NeuroSci最新文献

Until recently, research on the pathobiological substrate of psychosis has been focused on neurotransmitter perturbations. However, this scope has expanded to include new fields, such as the immune/redox/metabolic/neuroendocrine/stress systems. Indeed, basic research in the stress field showed that the systems above can represent components of a general inflammatory process as tightly interconnected as a Gordian knot. Based on the inflammatory hypothesis concerning the psychosis etiopathology, the findings from psychotic cohort studies on each one of the immune/redox/metabolic/neuroendocrine/stress systems have started to accumulate. The evidence favors the involvement of these systems in the formation of the pathobiological psychotic substrate, yet little is known concerning their interplay. This review attempts to establish a frame of reference for the evidence concerning intersystemic interactions, starting with the basic research on the stress field and expanding to clinical studies with psychosis cohorts, hoping to instigate new avenues of research.

The extracranial-intracranial (EC-IC) bypass is a complex neurosurgical procedure performed for cerebral flow augmentation or flow replacement. Anesthetic management of these patients poses significant challenges due to the delicate balance required to maintain cerebral perfusion, often complicated by extensive cardiovascular comorbidities. Despite the complexity of these cases, current literature offers limited guidance on optimal anesthetic strategies. At our high-volume academic institution, we developed a standardized multimodal anesthetic protocol aimed at achieving intraoperative hemodynamic stability and facilitating timely postoperative emergence. A dedicated team of neuroanesthesiologists manages these cases in constant communication with the surgical team, ensuring real-time adjustments aligned with surgical needs and patient physiology. Our experience highlights the importance of individualized anesthetic planning and interdisciplinary coordination. Given the scarcity of published data and the specialized nature of EC-IC bypass procedures, we believe our institutional approach may serve as a useful reference for other centers, particularly those with limited exposure to this complex patient population, and lay the foundation for future prospective trials on optimal anesthetic care for this patient population.

Background: attention-deficit/hyperactivity disorder (ADHD) and Alzheimer's disease (AD) are distinct neurological conditions that may share genetic and molecular underpinnings. ADHD, a neurodevelopmental disorder, affects approximately 5% of children and 3% of adults globally, while AD, a neurodegenerative disorder, is the leading cause of dementia in older adults. Emerging evidence suggests potential overlapping contributors, including pathways related to synaptic plasticity, neuroinflammation, and oxidative stress.

Methods: this systematic review investigated potential genetic predispositions linking Attention-Deficit/Hyperactivity Disorder (ADHD) and Alzheimer's Disease (AD). Following PRISMA guidelines, a search was conducted in Web of Science, Embase, PsycINFO, and PubMed using keywords related to ADHD, AD, and genetic factors. Studies included were original human studies utilizing genetic analyses and ADHD polygenic risk scores (PRS), with AD confirmed using established diagnostic criteria. Exclusion criteria comprised non-original studies, animal research, and articles not addressing genetic links between ADHD and AD. Screening was conducted with Rayyan software (version 1.4.3), assessing relevance based on titles, abstracts, and full texts.

Results: . The search identified 1450 records, of which 1092 were screened after duplicates were removed. Following exclusions, two studies met inclusion criteria. One study analyzed ADHD-PRS in 212 cognitively unimpaired older adults using amyloid-beta (Aβ) PET imaging and tau biomarkers. The findings revealed that ADHD-PRS was associated with progressive cognitive decline, increased tau pathology, and frontoparietal atrophy in Aβ-positive individuals, suggesting that ADHD genetic liability may exacerbate AD pathology. Another study assessed ADHD-PRS in a cohort of 10,645 Swedish twins, examining its association with 16 somatic conditions. The results showed modest risk increases for cardiometabolic, autoimmune, and neurological conditions, with mediation effects through BMI, education, tobacco use, and alcohol misuse, but no direct link between ADHD-PRS and dementia.

Discussion and conclusions: this review highlights preliminary but conflicting evidence for a genetic intersection between ADHD and AD. One study suggests that ADHD genetic liability may exacerbate AD-related pathology in Aβ-positive individuals, whereas another large registry-based study finds no direct link to dementia, with associations largely mediated by lifestyle factors. The potential ADHD-AD relationship is likely complex and context-dependent, influenced by biomarker status and environmental confounders. Longitudinal studies integrating genetics, biomarkers, and detailed lifestyle data are needed to clarify this relationship.

