The Immunomodulatory Potential of Short-Chain Fatty Acids in Multiple Sclerosis.

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.

Long-Term Disability Outcomes in Relapsing-Remitting Multiple Sclerosis Patients: Impact of Clinical and Demographic Factors on Disease Progression.

Background: Multiple sclerosis (MS) is a prevalent chronic inflammatory and neurodegenerative disease of the central nervous system. The main evolving forms, relapsing-remitting MS (RRMS) and secondary progressive MS (SPMS), lack clear delineation. Methods: We conducted an observational study on 523 Caucasian RRMS patients receiving first-line disease-modifying therapies (DMTs), analyzing demographic, clinical, and geographical data. Results: RRMS patients experienced a statistically significant reduction in relapse rates post-DMT initiation. Significant differences in time to reach an Expanded Disability Status Score (EDSS) of 3.0 and 6.0 were observed based on demographics and onset topography. Kaplan-Meier analysis revealed that the onset with optic or supratentorial symptoms is linked to a longer time until EDSS = 3.0 is reached. Urban origin correlated with a prolonged time until EDSS = 3.0. Gender and environment showed no significant associations with the hazard of reaching an EDSS = 6.0. Cox regression analysis revealed no significant impact of relapses on the time to reach EDSS scores of 3.0 and 6.0 in our study cohort. Conclusions: Multivariate analysis identified several predictive factors for disability progression, including environment, age at onset, and disability level at DMT initiation.

Astrocyte Involvement in Blood-Brain Barrier Function: A Critical Update Highlighting Novel, Complex, Neurovascular Interactions.

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.

The Benefits of Combining Bobath and Vojta Therapies in Infants with Motor Development Impairment-A Pilot Study.

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.

The peripheral profile of the chitinase 3-like-1 in benign multiple sclerosis - a single centre's experience.

BACKGROUND: A limited subgroup of multiple sclerosis (MS) patients present with a long-term disease evolution characterized by a limited disease progression, known as benign MS (BMS). Chitinase 3-like-1 (CHI3L1) levels are sensitive to inflammatory processes and may play a role in the pathogenesis of MS. In this observational, cross-sectional study, we aimed to evaluate the implications of serum CHI3L1 and inflammatory cytokines in BMS patients treated with interferon ß-1b for over a decade. METHODS: We collected serum samples from 17 BMS patients and 17 healthy controls (HC) to measure serum CHI3L1 levels and a Th17 panel of inflammatory cytokines. Serum levels of CHI3L1 were analysed using the sandwich ELISA method and the Th17 panel was assessed using the multiplex XMap technology on a Flexmap 3D Analyzer. RESULTS: Serum CHI3L1 levels did not differ significantly from HC. We identified a positive correlation between CHI3L1 levels and relapses during treatment. CONCLUSIONS: Our findings suggest that there are no differences in serum CHI3L1 levels between BMS patients and HC. However, serum CHI3L1 levels are sensitive to clinical inflammatory activity and may be associated with relapses in BMS patients.

Recent Progress in the Identification of Early Transition Biomarkers from Relapsing-Remitting to Progressive Multiple Sclerosis.

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.

Oxidative Stress in Amyotrophic Lateral Sclerosis: Synergy of Genetic and Environmental Factors.

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.

Autoimmune Encephalitis in COVID-19 Infection: Our Experience and Systematic Review of the Literature.

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.

Neuroprotection in Stroke-Focus on the Renin-Angiotensin System: A Systematic Review.

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.

Treatment With Cladribine Selects IFNγ+IL17+ T Cells in RRMS Patients - An In Vitro Study.

Background: Multiple 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. Methods: An 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. Results: Ex 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. Conclusions: CD3+ 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.

Severe Acute Motor Axonal Neuropathy associated with Influenza-A (H1N1) Infection and Prolonged Respiratory Failure - A Case Report.

Acute Motor Axonal Neuropathy (AMAN) is an immune-mediated disorder of the peripheral nervous system, part of the spectrum of the Guillain-Barre syndrome (GBS). An infectious event most often triggers it reported a few weeks before the onset. The reported case is of a 56 years-old woman who developed acute motor axonal neuropathy three weeks after respiratory infection with influenza A virus subtype H1N1. Despite early treatment with plasmapheresis and intravenous immunoglobulins, the patient remained tetraplegic, mechanically ventilated for five months, with repetitive unsuccessful weaning trails. The probable cause was considered to be phrenic nerve palsy in the context of acute motor axonal neuropathy. This case highlights that acute motor axonal neuropathy is a severe and life-threatening form of Guillain-Barre syndrome associated with significant mortality and morbidity. Neurological and physical recovery strongly depend on the inter-professional effort in an intensive care unit and neurology professionals.

Postpartum Acute Basilar Artery Occlusion Secondary to Vertebral Artery Dissection. Case Report and Literature Review.

