European Neurology最新文献

Background: Over the past decades, marked progress has been made in detecting vascular dementia (VD) both through maturation of diagnostic concepts and advances in brain imaging, especially MRI. We summarized the imaging, genetic, and pathological features of VD in this review.

Summary: It is a challenge for the diagnosis and treatment of VD, particularly in patients where there is no evident temporal relation between cerebrovascular events and cognitive dysfunction. In patients with cognitive dysfunction with poststroke onset, the etiological classification is still complicated.

Key messages: In this review, we summarized the clinical, imaging, and genetic as well as pathological features of VD. We hope to offer a framework to translate diagnostic criteria to daily practice, address treatment, and highlight some future perspectives.

Introduction: Ingesting some foods can trigger headache attacks in migraine patients. Diet-sourced citrulline activates the l-arginine-nitric oxide pathway, acting on the pathophysiology of migraine.

Methods: The study was a clinical trial, interventional, controlled, and with group comparison. The sample was non-random, composed of 38 volunteers with migraine and 38 without headache (control). Both groups ingested a portion of watermelon to determine the onset of headache attacks. Before and after ingesting watermelon, they underwent blood collections to determine serum nitrite levels.

Results: There were 38 volunteers diagnosed with migraine without aura and 38 controls, whose mean age was, respectively, 22.4 ± 1.5 and 22.9 ± 3.1 years (p = 0.791). Headache was triggered by watermelon ingestion after 124.3 ± 20.5 min of ingestion in 23.7% (9/38) of the migraine volunteers and in none of the controls (p = 0.002). There was an increase in serum nitrite levels, both in migraine volunteers (23.4%) and in the control group (24.3%), after watermelon ingestion. This difference was significant (p < 0.001).

Discussion: Watermelon ingestion triggered headache attacks in migraine patients and increased serum nitrite levels, attesting to a possible activation of the l-arginine-nitric oxide pathway.

Introduction: Clinical prediction rule (CPR) using decision tree analysis is able to show the branching of the variables under consideration in a clear, hierarchical manner, including specific reference values, which can be used as classifiers in clinical practice. However, CPRs developed by decision tree analysis for predicting the degree of independent living of patients with thoracic spinal cord injury (SCI) are few. The purpose of this study was to develop a simplified CPR for prognosticating dependent daily living in patients with thoracic SCI.

Methods: We extracted data on patients with thoracic SCI from a national multicenter registry database, the Japan Rehabilitation Database (JRD). All patients with thoracic SCI who were hospitalized within 30 days after the injury onset were included. The independent living was categorized in the JRD as follows: independent socially, independent at home, needing care at home, independent at the facility, and needing care at the facility. These categories were used as the objective variables in classification and regression tree (CART) analysis. The CART algorithm was applied to develop the CPR for predicting whether patients with thoracic SCI achieve independent living at hospital discharge.

Results: Three hundred ten patients with thoracic SCI were included in the CART analysis. The CART model identified, in a hierarchical order, patient's age, residual function level, and the bathing sub-score of Functional Independence Measure as the top three factors with moderate classification accuracy and area under the curve.

Conclusions: We developed a simplified, moderately accurate CPR for predicting whether patients with thoracic SCI achieve independent living at hospital discharge.

The first author is a left-handed, 51-year-old nephrologist who experienced a neurologic event. She underwent neurosurgery complicated by hemorrhage. Postoperatively, she developed persistent vertigo and unilateral tongue pain which persisted for over 5 years. Early neuroimaging revealed expected encephalomalacia but no neuroanatomical basis for her symptoms. A functional neurological disorder was suspected, and she was seen by several psychiatrists and psychotherapists. However, she suspected a neuroanatomical lesion would better explain her unrelenting symptoms. After seeing many neurologists, a neuroanatomical diagnosis was finally made. The theory and practice of medicine mandate that subjective complaint guides the modality and interpretation of objective evidence. The final neurologist knew where on neuroimaging to look because she was guided by the patient's complaints - vertigo and unilateral tongue pain. In this case, detailed scrutiny of neuroimaging by a neurologist, after encephalomalacia and gliosis were fully completed, gave a more accurate neuroanatomical diagnosis and a more realistic prognosis.

