Restorative neurology and neuroscience Journal Impact Factor & Information

Publisher: IOS Press

Journal description

The journal is interdisciplinary. Papers relating the plasticity and response of the nervous system to accidental of experimental injuries or in-terventions, transplantation, neurodegenerative disorders, and experimental strategies to improve regeneration or functional recovery will be considered for publication. Experimental and clinical research papers adopting fresh conceptual approaches are encouraged. The overriding criteria for publication are novelty, significant experimental or clinical relevance, and interest to a multidisciplinary audience. Experiments on unanesthetized animals should conform with the standards for the use of laboratory animals as established by the Institute of Laboratory Animal Resources, US National Academy of Sciences. Experiments in which paralytic agents are used must be justified. Patient identity should be concealed. All manuscripts are sent out for blind "peer review" to editorial board members or outside reviewers.

Current impact factor: 4.18

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 Impact Factor 4.179
2012 Impact Factor 2.929
2011 Impact Factor 2.51
2010 Impact Factor 3.349
2009 Impact Factor 3.714
2008 Impact Factor 1.978
2007 Impact Factor 1.415
2006 Impact Factor 2.862
2005 Impact Factor 1.825
2004 Impact Factor 1.412
2003 Impact Factor 1.623
2002 Impact Factor 0.836
2001 Impact Factor 0.678
2000 Impact Factor 0.911
1999 Impact Factor 0.5
1998 Impact Factor 1.196
1997 Impact Factor 1.117
1996 Impact Factor 0.56
1995 Impact Factor 0.915
1994 Impact Factor 1.435
1993 Impact Factor 2.609

Impact factor over time

Impact factor
Year

Additional details

5-year impact 3.41
Cited half-life 5.40
Immediacy index 0.42
Eigenfactor 0.00
Article influence 1.10
Website Restorative Neurology and Neuroscience website
Other titles Restorative neurology and neuroscience (Online)
ISSN 0922-6028
OCLC 47094437
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

IOS Press

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • On author's personal website, institutional website or funder's website, including PubMed Central
    • Non-commercial use only
    • Publisher copyright and source must be acknowledged
    • Author's version can be used
    • Publisher's pdf can be used on institutional website, company website or funding agency website for a fee
  • Classification
    ​ green

