Search

Background: The identification of biomarkers for the early diagnosis of Alzheimer's disease (AD) is a crucial goal of the current research. Blood biomarkers are less invasive, easier to obtain and achievable by a cheaper means than those on cerebrospinal fluid (CSF) and significantly more economic than functional neuroimaging investigations; thus, a great interest is focused on blood isoforms of the phosphorylated Tau protein (pTau), indicators of ongoing tau pathology (i.e. neurofibrillary tangles, NFTs, an AD neuropathological hallmark) in the central nervous system (CNS). However, current data often highlight discordant results about the ability of blood pTau to predict CSF status. Objective: We aim to synthesise the studies that compared pTau levels on CSF and blood to assess their correlation in AD continuum. Methods: We performed a narrative literature review using, first, MEDLINE (via PubMed) by means of MeSH terms, and then, we expanded the reults by means of Scopus and Web of Sciences to be as inclusive as possible. Finally, we added work following an expert opinion. Only papers presenting original data on pTau values on both blood and CSF were included. Results: The 33 included studies show an extreme heterogeneity in terms of pTau isoform (pTau181, 217 and 231), laboratory methods, diagnostic criteria and choice of comparison groups. Most studies evaluated plasma pTau181, while data on other isoforms and serum are scarcer. Discussion: Most papers identify a correlation between CSF and blood measurements. Furthermore, even when not specified, it is often possible to show an increase in blood pTau values as AD-related damage progresses in the AD continuum and higher values in AD than in other neurodegenerative diseases. Notably, plasma pTau231 seems the first biomarker to look for in the earliest and pre-clinical stages, quickly followed by pTau217 and, finally, by pTau181. Conclusions: Our results encourage the use of blood pTau for the early identification of patients with AD continuum. [ABSTRACT FROM AUTHOR]

Leukoencephalopathy with calcifications and cysts (LCC; OMIM #614561) is a rare disease and at present there are less than 100 cases reported worldwide. Mutations in the SNORD118 gene is now known to be the cause of LCC. We present a case who was heterozygous for the n.70G>A and n.6C>T sequence variants of the SNORD118 gene, variants which to date have not been described. Compared with the cases that we reviewed, our patient had the second longest time to diagnosis (age 56) from onset of symptoms 40 years prior. Moreover, his cousin's family has a high prevalence of epilepsy. This paper reviewed all published reports to date that had descriptive cases involving LCC as well as testing for the SNORD118 gene. Since 1996 only 85 patients have been described in 59 case reports. In this review, we summarize their clinical features, especially central nervous system symptoms, treatment, pathology, and gene testing results. [ABSTRACT FROM AUTHOR]

Steroid-responsive encephalopathy is a general term for diseases that are characterized by diffuse brain injury and respond well to corticosteroids or immunosuppressive agents, including Hashimoto's encephalopathy (HE), limbic encephalitis (LE), systemic lupus erythematosus encephalopathy (SLEE), antineutrophil cytoplasmic antibodies (ANCA)-associated systemic vasculitis encephalopathy (AASV), viral encephalitis (VE), and primary central nervous system lymphoma (PCNSL). Epilepsy and status epilepticus are the main manifestations of steroid-responsive encephalopathy. The spectrum of "autoimmune epilepsy" diseases, which has been approved by the epilepsy diagnostic recommendations of the International Antiepileptic League, is characterized by a high prevalence of epilepsy in central nervous system (CNS) autoimmune diseases and a variety of neuron-specific autoantibodies. Steroid-responsive encephalopathy with different causes may have different pathogeneses and has been suggested to be associated with some internal commonality producing seizure as the main symptom. Determining the regularity of seizures caused by steroid-responsive encephalopathy and implementing appropriate measures will help us improve the prognosis of patients. This paper summarizes the epidemiology, seizure onset, seizure type, and other characteristics of seizures in steroid-responsive encephalopathy (including HE, LE, SLEE, ANCA-associated systemic vasculitis encephalopathy, VE, and PCNSL) and then discusses the use of antiepileptic drugs to treat steroid-responsive encephalopathy. [ABSTRACT FROM AUTHOR]

