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Journal of Neurology
Journal Prestige (SJR): 1.626
Citation Impact (citeScore): 3
Number of Followers: 19  
 
  Hybrid Journal Hybrid journal (It can contain Open Access articles)
ISSN (Print) 1432-1459 - ISSN (Online) 0340-5354
Published by Springer-Verlag Homepage  [2658 journals]
  • Correction to: Sleep disturbances in craniopharyngioma: a challenging
           diagnosis

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      PubDate: 2021-11-01
       
  • Correction to: Prevalence of freezing of gait in Parkinson’s disease: a
           systematic review and meta-analysis

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      PubDate: 2021-11-01
       
  • Gaetano Perusini (1879–1915)

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      PubDate: 2021-11-01
       
  • Correction to: Long-term psychosocial outcome following mild traumatic
           brain injury and minor stroke: a direct longitudinal comparison

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      PubDate: 2021-11-01
       
  • Richard Stern (1878–1942)

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      PubDate: 2021-11-01
       
  • A dorsolateral medullary lesion causing persistent down-beating nystagmus

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      PubDate: 2021-11-01
       
  • Spontaneous spinal cord ischemia during COVID-19 infection

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      PubDate: 2021-11-01
       
  • CMV meningitis associated with dimethyl fumarate therapy-induced
           lymphopenia in a multiple sclerosis patient

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      PubDate: 2021-11-01
       
  • Neurosensory dysphagia in a COVID-19 patient

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      PubDate: 2021-11-01
       
  • Comment on the paper Negative anti-SARS-CoV-2 S antibody response
           following Pfizer SARS-CoV-2 vaccination in a patient on ocrelizumab: the
           likely explanation for this phenomenon based on our observations

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      PubDate: 2021-11-01
       
  • Cutaneous diseases related to a hyperactive T-cell response in
           ocrelizumab-treated multiple sclerosis patients

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      PubDate: 2021-11-01
       
  • Palilalia as a prominent feature of anti-NMDA receptor encephalitis in a
           woman with COVID-19

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      PubDate: 2021-11-01
       
  • Management considerations for stroke-like episodes in MELAS with
           concurrent COVID-19 infection

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      Abstract: There have been considerations since the beginning of the Coronavirus pandemic that COVID-19 infection, like any other viral illness, can trigger neurological and metabolic decompensation in patients with mitochondrial diseases. At the time of writing, there were no published reports reviewing experiences and guidelines about management of COVID-19 infection in this patient population. We present a challenging case of an adult patient with a known diagnosis of Mitochondrial Encephalomyopathy, Lactic Acidosis and Stroke-like Episodes (MELAS) complicated by COVID-19 infection. She initially presented with altered mental status and vomiting and went on to develop a stroke-like episode, pancreatitis, and pneumatosis intestinalis. We review salient features of her hospitalization, including initiation of thromboprophylaxis in relation to intravenous arginine therapy, caution regarding medications such as remdesivir, and the incidence of gastrointestinal complications.
      PubDate: 2021-11-01
       
  • John Langdon Haydon Down (1828–1896)

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      PubDate: 2021-11-01
       
  • Disease-modifying therapies and SARS-CoV-2 vaccination in multiple
           sclerosis: an expert consensus

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      Abstract: Coronavirus disease (COVID-19) appeared in December 2019 in the Chinese city of Wuhan and has quickly become a global pandemic. The disease is caused by the severe acute respiratory syndrome coronavirus type-2 (SARS-CoV-2), an RNA beta coronavirus phylogenetically similar to SARS coronavirus. To date, more than 132 million cases of COVID19 have been recorded in the world, of which over 2.8 million were fatal (https://coronavirus.jhu.edu/map.html). A huge vaccination campaign has started around the world since the end of 2020. The availability of vaccines has raised some concerns among neurologists regarding the safety and efficacy of vaccination in patients with multiple sclerosis (MS) taking immunomodulatory or immunosuppressive therapies.
      PubDate: 2021-11-01
       
  • Assessment of muscular strength and functional capacity in the juvenile
           and adult myotonic dystrophy type 1 population: a 3-year follow-up study

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      Abstract: Introduction Myotonic dystrophy type 1 (DM1) is a progressive, multisystemic, and autosomal dominant disease. Muscle wasting and weakness have been associated with impaired functional capacity and restricted social participation in affected individuals. The disease’s presentation is very heterogenous and its progression is still under-documented. Objective The aim of the study was to document the progression of muscular strength and functional capacity in the DM1 population over a 3-year period. Methods Twenty-three individuals with juvenile or adult phenotypes of DM1 were recruited to complete clinical assessments in 2016 and 2019. Maximal isometric muscle strength (MIMS) was evaluated with quantified muscle testing and functional capacity was evaluated with the Mini-BESTest, the 10-m walk test at comfortable and maximal speeds, the Timed Up and Go and the 6-min walk test. Participants also completed three questionnaires: DM1-Activ, Upper Extremity Functional Index and Lower Extremity Functional Scale (LEFS). Subgroup analyses were evaluated for sex, phenotype, and type of physical activity practiced during the 3-year period. Results For the whole group, there was a significant decline in the scores of the Mini-BESTest and the LEFS. Also, MIMS significantly declined for prehension, lateral pinch as well as for hip abductors, knee extensors and ankle dorsiflexors muscle groups. Subgroups analyses revealed that men lost more MIMS than women, and that adult phenotype lost more MIMS than juvenile phenotype. Conclusion Quantified muscle testing is a better indicator of disease progression over a 3-year period than functional tests. Phenotype and sex are important factors that influence the progression of DM1.
      PubDate: 2021-11-01
       
