Neurology International最新文献

{"title":"Albuminocytologic Dissociation and the Impact of Age-Adjusted Cerebrospinal Fluid Protein Levels in Guillain-Barré Syndrome.","authors":"Nithisha Thatikonda, Alexandru Lerint, Chaitra Takle, Xiang Fang, Chilvana Patel","doi":"10.3390/neurolint17020018","DOIUrl":"10.3390/neurolint17020018","url":null,"abstract":"<p><p><b>Background:</b> This study examined the impact of age-adjusted cerebrospinal fluid (CSF) protein levels on clinical characteristics, disease severity, and outcomes in Guillain-Barré Syndrome (GBS) patients. <b>Methods:</b> This retrospective study included 71 GBS patients at UTMB Galveston. Albuminocytologic dissociation (ACD) was defined as CSF-total protein (CSF-TP) >0.45 g/L with a cell count of <50 cells/L. Patients were grouped using the conventional cutoff (>0.45 g/L) and age-adjusted upper limits (URLs) for CSF-TP levels, comparing clinical, CSF, and electrophysiological characteristics across groups. <b>Results:</b> The mean age was 50 years (SD = 14.5). The mean age of patients with a CSF-TP > 45 g/L was higher (53 vs. 39 years, <i>p</i> = 0.000), whereas no such difference was noted using age-dependent URLs. Using age-adjusted CSF-TP URLs reduced the sensitivity for detecting ACD by 20%. CSF-TP > age-adjusted URLs were associated with lower MRC sum scores (39 vs. 47.43, <i>p</i> = 0.000), higher ICU admission rates (34% vs. 20%, <i>p</i> = 0.003), and the need for second-line treatment (41% vs. 17%, <i>p</i> = 0.049), and the trends were not observed with the conventional cutoff of 0.45 g/L. CSF-TP was an independent predictor of lower MRC sum scores (<i>p</i> = 0.009, 95% CI -0.058, -0.009) and higher GBS disability scores (<i>p</i> = 0.015, 95% CI 0.000, 0.004). <b>Conclusions:</b> ACD is a common finding in GBS, but normal protein levels do not exclude the diagnosis. Using age-adjusted URLs might improve specificity but reduce sensitivity for ACD detection, potentially increasing false negatives. CSF-TP levels exceeding age-adjusted URLs were more strongly associated with greater disease severity and poorer outcomes compared to the conventional cutoff of 0.45 g/L.</p>","PeriodicalId":19130,"journal":{"name":"Neurology International","volume":"17 2","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11858027/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143493026","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Proprioceptive Neuromuscular Facilitation and/or Electrical Stimulation in Patients with Peripheral Facial Paralysis: A Systematic Review.","authors":"Nerea Dominguez-Defez, Juan Lopez-Barreiro, Pablo Hernandez-Lucas, Ana González-Castro","doi":"10.3390/neurolint17020017","DOIUrl":"10.3390/neurolint17020017","url":null,"abstract":"<p><strong>Background: </strong>Peripheral facial paralysis (PFP) affects the facial nerve, the seventh cranial nerve. It has an incidence rate of 20-30 cases per 100,000 habitants. The diagnosis is clinical, though imaging tests may be required in some cases. The treatment protocol includes medication, physiotherapy, and, in certain cases, surgery. Proprioceptive neuromuscular facilitation (PNF) techniques and electrical stimulation have been shown to be significant for recovery. Although PFP has a high recovery rate, up to 40% of patients may experience permanent sequelae.</p><p><strong>Objective: </strong>to assess the efficacy of treatment based on electrical stimulation and/or PNF in patients affected by PFP.</p><p><strong>Methods: </strong>A systematic search was conducted across six databases (PubMed, Medline, SportDiscus, CINAHL, Scopus, and Web of Science) in November 2024. Randomized controlled trials were included.</p><p><strong>Results: </strong>Fourteen articles were analyzed, applying PNF and/or electrical stimulation methods, pharmacological treatment, low-level laser treatment, subcutaneous collagen injections, and physiotherapy protocols involving facial expression exercises, yielding evidence for the variables assessed.</p><p><strong>Conclusions: </strong>PNF and/or electrical stimulation treatment in patients with PFP can be effective when employed early with appropriate parameters, showing promising results in improving quality of life, facial movement quality, and CMAP and reducing both the incidence and degree of synkinesis.</p>","PeriodicalId":19130,"journal":{"name":"Neurology International","volume":"17 2","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11858216/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143492470","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pituitary Spindle Cell Oncocytoma: More than a Grade 1 Tumor?","authors":"Jonathan Hammond, Zacharie Gagne, Bojana Mitrovic, Stefano M Priola","doi":"10.3390/neurolint17020016","DOIUrl":"10.3390/neurolint17020016","url":null,"abstract":"<p><strong>Background/objectives: </strong>Spindle cell oncocytomas (SCOs) of the pituitary gland are rare tumors often misdiagnosed for nonfunctioning pituitary macroadenomas. Although classified as grade 1, they are often challenging in terms of diagnosis and treatment. Pituitary SCOs harbor peculiar features such as hypervascularity and stronger adherence to surrounding structures, with increased risk of hemorrhage, partial resection, and significantly higher recurrence rate. Almost 100 cases have been reported so far. The role of surgery is still crucial for the decompression of the optic chiasm as well as for achieving diagnosis. However, given the higher tendency of recurrence, the role of postoperative radiotherapy has been investigated over the last few years.