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BackgroundKearns-Sayre syndrome (KSS) is classified as one of the mitochondrial DNA (mtDNA) deletion syndromes with multisystemic involvement. Additionally, the negative prognosis is associated with inherited thrombophilia, which includes the presence of homozygous Factor V G1691A Leiden mutation, MTHFR gene polymorphisms C677T and A1298C, and PAI-1 675 homozygous genotype 5G/5G.Case presentationThis case report presents a 48-year-old man with chronic progressive external ophthalmoplegia, bilateral ptosis, cerebellar ataxia, cardiovascular signs (syncope, dilated cardiomyopathy, and cardiac arrest) with electrocardiographic abnormalities (first-degree atrioventricular block and major right bundle branch block), endocrine dysfunction (short stature, growth hormone insufficiency, primary gonadal insufficiency, hypothyroidism, and secondary hyperparathyroidism), molecular genetic tests (MT-TL2 gene), and abnormal MRI brain images, thus leading to the diagnosis of KSS. The patient came back 4 weeks after the diagnosis to the emergency department with massive bilateral pulmonary embolism with syncope at onset, acute cardiorespiratory failure, deep left femoral-popliteal vein thrombophlebitis, and altered neurological status. In the intensive care unit, he received mechanical ventilation through intubation. Significant improvement was seen after 2 weeks. The patient tested positive for inherited thrombophilia and was discharged in stable conditions on a new treatment with Rivaroxaban 20 mg/day. At 6 months of follow-up, ECG-Holter monitoring and MRI brain images remained unchanged. However, after 3 months, the patient died suddenly while sleeping at home.ConclusionThe genetic tests performed on KSS patients should also include those for inherited thrombophilia. By detecting these mutations, we can prevent major complications such as cerebral venous sinus thrombosis, coronary accidents, or sudden death.

Cerebrovascular disease accounts for major neurologic disabilities in patients with type 2 diabetes mellitus (DM). A potential association of mitochondrial DNA (mtDNA) and inflammation with cerebral vessel remodeling in patients with type 2 DM was evaluated. A cohort of 150 patients and 30 healthy controls were assessed concerning urinary albumin/creatinine ratio (UACR), synaptopodin, podocalyxin, kidney injury molecule-1 (KIM-1), N-acetyl-β-(D)-glucosaminidase (NAG), interleukins IL-17A, IL-18, IL-10, tumor necrosis factor-alpha (TNFα), intercellular adhesion molecule-1 (ICAM-1). MtDNA-CN and nuclear DNA (nDNA) were quantified in peripheral blood and urine by qRT-PCR. Cytochrome b (CYTB) gene, subunit 2 of NADH dehydrogenase (ND2), and beta 2 microglobulin nuclear gene (B2M) were assessed by TaqMan assays. mtDNA-CN was defined as the ratio of the number of mtDNA/nDNA copies, through analysis of the CYTB/B2M and ND2/B2M ratio; cerebral Doppler ultrasound: intima-media thickness (IMT)—the common carotid arteries (CCAs), the pulsatility index (PI) and resistivity index (RI)- the internal carotid arteries (ICAs) and middle cerebral arteries (MCAs), the breath-holding index (BHI). The results showed direct correlations of CCAs-IMT, PI-ICAs, PI-MCAs, RI-ICAs, RI-MCAs with urinary mtDNA, IL-17A, IL-18, TNFα, ICAM-1, UACR, synaptopodin, podocalyxin, KIM-1, NAG, and indirect correlations with serum mtDNA, IL-10. BHI correlated directly with serum IL-10, and serum mtDNA, and negatively with serum IL-17A, serum ICAM-1, and NAG. In neurologically asymptomatic patients with type 2 DM cerebrovascular remodeling and impaired cerebrovascular reactivity may be associated with mtDNA variations and inflammation from the early stages of diabetic kidney disease.

Fatigue is a common non-motor symptom in Parkinson’s disease (PD), but even so, it may still be underdiagnosed or misdiagnosed in current practice due to its non-specific manifestations. The aims of this study were to investigate the prevalence of fatigue in PD patients compared to healthy controls and to identify the main characteristics and associations of fatigue with other non-motor symptoms and the impact of fatigue on sleep disturbances in Parkinson’s disease. Materials and methods: case–control study in which 131 PD patients and 131 age- and sex-matched controls were enrolled. Main characteristics of fatigue, sleep, and other non-motor symptoms were assessed using specific validated questionnaires. Results: According to the Chalder fatigue scale, fatigue is more prevalent in PD patients (38.16%) compared to healthy controls (26.71%). Fatigue was identified in 46.54% of the PD patients using the Parkinson’s Fatigue Scale (PFS-16). PD patients with fatigue presented a worse motor status, more sleep disturbances (insomnia, daytime sleepiness), a broader spectrum of non-motor symptoms (pain, anxiety, urinary disturbances), worse cognitive performances, a lower level of happiness, and worse quality of life compared to PD patients without fatigue. Conclusion: Fatigue is a common symptom of PD and needs to be assessed, considering its consequences on quality of life. Sleep disturbances have a great influence over fatigue in PD patients.