Publications in this journal

  • Restorative neurology and neuroscience 06/2015;
  • Restorative neurology and neuroscience 06/2015;
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    ABSTRACT: Background and Purpose: Previous studies demonstrated that administering extradural cortical stimulation (ECS) to rats during the acute phase of a photothrombotic infarct enhances motor recovery. However, the effect of ECS during the subacute phase was unknown. We aimed to evaluate the effects of ECS on motor recovery in a rat model of subacute photothrombotic stroke. Methods: Photothrombotic ischemic injury to the left sensorimotor cortex (SMC) was induced in 41 male Sprague-Dawley rats using Rose-bengal dye (20 mg/kg) and cold light. The rats were randomly divided into two groups: ECS on infarcted SMC (ECS group) and no ECS on infarcted SMC (non-stimulated group). The ECS group received continuous ECS for 14 days starting from day 5 after the stroke onset. Behavioral training with the single-pellet reaching task (SPRT) was performed daily for all of the rats from the fifth day after stroke onset. After 19 days, brain sections were immunostained to allow the quantification of infarct volumes and the evaluation of the neuronal markers. Results: The SPRT scores showed significantly faster and greater improvement in the ECS group than in the non-stimulated group. There were no significant differences in infarct size. However, in the ECS group, significantly more doublecortin-labeled cells were identified close to the penumbra region of the cerebral cortex. Conclusion: ECS in the subacute phase improved the behavior motor function in the stroke rat model, and induced a significant axonal sprouting in the peri-infarct area.
    Restorative neurology and neuroscience 03/2015; DOI:10.3233/RNN-140445
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    ABSTRACT: Purpose: The present study was conducted to determine changes in the expression of voltage-gated sodium channels (VGSCs) α-subunits after nerve injury and their relation with development of neuropathic pain. Methods: We used the crush injury model of regeneration of the sciatic nerve (Crush) and the spared nerve injury (SNI) model of neuropathic pain in the rat. Measurements of thermal and mechanical pain thresholds were performed until 3 months after injury. Real-time PCR and immunohistochemistry of VGSC α-subunits were used to evaluate the mRNA and protein expression in the DRG. Results: Both nerve injuries induced similar alterations in the VGSCs expression at 7 dpi, with upregulation of Nav1.3, and downregulation of Nav1.7, Nav1.8 and Nav1.9. These changes persisted until 28 days, when hyperalgesia was still present in SNI but not in Crush rats. At 90 days, mRNA expression of all analyzed α-subunits returned to basal levels in the Crush group. However, SNI rats still showed altered expression of VGSCs, and neuropathic pain responses. Immunohistochemical staining revealed that Nav1.8 and Nav1.9 were widely expressed in IB4-positive neurons of the DRG, relevant in pain processing. The population of neurons coexpressing each α-subunit and IB4 was also affected by the injury, more markedly after the Crush. Conclusion: Shifts in VGSCs expression occur in parallel to neuropathic pain behavior in rats early after injury, while at later times they appear to be more related to sensory nerve degeneration and regeneration processes.
    Restorative neurology and neuroscience 02/2015; DOI:10.3233/RNN-140444
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    ABSTRACT: Purpose: The aim of the present study was to explore the use of two-photon microscopy for investigating the therapeutic time window of methylprednisolone (MP) treatment after spinal cord injury (SCI). Methods: Twenty-four YFP H-line mice were subjected to hemisection SCI and then divided into four groups. Group 1 received MP at 30 min post-injury; group 2 received MP at 8 h post-injury; group 3 received MP at 24 h post-injury; and group 4 received saline at 30 min post-injury. Post-injury axonal dieback was imaged in vivo using two-photon microscopy. After all imaging sessions, histological examination of the surviving neurons and microglial/macrophage accumulation was performed. Results: Two-photon imaging revealed the degree of progressive axon damage after SCI. Group 1 exhibited a shorter axonal dieback distance and slower axonal dieback speed than groups 2, 3, and 4 (p < 0.01). MAP-2 staining revealed greater neuronal survival in group 1 than in groups 2, 3, and 4 (p < 0.05). F4/80 staining revealed greater microglial/macrophage density in groups 2, 3, and 4 than in group 1 (p < 0.05). Conclusion: MP therapy may help attenuate progressive axon damage, reduce neuronal death, and inhibit microglial/macrophage accumulation, especially when initiated shortly after SCI.
    Restorative neurology and neuroscience 02/2015; DOI:10.3233/RNN-140463
