In the years 2015–2016, several important advances in neurology and neurosciences have been published in Neurological Sciences. The Journal continues to attract an ever-increasing number of article submissions. Here, we report a brief review of the journal’s content in the 2015–2016 years.
Vascular disorders
Stroke pathophysiology, treatments and outcomes are an active field of interest. Copy number variants, specific genetic polymorphisms, toll-like receptors, inflammatory citochines, and chemokines represent factors of susceptibility for stroke [1,2,3,4,5,6]. Moreover, microRNAs appear to play a role in post-stroke excitotoxicity [7], while Brain-derived neurotrophic factor Val66Met polymorphism is associated with functional and cognitive outcomes of stroke [8]. A specific ACE gene polymorphism has been reported to predispose to hemorrhagic stroke [9]. Acid uric and antioxidants act as a neuroprotective agent for the ischemic stroke [10]. Granulocyte-colony stimulating factor (G-CSF) combined with repetitive transcranial magnetic stimulation (rTMS), administered in the early subacute phase of ischemic stroke, may exert a hazardous effect on functional recovery, possibly due to impaired angiogenic mechanism, decreased cell survival, and increased inflammation [11]. Single small subcortical infarction has been reported associated to early neurological deterioration [12]. Investigations on the influence of cognition changes during post-stroke rehabilitation is relevant [13], associated to post stroke depression and to the degree of neurological deficit [14], while long-term mortality after stroke is higher than after myocardial infarction [15]. Several articles discuss epidemiology and diagnosis. The incidence of hemorrhagic stroke in Japan has been reported higher than in the western countries [16]. Glial fibrillary acidic protein test is a promising technique for diagnosis of intracerebral hemorrhage from ischemic stroke and prediction of short-term functional outcomes [17]. In mice, lithium treatment exerted a neuroprotective effect on learning and memory by potentiating the Akt/GSK3β cell-signaling pathway [18].
Antiplatelet treatment is useful both in primary and secondary prevention, but poor response to aspirin or clopidogrel is a not rare condition [19, 20].
A public education campaign or health-related applications (app) could potentially reduce pre-hospital delay for ischemic stroke patients [21], and also a web-based telemedicine system for thrombolysis could give a growing number of patients access to treatment [22]. Stroke awareness in general population could improve public behavior in terms of prevention, symptom recognition, and timely response [23]. Creation of hospital-based registers may help to ameliorate stroke management [24]. Endovascular treatment (ET) has shown to be safe in acute stroke, but its superiority over intravenous thrombolysis is debated [25]. In murine models, the adenosine A2A receptor antagonist, administered soon after ischemia, has been shown to protect from neurological deficit in the first days but not later [26].
Stem cell-based therapy hold extensive potential in treating intracerebral hemorrhage, which should be further evaluated with more evidence-based animal studies [27].
Carotid ultrasounds and transcranial Doppler remain the most important diagnostic tools [28]. Chronic cerebral hypoperfusion due to carotid arteries stenosis leads to axonal damage over time [29]. Carotid endarterectomy implies a reduced blood flow to the brain, but protective mechanisms such as brain release of erythropoietin and nitric oxide represent an endogenous self-activated neuroprotective mechanism aimed at the prevention of ischemia/reperfusion damage [30].
Multiple sclerosis
Also multiple sclerosis (MS) represents an active field, with high social and economic impact worldwide [31]. Grey matter damage in MS is an acquired data, with relevant clinical implications [32]. Genetic and environmental factors are involved in the risk of developing the disease [33,34,35,36]; while in other cases this susceptibility has not been demonstrated [37,38,39]. Other factors, as alcohol consumption, present potential protective effect [40]. Elevated fibrinogen levels are associated with a worse prognosis [41]. Higher C-reactive protein values were associated with pregnancy-related co-morbidities but not with MS disease activity [42]. The management of disease-modifying or symptomatic therapies represent an active field of interest in MS. Autologous hematopoietic stem cell transplantation might represent a therapeutic possibility in MS patients unresponsive to approved therapies [43]. High-dose interferon-β therapy is associated with thrombocytopenia [44]. Natalizumab is extremely effective in reducing disease activity in MS patients but its long-term use has been reported associated with the risk of progressive multifocal leukoencephalopathy (PML). Early detection of PML is related to a favourable outcome [45]. Recurrence of disease activity Natalizumab discontinuations despite the treatment with immunomodulant or more aggressive therapy has been demonstrated [46]. New diagnostic tools for assessment of urinary dysfunction lead to identify lower urinary tract symptoms also in asymptomatic patients [47]. Efficacy and safety of nabiximols on spasticity in MS have been largely demonstrated [48]. Alternative and complementary medicines, such as herbal remedies, appears to be scares and presents potential risk of adverse reactions or interference with conventional treatments [49]. Cognitive and psychiatric aspects have been better defined with differentiation of various profiles [50,51,52,53,54]. Fatigue, quality of life, and working status have recently arisen great interest in MS patients [55,56,57]. Asymmetrical visual and brainstem auditory evoked potentials (VEP and BAEP) abnormalities were found in fatigued MS patients, with no relationships to disease-related variables, inducing to consider them as an electrophysiological marker of fatigue in MS patients [58]. Physical activity should be encouraged in all stages of disease [59, 60].
Migraine and headache
Headache is a very common neurological problem with a high impact on quality of life, also among children and adolescent [61, 62]. Physiopathology of cephalic pain is not clearly understood [63,64,65,66,67]. Studies of resting-state functional magnetic resonance imaging have detected a brain dysfunction affecting intrinsic connectivity of brain networks [68]. Headache represents also a critical problem in the emergency setting [69,70,71,72]. The elevated high-sensitivity C-reactive protein level and low Retinol-binding protein-4 level in migraine patients suggest that vitamin A might play a major role in the pathogenesis of migraine [73]. An association between inflammation and atherosclerosis in patients with migraine, even in children, have been hypothesized [74], but the absolute risk of ischemic stroke in migraineurs is relatively low and an antithrombotic primary prevention is not indicated [75]. Several non-controlled studies suggest that closure of the foramen ovale significantly reduces attack frequency in migraine patient, but the only prospective placebo-controlled trial does not support these results [76]. Natural menopause is associated with a lower incidence of migraine as compared with surgical menopause [77]. Idiopathic intracranial hypertension without papilledema should be considered in all patients with almost daily migraine pain, with evidence of sinus stenosis and unresponsive to medical treatment [78, 79]. Ocular pain, in same case, requires the exclusion of ophthalmologic diseases, as uveitis, angle closure glaucoma, neuritis [80]. Pathophysiology of vestibular migraine has been better defined with functional neuroimaging techniques [81]. The combination of cinnarizine and dimenhydrinate in the prophylactic therapy has been reported effective [82]. Acute confusional migraine still has an unclear pathophysiology, but dysfunction of dorsal anterior cingulated cortex probably plays a pathogenic role [83]. Women with migraine and phonophobia exhibited deficits in otoacoustic emissions suppression, which points to a disorder affecting the medial olivocochlear efferent system [84]. The choroidal thickness has been found to decrease significantly not only in patients with migraine with aura, but also in those without aura during the attack-free period [85]. Treatment of chronic migraine with medication overuse requires withdrawal from acute medications [86]. Triptans represent the most specific and effective therapy option for migraine attacks. Nevertheless, in clinical practice, they are often underused [87, 88]. Topiramate is an effective drug in migraine prophylaxis but paresthesia is a frequent adverse reaction in patient with migraine more than in epileptic patients [89, 90]. Onabotulinumtoxin A treatment is efficacious in refractory chronic migraine [91, 92]. Recently, several neuromodulatory surgical techniques have been developed for the management of headaches that are unresponsive to medical treatment [93]. Transcutaneous neurostimulation with the Cefaly(®) device has shown efficacy for migraine therapy [94] while both deep brain stimulation and occipital nerve stimulation are utilized in refractory migraine [95]. Lymphatic drainage has been suggested as a therapeutic option in the prophlaxys of migraine [96].