Diabetic kidney disease (DKD) is one of the most debilitating complications of type 2 diabetes mellitus (T2DM), as it progresses silently to end-stage renal disease (ESRD). The discovery of novel biomarkers of early DKD becomes acute, as its incidence is reaching catastrophic proportions. Our study aimed to quantify previously identified metabolites from serum and urine through untargeted ultra-high-performance liquid chromatography coupled with electrospray ionization-quadrupole-time of flight-mass spectrometry (UHPLC-QTOF-ESI+-MS) techniques, such as the following: arginine, dimethylarginine, hippuric acid, indoxyl sulfate, p-cresyl sulfate, L-acetylcarnitine, butenoylcarnitine and sorbitol. The study concept was based on the targeted analysis of selected metabolites, using the serum and urine of 20 healthy subjects and 90 T2DM patients with DKD in different stages (normoalbuminuria—uACR < 30 mg/g; microalbuminuria—uACR 30–300 mg/g; macroalbuminuria—uACR > 300 mg/g). The quantitative evaluation of metabolites was performed with pure standards, followed by the validation methods such as the limit of detection (LOD) and the limit of quantification (LOQ). The following metabolites from this study resulted as possible biomarkers of early DKD: in serum—arginine, dimethylarginine, hippuric acid, indoxyl sulfate, butenoylcarnitine and sorbitol and in urine—p-cresyl sulfate.

Complications due to type 2 diabetes mellitus (T2DM) such as diabetic kidney disease (DKD) and cerebral small vessel disease (CSVD) have a powerful impact on mortality and morbidity. Our current diagnostic markers have become outdated as T2DM-related complications continue to develop. The aim of the investigation was to point out the relationship between previously selected metabolites which are potentially derived from gut microbiota and indicators of endothelial, proximal tubule (PT), and podocyte dysfunction, and neurosonological indices. The study participants were 20 healthy controls and 90 T2DM patients divided into three stages: normoalbuminuria, microalbuminuria, and macroalbuminuria. Serum and urine metabolites were determined by untargeted and targeted metabolomic techniques. The markers of endothelial, PT and podocyte dysfunction were assessed by ELISA technique, and the neurosonological indices were provided by an ultrasound device with high resolution (MYLAB 8-ESAOTE Italy). The descriptive statistical analysis was followed by univariable and multivariable linear regression analyses. In conclusion, in serum, arginine (sArg), butenoylcarnitine (sBCA), and indoxyl sulfate (sIS) expressed a biomarker potential in terms of renal endothelial dysfunction and carotid atherosclerosis, whereas sorbitol (sSorb) may be a potential biomarker of blood–brain barrier (BBB) dysfunction. In urine, BCA and IS were associated with markers of podocyte damage, whereas PCS correlated with markers of PT dysfunction.

Diabetic kidney disease (DKD) is the leading cause of end-stage renal disease; however, few biomarkers of its early identification are available. The aim of the study was to assess new biomarkers in the early stages of DKD in type 2 diabetes mellitus (DM) patients. This cross-sectional pilot study performed an integrated metabolomic profiling of blood and urine in 90 patients with type 2 DM, classified into three subgroups according to albuminuria stage from P1 to P3 (30 normo-, 30 micro-, and 30 macroalbuminuric) and 20 healthy controls using high-performance liquid chromatography and mass spectrometry (UPLC-QTOF-ESI* MS). From a large cohort of separated and identified molecules, 33 and 39 amino acids and derivatives from serum and urine, respectively, were selected for statistical analysis using Metaboanalyst 5.0. online software. The multivariate and univariate algorithms confirmed the relevance of some amino acids and derivatives as biomarkers that are responsible for the discrimination between healthy controls and DKD patients. Serum molecules such as tiglylglycine, methoxytryptophan, serotonin sulfate, 5-hydroxy lysine, taurine, kynurenic acid, and tyrosine were found to be more significant in the discrimination between group C and subgroups P1–P2–P3. In urine, o-phosphothreonine, aspartic acid, 5-hydroxy lysine, uric acid, methoxytryptophan, were among the most relevant metabolites in the discrimination between group C and DKD group, as well between subgroups P1–P2–P3. The identification of these potential biomarkers may indicate their involvement in the early DKD and 2DM progression, reflecting kidney injury at specific sites along the nephron, even in the early stages of DKD.

