Neurology International最新文献

{"title":"Development of a Novel Method of Spinal Electrophysiological Assessment via Intrathecal Administration at Analgesic Doses.","authors":"Daisuke Uta, Takuya Yamane, Sosuke Yoneda, Erika Kasai, Toshiaki Kume","doi":"10.3390/neurolint17050078","DOIUrl":"10.3390/neurolint17050078","url":null,"abstract":"<p><p><b>Background/Objectives</b>: Chronic pain is a significant global health challenge and is associated with diverse conditions, such as diabetic neuropathic pain and spinal stenosis. Understanding the mechanisms of pain transmission is crucial, for both the peripheral and central pathways. However, there are limitations in spinal electrophysiological techniques in terms of the injection method. Traditional methods such as spinal injections may differ in the distributions and concentrations of drugs compared with intrathecal administration during the behavior test. So, we developed a new intrathecal administration method for electrophysiological recordings. <b>Methods</b>: Sprague-Dawley rats were injected with lidocaine intrathecally, and the analgesic effect was evaluated by the von Frey test. In vivo extracellular single-unit recordings of the superficial dorsal horn neurons were performed following a newly developed technique. Lidocaine was intrathecally injected into the arachnoid membrane after laminectomy. After that, the neural responses in the superficial dorsal horn were measured. <b>Results</b>: Newly developed intrathecally administered dye reached the spinal cord and the cauda equina. Intrathecally administrated lidocaine increased the paw withdrawal threshold and suppressed spinal neuronal firing. This suppression correlated with increases in paw withdrawal thresholds. <b>Conclusions</b>: This innovative method provides insights into the central effects of analgesics, which will help the development of therapies for chronic pain.</p>","PeriodicalId":19130,"journal":{"name":"Neurology International","volume":"17 5","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12114472/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144151132","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Medications for Managing Central Neuropathic Pain as a Result of Underlying Conditions-A Systematic Review.","authors":"Bjarke Kaae Houlind, Henrik Boye Jensen","doi":"10.3390/neurolint17050077","DOIUrl":"10.3390/neurolint17050077","url":null,"abstract":"<p><p><b>Background:</b> This systematic review assessed the current literature regarding the analgesic treatment of central neuropathic pain (CNP) in central nervous system (CNS) conditions, such as spinal cord injuries, multiple sclerosis, post-stroke disorders, and Parkinson's disease. The aim of this systematic review was to compare the current algorithmic treatment of CNP, which generally does not discriminate among underlying conditions, with RCTs investigating algorithm-recommended and non-algorithm-recommended drugs for differing underlying conditions. <b>Methods</b>: The PubMed and EMBASE databases were used to identify relevant randomized control trials (RCTs). MeSH terms and EmTree terms were searched as well as free text words in the title/abstract of the studies. A risk of bias tool was used to assess all included studies. <b>Results</b>: A total of 903 RCTs were identified from the initial search. Thirty-eight RCTs published between January 2002 and November 2024 fulfilled all the inclusion criteria and none of the exclusion criteria. The review investigated progressive and stable neurological diseases and conditions with associated CNP. <b>Conclusions</b>: From the majority of the included studies, the current recommended treatment algorithm seems to be effective and safe; however, the underlying condition seems to influence how the patient responds to tier-appropriate medication.</p>","PeriodicalId":19130,"journal":{"name":"Neurology International","volume":"17 5","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12114137/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144151221","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Second Exteroceptive Suppression Period of the Temporalis Muscle Is Altered in Migraine Patients with Allodynia.","authors":"Eugenia Rota, Paolo Immovilli, Marco Aguggia, Maria Gabriella Saracco, Elisabetta Ghiglione, Antonella Melotti, Nicola Morelli","doi":"10.3390/neurolint17050076","DOIUrl":"10.3390/neurolint17050076","url":null,"abstract":"<p><p><b>Background/Objectives:</b> Studying the second exteroceptive suppression period (ES2) of the temporalis muscle may well shed some light on the brainstem neural circuits involved in migraine pathophysiology. It is known that allodynia is related to an increased sensitization of second-/third-order neurons both in the trigeminal nucleus caudalis and sensory thalamus. This pilot, observational study was carried out in the interictal period on female migraineurs with/without allodynia to assess the ES2 of the temporalis muscle compared to