Tumors
Cerebral tumors remains an important cause of death and disability [97]. The investigation of genetic and molecular mechanism on proliferation, apoptosis, invasion, and angiogenesis may help to focus potential therapeutic targets [98, 99]. As a class of small non-coding RNAs, microRNAs (miRNAs) has been discovered to be closely involved in carcinogenesis and might also be connected with glioma diagnosis and prognosis [100,101,102]. Metastasis-associated protein 3 (MTA3) expression was decreased in human glioma and negatively associated with prognosis of patients, suggesting that MTA3 may play a tumor suppressor role in glioma [103].
Alzheimer’s disease
Alzheimer’s disease (AD) is the principal cause of dementia in elderly, with high cost of treatment and care [104].
Accumulating evidence has indicated the role of insulin deficiency and insulin resistance as mediators of AD neurodegeneration, calling AD as “type 3 diabetes” [105], while a negative association between AD and cancer is an evidence that needs to be clarified [106]. Vitamin D deficiency presents a greater risk for ApoEɛ4 non-carrier AD patients than for ɛ4 carriers [107]. N-methyl-d-aspartate receptors (NMDARs) play a pivotal role in the synaptic transmission and synaptic plasticity thought to underlie learning and memory and have been recently implicated in Alzheimer’s disease [108]. Retinal nerve fiber layer (RNFL) thickness by optical coherence tomography (OCT) has been evaluated and correlated with cognitive impairment, but further studies are needed to optimize the utility of this method as an ocular biomarker in AD [109].
Edaravone, a potent free radical scavenger with antioxidant effects, may be developed as a novel agent for the treatment of AD for improving cholinergic system and protecting neurons from oxidative toxicity [110]. The mammalian target of rapamycin (mTOR) pathway has been reported to mediate Aβ clearance through autophagy and may represent an important therapeutic target for AD [111].
Parkinson’s disease
Parkinson’s disease (PD) is a major worldwide public health problem with a prevalence that is expected to increase dramatically in the coming decades [112]. Inflammatory markers as carcinoembryonic antigen, high-sensitivity C-reactive protein (hs-CRP), and Neutrophil/lymphocyte ratio (NLR) are significantly higher in the PD patients than in the normal controls [113]. Oxidative stress is considered as a contributing factor to the development of PD. Decreased nitric oxide (NO) level and negative correlation observed between NO level and disease rating scale implicated a role for NO in the disease process [114]. An inverse relation between uric acid levels and l-Dopa treatment and PD stages may be due to the fact that high serum uric acids levels may decrease the oxidative stress taking part in the pathogenesis of PD [115]. The levels of oligomeric form of α-synuclein of red blood cells in ischemic stroke and in Parkinson’s disease patients were both significantly higher than in normal people [116]. Corneal thickness may decrease in patients with PD [117], and colour and contrast dysfunction are present as the earliest symptoms of disease [118]. Minor salivary gland biopsy is a potential pathological biomarker for PD, but with a lower diagnostic accuracy than DAT-PET scan [119]. [(18)F] fluorinated-N-3-fluoropropyl-2-β-carboxymethoxy-3-β-(4-iodophenyl)nortropane (FP-CIT) positron emission tomography (PET) scans are able to differentiate PD and drug-induced parkinsonism [120]. Robertson dysarthria profile may be a valuable tool to detect speech/voice disturbances in Parkinson’s disease [121]. Indoor and outdoor falls among people with PD often result in activity limitations, participation restrictions, social isolation or premature mortality [122]. Oropharyngeal bradykinesia may be responsible for drooling in PD [123]. Botulinum toxin is a safe and effective therapy for the treatment of sialorrhea, applied without the requirement of ultrasound guidance [124]. Non-motor symptoms of idiopathic Parkinson’s disease, specifically pain, olfactory dysfunction, fatigue, depression, anxiety, and sleep disturbances, are important contributors for worsening the quality of life and poor patient outcomes [125,126,127,128,129].
Neuromuscular disorders
Amyotrophic lateral sclerosis (ALS) is the most common degenerative disease of the motor neuron system. Genetic and epigenetic factors play a role on the pathogenesis and the evolution of the clinical course [130,131,132]. Despite scientific efforts, pathophysiological mechanisms are not fully understood [133]. Modern MR techniques are helpful in ALS diagnosis, in assessment of clinical course, or even in the effects of new drugs [134, 135].
Spinal muscular atrophy (SMA) is a hereditary neuromuscular disorder with genetic heterogeneity [136]. Duchenne muscular dystrophy (DMD) and Becker muscular dystrophy (BMD) are the most frequent muscular dystrophies with different genetic profiles [137].
Genetic and clinical heterogeneity in genetic neuropathies and in Charcot–Marie–Tooth disease is notable [138].
Electrophysiological study is a fundamental diagnostic tool for all neuromuscular disorders [139,140,141]. For Guillain–Barrè syndrome (GBS), a correct and prompt diagnosis may be sometimes hard [142, 143]. A correlation between ubiquitin carboxy-terminal hydrolase-L1 (UCH-L1), a neuron-specific protein, in the cerebrospinal fluid of patients with GBS and severity of the disease at the acute phase has been suggested [144]. Facial onset sensory and motor neuronopathy (FOSMN) is a recently defined slowly progressive motor neuron disorder [145]. Brachial plexus injury (BPI) causes functional changes in the brain, but the structural changes resulting from BPI remain unknown [146]. Neuromyotoxicity due to therapy with hydroxychloroquine has been reported in a case [147].
Epilepsy
Epilepsy is a frequent cause of hospitalization, especially in pediatric age [148]. Seizure outcome in patients with juvenile absence epilepsy is not clear [149], and cognitive deterioration is not rare [150]. A prospective case–control study has shown that pregnancy does not affect seizure frequency in women with epilepsy [151]. Psychogenic nonepileptic seizures are more frequent among women and have possible biological basis [152, 153].
Electroencephalogram (EEG) is a fundamental diagnostic tool in epilepsy [154]. Focal changes in EEG have been reported in idiopathic generalized epilepsies [155].
Interesting articles report data on treatment. Phenytoin mainly metabolized by hepatic cytochrome P450 enzymes (CYP) and genetic polymorphism of CYP is related to therapeutic response [156]. The best withdrawal rate of antiepileptic monotherapy in seizure-free adult patients with epilepsy is questionable [157]. Ketogenic diet (KD) is one of the most effective therapies for intractable epilepsy, and, even if rich in olive oil, high-fat KD causes significant increase in LDL-cholesterol and triglyceride levels [158].
Vagus nerve stimulation therapy is the most frequently used neurostimulation modality for patients with drug-resistant epilepsy who are not eligible for seizure surgery [159].
Neurogenetics
Molecular genetics has an important role in all neurological diseases with the possibility to discover new mutations and new phenotypic presentations [160,161,162,163,164,165,166] also with investigations related to eye movements [167, 168]. Enzyme replacement therapy (ERT) is possible in a growing number of diseases: an open pilot study has been reported in late onset Pompe disease [169]. Allogenic hematopoietic stem cell transplantation and, more recently, liver transplantation are therapeutic options for mitochondrial neuro-gastro-intestinal encephalomyopathy (MNGIE) [170]. Llama single domain antibodies (VHH) directed against mutant huntingtin are interesting candidates as therapeutic agents or research tools in Huntington disease because of their small size, high thermostability, low cost of production, possibility of intracellular expression, and potency of blood–brain barrier crossing [171].
