1.3,"publicationDate":"2019-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2217/FNL-2018-0032","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48008808","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}
L. Mahmudi, Moslem Moslemirad, Bafrin Dabestani, M. Shohani, M. Azami
Aim: This study was conducted to determine the clinical and demographic features in Iranian multiple sclerosis (MS) patients including clinical courses, positive MS family history, disability and age of disease onset. Materials & methods: All stages of the study were reported according to the PRISMA guidelines. A systematic review of published literature in Persian and English journals with a comprehensive search was conducted on English international databases including Scopus, PubMed/Medline, Cochrane Library, Science Direct, Web of Science, Embase, PsycINFO, as well as the Google Scholar search engine and national databases. Results: The prevalence of clinical courses of relapsing remitting, primary progressive, secondary progressive and relapsing progressive in Iranian patients with MS was 77.1% (95% CI: 72.2–81.3), 6.2% (95% CI: 4.1–9.2), 9.5% (95% CI: 6.8–13.1) and 0.4% (95% CI: 0.2–0.8), respectively. Positive family history of MS in Iranian MS patients was 8.9% (95% CI: 6.9–11.4). The mean age of disease onset was 28.9 years (95% CI: 27.8–30.1). Conclusion: The results of this meta-analysis in an Iranian population can provide useful information for neurologists and healthcare.
{"title":"Clinical and demographic features in Iranian multiple sclerosis patients: a systematic review and meta-analysis","authors":"L. Mahmudi, Moslem Moslemirad, Bafrin Dabestani, M. Shohani, M. Azami","doi":"10.2217/FNL-2018-0025","DOIUrl":"https://doi.org/10.2217/FNL-2018-0025","url":null,"abstract":"Aim: This study was conducted to determine the clinical and demographic features in Iranian multiple sclerosis (MS) patients including clinical courses, positive MS family history, disability and age of disease onset. Materials & methods: All stages of the study were reported according to the PRISMA guidelines. A systematic review of published literature in Persian and English journals with a comprehensive search was conducted on English international databases including Scopus, PubMed/Medline, Cochrane Library, Science Direct, Web of Science, Embase, PsycINFO, as well as the Google Scholar search engine and national databases. Results: The prevalence of clinical courses of relapsing remitting, primary progressive, secondary progressive and relapsing progressive in Iranian patients with MS was 77.1% (95% CI: 72.2–81.3), 6.2% (95% CI: 4.1–9.2), 9.5% (95% CI: 6.8–13.1) and 0.4% (95% CI: 0.2–0.8), respectively. Positive family history of MS in Iranian MS patients was 8.9% (95% CI: 6.9–11.4). The mean age of disease onset was 28.9 years (95% CI: 27.8–30.1). Conclusion: The results of this meta-analysis in an Iranian population can provide useful information for neurologists and healthcare.","PeriodicalId":12606,"journal":{"name":"Future Neurology","volume":" ","pages":""},"PeriodicalIF":1.3,"publicationDate":"2019-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2217/FNL-2018-0025","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46448181","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}
Aim: The molecular mechanism of gabapentin (GBP)–morphine combinational function and its neuro-anatomical sites of action to prevent, to neutralize morphine side effects and also the enhancement its analgesic effect of morphine is unknown. Methods: Morphine (10 mg/kg), saline, co-injection: GBP (150 mg/kg) with morphine (10 mg/kg) were injected by intraperitoneal injection in rats under deep anaesthesia. C-Fos immunohistochemistry technique was used to locate c-Fos expression in rat hypothalamus. Results: Gabapentin in combination with morphine significantly (p < 0.01) attenuated the acute morphine induced c-Fos immunoreactive neuron in hypothalamus. Conclusion: GBP neutralized the morphine sensitization in rat hypothalamus. GBP might neuromodulate and or antagonize the receptor regulatory machinery of morphine sensitization circuit which might work for drug discovery of morphine abuse.