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    ABSTRACT: Purpose: Several clinical trials have highlighted general favorable outcomes of intravenous tissue type plasminogen activator (rt-PA) in acute ischemic stroke using different measures including, National Institutes of Health Stroke Scale (NIHSS) and modified Rankin Scale (mRS). Findings from most of these measures indicate that the benefits of rt-PA are time dependent, thus, supporting intensive efforts to fast-track hospital thrombolytic treatment in patients with stroke. Despite the widespread benefits of rt-PA, the effectiveness of this therapy on specific functions such as ambulatory performance of the recovering stroke patient is not fully investigated. We aim to investigate this issue in the current study. Methods: We analyzed data from a retrospective cohort of acute ischemic stroke patients admitted to Greenville Health System (GHS) between 2010-2013. We identified patients who received rt-PA within a 4.5 hour time frame following the onset of acute ischemic stroke symptoms. Our analysis compared ambulatory variables and hospital-level characteristics in proportions of patients receiving rt-PA with those not receiving rt-PA. This analysis determined whether early treatment with rt-PA is associated with favorable changes in ambulatory status from admission to discharge following acute ischemic stroke. Results: Among 663 patients with ischemic stroke who were eligible to receive rt-PA, 241 patients received rt-PA and 422 patients did not due to several risk factors. We found a statistically significant difference (P < 0.001) for changes in ambulation status from hospital admission to discharge between patients receiving rt-PA and patients who did not receive rt-PA. Among patients who received rt-PA, 27.8% improved in their ambulation status, 41.9% saw no change in their ambulation status, 0.4% worsened in their ambulation status, and 29.9% were unable to be determined. Of the patients who did not receive rt-PA, 20.1% improved in their ambulation status, 61.8% saw no change in their ambulation status, 1.4% worsened in their ambulation status, and 16.6% were unable to be determined. Conclusion: Our current study indicates that early treatment with rt-PA may be associated with favorable changes in ambulatory status from admission to discharge following acute ischemic stroke.
    Restorative neurology and neuroscience 02/2015; DOI:10.3233/RNN-140480
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    ABSTRACT: Background: Transcranial Electrical Stimulation (tES) methods have been shown to enhance performance across a range of cognitive tasks. It is thought that tES can be used to enhance the treatment-effects of cognitive training (CT), leading to lasting improvements in neurocognitive function. Recently, a small number of studies have investigated the effects of tES combined with CT in healthy and cognitively impaired subjects. Objective: To evaluate the effects of tES + CT on both CT task performance and on non-trained cognitive outcomes. Methods: A systematic review was conducted in accordance with PRISMA guidelines. Databases (PsycINFO, EMBASE, PubMed and Medline) were searched for all randomized, controlled and naturalistic prospective studies up until June 2014, combining tES and CT. Results: 13 studies comprising 465 participants met the inclusion criteria. Findings indicated that tES + CT enhanced performance on the majority of CT tasks. The effects on non-trained tasks were mixed, with some evidence for improvements in working memory, cognitive control, approximate number sense and arithmetic processing. Conclusions: tES + CT enhances performance on CT tasks across a range of cognitive functions. Preliminary evidence suggests that tES may also increase transfer effects to non-trained tasks in some domains. Recommendations for future studies are provided.
    Restorative neurology and neuroscience 01/2015; DOI:10.3233/RNN-140473
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    ABSTRACT: Purpose: Most pre-clinical stroke studies address the acute phase after injury, with less attention to long-term effects of injury, treatment, and experimental testing itself. We addressed these questions: 1) Will functional deficits persist up to 8 weeks following transient stroke in older animals? 2) Will functional deficits resolve spontaneously, with time and/or repeated behavioral testing? Methods: Male Sprague-Dawley rats (12 months) were pre-trained on behavioral tasks to provide baseline data and then underwent transient middle artery occlusion (tMCAO) or sham surgery. We measured motor, sensory, cognitive and gait impairments over 8 weeks, and the extent of hemispheric brain infarction. One cohort underwent behavioral testing once at 8 weeks post-stroke (LT); a second cohort (RLT) was tested at 3, 6 and 8 weeks post-stroke. Results: Significant deficits were exhibited in all functional outcomes in both cohorts after 8 weeks. We observed some recovery in some behavioral parameters in both cohorts at 8 weeks. Conclusions: Deficits persist for at least 8 weeks after tMCAO. The greater spontaneous recovery seen in the RLT groups suggest that repeated testing did reduce the severity of these stroke-induced impairments. These findings have implications for designing future studies of agents to induce long-term functional recovery following stroke.
    Restorative neurology and neuroscience 01/2015; DOI:10.3233/RNN-140450
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    ABSTRACT: Purpose: In previous studies, collagen based matrices have been implanted into the site of lesion in different models of brain injury. We hypothesized that semisynthestic collagen matrix can have neuroprotective function in the setting of traumatic brain injury. Methods: Rats were subjected to sham injury or controlled cortical impact. They either received extracellular matrix graft (DuraGen) over the injury site or did not receive any graft and underwent beam balance/beam walking test at post injury days 1-5 and Morris water maze at post injury days 14-18. Animals were sacrificed at day 18 for tissue analysis. Results: Collagen matrix implantation in injured rats did not affect motor function (beam balance test: p = 0.627, beam walking test: p = 0.921). However, injured group with collagen matrix had significantly better spatial memory acquisition (p < 0.05). There was a significant reduction in lesion volume, as well as neuronal loss in CA1 (p < 0.001) and CA3 (p < 0.05) regions of the hippocampus in injured group with collagen matrix (p < 0.05). Conclusions: Collagen matrix reduces contusional lesion volume, neuronal loss, and cognitive deficit after traumatic brain injury. Further studies are needed to demonstrate the mechanisms of neuroprotection by collagen matrix.