Introduction: Currently, it is still controversial to treat stroke with ticagrelor alone. The purpose of our study was to systematically review and analyze the efficacy and safety of ticagrelor on cerebrovascular outcomes in patients with vascular risk factors.

Methods: The PubMed, Cochrane Library, and Embase databases were systematically searched using the keywords stroke, ticagrelor, clopidogrel, and aspirin to identify randomized controlled trials (RCTs). Primary outcomes included reported stroke, ischemic stroke, and complex events; the secondary outcome was hemorrhagic stroke. The safety outcomes included major bleeding events, major or minor bleeding, and intracranial bleeding. The pooled odds ratio (OR), hazard ratios (HRs), and 95% confidence interval (CI) were calculated. We used I2 statistics to assess statistical heterogeneity.

Results: This meta-analysis included 15 RCTs involving 63,865 patients. Compared to the control group, ticagrelor reduced the risk of stroke (OR: 0.90; 95% CI: 0.81-0.99, p = 0.03; I2 = 3%), ischemic stroke (OR: 0.81; 95% CI: 0.74-0.90, p < 0.0001; I2 = 0%). Ticagrelor was not associated with an increased risk of all-cause mortality (OR: 0.94; 95% CI: 0.84-1.06, p = 0.31; I2 = 62%), major bleeding (OR: 1.06; 95% CI: 0.97-1.15, p = 0.20; I2 = 17%), hemorrhagic strokes (OR: 1.22, 95% CI: 0.76-1.96, p = 0.41; I2 = 0%), and intracranial hemorrhage (OR: 1.06; 95% CI: 0.78-1.43, p = 0.71; I2 = 12%). There was an increased risk of major or minor bleeding with ticagrelor compared to the control group (OR: 1.40; 95% CI: 1.19-1.66, p < 0.0001; I2 = 56%). Additional analyses demonstrated that ticagrelor reduced the risk of incident recurrent stroke (HR: 0.83; 95% CI: 0.75-0.93, p = 0.0009; I2 = 0%), recurrent ischemic stroke (HR: 0.79; 95% CI: 0.71-0.89, p < 0.0001; I2 = 0%) among patients with a history of acute ischemic stroke (AIS) or transient ischemic attack (TIA). There were no significant differences in safety outcomes.

Conclusion: Ticagrelor is slightly better than clopidogrel and aspirin in preventing stroke, especially ischemic stroke, with significant safety risks. For patients with a history of AIS/TIA, the use of ticagrelor was superior to the use of clopidogrel or aspirin in reducing the risk of subsequent stroke. We believe that ticagrelor is a potential alternative to aspirin or clopidogrel in some cases, especially for patients with CYP2C19 deficiency.

Background: Integrin β1, as a member of the adhesion molecule family, is widely distributed in many kinds of cells and participates in multiple biological functions of the nervous system, including cytoskeleton reorganization, axon growth, and inflammatory injury.

Summary: After nervous system injury, integrin β1 expressed by microglia is mainly involved in promoting inflammatory damage; integrin β1 expressed by astrocytes plays an important role in axon regeneration; integrin β1 expressed by endothelial cells mainly participates in vascular remodeling. We concluded that the function of integrin β1 depends on the location of the receptor cells. The mechanism of integrin β1, which is involved in the inflammatory response of immune regulatory cells and affects the axonal regeneration of neuronal cells, is the key to explore the repair after nervous system injury. The development of drugs targeting integrin β1 is expected to bring a breakthrough in the treatment of nervous system injury.

Key messages: This paper expounds the important role of integrin β1 in neurons of the nervous system and emphasizes the central role of integrin β1 in regulating non-neuronal cells after nervous system damage.