Conclusions
In summary, this 2 years review of what we learned by Neurologic Sciences Journal is an useful update of the main data published in the journal in the different fields of neurology, confirming the good quality of the journal, the modern and the international approach reporting all the new diagnostic, therapeutic and research strategies.
References
Vascular disorders
Colaianni V, Mazzei R, Cavallaro S (2016) Copy number variations and stroke. Neurol Sci Neurol Sci 37(12):1895–1904. doi:10.1007/s10072-016-2658-y
Zhang M, Wu JM, Zhang QS, Yan DW, Ren LJ, Li WP (2016) The association of CYP1A1 genetic polymorphisms and additional gene-gene interaction with ischemic stroke in the eastern Han of China. Neurol Sci 37(10):1679–1684
Gu L, Huang J, Tan J, Wei Q, Jiang H, Shen T, Liang B, Tang N (2016) Impact of TLR5 rs5744174 on stroke risk, gene expression and on inflammatory cytokines, and lipid levels in stroke patients. Neurol Sci 37(9):1537–1544
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Rezaei S, Asgari Mobarake K, Saberi A, Keshavarz P, Leili EK (2016) Brain-derived neurotrophic factor (BDNF) Val66Met polymorphism and post-stroke dementia: a hospital-based study from northern Iran. Neurol Sci 37(6):935–942
Das S, Roy S, Sharma V, Kaul S, Jyothy A, Munshi A (2015) Association of ACE gene I/D polymorphism and ACE levels with hemorrhagic stroke: comparison with ischemic stroke. Neurol Sci 36(1):137–142
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Beom J, Kim W, Han TR, Seo KS, Oh BM (2015) Concurrent use of granulocyte-colony stimulating factor with repetitive transcranial magnetic stimulation did not enhance recovery of function in the early subacute stroke in rats. Neurol Sci 36(5):771–777. doi:10.1007/s10072-014-2046-4
Duan Z, Fu C, Chen B, Xu G, Tao L, Tang T, Hou H, Fu X, Yang M, Liu Z, Zhang X (2015) Lesion patterns of single small subcortical infarct and its association with early neurological deterioration. Neurol Sci 36(10):1851–1857. doi:10.1007/s10072-015-2267-1
Pérez LM, Inzitari M, Roqué M, Duarte E, Vallés E, Rodó M, Gallofré M (2015) Change in cognitive performance is associated with functional recovery during post-acute stroke rehabilitation: a multi-centric study from intermediate care geriatric rehabilitation units of Catalonia. Neurol Sci 36(10):1875–1880. doi:10.1007/s10072-015-2273-3
Wang L, Tao Y, Chen Y, Wang H, Zhou H, Fu X (2016) Association of post stroke depression with social factors, insomnia, and neurological status in Chinese elderly population. Neurol Sci 37(8):1305–1310
Chwojnicki K, Wierucki Ł, Zagożdżon P, Wojtyniak B, Nyka WM, Zdrojewski T (2016) Long-term mortality after stroke is higher than after myocardial infarction. Neurol Sci 37(6):891–898
Suzuki K, Izumi M (2015) The incidence of hemorrhagic stroke in Japan is twice compared with western countries: the Akita stroke registry. Neurol Sci 36(1):155–160. doi:10.1007/s10072-014-1917-z
Xiong L, Yang Y, Zhang M, Xu W (2015) The use of serum glial fibrillary acidic protein test as a promising tool for intracerebral hemorrhage diagnosis in Chinese patients and prediction of the short-term functional outcomes. Neurol Sci 36(11):2081–2087
Fan M, Song C, Wang T, Li L, Dong Y, Jin W, Lu P (2015) Protective effects of lithium chloride treatment on repeated cerebral ischemia-reperfusion injury in mice. Neurol Sci 36(2):315–321. doi:10.1007/s10072-014-1943-x
Cai G, Zhou W, Lu Y, Chen P, Lu Z, Fu Y (2016) Aspirin resistance and other aspirin-related concerns. Neurol Sci 37(2):181–189. doi:10.1007/s10072-015-2412-x
Lv HH, Wu S, Liu X, Yang XL, Xu JF, Guan YT, Dong Q, Zheng SL, Jiang JM, Li SX, Luo Z, Li L, An LX, Han Y (2016) Comparison of VerifyNow P2Y12 and thromboelastography for assessing clopidogrel response in stroke patients in China. Neurol Sci 37(2):277–282. doi:10.1007/s10072-015-2407-7
Nishijima H, Kon T, Ueno T, Haga R, Yamazaki K, Yagihashi K, Funamizu Y, Arai A, Suzuki C, Nunomura J, Baba M, Tomiyama M (2016) Effect of educational television commercial on pre-hospital delay in patients with ischemic stroke. Neurol Sci 37(1):105–109
Baldereschi M, Di Carlo A, Piccardi B, Inzitari D (2016) The Italian stroke-app: ICTUS3R. Neurol Sci 37(6):991–994
Nardetto L, Dario C, Tonello S, Brunelli MC, Lisiero M, Carraro MG, Saccavini C, Scannapieco G, Giometto B (2016) A one-to-one telestroke network: the first Italian study of a web-based telemedicine system for thrombolysis delivery and patient monitoring. Neurol Sci 37(5):725–730
Baldereschi M, Di Carlo A, Vaccaro C, Polizzi B, Inzitari D, Promotion Implementation of Stroke Care in Italy Project Working Group (2015) Stroke knowledge in Italy. Neurol Sci 36(3):415–421. doi:10.1007/s10072-014-1964-5
Iacoviello L, Costanzo S, Persichillo M, Sparano A, Bartolo M, Polizzi BM, Donati MB, de Gaetano G (2016) Hospital-based register of stroke in the Molise Region: focus on main subtypes of stroke. Years 2009–2013. Neurol Sci 37(2):191–198
Mangiafico S, Pracucci G, Saia V, Nencini P, Inzitari D, Nappini S, Vallone S, Zini A, Fuschi M, Cerone D, Bergui M, Cerrato P, Gandini R, Sallustio F, Saletti A, De Vito A, Romano DG, Tassi R, Causin F, Baracchini C, Piano M, Motto C, Ciccone A, Gasparotti R, Magoni M, Giorgianni A, DeLodovici M, Cavasin N, Critelli A, Gallucci M, Carolei A, Meloni T, Corso G, Vaudano G, Duc E, Zappoli F, Cavallini A, Padolecchia R, Tassinari T, Longoni M, Salmaggi A, Zampieri P, Bovi P, Puglioli M, Chiti A, Guidetti G, Simonetti L, Procaccianti G, Menozzi R, Scoditti U, Ricciardi F, Pezzella FR, Guarnieri G, Andreone V, Toni D (2015) The Italian Registry of Endovascular Treatment in Acute Stroke: rationale, design and baseline features of patients. Neurol Sci 36(6):985–993. doi:10.1007/s10072-014-2053-5
Ma X, Qin J, Song B, Shi C, Zhang R, Liu X, Ji Y, Ji W, Gong G, Xu Y (2015) Stem cell-based therapies for intracerebral hemorrhage in animal model: a meta-analysis. Neurol Sci 36(8):1311–1317
Dormanesh B, Vosoughi K, Akhoundi FH, Mehrpour M, Fereshtehnejad SM, Esmaeili S, Sabet AS (2016) Carotid duplex ultrasound and transcranial Doppler findings in commercial divers and pilots. Neurol Sci 37(12):1911–1916
