Canan Duman İlki, Zerin Özaydın Aksun, Hüseyin Özden Şener
{"title":"Diagnostic Utility of 2L-IO Latency Difference in Carpal Tunnel Syndrome: An Electrophysiologic Perspective.","authors":"Canan Duman İlki, Zerin Özaydın Aksun, Hüseyin Özden Şener","doi":"10.1097/WNP.0000000000001225","DOIUrl":"10.1097/WNP.0000000000001225","url":null,"abstract":"<p><strong>Purpose: </strong>This study aimed to evaluate the diagnostic value of the second lumbrical-interosseous distal motor latency (2L-IO distal motor latency [DML]) difference in the diagnosis of carpal tunnel syndrome, and to assess its utility across different stages of the disease.</p><p><strong>Methods: </strong>A total of 145 carpal tunnel syndrome-affected hands from 89 patients and 52 hands from 31 healthy volunteers were evaluated between January and August 2023. In addition to standard electrophysiologic tests, the DML difference between the 2L and interosseous muscles was recorded. Carpal tunnel syndrome severity was classified according to the Bland scale. The diagnostic sensitivity and specificity of the 2L-IO DML difference were analyzed using receiver operating characteristic analysis.</p><p><strong>Results: </strong>The 2L-IO DML difference was significantly prolonged in the carpal tunnel syndrome group compared with healthy controls (1.85 ± 1.41 ms vs. 0.25 ± 0.28 ms; P < 0.001). With a cutoff value of 0.45 ms, the sensitivity and specificity of the method were calculated as 98.6 and 98.1%, respectively. Although the diagnostic accuracy of conventional tests was 84%, it increased to 98% with the 2L-IO DML difference. Diagnosis was achieved in 85% of early stage (Grade 0-1) cases and in 90% of advanced cases in which the abductor pollicis brevis response was absent.</p><p><strong>Conclusions: </strong>The 2L-IO DML difference offers high diagnostic value in carpal tunnel syndrome, serving as a complementary test in early stages and a decisive tool in advanced stages. Preferentially recording from the 2L muscle instead of the abductor pollicis brevis may facilitate electrophysiologic evaluation, especially in challenging cases.</p>","PeriodicalId":15516,"journal":{"name":"Journal of Clinical Neurophysiology","volume":" ","pages":"463-467"},"PeriodicalIF":1.8,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145541053","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}
Dayna D Whitcombe, Diana Escalona-Vargas, Hari Eswaran, Heather Moody, Luis Mercado, Nafisa K Dajani, Debopam Samanta
{"title":"Magnetoencephalography as a Novel Tool for Prenatal Diagnosis of Fetal Seizures.","authors":"Dayna D Whitcombe, Diana Escalona-Vargas, Hari Eswaran, Heather Moody, Luis Mercado, Nafisa K Dajani, Debopam Samanta","doi":"10.1097/WNP.0000000000001253","DOIUrl":"10.1097/WNP.0000000000001253","url":null,"abstract":"<p><strong>Summary: </strong>Fetal seizures represent one of the rarest phenomena in prenatal medicine, with fewer than 50 documented cases. Diagnosis has traditionally relied on maternal reports and ultrasound visualization of abnormal movements, lacking the neurophysiologic confirmation available in neonatal care. This case report presents the first neurophysiologic assessment of fetal seizures using fetal magnetoencephalography (fMEG), demonstrating a novel diagnostic approach for prenatal neurologic evaluation. A 22-year-old primigravida with controlled epilepsy presented with a fetus showing severe growth restriction and multiple anomalies at 23 weeks gestation. At 32 weeks, repetitive rhythmic jerking movements suggested in utero seizures and were confirmed with real-time ultrasound. fMEG was performed using the SQUID Array for Reproductive Assessment (SARA) system, revealing immature patterns indicative of encephalopathy with alternating periods of severe bilateral suppression and low-amplitude activity. Bursts lasting up to 6 seconds coincided with erratic body movements confirmed by actogram. The infant was delivered at 37 weeks weighing 1,200 g and continued to exhibit myoclonic and clonic seizures postnatally. Postmortem whole exome sequencing identified biallelic pathogenic variants in PSAT1 , confirming Neu-Laxova syndrome. The infant died on the fifth day of life after transition to comfort care. This case demonstrates the feasibility of direct neurophysiologic assessment of fetal brain activity using fMEG, providing objective confirmation of fetal seizures for the first time. The technology offers potential for distinguishing true fetal seizures from other conditions that mimic seizure-like movements, enabling more accurate prenatal counseling and informed decision making. This represents a significant advancement in prenatal neurologic assessment, with implications for early diagnosis and targeted interventions.