In this review, we provide an update on the pathogenesis, diagnosis, and management of adults with idiopathic intracranial hypertension (IIH) and implications of the cerebral venous system, highlighting the progress made during the past decade with regard to mechanisms of the venous outflow pathway and its connection with the cerebral glymphatic and lymphatic network in genesis of IIH. Early diagnosis and treatment are crucial for favorable visual outcomes and to avoid vision loss, but there is also a risk of overdiagnosis and misdiagnosis in many patients with IIH. We also present details about treatment of intracranial hypertension, which is possible in most cases with a combination of weight loss and drug treatments, but also in selected cases with surgical interventions such as optic nerve sheath fenestration, cerebral spinal fluid (CSF) diversion, or dural venous sinus stenting for some patients with cerebral venous sinus stenosis, after careful analysis of mechanisms of intracranial hypertension, patient clinical profile, and method risks.

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.

Background and aims: Orphan diseases, or rare diseases, are defined in Europe as diseases that affect less than 5 out of every 10,000 citizens. Given the small number of cases and the lack of profit potential, pharmaceutical companies have not invested much in the development of possible treatments. However, over the last few years, new therapies for rare diseases have emerged, giving physicians a chance to offer personalized treatment. With this paper, we aim to present some of the orphan neurological diseases for which new drugs have been developed lately. Methods: We have conducted a literature review of the papers concerning rare diseases and their treatment, and we have analyzed the existing studies for each orphan drug. For this purpose, we have used the Google Scholar search engine and the Orphanet. We have selected the studies published in the last 15 years. Results. Since the formation of the National Organization for Rare Diseases, the Orphan Drug Act, and the National Institutes of Health Office of Rare Diseases, pharmacological companies have made a lot of progress concerning the development of new drugs. Therefore, diseases that until recently were without therapeutic solutions benefit today from personalized treatment. We have detailed in our study over 15 neurological and systemic diseases with neurological implications, for which the last 10–15 years have brought important innovations regarding their treatment. Conclusions: Many steps have been taken towards the treatment of these patients, and the humanity and professionalism of the pharmaceutical companies, along with the constant support of the patient’s associations for rare diseases, have led to the discovery of new treatments and useful future findings.

Diagnosis in stroke patients is based mainly on clinical and radiological findings; therefore, there is a need for serological markers that can orient the clinician. Copeptin is a new blood marker for diagnosis and prognosis in several neurological conditions, such as ischemic stroke, hemorrhagic stroke, aneurysmal subarachnoid hemorrhage, and multiple sclerosis. The aim of our study was to highlight the diagnostic value of copeptin in differentiating between stroke subtypes and stroke mimics. We performed a literature review by searching the PubMed and Scopus databases for papers with the following keywords: “stroke AND copeptin AND differential”. The PRISMA criteria were used. We identified 29 papers that met the criteria. We analyzed only original research articles, excluding reviews and only including those in English. Some studies did not find any significant differences between cerebral infarction, intracerebral hemorrhage, and subarachnoid hemorrhage, but one study demonstrated significant correlations. All studies agreed that copeptin levels can help in differentiating stroke patients from stroke-free patients. Copeptin levels were correlated with prognostic scales For stroke mimics, copeptin levels were extremely broad and for vestibular disorders; it was shown that a normal level of copeptin excludes stroke. Copeptin is a new blood marker that can help clinicians in the acute neurological field. It may help in diagnosing stroke, in differentiating between stroke subtypes and stroke mimics, and in evaluating the prognosis of these patients, but further studies are needed.

A complex interplay of factors reflecting the general biological, cardiovascular, neurological, renal, and metabolic status of patients influences the outcome of thrombolysis in stroke patients. This is a retrospective cohort observational study aimed to determine the importance of kidney dysfunction among these factors. Data (demographic, lifestyle, physical examination, laboratory, imaging, including metabolic and cardiovascular risk factors and comorbidities, neurological scores, and outcomes) of all stroke patients who underwent thrombolysis have been registered since January 1, 2016, in an online database. A total of 296 patients registered until December 31, 2020, were included in the study. The National Institutes of Health Stroke Scale, modified Rankin scale, Barthel index, percentage of hemorrhagic transformation, and in hospital death were used to evaluate the neurological status and outcomes of the patients. Regression analysis, Mann–Whitney test, Fisher exact test, logistic regression, and multivariate analysis were used for statistical analysis. Kidney dysfunction, as reflected by the estimated glomerular filtration rate, was associated with in hospital death and all but one of the neurological scores. Other risk factors most frequently associated with neurological scores were age, international normalized ratio, and cognitive decline. Multivariate analysis revealed estimated glomerular filtration rate (as determined by chronic kidney disease-EPI equation) as a determinant for all but one of these scores, and as the most important determinant for most of them, except for those reflecting the pre-intervention neurological status of the patient. Kidney dysfunction seems to be the most important determinant of the outcome of thrombolysed stroke patients, a result obtained by no other study.

Background and Clinical Significance: Statins are a widely used drug class associated with a plethora of muscular side effects ranging from the subclinical elevation of creatine kinase to fulminant rhabdomyolysis. Cardiac myopathy secondary to statin treatment is rare and was recently reported as a part of statin-induced necrotizing autoimmune myopathy (SINAM). Its occurrence outside of this context is still debated. Case Presentation: We present the case of a 60-year-old male who developed atorvastatin-induced rhabdomyolysis, without associated hydroxymethyl glutaryl coenzyme A reductase (HMGCR) antibodies, with clinical findings of cardiac failure and severe ECG anomalies. The symptoms slowly regressed with statin withdrawal, and the patient made a full recovery. We discuss the recently proposed statin-associated cardiomyopathy (SACM) and the possible mechanisms. We compare our case to the three other cases of statin-induced cardiac myositis found in the literature. Conclusions: We believe that in vulnerable patients, as was our case, statins can determine significant subacute cardiac toxicity. This would seem to occur in the context of severe skeletal muscle injury, probably due to higher metabolic resistance on the part of the myocardium. Also, the available evidence suggests myocardial involvement should be actively investigated in SINAM patients, preferably by cardiac MRI.