Pub Date : 2025-12-02DOI: 10.1016/j.clinph.2025.2111468
Zhongke Mei , Anna-Sophie Hofer , Christian Baumann , Mechtild Uhl , Navrag Singh , William R. Taylor , Lennart Stieglitz , Deepak K. Ravi
Objective
To investigate the relationship between the spatial location of active electrode contacts in subthalamic nucleus deep brain stimulation (STN-DBS) and changes in gait performance in patients with Parkinson’s disease (PwPD).
Methods
This observational study included 49 PwPD who underwent bilateral STN-DBS. Spatiotemporal gait parameters were assessed before surgery and six months post-implantation using motion capture. Both mean values and variability of gait parameters were analyzed. Active contact locations were normalized using a voxel-based approach and statistically associated with gait outcomes.
Results
STN-DBS led to significant reductions in stride time, stance time, swing time, and step time, alongside increased step width and temporal gait variability. Gait improvements were associated with specific stimulation sites: the postero-superior STN region was most effective for enhancing mean spatial parameters (e.g., stride length, walking speed), while the antero-superior region was optimal for reducing temporal variability. Patients stimulated in these regions showed significantly better gait outcomes than those stimulated elsewhere.
Conclusions
Gait improvements were differentially associated with the spatial location of stimulation electrode within the STN, suggesting region-specific modulation of mean spatial and temporal variability gait parameters.
Significance
These findings support precision targeting of stimulation sites to optimize patient-specific gait outcomes, advancing personalized DBS therapy in Parkinson’s disease.
{"title":"The role of electrode placement in subthalamic nucleus deep brain stimulation for improving gait in Parkinson’s Disease","authors":"Zhongke Mei , Anna-Sophie Hofer , Christian Baumann , Mechtild Uhl , Navrag Singh , William R. Taylor , Lennart Stieglitz , Deepak K. Ravi","doi":"10.1016/j.clinph.2025.2111468","DOIUrl":"10.1016/j.clinph.2025.2111468","url":null,"abstract":"<div><h3>Objective</h3><div>To investigate the relationship between the spatial location of active electrode contacts in subthalamic nucleus deep brain stimulation (STN-DBS) and changes in gait performance in patients with Parkinson’s disease (PwPD).</div></div><div><h3>Methods</h3><div>This observational study included 49 PwPD who underwent bilateral STN-DBS. Spatiotemporal gait parameters were assessed before surgery and six months post-implantation using motion capture. Both mean values and variability of gait parameters were analyzed. Active contact locations were normalized using a voxel-based approach and statistically associated with gait outcomes.</div></div><div><h3>Results</h3><div>STN-DBS led to significant reductions in stride time, stance time, swing time, and step time, alongside increased step width and temporal gait variability. Gait improvements were associated with specific stimulation sites: the postero-superior STN region was most effective for enhancing mean spatial parameters (e.g., stride length, walking speed), while the antero-superior region was optimal for reducing temporal variability. Patients stimulated in these regions showed significantly better gait outcomes than those stimulated elsewhere.</div></div><div><h3>Conclusions</h3><div>Gait improvements were differentially associated with the spatial location of stimulation electrode within the STN, suggesting region-specific modulation of mean spatial and temporal variability gait parameters.</div></div><div><h3>Significance</h3><div>These findings support precision targeting of stimulation sites to optimize patient-specific gait outcomes, advancing personalized DBS therapy in Parkinson’s disease.</div></div>","PeriodicalId":10671,"journal":{"name":"Clinical Neurophysiology","volume":"182 ","pages":"Article 2111468"},"PeriodicalIF":3.6,"publicationDate":"2025-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145713210","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-01DOI: 10.1016/j.clinph.2025.2111467
Rocio Rodriguez Capilla , Aislinn M. Hurley , Karthik Kumaravelu , Jennifer J. Peters , Hui-Jie Lee , Dennis A. Turner , Warren M. Grill , Stephen L. Schmidt
Background
Deep brain stimulation reduces the motor symptoms of Parkinson’s disease (PD). Dual target deep brain stimulation (DT DBS) may better reduce symptoms and minimize side effects than single target, but the optimal parameters of DT DBS are unknown.
Objective
To quantify the frequency response of DT DBS on bradykinesia and beta oscillations, and to explore intrahemispheric pulse delay shifts as a means to reduce total energy delivered.
Methods
We applied DT DBS using the Summit RC + S in six participants with PD, varying DBS frequency. We further examined the effects of frequency in a biophysical model.