</p>","PeriodicalId":15516,"journal":{"name":"Journal of Clinical Neurophysiology","volume":" ","pages":"468-472"},"PeriodicalIF":1.8,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147512314","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":"Rhythmic and Periodic Patterns and Seizures in Hypoxic-Ischemic Encephalopathy.","authors":"Pia De Stefano, Nicolas Gaspard","doi":"10.1097/WNP.0000000000001235","DOIUrl":"10.1097/WNP.0000000000001235","url":null,"abstract":"<p><strong>Summary: </strong>Cardiac arrest is a major cause of hypoxic-ischemic brain injury, often resulting in coma even after the return of spontaneous circulation. In this severely ill population, accurate neurologic prognostication is essential for guiding treatment decisions. Continuous electroencephalography (EEG) has become a cornerstone of postcardiac arrest care, offering real-time monitoring of cerebral activity and facilitating early detection of electrographic seizures and other pathologic patterns. This narrative review focuses on the standardized interpretation of EEG findings using the 2021 American Clinical Neurophysiology Society Critical Care EEG terminology. Key EEG patterns-such as generalized periodic discharges, suppression-burst, and status epilepticus (SE)-are discussed in the context of their prognostic significance and therapeutic implications. Particular attention is given to the progressive restoration of background EEG continuity and amplitude over the first 24 hours after the arrest, which is increasingly recognized as a marker of the extent of neuronal damage and potential for recovery. Seizure and SE management remains complex in comatose postcardiac arrest patients, with recent studies highlighting variable outcomes and the potential risks of both under- and overtreatment. We underscore the importance of individualized treatment strategies informed by EEG characteristics and integrated with clinical examination, neuroimaging, and serum biomarkers. Multimodal prognostication helps identify patients with a potential for meaningful recovery while avoiding unnecessary interventions in those with poor neurologic prognosis. EEG-guided care is crucial in optimizing outcomes after cardiac arrest and enhancing the precision of neurocritical care.</p>","PeriodicalId":15516,"journal":{"name":"Journal of Clinical Neurophysiology","volume":" ","pages":"410-417"},"PeriodicalIF":1.8,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13317903/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148329933","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Spencer Nam, Olivia Marais, Manveer Dilts-Garcha, Fanglin Zhang, Alexandria Jensen, Robert S Fisher
{"title":"Focal Spikes Versus Sharp Waves: Do They Differ?","authors":"Spencer Nam, Olivia Marais, Manveer Dilts-Garcha, Fanglin Zhang, Alexandria Jensen, Robert S Fisher","doi":"10.1097/WNP.0000000000001223","DOIUrl":"10.1097/WNP.0000000000001223","url":null,"abstract":"<p><strong>Introduction: </strong>Conventional EEG interpretation distinguishes spikes (20-70 ms) versus sharp waves (70-200 ms), but the rationale for this distinction is unclear. This preliminary study endeavors to correlate discharge duration with some clinical outcomes.</p><p><strong>Methods: </strong>We measured spike and sharp wave duration for up to 10 discharges in 100 patients referred for routine, inpatient, or ambulatory EEGs. Excluded were generalized spikes, spike waves, polyspikes, seizures, or lateralized periodic discharges (LPDs).</p><p><strong>Results: </strong>We measured 882 interictal discharges in 100 patients, comprising structural, genetic, autoimmune, and unknown etiologies. Epileptiform discharges, mainly temporal, were unilateral in 64 and bilateral or multifocal in 36 patients. Each record presented 3 to 10 discharges, with 74% having 10 or more. Mean discharge duration was 71.9 ± 31.4, range 15 to 200 ms. Most patients (87%) had mixed sharps and spikes, with 6% having only sharps and 7% having only spikes. Discharge durations within an individual patient were highly variable. Mean discharge duration and seizure frequency were poorly correlated ( r = -0.023, P = 0.82), as were discharge duration and number of antiseizure medications ( r = -0.027, P = 0.80).</p><p><strong>Conclusions: </strong>In our series, discharge duration did not correlate with seizure frequency or number of antiseizures medicines. Only 13% of patients had exclusive spikes or sharp waves, suggesting that duration of an individual discharge is not a defining characteristic of that person's epilepsy. Although this study is small and preliminary, it suggests that the distinction between spike and sharp waves at 70 ms may not be clinically relevant and perhaps all epileptiform discharges could be called spikes.