Calcitonin gene-related peptide (CGRP) is a key signaling molecule involved in migraine pathophysiology. Efficacy of CGRP monoclonal antibodies and antagonists in migraine treatment has fueled an increasing interest in the prospect of treating cluster headache (CH) with CGRP antagonism. The exact role of CGRP and its mechanism of action in CH have not been fully clarified. A search for original studies and randomized controlled trials (RCTs) published in English was performed in PubMed and in ClinicalTrials.gov . The search term used was "cluster headache and calcitonin gene related peptide" and "primary headaches and calcitonin gene related peptide." Reference lists of identified articles were also searched for additional relevant papers. Human experimental studies have reported elevated plasma CGRP levels during both spontaneous and glyceryl trinitrate-induced cluster attacks. CGRP may play an important role in cluster headache pathophysiology. More refined human studies are warranted with regard to assay validation and using larger sample sizes. The results from RCTs may reveal the therapeutic potential of CGRP monoclonal antibodies and antagonists for cluster headache treatment. [ABSTRACT FROM AUTHOR]

The paper wants to be a tracking shot of the main recent acquisitions on the function and significance of microglia/macrophages in gliomas. The observations have been principally carried out on in vitro cultures and on tumor transplants in animals. Contrary to what is deduced from microglia in non-neoplastic pathologic conditions of central nervous system (CNS), most conclusions indicate that microglia acts favoring tumor proliferation through an immunosuppression induced by glioma cells. By immunohistochemistry, different microglia phenotypes are recognized in gliomas, from ramified microglia to frank macrophagic aspect. One wonders whether the functional conclusions drawn from many microglia studies, but not in conditions of human pathology, apply to all the phenotypes recognizable in them. It is difficult to verify in human pathology a prognostic significance of microglia. Only CD163-positive microglia/macrophages inversely correlate with glioma patients' survival, whereas the total number of microglia does not change with the malignancy grade. [ABSTRACT FROM AUTHOR]

Introduction: Primary central nervous system lymphoma (PCNSL) is a rare extranodal lymphomatous malignancy that affects the brain, spinal cord, leptomeninges, or eyes, in the absence of systemic diffusion. Myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD) is a newly identified benign immune-mediated CNS inflammatory disorder with specific anti-MOG antibody seropositivity. These two seemingly unrelated nosological entities both have abundant clinical and radiological manifestations, and whether there is a potential link between them is unclear. Case report: We describe a 49-year-old man who presented progressive headache, dizziness, and unsteady gait with multifocal scattered T2 hyperintensities with contrast enhancement. The serum anti-MOG antibody test was positive, and a brain biopsy showed inflammatory infiltration. Initially, he was diagnosed with MOGAD and his condition improved after corticosteroid therapy. The patient relapsed with exacerbation of symptoms and neuroimaging showed new mass-forming lesions four months later. A second brain biopsy confirmed PCNSL. Discussion: This is the first report of histologically confirmed successive MOGAD and PCNSL. Our case broadens the phenotypic spectrum of sentinel lesions in PCNSL. Though rare, PCNSL should be considered in patients diagnosed with benign CNS inflammatory disorder and responding well to steroid treatment when their clinical symptoms worsen and the imaging deteriorates. A timely biopsy is critical for accurate diagnosis and appropriate therapy. [ABSTRACT FROM AUTHOR]