{"title":"Gabapentin completely neutralized the acute morphine activation in the rat hypothalamus: a c-Fos study","authors":"J. Kazi, Rasdi Zatilfarihiah","doi":"10.2217/FNL-2018-0037","DOIUrl":"https://doi.org/10.2217/FNL-2018-0037","url":null,"abstract":"Aim: The molecular mechanism of gabapentin (GBP)–morphine combinational function and its neuro-anatomical sites of action to prevent, to neutralize morphine side effects and also the enhancement its analgesic effect of morphine is unknown. Methods: Morphine (10 mg/kg), saline, co-injection: GBP (150 mg/kg) with morphine (10 mg/kg) were injected by intraperitoneal injection in rats under deep anaesthesia. C-Fos immunohistochemistry technique was used to locate c-Fos expression in rat hypothalamus. Results: Gabapentin in combination with morphine significantly (p < 0.01) attenuated the acute morphine induced c-Fos immunoreactive neuron in hypothalamus. Conclusion: GBP neutralized the morphine sensitization in rat hypothalamus. GBP might neuromodulate and or antagonize the receptor regulatory machinery of morphine sensitization circuit which might work for drug discovery of morphine abuse.","PeriodicalId":12606,"journal":{"name":"Future Neurology","volume":" ","pages":""},"PeriodicalIF":1.3,"publicationDate":"2019-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2217/FNL-2018-0037","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42571527","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 rise and rise of cerebral small vessel disease: implications for vascular cognitive impairment and dementia","authors":"R. Kalaria, Y. Hase, M. Ihara","doi":"10.2217/FNL-2019-0004","DOIUrl":"https://doi.org/10.2217/FNL-2019-0004","url":null,"abstract":"","PeriodicalId":12606,"journal":{"name":"Future Neurology","volume":" ","pages":""},"PeriodicalIF":1.3,"publicationDate":"2019-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2217/FNL-2019-0004","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46505530","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}
Jairo Alexander Carmona Arroyave, Carlos Andrés Tobón Quintero, Jasmín Jimena Suárez Revelo, J. F. Gómez, Yamile Bocanegra García, Leonardo Moreno Gómez, David Antonio Pineda Salazar
Objective: Parkinson’s disease (PD) is characterized by cognitive deficits. There is not clarity about electroencephalogram (EEG) connectivity related to the cognitive profile of patients. Our objective was to evaluate connectivity over resting EEG in nondemented PD. Methods: PD subjects with and without mild cognitive impairment (MCI) were assessed using coherence from resting EEG for local, intra and interhemispheric connectivity. Results: PD subjects without MCI (PD-nMCI) had lower intra and interhemispheric coherence in alpha2 compared with controls. PD with MCI (PD-MCI) showed higher intra and posterior interhemispheric coherence in alpha2 and beta1, respectively, in comparison to PD-nMCI. PD-MCI presented lower frontal coherence in beta frequencies compared with PD-nMCI. Conclusion: EEG coherence measures indicate distinct cortical activity in PD with and without MCI.
