Some respiratory viruses have long been known to cause neurological involvement. A novel coronavirus, leading to severe acute respiratory syndrome, also called coronavirus disease 19 (COVID-19), seems to be a new member of neuroinvasive viruses. While severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) keeps on spreading around the world rapidly, reports about the neurological manifestations associated with SARS-CoV-2, increases day by day. It is reported that a variety of symptoms and syndromes such as headache, dizziness, confusion, ataxia, epilepsy, ischemic stroke, neuropathic pain and myopathy are common especially in more severe COVID-19 patients. It is also suggested that the development of neurological complications is strongly associated with a poor outcome. On the other hand, hyposmia can be the unique symptom in COVID-19 carriers and this can serve as a marker for identifying the otherwise asymptomatically infected patients. It is thought that SARS-CoV-2 may cause neurological symptoms through direct or indirect mechanisms. Nevertheless, neuroinvasion capability of SARS-CoV2 is confirmed by the presence of the virus, in the cerebrospinal fluid of a COVID-19 patient with encephalitis, and this is proven by gene sequencing. In conclusion, during the COVID-19 pandemic, it is crucial to be aware of the possible neurological complications of the disease. Therefore, in this review, we aimed to report neurological manifestations associated with SARS-CoV-2 and possible underlying pathophysiological mechanisms. Due to the high homology of SARS-CoV-2 with other human coronaviruses such as SARS-CoV or Middle East Respiratory Syndrome (MERS)-CoV, reviewing the neurological involvement also associated with these coronaviruses will provide an idea about the longterm complications of COVID-19.

Background Although specific role players are currently unknown, contribution of inflammatory mediators has been suggested in the pathophysiology of idiopathic intracranial hypertension (IIH), which is a disease more prevalent in obese female individuals of childbearing age. We aimed to investigate the levels of adipokines and cytokines to demonstrate possible markers for inflammation that participate in IIH pathophysiology and their association with clinical features of IIH. Methods IIH patients, diagnosed according to the revised criteria, and age-, gender- and body mass index (BMI)-matched healthy controls were enrolled in this study. Serum samples were evaluated for insulin-like growth factor 1, insulin, nesfatin, adiponectin, interleukin (IL)-1β, IL-6, IL-8, leptin, plasminogen activator inhibitor type-1, resistin, tumour necrosis factor-alpha (TNF-α) and monocyte chemotactic protein 1 via enzyme-linked immunosorbent assay or multiplex immunoassays. Results IL-1β level was significantly higher ( p = 0.012), and IL-8 and TNF-α levels were significantly lower in the IIH group ( p < 0.001 and p = 0.008, respectively) compared to the control group. There were no correlations between the cytokine/adipokine levels and age, BMI, disease duration, and cerebrospinal fluid oligoclonal bands. There were also no significant differences in cytokine and adipokine levels between IIH patients regarding visual impairment. However, statistically significant differences were found between IIH patients with relapse versus healthy controls regarding IL-1β ( p = 0.007), IL-8 ( p = 0.001) and TNF-α ( p = 0.017) levels. Other investigated cytokines and adipokines showed no significant alterations in IIH patients investigated in the remission period. Conclusion Altered serum levels of IL-1β, IL-8 and TNF-α seem to be associated with IIH pathogenesis, and these cytokines may be used as prognostic markers in IIH to predict relapse.

Background: Right temporal variant frontotemporal dementia (rtvFTD) has been generally considered as a right sided variant of semantic variant primary progressive aphasia (svPPA), which is a genetically sporadic disorder. Recently, we have shown that rtvFTD has a unique clinical syndrome compared to svPPA and behavioral variant frontotemporal dementia. Objective: We challenge the assumption that rtvFTD is a sporadic, non-familial variant of FTD by identifying potential autosomal dominant inheritance and related genes in rtvFTD. Methods: We collected all subjects with a diagnosis of FTD or primary progressive aphasia who had undergone genetic screening (n = 284) and subsequently who had a genetic variant (n = 48) with a diagnosis of rtvFTD (n = 6) in 2 specialized memory clinics. Results: Genetic variants in FTD related genes were found in 33% of genetically screened rtvFTD cases; including MAPT (n = 4), GRN (n = 1), and TARDBP (n = 1) genes, whereas only one svPPA case had a genetic variant in our combined cohorts. Additionally, 4 out of 6 rtvFTD subjects had a strong family history for dementia. Conclusion: Our results demonstrate that rtvFTD, unlike svPPA, is not a pure sporadic, but a heterogeneous potential genetic variant of FTD, and screening for genetic causes for FTD should be performed in patients with rtvFTD.

No abstract

Although formerly considered as a "benign" disease, the presence of some important problems such as vision loss, resistance to appropriate medical treatment and relapses suggests that neuronal damage might play a role in the pathophysiology of IIH. In order to demonstrate possible neuronal damage/dysfunction participating in IIH pathophysiology, we aimed to investigate the relationship between serum neuron-specific enolase (NSE) levels and clinical features in patients with idiopathic intracranial hypertension (IIH). Thirty-six patients with IIH, diagnosed according to the revised criteria, and 40 age, gender and body mass index-matched healthy controls were enrolled in this study after their consent. Serum samples were evaluated for NSE via enzyme-linked immunosorbent assay method. NSE levels were higher in the IIH group (23.7 ± 14.53 ng/ml) compared to the control group (22.7 ± 13.11 ng/ml), but the difference was not statistically significant (p = 0.824). There were also no statistically significant differences in NSE levels in IIH patients regarding the presence of visual loss, relapse, oligoclonal bands and papilledema. We could not demonstrate any correlations between NSE levels and age, body mass index, cerebrospinal fluid opening pressure and disease duration. The present study is the first to analyze NSE levels in IIH patients and showed no significant difference between patients and controls, and also between different clinical subgroups of IIH patients.