Neurology (Neurology)

Publisher: American Academy of Neurology, American Academy of Neurology

Journal description

Current impact factor: 8.30

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 Impact Factor 8.303
2012 Impact Factor 8.249
2011 Impact Factor 8.312
2010 Impact Factor 8.017
2009 Impact Factor 8.172
2008 Impact Factor 7.043
2007 Impact Factor 6.014
2006 Impact Factor 5.69
2005 Impact Factor 4.947
2004 Impact Factor 5.973
2003 Impact Factor 5.678
2002 Impact Factor 5.34
2001 Impact Factor 5.212
2000 Impact Factor 4.781
1999 Impact Factor 5.232
1998 Impact Factor 4.972
1997 Impact Factor 4.526
1996 Impact Factor 4.612
1995 Impact Factor 4.633
1994 Impact Factor 4.347
1993 Impact Factor 3.99
1992 Impact Factor 4.355

Impact factor over time

Impact factor
Year

Additional details

5-year impact 8.40
Cited half-life 9.00
Immediacy index 1.82
Eigenfactor 0.13
Article influence 2.91
Other titles Neurology (Online), Neurology, Neurology online
ISSN 1526-632X
OCLC 40802116
Material type Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

American Academy of Neurology

  • Pre-print
    • Author cannot archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Conditions
    • NIH, Wellcome Trust, HHMI, CIHR, MRC, BBSRC, NERC, ESRC and STFC authors will on their behalf have the Publisher's version/PDF deposited in PubMed Central for release 12 months embargo after publication
    • If required by institutional policy, Publisher's version/PDF deposited available in PubMed Central may be deposited in institutional repository12 months embargo after publication
    • Publisher last reviewed on 09/04/2014
  • Classification
    ​ white