Vanishing white matter disease (VWM; MIM #603896), also known as childhood ataxia with central nervous system hypomyelination (CACH) syndrome, is an autosomal recessive transmitted leukoencephalopathy related to mutations in each of the 5 genes ( EIF2B1, EIF2B2, EIF2B3, EIF2B4 and EIF2B5) encoding for the 5 subunits of eukaryotic translation initiation factor 2B (eIF2B), essential for protein synthesis. VWM is characterised by ataxia, spasticity, variable optic atrophy and intermittent episodes of acute regression of clinical and neurological status. Another key step in diagnosis, besides clinical picture and gene sequencing, is magnetic resonance imaging (MRI), which typically shows a progressive rarefaction of the brain white matter, and its replacement by cerebrospinal fluid (CSF). In the present paper we summarise the up-to-date knowledge about VWM and include the full list of known mutations. [ABSTRACT FROM AUTHOR]

Background: Primary central nervous system lymphoma (PCNSL) is an aggressive extranodal lymphoma exclusively occurring within the central nervous system. Inflammatory brain lesions as "sentinel lesions" of PCNSL are very rare. We present a rare case of PCNSL with preceding inflammatory lesions in an immunocompetent patient who underwent two biopsies, one craniotomy and two genetic testing. Case report: A 66-year-old male patient presented with left limb weakness and ataxia. Brain magnetic resonance imaging showed a contrast-enhancing lesion with perifocal brain edema in the near midline of right frontal lobe. Histological examination of a brain biopsy specimen revealed inflammatory lesion characteristics with infiltration of T-cell dominant lymphocytes and few B-cell. Given that the patient developed cerebral hematoma after biopsy, lesion resection by craniotomy was performed. An excised sample demonstrated mixed T-cell and B-cell infiltrating inflammatory lesions. Four months after total resection of the right frontal lobe lesion, another lesion appeared in the left frontal parietal lobe, which was diagnosed as diffuse large B-cell lymphoma by biopsy. In addition, genetic testing of the lesions at two different locations was performed, and the results showed that the inflammatory lesions had the same three gene (RELN, PCLO, and CREBBP) mutations as PCNSL. Interestingly, the three mutated genes are associated with tumor. Conclusion: Our present case is the first to demonstrate inflammatory brain lesions heralding PCNSL from genetic and pathological perspectives. This may help clinicians to select new auxiliary diagnostic methods for timely diagnosis of patients with suspected PCNSL. [ABSTRACT FROM AUTHOR]

Not all patients presenting with their first attack of multiple sclerosis (MS) or early thereafter are necessarily in the same phase of disease; some truly present early with minimal disease, whereas others present late, having accumulated already considerable damage to the central nervous system (CNS). This beckons a different approach to therapy depending on “where” a patient may be in the course of disease. If early, then any of the current first line immunomodulating agents may be appropriate, whereas later disease calls for a more aggressive approach entailing either induction with a more powerful but riskier treatment or an escalation approach, moving through first line agents and stepping up to more aggressive treatments. This paper discusses the rationale for either regimen. [ABSTRACT FROM AUTHOR]

Objective: Whipple's disease (WD) is a systemic, chronic, relapsing disease caused by Tropheryma whipplei, which can mimic signs and symptoms of various clinical entities. Typical manifestations are represented by gastrointestinal and systemic symptoms, among which neurological ones are frequent. We present the case of a patient with WD and rapidly progressive cognitive impairment and a review of literature aimed to report epidemiological, clinical, neuroimaging, and laboratory findings of cognitive impairment associated with WD.Methods: A systematic review of medical literature published until November 22, 2020, was performed. Full-text, peer-reviewed case reports and series in English language presenting patients with WD and cognitive impairment were included. Data concerning demographic, clinical, neuroimaging, and laboratory characteristics were collected and synthesized qualitatively.Results: The patient was a 54-year-old male who developed rapidly progressive dementia, fluctuating arousal disturbances, and supranuclear ophthalmoparesis associated with chronic diarrhea and fever spikes. T. whipplei was detected in the cerebrospinal fluid, and appropriate antimicrobial therapy was given with progressive clinical benefit. The systematic review of 114 case reports/series identified 147 patients with WD and cognitive impairment; this latter was rarely isolated. Neurological symptoms associated with cognitive decline were psychiatric disturbances, supranuclear ophthalmoplegia, hypothalamic involvement, and consciousness disorders. Brain imaging and cerebrospinal fluid findings were heterogeneous and nonspecific.Conclusions: Cognitive impairment represents one of the most common neurological features associated with WD. The clinical suspicion of this disease in patients with rapidly progressive dementia is crucial to guide diagnostic strategies and proper antimicrobial therapy, which may revert the clinical deterioration. [ABSTRACT FROM AUTHOR]