Results
DT DBS at 50 Hz was effective at reducing bradykinesia, whereas increasing DT DBS frequency up to 125 Hz also led to significantly lower beta power. This frequency effect on beta power was replicated in a biophysical model. The model suggested that 22 Hz DT DBS, with an intrahemispheric delay of 40 ms, can reduce beta power by 87 %.
Conclusion
This exploratory study (n = 6) suggests that 125 Hz DT DBS best reduced bradykinesia. However, low frequency DBS with an appropriate intrahemispheric delay could also improve symptom relief.
Significance
Both 125 Hz and tailored low-frequency DT DBS may achieve equivalent symptomatic control of PD symptoms.
{"title":"Effect of frequency on dual target deep brain stimulation","authors":"Rocio Rodriguez Capilla , Aislinn M. Hurley , Karthik Kumaravelu , Jennifer J. Peters , Hui-Jie Lee , Dennis A. Turner , Warren M. Grill , Stephen L. Schmidt","doi":"10.1016/j.clinph.2025.2111467","DOIUrl":"10.1016/j.clinph.2025.2111467","url":null,"abstract":"<div><h3>Background</h3><div>Deep brain stimulation reduces the motor symptoms of Parkinson’s disease (PD). Dual target deep brain stimulation (DT DBS) may better reduce symptoms and minimize side effects than single target, but the optimal parameters of DT DBS are unknown.</div></div><div><h3>Objective</h3><div>To quantify the frequency response of DT DBS on bradykinesia and beta oscillations, and to explore intrahemispheric pulse delay shifts as a means to reduce total energy delivered.</div></div><div><h3>Methods</h3><div>We applied DT DBS using the Summit RC + S in six participants with PD, varying DBS frequency. We further examined the effects of frequency in a biophysical model.</div></div><div><h3>Results</h3><div>DT DBS at 50 Hz was effective at reducing bradykinesia, whereas increasing DT DBS frequency up to 125 Hz also led to significantly lower beta power. This frequency effect on beta power was replicated in a biophysical model. The model suggested that 22 Hz DT DBS, with an intrahemispheric delay of 40 ms, can reduce beta power by 87 %.</div></div><div><h3>Conclusion</h3><div>This exploratory study (n = 6) suggests that 125 Hz DT DBS best reduced bradykinesia. However, low frequency DBS with an appropriate intrahemispheric delay could also improve symptom relief.</div></div><div><h3>Significance</h3><div>Both 125 Hz and tailored low-frequency DT DBS may achieve equivalent symptomatic control of PD symptoms.</div></div>","PeriodicalId":10671,"journal":{"name":"Clinical Neurophysiology","volume":"182 ","pages":"Article 2111467"},"PeriodicalIF":3.6,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145682016","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-01DOI: 10.1016/j.clinph.2025.2111466
Minsoo Kim , Soung Wook Park , Hyun Seok Lee , Sang-Ku Park , Kwan Park
Objective
To determine whether intraoperative lateral spread response (LSR) amplitudes reflect vascular burden and configuration in hemifacial spasm.
Methods
We retrospectively reviewed consecutive microvascular decompressions at a single center. LSR I (mentalis) and LSR II (frontalis) were recorded using a standardized protocol. The primary exposure was arterial vessel count (single vs. multiple); vein-only cases were exploratory owing to imbalance. Amplitudes and derived indices (I/II ratio, I–II difference) were compared using variance-aware parametric and nonparametric tests.
Results
LSRs were obtained in most patients. LSR I exceeded LSR II with a significant paired effect. Arterial burden showed a graded pattern in LSR I, with higher amplitudes in multiple-vessel compression; however, differences across vessels counts were not significant after adjustment. No differences were observed for LSR II. Derived indices better reflected vascular burden, showing significant contrasts where raw amplitudes did not, including single-versus-multiple comparisons. Vein-only cases appeared lower but remained exploratory.
Conclusions
Intraoperative LSR amplitudes, especially at the mentalis muscle, reflect arterial burden, and derived indices improve discrimination. Findings support amplitude-based monitoring, with multicenter studies needed to confirm underlying mechanisms and predictive utility.
Significance
LSR monitoring offers a practical marker of vascular burden, potentially guiding surgical decisions and improving outcomes.