(1) Background: Cerebral venous and dural sinus thrombosis (CVT) rarely appears in the adult population. It is difficult to diagnosis because of its variable clinical presentation and the overlapping signal intensities of thrombosis and venous flow on conventional MR images and MR venograms. (2) Case presentation: A 41-year-old male patient presented with an acute isolated intracranial hypertension syndrome. The diagnosis of acute thrombosis of the left lateral sinus (both transverse and sigmoid portions), the torcular Herophili, and the bulb of the left internal jugular vein was established by neuroimaging data from head-computed tomography, magnetic resonance imaging (including Contrast-enhanced 3D T1-MPRAGE sequence), and magnetic resonance venography (2D-TOF MR venography). We detected different risk factors (polycythemia vera-PV with JAK2 V617F mutation and inherited low-risk thrombophilia). He was successfully treated with low-molecular-weight heparin, followed by oral anticoagulation. (3) Conclusions: In the case of our patient, polycythemia vera represented a predisposing risk factor for CVT, and the identification of JAK2 V617F mutation was mandatory for the etiology of the disease. Contrast-enhanced 3D T1-MPRAGE sequence proved superior to 2D-TOF MR venography and to conventional SE MR imaging in the diagnosis of acute intracranial dural sinus thrombosis.

Chronic kidney disease (CKD) has emerged as one of the most progressive diseases with increased mortality and morbidity. Metabolomics offers new insights into CKD pathogenesis and the discovery of new biomarkers for the early diagnosis of CKD. The aim of this cross-sectional study was to assess metabolomic profiling of serum and urine samples obtained from CKD patients. Untargeted metabolomics followed by multivariate and univariate analysis of blood and urine samples from 88 patients with CKD, staged by estimated glomerular filtration rate (eGFR), and 20 healthy control subjects was performed using ultra-high-performance liquid chromatography coupled with electrospray ionization-quadrupole-time of flight-mass spectrometry. Serum levels of Oleoyl glycine, alpha-lipoic acid, Propylthiouracil, and L-cysteine correlated directly with eGFR. Negative correlations were observed between serum 5-Hydroxyindoleacetic acid, Phenylalanine, Pyridoxamine, Cysteinyl glycine, Propenoylcarnitine, Uridine, and All-trans retinoic acid levels and eGFR. In urine samples, the majority of molecules were increased in patients with advanced CKD as compared with early CKD patients and controls. Amino acids, antioxidants, uremic toxins, acylcarnitines, and tryptophane metabolites were found in all CKD stages. Their dual variations in serum and urine may explain their impact on both glomerular and tubular structures, even in the early stages of CKD. Patients with CKD display a specific metabolomic profile. Since this paper represents a pilot study, future research is needed to confirm our findings that metabolites can serve as indicators of early CKD.

Vascular cognitive impairment (VCI) is a heterogeneous group of cognitive disorders that share a presumed vascular cause, and it is the second most common cause of cognitive impairment in the elderly after Alzheimer’s disease. Its prevalence is estimated to double over the next 30 years. Vascular cognitive impairment encompasses cases related to multiple cortico-subcortical infarcts, silent infarcts, strategic infarcts, small vessel disease, as well as mixed pathology. It is important to emphasize that some of the risk factors for vascular dementia are the same as for stroke, including high blood pressure, diabetes, heart disease and cigarette smoking. Compared with Alzheimer’s disease, vascular dementia has a higher rate of mortality and a slower rate of cognitive decline. The aim of the treatment in vascular cognitive impairment is mainly to identify and reduce the effect of the vascular risk factors. This article aims to resume the most important data regarding VCI.