The authors seek to clarify the nomenclature used to describe cervical spinal cord injuries, particularly the use of the terms 'tetraplegia', 'quadriplegia', 'quadriparesis', 'tetraparesis', 'incomplete quadriplegia' or 'incomplete tetraplegia' when applied to patients with lower cervical cord injuries. A review of the origin of the terms and nomenclature used currently to describe the neurological status of patients with SCI in the literature was performed. The terms 'tetraplegia', 'quadriplegia', 'quadriparesis', 'tetraparesis', 'incomplete quadriplegia' or 'incomplete tetraplegia' have been used very often to describe patients with complete lower cervical SCI despite the fact that the clinical scenario is all the same for most of these patients. Most of these patients have total loss of the motor voluntary movements of their lower trunk and inferior limbs, and partial impairment of movement of their superior limbs, preserving many motor functions of the proximal muscles of their arms (superior limbs). A potentially better descriptive term may be 'paraplegia with brachial diparesis'. In using the most appropriate terminology, the patients with lower cervical SCI currently referred as presenting with 'tetraplegia', 'quadriplegia', 'quadriparesis', 'tetraparesis', 'incomplete quadriplegia' or 'incomplete tetraplegia', might be better described as having 'paraplegia with brachial diparesis'. [ABSTRACT FROM AUTHOR]

Patients with COVID-19 are increasingly reported to suffer from a wide range of neurological complications, affecting both the central and peripheral nervous system. Among central manifestations, cognitive and behavioral symptoms are to date not exhaustively detailed. Furthermore, it is not clear whether these represent a combination of non-specific complications of a severe systemic disease, not differing from those usually seen in patients suffering from heterogenous pathological conditions affecting the central nervous system, or instead, they are a peculiar expression of COVID-19 neurotropism; in other words, if the infection has a coincidental or causal role in such patients. We examined both hypotheses, reporting opposite points of view, with the aim to stimulate discussion and raise awareness of the topic. [ABSTRACT FROM AUTHOR]

Purpose: Developmental venous anomalies (DVAs) have been found to be more prevalent in patients with multiple sclerosis (MS). The aim of the study was to compare the prevalence of DVAs in a large population of patients with MS compared with controls and to investigate the correlation of 3D Fluid Attenuated Inversion Recovery (FLAIR) hyperintense signal abnormalities adjacent to DVAs between MS patients and controls having DVAs, as well as DVA potential role in differential diagnosis.Methods: Between January 2001 and December 2019, 349 patients who met the McDonald criteria for MS diagnosis (249 females, 100 males, age range 18-70 years) were retrospectively included in the study. All patients and 340 age-matched healthy controls had brain MRIs performed on a 1.5 Tesla MR system. Two radiologists reviewed all images to identify DVAs; their presence was compared between the MS and control groups. Among the subjects having DVAs, age, gender, adjacent FLAIR anomalies, and DVA location were compared between the two groups.Results: Fifty (14.3%) out 349 patients presented 51 DVAs (35 supratentorial and 16 infratentorial), in comparison to 21/340 (6.2%) controls (P = 0.0005). One patient showed 2 simultaneous DVAs, while 3 patients had coexisting pontine capillary telangiectasias. FLAIR white matter changes adjacent to DVAs were found in 46.2% of patients and in 28.1% of controls (P = 0.0001).Conclusions: DVAs demonstrated a higher prevalence in the MS group in comparison to controls. We confirmed the association between DVAs and FLAIR anomalies in MS patients. However, currently there are no evidences that the presence of DVAs may be used in MS differential diagnosis. [ABSTRACT FROM AUTHOR]