controls. <b>Methods:</b> Forty-nine non-consecutive female patients were enrolled, as they met the diagnostic criteria for migraine (26 episodic and 23 chronic), alongside 23 healthy controls. The inclusion criteria encompassed no ongoing pharmacological prophylactic treatment, and the exclusion criteria included any relevant comorbidities. In line with international standards, the exteroceptive suppression of the temporalis muscle activity was registered on the left side, assessing ES2 latency and duration in the interictal period. <b>Results:</b> Allodynia was observed in 24 patients (50%), and 16/24 (67%) were chronic migraineurs. No statistically significant differences in ES2 latency or its duration between the migraine patients and controls were detected. However, there was a significantly longer ES2 duration in allodynic migraineurs than in the controls (<i>p</i> = 0.04; effect size: 0.71) and in allodynic compared to non-allodynic migraineurs (<i>p</i> = 0.04; effect size: 0.63). <b>Conclusions:</b> The increased duration of ES2 observed in allodynic migraineurs might be related to the impaired activity of brainstem circuits and, in our opinion, it seems reasonable to hypothesize that this change may be a neurophysiological correlate of central sensitization in migraine allodynic patients.</p>","PeriodicalId":19130,"journal":{"name":"Neurology International","volume":"17 5","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12114357/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144151235","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Role of Tau in Neuronal Function and Neurodegeneration.","authors":"Gonzalo Emiliano Aranda-Abreu, Fausto Rojas-Durán, María Elena Hernández-Aguilar, Deissy Herrera-Covarrubias, Luis Isauro García-Hernández, María Rebeca Toledo-Cárdenas, Donají Chi-Castañeda","doi":"10.3390/neurolint17050075","DOIUrl":"10.3390/neurolint17050075","url":null,"abstract":"<p><p>Tau protein plays a pivotal role in maintaining neuronal structure and function through its regulation of microtubule stability and neuronal polarity. Encoded by the <i>MAPT</i> gene, Tau exists in multiple isoforms due to alternative mRNA splicing, with differential expression in the central and peripheral nervous systems. In healthy neurons, <i>tau</i> mRNA is selectively localized and translated in axons, a process tightly regulated by untranslated regions (UTRs) and RNA-binding proteins such as HuD and FMRP. Pathologically, Tau undergoes hyperphosphorylation, misfolding, and aggregation, which contribute to neurodegeneration in a range of disorders collectively known as tauopathies. Alzheimer's disease (AD) is the most prevalent tauopathy, where abnormal Tau accumulation in the temporal and frontal lobes correlates with cognitive decline and behavioral symptoms. Other tauopathies, including Progressive Supranuclear Palsy (PSP), Corticobasal Degeneration (CBD), Frontotemporal Dementia with Parkinsonism (FTDP-17), and Pick's disease, are distinguished by the predominance of specific Tau isoforms (3R or 4R), cellular distribution, and affected brain regions. Notably, astroglial tauopathies highlight the pathological role of Tau accumulation in glial cells, expanding the understanding of neurodegeneration beyond neurons. Despite advances in imaging biomarkers (e.g., Tau-PET) and molecular diagnostics, effective disease-modifying therapies for tauopathies remain elusive. Ongoing research targets Tau through immunotherapies, splicing modulators, kinase inhibitors, and antisense oligonucleotides, aiming to mitigate Tau pathology and its deleterious effects. Understanding the multifaceted roles of Tau in neuronal and glial contexts is critical for developing future therapeutic strategies against tauopathies.</p>","PeriodicalId":19130,"journal":{"name":"Neurology International","volume":"17 5","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12114167/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144151232","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cardiac Autonomic Modulation and Cognitive Performance in Community-Dwelling Older Adults: A Preliminary Study.","authors":"Paula Andreatta Maduro, Luiz Alcides Ramires Maduro, Polyana Evangelista Lima, Ana Clara Castro Silva, Rita de Cássia Montenegro da Silva, Alaine Souza Lima Rocha, Maria Jacqueline Silva Ribeiro, Juliana Magalhães Duarte Matoso, Bruno Bavaresco Gambassi, Paulo Adriano Schwingel","doi":"10.3390/neurolint17050074","DOIUrl":"10.3390/neurolint17050074","url":null,"abstract":"<p><strong>Background/objectives: </strong>Cognitive decline has been increasingly linked to cardiac autonomic regulation; however, its specific associations with cognitive domains, such as information processing speed and executive function, remain unclear. This preliminary study examined the relationship between cardiac autonomic modulation and cognitive performance in older adults.