{"title":"Resting functional connectivity and mild cognitive impairment in Parkinson’s disease. An electroencephalogram study","authors":"Jairo Alexander Carmona Arroyave, Carlos Andrés Tobón Quintero, Jasmín Jimena Suárez Revelo, J. F. Gómez, Yamile Bocanegra García, Leonardo Moreno Gómez, David Antonio Pineda Salazar","doi":"10.2217/FNL-2018-0048","DOIUrl":"https://doi.org/10.2217/FNL-2018-0048","url":null,"abstract":"Objective: Parkinson’s disease (PD) is characterized by cognitive deficits. There is not clarity about electroencephalogram (EEG) connectivity related to the cognitive profile of patients. Our objective was to evaluate connectivity over resting EEG in nondemented PD. Methods: PD subjects with and without mild cognitive impairment (MCI) were assessed using coherence from resting EEG for local, intra and interhemispheric connectivity. Results: PD subjects without MCI (PD-nMCI) had lower intra and interhemispheric coherence in alpha2 compared with controls. PD with MCI (PD-MCI) showed higher intra and posterior interhemispheric coherence in alpha2 and beta1, respectively, in comparison to PD-nMCI. PD-MCI presented lower frontal coherence in beta frequencies compared with PD-nMCI. Conclusion: EEG coherence measures indicate distinct cortical activity in PD with and without MCI.","PeriodicalId":12606,"journal":{"name":"Future Neurology","volume":" ","pages":""},"PeriodicalIF":1.3,"publicationDate":"2019-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2217/FNL-2018-0048","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47111915","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}
M. Scarpino, R. Carrai, F. Lolli, G. Lanzo, M. Spalletti, D. Audenino, C. Callegarin, M. Celani, M. Lombardi, A. Marrelli, O. Mecarelli, C. Minardi, F. Minicucci, L. Motti, L. Politini, F. Valzania, E. Vitelli, A. Peris, A. Amantini, A. Grippo
Aim: Hypoxic-ischemic-encephalopathy is a severe and frequent neurological complication of successful cardiopulmonary-resuscitation after cardiac arrest. Prognosticating neurological outcomes in patients with hypoxic-ischemic-encephalopathy is challenging and recent guidelines suggest a multimodal approach. Only few studies have analyzed the prognostic power of the association between instrumental tests and, in addition, most of them were monocentric, retrospective and evaluating only poor outcome. Methods/design: We designed a multicenter prospective cohort study to assessing the prognostic power of the association of electroencephalogram and somatosensory evoked potentials for the prediction of both poor and good neurological outcomes at different times after cardiac arrest. Discussion: The results of our study will provide a high level of evidence for the use of neurophysiological evaluation in the current clinical practice.
{"title":"Electroencephalogram and somatosensory evoked potential evaluation for good and poor neurological prognosis after cardiac arrest: a prospective multicenter cohort trial (ProNeCA)","authors":"M. Scarpino, R. Carrai, F. Lolli, G. Lanzo, M. Spalletti, D. Audenino, C. Callegarin, M. Celani, M. Lombardi, A. Marrelli, O. Mecarelli, C. Minardi, F. Minicucci, L. Motti, L. Politini, F. Valzania, E. Vitelli, A. Peris, A. Amantini, A. Grippo","doi":"10.2217/FNL-2018-0036","DOIUrl":"https://doi.org/10.2217/FNL-2018-0036","url":null,"abstract":"Aim: Hypoxic-ischemic-encephalopathy is a severe and frequent neurological complication of successful cardiopulmonary-resuscitation after cardiac arrest. Prognosticating neurological outcomes in patients with hypoxic-ischemic-encephalopathy is challenging and recent guidelines suggest a multimodal approach. Only few studies have analyzed the prognostic power of the association between instrumental tests and, in addition, most of them were monocentric, retrospective and evaluating only poor outcome. Methods/design: We designed a multicenter prospective cohort study to assessing the prognostic power of the association of electroencephalogram and somatosensory evoked potentials for the prediction of both poor and good neurological outcomes at different times after cardiac arrest. Discussion: The results of our study will provide a high level of evidence for the use of neurophysiological evaluation in the current clinical practice.","PeriodicalId":12606,"journal":{"name":"Future Neurology","volume":" ","pages":""},"PeriodicalIF":1.3,"publicationDate":"2019-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2217/FNL-2018-0036","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42166156","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}