</p><p><strong>Case presentation: </strong>Here, we reported a case of a 48-year-old female with a pituitary SCO treated at our institution, in which we focused on diagnosis, treatment, and follow-up.</p><p><strong>Conclusions: </strong>This type of tumor presents a challenge related to its higher vascularity and strong adherence to the surrounding structures. Adjuvant radiotherapy is something that should be considered, especially when gross total resection is not achieved, and finally, SCOs require diligent follow-up to monitor for any signs of disease recurrence or progression.</p>","PeriodicalId":19130,"journal":{"name":"Neurology International","volume":"17 2","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11858046/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143493034","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"fMRI Insights into Visual Cortex Dysfunction as a Biomarker for Migraine with Aura.","authors":"Damian Pikor, Natalia Banaszek-Hurla, Alicja Drelichowska, Mikołaj Hurla, Jolanta Dorszewska, Tomasz Wolak, Wojciech Kozubski","doi":"10.3390/neurolint17020015","DOIUrl":"10.3390/neurolint17020015","url":null,"abstract":"<p><p>Migraine with aura (MwA) is a common and severely disabling neurological disorder, characterised by transient yet recurrent visual disturbances, including scintillating scotomas, flickering photopsias, and complex geometric patterns. These episodic visual phenomena significantly compromise daily functioning, productivity, and overall quality of life. Despite extensive research, the underlying pathophysiological mechanisms remain only partially understood. Cortical spreading depression (CSD), a propagating wave of neuronal and glial depolarisation, has been identified as a central process in MwA. This phenomenon is triggered by ion channel dysfunction, leading to elevated intracellular calcium levels and excessive glutamate release, which contribute to widespread cortical hyperexcitability. Genetic studies, particularly involving the <i>CACNA gene</i> family, further implicate dysregulation of calcium channels in the pathogenesis of MwA. Recent advances in neuroimaging, particularly functional magnetic resonance imaging (fMRI), have provided critical insights into the neurophysiology of MwA. These results support the central role of CSD as a basic mechanism behind MwA and imply that cortical dysfunction endures beyond brief episodes, possibly due to chronic neuronal dysregulation or hyperexcitability. The visual cortex of MwA patients exhibits activation patterns in comparison to other neuroimaging studies, supporting the possibility that it is a disease-specific biomarker. Its distinctive sensory and cognitive characteristics are influenced by a complex interplay of cortical, vascular, and genetic factors, demonstrating the multifactorial nature of MwA. We now know much more about the pathophysiology of MwA thanks to the combination of molecular and genetic research with sophisticated neuroimaging techniques like arterial spin labelling (ASL) and fMRI. This review aims to synthesize current knowledge and analyse molecular and neurophysiological targets, providing a foundation for developing targeted therapies to modulate cortical excitability, restore neural network stability, and alleviate the burden of migraine with aura. The most important and impactful research in our field has been the focus of this review, which highlights important developments and their contributions to the knowledge and treatment of migraine with aura.</p>","PeriodicalId":19130,"journal":{"name":"Neurology International","volume":"17 2","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11858725/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143493030","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Electroencephalographic and Epilepsy Findings in ZNF711 Variants: A Case Series of Two Siblings.","authors":"Michele Minerva, Lorenzo Perilli, Samanta Carbone, Margherita Maria Rossi, Federica Lotti, Luisa Lonoce, Maria Rosaria Curcio, Salvatore Grosso","doi":"10.3390/neurolint17010014","DOIUrl":"10.3390/neurolint17010014","url":null,"abstract":"<p><strong>Background/objectives: </strong>ZNF711(Zinc finger protein 711) encodes a zinc finger protein of currently undefined function, located on the X chromosome. Current knowledge includes a limited number of case reports where this gene has been exclusively associated with X-linked intellectual disability (XLID). As far as we are aware, we report the first cases of epilepsy associated with this particular variant. Our aim is to further delineate the phenotypic spectrum of ZNF711 gene pathogenic variants, adding clinical features to this rare condition, following a genotype-first approach.