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Multiple sclerosis (MS) is a chronic inflammatory and neurodegenerative central nervous system (CNS) disorder, characterized by focal inflammation, demyelination, irreversible axonal loss and neurodegeneration. The proposed mechanism involves auto-reactive T lymphocytes crossing the blood–brain barrier (BBB), contributing to inflammation and demyelination. Pro-inflammatory Th1 and Th17 lymphocytes are pivotal in MS pathogenesis, highlighting an imbalanced interaction with regulatory T cells. Dysbiosis in the gut microbiota, characterized by microbial imbalance is implicated in systemic inflammation, yet its exact role in MS remains elusive. Short-chain fatty acids (SCFAs), including valerate, butyrate, propionate, and acetate, produced through dietary fiber fermentation by the gut microbiota, modulate inflammation and immune responses. Particularly, butyrate and propionate exhibit pronounced anti-inflammatory effects in both the gut and CNS. These SCFAs influence regulatory T lymphocyte expression and BBB permeability. This review discusses the potential therapeutic implications of SCFA in MS, highlighting their ability to modulate the gut–brain axis and restore immune balance.

Neurological disorders have been linked to a defective blood–brain barrier (BBB), with dysfunctions triggered by stage-specific disease mechanisms, some of these being generated through interactions in the neurovascular unit (NVU). Advanced knowledge of molecular and signaling mechanisms in the NVU and the emergence of improved experimental models allow BBB permeability prediction and the development of new brain-targeted therapies. As NVU constituents, astrocytes are the most numerous glial cells, characterized by a heterogeneity that occurs as a result of developmental and context-based gene expression profiles and the differential expression of non-coding ribonucleic acids (RNAs). Due to their heterogeneity and dynamic responses to different signals, astrocytes may have a beneficial or detrimental role in the BBB’s barrier function, with deep effects on the pathophysiology of (and on the progression of) central nervous system diseases. The implication of astrocytic-derived extracellular vesicles in pathological mechanisms, due to their ability to pass the BBB, must also be considered. The molecular mechanisms of astrocytes’ interaction with endothelial cells at the BBB level are considered promising therapeutic targets in different neurological conditions. Nevertheless, a personalized and well-founded approach must be addressed, due to the temporal and spatial heterogeneity of reactive astrogliosis states during disease.

Dissection of the cervical arteries is the leading cause of stroke in young adults, yet the aetiology and pathogenesis of this event remain unclear. However, a growing number of data in the literature support the potential implications of immunological mechanisms in the pathogenesis. Several large patient groups and multicentre cohorts have reported significant associations with recent infections and elevated inflammatory markers. There are also several case reports and case series suggesting an association with various autoimmune disorders and viral infections. Some case reports have also detailed cervical artery dissections linked to the use of biological therapies for other pathologies. In the present case, a 38-year-old female patient with triple spontaneous cervical artery dissection presented multiple potential trigger factors as recent infection, autoimmune thyroid disease, primary thrombophilia and hyperhomocysteinemia. This report sought first presents this case, and then reviews the existing relevant literature data regarding the potential immunological mechanisms implicated in the pathogenesis of cervical artery dissection.

Background: In infants presenting with motor development impairment, early kinesiotherapeutic interventions aim to normalise the pattern of movements and improve recovery. By applying Bobath and Vojta methods, we aimed to identify a combined approach regarding motor deficit in infants with neurological disabilities. Methods: We designed a prospective interventional study on 108 infants with motor developmental delay and applied Bobath, Vojta, or combined Bobath and Vojta therapy in three equal groups. Results: In the combined Bobath and Vojta group, complete motor recovery was achieved for 50% of the participants, with full recovery after six months, whereas in Bobath- or Vojta-only therapy groups, the total recovery for all participants was achieved at seven months. Regarding infants with muscular hypertonia, Bobath therapy initiation demonstrated complete recovery in 5 months in more than 50% of the cases, while for Vojta this was achieved in only 33.57% of the cases. Conclusions: The comparative evaluation conducted by analysing the data regarding the application of the Bobath and Vojta methods showed that combining these two therapies results in a shorter motor deficit recovery time than if a single therapy is applied. These findings have important implications for the selection of rehabilitation therapies in infants with neurological motor development issues.

