Frontiers in Neurology 

About: Frontiers in Neurology is an academic journal published by Frontiers Media. The journal publishes majorly in the area(s): Medicine & Internal medicine. It has an ISSN identifier of 1664-2295. It is also open access. Over the lifetime, 13217 publications have been published receiving 168178 citations.

Behavioral and Psychological Symptoms of Dementia

Abstract: Behavioral and psychological symptoms of dementia (BPSD), also known as neuropsychiatric symptoms, represent a heterogeneous group of non-cognitive symptoms and behaviors occurring in subjects with dementia. BPSD constitute a major component of the dementia syndrome irrespective of its subtype. They are as clinically relevant as cognitive symptoms as they strongly correlate with the degree of functional and cognitive impairment. BPSD include agitation, aberrant motor behavior, anxiety, elation, irritability, depression, apathy, disinhibition, delusions, hallucinations, and sleep or appetite changes. It is estimated that BPSD affect up to 90% of all dementia subjects over the course of their illness, and is independently associated with poor outcomes, including distress among patients and caregivers, long-term hospitalization, misuse of medication, and increased health care costs. Although these symptoms can be present individually it is more common that various psychopathological features co-occur simultaneously in the same patient. Thus, categorization of BPSD in clusters taking into account their natural course, prognosis, and treatment response may be useful in the clinical practice. The pathogenesis of BPSD has not been clearly delineated but it is probably the result of a complex interplay of psychological, social, and biological factors. Recent studies have emphasized the role of neurochemical, neuropathological, and genetic factors underlying the clinical manifestations of BPSD. A high degree of clinical expertise is crucial to appropriately recognize and manage the neuropsychiatric symptoms in a patient with dementia. Combination of non-pharmacological and careful use of pharmacological interventions is the recommended therapeutic for managing BPSD. Given the modest efficacy of current strategies, there is an urgent need to identify novel pharmacological targets and develop new non-pharmacological approaches to improve the adverse outcomes associated with BPSD.

Cognitive dysfunction in multiple sclerosis.

Abstract: In Multiple Sclerosis (MS) prevalence studies of community and clinical samples, indicate that 45–60% of patients are cognitively impaired. These cognitive dysfunctions have been traditionally described as heterogeneous, but more recent studies suggest that there is a specific pattern of MS-related cognitive dysfunctions. With the advent of disease-modifying medications for MS and emphasis on early intervention and treatment, detection of cognitive impairment at its earliest stage becomes particularly important. In this review the authors address: the cognitive domains most commonly impaired in MS (memory, attention, executive functions, speed of information processing, and visual–spatial abilities); the pathophysiological mechanism implied in MS cognitive dysfunction and correlated brain MRI features; the importance of neuropsychological assessment of MS patients in different stages of the disease and the influence of its course on cognitive performance; the most used tests and batteries for neuropsychological assessment; therapeutic strategies to improve cognitive abilities.

Traumatic Spinal Cord Injury: An Overview of Pathophysiology, Models and Acute Injury Mechanisms.

Abstract: Traumatic spinal cord injury (SCI) is a life changing neurological condition with substantial socioeconomic implications for patients and their care-givers. Recent advances in medical management of SCI has significantly improved diagnosis, stabilization, survival rate and well-being of SCI patients. However, there has been small progress on treatment options for improving the neurological outcomes of SCI patients. This incremental success mainly reflects the complexity of SCI pathophysiology and the diverse biochemical and physiological changes that occur in the injured spinal cord. Therefore, in the past few decades, considerable efforts have been made by SCI researchers to elucidate the pathophysiology of SCI and unravel the underlying cellular and molecular mechanisms of tissue degeneration and repair in the injured spinal cord. To this end, a number of preclinical animal and injury models have been developed to more closely recapitulate the primary and secondary injury processes of SCI. In this review, we will provide a comprehensive overview of the recent advances in our understanding of the pathophysiology of SCI. We will also discuss the neurological outcomes of human SCI and the available experimental model systems that have been employed to identify SCI mechanisms and develop therapeutic strategies for this condition.

The role of markers of inflammation in traumatic brain injury.

Abstract: Within minutes of a traumatic impact, a robust inflammatory response is elicited in the injured brain. The complexity of this post-traumatic squeal involves a cellular component, comprising the activation of resident glial cells, microglia, and astrocytes, and the infiltration of blood leukocytes. The second component regards the secretion immune mediators, which can be divided into the following sub-groups: the archetypal pro-inflammatory cytokines (Interleukin-1, Tumor Necrosis Factor, Interleukin-6), the anti-inflammatory cytokines (IL-4, Interleukin-10, and TGF-beta), and the chemotactic cytokines or chemokines, which specifically drive the accumulation of parenchymal and peripheral immune cells in the injured brain region. Such mechanisms have been demonstrated in animal models, mostly in rodents, as well as in human brain. Whilst the humoral immune response is particularly pronounced in the acute phase following Traumatic brain injury (TBI), the activation of glial cells seems to be a rather prolonged effect lasting for several months. The complex interaction of cytokines and cell types installs a network of events, which subsequently intersect with adjacent pathological cascades including oxidative stress, excitotoxicity, or reparative events including angiogenesis, scarring, and neurogenesis. It is well accepted that neuroinflammation is responsible of beneficial and detrimental effects, contributing to secondary brain damage but also facilitating neurorepair. Although such mediators are clear markers of immune activation, to what extent cytokines can be defined as diagnostic factors reflecting brain injury or as predictors of long term outcome needs to be further substantiated. In clinical studies some groups reported a proportional cytokine production in either the cerebrospinal fluid or intraparenchymal tissue with initial brain damage, mortality, or poor outcome scores. However, the validity of cytokines as biomarkers is not broadly accepted. This review article will discuss the evidence from both clinical and laboratory studies exploring the validity of immune markers as a correlate to classification and outcome following TBI.

EEG Source Imaging: A Practical Review of the Analysis Steps.

Abstract: The electroencephalogram (EEG) is one of the oldest technologies to measure neuronal activity of the human brain. It has its undisputed value in clinical diagnosis, particularly (but not exclusively) in the identification of epilepsy and sleep disorders and in the evaluation of dysfunctions in sensory transmission pathways. With the advancement of digital technologies, the analysis of EEG has moved from pure visual inspection of amplitude and frequency modulations over time to a comprehensive exploration of the temporal and spatial characteristics of the recorded signals. Today, EEG is accepted as a powerful tool to capture brain function with the unique advantage of measuring neuronal processes in the time frame in which these processes occur, namely in the sub-second range. However, it is generally stated that EEG suffers from a poor spatial resolution that makes it difficult to infer to the location of the brain areas generating the neuronal activity measured on the scalp. This statement has challenged a whole community of biomedical engineers to offer solutions to localize more precisely and more reliably the generators of the EEG activity. High-density EEG systems combined with precise information of the head anatomy and sophisticated source localization algorithms now exist that convert the EEG to a true neuroimaging modality. With these tools in hand and with the fact that EEG still remains versatile, inexpensive and portable, electrical neuroimaging has become a widely used technology to study the functions of the pathological and healthy human brain. However, several steps are needed to pass from the recording of the EEG to 3-dimensional images of neuronal activity. This review explains these different steps and illustrates them in a comprehensive analysis pipeline integrated in a stand-alone freely available academic software: Cartool. The information about how the different steps are performed in Cartool is only meant as a suggestion. Other EEG source imaging software may apply similar or different approaches to the different steps.