</p><p><strong>Methods: </strong>A cross-sectional study was conducted with 101 older adults (aged ≥60 years) attending a university hospital outpatient clinic. Participants were classified as without cognitive impairment (WCI) or cognitively impaired and not demented (CIND) based on neuropsychological assessments. Heart rate variability (HRV) was measured at rest, focusing on the time-domain parameters (SDNN, rMSSD, and pNN50). Trail making test parts A and B (TMT-A and TMT-B) were used to assess information processing speed and executive function, respectively. Analyses of covariance (ANCOVAs) were performed, adjusting for confounding variables including age, sex, and comorbidities.</p><p><strong>Results: </strong>Participants in the CIND group had significantly lower HRV indices than those in the WCI group (SDNN, <i>p</i> < 0.05, <i>d</i> = 0.44; rMSSD, <i>p</i> < 0.05, <i>d</i> = 0.39; pNN50, <i>p</i> < 0.05, <i>d</i> = 0.40), indicating reduced parasympathetic modulation. Higher HRV values were observed in individuals with preserved processing speed and executive function. Specifically, pNN50 was significantly associated with processing speed (<i>p</i> = 0.04), and SDNN was significantly correlated with executive function (<i>p</i> = 0.02). These associations persisted even after adjusting for confounding factors.</p><p><strong>Conclusions: </strong>Reduced cardiac autonomic modulation, especially lower parasympathetic activity, is significantly associated with cognitive impairment in older adults. Lower pNN50 values were correlated with slower information processing speed, and lower SDNN was associated with poorer executive function. These findings support the potential use of HRV as a physiological biomarker to detect cognitive changes during ageing.</p>","PeriodicalId":19130,"journal":{"name":"Neurology International","volume":"17 5","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12113867/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144150187","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impaired DNAJB2 Response to Heat Shock in Fibroblasts from a Neuropathy Patient with <i>DNAJB2/HSJ1</i> Mutation: Cystamine as a Potential Therapeutic Intervention.","authors":"Raj Kumar Pradhan, Nikolas G Kinney, Brigid K Jensen, Hristelina Ilieva","doi":"10.3390/neurolint17050073","DOIUrl":"10.3390/neurolint17050073","url":null,"abstract":"<p><p><b>Background and Objectives:</b> Neuropathy is a debilitating disorder characterized by peripheral nerve dysfunction and damage to sensory, motor, and autonomic neurons and their axons. While homozygous mutations in DNAJB2/HSJ1 have been linked to early-onset neuropathy, a heterozygous DNAJB2 c.823+6C>T was discovered in an adult patient with severe sensory-motor polyneuropathy. This mutation is predicted to affect both isoforms of the protein. DNAJB2 (HSP40), a key member of the heat shock protein family, plays a critical role in cellular protection and stress, including response to heat shock. DNAJB2 traffics unfolded proteins to another heat shock protein, HSP70, and activates its ATPase activity to result in a correctly folded protein(s). In this study, we aimed to investigate the effects of the heterozygous DNAJB2 c.823+6C>T mutation on the stress response of DNAJB2 in fibroblasts obtained from the neuropathy patient. <b>Methods:</b> The fibroblasts were subjected to one hour of heat shock at 42 °C, and the time course of expression levels of DNAJB2 was established. Additionally, we evaluated the therapeutic efficacy of Cystamine, which has been shown to modulate DNAJB2 levels in cellular and animal models of Huntington's disease. <b>Results:</b> Our results revealed reduced baseline levels of DNAJB2 between the mutant and control fibroblasts. Importantly the mutant cells exhibited a diminished response to heat shock. Thus, the mutation affects the upregulation of DNAJB2 under stress, possibly contributing to the pathogenesis of sensory-motor polyneuropathy. A 48-h pretreatment with 150 μM of Cystamine increased the levels of DNAJB2 in both the control and patient's fibroblasts. <b>Conclusions:</b> To the best of our knowledge, this is the first study to explore this mutant form of DNAJB2 in neuropathy. The study demonstrated that the heterozygous DNAJB2 c.823+6C>T mutation leads to impaired DNAJB2 response to heat shock in the fibroblasts. Cystamine showed promise in restoring DNAJB2 expression, highlighting the need for further research into targeted therapeutic strategies for DNAJB2-related disorders.