Baracchini C, Anzola GP, Cenciarelli S, Diomedi M, Bella R, Tonon A, Braga M, Zedde ML, Zanferrari C, Del Sette M, Caliandro P, Gandolfo C, Ricci S, Meneghetti G (2016) Italian symptomatic intracranial atherosclerosis study (ISIDE): a multicenter transcranial ultrasound evaluation. Neurol Sci 37(10):1645–1651. doi:10.1007/s10072-016-2642-6
Liang W, Zhang W, Zhao S, Li Q, Liang H, Ceng R (2015) Altered expression of neurofilament 200 and amyloid-β peptide (1-40) in a rat model of chronic cerebral hypoperfusion. Neurol Sci 36(5):707–712. doi:10.1007/s10072-014-2014-z
Carelli S, Ghilardi G, Bianciardi P, Latorre E, Rubino F, Bissi M, Di Giulio AM, Samaja M, Gorio A (2016) Enhanced brain release of erythropoietin, cytokines and NO during carotid clamping. Neurol Sci 37(2):243–252. doi:10.1007/s10072-015-2398-4
Multiple sclerosis
Ponzio M, Gerzeli S, Brichetto G, Bezzini D, Mancardi GL, Zaratin P, Battaglia MA (2015) Economic impact of multiple sclerosis in Italy: focus on rehabilitation costs. Neurol Sci 36(2):227–234. doi:10.1007/s10072-014-1925-z
Tavazzi E, Laganà MM, Bergsland N, Tortorella P, Pinardi G, Lunetta C, Corbo M, Rovaris M (2015) Grey matter damage in progressive multiple sclerosis versus amyotrophic lateral sclerosis: a voxel-based morphometry MRI study. Neurol Sci 36(3):371–377. doi:10.1007/s10072-014-1954-7
Nicoletti A, Messina S, Bruno E, Mostile G, Quattrocchi G, Raciti L, Dibilio V, Cappellani R, D’Amico E, Sciacca G, Lo Fermo S, Paradisi V, Patti F, Zappia M (2016) Risk factors in multiple sclerosis: a population-based case-control study in Sicily. Background and methods. Neurol Sci 37(12):1931–1937
Nasr Z, Majed M, Rostami A, Sahraian MA, Minagar A, Amini A, McGee JC, Etemadifar M (2016) Prevalence of multiple sclerosis in Iranian emigrants: review of the evidence. Neurol Sci 37(11):1759–1763
Cristiano E, Patrucco L, Miguez J, Giunta D, Peroni J, Rojas JI (2016) Increasing incidence of multiple sclerosis among women in Buenos Aires: a 22 year health maintenance organization based study. Neurol Sci 37(10):1621–1626
Wu S, Liu Q, Zhu JM, Wang MR, Li J, Sun MG (2016) Association between the IL7R T244I polymorphism and multiple sclerosis risk: a meta analysis. Neurol Sci 37(9):1467–1474
Lorefice L, Tranquilli S, Fenu G, Murru MR, Frau J, Rolesu M, Coghe GC, Marrosu F, Marrosu MG, Cocco E (2015) A genetic study of the FMR1 gene in a Sardinian multiple sclerosis population. Neurol Sci 36(12):2213–2220. doi:10.1007/s10072-015-2339-2
Ristić S, Čizmarević NS, Sepčić J, Kapović M, Peterlin B (2016) Angiotensin-converting enzyme insertion/deletion gene polymorphism in multiple sclerosis: a meta-analysis. Neurol Sci 37(12):1955–1959
Agnello L, Scazzone C, Ragonese P, Salemi G, Lo Sasso B, Schillaci R, Musso G, Bellia C, Ciaccio M (2016) Vitamin D receptor polymorphisms and 25-hydroxyvitamin D in a group of Sicilian multiple sclerosis patients. Neurol Sci 37(2):261–267
Zhu T, Ye X, Zhang T, Lin Z, Shi W, Wei X, Liu Y, He J (2015) Association between alcohol consumption and multiple sclerosis: a meta-analysis of observational studies. Neurol Sci 36(9):1543–1550. doi:10.1007/s10072-015-2326-7
Zhang Y, Zhang X, Liu D, Wang H, Pan S, Wang D, Chen X (2016) Elevated fibrinogen levels in neuromyelitis optica is associated with severity of disease. Neurol Sci 37(11):1823–1829
Jalkanen A, Kauko T, Koskinen JO, Waris ME, Airas L (2015) Elevated concentration of C-reactive protein is associated with pregnancy-related co-morbidities but not with relapse activity in multiple sclerosis. Neurol Sci 36(3):441–447. doi:10.1007/s10072-014-1980-5
Currò D, Mancardi G (2016) Autologous hematopoietic stem cell transplantation in multiple sclerosis: 20 years of experience. Neurol Sci 37(6):857–865
Koudriavtseva T, Plantone D, Renna R, Mandoj C, Giannarelli D, Mainero C (2015) Interferon-β therapy and risk of thrombocytopenia in multiple sclerosis patients. Neurol Sci 36(12):2263–2268. doi:10.1007/s10072-015-2348-1
Cordioli C, De Rossi N, Rasia S, Lodoli G, Capra R (2015) Early detection and favourable outcome of natalizumab-related progressive multifocal leukoencephalopathy (PML) in two multiple sclerosis patients. Neurol Sci 36(3):489–491
Ferrè L, Moiola L, Sangalli F, Radaelli M, Barcella V, Comi G, Martinelli V (2015) Recurrence of disease activity after repeated Natalizumab withdrawals. Neurol Sci 36(3):465–467. doi:10.1007/s10072-014-1960-9
Ghezzi A, Mutta E, Bianchi F, Bonavita S, Buttari F, Caramma A, Cavarretta R, Centonze D, Coghe GC, Coniglio G, Del Carro U, Ferrò MT, Marrosu MG, Patti F, Rovaris M, Sparaco M, Simone I, Tortorella C, Bergamaschi R (2016) Diagnostic tools for assessment of urinary dysfunction in MS patients without urinary disturbances. Neurol Sci 37(3):437–442
Ferrè L, Nuara A, Pavan G, Radaelli M, Moiola L, Rodegher M, Colombo B, Keller Sarmiento IJ, Martinelli V, Leocani L, Martinelli Boneschi F, Comi G, Esposito F (2016) Efficacy and safety of nabiximols (Sativex(®)) on multiple sclerosis spasticity in a real-life Italian monocentric study. Neurol Sci 37(2):235–242
Loraschi A, Bellantonio P, Bortolon F, Capra R, Cavalla P, Costantino G, Lugaresi A, Martinelli V, Marrosu MG, Patti F, Rottoli M, Salvetti M, Sola P, Solaro C, Klersy C, Marino F, Zaffaroni M, Cosentino M (2016) Use of herbal remedies by multiple sclerosis patients: a nation-wide survey in Italy. Neurol Sci 37(4):613–622
Migliore S, Ghazaryan A, Simonelli I, Pasqualetti P, Landi D, Palmieri MG, Moffa F, Rinaldi P, Vernieri F, Filippi MM (2016) Validity of the minimal assessment of cognitive function in multiple sclerosis (MACFIMS) in the Italian population. Neurol Sci 37(8):1261–1270
Vollmer T, Huynh L, Kelley C, Galebach P, Signorovitch J, DiBernardo A, Sasane R (2016) Relationship between brain volume loss and cognitive outcomes among patients with multiple sclerosis: a systematic literature review. Neurol Sci 37(2):165–179
Magnano I, Pes GM, Cabboi MP, Pilurzi G, Ginatempo F, Achene A, Salis A, Conti M, Deriu F (2016) Comparison of brainstem reflex recordings and evoked potentials with clinical and MRI data to assess brainstem dysfunction in multiple sclerosis: a short-term follow-up. Neurol Sci 37(9):1457–1465