Spinal muscular atrophy (SMA) is a devastating neuromuscular disorder and is the leading genetic cause of infant mortality [1,2]. SMA is a monogenic disease caused by complete loss of the SMN1 gene and the full-length (FL) functional SMN protein it produces [3]. A recent duplication in the human genome, however, has resulted in a second almost identical copy of SMN1, called SMN2, which, due to a silent point mutation, mostly produces a truncated nonfunctional protein [4]. The SMN2 gene nevertheless retains the ability to generate a small amount of FL protein, thus allowing the survival of individuals born with homozygous deletions/mutations within SMN1 [4]. A total absence of SMN protein is indeed not compatible with life [5]. Furthermore, the number of SMN2 copies varies from person to person and there is a clear and accepted negative correlation between the number of SMN2 copies (i.e., FL SMN protein produced) and severity of disease manifestation [6]. The identification of SMN as the gene that causes SMA dates back to 1995 [3]. Since that seminal discovery, a series of fundamental, pre-clinical and clinical research endeavours have been aimed at identifying and developing pharmacological strategies that could increase SMN abundance, either by exogenously re-introducing the SMN1 gene or by promoting the production of FL SMN protein from the SMN2 gene [7]. This arduous and approximately 25-year journey, which was supported by the entire SMA community (fundamental researchers, clinicians, families, patients and funders), reached its intended goal in December 2016, when the first gene therapy for SMA was approved by the US FDA for all SMA patients. It was subsequently approved by the European Medicines Agency (EMA) in June 2017. The drug, an antisense oligonucleotide that promotes FL SMN expression from SMN2, is sold under the commercial name of SpinrazaTM by Ionis and Biogen [8]. Saying that the approval of SpinrazaTM has changed SMA research would be quite an understatement. It has in fact completely transformed both the SMA therapeutic landscape and the SMA patient population [7,8]. Indeed, in a blink of an eye, we went from having no available therapies to having one with the potential to completely alter the fate of SMA children. Newly diagnosed patients that typically could not expect to live beyond their second birthday, now not only live beyond that timeframe, but do so by reaching motor function milestones that surpass what was ever thought possible [9,10]. Our research and clinical priorities had to therefore naturally adapt and shift overnight [11]. Shift yes, but not stop. Spinraza is an incredible life-changing treatment but, unfortunately, not a cure [8]. Indeed, treated SMA patients can still display neuromuscular symptoms and decline, and for reasons still unknown, patients respond differently to the treatment, roughly dividing into groups of responders that improve, responders that plateau and non-responders [8,12–15]. While recen
{"title":"Funding for spinal muscular atrophy research must continue","authors":"M. Bowerman","doi":"10.2217/FNL-2019-0001","DOIUrl":"https://doi.org/10.2217/FNL-2019-0001","url":null,"abstract":"Spinal muscular atrophy (SMA) is a devastating neuromuscular disorder and is the leading genetic cause of infant mortality [1,2]. SMA is a monogenic disease caused by complete loss of the SMN1 gene and the full-length (FL) functional SMN protein it produces [3]. A recent duplication in the human genome, however, has resulted in a second almost identical copy of SMN1, called SMN2, which, due to a silent point mutation, mostly produces a truncated nonfunctional protein [4]. The SMN2 gene nevertheless retains the ability to generate a small amount of FL protein, thus allowing the survival of individuals born with homozygous deletions/mutations within SMN1 [4]. A total absence of SMN protein is indeed not compatible with life [5]. Furthermore, the number of SMN2 copies varies from person to person and there is a clear and accepted negative correlation between the number of SMN2 copies (i.e., FL SMN protein produced) and severity of disease manifestation [6]. The identification of SMN as the gene that causes SMA dates back to 1995 [3]. Since that seminal discovery, a series of fundamental, pre-clinical and clinical research endeavours have been aimed at identifying and developing pharmacological strategies that could increase SMN abundance, either by exogenously re-introducing the SMN1 gene or by promoting the production of FL SMN protein from the SMN2 gene [7]. This arduous and approximately 25-year journey, which was supported by the entire SMA community (fundamental researchers, clinicians, families, patients and funders), reached its intended goal in December 2016, when the first gene therapy for SMA was approved by the US FDA for all SMA patients. It was subsequently approved by the European Medicines Agency (EMA) in June 2017. The drug, an antisense oligonucleotide that promotes FL SMN expression from SMN2, is sold under the commercial name of