Female patients in the peripartum and postpartum periods have an increased risk of stroke than nonpregnant women. Cerebrovascular complications of pregnancy represent a significant cause of maternal mortality and morbidity and are potentially disabling. Acute basilar artery occlusion secondary to spontaneous vertebral artery dissection in the postpartum period is an infrequent entity and a major diagnostic and treatment challenge. In the present case, a 37-year-old female patient, eight weeks after caesarean delivery, presented with a history of sudden cervical pain, followed by headache and dizziness. Some hours later, she was found unconscious by her family and was transferred to the emergency department, where a neurological status assessment suggested vertebrobasilar stroke. The imagistic workup revealed right vertebral artery dissection and basilar artery occlusion without constituted ischemic lesions. The patient underwent endovascular intervention with dilation of the narrowed vertebral artery and stent retriever basilar artery thrombectomy, with a favourable clinical outcome. This report first presents the details of this case and the relevant literature data on postpartum arterial dissections and the subsequent ischemic complications and available treatment options.

Prevalence and Clinical Characteristics of Subclavian Steal Phenomenon/Syndrome in Patients with Acute Ischemic Stroke.

There are no published clinical studies regarding the prevalence of subclavian steal among acute ischemic stroke patients. The aim of this study was to evaluate the prevalence and clinical significance of subclavian steal among a large number of consecutive ischemic stroke patients. MATERIALS AND METHODS: We reviewed the medical records of 2192 consecutive cases of acute ischemic stroke at a tertiary neurology clinic in Targu Mures, Romania, between 2018 and 2020. In total, 47 patients (2.2%) were diagnosed with subclavian steal phenomenon/syndrome. RESULTS: Stroke patients with associated steal phenomenon were significantly younger (64.2 ± 11.1 versus 70.2 ± 12.8, p = 0.005) and predominantly male (68.1%). From among the 47 patients with subclavian steal phenomenon, nine (19.1%) presented stroke symptomatology in the vertebrobasilar territory. Overall, 83.3% of the stroke patients with associated steal phenomenon presented cerebral infarction and 16.7% presented TIA. There was no difference between groups regarding the affected vascular territory (VB versus carotid). Large artery atherosclerosis was more frequent in the stroke group with associated steal phenomenon (81.3% versus 43.5%, p = 0.0033). The NIHSS score at admission was higher in the patient group with associated steal phenomenon, but there was no difference in mRS at discharge. Associated carotid artery occlusion was more frequent in the stroke group with steal phenomenon (p < 0.01). Smoking and peripheral arteriopathy were more frequent in the patient group with associated steal phenomenon. Of the nine symptomatic patients, five underwent revascularization treatment. CONCLUSIONS: The prevalence of subclavian steal phenomenon among acute ischemic stroke patients was not higher than in other cohorts with heterogenous peripheral vascular pathologies. Similar to the general population, in acute ischemic stroke patients, the associated subclavian steal behaved like a benign hemodynamical condition, without severe consequences.

Autonomic and Somatic Nerve Functions in Type 2 Diabetes Mellitus Patients: Electrophysiological Aspects.

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.

Ischemic Stroke in Patients with Cancer: a Retrospective Cross-Sectional Study.

INTRODUCTION: An increasing trend of cancer associated stroke has been noticed in the past decade. OBJECTIVES: To evaluate the risk factors and the incidence of neoplasia in stroke patients. MATERIAL AND METHOD: A retrospective, observational study was undertaken on 249 patients with stroke and active cancer (SAC) and 1563 patients with stroke without cancer (SWC). The general cardiovascular risk factors, the site of cancer, and the general clinical data were registered and evaluated. According to the "Oxfordshire Community Stroke Project" (OCSP) classification, all patients were classified into the clinical subtypes of stroke. The aetiology of stroke was considered as large-artery atherosclerosis, small vessel disease, cardio-embolic, cryptogenic or other determined cause. RESULTS: The severity of neurological deficits at admission were significantly higher in the SAC group (p<0.01). The haemoglobin level was significantly lower, and platelet level and erythrocyte sedimentation rate were significantly higher in the SAC group. Glycaemia, cholesterol and triglycerides levels were significantly higher in the SWC group. The personal history of hypertension was more frequent in the SWC group. In the SAC group, 28.9% had a cryptogenic aetiology, compared to 9.1% in SWC group. Cardio-embolic strokes were more frequent in the SAC group (24%) than the SWC group (19.6%). In the SAC group, 15,6% were diagnosed with cancer during the stroke hospitalization, and 78% of the SAC patients were without metastasis. CONCLUSIONS: The most frequent aetiologies of stroke in cancer patients were cryptogenic stroke, followed by large-artery atherosclerosis. SAC patients had more severe neurological deficits and worse clinical outcomes than SWC patients. Stroke in cancer patients appears to be more frequently cryptogenic, probably due to cancer associated thrombosis. The association between stroke and cancer is important, especially in stroke of cryptogenic mechanism, even in the presence of traditional cardiovascular risk factors.