</p>","PeriodicalId":15516,"journal":{"name":"Journal of Clinical Neurophysiology","volume":" ","pages":"446-454"},"PeriodicalIF":1.8,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145438227","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":"Neurophysiologic Mechanisms of Cerebral Ischemia and the EEG.","authors":"Michel J A M van Putten, Jeannette Hofmeijer","doi":"10.1097/WNP.0000000000001227","DOIUrl":"10.1097/WNP.0000000000001227","url":null,"abstract":"<p><strong>Summary: </strong>Cerebral ischemia rapidly disturbs neuronal function through failure of synaptic transmission and, with ongoing energy deprivation, loss of ion gradients. Adenosine-mediated inhibition of presynaptic release leads to an early and reversible loss of synaptic transmission, reflected in the EEG by slowing and eventual suppression of rhythmic activity. With more severe or prolonged energy failure, Na + /K + -ATPase failure results in membrane depolarization, cytotoxic swelling, and irreversible injury. Secondary injury mechanisms include spreading depolarizations, inflammation, and oxidative stress. The EEG primarily reflects extracellular currents resulting from synaptic input on pyramidal neurons, providing a real-time readout of cerebral function. Recovery of continuous background activity with physiologic rhythms within 12 to 24 hours indicates preserved and reversible synaptic function, whereas persistent suppression or burst suppression with identical bursts beyond 24 hours is consistently associated with extensive structural injury and poor neurologic outcome.</p>","PeriodicalId":15516,"journal":{"name":"Journal of Clinical Neurophysiology","volume":" ","pages":"375-383"},"PeriodicalIF":1.8,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148329905","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":"Neuroprotective Treatment of Postanoxic Encephalopathy: Review of the Literature and Ongoing Trials.","authors":"Jong Woo Lee, Jeannette Hofmeijer","doi":"10.1097/WNP.0000000000001251","DOIUrl":"10.1097/WNP.0000000000001251","url":null,"abstract":"<p><strong>Summary: </strong>Postanoxic encephalopathy is a common consequence of cardiac arrest, characterized by varying degrees of global cerebral hypoxic-ischemic injury. Despite advances in resuscitation science and critical care, neurologic outcome is essentially unchanged over the past decades. Although various treatment approaches to mitigate brain injury have been proposed, none of these has been unequivocally associated with improved neurologic outcome. This review provides an overview of the evidence from previous studies and ongoing clinical trials. Based on successes and limitations in recent research, we recommend EEG-based patient stratification and sufficiently powered subgroups for future trials. We also recommend outcome measures that provide more granularity than the current ordinal outcome scales, such as screening instruments for cognitive and emotional functioning. Adaptive randomized trial designs using a single master protocol and Bayesian statistics can provide an efficient platform for testing multiple treatments against a common control group, simultaneously. Treatments based on active stimulation of neuro- and synaptogenesis instead of prevention of secondary injury are promising.</p>","PeriodicalId":15516,"journal":{"name":"Journal of Clinical Neurophysiology","volume":" ","pages":"432-440"},"PeriodicalIF":1.8,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148330027","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":"Neurophysiology in Postanoxic Encephalopathy: Pathophysiology, Prognosis, and Treatment.","authors":"Michel J A M van Putten","doi":"10.1097/WNP.0000000000001270","DOIUrl":"10.1097/WNP.0000000000001270","url":null,"abstract":"","PeriodicalId":15516,"journal":{"name":"Journal of Clinical Neurophysiology","volume":" ","pages":"373-374"},"PeriodicalIF":1.8,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148330057","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}
David Burdette, Sanjay Patra, Martha Morrell, Lise Johnson