It has been almost a decade since the multinodular and vacuolating neuronal tumor (MVNT) was first described. In 2021, WHO classified it as a defined entity, and it is considered one of the glioneuronal and neuronal tumors. Due to its similarities with dysembryoplastic neuroepithelial tumors (DNET), some authors consider it a variant of these, ranking in the category of malformations, but genetic alterations favor a neoplastic origin. We present a 29-year-old male with a generalized onset tonic-clonic seizure after a nightclub party. Imaging studies revealed a right temporal multinodular and vacuolating neuronal tumor confirmed by biopsy. It is considered a nonaggressive, “leave me alone” brain lesion, which does not require biopsy because of well-defined MRI characteristics. Surgery is indicated only in symptomatic cases. We consider that this lesion was revealed by his seizure, most probably provoked (with normal video EEG recording) by the consumption of a lot of alcohol, illicit drugs, and sleep loss after a club party. We recommended close monitoring, but our patient preferred the surgery. Our case added more imaging details corroborated with the histopathology features of MVNT. FLAIR images revealed hypointense nodules surrounded by hyperintense peripheral rings and areas of high signal intensity between the nodules, which correspond to the histopathological architecture. To our knowledge, this is the first case of MVNT with diffusion tensor imaging and fiber tractography imaging studies.

Aphasia is an acquired central disorder of language that affects a person’s ability to understand and/or produce spoken and written language, caused by lesions situated usually in the dominant (left) cerebral hemisphere. On one hand aphasia has a prevalence of 25–30% in acute ischemic stroke, especially in arterial infarcts. On the other hand, cerebral venous and dural sinuses thrombosis (CVT) remains a less common and underdiagnosed cause of ischemic stroke (0.5–1% of all strokes). Aphasia has been observed in almost 20% of patients who suffered CVT. The presence of aphasia is considered a negative predictive factor in patients with stroke, severe language disorders corresponding to arduous recovery. Taking into consideration data from the literature, aphasia is also considered a predictive factor for patients with CVT; its absences, together with the absence of worsening after admission, are determinants of complete recovery after CVT. This review has as the principal role of gathering current information from the literature (PubMed database 2012–2022) regarding the clinical features of aphasic syndromes and its incidence in patients with CVT. The main conclusion of this review was that aphasic syndromes are not usually the consequence of isolated thrombosis of dural sinuses or cerebral veins thrombosis. The most frequent form of CVT that determines aphasia is represented by the left transverse sinus thrombosis associated with a posterior left temporal lesion (due to left temporal cortical veins thrombosis), followed by the superior sagittal sinus thrombosis associated with a left frontal lesion (due to left frontal cortical veins thrombosis). Only a few cases are presenting isolated cortical veins thrombosis and left thalamus lesions due to deep cerebral vein thrombosis. We also concluded that the most important demographic factor was the gender of the patients, women being more affected than men, due to their postpartum condition.

Background and Objectives: The purpose of this paper was to perform a literature review on the effects of the COVID-19 pandemic on cardiothoracic and vascular surgery care and departments. Materials and Methods: To conduct this evaluation, an electronic search of many databases was conducted, and the resulting papers were chosen and evaluated. Results: Firstly, we have addressed the impact of COVID-19 infection on the cardiovascular system from the pathophysiological and treatment points of view. Afterwards, we analyzed every cardiovascular disease that seemed to appear after a COVID-19 infection, emphasizing the treatment. In addition, we have analyzed the impact of the pandemic on the cardiothoracic and vascular departments in different countries and the transitions that appeared. Finally, we discussed the implications of the cardiothoracic and vascular specialists’ and residents’ work and studies on the pandemic. Conclusions: The global pandemic caused by SARS-CoV-2 compelled the vascular profession to review the treatment of certain vascular illnesses and find solutions to address the vascular consequences of COVID-19 infection. The collaboration between vascular surgeons, public health specialists, and epidemiologists must continue to investigate the impact of the pandemic and the response to the public health issue.

Cerebral venous thrombosis is a rare cause of stroke. Imaging is essential for diagnosis. Although digital subtraction angiography is still considered by many to be the gold standard, it no longer plays a significant role in the diagnosis of cerebral venous thrombosis. MRI, which allows for imaging the parenchyma, vessels and clots, and CT are the reference techniques. CT is useful in case of contraindication to MRI. After presenting the radio-anatomy for MRI, we present the different MRI and CT acquisitions, their pitfalls and their limitations in the diagnosis of cerebral venous thrombosis.

