Small cell lung cancer (SCLC) is the most malignant pathological type of lung cancer with the highest mortality, and the incidence of brain metastasis (BM) is in high frequency. So far, prophylactic cranial irradiation (PCI) has been suggested as an effective treatment for preventing brain metastasis of SCLC. PCI has long been applied to limited-stage SCLC (LS-SCLC) patients who have achieved complete remission after radiotherapy and chemotherapy as a standard treatment. However, the neurocognitive decline is a major concern surrounding PCI. New therapeutic approaches targeting PCI-induced neurotoxicity, including hippocampal protection or memantine, have been increasingly incorporated into the therapeutic interventions of PCI. Helical tomotherapy, RapidArc, and Volumetric-modulated arc therapy (VMAT) with a head-tilting baseplate are recommended for hippocampal protection. Besides, in the MRI and immunotherapy era, the significance of PCI in SCLC patients is controversial. SCLC patients with PCI should be recruited in clinical trials since this is the only way to improve the existing standard of care. This review summarizes the current therapeutic strategy and dilemma over PCI for SCLC, providing a theoretical basis for clinical decision-making and suggestions for PCI practice in clinical.

Encephalopathy is part of the clinical triad of Susac syndrome, but a detailed understanding of the neurocognitive and neuropsychiatric profile of this condition is lacking. Existing literature indicates that cognitive deficits range in severity from subtle to profound. Executive function and short-term recall are affected frequently. Psychiatric manifestations may be absent or may include anxiety, mood disorders or psychosis. If psychiatric phenomena develop during the disease course, it can be hard to disentangle whether symptoms directly relate to the pathology of Susac syndrome or are secondary to treatment-related side effects. In this article, we review what is known about the cognitive and psychiatric morbidity of Susac syndrome and identify areas where knowledge is deficient. Importantly, we also provide a framework for future research, arguing that better phenotyping, understanding of pathophysiology, evaluation of treatments on cognitive and psychiatric outcomes, and longitudinal data capture are vital to improving patient outcomes.

Olfactory dysfunction (OD) is one of the most common symptoms in COVID-19 patients and can impact patients\' lives significantly. The aim of this review was to investigate the multifaceted impact of COVID-19 on the olfactory system and to provide an overview of magnetic resonance (MRI) findings and neurocognitive disorders in patients with COVID-19-related OD. Extensive searches were conducted across PubMed, Scopus, and Google Scholar until 5 December 2023. The included articles were 12 observational studies and 1 case report that assess structural changes in olfactory structures, highlighted through MRI, and 10 studies correlating the loss of smell with neurocognitive disorders or mood disorders in COVID-19 patients. MRI findings consistently indicate volumetric abnormalities, altered signal intensity of olfactory bulbs (OBs), and anomalies in the olfactory cortex among COVID-19 patients with persistent OD. The correlation between OD and neurocognitive deficits reveals associations with cognitive impairment, memory deficits, and persistent depressive symptoms. Treatment approaches, including olfactory training and pharmacological interventions, are discussed, emphasizing the need for sustained therapeutic interventions. This review points out several limitations in the current literature while exploring the intricate effects of COVID-19 on OD and its connection to cognitive deficits and mood disorders. The lack of objective olfactory measurements in some studies and potential validity issues in self-reports emphasize the need for cautious interpretation. Our research highlights the critical need for extensive studies with larger samples, proper controls, and objective measurements to deepen our understanding of COVID-19\'s long-term effects on neurological and olfactory dysfunctions.