Background: Recognition of secondary movement disorders (SMDs) is fundamental either to alleviate disabling disturbances or to treat potentially life-threatening conditions, such as brain tumors. Primary CNS lymphoma (PCNSL) is a rare form of CNS cancer that is often located in subcortical areas, accounting for both neuropsychiatric and motoric disorders. Nevertheless, an overview on PCNSL-related movement disorders (MDs) phenomenology has not been provided yet. Objective: To outline the main features of PCNSL-related MDs. Methods: A retrospective analysis was conducted on a cohort of patients with PCNSL presenting with MDs, including all existing cases identified by a systematic literature review (source: Medline; period: 1946–2020) and two unreported cases. Data on phenomenology, neuroimaging, histology, and clinical course were collected. Results: A total cohort of fifteen subjects was defined, enrolling thirteen previously described patients extracted from eleven published studies, and our two unreported cases. A parkinsonian syndrome appearing at about 60 years of age, unresponsive to levodopa, associated to other neurological signs, resulted as the most common presentation of PCNSL-related MD. Chorea, dystonia, and dyskinesia occurred less frequently, with some degree of responsiveness to symptomatic treatments. Basal ganglia were involved in most cases and motoric disturbances often ameliorated after tumor mass reduction. Conclusions: This study identified those features of PCNSL-related MDs that could support an appropriate approach to such a rare condition. In fact, while the outcome remains still poor, the therapeutic scenario of PCNSL is changing; an early diagnosis together with an adequate management will be thus crucial for timely and successful interventions. [ABSTRACT FROM AUTHOR]

Background: Human serum paraoxonase (PON) is an enzyme that is synthesized by the liver and enters the bloodstream, and it is transmitted by high-density lipoproteins (HDL). Paraoxonase 1 (PON1) is a hydrolytic enzyme with a wide range of substrates and the ability to protect against lipid oxidation. In this study, due to the activity of PON1 in the brain and its antioxidant effects on the reduction of neurological disorders in the central nervous system, the role of PON1 and its polymorphisms related to multiple sclerosis has been examined to enhance treatment methods. Methods: This article is a systematic review. In this study, the role of PON1 and its polymorphisms in multiple sclerosis (MS) has been investigated. Articles published in Persian and international databases of SID, Google Scholar, ISI (WoS), Magiran, PubMed, Scopus, IranDoc, Science Direct, and Iran Medix were examined, using the search keywords of Paraoxonase 1, polymorphism, multiple sclerosis, and PON1. Results: PON1 is undoubtedly a potential factor in the pathogenesis of multiple sclerosis, and it plays an important role in protecting antioxidants in the blood. Oxidative stress and lipid peroxidation are factors in the pathogenesis of MS. Both inflammatory cytokines and oxidative stress have a detrimental effect on PON1. However, reducing the activity of PON1 may help to restore the pathogenesis of the disease. Conclusion: Decreased PON1 activity and PON1 polymorphism are associated with several neurological diseases, including ischemic stroke, white matter lesions (WMLs), amyotrophic lateral sclerosis (ALS), dementia, and Parkinson's disease. PON1-55M alleles in Italians and PON1-192Q alleles in Poles were associated with a high risk of MS. Moreover, PON1-55 and PON1-192 polymorphisms were not associated with MS onset age, nor its evolutionary type. [ABSTRACT FROM AUTHOR]