{"title":"Quantitative intraoperative lateral spread response amplitudes in hemifacial Spasm: Associations with vascular burden","authors":"Minsoo Kim , Soung Wook Park , Hyun Seok Lee , Sang-Ku Park , Kwan Park","doi":"10.1016/j.clinph.2025.2111466","DOIUrl":"10.1016/j.clinph.2025.2111466","url":null,"abstract":"<div><h3>Objective</h3><div>To determine whether intraoperative lateral spread response (LSR) amplitudes reflect vascular burden and configuration in hemifacial spasm.</div></div><div><h3>Methods</h3><div>We retrospectively reviewed consecutive microvascular decompressions at a single center. LSR I (mentalis) and LSR II (frontalis) were recorded using a standardized protocol. The primary exposure was arterial vessel count (single vs. multiple); vein-only cases were exploratory owing to imbalance. Amplitudes and derived indices (I/II ratio, I–II difference) were compared using variance-aware parametric and nonparametric tests.</div></div><div><h3>Results</h3><div>LSRs were obtained in most patients. LSR I exceeded LSR II with a significant paired effect. Arterial burden showed a graded pattern in LSR I, with higher amplitudes in multiple-vessel compression; however, differences across vessels counts were not significant after adjustment. No differences were observed for LSR II. Derived indices better reflected vascular burden, showing significant contrasts where raw amplitudes did not, including single-versus-multiple comparisons. Vein-only cases appeared lower but remained exploratory.</div></div><div><h3>Conclusions</h3><div>Intraoperative LSR amplitudes, especially at the mentalis muscle, reflect arterial burden, and derived indices improve discrimination. Findings support amplitude-based monitoring, with multicenter studies needed to confirm underlying mechanisms and predictive utility.</div></div><div><h3>Significance</h3><div>LSR monitoring offers a practical marker of vascular burden, potentially guiding surgical decisions and improving outcomes.</div></div>","PeriodicalId":10671,"journal":{"name":"Clinical Neurophysiology","volume":"182 ","pages":"Article 2111466"},"PeriodicalIF":3.6,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145682018","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-29DOI: 10.1016/j.clinph.2025.2111461
Mariem Ben Mahmoud , Adrien Benard , Delphine Taussig , Pascale Trebon , Dan Cristian Chiforeanu , Yves Sahler , Arnaud Biraben , Anca Nica , Mihai Dragos Maliia
Objective
Distinguishing drug-resistant temporal lobe epilepsy (TLE) caused by isolated hippocampal sclerosis (iHS) from focal cortical dysplasia type IIIa (FCD IIIa) remains a presurgical challenge. This study aimed to compare the clinical characteristics, electrophysiological data, and postsurgical seizure outcomes between these pathologies.
Methods
We retrospectively analyzed a cohort of 50 consecutive TLE patients (mean duration of disease of 22 years) who underwent surgery. The histopathology confirmed either iHS (n = 22) or FCD IIIa (n = 28) and a minimum follow-up of 12 months. The groups were compared on complex presurgical data, surgery type, and outcome.
Results
A history of febrile seizures (p = 0.02, OR = 4.7) was more frequent in the FCD IIIa group, which also had significantly lower intelligence quotient (IQ) scores in all domains. The mean total IQ score for FCD IIIa/iHS was 86/94 (p = 0.02); verbal IQ was 85/92 (p = 0.03); performance IQ was 89/98 (p = 0.02). The effect size was considered medium for all three (Cohen’s d = 0.7, 0.63 and 0.68 respectively). Scalp EEG showed shorter seizures in FCD IIIa (p = 0.03), in SEEG, the temporal pole was more implanted in this group (p = 0.02, 50 % difference, OR = ∞). At a mean follow-up of 8.5 years, similar seizure-freedom rates was found between groups (82 % for FCD IIIa, 95 % for iHS; p = 0.48). Follow-up EEG and neuropsychological assessment at 6 months post-surgery showed no statistical differences.
Significance
FCD IIIa and iHS exhibit several distinct electro-clinical features. The most important is a more impaired general cognitive profile associated with FCD IIIa, without differences in language or global memory.