The presence of neurological symptoms within the clinical range of COVID-19 disease infection has increased. This paper presents the situation of a 45-year-old man having the medical antecedent diabetes mellitus, who presented to the emergency department with fever, headache, and respiratory symptoms, nine days following vaccination with the Ad26.COV2-S COVID-19 vaccine. The patient tested positive for SARS-CoV-2 based on nasal polymerase chain reaction (RT-PCR). Two weeks after the presentation, he developed Tolosa–Hunt Syndrome, an autoimmune phenomenon, with painful left ophthalmoplegia. Significant improvement was seen in terms of his discomfort; however, ptosis and ocular mobility improved only moderately after treatment with intravenous methylprednisolone, and the patient was discharged on a new insulin regimen. The patient returned after four weeks and the neurological exam results showed significant signs of right hemiparesis, mixed aphasia, incomplete left ophthalmoplegia, severe headache, and agitation; after a few days, the patient experienced a depressed level of consciousness and coma. The patient’s clinical condition worsened and, unfortunately, he died. MRI brain images revealed multiple ischemic strokes, meningitis, infectious vasculitis, and hemorrhagic encephalitis, which are all serious complications of COVID-19.

OBSERVE-PD was a cross-sectional, multicountry, observational study conducted in 128 Movement Disorders Centers (MDCs) in 18 countries. Overall, the study enrolled 2615 patients. The aim was to determine the proportion of patients with advanced Parkinson’s disease (APD) versus non-APD from MDCs and to uncover the clinical burden of APD, as well as a correlation between overall assessment of APD and several indicators of APD. The advanced stage of the disease and severity were assessed by investigators using their clinical judgement. Data were collected during a single visit between February 2015 and January 2016. Agreement on physician judgement of APD diagnosis and fulfillment of at least one previously established APD indicator was calculated. Motor and nonmotor symptoms (NMSs), activities of daily living, treatment complications, quality of life (QoL), conventional treatments, and device-aided therapy (DAT) eligibility were assessed. Here, country-specific results of 161 Romanian patients with PD are presented. In total, 59.0% of patients were diagnosed with APD and 78.8% met at least one APD indicator. There was only moderate agreement between clinical judgement of APD and overall fulfillment of APD indicators. All scores related to motor symptoms, NMSs, and treatment complications, as well as to QoL, showed a higher disease burden for patients with APD versus non-APD. Physicians considered 73.7% of patients with APD eligible for DAT. The majority of patients eligible for DAT (54.3%) did not receive such treatment. Our results highlight the importance of earlier recognition of APD, by combining clinical judgement with more standardized clinical tools, such as generally recognized APD criteria. However, timely diagnosis of APD alone is not enough to improve patient outcomes. Other critical factors include patient acceptance and access to appropriate treatment.

(1) Objective: This review paper aims to discuss multiple aspects of cerebral venous thrombosis (CVT), including epidemiology, etiology, pathophysiology, and clinical presentation. Different neuroimaging methods for diagnosis of CVT, such as computer tomography CT/CT Venography (CTV), and Magnetic Resonance Imaging (MRI)/MR Venography (MRV) will be presented. (2) Methods: A literature analysis using PubMed and the MEDLINE sub-engine was done using the terms: cerebral venous thrombosis, thrombophilia, and imaging. Different studies concerning risk factors, clinical picture, and imaging signs of patients with CVT were examined. (3) Results: At least one risk factor can be identified in 85% of CVT cases. Searching for a thrombophilic state should be realized for patients with CVT who present a high pretest probability of severe thrombophilia. Two pathophysiological mechanisms contribute to their highly variable clinical presentation: augmentation of venular and capillary pressure, and diminution of cerebrospinal fluid absorption. The clinical spectrum of CVT is frequently non-specific and presents a high level of clinical suspicion. Four major syndromes have been described: isolated intracranial hypertension, seizures, focal neurological abnormalities, and encephalopathy. Cavernous sinus thrombosis is the single CVT that presents a characteristic clinical syndrome. Non-enhanced CT (NECT) of the Head is the most frequently performed imaging study in the emergency department. Features of CVT on NECT can be divided into direct signs (demonstration of dense venous clot within a cerebral vein or a cerebral venous sinus), and more frequently indirect signs (such as cerebral edema, or cerebral venous infarct). CVT diagnosis is confirmed with CTV, directly detecting the venous clot as a filling defect, or MRI/MRV, which also realizes a better description of parenchymal abnormalities. (4) Conclusions: CVT is a relatively rare disorder in the general population and is frequently misdiagnosed upon initial examination. The knowledge of wide clinical aspects and imaging signs will be essential in providing a timely diagnosis.