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: To find the strongest neuroimaging predictors for motor dysfunction using conventional and quantitative imaging measures focusing on the corticospinal tract (CST) in a large cohort of patients with long-standing multiple sclerosis (MS). In this cross-sectional study, a wide spectrum of neuroimaging measures at the whole-brain, cervical, and CST level were analyzed in 195 patients with MS and 54 healthy controls. Motor function was assessed using the Expanded Disability Status Scale (EDSS), 9-Hole Peg Test, Timed 25-Foot Walk Test, and Multiple Sclerosis Walking Scale. Associations between damage in different parts of the motor system and motor functioning were assessed using stepwise linear regression. Patients had an average disease duration of 19.98 (±6.99) years and a median EDSS score of 4 (range: 1.0-8.0). EDSS score was associated with number of infratentorial and cervical cord lesions, lesion volume in the CST, and mean upper cervical cord area (adjusted R(2) = 0.403). Timed 25-Foot Walk Test score was associated with number of infratentorial lesions and cerebellar volume (adjusted R(2) = 0.150), 9-Hole Peg Test score with number of infratentorial lesions and thickness of the cortex connected to the CST (adjusted R(2) = 0.245), and Multiple Sclerosis Walking Scale with number of infratentorial and cervical lesions, thickness of the cortex connected to the CST, and mean upper cervical cord area (adjusted R(2) = 0.354). Motor dysfunction in MS has a complex substrate that cannot be ascribed to a single neuroimaging finding, but is the consequence of infratentorial and spinal cord damage, as well as damage in the CST. © 2015 American Academy of Neurology.
    Neurology 06/2015; DOI:10.1212/WNL.0000000000001756
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    ABSTRACT: To describe the clinical and neurophysiologic patterns of patients with neuronal ceroid lipofuscinoses associated with CLN6 mutations. We reviewed the features of 11 patients with different ages at onset. Clinical disease onset occurred within the first decade of life in 8 patients and in the second and third decades in 3. All children presented with progressive cognitive regression associated with ataxia and pyramidal and extrapyramidal signs. Recurrent seizures, visual loss, and myoclonus were mostly reported after a delay from onset; 7 children were chairbound and had severe dementia less than 4 years from onset. One child, with onset at 8 years, had a milder course. Three patients with a teenage/adult onset presented with a classic progressive myoclonic epilepsy phenotype that was preceded by learning disability in one. The EEG background was slow close to disease onset in 7 children, and later showed severe attenuation; a photoparoxysmal response (PPR) was present in all. The 3 teenage/adult patients had normal EEG background and an intense PPR. Early attenuation of the electroretinogram was seen only in children with onset younger than 5.5 years. Somatosensory evoked potentials were extremely enlarged in all patients. In all patients, multifocal myoclonic jerks and seizures were a key feature, but myoclonic seizures were an early and prominent sign in the teenage/adult form only. Conversely, the childhood-onset form was characterized by initial and severe cognitive impairment coupled with electroretinogram and EEG attenuation. Cortical hyperexcitability, shown by the PPR and enlarged somatosensory evoked potentials, was a universal feature. © 2015 American Academy of Neurology.
    Neurology 06/2015; DOI:10.1212/WNL.0000000000001784
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    ABSTRACT: The ability to name objects or abstract entities is an essential feature of speech and language, being commonly considered a central component of normal neurologic function. For this reason, the bedside testing of naming performance is part of the neurologic examination, especially since naming impairments can signify the early onset of a progressive disease or the occurrence of a more established problem. Modern neuroscience research suggests that naming relies on specific and distributed networks that operate in concert to support various processing stages, spanning from object recognition to spoken words. Likewise, studies evaluating the types of naming impairments in patients with neurologic conditions have contributed to the understanding of acquired forms of naming impairments and the underlying stages during normal language processing. In this article, we review the neurobiological mechanisms supporting naming, with a focus on the clinical application of these concepts. We provide an overview of the stages of cognitive processing that are hypothesized to support naming. For each stage, we explore the evidence revealing its neural basis, drawing parallels to clinical syndromes that commonly disrupt each stage. We review the patterns of naming impairment across various neurologic conditions, including classic language disorders, such as poststroke aphasia or primary progressive aphasia, as well as other diseases where language impairments may be subtle but helpful for the appropriate diagnosis. In this context, we provide a structured and practical guide for the bedside naming assessments rooted in modern neuroscience, aimed at supporting the evaluation and diagnosis of neurologic conditions that affect language. © 2015 American Academy of Neurology.
    Neurology 06/2015; DOI:10.1212/WNL.0000000000001765