</p><p><strong>Case presentation: </strong>We describe the familiar case of two male siblings presenting with moderate intellectual disability (ID), language delay, and motor stereotypies. Additionally, they experienced generalized tonic-clonic seizures (GTCSs) and myoclonic seizures with interictal electroencephalographic abnormalities. Both children underwent various genetic testing and counselling, including an extended next-generation sequencing (NGS) panel, revealing a hemizygous c.657C > G pathogenic variant in the ZNF711 gene from maternal inheritance.</p><p><strong>Conclusions: </strong>This case expands the clinical range of ZNF711 variants by highlighting epilepsy as a potential comorbidity and suggesting other possible causal candidates for generalized epilepsy. Moreover, it emphasizes the need for further research into the phenotypic spectrum associated with this variant.</p>","PeriodicalId":19130,"journal":{"name":"Neurology International","volume":"17 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11767995/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143033729","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Optical Coherence Tomography in Huntington's Disease-A Potential Future Biomarker for Neurodegeneration?","authors":"Clancy Cerejo, Nicolas De Cleene, Elias Mandler, Katarina Schwarzová, Samuel Labrecque, Philipp Mahlknecht, Florian Krismer, Atbin Djamshidian, Klaus Seppi, Beatrice Heim","doi":"10.3390/neurolint17010013","DOIUrl":"10.3390/neurolint17010013","url":null,"abstract":"<p><p>Huntington's disease (HD) is a progressive neurodegenerative disorder for which, until now, only symptomatic treatment has been available. Lately, there have been multiple ongoing clinical trials targeting therapeutic agents for preventing disease onset or slowing disease progression in HD. These studies are in constant need of reliable biomarkers for neurodegeneration in HD. In recent years, retinal biomarkers have attracted significant attention in neurodegenerative disorders. Likewise, optical coherence tomography (OCT) is being evaluated as a potential biomarker in HD. In this article, we review the existing literature on OCT as a biomarker for neurodegeneration in HD.</p>","PeriodicalId":19130,"journal":{"name":"Neurology International","volume":"17 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11767877/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143033746","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Analysis of Upper Facial Weakness in Central Facial Palsy Following Acute Ischemic Stroke.","authors":"Monton Wongwandee, Kantham Hongdusit","doi":"10.3390/neurolint17010012","DOIUrl":"10.3390/neurolint17010012","url":null,"abstract":"<p><strong>Background: </strong>Central facial palsy (CFP), resulting from upper motor neuron lesions in the corticofacial pathway, is traditionally characterized by the sparing of the upper facial muscles. However, reports of upper facial weakness in CFP due to acute ischemic stroke have challenged this long-held assumption. This study aimed to determine the prevalence of upper facial weakness in CFP and identify its associated clinical factors.</p><p><strong>Methods: </strong>In this cross-sectional study, we evaluated consecutive patients with acute ischemic stroke admitted to a university hospital in Thailand from January 2022 to June 2023. Full-face video recordings were analyzed using the Sunnybrook Facial Grading System. Upper facial weakness was defined as asymmetry in at least one upper facial expression. Multivariable logistic regression was performed to identify factors associated with upper facial weakness.</p><p><strong>Results: </strong>Of 108 patients with acute ischemic stroke, 92 had CFP, and among these, 70 (76%) demonstrated upper facial weakness. Tight eye closure (force and wrinkle formation, both 42%) was the most sensitive indicator for detecting upper facial weakness. Greater stroke severity, as reflected by higher NIHSS scores (adjusted odds ratio [aOR], 1.42; 95% CI 1.07-1.88) and the presence of lower facial weakness (aOR, 6.56; 95% CI 1.85-23.29) were significantly associated with upper facial involvement. Although upper facial weakness was generally milder than lower facial weakness, its severity correlated with increasing lower facial asymmetry during movement.</p><p><strong>Conclusions: </strong>Contrary to traditional teaching, upper facial weakness is common in CFP due to acute ischemic stroke. The severity of stroke and the presence of lower facial weakness are key predictors of upper facial involvement. These findings underscore the need for clinicians to reconsider the diagnostic paradigm, recognizing that upper facial weakness can occur in CFP. Enhanced awareness may improve diagnostic accuracy, inform treatment decisions, and ultimately lead to better patient outcomes.