BACKGROUND: Extracorporeal membrane oxygenation (ECMO) has been widely used in severe neonatal diseases for approximately 50 years, while few studies have concentrated on the long-term follow-up of its neuropsychological development.
OBJECTIVE: To assess the long-term neuropsychological complications in children who underwent ECMO in infancy.
METHODS: The PubMed, Web of Science, Cochrane, and EMBASE databases were searched for retrieving studies published in the recent 10 years (until June 10, 2022). All studies were eligible that concentrated on the long-term follow-up of neuropsychological complications in neonates undergoing ECMO. Excluding animal studies, neonates with congenital craniocerebral dysplasia and studies with data from the same center performed at different times. Statistical analysis was performed using RevMan 5.3 and Stata/SE 12.0 software. A random-effects model was used to report results. The sensitivity analysis was utilized to identify sources of heterogeneity.
RESULTS: The meta-analysis of 10 studies that enrolled 1199 patients was conducted, showing the pooled morbidity of intelligence (pooled morbidity: 20.3%, 95% CI: 0.16-0.25, I2: 9.5%, P=0.33), motor activity (pooled morbidity: 10.3%, 95%CI: 0.07-0.14, I2: 43.5%, P=0.15), learning (pooled morbidity: 9.0%, 95%CI: -0.03-0.21, I2: 63.2%, P=0.10), hearing (pooled morbidity: 15.7%, 95%CI: 0.02-0.29, I2: 94.2%, P=0.00), vision (pooled morbidity: 18.5%, 95%CI: 0.12-0.25, I2: 0%, P=0.46), cognition (pooled morbidity: 26.3%, 95%CI: 0.19-0.34, I2: 0%, P=0.32), attention (pooled morbidity: 7.4%, 95%CI: 0.02-0.13, I2: 38.9%, P=0.20), speed in attention (pooled morbidity: 69.9%, 95%CI: 0.62-0.78), and accuracy in attention (pooled morbidity: 39.0%, 95%CI: 0.30-0.48) in neonates undergoing ECMO. The results of the Begg\'s test and sensitivity analysis indicated that the heterogeneity was originated from factors other than sample size.
CONCLUSIONS: This systematic review and meta-analysis showed that neonates undergoing ECMO were associated with various neuropsychological complications. Additional randomized controlled trials (RCTs) with a larger sample size and a higher quality are needed.

It has been more than three years since COVID-19 impacted the lives of millions of people, many of whom suffer from long-term effects known as long-haulers. Notwithstanding multiorgan complaints in long-haulers, signs and symptoms associated with cognitive characteristics commonly known as \"brain fog\" occur in COVID patients over 50, women, obesity, and asthma at excessive. Brain fog is a set of symptoms that include cognitive impairment, inability to concentrate and multitask, and short-term and long-term memory loss. Of course, brain fog contributes to high levels of anxiety and stress, necessitating an empathetic response to this group of COVID patients. Although the etiology of brain fog in COVID-19 is currently unknown, regarding the mechanisms of pathogenesis, the following hypotheses exist: activation of astrocytes and microglia to release pro-inflammatory cytokines, aggregation of tau protein, and COVID-19 entry in the brain can trigger an autoimmune reaction. There are currently no specific tests to detect brain fog or any specific cognitive rehabilitation methods. However, a healthy lifestyle can help reduce symptoms to some extent, and symptom-based clinical management is also well suited to minimize brain fog side effects in COVID-19 patients. Therefore, this review discusses mechanisms of SARS-CoV-2 pathogenesis that may contribute to brain fog, as well as some approaches to providing therapies that may help COVID-19 patients avoid annoying brain fog symptoms.

Atrial fibrillation is associated with neurocognitive comorbidities such as stroke and dementia. Evidence suggests that rhythm control-especially if implemented early-may reduce the risk of cognitive decline. Catheter ablation is highly efficacious for restoring sinus rhythm in the setting of atrial fibrillation; however, ablation within the left atrium has been shown to result in MRI-detected silent cerebral lesions. In this state-of-the-art review article, we discuss the balance of risk between left atrial ablation and rhythm control. We highlight suggestions to lower the risk, as well as the evidence behind newer forms of ablation such as very high power short duration radiofrequency ablation and pulsed field ablation.

Adolescence is a transitional stage marked by continued brain development. This period is accompanied by physical and neurochemical modifications in the shape and function of the hippocampus, prefrontal cortex, and other limbic system structures. Brain maturation during adolescence, which is typically governed by intrinsic factors, can be dramatically altered by environmental influences such as drugs and alcohol. Unlike many other addictive substances, binge drinking is very common and normative among teenagers and young adults. This repeated pattern of excessive alcohol consumption in adolescents has been shown to cause behavioral changes and neurocognitive impairments that include increased anxiety, risky decision-making, and learning deficits, which could lead to the development of alcohol use disorder (AUD). This manuscript highlights factors that lead to adolescent binge drinking, discusses maturational changes that occur in an adolescent\'s brain, and then evaluates the effect of adolescent alcohol consumption on brain structure, function, and neurocognitive abilities in both human studies and animal models. The impact of gender/sex and COVID-19 are briefly discussed. Understanding the factors that promote the onset of adolescent binge drinking and its undesirable consequences could serve as a catalyst for developing therapeutic agents that would decrease or eradicate the damaging effects of alcohol on an adolescent brain.