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    ABSTRACT: To systematically review temporal changes in perioperative safety of carotid endarterectomy (CEA) in asymptomatic individuals in trial and registry studies. The MEDLINE and EMBASE databases were searched using the terms "carotid" and "endarterectomy" and "asymptomatic" from 1947 to August 23, 2014. Articles dealing with 50%-99% stenosis in asymptomatic individuals were included and low-volume studies were excluded. The primary endpoint was 30-day stroke or death and the secondary endpoint was 30-day all-cause mortality. Statistical analysis was performed using random-effects meta-regression for registry data and for trial data graphical interpretation alone was used. Six trials (n = 4,431 procedures) and 47 community registries (n = 204,622 procedures) reported data between 1983 and 2013. Registry data showed a significant decrease in postoperative stroke or death incidence over the period 1991-2010, equivalent to a 6% average proportional annual reduction (95% credible interval [CrI] 4%-7%; p < 0.001). Considering postoperative all-cause mortality, registry data showed a significant 5% average proportional annual reduction (95% CrI 3%-9%; p < 0.001). Trial data showed a similar visual trend. CEA is safer than ever before and high-volume registry results closely mirror the results of trials. New benchmarks for CEA are a stroke or death risk of 1.2% and a mortality risk of 0.4%. This information will prove useful for quality improvement programs, for health care funders, and for those re-examining the long-term benefits of asymptomatic revascularization in future trials. © 2015 American Academy of Neurology.
    Neurology 06/2015; DOI:10.1212/WNL.0000000000001781
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    ABSTRACT: Genetic variants ε2/ε4 within the APOE gene are established risk factors for lobar intracerebral hemorrhage (ICH). Published preliminary data suggest a potential role for APOE ε4 in risk of nonlobar ICH. We therefore investigated the role of APOE in recurrent nonlobar ICH, and sought to clarify whether effects of APOE on circulating lipids mediate this association. Three hundred sixty-three survivors of nonlobar ICH were followed prospectively for ICH recurrence, with APOE genotype determined at enrollment. All participants had clinical, demographic, and laboratory data captured at time of index ICH and during follow-up. Using a multivariate model, we performed association and interaction analyses of the relationships among APOE genotype, lipid levels, and recurrent nonlobar ICH. We observed 29 nonlobar ICH recurrences among 363 survivors. APOE ε4 was associated with recurrent nonlobar ICH (hazard ratio = 1.31; 95% confidence interval = 1.02-2.69; p = 0.038) after adjustment for age/sex/ethnicity and cardiovascular risk factors. Increasing low-density lipoprotein (LDL) levels were associated with decreased risk of recurrent nonlobar ICH (p = 0.027), as were decreasing HDL levels (p = 0.046). LDL levels modified the association of APOE ε4 with recurrent nonlobar ICH (mediation p < 0.05). No associations were identified between APOE ε2 and recurrent nonlobar ICH. APOE ε4 is associated with recurrent ICH in nonlobar brain regions, providing further evidence for its causal role in ICH unrelated to cerebral amyloid angiopathy. LDL levels modulated this effect, suggesting that circulating lipid levels may mediate a portion of the role of APOE ε4 in nonlobar ICH. © 2015 American Academy of Neurology.
    Neurology 06/2015; DOI:10.1212/WNL.0000000000001790
  • Neurology 06/2015; DOI:10.1212/WNL.0000000000001793
  • Neurology 06/2015; DOI:10.1212/WNL.0000000000001776
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    ABSTRACT: To determine the frequency and range of paraneoplastic neurologic disorders (PNDs) and neuronal antibodies in small cell lung carcinoma (SCLC). Two hundred sixty-four consecutive patients with biopsy-proven SCLC were recruited at the time of tumor diagnosis. All patients underwent full neurologic examination. Serum samples were taken prior to chemotherapy and analyzed for 15 neuronal antibodies. Thirty-eight healthy controls were analyzed in parallel. PNDs were quite prevalent (n = 24, 9.4%), most frequently Lambert-Eaton myasthenic syndrome (3.8%), sensory neuronopathy (1.9%), and limbic encephalitis (1.5%). Eighty-seven percent of all patients with PNDs had antibodies to SOX2 (62.5%), HuD (41.7%), or P/Q VGCC (50%), irrespective of their syndrome. Other neuronal antibodies were found at lower frequencies (GABAb receptor [12.5%] and N-type VGCC [20.8%]) or very rarely (GAD65, amphiphysin, Ri, CRMP5, Ma2, Yo, VGKC complex, CASPR2, LGI1, and NMDA receptor [all <5%]). The spectrum of PNDs is broader and the frequency is higher than previously appreciated, and selected antibody tests (SOX2, HuD, VGCC) can help determine the presence of an SCLC. © 2015 American Academy of Neurology.
    Neurology 06/2015; DOI:10.1212/WNL.0000000000001721