Dackovic J, Pekmezovic T, Mesaros S, Dujmovic I, Stojsavljevic N, Martinovic V, Drulovic J (2016) The Rao’s Brief Repeatable Battery in the study of cognition in different multiple sclerosis phenotypes: application of normative data in a Serbian population. Neurol Sci 37(9):1475–1481
Bruno D, Torralva T, Marenco V, Ardilla JT, Baez S, Gleichgerrcht E, Sinay V, Roca M (2015) Utility of the INECO frontal screening (IFS) in the detection of executive dysfunction in patients with relapsing-remitting multiple sclerosis (RRMS). Neurol Sci 36(11):2035–2041. doi:10.1007/s10072-015-2299-6
Pokryszko-Dragan A, Zagrajek M, Slotwinski K, Bilinska M, Gruszka E, Podemski R (2016) Event-related potentials and cognitive performance in multiple sclerosis patients with fatigue. Neurol Sci 37(9):1545–1556
Ponzio M, Brichetto G, Zaratin P, Battaglia MA (2015) Workers with disability: the case of multiple sclerosis. Neurol Sci 36(10):1835–1841. doi:10.1007/s10072-015-2265-3
Devy R, Lehert P, Varlan E, Genty M, Edan G (2015) Improving the quality of life of multiple sclerosis patients through coping strategies in routine medical practice. Neurol Sci 36(1):85–90. doi:10.1007/s10072-014-1900-8
Pokryszko-Dragan A, Bilinska M, Gruszka E, Kusinska E, Podemski R (2015) Assessment of visual and auditory evoked potentials in multiple sclerosis patients with and without fatigue. Neurol Sci 36(2):235–242. doi:10.1007/s10072-014-1953-8
Neven A, Vanderstraeten A, Janssens D, Wets G, Feys P (2016) Understanding walking activity in multiple sclerosis: step count, walking intensity and uninterrupted walking activity duration related to degree of disability. Neurol Sci 37(9):1483–1490
Frau J, Coghe G, Lorefice L, Fenu G, Cadeddu B, Marrosu MG, Cocco E (2015) Attitude towards physical activity in patients with multiple sclerosis: a cohort study. Neurol Sci 36(6):889–893. doi:10.1007/s10072-015-2100-x
Migraine and headache
Zargaran A, Borhani-Haghighi A, Faridi P, Daneshamouz S, Mohagheghzadeh A (2016) A review on the management of migraine in the Avicenna’s Canon of Medicine. Neurol Sci 37(3):471–478
Leonardi M (2015) Burden of migraine: what should we say more? Neurol Sci 36(Suppl 1):1–3. doi:10.1007/s10072-015-2188-z
Panerai AE (2015) Physiopathology of cephalic pain: where are we? Neurol Sci 36(Suppl 1):13–16. doi:10.1007/s10072-015-2178-1
D’Andrea G, Cevoli S, Colavito D, Leon A (2015) Biochemistry of primary headaches: role of tyrosine and tryptophan metabolism. Neurol Sci 36(Suppl 1):17–22. doi:10.1007/s10072-015-2131-3
Gumusyayla S, Vural G, Bektas H, Neselioglu S, Deniz O, Erel O (2016) A novel oxidative stress marker in migraine patients: dynamic thiol-disulphide homeostasis. Neurol Sci 37(8):1311–1317
Wang F, He Q, Ren Z, Li F, Chen W, Lin X, Zhang H, Tai G (2015) Association of serum levels of intercellular adhesion molecule-1 and interleukin-6 with migraine. Neurol Sci 36(4):535–540. doi:10.1007/s10072-014-2010-3
Duarte H, Teixeira AL, Rocha NP, Domingues RB (2015) Increased interictal serum levels of CXCL8/IL-8 and CCL3/MIP-1α in migraine. Neurol Sci 36(2):203–208. doi:10.1007/s10072-0141931-1
Colombo B, Rocca MA, Messina R, Guerrieri S, Filippi M (2015) Resting-state fMRI functional connectivity: a new perspective to evaluate pain modulation in migraine? Neurol Sci 36(Suppl 1):41–45. doi:10.1007/s10072-015-2145-x
Schuster NM, Vollbracht S, Rapoport AM (2015) Emerging treatments for the primary headache disorders. Neurol Sci 36(Suppl 1):109–113. doi:10.1007/s10072-015-2133-1
Iurlaro S, Silvani A, Mauri M, Truci G, Beretta S, Zilioli A, Guidotti M, Salmaggi A, Ferrarese C, Comi G, Riva M (2015) Headache in cerebral venous thrombosis associated with extracranial tumors: a clinical series. Neurol Sci 36(Suppl 1):149–151. doi:10.1007/s10072-015-2174-5
Pari E, Rinaldi F, Gipponi S, Venturelli E, Liberini P, Rao R, Padovani A (2015) Management of headache disorders in the Emergency Department setting. Neurol Sci 36(7):1153–1160. doi:10.1007/s10072-015-2148-7
Granato A, Belluzzo M, Fantini J, Zorzon M, Koscica N (2015) SUNCT-like syndrome attributed to varicella-zoster virus meningoencephalitis. Neurol Sci 36(5):807–808
Tanik N, Celikbilek A, Metin A, Gocmen AY, Inan LE (2015) Retinol-binding protein-4 and hs-CRP levels in patients with migraine. Neurol Sci 36(10):1823–1827. doi:10.1007/s10072-015-2262-6
Poyrazoglu HG, Vurdem UE, Arslan A, Uytun S (2016) Evaluation of carotid intima-media thickness in children with migraine: a marker of subclinical atherosclerosis. Neurol Sci 37(10):1663–1669
de Falco FA, de Falco A (2015) Migraine with aura: which patients are most at risk of stroke? Neurol Sci 36(Suppl 1):57–60. doi:10.1007/s10072-015-2132-2
Finocchi C, Del Sette M (2015) Migraine with aura and patent foramen ovale: myth or reality? Neurol Sci 36(Suppl 1):61–66. doi:10.1007/s10072-015-2163-8
Allais G, Bussone G, Tullo V, Cortelli P, Valguarnera F, Barbanti P, Sette G, Frediani F, D’Arrigo G, d’Onofrio F, Comi G, Curone M, Colombo B, Omboni S, Benedetto C (2015) Early (≤1-h) vs. late (>1-h) administration of frovatriptan plus dexketoprofen combination vs. frovatriptan monotherapy in the acute treatment of migraine attacks with or without aura: a post hoc analysis of a double-blind, randomized, parallel group study. Neurol Sci 36(Suppl 1):161–167. doi:10.1007/s10072-015-2165-6
De Simone R, Ranieri A (2015) The role of intracranial hypertension in the chronification of migraine. Neurol Sci 36(Suppl 1):23–28. doi:10.1007/s10072-015-2164-7
Curone M, Peccarisi C, Bussone G (2015) Headache attributed to intracranial pressure alterations: applicability of the International Classification of Headache Disorders ICHD-3 beta version versus ICHD-2. Neurol Sci 36(Suppl 1):137–139. doi:10.1007/s10072-015-2202-5
Marzoli SB, Criscuoli A (2015) Headaches attributed to visual disturbances. Neurol Sci 36(Suppl 1):85–88. doi:10.1007/s10072-015-2167-4