Despite extensive research into the pathophysiology of multiple sclerosis (MS) and recent developments in potent disease-modifying therapies (DMTs), two-thirds of relapsing-remitting MS patients transition to progressive MS (PMS). The main pathogenic mechanism in PMS is represented not by inflammation but by neurodegeneration, which leads to irreversible neurological disability. For this reason, this transition represents a critical factor for the long-term prognosis. Currently, the diagnosis of PMS can only be established retrospectively based on the progressive worsening of the disability over a period of at least 6 months. In some cases, the diagnosis of PMS is delayed for up to 3 years. With the approval of highly effective DMTs, some with proven effects on neurodegeneration, there is an urgent need for reliable biomarkers to identify this transition phase early and to select patients at a high risk of conversion to PMS. The purpose of this review is to discuss the progress made in the last decade in an attempt to find such a biomarker in the molecular field (serum and cerebrospinal fluid) between the magnetic resonance imaging parameters and optical coherence tomography measures.

Vertebrobasilar dolichoectasia (VBD) is a rare condition characterized by a significant dilation, elongation and tortuosity of the arteries emerging from the vertebrobasilar system. In this study, we report a 57-year-old male, with medical history of recurrent migraines and right peroneal nerve palsy, which presents the sudden onset of clinical signs of brainstem and cerebellar stroke. The brain CT scan revealed an inhomogeneous, hyperdense prepontine lesion, situated in the area of basilar artery (BA) projection. The cerebral angiography showed in the V4 segment of the left vertebral artery (VA) a focal, concentric stenosis of 70%, followed by a fusiform dilation extended to the BA bifurcation, a saccular aneurysmal dilation in the communicant segment of the internal carotid artery and tortuous trajectory of the abdominal and thoracic aorta, including the supra-aortic vessels. The brain MRI revealed a bulbopontin and left cerebellum infarction. Patient developed at 48 hours after hospitalization livedo reticularis at the level of the right thoracic wall and thighs. The nerve conduction studies revealed mononeuritis multiplex. The vascular anomaly that was identified in the presented case respects the criteria for a VBD, however the involvement of the aorta with the presence of tortuosities, the simultaneous presence of the internal carotid artery aneurysm, together with the presence of the mononeuritis multiplex and the skin condition (livedo reticularis) suggest the possibility of coexistence of a systemic vasculitis, possible polyarteritis nodosa.

Amyotrophic lateral sclerosis (ALS) is a grievous neurodegenerative disease whose survival is limited to only a few years. In spite of intensive research to discover the underlying mechanisms, the results are fairly inconclusive. Multiple hypotheses have been regarded, including genetic, molecular, and cellular processes. Notably, oxidative stress has been demonstrated to play a crucial role in ALS pathogenesis. In addition to already recognized and exhaustively studied genetic mutations involved in oxidative stress production, exposure to various environmental factors (e.g., electromagnetic fields, solvents, pesticides, heavy metals) has been suggested to enhance oxidative damage. This review aims to describe the main processes influenced by the most frequent genetic mutations and environmental factors concurring in oxidative stress occurrence in ALS and the potential therapeutic molecules capable of diminishing the ALS related pro-oxidative status.

The neurologic complications of COVID-19 infection are frequent in hospitalized patients; a high percentage of them present neurologic manifestations at some point during the course of their disease. Headache, muscle pain, encephalopathy and dizziness are among the most common complications. Encephalitis is an inflammatory condition with many etiologies. There are several forms of encephalitis associated with antibodies against intracellular neuronal proteins, cell surfaces or synaptic proteins, referred to as autoimmune encephalitis. Several case reports published in the literature document autoimmune encephalitis cases triggered by COVID-19 infection. Our paper first presents our experience in this issue and then systematically reviews the literature on autoimmune encephalitis that developed in the background of SARS-CoV-2 infections and also discusses the possible pathophysiological mechanisms of auto-immune-mediated damage to the nervous system. This review contributes to improve the management and prognosis of COVID-19-related autoimmune encephalitis.