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    ABSTRACT: To evaluate whether diffusion tensor imaging (DTI) will noninvasively reveal white matter changes not present on conventional MRI in acute blast-related mild traumatic brain injury (mTBI) and to determine correlations with clinical measures and recovery. Prospective observational study of 95 US military service members with mTBI enrolled within 7 days from injury in Afghanistan and 101 healthy controls. Assessments included Rivermead Post-Concussion Symptoms Questionnaire (RPCSQ), Post-Traumatic Stress Disorder Checklist Military (PCLM), Beck Depression Inventory (BDI), Balance Error Scoring System (BESS), Automated Neuropsychological Assessment Metrics (ANAM), conventional MRI, and DTI. Significantly greater impairment was observed in participants with mTBI vs controls: RPCSQ (19.7 ± 12.9 vs 3.6 ± 7.1, p < 0.001), PCLM (32 ± 13.2 vs 20.9 ± 7.1, p < 0.001), BDI (7.4 ± 6.8 vs 2.5 ± 4.9, p < 0.001), and BESS (18.2 ± 8.4 vs 15.1 ± 8.3, p = 0.01). The largest effect size in ANAM performance decline was in simple reaction time (mTBI 74.5 ± 148.4 vs control -11 ± 46.6 milliseconds, p < 0.001). Fractional anisotropy was significantly reduced in mTBI compared with controls in the right superior longitudinal fasciculus (0.393 ± 0.022 vs 0.405 ± 0.023, p < 0.001). No abnormalities were detected with conventional MRI. Time to return to duty correlated with RPCSQ (r = 0.53, p < 0.001), ANAM simple reaction time decline (r = 0.49, p < 0.0001), PCLM (r = 0.47, p < 0.0001), and BDI (r = 0.36 p = 0.0005). Somatic, behavioral, and cognitive symptoms and performance deficits are substantially elevated in acute blast-related mTBI. Postconcussive symptoms and performance on measures of posttraumatic stress disorder, depression, and neurocognitive performance at initial presentation correlate with return-to-duty time. Although changes in fractional anisotropy are uncommon and subtle, DTI is more sensitive than conventional MRI in imaging white matter integrity in blast-related mTBI acutely. © 2015 American Academy of Neurology.
    Neurology 06/2015; DOI:10.1212/WNL.0000000000001758
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    ABSTRACT: To examine the relation of performance on brief cognitive tests to development of clinically diagnosed Alzheimer disease (AD) dementia over the following 18 years in a sample of African Americans and European Americans. A composite cognitive test score based on tests of episodic memory, executive function, and global cognition was constructed in a prospective population-based sample of 2,125 participants (55% African American and 61% female) aged 65 years and older residing in 4 Chicago neighborhoods. Time before AD dementia diagnosis was categorized into 6 groups corresponding to data collection periods: 0.1-0.9, 1.0-3.9, 4.0-6.9, 7.0-9.9, 10.0-12.9, and 13.0-17.9 years. Of 2,125 participants without clinical AD dementia, 442 (21%) developed clinical AD dementia over 18 years of follow-up. Lower composite cognitive test scores were associated with the development of AD dementia over the duration of the study. The magnitude of association between composite cognitive test score and development of AD dementia increased from an odds ratio of 3.39 (95% confidence interval 1.72, 6.67; p < 0.001) at 13.0-17.9 years to 9.84 (95% confidence interval 7.41, 13.06; p < 0.001) at 0.1-0.9 years, per SD increment. These associations were consistently larger among European Americans than among African Americans. Performance on individual cognitive tests of episodic memory, executive function, and global cognition also significantly predicted the development of AD dementia, with associations exhibiting a similar trend over 18 years. Our findings suggest that cognitive impairment may manifest in the preclinical phase of AD dementia substantially earlier than previously established. © 2015 American Academy of Neurology.
    Neurology 06/2015; DOI:10.1212/WNL.0000000000001774
  • Neurology 06/2015; DOI:10.1212/WNL.0000000000001771
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    ABSTRACT: We evaluated the frequency and predictive value of ocular fundus abnormalities among patients who presented to the emergency department (ED) with focal neurologic deficits to determine the utility of these findings in the evaluation of patients with suspected TIA and stroke. In this cross-sectional pilot study, ocular fundus photographs were obtained using a nonmydriatic fundus camera. Demographic, neuroimaging, and ABCD(2) score components were collected. Photographs were reviewed for retinal microvascular abnormalities. The results were analyzed using univariate statistics and logistic regression modeling. Two hundred fifty-seven patients presented to the ED with focal neurologic deficits, of whom 81 patients (32%) had cerebrovascular disease (CVD) and 144 (56%; 95% confidence interval: 50%-62%) had retinal microvascular abnormalities. Focal and general arteriolar narrowing increased the odds of clinically diagnosed CVD by 5.5 and 2.6 times, respectively, after controlling for the ABCD(2) score and diffusion-weighted imaging. These fundus findings also significantly differentiated TIA from non-CVD, even after controlling for the ABCD(2) score. Focal and general arteriolar narrowing were independent predictors of CVD overall, and TIA alone, even after controlling for the ABCD(2) score and diffusion-weighted imaging lesions. The inclusion of nonmydriatic ocular fundus photographs in the evaluation of patients presenting to the ED with focal neurologic deficits may assist in the differentiation of stroke and TIA from other causes of focal neurologic deficits. © 2015 American Academy of Neurology.
    Neurology 06/2015; DOI:10.1212/WNL.0000000000001759