Considering the valuable information provided by glycosphingolipids as molecular markers and the limited data available for their detection and characterization in patients suffering from Type 2 diabetic kidney disease (DKD), we developed and implemented a superior method based on high-resolution (HR) mass spectrometry (MS) and tandem MS (MS/MS) for the determination of gangliosides in the urine of DKD patients. This study was focused on: (i) testing of the HR MS and MS/MS feasibility and performances in mapping and sequencing of renal gangliosides in Type 2 DM patients; (ii) determination of the changes in the urine gangliosidome of DKD patients in different stages of the disease—normo-, micro-, and macroalbuminuria—in a comparative assay with healthy controls. Due to the high resolution and mass accuracy, the comparative MS screening revealed that the sialylation status of the ganglioside components; their modification by O-acetyl, CH3COO−, O-fucosyl, and O-GalNAc; as well as the composition of the ceramide represent possible markers for early DKD detection, the assessment of disease progression, and follow-up treatment. Moreover, structural investigation by MS/MS demonstrated that GQ1d(d18:1/18:0), GT1α(d18:1/18:0) and GT1b(d18:1/18:0) isomers are associated with macroalbuminuria, meriting further investigation in relation to their role in DKD.

The COVID-19 disease, caused by infection with SARS-CoV-2, rapidly transformed into a pandemic following its emergence, and it continues to affect the population at a global level. This disease is associated with high mortality rates and mainly affects the pulmonary spectrum, with signs of interstitial pneumonia or other pathological modifications. Signs indicative of SARS-CoV-2 infection can be observed using pulmonary radiography or computed tomography scans and are closely linked to acute respiratory distress; however, there is accumulating evidence that the virus affects the central nervous system. Several symptoms, such as headaches, cough, fatigue, myalgia, ageusia, and anosmia, have also been reported along with neurological syndromes such as stroke, encephalopathy, Guillain–Barre syndrome, convulsions, and coma; the most frequent associated complication is ischemic stroke. Diagnosis of infection with SARS-CoV-2 virus is based on a positive RT-PCR test. Imaging investigations, such as thoracic computed tomography scans, are not used to diagnose COVID-19, monitor for pulmonary disease, or follow dynamic disease evolution, but they may be used in the case of a negative RT-PCR test. This paper presents the research performed on a group of 150 cases of patients affected by neurological disorders and that were subsequently confirmed to be infected with SARS-CoV-2, which was carried out over a period of 10 months within the Neurology Department and Laboratory of Magnetic Resonance Imaging of “Sf. Andrei” Emergency Hospital in Constanta. The collected data are observational and provide perspectives on the neurological pathology associated with the SARS-CoV-2 virus, and on the frequently associated risk factors, associated comorbidities, and the ages of patients who were affected by the virus, as well as the clinical and paraclinical manifestations of the patients admitted to the hospital’s neurology department.

In the first months of the COVID-19 pandemic, several research studies focused on understanding the damage to the respiratory and circulatory systems. However, the evidence of neurological manifestations as part of the clinical spectrum of the disease has increased. The aim of this retrospective study was to determine the potential association of neurological disorders with concomitant COVID-19 infection. We reviewed 101 patients (mean age, 70.05 years; 62.37% men) diagnosed with different neurological disorders and COVID-19 who were referred to the Department of Neurology between March 2020 and May 2021. The protocol included demographic, clinical, and neuroimagistic features, biochemical evaluation data, and prognosis. In the first group of patients with non-severe COVID-19 infection (50% lung damage). Severe COVID-19 infection was significantly correlated with an increased highly sensitive C-reactive protein level (hsCRP) (p < 0.05), lactate dehydrogenase level (LDH) (p < 0.05), erythrocyte sedimentation rate (ESR) (p < 0.05), D-dimer (p < 0.05), fibrinogen level (p < 0.05), and blood glucose (p < 0.05) when compared to the first group. These biochemical parameters were increased in both groups, but the levels were much higher in the second group. Headaches (72.27%) and dizziness (14.85%) were present in the early stage of infection. Cerebrovascular events were also reported: ischemic stroke (48% vs. 57.69%; p < 0.05), cerebral hemorrhage (4.95%), and cerebral venous sinus thrombosis (1.98%). Encephalitis (1.98%) and Guillain–Barré Syndrome (1.98%) were found but less frequently. Cranial nerve abnormalities were statistically more common in the non-severe group: anosmia (32% vs. 26.92%; p < 0.05), dysgeusia/ageusia (48% vs. 42.30%; p < 0.05), impaired eye movement (1.33% vs. 0%), and facial nerve palsy (2.66% vs. 0%). Seizures (13.33% vs. 11.53%; p < 0.05) and a depressed level of consciousness (31.68%) occurred commonly. We detected the neuropsychiatric symptoms of anxiety (23.76%) and depression (14.85%). Mortality was increased in both groups but was much higher in the second group (46.15% vs. 21.33%). Neurological complications during COVID-19 infection are common in hospitalized patients, but the mechanism of these complications is not fully understood, representing a continuous challenge for neurologists.