Stroke is the primary cause of disability in the adult population. Hypertension represents the leading risk factor being present in almost half the patients. The renin-angiotensin system is involved in the physiopathology of stroke and has an essential impact on hypertension as a risk factor. This article targeted the role of the renin-angiotensin system in stroke neuroprotection by reviewing the current literature available. The mechanism of action of the renin-angiotensin system was observed through the effects on AT1, AT2, and Mas receptors. The neuroprotective properties ascertained by angiotensin in stroke seem to be independent of the blood pressure reduction mechanism, and include neuroregeneration, angiogenesis, and increased neuronal resistance to hypoxia. The future relationship of stroke and the renin-angiotensin system is full of possibilities, as new agonist molecules emerge as potential candidates to restrict the impairment caused by stroke.

Isolated cerebral infarction in a small vascular territory such as the posterior limb of the internal capsule rarely represents the first clinical manifestation of systemic lupus erythematosus, and represents a diagnostic challenge, especially if other organ systems are not affected. We report the case of a 28-year-old woman who was admitted to the emergency room with acute onset left-sided hemiparesis. She was diagnosed with acute ischaemic stroke and treated with intravenous thrombolysis, without improvement. The localisation of the lesion in the posterior limb of the internal capsule was based on MRI with DWI sequences, performed after thrombolysis. After extensive workup, a diagnosis of lupus was established. The functional outcome was unfavourable. AChA territory infarction is a special entity, which is increasingly recognised owing to extensive use of MRI in stroke care, with particular clinical characteristics. Cerebrovascular events can be the first clinical manifestation of lupus and contribute to premature morbidity and disability.

Objectives: To investigate the relationship between neurophysiological sensory and motor nerve function parameters, assessed by nerve conduction studies (NCS) with parasympathetic autonomic function and by heart rate variability (HRV) tests in patients with type 2 diabetes mellitus (T2DM). Material and Methods: A total of 161 T2DM patients underwent NCS. Cardiac autonomic response was assessed by HRV tests to deep breathing (HRV DB), to Valsalva manoeuvre, and during postural change from lying to standing. Results: The amplitude of motor response in the median nerve, tibial nerve, and peroneal nerve was associated with reduced HRV DB (p = 0.0001). The amplitude of motor response in the median nerve, tibial nerve, and peroneal nerve was associated with reduced HRV Valsalva (p = 0.0001). The correlation between the amplitude of response in all sensory nerves (sural, median, and ulnar) and HRV DB was statistically significant (p = 0.0001). Conclusion: The results indicate that there is a correlation in T2DM patients between the damage of small myelinated and unmyelinated nerve fibres from cardiac autonomic nerves, assessed by HRV tests and damage of large motor and sensory fibres, assessed by NCS. Based on the above results, a combination of NCS and HRV tests should be considered in the neurophysiological approach to diabetic neuropathy.

The disruption of blood–brain barrier (BBB) for multiple sclerosis (MS) pathogenesis has a double effect: early on during the onset of the immune attack and later for the CNS self-sustained ‘inside-out’ demyelination and neurodegeneration processes. This review presents the characteristics of BBB malfunction in MS but mostly highlights current developments regarding the impairment of the neurovascular unit (NVU) and the metabolic and mitochondrial dysfunctions of the BBB’s endothelial cells. The hypoxic hypothesis is largely studied and agreed upon recently in the pathologic processes in MS. Hypoxia in MS might be produced per se by the NVU malfunction or secondary to mitochondria dysfunction. We present three different but related terms that denominate the ongoing neurodegenerative process in progressive forms of MS that are indirectly related to BBB disruption: progression independent of relapses, no evidence of disease activity and smoldering demyelination or silent progression. Dimethyl fumarate (DMF), modulators of S1P receptor, cladribine and laquinimode are DMTs that are able to cross the BBB and exhibit beneficial direct effects in the CNS with very different mechanisms of action, providing hope that a combined therapy might be effective in treating MS. Detailed mechanisms of action of these DMTs are described and also illustrated in dedicated images. With increasing knowledge about the involvement of BBB in MS pathology, BBB might become a therapeutic target in MS not only to make it impenetrable against activated immune cells but also to allow molecules that have a neuroprotective effect in reaching the cell target inside the CNS.