Background: The consequences of median nerve compression at the carpal tunnel level require a precise diagnostic evaluation before a frequently applied surgical intervention. Positive Tinel or Phalen signs are not always related to abnormal results in electroneurographic examinations of sensory and motor nerve fibers, which are intended to confirm final diagnoses, thereby confusing both surgeons and neurophysiologists. In the face of contradictory data, this study aims to reinvestigate these correlations in a randomly chosen population of patients with a primary diagnosis of carpal tunnel syndrome (CTS).

Methods: Seventy-five randomly chosen patients with clinically detected CTS underwent neurophysiological studies of median nerve sensory (SNAP) and motor (CMAP) fibers conduction at the wrist. Both the median and ulnar nerves were assessed to reduce the risk of misinterpretation related to anatomical variations.

Results: This study provides evidence on the relatively high utility of Phalen's test in the early clinical detection of CTS within a general population of patients, whose positive results moderately correlate (rho = -0.327) with abnormalities in amplitudes rather than the distal latency parameters of SNAP recordings. The axonal injury type is more distinct than slowing-down impulses at the wrist following compression of the sensory nerve fibers in the early course of CTS. Positive Tinel's test results are useful in diagnosing CTS patients with advanced axonal and demyelinating changes in the motor fibers at the wrist, which weakly correlate with prolonged latency and decreased amplitude in SNAP recordings (rho = -0.214 and rho = -0.235, respectively), but not with abnormalities in recordings of both amplitudes and latencies in CMAP electroneurography.

Conclusions: The correlations between clinical signs and neurophysiological findings in CTS indicate that provocative tests, such as Phalen's and Tinel's, have limited diagnostic value, demonstrating only weak-to-moderate associations with neural conduction parameters. A positive Tinel's sign should be regarded mainly as a marker of severe or chronic sensory impairment, often accompanied by motor fibers involvement in advanced pathological stages, rather than as an indicator of motor damage alone. Nerve conduction studies remain essential for confirming CTS, assessing its severity, and guiding treatment decisions, including surgical qualification. The presented correlation of clinical and functional neurophysiological results in CTS diagnosis allows us not only to specify the source and severity of the pathology of the median nerve fibers but also may influence the personalization of physiotherapeutic and surgical treatments.

Background: Sciatic nerve schwannomas are rare benign tumors that can develop along the nerve's course, from the pelvis to the thigh. Giant schwannomas, defined as those exceeding 5 cm, are particularly rare and may alter the tumor's anatomical relationship with the nerve, impacting surgical strategy.

Methods: A PRISMA 2020-compliant systematic review was conducted using the terms ("sciatic" AND "schwannoma") for publications from 2000 to October 2024. Of 166 identified articles, we excluded those lacking giant schwannoma cases or involving syndromic associations. We also report a novel case from our center.

Results: Our patient, a 35-year-old woman, presented with tingling and discomfort while sitting, localized to the left thigh, without radicular pain or motor deficits. MRI revealed a 14 × 7 cm mass. This is, to our knowledge, the first reported case of a giant solitary sciatic schwannoma of these dimensions located exclusively in the thigh, resected via intracapsular dissection with nerve monitoring, that was fully documented and reported. The review yielded 22 relevant articles, most involving pelvic or pelvic-thigh junction locations, with low recurrence rates.

Conclusions: Giant sciatic schwannomas may be asymptomatic and slow-growing. This case is notable for tumor's location, large size, and successful nerve-sparing surgical outcome.

Patients with Parkinson's disease frequently suffer from complicated anxiety disorders that are entwined with their attitudes and behaviors. In regard to this population, cognitive behavioral therapy (CBT) has been attracting an increasing amount of attention as a potentially effective treatment for mental health issues like anxiety. CBT helps patients manage stress and improve their psychological well being through behavioral, relaxation, and cognitive techniques. Even though there is already evidence that cognitive behavioral therapy (CBT) can dramatically reduce psychological symptoms in Parkinson's patients, more thorough research is required to determine its exact role in comprehensive anxiety treatment and prove its long-term efficacy. The purpose of this study is to examine the body of research on the use of cognitive behavioral therapy (CBT) to treat anxiety in patients with Parkinson's disease, looking at its limitations and challenges as well as clinical characteristics, advantages, and possible behavioral and psychological impacts.