{"title":"Isolated hippocampal sclerosis and focal dysplasia type IIIa: Comparative study of anatomo-electro-clinical profile and seizure outcome","authors":"Mariem Ben Mahmoud , Adrien Benard , Delphine Taussig , Pascale Trebon , Dan Cristian Chiforeanu , Yves Sahler , Arnaud Biraben , Anca Nica , Mihai Dragos Maliia","doi":"10.1016/j.clinph.2025.2111461","DOIUrl":"10.1016/j.clinph.2025.2111461","url":null,"abstract":"<div><h3>Objective</h3><div>Distinguishing drug-resistant temporal lobe epilepsy (TLE) caused by isolated hippocampal sclerosis (iHS) from focal cortical dysplasia type IIIa (FCD IIIa) remains a presurgical challenge. This study aimed to compare the clinical characteristics, electrophysiological data, and postsurgical seizure outcomes between these pathologies.</div></div><div><h3>Methods</h3><div>We retrospectively analyzed a cohort of 50 consecutive TLE patients (mean duration of disease of 22 years) who underwent surgery. The histopathology confirmed either iHS (n = 22) or FCD IIIa (n = 28) and a minimum follow-up of 12 months. The groups were compared on complex presurgical data, surgery type, and outcome.</div></div><div><h3>Results</h3><div>A history of febrile seizures (p = 0.02, OR = 4.7) was more frequent in the FCD IIIa group, which also had significantly lower intelligence quotient (IQ) scores in all domains. The mean total IQ score for FCD IIIa/iHS was 86/94 (p = 0.02); verbal IQ was 85/92 (p = 0.03); performance IQ was 89/98 (p = 0.02). The effect size was considered medium for all three (Cohen’s <em>d =</em> 0.7, 0.63 and 0.68 respectively<em>).</em> Scalp EEG showed shorter seizures in FCD IIIa (p = 0.03), in SEEG, the temporal pole was more implanted in this group (p = 0.02, 50 % difference, OR = ∞). At a mean follow-up of 8.5 years, similar seizure-freedom rates was found between groups (82 % for FCD IIIa, 95 % for iHS; p = 0.48). Follow-up EEG and neuropsychological assessment at 6 months post-surgery showed no statistical differences.</div></div><div><h3>Significance</h3><div>FCD IIIa and iHS exhibit several distinct electro-clinical features. The most important is a more impaired general cognitive profile associated with FCD IIIa, without differences in language or global memory.</div></div>","PeriodicalId":10671,"journal":{"name":"Clinical Neurophysiology","volume":"182 ","pages":"Article 2111461"},"PeriodicalIF":3.6,"publicationDate":"2025-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145682019","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-26DOI: 10.1016/j.clinph.2025.2111459
Alberto Benussi , Steve Vucic
This chapter examines how emerging neurophysiological technologies are transforming the early and differential diagnosis of neurological disorders. While imaging and fluid biomarkers have greatly advanced the field, they remain limited by cost, invasiveness, and their inability to directly capture dynamic brain activity. Neurophysiological techniques, particularly transcranial magnetic stimulation (TMS) and TMS combined with EEG, offer a unique, non-invasive means of probing cortical excitability, connectivity, and plasticity with millisecond precision.
Recent technological and analytical breakthroughs are moving these approaches from research laboratories into clinical practice. By detecting subtle network dysfunctions that precede structural degeneration, they open the possibility of identifying disease in its prodromal or even presymptomatic stages, when interventions may be most effective. This chapter outlines the principles of advanced TMS paradigms and TMS-EEG and explores their application across a range of conditions, including amyotrophic lateral sclerosis, dementias, and movement disorders. It also highlights how integrating neurophysiological measures with blood-based biomarkers and computational tools, such as machine learning, can enhance diagnostic accuracy and guide individualized treatment strategies.
Together, these innovations establish neurophysiology as a cornerstone of precision neurology, linking mechanistic insights to clinical decision-making and enabling earlier diagnosis, improved patient stratification, and more targeted therapeutic interventions.
{"title":"Emergent technologies and applications of TMS and TMS-EEG in clinical neurophysiology for early and differential diagnosis: IFCN handbook chapter","authors":"Alberto Benussi , Steve Vucic","doi":"10.1016/j.clinph.2025.2111459","DOIUrl":"10.1016/j.clinph.2025.2111459","url":null,"abstract":"<div><div>This chapter examines how emerging neurophysiological technologies are transforming the early and differential diagnosis of neurological disorders. While imaging and fluid biomarkers have greatly advanced the field, they remain limited by cost, invasiveness, and their inability to directly capture dynamic brain activity. Neurophysiological techniques, particularly transcranial magnetic stimulation (TMS) and TMS combined with EEG, offer a unique, non-invasive means of probing cortical excitability, connectivity, and plasticity with millisecond precision.</div><div>Recent technological and analytical breakthroughs are moving these approaches from research laboratories into clinical practice. By detecting subtle network dysfunctions that precede structural degeneration, they open the possibility of identifying disease in its prodromal or even presymptomatic stages, when interventions may be most effective. This chapter outlines the principles of advanced TMS paradigms and TMS-EEG and explores their application across a range of conditions, including amyotrophic lateral sclerosis, dementias, and movement disorders. It also highlights how integrating neurophysiological measures with blood-based biomarkers and computational tools, such as machine learning, can enhance diagnostic accuracy and guide individualized treatment strategies.</div><div>Together, these innovations establish neurophysiology as a cornerstone of precision neurology, linking mechanistic insights to clinical decision-making and enabling earlier diagnosis, improved patient stratification, and more targeted therapeutic interventions.</div></div>","PeriodicalId":10671,"journal":{"name":"Clinical Neurophysiology","volume":"182 ","pages":"Article 2111459"},"PeriodicalIF":3.6,"publicationDate":"2025-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145616624","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-25DOI: 10.1016/j.clinph.2025.2111460
Thaera Arafat , Zhengchen Cai , Jean Gotman
Simultaneous EEG-fMRI is a unique, noninvasive neuroimaging technique that enables high spatial resolution mapping of metabolic changes linked to EEG epileptic discharges in focal and generalized epilepsy, reflected through fMRI signals. It is increasingly recognized as a valuable tool in the presurgical evaluation of drug-resistant epilepsy, supporting the localization of epileptogenic zones, guiding electrode implantation, and informing surgical strategies and outcome prediction, while also revealing important insights into the networks involved in epileptic activity.