Background: Cerebral venous thrombosis (CVT) is a rare variant of stroke in the general population, but an important subtype among pregnancy- and puerperium-related cases. Studies describing its risk factors and clinical characteristics are limited. The aim of our study is to disclose these aspects and compare with cases unrelated to pregnancy and puerperium. Materials and Methods: We performed a retrospective analysis including 88 consecutive cases from a tertiary neurology clinic with a diagnosis of CVT. Ten of the 88 cases (11.3%) appeared during the postpartum period. Results: The mean age of the puerperal CVT cases was 26.5 years. The main pregnancy-related risk factors besides puerperium were cesarean delivery (5/10), preeclampsia (2/10), and stillbirth (1/10). General risk factors for thrombosis, i.e., infection, smoking, and primary hypercoagulability, were identified in 50% of cases. Onset was in the first 3 weeks after delivery, with a mean value of 9.6 ± 5.6 days. Headache was present in 90% of postpartum CVT cases and in 76.1% of non-postpartum female cases. Seizures were more frequent in the postpartum group (60% vs. 34.8%). Onset was acute (p = 0.02), suggesting a more favorable short-term outcome. Conclusions: The early postpartum period represents an important risk for the development of CVT. Cesarean delivery and preeclampsia, besides general risk factors such as infection, smoking, and primary thrombophilia, contribute to enhanced risk. Puerperium-related CVT presents a more favorable outcome compared with CVT with other etiologies.

Introduction. Cardiovascular Autonomic Neuropathy (CAN), also known as the “silent killer”, represents a serious complication of diabetes mellitus and is most of the times ignored. This is a highly topical issue, given the increased number of patients diagnosed with type 2 diabetes mellitus (T2DM). The purpose of this study was to determine the association between the severity of CAN and the severity of other microvascular complications, such as diabetic sensory-motor polyneuropathy (DSMP), diabetic retinopathy (DR) and macrovascular complications (carotid and peripheral vascular atherosclerosis) in patients with T2DM. Methods. A total of 149 patients with T2DM were assessed for CAN using the Ewing’s battery of cardiovascular autonomic function tests. The patients were evaluated for diabetic microvascular complications (DSMP, RD), respectively macrovascular complications (carotid atherosclerosis by intima media thickness and peripheral vascular atherosclerosis by ankle-brachial index). Results. Of the 45 patients with intermediate CAN, 35.55% were without DR, 51.11% had non-proliferative DR and 13.33% had proliferative DR. From the 13 patients with severe CAN, 76.92% had non-proliferative DR and 23.07% had proliferative DR. From the 56 patients with subclinical CAN, 26.7% had no DSMP, 48.2% had subclinical DSMP and 25% had clinical DSMP. Of the 45 patients with intermediate CAN, 11.2% had subclinical DSMP and 80% had clinical DSMP. Conclusion. In T2DM we demonstrated that an increase in the severity of cardiovascular autonomic injury is associated with an increase in the prevalence and severity of DSMP and DR, respectively carotid and peripheral atherosclerosis.

Natalizumab (NAT) was the first disease modifying therapy used for the treatment of relapsing-remitting multiple sclerosis (MS) that was designed with a specific mechanism of action that targets an important step of the MS immunopathology, directly blocking the T lymphocyte intrusion in the central nervous system. Initially, it was considered that NAT carried no biological effects on the peripheral immune response. The purpose of our study was to assess the effects of NAT on the peripheral pro and anti-inflammatory cytokines and to reveal possible correlations between them and the clinical activity of the disease. We noticed a significant decrease in interleukin (IL)-17, tumor necrosis factor-alpha (TNF-α) and IL-31 serum levels in treated patients. The lack of relapses during the study was associated with low baseline IL-17 level. The patients that had an increase in the disability score during the study had significantly lower IL-17 and higher IL-1β baseline levels. IL-17 can be used as a biomarker for disease activity but also for progression assessment in NAT treated patients. NAT has a far more complex mechanism compared to what was initially believed, besides modulating lymphocyte trafficking through the blood–brain barrier, it also changes the peripheral levels of pro and anti-inflammatory cytokines in MS patients.

Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disease characterized by progressive loss of motor neurons. Emerging evidence suggests a potential link between metabolic dysregulation and ALS pathogenesis. This study aimed to investigate the relationship between metabolic hormones and disease progression in ALS patients. A cross-sectional study was conducted involving 44 ALS patients recruited from a tertiary care center. Serum levels of insulin, total amylin, C-peptide, active ghrelin, GIP (gastric inhibitory peptide), GLP-1 active (glucagon-like peptide-1), glucagon, PYY (peptide YY), PP (pancreatic polypeptide), leptin, interleukin-6, MCP-1 (monocyte chemoattractant protein-1), and TNFα (tumor necrosis factor alpha) were measured, and correlations with ALSFRS-R, evolution scores, and biomarkers were analyzed using Spearman correlation coefficients. Subgroup analyses based on ALS subtypes, progression pattern of disease, and disease progression rate patterns were performed. Significant correlations were observed between metabolic hormones and ALS evolution scores. Insulin and amylin exhibited strong correlations with disease progression and clinical functional outcomes, with insulin showing particularly robust associations. Other hormones such as C-peptide, leptin, and GLP-1 also showed correlations with ALS progression and functional status. Subgroup analyses revealed differences in hormone levels based on sex and disease evolution patterns, with male patients showing higher amylin and glucagon levels. ALS patients with slower disease progression exhibited elevated levels of amylin and insulin. Our findings suggest a potential role for metabolic hormones in modulating ALS progression and functional outcomes. Further research is needed to elucidate the underlying mechanisms and explore the therapeutic implications of targeting metabolic pathways in ALS management.

Fatigue is the most common and disabling symptom in patients with multiple sclerosis (PwMS), representing one of the main determinants of reduced quality of life among PwMS due to its interference with social activities and work capacity. This study aimed to identify the sociodemographic determinants of fatigue in a cohort of 150 PwMS and 100 healthy controls (HCs). Fatigue was assessed using one of the most suitable and appropriate tools for measuring the degree of fatigue: the Modified Fatigue Impact Scale (MFIS). By comparing the median scores for the MFIS, we observed that the PwMS group had significantly higher MFIS scores than the HCs (p = 0.0001). In PwMS, MFIS scores correlated positively with age, total number of relapses, total disease duration, disability status, and Beck Depression Inventory-II score and negatively with cognitive performance. Patients with relapsing-remitting MS had significantly lower fatigue levels than those with secondary progressive MS (p = 0.0010). Fatigue levels were significantly lower among male than female PwMS (p = 0.0120). Other determinant factors of fatigue in our study proved to be the marital and occupational status, as well as the presence of children, but in a linear multivariate regressions analysis with MFIS score as the dependent variable, the fatigue levels were influenced only by sex, occupational status, marital status, children status, and BDI-II test results. Considering the significant impact of fatigue on the quality of life of PwMS, clinicians must diagnose fatigue as early as possible, identify its modifiable determinants, and manage it effectively to increase their quality of life.

Stroke prevention, a significant public-health concern, begins with recognizing and addressing risk factors. Interventions targeted at modifiable risk factors can effectively prevent ischemic stroke, while Omega-3 fatty acids have been shown to improve stroke outcomes. Our study aimed to investigate the relationship between ischemic-stroke risk factors and fatty acids using a prospective observational study with 274 patients. We collected clinical data on risk factors and measured fatty-acid levels using high-performance liquid chromatography coupled with mass spectrometry. We found that several risk factors, including age, sex, smoking, atrial fibrillation, dyslipidemia, and previous stroke history, had a direct relationship with fatty acids. Of these, smoking had the most significant impact, negatively impacting levels of docosahexaenoic and eicosapentaenoic acid. Conversely, dyslipidemia and atrial fibrillation positively correlated with fatty acids, particularly in female patients and those with recurrent strokes. Age was found to directly correlate with other risk factors and variations in fatty-acid ratios. The stroke rate was higher in males than females before the age of 70, but this trend reversed. Our findings suggest that better management of risk factors, particularly modifiable lifestyle factors, could improve fatty-acid profiles and the balance of Omega-3 and Omega-6 in patients with ischemic stroke.