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    ABSTRACT: To investigate the effects of NEFL Glu396Lys mutation on the expression and assembly of neurofilaments (NFs) in cutaneous nerve fibers of patients with Charcot-Marie-Tooth disease type 2E (CMT2E). A large family with CMT2E underwent clinical, electrophysiologic, and skin biopsy studies. Biopsies were processed by indirect immunofluorescence (IF), electron microscopy (EM), and Western blot analysis. The clinical features demonstrated intrafamilial phenotypic variability, and the electrophysiologic findings revealed nerve conductions that were either slow or in the intermediate range. All patients had reduced or absent compound muscular action potential amplitudes. Skin biopsies showed axons labeled with the axonal markers protein gene product 9.5 and α-tubulin, but not with NFs. The results of Western blot analysis were consistent with those of IF, showing reduced or absent NFs and normal expression of α-tubulin. EM revealed clusters of regenerated fibers, in absence of myelin sheath abnormalities. Both IF and EM failed to show NF aggregates in dermal axons. The morphometric analysis showed a smaller axonal caliber in patients than in controls. The study of the nodal/paranodal architecture demonstrated that sodium channels and Caspr were correctly localized in patients with CMT2E. Decrease in NF abundance may be a pathologic marker of CMT2E. The lack of NF aggregates, consistent with prior studies, suggests that they occur proximally leading to subsequent alterations in the axonal cytoskeleton. The small axonal caliber, along with the normal molecular architecture of nodes and paranodes, explain the reduced velocities detected in patients with CMT2E. Our results also demonstrate that skin biopsy can provide evidence of pathologic and pathogenic abnormalities in patients with CMT2E. © 2015 American Academy of Neurology.
    Neurology 06/2015; DOI:10.1212/WNL.0000000000001773
  • Neurology 06/2015; DOI:10.1212/WNL.0000000000001769
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    ABSTRACT: Inflammation-related epilepsy is increasingly recognized; however, studies on status epilepticus (SE) are very infrequent. We therefore aimed to determine the frequency of inflammatory etiologies in adult SE, and to assess related demographic features and outcomes. This was a retrospective analysis of a prospective registry of adult patients with SE treated in our center, from January 2008 to June 2014, excluding postanoxic causes. We classified SE episodes into 3 etiologic categories: infectious, autoimmune, and noninflammatory. Demographic and clinical variables were analyzed regarding their relationship to etiologies and functional outcome. Among the 570 SE consecutive episodes, 33 (6%) were inflammatory (2.5% autoimmune; 3.3% infectious), without any change in frequency over the study period. Inflammatory SE episodes involved younger patients (mean age 53 vs 61 years, p = 0.015) and were more often refractory to initial antiepileptic treatment (58% vs 38%, odds ratio = 2.19, 95% confidence interval = 1.07-4.47, p = 0.041), despite similar clinical outcome. Subgroup analysis showed that, compared with infectious SE episodes, autoimmune SE involved younger adults (mean age 44 vs 60 years, p = 0.017) and was associated with lower morbidity (return to baseline conditions in 71% vs 32%, odds ratio = 5.41, 95% confidence interval = 1.19-24.52, p = 0.043) without any difference in mortality. Despite increasing awareness, inflammatory SE etiologies were relatively rare; their occurrence in younger individuals and higher refractoriness to treatment did not have any effect on outcome. Autoimmune SE episodes also occurred in younger patients, but tended to have better outcomes in survivors than infectious SE. © 2015 American Academy of Neurology.
    Neurology 06/2015; DOI:10.1212/WNL.0000000000001717
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    ABSTRACT: To evaluate the appropriateness of dopamine receptor antagonist prescriptions in hospitalized patients with dopamine-requiring diseases after implementation of an automated prescription alert system. We examined dopamine receptor antagonist prescriptions in hospitalized patients with dopamine-requiring diseases and physician response to an automated drug contraindication alert system at Barnes-Jewish Hospital from 2009 to 2013. A detailed review of patient medical records was performed for all alert events generated when a physician prescribed a dopamine receptor antagonist concurrently with a dopamine receptor agonist in hospitalized patients. Two movement disorders neurologists determined the appropriateness of each prescription, based on patient medical history, through consensus. Physician response to alert was compared by indication for the prescription and physician specialty. Of 237 orders, 197 (83.1%) prescriptions for dopamine receptor antagonists were considered inappropriate. The prevalence of inappropriate dopamine receptor antagonist prescriptions per levodopa prescriptions was 16.10% (95% confidence interval 9.47, 22.73) in psychiatry, 7.51% (6.16, 8.86) in general medicine, 6.14% (4.49, 7.79) in the surgical specialties, and 0.85% (0.46, 1.25) in the neurologic/neurosurgical specialties. Of the inappropriate prescriptions, 146 (74.1%) were continued despite the alert. The strongest predictor of discontinuation of dopamine receptor antagonist medications was use of the medication to treat nausea or emesis (p < 0.001). Despite successfully identifying instances when dopamine antagonists were prescribed to patients with dopamine-requiring diseases, the alert system modestly affected physician prescribing behavior, highlighting the need for improved education of health care providers. © 2015 American Academy of Neurology.
    Neurology 06/2015; DOI:10.1212/WNL.0000000000001745