Advances in artifact removal, automated spike detection, and statistical modeling have improved EEG-fMRI’s data quality and clinical utility. It is particularly valuable in diagnostically challenging cases where standard EEG is not localizing, or MRI findings are negative. However, its routine clinical adoption is limited by the complexity of the procedure, the lack of standardized protocols, interpretation criteria, and broader validation across diverse epilepsy populations.
This review highlights EEG-fMRI’s evolving role in localizing epileptic discharges, emphasizing both methodological and clinical aspects. It covers the process from data acquisition through analysis to statistical interpretation and decision-making, with its application in distinguishing generalized from widespread activity, assessing thalamic involvement in focal epilepsy, evaluating status epilepticus, mapping blood oxygen–level dependent responses in relation to structural lesions, and supporting presurgical planning in complex cases, demonstrating its potential to improve diagnostic precision and treatment outcomes.
{"title":"Clinical and methodological advances in EEG-fMRI for epilepsy: a focused review","authors":"Thaera Arafat , Zhengchen Cai , Jean Gotman","doi":"10.1016/j.clinph.2025.2111460","DOIUrl":"10.1016/j.clinph.2025.2111460","url":null,"abstract":"<div><div>Simultaneous EEG-fMRI is a unique, noninvasive neuroimaging technique that enables high spatial resolution mapping of metabolic changes linked to EEG epileptic discharges in focal and generalized epilepsy, reflected through fMRI signals. It is increasingly recognized as a valuable tool in the presurgical evaluation of drug-resistant epilepsy, supporting the localization of epileptogenic zones, guiding electrode implantation, and informing surgical strategies and outcome prediction, while also revealing important insights into the networks involved in epileptic activity.</div><div>Advances in artifact removal, automated spike detection, and statistical modeling have improved EEG-fMRI’s data quality and clinical utility. It is particularly valuable in diagnostically challenging cases where standard EEG is not localizing, or MRI findings are negative. However, its routine clinical adoption is limited by the complexity of the procedure, the lack of standardized protocols, interpretation criteria, and broader validation across diverse epilepsy populations.</div><div>This review highlights EEG-fMRI’s evolving role in localizing epileptic discharges, emphasizing both methodological and clinical aspects. It covers the process from data acquisition through analysis to statistical interpretation and decision-making, with its application in distinguishing generalized from widespread activity, assessing thalamic involvement in focal epilepsy, evaluating status epilepticus, mapping blood oxygen–level dependent responses in relation to structural lesions, and supporting presurgical planning in complex cases, demonstrating its potential to improve diagnostic precision and treatment outcomes.</div></div>","PeriodicalId":10671,"journal":{"name":"Clinical Neurophysiology","volume":"182 ","pages":"Article 2111460"},"PeriodicalIF":3.6,"publicationDate":"2025-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145682020","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
In contrast to needle electromyography, the diagnostic performance of muscle ultrasound (MUS) for differentiating neurogenic from myopathic disorders remains unclear. We examined the clinical utility of “fascicular twitch,” a visible movement of muscle bundles during isometric contraction, and evaluated its ability to differentiate neurogenic from myopathic changes.
Methods
We quantified fascicular twitches on MUS during isometric contraction as normalized twitch pixels (nTP) using an original image analysis method based on background subtraction. We analyzed echogenicity and nTP values in the biceps brachii muscle of 89 patients with neuromuscular disorders and 42 controls.
Results
The neurogenic group demonstrated substantially higher nTP values than the myopathic group and controls, achieving a sensitivity of 90.5% and specificity of 88.1% at an nTP cutoff of 0.04. Although echogenicity distinguished patients with neuromuscular disorders from controls, it failed to discriminate between the neurogenic and myopathic groups.
