{"title":"Changes in brain functional connectivity associated with ongoing neuropathic pain in patients with painful polyneuropathies","authors":"Julie Bismuth , Renaud Lopes , Jérôme Hodel , Jean-Pascal Lefaucheur","doi":"10.1016/j.neucli.2025.103102","DOIUrl":"10.1016/j.neucli.2025.103102","url":null,"abstract":"<div><h3>Objective</h3><div>To assess changes in brain functional connectivity associated with the painful nature of peripheral polyneuropathy.</div></div><div><h3>Methods</h3><div>Resting-state functional magnetic resonance imaging (rs-fMRI) was performed in 26 patients with painful or painless polyneuropathy. According to previously published results, connectivity was studied regarding the default mode network (DMN), intrathalamic and thalamocortical connections, and, the different brain networks (pain matrices) involved in the \"nociceptive\", \"attentional\" and \"emotional\" aspects of the chronic pain experience.</div></div><div><h3>Results</h3><div>No change in DMN connectivity was found between groups. Thalamocortical connectivity was reduced in patients with painful polyneuropathy, especially for the thalamic cluster connected to the motor cortex, while intra-thalamic (mediolateral) connectivity was increased in patients with painless polyneuropathy. Intra-connectivity was increased within the pain matrices, especially the \"nociceptive\" matrix, in patients with painful polyneuropathy, while inter-connectivity was increased between the \"attentional\" and \"emotional\" pain matrices in patients with painless polyneuropathy. Increased connectivity between the posterior insula and parietal operculum positively correlated with the neuropathic pain symptom score and impact of pain on daily functioning.</div></div><div><h3>Conclusions</h3><div>Painful polyneuropathy was characterized by increased intra-connectivity within each pain matrix and reduced thalamocortical connectivity of certain thalamic clusters, notably linked to the motor cortex. Conversely, painless polyneuropathy was characterized by increased connectivity within the thalamus and between the different pain matrices. Although various methodological limitations must be acknowledged (small sample size, lack of a control group of healthy subjects or measurement of pain intensity during neuroimaging examination), these results provide new information on the changes in brain connectivity associated with painful polyneuropathies. This study also brings new arguments to explain the efficacy of motor cortex stimulation in the treatment of chronic neuropathic pain.</div></div>","PeriodicalId":19134,"journal":{"name":"Neurophysiologie Clinique/Clinical Neurophysiology","volume":"55 5","pages":"Article 103102"},"PeriodicalIF":2.4,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145044356","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The neurophysiology of aggressiveness: From adaptive behavior to pathology and deep brain stimulation","authors":"Marie des Neiges Santin","doi":"10.1016/j.neucli.2025.103090","DOIUrl":"10.1016/j.neucli.2025.103090","url":null,"abstract":"<div><h3>Objectives</h3><div>Aggressiveness is a complex social behavior that ranges from adaptive to pathological forms. This review synthesizes current knowledge of the neural circuits underlying aggression and explores how this informs neurosurgical strategies for severe, treatment-resistant cases.</div></div><div><h3>Methods</h3><div>We reviewed recent experimental and clinical studies of the anatomical, functional, and neurochemical bases of aggression, focusing on reactive and proactive subtypes. Emphasis was placed on animal models, optogenetics, and human deep brain stimulation (DBS) approaches.</div></div><div><h3>Results</h3><div>Internal states – such as hormonal status, energy balance, and prior experience – modulate the threshold for aggression. The ventrolateral part of the ventromedial nucleus of the hypothalamus (VMHvl), particularly its ERα-expressing neurons, plays a central role in triggering aggressive behavior. The core aggression circuit (CAC) includes the VMHvl, amygdala, bed nucleus of the stria terminalis, and ventral premammillary nucleus, under modulation by prefrontal inputs. Aggression is expressed through a direct VMHvl–periaqueductal gray (PAG) pathway for innate actions and an indirect, dopamine-dependent striatal pathway for learned aggression. Serotonin inhibits, while dopamine promotes, proactive aggression.