Teggi R, Colombo B, Rocca MA, Bondi S, Messina R, Comi G, Filippi M (2016) A review of recent literature on functional MRI and personal experience in two cases of definite vestibular migraine. Neurol Sci 37(9):1399–1402
Teggi R, Colombo B, Gatti O, Comi G, Bussi M (2015) Fixed combination of cinnarizine and dimenhydrinate in the prophylactic therapy of vestibular migraine: an observational study. Neurol Sci 36(10):1869–1873. doi:10.1007/s10072-015-2270-6
Kim DE, Shin JH, Kim YH, Eom TH, Kim SH, Kim JM (2016) Source localization of intermittent rhythmic delta activity in a patient with acute confusional migraine: cross-spectral analysis using standardized low-resolution brain electromagnetic tomography (sLORETA). Neurol Sci 37(1):89–95
Joffily L, de Melo Tavares de Lima MA, Vincent MB, Frota SM (2016) Assessment of otoacoustic emission suppression in women with migraine and phonophobia. Neurol Sci 37(5):703–709
Karaca EE, Koçer EB, Özdek Ş, Akçam HT, Ercan MB (2016) Choroidal thickness measurements in migraine patients during attack-free period. Neurol Sci 37(1):81–88
Raggi A, Schiavolin S, Leonardi M, Grazzi L, Usai S, Curone M, D’Amico D (2015) Approaches to treatments of chronic migraine associated with medication overuse: a comparison between different intensity regimens. Neurol Sci 36(Suppl 1):5–8. doi:10.1007/s10072-015-2134-0
Viticchi G, Falsetti L, Buratti L, Plutino A, Provinciali L, Silvestrini M, Bartolini M (2015) Triptan use among hospital workers affected by migraine. Neurol Sci 36(Suppl 1):157–159. doi:10.1007/s10072-015-2143-z
Allais G, Chiarle G, Bergandi F, Benedetto C (2015) Migraine in perimenopausal women. Neurol Sci 36(Suppl 1):79–83. doi:10.1007/s10072-015-2155-8
Sedighi B, Shafiei K, Azizpour I (2016) Topiramate-induced paresthesia is more frequently reported by migraine than epileptic patients. Neurol Sci 37(4):585–589
Raggi A, Covelli V, Schiavolin S, Giovannetti AM, Cerniauskaite M, Quintas R, Leonardi M, Sabariego C, Grazzi L, D’Amico D (2016) Psychosocial difficulties in patients with episodic migraine: a cross-sectional study. Neurol Sci 37(12):1979–1986
Demiryurek BE, Ertem DH, Tekin A, Ceylan M, Aras YG, Gungen BD (2016) Effects of onabotulinumtoxin A treatment on efficacy, depression, anxiety, and disability in Turkish patients with chronic migraine. Neurol Sci 37(11):1779–1784
Butera C, Colombo B, Bianchi F, Cursi M, Messina R, Amadio S, Guerriero R, Comi G, Del Carro U (2016) Refractory chronic migraine: is drug withdrawal necessary before starting a therapy with onabotulinum toxin type A? Neurol Sci 37(10):1701–1706
Lambru G, Giakoumakis E, Al-Kaisy A (2015) Advanced technologies and novel neurostimulation targets in trigeminal autonomic cephalalgias. Neurol Sci 36(Suppl 1):125–129. doi:10.1007/s10072-015-2171-8
Didier HA, Di Fiore P, Marchetti C, Tullo V, Frediani F, Arlotti M, Giannì AB, Bussone G (2015) Electromyography data in chronic migraine patients by using neurostimulation with the Cefaly® device. Neurol Sci 36(Suppl 1):115–119. doi:10.1007/s10072-015-2154-9
Franzini A, Messina G (2015) Surgery for treatment of refractory chronic cluster headache: toward standard procedures. Neurol Sci 36(Suppl 1):131–135. doi:10.1007/s10072-015-2179-0
Happe S, Peikert A, Siegert R, Evers S (2016) The efficacy of lymphatic drainage and traditional massage in the prophylaxis of migraine: a randomized, controlled parallel group study. Neurol Sci 37(10):1627–1632
Tumors
Aprile I, Chiesa S, Padua L, Di Blasi C, Arezzo MF, Valentini V, Di Stasio E, Balducci M (2015) Occurrence and predictors of the fatigue in high-grade glioma patients. Neurol Sci 36(8):1363–1369. doi:10.1007/s10072-015-2111-7
Wang B, Wang D, Zhu Z, Wang W, Zhang X, Tang F, Zhou Y, Wang H, Liu M, Yao X, Yan X (2016) The role of extracellular-5′-nucleotidase/CD73 in glioma peritumoural brain edema. Neurol Sci 37(4):603–611
Rudà R, Pellerino A, Magistrello M, Franchino F, Pinessi L, Soffietti R (2015) Molecularly based management of gliomas in clinical practice. Neurol Sci 36(9):1551–1557. doi:10.1007/s10072-015-2332-9
Ye Z, Zhang Z, Wu L, Liu C, Chen Q, Liu J, Wang X, Zhuang Z, Li W, Xu S, Hang C (2016) Upregulation of miR-183 expression and its clinical significance in human brain glioma. Neurol Sci 37(8):1341–1347
Shao N, Wang L, Xue L, Wang R, Lan Q (2015) Plasma miR-454-3p as a potential prognostic indicator in human glioma. Neurol Sci 36(2):309–313. doi:10.1007/s10072-014-1938-7
Chen T, Wang XY, Li C, Xu SJ (2015) Downregulation of microRNA-124 predicts poor prognosis in glioma patients. Neurol Sci 36(1):131–135. doi:10.1007/s10072-014-1895-1
Shan S, Hui G, Hou F, Shi H, Zhou G, Yan H, Wang L, Liu J (2015) Expression of metastasis-associated protein 3 in human brain glioma related to tumor prognosis. Neurol Sci 36(10):1799–1804. doi:10.1007/s10072-015-2252-8
Alzheimer’s disease and other cognitive disorders
Marešová P, Zahálková V (2016) The economic burden of the care and treatment for people with Alzheimer’s disease: the outlook for the Czech Republic. Neurol Sci 37(12):1917–1922
Ahmed S, Mahmood Z, Zahid S (2015) Linking insulin with Alzheimer’s disease: emergence as type III diabetes. Neurol Sci 36(10):1763–1769. doi:10.1007/s10072-015-2352-5
Zhang Q, Guo S, Zhang X, Tang S, Shao W, Han X, Wang L, Du Y (2015) Inverse relationship between cancer and Alzheimer’s disease: a systemic review meta-analysis. Neurol Sci 36(11):1987–1994. doi:10.1007/s10072-015-2282-2
Dursun E, Alaylıoğlu M, Bilgiç B, Hanağası H, Lohmann E, Atasoy IL, Candaş E, Araz ÖS, Önal B, Gürvit H, Yılmazer S, Gezen-Ak D (2016) Vitamin D deficiency might pose a greater risk for ApoEɛ4 non-carrier Alzheimer’s disease patients. Neurol Sci 37(10):1633–1643. doi:10.1007/s10072-016-2647-1
Zhang Y, Li P, Feng J, Wu M (2016) Dysfunction of NMDA receptors in Alzheimer’s disease. Neurol Sci 37(7):1039–1047. doi:10.1007/s10072-016-2546-5
Oktem EO, Derle E, Kibaroglu S, Oktem C, Akkoyun I, Can U (2015) The relationship between the degree of cognitive impairment and retinal nerve fiber layer thickness. Neurol Sci 36(7):1141–1146. doi:10.1007/s10072-014-2055-3
Yang R, Wang Q, Li F, Li J, Liu X (2015) Edaravone injection ameliorates cognitive deficits in rat model of Alzheimer’s disease. Neurol Sci 36(11):2067–2072. doi:10.1007/s10072-015-2314-y