Conclusions
Quantification of fascicular twitch via nTP effectively differentiates neurogenic from myopathic disorders, thereby demonstrating that MUS is a valuable, noninvasive diagnostic method for assessing neuromuscular diseases.
Significance
This study introduces fascicular twitch quantification as a novel ultrasound biomarker that uniquely discriminates neurogenic from myopathic pathology, offering a high‑performance, noninvasive approach to neuromuscular diagnosis.
{"title":"“Fascicular twitch” on muscle ultrasonography in neuromuscular disorders: quantitative video-image analysis","authors":"Shun Matoba , Kenji Sekiguchi , Yoshikatsu Noda , Ryosuke Sugisawa , Hirotomo Suehiro , Katsuya Nishida , Riki Matsumoto","doi":"10.1016/j.clinph.2025.2111447","DOIUrl":"10.1016/j.clinph.2025.2111447","url":null,"abstract":"<div><h3>Objective</h3><div>In contrast to needle electromyography, the diagnostic performance of muscle ultrasound (MUS) for differentiating neurogenic from myopathic disorders remains unclear. We examined the clinical utility of “fascicular twitch,” a visible movement of muscle bundles during isometric contraction, and evaluated its ability to differentiate neurogenic from myopathic changes.</div></div><div><h3>Methods</h3><div>We quantified fascicular twitches on MUS during isometric contraction as normalized twitch pixels (nTP) using an original image analysis method based on background subtraction. We analyzed echogenicity and nTP values in the biceps brachii muscle of 89 patients with neuromuscular disorders and 42 controls.</div></div><div><h3>Results</h3><div>The neurogenic group demonstrated substantially higher nTP values than the myopathic group and controls, achieving a sensitivity of 90.5% and specificity of 88.1% at an nTP cutoff of 0.04. Although echogenicity distinguished patients with neuromuscular disorders from controls, it failed to discriminate between the neurogenic and myopathic groups.</div></div><div><h3>Conclusions</h3><div>Quantification of fascicular twitch via nTP effectively differentiates neurogenic from myopathic disorders, thereby demonstrating that MUS is a valuable, noninvasive diagnostic method for assessing neuromuscular diseases.</div></div><div><h3>Significance</h3><div>This study introduces fascicular twitch quantification as a novel ultrasound biomarker that uniquely discriminates neurogenic from myopathic pathology, offering a high‑performance, noninvasive approach to neuromuscular diagnosis.</div></div>","PeriodicalId":10671,"journal":{"name":"Clinical Neurophysiology","volume":"182 ","pages":"Article 2111447"},"PeriodicalIF":3.6,"publicationDate":"2025-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145616691","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-23DOI: 10.1016/j.clinph.2025.2111436
Andrea Antal, Jovana Bjekić, Ana Ganho-Ávila, Ivan Alekseichuk, Sara Assecondi, Til Ole Bergmann, Marom Bikson, Jerome Brunelin, Andre R Brunoni, Leigh Charvet, Robert Chen, Roi Cohen Kadosh, Lukas Diedrich, Giordano D'Urso, Roberta Ferrucci, Saša R Filipović, Paul B Fitzgerald, Agnes Flöel, Flavio Fröhlich, Mark S George, Roy H Hamilton, Jens Haueisen, Mark Hallett, Christoph S Herrmann, Friedhelm C Hummel, Shapour Jaberzadeh, Berthold Langguth, Michal Lavidor, Jean-Pascal Lefaucheur, Carlo Miniussi, Vera Moliadze, Mika Nikander, Stevan Nikolin, Michael A Nitsche, Alexander Opitz, Jacinta O'Shea, Frank Padberg, Christian Plewnia, Alberto Priori, Perianen Ramasawmy, Lais B Razza, Simone Rossi, John Rothwell, Maria A Rueger, Giulio Ruffini, Alexander T Sack, Ricardo Salvador, Klaus Schellhorn, Teresa Schuhmann, Yuichiro Shirota, Hartwig Roman Siebner, Axel Thielscher, Yoshikazu Ugawa, Susanne Uusitalo, Anna Wexler, Walter Paulus, Marie-Anne Vanderhasselt, Vincent Van Waes, Maximilian J Wessel, Miles Wischnewski, Chris Baeken, Ulf Ziemann
This guideline summarizes updated safety data (2017-2025) and provides expert recommendations on the use of low intensity transcranial electrical stimulation (tES) in humans. tES encompasses several techniques including transcranial direct current stimulation (tDCS), oscillatory transcranial direct current stimulation (otDCS), transcranial alternating current stimulation (tACS), transcranial random noise stimulation (tRNS), transcranial temporal interference stimulation (tTIS), and their combinations or variations. Across over 300,000 sessions involving healthy individuals, patients with neuropsychiatric conditions, and other clinical populations, no tES-related serious adverse events (AEs) have been reported. Moderate AEs are rare and limited to a small range of specific applications. Mild AEs are common and include transient symptoms such as localized sensations (e.g., tingling or burning), headaches, and fatigue. Similar mild AEs are also reported by individuals receiving placebo stimulation. The frequency, magnitude, and type of AEs are comparable across healthy, clinical, and vulnerable groups, including children, elderly, or pregnant women. Combined interventions (e.g., co-application with EEG, TMS, or neuroimaging) have not shown increased safety risks. Safety is well-established for both bipolar and multichannel tES when applied up to 4 mA and up to 60 min per day. Higher intensities and longer stimulation durations may also be safe. Nevertheless, the number of studies using intensities above 4 mA or stimulating longer than 60 min is low. Home-based use of treatments is growing rapidly, leveraging remote supervision to provide patients with greater access and enable repeated, sustained dosing paradigms. We recommend using screening and AE questionnaires in future controlled studies, in particular when planning to extend the stimulation parameters applied. We discuss recent regulatory and ethical issues.