</div></div><div><h3>Discussion</h3><div>Pathological impulsive aggression, often linked to neurodevelopmental disorders and intellectual disability, may become refractory to pharmacotherapy. In such cases, neurosurgical approaches targeting the Sano triangle—originally described as part of the posterior hypothalamus—have shown promise. Understanding the connectivity and functional role of this region is essential for optimizing targeted interventions. Viewing aggression as a disorder of internal state regulation within defined circuits provides a framework for ethical and effective neuromodulation.</div></div>","PeriodicalId":19134,"journal":{"name":"Neurophysiologie Clinique/Clinical Neurophysiology","volume":"55 5","pages":"Article 103090"},"PeriodicalIF":2.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144534355","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Eva Diab , William Gacquer , Carole Nouboue , Derambure Philippe , Bertille Périn , Simone Chen , Julien De Jonckheere , William Szurhaj
{"title":"Electrocardiogram (ECG)-based seizure detection using supervised machine-learning","authors":"Eva Diab , William Gacquer , Carole Nouboue , Derambure Philippe , Bertille Périn , Simone Chen , Julien De Jonckheere , William Szurhaj","doi":"10.1016/j.neucli.2025.103098","DOIUrl":"10.1016/j.neucli.2025.103098","url":null,"abstract":"<div><h3>Background</h3><div>We conducted a pilot study utilizing automatic delineation of electrocardiogram (ECG) and machine learning that considered all components of the ECG complex for seizure detection. The primary outcome was to assess the feasibility of this method. The secondary outcome was to identify the most effective machine learning algorithm.</div></div><div><h3>Methods</h3><div>We screened ECG recordings from patients included in the EPICARD cohort who underwent video-electroencephalogram monitoring. A total of 47 seizures from 32 patients were selected. Epochs of 90 min surrounding the seizures were retained. Each ECG was converted into a sequence of heartbeats modeled as a P-Q-R-S-T succession. Derivative quantities measuring time variations between the inner and outer components of heartbeats were computed, designated as δ<sub>X</sub> and ΔX. Our algorithm monitored 3 to 60 successive heartbeats within a sliding window. An alarm was triggered when more than N heartbeats were classified as in-seizure (N between 3 and 20). Heartbeats were categorized as in-seizure by trained neurophysiologists. We used automated machine learning (auto-ML) platforms (Dataiku & Flaml) to assess six different algorithms: Random Forest, LightGBM, XGBoost, Decision Tree, K-Nearest Neighbors, and Extra Trees.</div></div><div><h3>Results</h3><div>The Extra Trees algorithm provided the best seizure detection performance regardless of the validation method used. Although longer-window models enhance detection sensitivity, they do so at the cost of delayed identification. A model analyzing 60 heartbeats with a trigger of 20 achieved 86 % sensitivity and 99.9 % specificity.</div></div><div><h3>Discussion</h3><div>Automatic delineation is reliable, however the false alarm rate remains high (1.5 per hour). Future work should focus on personalizing detection algorithms to improve this false alarm rate.</div></div>","PeriodicalId":19134,"journal":{"name":"Neurophysiologie Clinique/Clinical Neurophysiology","volume":"55 5","pages":"Article 103098"},"PeriodicalIF":2.4,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144887027","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Effect of reference electrode position on diagnostic accuracy of split hand index in ALS","authors":"Sepideh Omidbakhsh , Hatice Tankisi","doi":"10.1016/j.neucli.2025.103101","DOIUrl":"10.1016/j.neucli.2025.103101","url":null,"abstract":"","PeriodicalId":19134,"journal":{"name":"Neurophysiologie Clinique/Clinical Neurophysiology","volume":"55 5","pages":"Article 103101"},"PeriodicalIF":2.4,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145026677","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cristina Mariscal , Javier Navallas , Armando Malanda , Silvia Recalde-Villamayor , Javier Rodriguez-Falces