Cerebral venous sinus thrombosis (CVST), accounting for less than 1% of stroke cases, is characterized by various causes, heterogeneous clinical presentation and different outcome. The plasminogen activator inhibitor-1 (PAI-1) gene polymorphisms has been found to be associated with CVST. The aim of this retrospective study was to determine the potential association of PAI-1 675 4G/5G polymorphisms and homocysteine levels with cardiovascular risk factors in a group of young patients with CVST. Eighty patients with CVST and an equal number of age and sex matched controls were enrolled. The protocol included demographic and clinical baseline characteristics, neuroimagistic aspects, genetic testing (PAI-1 675 4G/5G polymorphisms), biochemical evaluation (homocysteine—tHcy, the lipid profile, blood glucose, glycohemoglobin—HbA1c, high-sensitive C-reactive protein—hsCRP) data, therapy and prognosis. The PAI-1 675 4G/5G gene polymorphisms were significantly correlated with increased homocysteine level (tHcy) (p < 0.05), higher total cholesterol (TC) (p < 0.05), low- density lipoprotein cholesterol (LDLc) (p = 0.05) and high- sensitive C- reactive protein (hsCRP) (p < 0.05) in patients with CVST when compared with controls. From the PAI-1 gene polymorphisms, the PAI-1 675 4G/5G genotype presented statistically significant values regarding the comparisons of the blood lipids values between the CVST group and control group. The homocysteine (tHcy) was increased in both groups, patients versus controls, in cases with the homozygous variant 4G/4G but the level was much higher in the group with CVST (50.56 µmol/L vs. 20.22 µmol/L; p = 0.03). The most common clinical presentation was headache (91.25%), followed by seizures (43.75%) and focal motor deficits (37.5%). The superior sagittal sinus (SSS) was the most commonly involved dural sinus (56.25%), followed by the lateral sinus (LS) (28.75%). Intima—media thickness (IMT) values were higher in the patients’ group with CVST (0.95 mm vs. 0.88 mm; p < 0.05). The fatal outcome occurred 2.5% of the time. PAI-1 675 4G/5G gene polymorphisms and higher homocysteine concentrations were found to be significantly associated with CVST in young patients.

Thrombophilia is characterized by an increased tendency to arterial and venous thrombus formation. Inherited thrombophilia can be secondary to protein S deficiency. Concomitant use of oral contraceptive pills increases the risk of venous thromboembolism and arterial thrombosis. We report a case of a 34-year-old female who used oral contraceptive pills for many years, who developed acute ischemic stroke of right occipital lobe with secondary left superior homonymous quadrantanopia. We have run several tests to establish the ischemic stroke etiology: unenhanced brain and cervical spine computed tomography, brain magnetic resonance imaging and magnetic resonance angiography (including MR venography), computed tomographic angiography, echocardiography, extracranial duplex ultrasound and laboratory data (including thrombophilia testing). The laboratory investigations confirmed that the ischemic stroke of our patient resulted from a severe inherited thrombophilia secondary to protein S deficiency.

Cerebral venous sinus thrombosis (CVST) as a severe neurological emergency, is represented by variable conditions in its clinic presentation, onset, risk factors, neuroimagistic features and outcome. The genetic polymorphism of the methylenetetrahydrofolate reductase (MTHFR) gene C677T and A1298C was associated with CVST. We aimed to characterize the prevalence of MTHFR gene polymorphisms associated with cardiovascular risk factors in the group of patients with CVST. Also, we studied additional causes associated with CVST including local infections, general infections, obstetric causes (pregnancy, puerperium) and head injury. This is a retrospective study including 114 patients which referred to our hospital between February 2012–February 2020. The protocol included demographic (age, sex), clinical, neuroimagistic features, paraclinic (genetic polymorphism of MTHFR, factor V G1691A—Leiden, prothrombin G20210A, PAI-1 675 4G/5G; Homocysteine level, the lipid profile, blood glucose and Glycohemoglobin HbA1c, high- sensitive C- reactive protein- hsCRP) data, as well as treatment and outcome. The mean age was 37.55 years with a female predominance (65.79%). In the first group of patients with inherited thrombophilia (60 cases; 52.63%) we found genetic mutation includes MTHFR C677T (38.59%) and A1298C (14.03%), factor V G1691A- Leiden (15.78%), prothrombin G20210A (2.63%), PAI-1 675 4G/5G (42.98%), and hyperhomocysteinemia (35.08%). At the second group with other etiology of CVST, except thrombophilia, we included 54 patients (47.36%). The most common sites of thrombosis were the superior sagittal sinus (52.63%). Headache was the most common symptom (91.22%) and seizures were the main clinical presentation (54.38%). The MTHFR polymorphism was significantly correlated with higher total cholesterol (TC) (p = 0.023), low- density lipoprotein cholesterol (LDL) (p = 0.008), homocysteine level (tHcy) (p < 0.001). Inside the first group with MTHFR polymorphism we have found a significant difference between the levels of homocysteine at the patients with MTHFR C677T versus MTHFR A1298C polymorphism (p < 0.001). The high-sensitive C-reactive protein (hsCRP) was increased in both groups of patients, but the level was much higher in the second group (p = 0.046). Mortality rate was of 2.63%. Demographic, clinical and neuroimagistic presentation of CVST in our study was similar with other studies on the matter, with a high frequency of thrombophilia causes. MTHFR gene polymorphisms (C677T and A1298C) are increased in prevalence in CVST. PAI-1 675 4G/5G gene mutation seems to be involved in CVST etiology. Plasma C-reactive protein level and hyperhomocysteinemia should be considered as a prognostic factor in CVST.