</p>","PeriodicalId":19130,"journal":{"name":"Neurology International","volume":"17 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11767383/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143033725","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Early Polytherapy for Probably Benzodiazepine Refractory Naïve Status Epilepticus (Stage 1 Plus).","authors":"Giuseppe Magro","doi":"10.3390/neurolint17010011","DOIUrl":"10.3390/neurolint17010011","url":null,"abstract":"<p><p>Stage 1 Plus is defined here as a naïve, previously untreated, status epilepticus (SE) that is probably refractory to Benzodiazepines (BDZ). These cases include not only prolonged SE as previously proposed by the author (SE lasting > 10 min) but also other cases notoriously associated with BDZ refractoriness such as the absence of prominent motor phenomena and acute etiology (especially primary central nervous system etiology). Interestingly, the absence of prominent motor phenomena as is the case of non convulsive SE might implicitly fall in the category of prolonged SE due to the delay in recognition and treatment. Future studies should help identify other factors associated with BDZ refractoriness, therefore widening the definition of Stage 1 Plus. The appropriate timing for defining prolonged SE may also differ depending on different etiology. Consequently, in future tailored models of SE, the definition of prolonged SE could be enhanced by defining it for a longer duration than Tx, a time point that changes based on different etiologies (x), Tx being much shorter than 10 min in acute etiologies. These cases of naïve probably BDZ refractory SE (Stage 1 Plus) might require a different approach: combined polytherapy from the start. The objective of this review is to provide pathophysiological and pre-clinical evidence, mostly from animal studies, for the different approach of combined polytherapy from the start for those cases of SE falling in the definition of Stage 1 Plus.</p>","PeriodicalId":19130,"journal":{"name":"Neurology International","volume":"17 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11767287/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143033728","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Initial Contact with Forefoot or Rearfoot in Spastic Patients After Stroke-Three-Dimensional Gait Analysis.","authors":"Inês Mendes-Andrade, Miguel Reis E Silva, Jorge Jacinto","doi":"10.3390/neurolint17010010","DOIUrl":"10.3390/neurolint17010010","url":null,"abstract":"<p><strong>Background/objectives: </strong>Post-stroke hemiparetic gait often presents with asymmetric patterns to compensate for stability deficits. This study examines gait differences in chronic stroke patients with spastic hemiparesis based on initial foot contact type-forefoot versus rearfoot.</p><p><strong>Methods: </strong>Thirty-four independently walking spastic hemiparetic patients were retrospectively analyzed. Using 3D gait analysis, patients were categorized by initial contact type. Spatiotemporal descriptors, joint kinematics, kinetics, and EMG patterns were compared across groups.</p><p><strong>Results: </strong>Patients with rearfoot initial contact (G1) showed higher cadence, longer single-limb support time and shorter stride times than those with forefoot contact (G0). G1 patients also demonstrated greater knee flexion during stance, enhancing stability. Additionally, G1 patients with abnormal lateral gastrocnemius activation in the swing phase showed increased ankle power at the end of the stance phase.</p><p><strong>Conclusions: </strong>In post-stroke spastic hemiparetic patients, the type of initial foot contact-forefoot or rearfoot-appears to influence gait characteristics, with rearfoot contact associated with a trend toward improved gait parameters, such as increased cadence and longer single-limb support.</p>","PeriodicalId":19130,"journal":{"name":"Neurology International","volume":"17 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-01-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11768022/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143033731","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Non-Thrombotic Filling Defects in Cerebral Veins and Sinuses: When Normal Structures Mimic a Disease.","authors":"Marialuisa Zedde, Rosario Pascarella","doi":"10.3390/neurolint17010009","DOIUrl":"10.3390/neurolint17010009","url":null,"abstract":"<p><p>Cerebral venous thrombosis (CVT) is a rare and potentially critical cerebrovascular disease involving intracranial dural sinuses and veins. The diagnosis is a stepwise pathway starting from clinical suspicion and employing several neuroradiological techniques, mainly Computed Tomography (CT)-based and Magnetic Resonance Imaging (MRI)-based modalities. The neuroradiological findings, both in the diagnostic phase and in the follow-up phase, may provide some results at risk for misdiagnosis. Non-thrombotic filling defects of intracranial dural sinuses are among them, and the potential sources are artefactual and or anatomical (venous septa and arachnoid granulations). The misdiagnosis of these findings as CVT is potentially linked to dangerous consequences. A potential strategy to avoid this is to increase the knowledge about technical and anatomical reasons for non-thrombotic filling defects of intracranial dural sinuses and their imaging features. The main aim of this review is to address these issues, including the variability of the intracranial venous pathways, providing the solutions for overcoming the above-cited potential misdiagnosis of non-thrombotic filling defects as CVT.</p>","PeriodicalId":19130,"journal":{"name":"Neurology International","volume":"17 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11767902/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143033745","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}