BackgroundMultiple sclerosis (MS) is an incurable autoimmune disease mediated by a heterogeneous T cell population (CD3+CD161+CXCR3−CCR6+IFNγ−IL17+, CD3+CXCR3+CCR6+IFNγ+IL17+, and CD3+CXCR3+IFNγ+IL17− phenotypes) that infiltrates the central nervous system, eliciting local inflammation, demyelination and neurodegeneration. Cladribine is a lymphocyte-depleting deoxyadenosine analogue recently introduced for MS therapy as a Disease Modifying Drug (DMD). Our aim was to establish a method for the early identification and prediction of cladribine responsiveness among MS patients.MethodsAn experimental model was designed to study the cytotoxic and immunomodulatory effect of cladribine. T cell subsets of naïve relapsing-remitting MS (RRMS) patients were analyzed ex vivo and in vitro comparatively to healthy controls (HC). Surviving cells were stimulated with rh-interleukin-2 for up to 14days. Cell proliferation and immunophenotype changes were analyzed after maximal (phorbol myristate acetate/ionomycin/monensin) and physiological T-cell receptor (CD3/CD28) activation, using multiparametric flow cytometry and xMAP technology.ResultsEx vivo CD161+Th17 cells were increased in RRMS patients. Ex vivo to in vitro phenotype shifts included: decreased CD3+CCR6+ and CD3+CD161+ in all subjects and increased CD3+CXCR3+ in RRMS patients only; Th17.1 showed increased proliferation vs Th17 in all subjects; CD3+IL17+ and CD3+IFNγ+IL17+ continued to proliferate till day 14, CD3+IFNγ+ only till day 7. Regarding cladribine exposure: RRMS CD3+ cells were more resistant compared to HC; treated CD3+ cells proliferated continuously for up to 14 days, while untreated cells only up to 7 days; both HC/RRMS CD3+CXCR3+ populations increased from baseline till day 14; in RRMS patients vs HC, IL17 secretion from cladribine-treated cells increased significantly, in line with the observed proliferation of CD3+IL17+ and CD3+IFNγ+IL17+ cells; in both HC/RRMS, cladribine led to a significant increase in CD3+IFNγ+ cells at day 7 only, having no further effect at day14. IFNγ and IL17 secreted in culture media decreased significantly from ex vivo to in vitro.ConclusionsCD3+ subtypes showed different responsiveness due to selectivity of cladribine action, in most patients leading to in vitro survival/proliferation of lymphocyte subsets known as pathogenic in MS. This in vitro experimental model is a promising tool for the prediction of individual responsiveness of MS patients to cladribine and other DMDs.

Objective. To determine the prevalence of suicidal concerns (SC) in a large multiple sclerosis (MS) patient group and to assess the major determinants that are implicated in their occurrence. Methods. A total of 349 patients were included in the study. They completed a survey about their demographic characteristics, psycho-socio-economic data, and disease-related information. Their disability level was assessed using the Expanded Disability Status Scale (EDSS) based on the neurological examination performed by the same doctor for every patient and the SC were documented with the Beck Depression Inventory-II questionnaire. Results. The study included 112 men and 237 women, with a mean age around 42 years old. Suicidal thoughts were more frequent in men, while suicidal intentions in women. Positive correlations were found between SC and depression, EDSS, total number of relapses, disease duration, and level of education. From the EDSS functional scores, only the pyramidal score and the cerebellar score presented a significant correlation with SC. None of the patients with clinically isolated syndrome had SC. The type of disease-modifying therapy, marital and occupational status, and the presence of children did not influence the presence of SC. Conclusions. The prevalence of SC is higher in patients with MS compared to the general population. Their occurrence is mostly influenced by the disease itself (duration, relapses, acquired disability) and also by depression and lack of education.