Background and objectives: cerebral vein and dural sinus thrombosis (CVT) present a variety of non-specific clinical signs, but, due to the development of neuroimaging techniques, especially magnetic resonance imaging, their identification has increased in recent years, due to the development of neuroimaging techniques, especially of magnetic resonance imaging. The aim of our study was to identify causes and risk factors, to describe the demographic, clinical, laboratory and neuroimaging data, and to evaluate the treatment and outcome of patients with C.V.T., comparing our experience with international literature. Patients and methods: we included 30 patients (pts) with CVT, between January 1998 and September 2010. The diagnosis was based in all cases on neuroimaging features. The pts were examined at admission and after three months, using the mRS scores. Results: mean age was 37.2 years (SD 8.6), sex ratio: male/female was 1/2. 80% of women were fertile. The main clinical manifestations were headache: 22 pts (73.3%), and papilledema: 16 pts (53.3%). The most frequent neurological syndrome at onset was intracranial hypertension with subacute evolution. CT showed direct signs of dural sinuses thrombosis: (dense triangle sign in 3 pts, delta sign in 7 cases); in 12 pts, we identified a venous cerebral infarct (indirect sign of dural sinuses thrombosis). MRI identified thrombosis of SSS in 21 pts, transverse sinus in 12 cases, cavernous sinus in 3 pts, cerebral edema in 18 pts. In 12 cases, we identified a venous cerebral infarct. 7 out of 30 MRI had a normal CT. DSA revealed isolated cortical veins occlusion, without sinus occlusion in 2 cases (CT, MRI, and MR-A were normal). Risk factors were identified in 22 pts (73.3%); congenital thrombophilia being the most common (9 pts). All pts received anticoagulant therapy. After 90 days from admission, complete resolution of symptoms was seen in 14 cases, minimal neurological deficits in 7 pts, and the death rate was 16.7% (5 pts). Conclusions: CVT appear to be underdiagnosed in our region, due to low percentage of admissions for benign intracranial hypertension. CVT was common in women of fertile age, but oral contraceptive was not an important risk factor. The outcome was favorable with adequate therapy.

Background. Giant cell arteritis is a primary vasculitis, that affects medium-sized arteries, especially branches of the ECA. Purpose. The main objective was to assess the role of CDI of retrobulbar vessels in the study of two patients with Horton’s disease with eye involvement. Methods. We have used a sonographer with 8-15 MHz linear probe for CDI of orbital vessels. Results. Both patients presented malaise, temporal headache, tender temporal arteries and laboratory signs of inflammation. The first patient had a left central retinal artery obstruction, and the second one had a left ischaemic optic neuropathy. They presented a painless, severe loss of vision of the left eye. Temporal artery histology was positive in both cases. Ultrasound investigation was performed before corticosteroid treatement. CDI of retrobulbar vessels detected low blood velocities, especially end-diastolic velocities and high resistance index in all retrobulbar vessels, in both orbits, for both patients (especially on the affected side). Typical sonographic features in temporal arteritis were ”dark halo sign” (vessel wall thickening), associated with stenoses or occlusions of branches of ECA. Interestingly, in both cases, the CCA and the ICA were, also, affected. Conclusions. Ultrasound technique is a valuable diagnostic tool to investigate giant cell arteritis.