Background: Primary angiitis of the CNS (PACNS) is a process causing variously combined neurological disturbances. Its rarity and kaleidoscopic presentation make it difficult to diagnose and even to suspect. Objective: (1) To provide an up-to-date review on PACNS and (2) to create a preliminary screening algorithm based on clinical and radiological first-level data, useful to suspect PACNS and guide further investigations. Methods: Review of PUBMED case series on PACNS, published from 2002 to 2017, collection of frequencies of clinical and neuroimaging features and calculation of median values. Classification of features as "major" or "minor" if frequency was higher or lower than median value. Combination of features in sets of criteria represented by all possible combinations of major and minor clinical and neuroradiological features. Application of criteria to published PACNS case reports and selection of the ones best identifying patients with definite PACNS. Results: We reviewed 24 case series. "Major" clinical features were headache, stroke, cognitive impairment, focal neurological deficits; "minor" were seizures, altered consciousness, psychiatric disorders. "Major" neuroradiological features were multiple parenchymal lesions, parenchymal/meningeal contrast enhancement, magnetic resonance angiography vessel abnormalities, vessel wall enhancement; "minor" were parenchymal/subarachnoid hemorrhage, single parenchymal lesion. The selected sets of criteria able to identify all PACNS patients were (1) one clinical (major/minor) + one major neuroradiological feature; and (2) Two clinical (≥ 1 major) + one minor neuroradiological feature. Conclusion: Our review provides a detailed clinical/neuroradiological picture of PACNS. The proposed algorithm should be regarded as a preliminary screening tool to move the first steps towards PACNS diagnosis that needs validation. [ABSTRACT FROM AUTHOR]

Huntington's disease (HD) is a rare neurodegenerative disorder of the central nervous system characterized by involuntary choreatic movements, cognitive, behavioral, and psychiatric disturbances. Most HD suffer from dysphagia and aspiration pneumonia is the leading cause of death. However, little is known about dysphagia management in HD. A revision of the literature was conducted to depict the state of the art on the assessment and treatment of dysphagia in HD. Literature search of the last 10 years was performed using PubMed and EMBASE. Twenty-four studies were included: 16 cross-sectional studies, 2 case reports, 2 case series, 2 open-label trials, 1 pre-post study, and 1 randomized controlled trial. Based on the studies retrieved, dysphagia should be assessed from the early stage of the disease, especially when specific clinical markers occur. Timing for dysphagia re-assessment should be based on the recommendation of the swallowing experts on the individual case. Instrumental assessment of swallowing by videofluoroscopy or videoendoscopy is feasible and recommended to diagnose dysphagia in patients with HD. Clinical assessment tools and patient-reported outcome measures may be used to complete the swallowing examination, but not to replace instrumental assessment. The impact of pharmacological and rehabilitative treatments on dysphagia in HD has been little studied in literature. While the effect of tetrabenazine on swallowing is still controversial, compensatory strategies seem to be applicable and efficacious. To date, there are no well-proven rehabilitative strategies to improve swallowing function in patients with HD. The topic of dysphagia in HD remains poorly studied compared with its clinical relevance. [ABSTRACT FROM AUTHOR]

Objective: To summarize the current understanding of neuronal intranuclear inclusion disease (NIID) and improve the understanding of the physician about this condition.Methods: We searched PubMed with keywords related to NIID and selected publications which seemed appropriate. We analyzed its clinical features, pathogenesis, evaluation methods, treatment options, and research prospectives.Results: NIID is a degenerative condition which can affect multiple organ systems especially central nervous system. Its clinical features greatly vary, and making the exact diagnosis is often difficult. There are several genes which have been associated with this disorder. Some specific signs on diffusion-weighted-imaging (DWI) sequence of magnetic resonance (MR) imaging are characteristics to NIID.Conclusion: Intranuclear inclusions have been found in various nonneural cells of the body; therefore, the term systemic intranuclear inclusion disease is, perhaps, better suited to explain this disorder. There are several disorders which need to be ruled out before making the diagnosis, and neuroimaging and biopsy analysis should be combined to support the diagnosis. [ABSTRACT FROM AUTHOR]