</p>","PeriodicalId":19130,"journal":{"name":"Neurology International","volume":"17 5","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12113656/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144151216","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cerebellar Contributions to Hypokinetic Symptoms in an Acute Lesion Parkinsonism Model.","authors":"Cristofer Zarate-Calderon, Gerardo Marín, Iraís Viveros-Martínez, Lizbeth Vásquez-Celaya, Porfirio Carrillo-Castilla, Gonzalo E Aranda-Abreu, Donaji Chi-Castañeda, Luis I García","doi":"10.3390/neurolint17050072","DOIUrl":"10.3390/neurolint17050072","url":null,"abstract":"<p><p><b>Background:</b> Parkinsonism, characterized by motor symptoms, is typically attributed to basal ganglia dysfunction. Recent evidence suggests that the cerebellum may also influence these symptoms. This study investigated Crus II, the dentate nucleus (DN), and the inferior olive (IO) in a rat model of parkinsonism induced by a bilateral ventrolateral striatal (VLS) lesion. <b>Materials and Methods:</b> Twenty-four male <i>Wistar</i> rats were divided into control (<i>n</i> = 12) and experimental (<i>n</i> = 12) groups. Monopolar electrodes were implanted in target structures. The experimental group received a bilateral VLS lesion. Animals underwent four weekly sessions of electrophysiological recordings and blind behavioral assessments (resting, grooming, locomotion, rearing, sniffing) via video tracking. Power spectral density (PSD) in the 300-500 Hz band was computed. Statistical analyses included Mann-Whitney U, Friedman with Wilcoxon post hoc, and Spearman correlation tests. <b>Results:</b> During weeks one and two, there were significant PSD increases in the experimental group compared to the control, particularly in Crus II-grooming (<i>p</i> = 0.005), locomotion (<i>p</i> = 0.007), and rearing (<i>p</i> = 0.026); in IO-sniffing (<i>p</i> = 0.0167); and in DN-grooming (<i>p</i> < 0.001) and locomotion (<i>p</i> = 0.0008). Additionally, intragroup analysis revealed significant PSD elevations relative to baseline in these structures. Significant correlations were observed only for grooming (negative correlations) and sniffing (positive correlations) across all cerebellar regions. <b>Conclusions:</b> These findings suggest compensatory cerebellar hyperactivity induced by VLS lesion, potentially modulating hypokinetic symptoms and highlighting dynamic network interactions. Interpretation warrants caution due to limitations inherent to the acute lesion model and experimental duration.</p>","PeriodicalId":19130,"journal":{"name":"Neurology International","volume":"17 5","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12113700/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144151124","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neurological Sequelae of Acute Hydrogen Sulfide Poisoning: A Literature Review, Controversies, and Knowledge Gaps.","authors":"Wilson K Rumbeiha, Dong-Suk Kim","doi":"10.3390/neurolint17050071","DOIUrl":"10.3390/neurolint17050071","url":null,"abstract":"<p><p>Hydrogen sulfide (H₂S) is a highly potent toxic gas, and the brain is a primary target organ following acute intoxications. Accidents and misuse of this gas for nefarious purposes, i.e., bioterrorism, are causes for concern regarding acute poisoning. The immediate effects of acute H₂S poisoning are well known. Numerous publications have reported neurological sequelae, including insomnia, persistent headaches, ataxia, cognition deficits, hearing impairment, dysarthria, and neuropsychiatric behaviors, among survivors of acute H₂S poisoning. However, this subject remains controversial. The goal of this study was to review the literature on acute H₂S-poisoning-induced neurological sequelae and on animal models to determine prevalence and knowledge gaps. We also reviewed the literature on cyanide-induced neurological sequelae. The results of large population studies indicate that the majority of victims of acute H₂S poisoning survive. There is a lack of patient follow-up and standardized neuropsychological, neurological, and neuroimaging for accurate assessments. We observed flaws in animal models that failed to recapitulate the severe neurotoxicity induced via the inhalation route. We observed a paucity of literature on cyanide-induced neurological sequelae. In contrast to cyanide-induced sequelae, predominantly characterized by Parkinsonian-like motor behavioral deficits, H₂S patients exhibit mostly cognition deficits, speech impairment, and neuropsychological effects. This first comprehensive review of neurological sequelae induced by H₂S and cyanide poisonings identified knowledge gaps in the prevalence of these sequelae and cellular and molecular mechanisms underlying them. It is unclear whether these sequelae are reversible. There are no FDA-approved drugs for the prevention or treatment of these sequelae. Notably, patients who received life-saving therapy still developed delayed neurological sequelae.