    Restorative neurology and neuroscience 01/2015; 33(2). DOI:10.3233/RNN-140430
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    ABSTRACT: Purpose: Acute hypobaric hypoxia (HH) causes persistent cognitive impairment, affecting memory function specifically. Mitochondrial dysfunction and synaptic morphological change were the prominent pathological features of HH exposure on brain. Quercetin, a flavonoid found in fruits, vegetables, leaves and grains, is reported to prevent ischemia induced by neuronal injury. This study investigated the efficacy of quercetin to ameliorate HH-induced memory deficit. Methods: Rats were exposed to HH equivalent to 5000 m for 7 days in a decompression chamber and received quercetin daily (50, 75 or 100 mg/kg·bw) via gavage during the period of exposure. Cognitive performance was assessed by the Morris water maze test. In vitro, the effect of quercetin was tested in hippocampus tissue. Results: Quercetin, especially at 100 mg/kg·bw, significantlyreduced HH-induced memory decline. Meanwhile, HH-induced hippocampus mitochondrial and synaptic lesions were ameliorated by quercetin. Furthermore, quercetin regulated the expression of sirtuin 1(Sirt1), PGC-1α, and the proteins related with mitochondrial biogenesis and dynamics. Moreover, quercetin increased expression of fibronectin type III domain-containing protein 5 (FNDC5) and brain-derived neurotrophic factor (BDNF), showing the PGC-1α/FNDC5/BNDF pathways might be involved in neuronal adaptation. Conclusions: The results suggest quercetin has prophylactic potential for amelioration of HH-induced memory impairment, which is associated with the mitochondrial and neuronal adaptation in hippocampus.
    Restorative neurology and neuroscience 01/2015; 33(2). DOI:10.3233/RNN-140446
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    ABSTRACT: Purpose: Disorders of consciousness (DOC) diagnosis relies on the presence or absence of purposeful motor responsiveness, which characterizes the minimally conscious state (MCS) and the unresponsive wakefulness syndrome (UWS), respectively. Functional neuroimaging studies have raised the question of possible residual conscious awareness also in clinically-defined UWS patients. The aim of our study was to identify electrophysiological parameters, by means of a transcranial magnetic stimulation approach, which might potentially express the presence of residual networks sustaining fragmentary behavioral patterns, even when no conscious behavior can be observed. Methods: We enrolled 25 severe DOC patients, following post-anoxic or traumatic brain injury and 20 healthy individuals (HC) as control group. Baseline electrophysiological evaluation evidenced, in comparison to HC, a partial preservation of cortical effective connectivity and excitability in clinically defined MCS, whereas these components were absent in clinically defined UWS. Then, we applied an anodal transcranial direct current stimulation (a-tDCS) protocol over the orbitofrontal cortex. Result: a-tDCS was able to boost cortical connectivity and excitability in all HC, MCS, and to unmask such excitability/connectivity in some UWS patients. Conclusion: a-tDCS could be useful in identifying residual connectivity markers in clinically-defined UWS, who may lack of purposeful behavior as a result of a motor-output failure.
    Restorative neurology and neuroscience 01/2015; 33(2). DOI:10.3233/RNN-140448
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    ABSTRACT: Purpose: The present work compared the behavioral outcomes of ACCS therapy delivered either intravenously (i.v.) or intracerebroventricularly (i.c.v.) after penetrating ballistic-like brain injury (PBBI). Histological markers for neuroinflammation and neurodegeneration were employed to investigate the potential therapeutic mechanism of ACCS. Methods: Experiment-1, ACCS was administered either i.v. or i.c.v. for 1 week post-PBBI. Outcome metrics included behavioral (rotarod and Morris water maze) and gross morphological assessments. Experiment-2, rats received ACCS i.c.v for either 1 or 2 weeks post-PBBI. The inflammatory response was determined by immunohistochemistry for neutrophils and microglia reactivity. Neurodegeneration was visualized using silver staining. Results: Both i.v. and i.c.v. delivery of ACCS improved motor outcome but failed to improve cognitive outcome or tissue sparing. Importantly, only i.c.v. ACCS treatment produced persistent motor improvements at a later endpoint. The i.c.v. ACCS treatment significantly reduced PBBI-induced increase in myeloperoxidase (MPO) and ionized calcium binding adaptor molecule 1 (Iba1) expression. Concomitant reduction of both Iba1 and silver staining were detected in corpus callosum with i.c.v. ACCS treatment. Conclusions: ACCS, as a treatment for TBI, showed promise with regard to functional (motor) recovery and demonstrated strong capability to modulate neuroinflammatory responses that may underline functional recovery. However, the majority of beneficial effects appear restricted to the i.c.v. route of ACCS delivery, which warrants future studies examining delivery routes (e.g. intranasal delivery) which are more clinically viable for the treatment of TBI.
    Restorative neurology and neuroscience 01/2015; 33(2). DOI:10.3233/RNN-140455