Addison\'s disease (AD) entails a chronic insufficient production of gluco- and mineralocorticoids. Fatigue and decreased quality of life are frequently reported symptoms, but little is known about its effects on cognition. This study aims to explore the existence of cognitive impairment in patients with AD and the influence of treatment regimens. We conducted a systematic review. Inclusion criteria were met by 10 articles, most of them ranked as intermediate quality. Three studies analyzed the relationship between AD and cognitive impairment; one explored the effect of delaying treatment showing no effect on cognitive performance, and another one studied the effect of fludrocortisone treatment. Episodic memory was the most frequent cognitive domain impaired across studies, in comparison to healthy controls. Two papers investigated the relationship between impaired sleep quality and poor cognitive performance. Two studies related cognitive impairments with hypocortisolism-derived brain neuroglycopenia. Two studies investigated the effect of DHEA substitution. In conclusion, patients exhibit a moderately reduced performance in verbal learning. The pathophysiology of this impairment is likely multifactorial. Future studies should include larger sample sizes, the use of comprehensive and multi-domain neuropsychological and behavioral protocols, and neuroimaging.

As one of the basic elements in acoustic events, timbre influences the brain collectively with other factors such as pitch and loudness. Research on timbre perception involve interdisciplinary fields, including physical acoustics, auditory psychology, neurocognitive science and music theory, etc. From the perspectives of psychology and physiology, this article summarizes the features and functions of timbre perception as well as their correlation, among which the multi-dimensional scaling modeling methods to define timbre are the focus; the neurocognition and perception of timbre (including sensitivity, adaptability, memory capability, etc.) are outlined; related experiment findings (by using EEG/ERP, fMRI, etc.) on the deeper level of timbre perception in terms of neural cognition are summarized. In the meantime, potential problems in the process of experiments on timbre perception and future possibilities are also discussed. Thought sorting out the existing research contents, methods and findings of timbre perception, this article aims to provide heuristic guidance for researchers in related fields of timbre perception psychology, physiology and neural mechanism. It is believed that the study of timbre perception will be essential in various fields in the future, including neuroaesthetics, psychological intervention, artistic creation, rehabilitation, etc.

Youth at clinical high-risk (CHR) for psychosis present with neuropsychological impairments relative to healthy controls (HC), but whether these impairments are distinguishable from those seen among putatively lower risk peers with other psychopathology remains unknown. We hypothesized that any excess impairment among CHR cohorts beyond that seen in other clinical groups is minimal and accounted for by the proportion who transition to psychosis (CHR-T).
We performed a systematic review and meta-analysis of studies comparing cognitive performance among CHR youth to clinical comparators (CC) who either sought mental health services but did not meet CHR criteria or presented with verified nonpsychotic psychopathology.
Twenty-one studies were included representing nearly 4000 participants. Individuals at CHR showed substantial cognitive impairments relative to HC (eg, global cognition: g = -0.48 [-0.60, -0.34]), but minimal impairments relative to CC (eg, global cognition: g = -0.13 [-0.20, -0.06]). Any excess impairment among CHR was almost entirely attributable to CHR-T; impairment among youth at CHR without transition (CHR-NT) was typically indistinguishable from CC (eg, global cognition, CHR-T: g = -0.42 [-0.64, -0.19], CHR-NT: g = -0.09 [-0.18, 0.00]; processing speed, CHR-T: g = -0.59 [-0.82, -0.37], CHR-NT: g = -0.12 [-0.25, 0.07]; working memory, CHR-T: g = -0.42 [-0.62, -0.22], CHR-NT: g = -0.03 [-0.14, 0.08]).
Neurocognitive impairment in CHR cohorts should be interpreted cautiously when psychosis or even CHR status is the specific clinical syndrome of interest as these impairments most likely represent a transdiagnostic vs psychosis-specific vulnerability.