Zhu Y, Wang J (2015) Wogonin increases β-amyloid clearance and inhibits tau phosphorylation via inhibition of mammalian target of rapamycin: potential drug to treat Alzheimer’s disease. Neurol Sci 36(7):1181–1188. doi:10.1007/s10072-015-2070-z
Parkinson’s disease
Baldacci F, Policardo L, Rossi S, Ulivelli M, Ramat S, Grassi E, Palumbo P, Giovannelli F, Cincotta M, Ceravolo R, Sorbi S, Francesconi P, Bonuccelli U (2015) Reliability of administrative data for the identification of Parkinson’s disease cohorts. Neurol Sci 36(5):783–786. doi:10.1007/s10072-015-2062-z
Akıl E, Bulut A, Kaplan İ, Özdemir HH, Arslan D, Aluçlu MU (2015) The increase of carcinoembryonic antigen (CEA), high-sensitivity C-reactive protein, and neutrophil/lymphocyte ratio in Parkinson’s disease. Neurol Sci 36(3):423–428. doi:10.1007/s10072-014-1976-1
Çubukçu HC, Yurtdaş M, Durak ZE, Aytaç B, Güneş HN, Çokal BG, Yoldaş TK, Durak İ (2016) Oxidative and nitrosative stress in serum of patients with Parkinson’s disease. Neurol Sci 37(11):1793–1798
Vieru E, Köksal A, Mutluay B, Dirican AC, Altunkaynak Y, Baybas S (2016) The relation of serum uric acid levels with l-Dopa treatment and progression in patients with Parkinson’s disease. Neurol Sci 37(5):743–747. doi:10.1007/s10072-015-2471-z
Zhao HQ, Li FF, Wang Z, Wang XM, Feng T (2016) A comparative study of the amount of α-synuclein in ischemic stroke and Parkinson’s disease. Neurol Sci 37(5):749–754. doi:10.1007/s10072-016-2485-1
Demirci S, Gunes A, Koyuncuoglu HR, Tok L, Tok O (2016) Evaluation of corneal parameters in patients with Parkinson’s disease. Neurol Sci 37(8):1247–1252. doi:10.1007/s10072-016-2574-1
Štenc Bradvica I, Bradvica M, Matić S, Reisz-Majić P (2015) Visual dysfunction in patients with Parkinson’s disease and essential tremor. Neurol Sci 36(2):257–262. doi:10.1007/s10072-014-1930-2
Gao L, Chen H, Li X, Li F, Ou-Yang Q, Feng T (2015) The diagnostic value of minor salivary gland biopsy in clinically diagnosed patients with Parkinson’s disease: comparison with DAT PET scans. Neurol Sci 36(9):1575–1580. doi:10.1007/s10072-015-2190-5
Shin HW, Kim JS, Oh M, You S, Kim YJ, Kim J, Kim MJ, Chung SJ (2015) Clinical features of drug-induced parkinsonism based on [18F] FP-CIT positron emission tomography. Neurol Sci 36(2):269–274. doi:10.1007/s10072-014-1945-8
Defazio G, Guerrieri M, Liuzzi D, Gigante AF, di Nicola V (2016) Assessment of voice and speech symptoms in early Parkinson’s disease by the Robertson dysarthria profile. Neurol Sci 37(3):443–449. doi:10.1007/s10072-015-2422-8
Gazibara T, Kisic-Tepavcevic D, Svetel M, Tomic A, Stankovic I, Kostic VS, Pekmezovic T (2016) Indoor and outdoor falls in persons with Parkinson’s disease after 1 year follow-up study: differences and consequences. Neurol Sci 37(4):597–602
Karakoc M, Yon MI, Cakmakli GY, Ulusoy EK, Gulunay A, Oztekin N, Ak F (2016) Pathophysiology underlying drooling in Parkinson’s disease: oropharyngeal bradykinesia. Neurol Sci 37(12):1987–1991
Gómez-Caravaca MT, Cáceres-Redondo MT, Huertas-Fernández I, Vargas-González L, Carrillo F, Carballo M, Mir P (2015) The use of botulinum toxin in the treatment of sialorrhea in parkinsonian disorders. Neurol Sci 36(2):275–279. doi:10.1007/s10072-014-1950-y
Dogan VB, Koksal A, Dirican A, Baybas S, Dirican A, Dogan GB (2015) Independent effect of fatigue on health-related quality of life in patients with idiopathic Parkinson’s disease. Neurol Sci 36(12):2221–2226
Jiang SM, Yuan YS, Tong Q, Zhang L, Xu QR, Ding J, Zhang KZ (2015) The association between clinically relevant anxiety and other non-motor symptoms in Parkinson’s disease. Neurol Sci 36(11):2105–2109
Ylikoski A, Martikainen K, Sieminski M, Partinen M (2015) Parkinson’s disease and insomnia. Neurol Sci 36(11):2003–2010
Erro R (2015) The non-motor heterogeneity of Parkinson disease. Neurol Sci 36(9):1705–1706
Zhang N, Liu W, Ye M, Cohen AD, Zhang Y (2015) The heterogeneity of non-motor symptoms of Parkinson’s disease. Neurol Sci 36(4):577–584
Neuromuscular disorders
Pan L, Deng X, Ding D, Leng H, Zhu X, Wang Z (2015) Association between the Angiogenin (ANG) K17I variant and amyotrophic lateral sclerosis risk in Caucasian: a meta-analysis. Neurol Sci 36(12):2163–2168. doi:10.1007/s10072-015-2344-5
Mandrioli J, Biguzzi S, Guidi C, Sette E, Terlizzi E, Ravasio A, Casmiro M, Salvi F, Liguori R, Rizzi R, Pietrini V, Borghi A, Rinaldi R, Fini N, Chierici E, Santangelo M, Granieri E, Mussuto V, De Pasqua S, Georgoulopoulou E, Fasano A; ERRALS Group, Ferro S, D’Alessandro R (2015) Heterogeneity in ALSFRS-R decline and survival: a population-based study in Italy. Neurol Sci 36(12):2243–2252. doi: 10.1007/s10072-015-2343-6
Santurtún A, Villar A, Delgado-Alvarado M, Riancho J (2016) Trends in motor neuron disease: association with latitude and air lead levels in Spain. Neurol Sci 37(8):1271–1275. doi:10.1007/s10072-016-2581-2
Ma X, Zhang J, Zhang Y, Chen H, Li R, Wang J, Chen H (2015) Altered cortical hubs in functional brain networks in amyotrophic lateral sclerosis. Neurol Sci 36(11):2097–2104. doi:10.1007/s10072-015-2319-6
Budrewicz S, Szewczyk P, Bladowska J, Podemski R, Koziorowska-Gawron E, Ejma M, Słotwiński K, Koszewicz M (2016) The possible meaning of fractional anisotropy measurement of the cervical spinal cord in correct diagnosis of amyotrophic lateral sclerosis. Neurol Sci 37(3):417–421. doi:10.1007/s10072-015-2418-4
Sako W, Abe T, Izumi Y, Harada M, Kaji R (2016) Fractional anisotropy in the supplementary motor area correlates with disease duration and severity of amyotrophic lateral sclerosis. Neurol Sci 37(4):573–577. doi:10.1007/s10072-016-2487-z
Theodorou L, Nicolaou P, Koutsou P, Georghiou A, Anastasiadou V, Tanteles G, Kyriakides T, Zamba-Papanicolaou E, Christodoulou K (2015) Genetic findings of Cypriot spinal muscular atrophy patients. Neurol Sci 36(10):1829–1834. doi:10.1007/s10072-015-2263-5
Zamani GR, Karami F, Mehdizadeh M, Movafagh A, Nilipour Y, Zamani M (2015) Analysis of dystrophin gene in Iranian Duchenne and Becker muscular dystrophies patients and identification of a novel mutation. Neurol Sci 36(11):2011–2017. doi:10.1007/s10072-015-2290-2