Contrast Medium-Induced Encephalopathy After Coronary Angiography- Case Report.

INTRODUCTION: Contrast-induced encephalopathy represents a rare, reversible complication that appears after intravenous or intra-arterial exposure to contrast agents. There is no consensus in the literature regarding the mechanism of action. However, the theoretical mechanism is set around the disruption of the blood-brain barrier and the contrast agents' chemical properties. CASE REPORT: The case of a 70-year-old patient, known to have hypertension and type 2 diabetes mellitus is reported. The patient had undergone a diagnostic coronary angiography during which he received 100ml of Ioversol (Optiray 350™). Soon after the procedure, the patient began experiencing a throbbing headache, followed by intense behavioural changes and aggressive tendencies. He was transferred to the Neurology Clinic. The neurological examination was without focal neurological signs; however, the patient was very aggressive and uncooperative. The CT scan revealed a mild hyper-density in the frontal lobes. MRI scan revealed no pathological changes. Conservative treatment with diuretics and hydration was administered, and the patient experienced a complete resolution of symptoms in 72 hours. CONCLUSION: Contrast-induced encephalopathy is a possible secondary complication to contrast agents and a diagnostic challenge, and it should not be overlooked, especially following procedures that use contrast agents.

Reviewing the Significance of Blood-Brain Barrier Disruption in Multiple Sclerosis Pathology and Treatment.

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.

Stroke secondary to giant-cell arteritis: A literature review.

Stroke is a leading cause of death and disability worldwide. In addition to the classical etiologies of stroke as atherosclerosis and cardioembolism there are many unusual, rare causes, which require a high level of clinical suspicion and further investigations for correct and early diagnosis and adequate treatment. Giant-cell arteritis or temporal arteritis, the most frequent vasculitis in the elderly population is one of the uncommon causes of stroke. In the setting of giant-cell arteritis, stroke more likely affects the vertebrobasilar territory and is the main cause of mortality. Duplex ultrasound examination is a routine investigation for stroke patients and may be key to the diagnosis if the classical hypoechoic 'halo sign' is recognized at the level of vertebral arteries. In this situation the ultrasound evaluation of temporal arteries and temporal artery biopsy are mandatory. The Giant-cell arteritis-related stroke is a rare condition; therefore, there are no evidence-based guidelines or standard recommendations for the treatment. In the present review, the main characteristics of giant-cell arteritis-related stroke are discussed.

Postpartum Cerebral Venous Thrombosis-A Single-Center Experience.

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 (<48 h) in 50% of postpartum cases and in 30.4% of the non-postpartum female group. The Rankin score at discharge was significantly lower in the postpartum group (0.22 vs. 0.7, 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.

Gender Differences in Risk Factor Profile and Clinical Characteristics in 89 Consecutive Cases of Cerebral Venous Thrombosis.

Gender has been shown to be an important variable in cerebral venous thrombosis (CVT) risk and significantly influences its clinical manifestations and outcome. The aim of our study was to investigate the gender-specific risk factor profile and clinical picture of this rare cerebrovascular disorder. MATERIALS AND METHODS: We retrospectively reviewed the medical records of 89 consecutive cases of CVT at a tertiary neurology clinic in Târgu Mures, Romania, between June 2009 and January 2021 to analyze the gender-related differences in etiology, clinical presentation, and outcome. RESULTS: Women comprised 62.5% of the cohort. Females were significantly younger than males (37.3 years versus 48.8 years, respectively, p = 0.001), and the main risk factors were hormone related in 37.9% of the cases, followed by primary thrombophilia (34.4%), smoking (25.8%), obesity (17.2%), infections (17.2%), mechanical factors (17.2%), cancer (8.6%), systemic autoimmune disorders (8.6%), and hematological disorders (8.6%). In male patients, the main risk factors were smoking (41.9%), primary thrombophilia (29%), infections (22.6%), heavy alcohol consumption (16.1%), and venous thromboembolism in the medical history (12.9%). Frequency of headache was higher in females than in males (75.9% versus 67.7%), whereas frequency of coma (6.5% in males versus 1.7% in females) and dizziness (19.4% in males versus 10.3% in females) was higher in males. CVT onset was acute in 41.4% of females and 38.7% of males. The Rankin score at discharge was significantly lower in females compared with males (0.6 versus 1.6), reflecting a more favorable short-term outcome. Mortality was 6.4% in males and 1.7% in females. CONCLUSIONS: CVT is a multifactorial disorder that has a broad spectrum of risk factors with important gender-related differences in clinical manifestation and prognosis. Female patients, especially those with hormone-related risk factors, have a more favorable outcome than male patients.