SpinrazaTM by Ionis and Biogen [8]. Saying that the approval of SpinrazaTM has changed SMA research would be quite an understatement. It has in fact completely transformed both the SMA therapeutic landscape and the SMA patient population [7,8]. Indeed, in a blink of an eye, we went from having no available therapies to having one with the potential to completely alter the fate of SMA children. Newly diagnosed patients that typically could not expect to live beyond their second birthday, now not only live beyond that timeframe, but do so by reaching motor function milestones that surpass what was ever thought possible [9,10]. Our research and clinical priorities had to therefore naturally adapt and shift overnight [11]. Shift yes, but not stop. Spinraza is an incredible life-changing treatment but, unfortunately, not a cure [8]. Indeed, treated SMA patients can still display neuromuscular symptoms and decline, and for reasons still unknown, patients respond differently to the treatment, roughly dividing into groups of responders that improve, responders that plateau and non-responders [8,12–15]. While recen","PeriodicalId":12606,"journal":{"name":"Future Neurology","volume":" ","pages":""},"PeriodicalIF":1.3,"publicationDate":"2019-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2217/FNL-2019-0001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48602001","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":"Could novel diagnostic technology Cognetivity accelerate dementia research? An interview with Dr Sina Habibi","authors":"Sina Habibi, Rachel Jenkins","doi":"10.2217/FNL-2019-0005","DOIUrl":"https://doi.org/10.2217/FNL-2019-0005","url":null,"abstract":"","PeriodicalId":12606,"journal":{"name":"Future Neurology","volume":" ","pages":""},"PeriodicalIF":1.3,"publicationDate":"2019-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2217/FNL-2019-0005","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47432377","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}
Medulloblastoma is the most common embryonal tumor in children. The current standard of care comprises surgical resection, radiation and chemotherapy. Patients are stratified into standard and high risk based on the degree of resection, presence of metastatic disease and histopathology. Cure rates dramatically improved during the past decades reaching 70–80% (high and average risk, respectively). Infant medulloblastoma has a worse outcome as the use of radiation therapy is very limited, a group of patients still has dismal outcome despite appropriate therapy, and the unacceptable long-term therapy side effects in survivors. Advanced molecular techniques have allowed scientists to discover four distinct molecular subgroups and correlate them with multiple factors such as histopathology, clinical behavior and possible therapeutic targets.
{"title":"Molecular genetics of medulloblastoma in children: diagnostic, therapeutic and prognostic implications","authors":"M. Doussouki, A. Gajjar, Omar Chamdine","doi":"10.2217/FNL-2018-0030","DOIUrl":"https://doi.org/10.2217/FNL-2018-0030","url":null,"abstract":"Medulloblastoma is the most common embryonal tumor in children. The current standard of care comprises surgical resection, radiation and chemotherapy. Patients are stratified into standard and high risk based on the degree of resection, presence of metastatic disease and histopathology. Cure rates dramatically improved during the past decades reaching 70–80% (high and average risk, respectively). Infant medulloblastoma has a worse outcome as the use of radiation therapy is very limited, a group of patients still has dismal outcome despite appropriate therapy, and the unacceptable long-term therapy side effects in survivors. Advanced molecular techniques have allowed scientists to discover four distinct molecular subgroups and correlate them with multiple factors such as histopathology, clinical behavior and possible therapeutic targets.","PeriodicalId":12606,"journal":{"name":"Future Neurology","volume":" ","pages":""},"PeriodicalIF":1.3,"publicationDate":"2019-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2217/FNL-2018-0030","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45708707","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":"Welcome to the 14th Volume of Future Neurology","authors":"Rachel Jenkins","doi":"10.2217/FNL-2018-0035","DOIUrl":"https://doi.org/10.2217/FNL-2018-0035","url":null,"abstract":"","PeriodicalId":12606,"journal":{"name":"Future Neurology","volume":" ","pages":""},"PeriodicalIF":1.3,"publicationDate":"2019-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2217/FNL-2018-0035","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42681600","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}
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