Xie C, Zhou X, Zhu D, Liu W, Wang X, Yang H, Li Z, Hao Y, Zhang GX, Guan Y (2016) CNS involvement in CMTX1 caused by a novel connexin 32 mutation: a 6-year follow-up in neuroimaging and nerve conduction. Neurol Sci 37(7):1063–1070. doi:10.1007/s10072-016-2537-6
Keskin G, Kahraman Koytak P, Bastan B, Tanridag T, Us O, Uluc K (2015) The reliability of medial and lateral plantar nerve recordings in healthy elderly individuals. Neurol Sci 36(6):883–888. doi:10.1007/s10072-014-2056-2
Wang Y, Wang H, Mi D, Gu X, Hu W (2015) Periodical assessment of electrophysiological recovery following sciatic nerve crush via surface stimulation in rats. Neurol Sci 36(3):449–456. doi:10.1007/s10072-014-2005-0
Won YH, Kim KW, Choi JT, Ko M, Park SH, Seo JH (2016) Correlation between muscle electrophysiology and strength after fibular nerve injury. Neurol Sci 37(8):1293–1298. doi:10.1007/s10072-016-2584-z
Squintani G, Basaldella F, Donato F, Silipo S, Moretto G (2016) Increase of distal sensory action potential duration as a sensitive electrophysiological parameter in atypical case of acute inflammatory demyelinating polyneuropathy. Neurol Sci 37(2):305–307. doi:10.1007/s10072-015-2416-6
Wu X, Liu K, Zhang HL (2015) Guillain–Barré syndrome and encephalitis/encephalopathy associated with acute severe hepatitis E infection. Neurol Sci 36(1):165–166
Nagamine S, Fujiwara Y, Shimizu T, Kawata A, Wada K, Isozaki E, Kabuta T (2015) Association of ubiquitin carboxy-terminal hydrolase-L1 in cerebrospinal fluid with clinical severity in a cohort of patients with Guillain–Barré syndrome. Neurol Sci 36(6):921–926. doi:10.1007/s10072-015-2137-x
Zheng Q, Chu L, Tan L, Zhang H (2016) Facial onset sensory and motor neuronopathy. Neurol Sci 37(12):1905–1909
Ginanneschi F, Cioncoloni D, Bigliazzi J, Bonifazi M, Lorè C, Rossi A (2015) Sensory axons excitability changes in carpal tunnel syndrome after neural mobilization. Neurol Sci 36(9):1611–1615. doi:10.1007/s10072-015-2218-x
Vinciguerra C, Sicurelli F, Fioravanti A, Malandrini A, Battisti C, Federico A (2015) Hydroxychloroquine neuromyotoxicity: a case with rapid course and complete recovery. Neurol Sci 36(12):2293–2294. doi:10.1007/s10072-015-2355-2
Epilepsy
Gabutti G, Kuhdari P, Ferioli S, Trucchi C (2015) Hospital admissions for seizure in Italy: a decennial retrospective analysis with a special focus on the burden in the pediatric age. Neurol Sci 36(9):1667–1673. doi:10.1007/s10072-015-2230-1
Asadi-Pooya AA, Farazdaghi M (2016) Seizure outcome in patients with juvenile absence epilepsy. Neurol Sci 37(2):289–292. doi:10.1007/s10072-015-2411-y
Cevik N, Koksal A, Dogan VB, Dirican AC, Bayramoglu S, Ozturk M, Baybas S (2016) Evaluation of cognitive functions of juvenile myoclonic epileptic patients by magnetic resonance spectroscopy and neuropsychiatric cognitive tests concurrently. Neurol Sci 37(4):623–627. doi:10.1007/s10072-015-2425-5
La Neve A, Boero G, Francavilla T, Plantamura M, De Agazio G, Specchio LM (2015) Prospective, case-control study on the effect of pregnancy on seizure frequency in women with epilepsy. Neurol Sci 36(1):79–83. doi:10.1007/s10072-014-1908-0
Asadi-Pooya AA (2016) Biological underpinnings of psychogenic nonepileptic seizures: directions for future research. Neurol Sci 37(7):1033–1038. doi:10.1007/s10072-016-2540-y
Asadi-Pooya AA (2016) Psychogenic nonepileptic seizures are predominantly seen in women: potential neurobiological reasons. Neurol Sci 37(6):851–855. doi:10.1007/s10072-016-2481-5
Janati AB, AlGhasab N, Umair M (2015) Focal triphasic sharp waves and spikes in the electroencephalogram. Neurol Sci 36(2):221–226. doi:10.1007/s10072-014-1923-1
Esmail EH, Nawito AM, Labib DM, Basheer MA (2016) Focal interictal epileptiform discharges in idiopathic generalized epilepsy. Neurol Sci 37(7):1071–1077. doi:10.1007/s10072-016-2538-5
Ozkaynakci A, Gulcebi MI, Ergeç D, Ulucan K, Uzan M, Ozkara C, Guney I, Onat FY (2015) The effect of polymorphic metabolism enzymes on serum phenytoin level. Neurol Sci 36(3):397–401. doi:10.1007/s10072-014-1961-8
Gasparini S, Ferlazzo E, Giussani G, Italiano D, Cianci V, Sueri C, Spina E, Beghi E, Aguglia U (2016) Rapid versus slow withdrawal of antiepileptic monotherapy in 2-year seizure-free adult patients with epilepsy (RASLOW) study: a pragmatic multicentre, prospective, randomized, controlled study. Neurol Sci 37(4):579–583. doi:10.1007/s10072-016-2483-3
Güzel O, Yılmaz U, Uysal U, Arslan N (2016) The effect of olive oil-based ketogenic diet on serum lipid levels in epileptic children. Neurol Sci 37(3):465–470. doi:10.1007/s10072-015-2436-2
Pakdaman H, Amini Harandi A, Abbasi M, Karimi M, Arami MA, Mosavi SA, Haddadian K, Rezaei O, Sadeghi S, Sharifi G, Gharagozli K, Bahrami P, Ashrafi F, Kasmae HD, Ghassemi A, Arabahmadi M, Behnam B (2016) Vagus nerve stimulation in drug-resistant epilepsy: the efficacy and adverse effects in a 5-year follow-up study in Iran. Neurol Sci 37(11):1773–1778
Neurogenetic
Da Pozzo P, Rubegni A, Rufa A, Cardaioli E, Taglia I, Gallus GN, Malandrini A, Federico A (2015) Sporadic PEO caused by a novel POLG variation and a Twinkle mutation: digenic inheritance? Neurol Sci 36(9):1713–1715. doi:10.1007/s10072-015-2247-5
Yu F, Liu XM, Chen YH, Zhang SQ, Wang K (2015) A novel CLN2/TPP1 mutation in a patient with late infantile neuronal ceroid lipofuscinosis. Neurol Sci 36(10):1917–1919
Mignarri A, Tessa A, Federico A, Santorelli FM, Dotti MT (2015) Ataxia with oculomotor apraxia type 2: not always an easy diagnosis. Neurol Sci 36(8):1505–1507. doi:10.1007/s10072-015-2119-z
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A. Federico: Editor in Chief Neurological Sciences.
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Di Donato, I., Federico, A. Advances in clinical neurology through the journal “Neurological Sciences” (2015–2016). Neurol Sci 38, 9–18 (2017). https://doi.org/10.1007/s10072-017-2815-y
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DOI: https://doi.org/10.1007/s10072-017-2815-y