Introduction: Migraine is a neurovascular disorder and is clinically characterized by episodic attacks of mild to severe headaches. Due to the involvement of multiple environmental and genetic factors, it has become a much more complex neurological condition to understand. Apart from the environmental variables, a plethora of genes have been implicated, and one such example is ESR1. The present study was focused to find out the association of two important polymorphisms, namely, PvuII and XbaI of the ESR1 with migraine in the population of Jammu and Kashmir (UT).

Methods: The PCR-RFLP genotyping method was utilized to detect PvuII and XbaI polymorphism, and the result was confirmed by statistical analysis.

Results: Although we did not find a signification association of ESR-PvuII polymorphism with migraine susceptibility {OR: 1.14 at 95% CI [0.76-1.71] (p value 0.5)}, a strong association was found with the clinical subtype of migraine; migraine with aura (MA) {OR: 2.014 at 95% CI [1.069-3.792] (p value 0.028)}. Furthermore, a significant association of ESR-XbaI polymorphism was observed with migraine {OR: 1.908 at 95% CI [1.252-2.907] (p value 0.002) and its both clinical subtypes; migraine without aura (MO) {OR: 1.870 at 95% CI [1.186-2.950] (p value 0.006)} and MA {OR: 2.014 at 95% CI [1.069-3.792] (p value 0.028)}.

Conclusion: In conclusion, ESR1-XbaI polymorphism is significantly associated with migraine risk including both subtypes (MA and MO) in the North Indian population of Jammu.

A solitary pontine lesion (SPL) is a single brainstem lesion on the trigeminal nerve pathway without any other central nervous system lesion. This research aimed to investigate the demographic and clinical features of nonpainful TNO patients with SPL and identify the most frequently affected anatomical areas using lesion mapping techniques. Demographic and clinical features were retrospectively reviewed from the patients' charts. Brain lesions were mapped using MRIcroGL software. The study included 6 patients (three females and three males) with an SPL. The median age of the patients was 57 (range: 46-68) years. Cranial MRI displayed lesions in the dorsolateral pons and the cerebellar peduncle. The lesion mapping revealed that the lesions were on the trigeminal nerve pathway. SPL is an uncommon cause of TNO. Nonpainful SPL patients have demographic, clinical, and radiological features similar to those of painful SPL patients. The lesion mapping showed that the same brainstem areas are affected in painful and nonpainful SPL patients.

Introduction: Many clinical studies reported the coexistence of Alzheimer's disease (AD) and multiple sclerosis (MS), but the common molecular signature between AD and MS remains elusive. The purpose of our study was to explore the genetic linkage between AD and MS through bioinformatic analysis, providing new insights into the shared signatures and possible pathogenesis of two diseases.

Methods: The common differentially expressed genes (DEGs) were determined between AD and MS from datasets obtained from Gene Expression Omnibus (GEO) database. Further, functional and pathway enrichment analysis, protein-protein interaction network construction, and identification of hub genes were carried out. The expression level of hub genes was validated in two other external AD and MS datasets. Transcription factor (TF)-gene interactions and gene-miRNA interactions were performed in NetworkAnalyst. Finally, receiver operating characteristic (ROC) curve analysis was applied to evaluate the predictive value of hub genes.

Results: A total of 75 common DEGs were identified between AD and MS. Functional and pathway enrichment analysis emphasized the importance of exocytosis and synaptic vesicle cycle, respectively. Six significant hub genes, including CCL2, CD44, GFAP, NEFM, STXBP1, and TCEAL6, were identified and verified as common hub genes shared by AD and MS. FOXC1 and hsa-mir-16-5p are the most common TF and miRNA in regulating hub genes, respectively. In the ROC curve analysis, all hub genes showed good efficiency in helping distinguish patients from controls.

Conclusion: Our study first identified a common genetic signature between AD and MS, paving the road for investigating shared mechanism of AD and MS.