{"title":"EMG filling analysis, a new method for the assessment of recruitment of motor units with needle EMG","authors":"Cristina Mariscal , Javier Navallas , Armando Malanda , Silvia Recalde-Villamayor , Javier Rodriguez-Falces","doi":"10.1016/j.neucli.2025.103059","DOIUrl":"10.1016/j.neucli.2025.103059","url":null,"abstract":"<div><h3>Objectives</h3><div>The progression of recruitment of motor unit potentials (MUPs) during increasing voluntary contraction can provide important information about the motor units (MUs) innervating a muscle. Here, we described a method to quantitate the recruitment level of the intramuscular electromyographic (iEMG) signal during an increasing force level.</div></div><div><h3>Methods</h3><div>Concentric needle EMG signals were recorded from the <em>tibialis anterior</em> of healthy subjects as force was gradually increased from 0 to maximum force. The iEMG filling process was analyzed by measuring the EMG filling factor (FF), calculated from the mean rectified iEMG and the root mean square iEMG.</div></div><div><h3>Results</h3><div>(1) The iEMG activity at low contraction forces was “discrete” (FF<0.3) for all participants. (2) The iEMG activity at maximal effort was “full” (FF>0.5) for 83 % of the participants, whereas it was “incompletely-reduced” (0.3<FF< 0.5) for 17 % of the participants. (3) The FF increased rapidly for forces up to 20 % MVC, and then levelled off for higher forces: thus, the FF curve had a typical exponential shape.</div></div><div><h3>Conclusions</h3><div>The iEMG filling method can be considered of general applicability since the FF increased over a wide range in all healthy participants.</div></div><div><h3>Significance</h3><div>The EMG filling analysis may have potential to detect scenarios of MU loss and remodelling in neurogenic and motor neuron diseases.</div></div>","PeriodicalId":19134,"journal":{"name":"Neurophysiologie Clinique/Clinical Neurophysiology","volume":"55 4","pages":"Article 103059"},"PeriodicalIF":2.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143453035","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Fear in the neuropsychiatric aspects of epilepsy: What role for the amygdala?","authors":"Alexis Tarrada , Yassine Jamal Eddine","doi":"10.1016/j.neucli.2025.103062","DOIUrl":"10.1016/j.neucli.2025.103062","url":null,"abstract":"<div><div>Fear is essential for survival; however, its dysregulation may lead to various neuropsychiatric disorders. Understanding the neural networks involved in the expression of fear is useful for elaborating therapeutic interventions (pharmacological or psychoeducation). We aimed to summarize suspected roles of amygdala, but also of other structures such as insula, frontal and temporal associative cortices, and brainstem. Three pathways can be distinguished leading to the expression of fear: indirect, direct and interoceptive, comprising the amygdala as a “hub of fear”. Moreover, temporal epilepsies that imply fear as a “spontaneous” symptom may constitute an interesting model for understanding physiological mechanisms of fear.</div></div>","PeriodicalId":19134,"journal":{"name":"Neurophysiologie Clinique/Clinical Neurophysiology","volume":"55 4","pages":"Article 103062"},"PeriodicalIF":2.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143637510","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jean-Baptiste Davion , Jérôme Devaux , Céline Tard , Armelle Magot , François Cassim , Yann Péréon