Traumatic brain injury (TBI), even when mild, has been associated with the presence of depression. Depression is a mood disorder characterized by persistent negative thoughts and sadness and is challenging to treat due to the multiple mechanisms involved in its pathophysiology, including increased nitric oxide (NO) levels. There are no completely safe and effective pharmacological strategies to treat this disorder. Mucuna pruriens (MP) has been shown to possess neuroprotective properties by regulating inflammatory responses and nitric oxide synthase activity. In this study, we evaluated the antidepressant-like effect of MP in male Wistar rats with induced mild traumatic brain injury (mTBI). MP extract (50 mg/kg i.p.) was administered immediately after mTBI and every 24 h for five days. We used the rats' preference for sucrose consumption to assess the presence of depression-like behavior and analyzed the nitrite and nitrate levels in their cerebral cortex, striatum, midbrain, and nucleus accumbens. Untreated animals with mTBI showed a reduced preference for sucrose than those treated with MP, whose preference for sucrose was similar to that of sham animals. Increased nitrite and nitrate levels were observed in different brain regions in the TBI subjects; however, this increase was not observed in MP-treated animals. MP reduces behavior associated with depression and the brain NO levels in rats with mTBI.

The antipsychotic drug haloperidol is found on the WHO list of essential drugs. In vitro, haloperidol demonstrates binding affinity for various receptors, including histamine H₂ receptors (H₂Rs). Several cardiac effects of haloperidol are known, but it remains unclear whether H₂Rs are involved. Here, the hypothesis was tested that haloperidol has the potential to act as either an agonist or an antagonist of human cardiac H₂Rs. The contractile effects of haloperidol were studied in isolated left and right atrial preparations from transgenic mice overexpressing human H₂Rs in the heart (H₂-TG), and compared to human atrial preparations from adult patients. Haloperidol reduced the histamine-stimulated force of contraction in the human atrial preparations as well as the histamine-stimulated force of contraction and beating rate in the left and right atrial preparations from the H₂-TG, respectively. Moreover, haloperidol reduced the isoprenaline-stimulated force of contraction in the human atrial preparations. In the wild-type mouse preparations, haloperidol only reduced the isoprenaline-stimulated beating rate in the right atria, but not the force in the left atria. Principally, haloperidol is capable of acting as an antagonist of both H₂Rs and β-adrenoceptors in the human heart. However, the effects are only relevant at very high doses of haloperidol, which are never or seldom achieved in practice.

Background: Systemic lupus erythematosus (SLE) is reported to be the most common rheumatological disorder associated with catatonia. To date, reports on catatonia manifestations in SLE patients are uncommon in published literature, which has often favored a fragmented vision. We performed a narrative review with the aim of identifying all published reports of catatonia in SLE patients to ascertain-in a comprehensive view-its clinical characteristics and to provide useful insights for daily clinical practice.

Methods: Comprehensive literature searches were carried out on 10 March 2025 (subsequently repeated ahead of draft on 6 June) in all main bibliographic databases: MEDLINE and EMBASE (OVID interface); PsycINFO (ProQuest); and PubMed, to capture within-text references. All searches combined controlled (MESH, Entree, and APA Headings) and free-text elements for both areas under observation: systemic lupus erythematosus (SLE) AND catatonia, with primary focus on case reports and series. Sets of findings were reviewed separately by the authors, and the full text of selected items was sourced. Further useful references were retrieved through citation lists.

Results: 39 cases of patients with SLE and catatonia were identified (35 females and 4 males), with a mean age of 22.64 years (range 11-46). Only three patients were over the age of 40; a total of 10 had catatonia at the same time of SLE onset and 5 within a month of SLE diagnosis. Antiphospholipid and anti-ribosomal P protein antibodies were rarely identified. Almost all the patients improved following treatment with lorazepam and/or electroconvulsive therapy. Only one case of malignant catatonia was reported. Finally, a large number of patients were Asian or Afro-American, at least in the reports where ethnicity was specified.

Conclusions: Catatonia can occur in patients with SLE, and it may be its first clinical manifestation, especially in young patients. Its prognosis is mostly favorable.

Advanced glycation end products (AGEs) are reactive compounds formed through non-enzymatic glycation in a process known as the Maillard reaction. While humans produce AGEs endogenously, these compounds can also enter the body through dietary sources, food preparation methods, and exposure to agricultural and food-related chemicals. AGEs can accumulate within cells and impair cellular function. In addition, when AGEs bind to receptors for advanced glycation end products (RAGE), they activate intracellular signaling pathways that promote the generation of reactive oxygen species (ROS), mitochondrial dysfunction, and inflammation. Sustained AGE-RAGE signaling drives chronic inflammation contributing to the development of various ailments, including neurodegenerative diseases. This review examines AGE formation, metabolism, and accumulation, with an emphasis on dietary sources as modifiable contributors to AGE-RAGE mediated pathology. We highlight the need for further research on dietary AGE restriction as a potential strategy to prevent or slow the progression of neurodegenerative and neuroinflammatory disorders.