  • RFC1 AAGGG repeat expansion masquerading as Chronic Idiopathic Axonal
           Polyneuropathy

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      Abstract: Background A biallelic intronic AAGGG repeat expansion in the Replication Factor C subunit 1 (RFC1) gene has been recently associated with Cerebellar Ataxia, Neuropathy, Vestibular Areflexia Syndrome, a disorder often presenting as a slowly evolving sensory neuropathy at the onset. “Chronic Idiopathic Axonal Polyneuropathy” (CIAP) is a common indolent axonal neuropathy of adulthood which remains without an identifiable cause despite thorough investigations. Methods We screened 234 probands diagnosed with CIAP for a pathogenic biallelic RFC1 AAGGG repeat expansion. Patients were selected from 594 consecutive patients with neuropathy referred to our tertiary-care center for a sural nerve biopsy over 10 years. Results The RFC1 AAGGG repeat expansion was common in patients with pure sensory neuropathy (21/40, 53%) and less frequent in cases with predominantly sensory (10/56, 18%, P < 0.001) or sensorimotor (3/138, 2%, P < 0.001) neuropathy. The mutation was associated with sensory ataxia (τb = 0.254, P < 0.001), autonomic disturbances (35% vs 8%, Prevalence Odds Ratio—POR 6.73 CI 95% 2.79–16.2, P < 0.001), retained deep tendon reflexes (score 18.0/24 vs 11.5/24, R = 0.275, P < 0.001). On pathology, we observed absent/scant regenerative changes (τb = − 0.362, P < 0.001), concomitant involvement of large (100% and 99%, n.s.), small myelinated (97% vs 81%, POR 7.74 CI 95% 1.03–58.4, P = 0.02) and unmyelinated nerve fibers (85% vs 41%, POR 8.52 CI 95% 3.17–22.9, P < 0.001). Cerebellar or vestibular involvement was similarly rare in the two groups. Conclusions This study highlights the frequent occurrence of the RFC1 AAGGG repeat expansion in patients diagnosed with CIAP and characterizes the clinical and pathological features of the related neuro(no)pathy.
      PubDate: 2021-11-01
       
  • The known burden of Huntington disease in the North of Scotland:
           prevalence of manifest and identified pre-symptomatic gene expansion
           carriers in the molecular era

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      Abstract: Background Huntington disease prevalence was first estimated in Grampian, northern Scotland in 1984. Molecular testing has since increased ascertainment. Objective To estimate the prevalence of manifest Huntington disease and identified pre-symptomatic gene expansion carriers (IPGEC) in northern Scotland, and estimate the magnitude of biases in prevalence studies that rely upon routine coding in primary care records. Methods Cases were ascertained using North of Scotland genetic laboratory, clinic, and hospital records. Prevalence was calculated for manifest and IPGEC on 01/07/2016 and 01/01/2020 and compared with local published data. Results The prevalence of manifest Huntington disease in northern Scotland in 2020 was 14.6 (95% CI 14.3–15.3) per 100,000, and of IPGEC was 8.3 (95% CI 7.8–9.2) per 100,000. Whilst the population of northern Scotland decreased by 0.05% between 2016 and 2020, the number of manifest and identified pre-symptomatic gene expansion carriers increased by 7.4% and 23.3%, respectively. Manifest disease in Grampian increased by 45.9% between 1984 and 2020. More women than men had a diagnosis. General Practice coding underestimated symptomatic molecularly confirmed prevalence by 2.2 per 100,000 people. Conclusion Even in an area with previously high ascertainment, there has been a 45.9% increase in manifest Huntington disease over the last 30 years. Within our catchment area, prevalence varies between health board regions with similar community-based services. Such variation in prevalence could have major drug cost and service delivery implications, especially if expensive, complexly administered therapies prove successful. Health services should gather accurate population-based data on a regional basis to inform service planning.
      PubDate: 2021-11-01
       
  • Baseline cognitive profile is closely associated with long-term motor
           prognosis in newly diagnosed Parkinson’s disease

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      Abstract: Objectives To investigate the association between cognitive function at baseline and the progression of motor disability in Parkinson’s disease (PD). Methods We consecutively enrolled 257 drug-naïve patients with early-stage PD (follow-up > 2 years) who underwent a detailed neuropsychological test at initial assessment. Factor analysis was conducted to yield four cognitive function factors and composite scores thereof: Factor 1 (visual memory/visuospatial), Factor 2 (verbal memory), Factor 3 (frontal/executive), and Factor 4 (attention/working memory/language). The global cognitive composite score of each patient was calculated based on these factors. Subsequently, we assessed the effect of baseline cognitive function on long-term motor outcomes, namely levodopa-induced dyskinesia (LID), wearing-off, freezing of gait (FOG), and rate of longitudinal increases in levodopa-equivalent dose (LED). Results Cox regression analysis demonstrated that higher Factor 3 (frontal/executive) composite scores (i.e., better cognitive performance) were associated with early development of LID [hazard ratio (HR), 1.507; p = 0.003], whereas higher Factor 1 (visual memory/visuospatial) composite scores (i.e., better cognitive performance) were associated with a lower risk for FOG (HR 0.683; p = 0.017). We noted that higher global cognitive composite scores were associated with a lower risk for developing FOG (HR 0.455; p = 0.045). The linear mixed model demonstrated that higher global cognitive composite scores and better cognitive performance in visual memory/visuospatial function were associated with slower longitudinal increases in LED. Conclusions These findings suggest that baseline cognitive profiles have prognostic implications on several motor aspects in patients with PD.
      PubDate: 2021-11-01
       
  • Vaccine-induced immune thrombosis and thrombocytopaenia: incidence,
           mechanism and treatment

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      PubDate: 2021-10-06
       
 
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