Functional neurological disorder (FND), formerly called conversion disorder, is a condition characterized by neurological symptoms that lack an identifiable organic purpose. These signs, which can consist of motor, sensory, or cognitive disturbances, are not deliberately produced and often vary in severity. Its diagnosis is predicated on clinical evaluation and the exclusion of other medical or psychiatric situations. Its treatment typically involves a multidisciplinary technique addressing each of the neurological symptoms and underlying psychological factors via a mixture of medical management, psychotherapy, and supportive interventions. Recent advances in neuroimaging and a deeper exploration of its epidemiology, pathophysiology, and clinical presentation have shed new light on this disorder. This paper synthesizes the current knowledge on FND, focusing on its epidemiology and underlying mechanisms, neuroimaging insights, and the differentiation of FND from feigning or malingering. This review highlights the phenotypic heterogeneity of FND and the diagnostic challenges it presents. It also discusses the significant role of neuroimaging in unraveling the complex neural underpinnings of FND and its potential in predicting treatment response. This paper underscores the importance of a nuanced understanding of FND in informing clinical practice and guiding future research. With advancements in neuroimaging techniques and growing recognition of the disorder’s multifaceted nature, the paper suggests a promising trajectory toward more effective, personalized treatment strategies and a better overall understanding of the disorder.

Ischemic strokes occur when the blood supply to a part of the brain is interrupted or reduced due to arterial blockage, and it often leads to damage to brain cells or death. According to a myriad of experimental studies, oxidative stress is an important pathophysiological mechanism of ischemic stroke. In this narrative review, we aimed to identify how the alterations of oxidative stress biomarkers could suggest a severity-reflecting diagnosis of ischemic stroke and how these interactions may provide new molecular targets for neuroprotective therapies. We performed an eligibility criteria-based search on three main scientific databases. We found that patients with acute ischemic stroke are characterized by increased oxidative stress markers levels, such as the total antioxidant capacity, F2-isoprostanes, hydroxynonenal, total and perchloric acid oxygen radical absorbance capacity (ORAC_TOT and ORAC_PCA), malondialdehyde (MDA), myeloperoxidase, and urinary 8-oxo-7,8-dihydro-2′-deoxyguanosine. Thus, acute ischemic stroke is causing significant oxidative stress and associated molecular and cellular damage. The assessment of these molecular markers could be useful in diagnosing ischemic stroke, finding its causes, predicting its severity and outcomes, reducing its impact on the cellular structures of the brain, and guiding preventive treatment towards antioxidant-based therapy as novel therapeutic alternatives.

Mild traumatic brain injury (mTBI) accounts for most TBI cases, the leading cause of morbidity and mortality worldwide. Despite its high incidence, mTBI pathophysiology remains largely unknown. Recent studies have shown that the inflammatory response is activated early after mTBI and can persist for several weeks or months. However, limited evidence on the utility of inflammatory biomarkers as predictors of clinical outcomes in mTBI has been previously provided. Thus, this systematic review and meta-analysis aims to provide an overview of the current knowledge on the role of inflammation in the pathogenesis of mTBI and the potential of some inflammatory biomolecules as biomarkers of mTBI. In this regard, eight studies comprising 1184 individuals were selected. Thus, it was shown that the increase in IL-6, TNF-α, and IL-1β plasma levels could be implicated in the development of early post-concussion symptoms. On the other hand, the persistence of the increased plasmatic concentrations of IL-10 and IL-8 for as long as six months following the brain injury event could suggest chronic inflammation leading to neuroinflammation and late or persistent symptoms. In this context, our findings showed that inflammatory biomarkers could be relevant in diagnosing or predicting recovery or long-term outcomes of mTBI.

Harlequin syndrome (HS) is a rare autonomic disorder. The causes and risk factors of the disease are not fully understood. Some cases of HS are associated with traumatic injuries, tumors, or vascular impairments of the head. Symptoms of HS can also occur in some autoimmune disorders, ophthalmic disorders, sleep disorders, and with certain organic lesions. In this context, a thorough review of the pathophysiology of HS in relation to neurological, ophthalmological, and dermatological conditions is necessary. In this mini-review, we aim to review the pathophysiological changes and underlying mechanisms in primary and secondary HS. Additionally, we discuss possible management approaches for patients with HS in light of the discussed pathological mechanisms. The main symptoms of HS that are correlated with autonomic nervous system impairments include sudden unilateral flushing of the face, neck, chest, and rarely arm, with concurrent contralateral anhidrosis. Despite reported co-occurring syndromes (such as cluster headaches), several studies have shown that HS could frequently overlap with other syndromes that are disruptive to the idiopathic nerve pathways. HS usually does not require any medical treatment. In some severe cases, symptomatic treatments could be needed. However, total symptomatic relief may not be achieved in many cases of HS. We therefore suggest an approach to comprehensive management of HS, which may lead to better long-term control of HS.

Childhood obesity has become a global public health issue and its assessment is essential, as an obese child is a future overweight or obese adult. Obesity is no longer a matter of exercising more and eating less, with several factors coming into play and dictating the pattern of fat accumulation and the ease/difficulty of reducing it. In the current paper, we aimed to analyze the cardiovascular impact of obesity in a large number of patients alongside the paraclinical changes that occur due to weight gain, and to perform an analysis on the increase in prevalence throughout our research. The main cardiovascular conditions identified were hypertension (15.36%), septal or concentric hypertrophic cardiomyopathy (11.15%), atherosclerosis risk (13.04%), and hypercholesterolemia (20.94%). We have used echocardiography to measure the thickness of epicardial adipose tissue (useful for assessing the patient’s cardiovascular risk), and we observed that it was greater in children with moderate and severe obesity alongside diastolic dysfunction of the left ventricle in the whole group, without any connection with hypertension or coronary impairment. Obese children will be affected by increased cardiovascular mortality and morbidity in adulthood and they may experience early cardiovascular dysfunction. We want to strongly underline the importance and necessity of programs for the early detection and prevention of obesity and its complications, especially since interesting phenomena such as the “obesity paradox” exist and prove that obesity is far less understood than it is at a first glance.

Traumatic brain injury (TBI) is currently a problematic issue of public health due to its frequency, and many of the mild cases often remain undiagnosed despite the possible predisposition to prolonged or persistent post-concussive symptomatology. It was shown here that the severity and persistence of grey matter (GM) changes following TBI could predict disease outcomes. Our aim was to conduct a voxel-wise meta-analysis to detect significant GM changes following mild TBI (mTBI) and to investigate whether these changes are associated with the duration and severity of post-concussion syndrome (PCS). A voxel-wise meta-analysis was conducted regarding the GM and white matter (WM) changes in mTBI adult patients versus healthy controls, and Seed-based d Mapping was used to correlate the data. Standard meta-analysis statistical processing was used to assess heterogeneity and publication bias. Our analysis showed significant GM volume increases in the left medial cingulate/paracingulate gyri, the middle frontal gyrus, and the right caudate nucleus of the mTBI patients and significant volume loss in the thalamus, the frontal lobe, and the temporal lobe. These changes could potentially be associated with PCS that some mTBI later patients develop as a result to the injury or other compensatory changes. Additional studies considering long-term GM changes in mTBI patients and their potential relationship to PCS could provide further insight into the pathophysiological similarities and correlations between mTBI and PCS.