Melatonin is a neurohormone mainly produced by the pineal gland following a circadian rhythm. It is characterized as a pleiotropic factor because it not only regulates the wake-sleep rhythm but also exerts antinociceptive, antidepressant, anxiolytic, and immunomodulating properties. Recent studies suggest that dysregulation of melatonin secretion is associated with the pathogenesis of various autoimmune diseases, such as, rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and multiple sclerosis (MS). MS is an autoimmune disorder characterized by an abnormal immune response directed against the myelin sheath in the central nervous system, demyelination, oligodendrocyte death, and axonal degeneration. Recent evidence reveals that melatonin secretion is dysregulated in MS patients, suggesting that melatonin could be a potential target for therapeutic intervention. Here, we summarize the available literature regarding the role of melatonin in immune processes relevant for experimental autoimmune encephalomyelitis (EAE), MS, and the current clinical trials of melatonin supplementation in MS patients. [ABSTRACT FROM AUTHOR]

Aquaporin 4 (AQP4) is a primary water channel found on astrocytes in the central nervous system (CNS). Besides its function in water and ion homeostasis, AQP4 has also been documented to be involved in a myriad of acute and chronic cerebral pathologies, including autoimmune neurodegenerative diseases. AQP4 has been postulated to be associated with the incidence of a progressive neurodegenerative disorder known as amyotrophic lateral sclerosis (ALS), a disease that targets the motor neurons, causing muscle weakness and eventually paralysis. Raised AQP4 levels were noted in association with vessels surrounded with swollen astrocytic processes as well as in the brainstem, cortex, and gray matter in patients with terminal ALS. AQP4 depolarization may lead to motor neuron degeneration in ALS via GLT-1. Besides, alterations in AQP4 expression in ALS may result in the loss of blood-brain barrier (BBB) integrity. Changes in AQP4 function may also disrupt K+ homeostasis and cause connexin dysregulation, the latter of which is associated to ALS disease progression. Furthermore, AQP4 suppression augments recovery in motor function in ALS, a phenomenon thought to be associated to NGF. No therapeutic drug targeting AQP4 has been developed to date. Nevertheless, the plethora of suggestive experimental results underscores the significance of further exploration into this area. [ABSTRACT FROM AUTHOR]

Multiple sclerosis (MS) is a chronic, inflammatory, autoimmune disease of the central nervous system, and is an important cause of disability in young adults. In genetically susceptible individuals, several environmental factors may play a partial role in the pathogenesis of MS. Some studies suggests that high-salt diet (>5 g/day) may contribute to the MS and other autoimmune disease development through the induction of pathogenic Th17 cells and pro-inflammatory cytokines in both humans and mice. However, the precise mechanisms of pro-inflammatory effect of sodium chloride intake are not yet explained. The purpose of this review was to discuss the present state of knowledge on the potential role of environmental and dietary factors, particularly sodium chloride on the development and course of MS. [ABSTRACT FROM AUTHOR]

Rheumatological diseases can involve the central and the peripheral nervous system in many ways. Every structure—the brain, meninges, spinal cord, cranial nerves, peripheral nerves—can be affected. Early recognition of neurological abnormality can help achieving diagnosis of the underlying condition and prevent permanent sensorimotor or cognitive function loss. This review focuses on the clinical presentation of the neurological involvement in rheumatological diseases. [ABSTRACT FROM AUTHOR]

Astract. The present essay concisely analyses the contemporary neurobiological debate concerning the hypothesis of the “temporal correlation” advanced to solve the perceptual problem of linking different features in a unitary object or visual scene. Although fascinating and grounded on simulations and brain models, in addition to important electrophysiological findings on the sensory systems, this hypothesis is regarded as not conclusive, and it still excites numerous critical observations from different approaches. Nevertheless, it has contributed to an innovative use of the idea of cortical oscillations, as regards its usual employment in reference to the electrical activity of the brain. It also opens a new perspective in the assumption of the temporal pattern to read the neural code. [ABSTRACT FROM AUTHOR]