</p>","PeriodicalId":19130,"journal":{"name":"Neurology International","volume":"17 5","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12113851/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144151224","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Impact of Concurrent Chronic Heart Failure and Chronic Kidney Dysfunction on Post-Stroke Rehabilitation Outcomes.","authors":"Azadeh Fischer, Nadja Jauert, Martin Schikora, Michael Joebges, Wolfram Doehner","doi":"10.3390/neurolint17050070","DOIUrl":"10.3390/neurolint17050070","url":null,"abstract":"<p><p><b>Background/Objectives:</b> The aim of this study was to evaluate the impact of chronic heart failure (CHF), chronic kidney dysfunction (CKD), and the combined CHF-CKD comorbidity on the outcomes of rehabilitation in stroke patients. <b>Methods:</b> A total of 586 patients who had suffered a stroke (mean age, 70 ± 13; 47.6% female; 72.4% ischemic and 27.6% hemorrhagic strokes) and who were admitted immediately after acute stroke care to a rehabilitation center were included in this cohort study and followed up with until their death or discharge from the rehabilitation center. The clinical characteristics of the patients were obtained from their medical records. The relationship between the background comorbidities (CHF, CKD, and concurrent CHF-CKD) and fatal and non-fatal unfavorable outcomes (emergency readmission to a primary hospital or transfer to a long-term care facility in a vegetative or minimally conscious state) were investigated. <b>Results:</b> Unfavorable outcomes were more common in the groups with background CHF and/or CKD. From the Cox multivariate analysis, both CHF and CKD were independent prognostic factors for the occurrence of unfavorable outcomes, with a hazard ratio (HR) of 2.28 (95% CI = 1.2-4.29; <i>p</i>-value = 0.01) and 2.19 (95% CI = 1.24-3.87; <i>p</i>-value = 0.007), respectively. Moreover, the combined CHF-CKD comorbidity showed a more than 5-fold increased risk of an adverse post-stroke outcome (HR of 5.8; 95% CI = 2.5-13.44; <i>p</i>-value < 0.001). <b>Conclusions:</b> The combined CHF-CKD comorbidity is an important independent complicating factor that, along with other known influencing factors, can affect unfavorable post-stroke outcomes more than CHF or CKD alone, and necessitates critical attention to its diagnosis and management as a separate mixed syndrome.</p>","PeriodicalId":19130,"journal":{"name":"Neurology International","volume":"17 5","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12113819/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144151229","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of Cilostazol and Aspirin During Hyperacute Stroke Phase in Rats: An Experimental Research Study.","authors":"Christiana Anastasiadou, Anastasios Papapetrou, George Galyfos, Kostas Vekrellis, Patroklos Katafygiotis, Andreas Lazaris, George Geroulakos, Angelos Megalopoulos, Christos Liapis, Nikolaos Kostomitsopoulos, John Kakisis","doi":"10.3390/neurolint17050069","DOIUrl":"10.3390/neurolint17050069","url":null,"abstract":"<p><strong>Objective: </strong>The contralateral hippocampus, a critical region for cognitive function, is often overlooked in everyday clinical practice and stroke research. This study aimed to evaluate the effect of specific antiplatelet agents on the hippocampus (ipsilateral and contralateral) during the hyperacute phase of stroke.</p><p><strong>Materials and methods: </strong>Twelve-week-old rats were randomly assigned to four groups, each containing six rats: a cilostazol group, an aspirin group, an aspirin plus cilostazol group, and a control group. Each substance was administered for four weeks. Permanent brain ischemia was induced over 2 h using intraluminal middle cerebral artery occlusion. A neurologic examination was conducted, followed by euthanasia and histological examination of the CA1 hippocampal region. The hematoxylin and eosin stain was used to assess the total number of intact neuronal cell bodies and pyknotic nuclei, an indicator of early irreversible neuronal injury.</p><p><strong>Results: </strong>In the ipsilateral hippocampus, monotherapy with either aspirin or cilostazol significantly reduced pyknotic nuclei compared with the control group (<i>p</i> = 0.0016 and <i>p</i> = 0.0165, respectively). However, combination therapy showed no significant difference from the controls (<i>p</i> = 0.2375). In the contralateral hippocampus, cilostazol monotherapy demonstrated significantly reduced pyknotic nuclei (<i>p</i> = 0.0098), whereas aspirin monotherapy and combination therapy did not (<i>p</i> = 0.1009 and <i>p</i> = 0.9999, respectively). A cumulative analysis of both hemispheres revealed that monotherapy with aspirin or cilostazol markedly reduced injury markers (<i>p</i> = 0.0002 and <i>p</i> = 0.0001, respectively), whereas combined therapy revealed no significant benefit (<i>p</i> = 0.1984). A neurological assessment indicated that the most severe deficits were in the combination therapy group.</p><p><strong>Conclusions: </strong>To the best of our knowledge, this is the first study to compare acute histopathological changes in the affected and unaffected hippocampus after a stroke in a rat model. Dual antiplatelet therapy resulted in worse outcomes (histopathological and neurological) than monotherapy.</p>","PeriodicalId":19130,"journal":{"name":"Neurology International","volume":"17 5","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12114208/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144151071","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}