Background: Multiple sclerosis (MS), chronic, demyelinating disease of the central nervous system, is caused by an abnormal immune response in genetically susceptible individuals secondary to various environmental, infectious and genetic factors. The first immunomodulatory agent used for the treatment of MS was interferon beta-1b (IFN⊠-1b). Material and methods: In this study we included 67 patients treated continuously with IFN⊠-1b for more than 10 years. The patients were assessed based on their demographic data, clinical features: relapse rates, disability progression assessed by the expanded disability status scale (EDSS) and neuropsychiatric features: depression scores evaluated by the Hamilton scale, cognitive tests evaluated using SDMT test. A pro and anti inflammatory cytokine panel (IL-4, IL-19, IL-17A, Il17F etc) is being collected in our selected group of patients. We defined two groups: patients with an EDSS score < 4.0 in 2016 and patients with an EDSS score ≥ 4.0 in 2016. Results: The average age at the beginning of the treatment was 30.69 years. The mean duration of the disease was 12.34 years. By comparing the annual relapse rates before and after the treatment was initiated, in the first group we notice a statistical significant reduction in recurrences. An increase in the disability score positively correlated with a decrease in the intelectual performance. Conclusions: Long term treatment with disease modifying therapies such as IFN⊠-1b proved to have a favorable effect on patients with a recurrentremitting form of MS. [ABSTRACT FROM AUTHOR]

Background: Depression is the most common psychiatric disease seen in multiple sclerosis (MS) patients. It represents one of the most important determinants of the quality of life of MS patients having a significant negative impact on cognitive functions, vocational status, social and family relationships, adherence to treatment, and it also represents a risk factor for suicide. Material and methods: The study included a total of 351 patients with clinically isolated syndrome, relapsing-remitting and secondary progressive MS being in evidence in the Regional MS Center Targu Mures in the period September 2014-February 2015. Depression level was assessed by using the Beck Depression Inventory-Version II (BDI-II). All patients completed a questionnaire with data regarding the level of education, occupational status, marital status, presence or absence of children, demographic and medical informations. Neurological examination was performed in all patients and the level of disabilty was expressed by EDSS score. Results: In our group of patients, 191 had BDI-II scores within the normal range, 65 had mild mood disorders, 36 borderline depression, 35 moderate depression, and 24 severe and extreme depression. Age at disease onset, the actual age of the patient, disease duration, number of recurrences and the degree of disability were positively correlated with the severity of depression. Patients with low education levels, pensioners, patients with children had the highest values of the BDI-II scores. With regard to marital status, the highest levels of depression were retrieved in divorced and widowed patients, followed by married patients. Conclusions: The prevalence of depression in our group of patients was 27.05%. Determinant factors of depression in this group of patients were age, duration of illness, occupational and marital status, education level and degree of disability. Acknowledgments: This study was supported by the internal research Grant of The University of Medicine and Pharmacy Targu Mures, Grant Number 18/2015. [ABSTRACT FROM AUTHOR]

Background: Multiple sclerosis (MS) is a chronic autoimmune disease of the central nervous system, with only partially known immunopathogenesis. Interleukin 17 (IL-17) plays a major role in the immunopathogenesis of MS. Heterogeneity of MS determines the special attention to early determination of biomarkers of multiple pathological processes in MS. Material and methods: The study included 32 relapsing remitting MS patients and 32 healthy subjects (HS).10 patients were naive to IFN-beta1a, 10 were early treated and 12 late treated. Physical disability was evaluated by calculating the EDSS score. The serum levels of IL-17 were determined by ELISA at the beginning of the study, at 6 and 12 months respectively. All patients underwent a brain MRI examination at study onset and visit 12 months. Treatment response was evaluated by Rio score. Results: MS patients had higher IL-17 compared to HS. The lowest values ☒ of IL17 were found in the group of early treated patients. In naive group of patients, after one year of treatment, there was a significant reduction of IL-17 level. Baseline IL-17 serum levels were correlated significantly with the number of relapses during the study and with MRI disease activity and were negatively correlated with the total duration of the disease. 28.12% of patients in the study were nonresponders and 71.88% responders to IFN-beta1a treatment. Initially increased titers of IL-17 were significantly correlated with a Rio score of 3 (nonresponder). Conclusions: Early treatment with IFN-beta1a decreases the secretion of IL-17 at a level close to HS. IL-17 can be used as a predictive biomarker of MS evolution under treatment with IFN-beta1a. Acknowledgments: This study was supported by the internal research Grant of The University of Medicine and Pharmacy Targu Mures, Grant Number 18/2015 [ABSTRACT FROM AUTHOR]