{"title":"Guillain-Barré syndrome in patients with Charcot-Marie-Tooth type 1A disease, probably a non-random association","authors":"Jean-Baptiste Davion , Jérôme Devaux , Céline Tard , Armelle Magot , François Cassim , Yann Péréon","doi":"10.1016/j.neucli.2025.103071","DOIUrl":"10.1016/j.neucli.2025.103071","url":null,"abstract":"<div><h3>Objective</h3><div>To describe four cases of Charcot-Marie-Tooth disease type 1A (CMT1A) who developed Guillain-Barré syndrome (GBS), respectively the most frequent genetic and inflammatory neuropathies.</div></div><div><h3>Methods</h3><div>We described the patients’ clinical and electrodiagnostic characteristics.</div></div><div><h3>Results</h3><div>Our CMT1A patients developed typical GBS at various ages (3 to 76 years). GBS-related clinical manifestations were different within patients, with various severity degrees of seve (weakness, respiratory failure). Nerve conduction studies revealed more severe demyelinating features than expected in patients with no CMT1A. High cerebrospinal fluid protein level was found in 3 patients. GBS outcome was mainly good, although some patients only slowly improved.</div></div><div><h3>Conclusions</h3><div>Our cases are close to the previously described cases of acute worsening in CMT1A, and presented with many electrophysiological features of GBS. Overall, GBS prognosis does not seem worse in CMT1A patients than in other patients. If GBS and CMT1A were independent, the expected frequency of co-occurrence of GBS and CMT1A in our two French regions should be 1 case every 137 years. As we observed 4 cases in only 5 years, we suspect that CMT1A is a risk factor of GBS.</div></div><div><h3>Significance</h3><div>These cases bring further evidence for a non-random link between inflammatory and genetic neuropathies.</div></div>","PeriodicalId":19134,"journal":{"name":"Neurophysiologie Clinique/Clinical Neurophysiology","volume":"55 4","pages":"Article 103071"},"PeriodicalIF":2.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143679824","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ioannis Liampas , Dimitra Veltsista , Alexandra Germeni , Paraskevi Batzikosta , Emilia Michou , Zinovia Kefalopoulou , Elisabeth Chroni
{"title":"F waves in amyotrophic lateral sclerosis: A systematic review and meta-analysis","authors":"Ioannis Liampas , Dimitra Veltsista , Alexandra Germeni , Paraskevi Batzikosta , Emilia Michou , Zinovia Kefalopoulou , Elisabeth Chroni","doi":"10.1016/j.neucli.2025.103061","DOIUrl":"10.1016/j.neucli.2025.103061","url":null,"abstract":"<div><h3>Objective</h3><div>This systematic review and meta-analysis aimed to determine the pattern of F-wave abnormalities and their potential utility in the early diagnosis of amyotrophic lateral sclerosis (ALS).</div></div><div><h3>Methods</h3><div>Medline and Embase were thoroughly searched. We primarily emphasized F-wave recordings from the abductor digiti minimi, following stimulation of the ulnar nerve at the wrist. Data from case-control studies involving individuals with ALS versus healthy controls (HC) or other well-defined patient groups were reviewed and -if appropriate- quantitatively synthesized.</div></div><div><h3>Results</h3><div>Twenty-nine studies were included in this systematic review and 17 of them in the analytic part. The pattern of F-abnormalities in ALS compared to HC was as follows: decreased persistence (MD=20.25 %,15.67–24.84 %), mildly prolonged minimum latency (MD=1.59msec,1.11–2.06msec), increased maximum amplitude (MD=196μV,106–287μV) and elevated Index total Freps (MD=33.9 %,26.0–41.8 %). Affected limbs (with substantial weakness in clinical examination and/or muscle wasting and/or abnormal nerve conduction studies) exhibited more marked abnormalities in persistence, minimum latency, and Index total Freps, whereas abnormalities in these parameters were very mild in clinically unaffected limbs. More prominent increases in maximum amplitude accompanied pyramidal dysfunction. Of note, isolated upper motor neuron (UMN) disorders exhibited a comparable increase in Index total Freps without a decrease in persistence.</div></div><div><h3>Conclusions</h3><div>The pattern of F wave abnormalities may raise suspicion of involvement of the under-study lower motor neuron (LMN) pool in ALS. These findings may identify LMN dysfunction even at a preclinical stage and prompt extensive electromyographic investigations. UMN involvement may to some extent differentiate the profile of F wave abnormalities in ALS.</div></div>","PeriodicalId":19134,"journal":{"name":"Neurophysiologie Clinique/Clinical Neurophysiology","volume":"55 4","pages":"Article 103061"},"PeriodicalIF":2.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143609945","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}