{"title":"Low intensity transcranial electric stimulation: Safety, ethical, legal regulatory and application guidelines (2017-2025: An update) - endorsed by the European Society for Brain Stimulation (ESBS) and by the International Federation for Clinical Neurophysiology (IFCN).","authors":"Andrea Antal, Jovana Bjekić, Ana Ganho-Ávila, Ivan Alekseichuk, Sara Assecondi, Til Ole Bergmann, Marom Bikson, Jerome Brunelin, Andre R Brunoni, Leigh Charvet, Robert Chen, Roi Cohen Kadosh, Lukas Diedrich, Giordano D'Urso, Roberta Ferrucci, Saša R Filipović, Paul B Fitzgerald, Agnes Flöel, Flavio Fröhlich, Mark S George, Roy H Hamilton, Jens Haueisen, Mark Hallett, Christoph S Herrmann, Friedhelm C Hummel, Shapour Jaberzadeh, Berthold Langguth, Michal Lavidor, Jean-Pascal Lefaucheur, Carlo Miniussi, Vera Moliadze, Mika Nikander, Stevan Nikolin, Michael A Nitsche, Alexander Opitz, Jacinta O'Shea, Frank Padberg, Christian Plewnia, Alberto Priori, Perianen Ramasawmy, Lais B Razza, Simone Rossi, John Rothwell, Maria A Rueger, Giulio Ruffini, Alexander T Sack, Ricardo Salvador, Klaus Schellhorn, Teresa Schuhmann, Yuichiro Shirota, Hartwig Roman Siebner, Axel Thielscher, Yoshikazu Ugawa, Susanne Uusitalo, Anna Wexler, Walter Paulus, Marie-Anne Vanderhasselt, Vincent Van Waes, Maximilian J Wessel, Miles Wischnewski, Chris Baeken, Ulf Ziemann","doi":"10.1016/j.clinph.2025.2111436","DOIUrl":"https://doi.org/10.1016/j.clinph.2025.2111436","url":null,"abstract":"<p><p>This guideline summarizes updated safety data (2017-2025) and provides expert recommendations on the use of low intensity transcranial electrical stimulation (tES) in humans. tES encompasses several techniques including transcranial direct current stimulation (tDCS), oscillatory transcranial direct current stimulation (otDCS), transcranial alternating current stimulation (tACS), transcranial random noise stimulation (tRNS), transcranial temporal interference stimulation (tTIS), and their combinations or variations. Across over 300,000 sessions involving healthy individuals, patients with neuropsychiatric conditions, and other clinical populations, no tES-related serious adverse events (AEs) have been reported. Moderate AEs are rare and limited to a small range of specific applications. Mild AEs are common and include transient symptoms such as localized sensations (e.g., tingling or burning), headaches, and fatigue. Similar mild AEs are also reported by individuals receiving placebo stimulation. The frequency, magnitude, and type of AEs are comparable across healthy, clinical, and vulnerable groups, including children, elderly, or pregnant women. Combined interventions (e.g., co-application with EEG, TMS, or neuroimaging) have not shown increased safety risks. Safety is well-established for both bipolar and multichannel tES when applied up to 4 mA and up to 60 min per day. Higher intensities and longer stimulation durations may also be safe. Nevertheless, the number of studies using intensities above 4 mA or stimulating longer than 60 min is low. Home-based use of treatments is growing rapidly, leveraging remote supervision to provide patients with greater access and enable repeated, sustained dosing paradigms. We recommend using screening and AE questionnaires in future controlled studies, in particular when planning to extend the stimulation parameters applied. We discuss recent regulatory and ethical issues.</p>","PeriodicalId":10671,"journal":{"name":"Clinical Neurophysiology","volume":" ","pages":"2111436"},"PeriodicalIF":3.6,"publicationDate":"2025-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146099555","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-21DOI: 10.1016/j.clinph.2025.2111450
Cindy Shin-Yi Lin , Jowy Tani , Ting Wei Hsu , Yi-Chen Lin , Yun-Ru Liu , Jia-Ying Sung M.D. PhD.