{"title":"Clusters in Thalamic iEEG Spectral Features Reveal Sleep/Wake Differences Over Time.","authors":"David Burdette, Sanjay Patra, Martha Morrell, Lise Johnson","doi":"10.1097/WNP.0000000000001230","DOIUrl":"10.1097/WNP.0000000000001230","url":null,"abstract":"<p><strong>Purpose: </strong>The thalamus is a target for neurostimulation in epilepsy based on its extensive reciprocal connectivity with the cortex and subcortical areas and putative participation in a broader seizure network. In focal neocortical onset epilepsies, costimulation of the cortex and thalamus may provide an opportunity to modulate two nodes of a seizure network. Given the central role of the thalamus in sleep oscillations and regulation of consciousness, as well as the fundamental interaction between sleep and epilepsy, consideration of sleep/wake cycles may be important when treating patients with corticothalamic stimulation.</p><p><strong>Methods: </strong>This single-center retrospective study included 30 patients with focal seizures treated with cortical and thalamic responsive neurostimulation (NeuroPace RNS ® System). The thalamic leads were implanted in the centromedian, pulvinar, mediodorsal, or anterior nucleus depending on clinical characteristics, semiology, and localization testing. Changes in the average power of predefined frequency bands in the interictal thalamic iEEGs were evaluated in ambulatory daily recordings collected postimplant.</p><p><strong>Results: </strong>Two clusters in frequency characteristics were clearly distinguished by time of day (daytime vs. nighttime). The time series evolution for points in the two clusters was not generally correlated, and sometimes diverged. Clusters were more prominent on some channels than others, even between adjacent electrode contacts on the same leads, perhaps reflecting the anatomic location.</p><p><strong>Conclusions: </strong>These results suggest that thalamic iEEG data can potentially be used to identify wake/sleep states electrographically without traditional sleep studies. This could enable state-dependent neuromodulation therapy. The observed changes in sleep/wake clusters over time could represent neuromodulation-driven changes in thalamocortical networks and warrant further investigation.</p>","PeriodicalId":15516,"journal":{"name":"Journal of Clinical Neurophysiology","volume":" ","pages":"455-462"},"PeriodicalIF":1.8,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13317916/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145911727","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hunki Kwon, Edward M Merricks, Sarah Yi, Mark A Kramer, Catherine J Chu
{"title":"Sleep Microarchitecture, Epileptic Spikes, and Memory in Epilepsy: Implications for Developmental and Epileptic Encephalopathies.","authors":"Hunki Kwon, Edward M Merricks, Sarah Yi, Mark A Kramer, Catherine J Chu","doi":"10.1097/WNP.0000000000001278","DOIUrl":"10.1097/WNP.0000000000001278","url":null,"abstract":"<p><strong>Summary: </strong>Healthy sleep is electrographically defined by oscillations that drive alternating up- and down-states that regulate neuronal excitability. Slow oscillations-the hallmark rhythm of deep nonrapid eye movement sleep, temporally organize faster, more focal rhythms, including thalamocortical sleep spindles and hippocampal sharp-wave ripples. These cascading rhythms have been implicated as a critical activity-dependent mechanism that binds coordinated neuronal activity to support systems-level consolidation of previous experience into long-term memory. Epilepsy is a disease characterized by sporadic pathologic neuronal activity, including interictal epileptiform discharges and seizures. Epileptic activity is frequently potentiated during sleep, but the interactions with specific graphoelements that comprise sleep microarchitecture are complex. Critically, the diverse ways in which epileptic activity interdigitates with sleep microstructure imply that epileptiform activity can distort and disrupt the same sleep rhythms that normally support memory consolidation. Cognitive comorbidities are common in epilepsy, and impairments in memory consolidation are increasingly recognized. In this review, we synthesize leading evidence on the complex interactions between sleep microarchitecture and interictal epileptiform discharges. We first summarize electrophysiologic data on how slow oscillations interact with spindles and interictal epileptiform discharges and then assemble these findings into a unifying framework for interictal epileptiform discharge-slow oscillation-spindle dynamics. Finally, we review evidence on how disruption of these sleep oscillations can contribute to cognitive dysfunction in epilepsy and highlight implications for developmental and epileptic encephalopathies.</p>","PeriodicalId":15516,"journal":{"name":"Journal of Clinical Neurophysiology","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2026-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148295236","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}