Objective
This study aims to characterize sensory axonal changes in patients with non-painful and painful type 2 diabetes mellitus (T2DM) to explore the mechanisms underlying diabetic neuropathic pain in relation to pregabalin treatment.
Methods
Clinical evaluations, including nerve conduction studies, nerve excitability testing (NET) and visual analogue scale (VAS), were conducted on 200 T2DM, resulting 131 qualifying for inclusion. Cohort stratification utilized VAS scores: 43 had VAS ≥ 4 (painful), and 88 had VAS < 4 (non-painful). The painful cohort was categorized into low pain (4 ≤ VAS < 7) and high pain (VAS ≥ 7). A subgroup receiving pregabalin (15) was assessed to investigate neurophysiological differences.
Results
The painful cohort differed significantly from the non-painful cohort in sensory nerve excitability parameters including stimulus for 50% maximum amplitude, refractoriness, superexcitability, subexcitability, and depolarization thresholds. Higher VAS scores correlated with reduced TEd40(Accom) and TEh(overshoot). Pregabalin-treated patients demonstrated improved stimulus–response slope, S2 accommodation and TEd40(Accom) compared to untreated patients.
Conclusions
Our findings suggest that diabetic neuropathic pain may be associated with axonal hyperpolarization and accommodative properties with implications to potassium channel dysfunction.
Significance
These findings elucidate mechanisms of diabetic pain pathophysiology, highlighting the clinical significance of sensory NET and the role of potassium channel modulation in T2DM pain management.
{"title":"Potassium channel dysfunction and distinct sensory axonal profiles in painful type 2 diabetes","authors":"Cindy Shin-Yi Lin , Jowy Tani , Ting Wei Hsu , Yi-Chen Lin , Yun-Ru Liu , Jia-Ying Sung M.D. PhD.","doi":"10.1016/j.clinph.2025.2111450","DOIUrl":"10.1016/j.clinph.2025.2111450","url":null,"abstract":"<div><h3>Objective</h3><div>This study aims to characterize sensory axonal changes in patients with non-painful and painful type 2 diabetes mellitus (T2DM) to explore the mechanisms underlying diabetic neuropathic pain in relation to pregabalin treatment.</div></div><div><h3>Methods</h3><div>Clinical evaluations, including nerve conduction studies, nerve excitability testing (NET) and visual analogue scale (VAS), were conducted on 200 T2DM, resulting 131 qualifying for inclusion. Cohort stratification utilized VAS scores: 43 had VAS ≥ 4 (painful), and 88 had VAS < 4 (non-painful). The painful cohort was categorized into low pain (4 ≤ VAS < 7) and high pain (VAS ≥ 7). A subgroup receiving pregabalin (15) was assessed to investigate neurophysiological differences.</div></div><div><h3>Results</h3><div>The painful cohort differed significantly from the non-painful cohort in sensory nerve excitability parameters including stimulus for 50% maximum amplitude, refractoriness, superexcitability, subexcitability, and depolarization thresholds. Higher VAS scores correlated with reduced TEd<sup>40</sup>(Accom) and TEh(overshoot). Pregabalin-treated patients demonstrated improved stimulus–response slope, S2 accommodation and TEd<sup>40</sup>(Accom) compared to untreated patients.</div></div><div><h3>Conclusions</h3><div>Our findings suggest that diabetic neuropathic pain may be associated with axonal hyperpolarization and accommodative properties with implications to potassium channel dysfunction.</div></div><div><h3>Significance</h3><div>These findings elucidate mechanisms of diabetic pain pathophysiology, highlighting the clinical significance of sensory NET and the role of potassium channel modulation in T2DM pain management.</div></div>","PeriodicalId":10671,"journal":{"name":"Clinical Neurophysiology","volume":"182 ","pages":"Article 2111450"},"PeriodicalIF":3.6,"publicationDate":"2025-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145616618","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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