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The potassium-chloride co-transporter 2, KCC2, is a neuron-specific ion transporter that plays a multifunctional role in neuronal development. In mature neurons, KCC2 maintains a low enough intracellular chloride concentration essential for inhibitory neurotransmission. During recent years, pathogenic variants in the KCC2 encoding gene SLC12A5 affecting the functionality or expression of the transporter protein have been described in several patients with epilepsy of infancy with migrating focal seizures (EIMFS), a devastating early-onset developmental and epileptic encephalopathy. In this study, we identified a novel recessively inherited SLC12A5 c.692G>A, p. (R231H) variant in a patient diagnosed with severe and drug-resistant EIMFS and profound intellectual disability. The functionality of the variant was assessed in vitro by means of gramicidin-perforated patch-clamp experiments and ammonium flux assay, both of which indicated a significant reduction in chloride extrusion. Based on surface immunolabeling, the variant showed a reduction in membrane expression. These findings implicate pathogenicity of the SLC12A5 variant that leads to impaired inhibitory neurotransmission, increasing probability for hyperexcitability and epileptogenesis.

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Introduction: Sleep increases brain fluid transport and the power of pulsations driving the fluids. We investigated how sleep deprivation or electrophysiologically different stages of non-rapid-eye-movement (NREM) sleep affect the human brain pulsations. Methods: Fast functional magnetic resonance imaging (fMRI) was performed in healthy subjects (n = 23) with synchronous electroencephalography (EEG), that was used to verify arousal states (awake, N1 and N2 sleep). Cardiorespiratory rates were verified with physiological monitoring. Spectral power analysis assessed the strength, and spectral entropy assessed the stability of the pulsations. Results: In N1 sleep, the power of vasomotor (VLF < 0.1 Hz), but not cardiorespiratory pulsations, intensified after sleep deprived vs. non-sleep deprived subjects. The power of all three pulsations increased as a function of arousal state (N2 > N1 > awake) encompassing brain tissue in both sleep stages, but extra-axial CSF spaces only in N2 sleep. Spectral entropy of full band and respiratory pulsations decreased most in N2 sleep stage, while cardiac spectral entropy increased in ventricles. Discussion: In summary, the sleep deprivation and sleep depth, both increase the power and harmonize the spectral content of human brain pulsations.

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OBJECTIVE: Infra-slow fluctuations (ISF, 0.008-0.1 Hz) characterize hemodynamic and electric potential signals of human brain. ISFs correlate with the amplitude dynamics of fast (>1 Hz) neuronal oscillations, and may arise from permeability fluctuations of the blood-brain barrier (BBB). It is unclear if physiological rhythms like respiration drive or track fast cortical oscillations, and the role of sleep in this coupling is unknown. METHODS: We used high-density full-band electroencephalography (EEG) in healthy human volunteers (N = 21) to measure concurrently the ISFs, respiratory pulsations, and fast neuronal oscillations during periods of wakefulness and sleep, and to assess the strength and direction of their phase-amplitude coupling. RESULTS: The phases of ISFs and respiration were both coupled with the amplitude of fast neuronal oscillations, with stronger ISF coupling being evident during sleep. Phases of ISF and respiration drove the amplitude dynamics of fast oscillations in sleeping and waking states, with different contributions. CONCLUSIONS: ISFs in slow cortical potentials and respiration together significantly determine the dynamics of fast cortical oscillations. SIGNIFICANCE: We propose that these slow physiological phases play a significant role in coordinating cortical excitability, which is a fundamental aspect of brain function.

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Objective: Primary objective was to retrospectively examine the effects of patient age and carpal tunnel syndrome (CTS) related axon loss on median nerve (MN) high resolution ultrasound (HRUS) in younger and older patients. HRUS parameters evaluated in this study were MN cross sectional area at the wrist (CSA) and wrist-to-forearm ratio (WFR). Methods: The material comprised 467 wrists of 329 patients. The patients were categorized into younger (<65 years) and older (≥65 years) groups. Patients with moderate to extreme CTS were included in the study. Axon loss of the MN was assessed by needle EMG and graded by the interference pattern (IP) density. The association between axon loss and CSA and WFR was studied. Results: The older patients had smaller mean CSA and WFR values compared to the younger patients. CSA correlated positively to the CTS severity only in the younger group. However, WFR correlated positively to CTS severity in both groups. In both age groups, CSA and WFR correlated positively with IP reduction. Conclusions: Our study complemented recent findings on the effects of patient age on the CSA of the MN. However, although the MN CSA did not correlate with the CTS severity in older patients, the CSA increased in respect to the amount of axon loss. Also, as a new result, we presented the positive association of WFR with CTS severity among older patients. Significance: Our study supports the recently speculated need for different MN CSA and WFR cut-off values for younger and older patients in assessing the severity of CTS. With older patients, WFR may be a more reliable parameter to assess the CTS severity than the CSA. CTS related axonal damage of the MN is associated to additional nerve enlargement at the carpal tunnel intel site.

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The physiological underpinnings of the necessity of sleep remain uncertain. Recent evidence suggests that sleep increases the convection of cerebrospinal fluid (CSF) and promotes the export of interstitial solutes, thus providing a framework to explain why all vertebrate species require sleep. Cardiovascular, respiratory and vasomotor brain pulsations have each been shown to drive CSF flow along perivascular spaces, yet it is unknown how such pulsations may change during sleep in humans. To investigate these pulsation phenomena in relation to sleep, we simultaneously recorded fast fMRI, magnetic resonance encephalography (MREG), and electroencephalography (EEG) signals in a group of healthy volunteers. We quantified sleep-related changes in the signal frequency distributions by spectral entropy analysis and calculated the strength of the physiological (vasomotor, respiratory, and cardiac) brain pulsations by power sum analysis in 15 subjects (age 26.5 ± 4.2 years, 6 females). Finally, we identified spatial similarities between EEG slow oscillation (0.2-2 Hz) power and MREG pulsations. Compared with wakefulness, nonrapid eye movement (NREM) sleep was characterized by reduced spectral entropy and increased brain pulsation intensity. These effects were most pronounced in posterior brain areas for very low-frequency (≤0.1 Hz) vasomotor pulsations but were also evident brain-wide for respiratory pulsations, and to a lesser extent for cardiac brain pulsations. There was increased EEG slow oscillation power in brain regions spatially overlapping with those showing sleep-related MREG pulsation changes. We suggest that reduced spectral entropy and enhanced pulsation intensity are characteristic of NREM sleep. With our findings of increased power of slow oscillation, the present results support the proposition that sleep promotes fluid transport in human brain.SIGNIFICANCE STATEMENT We report that the spectral power of physiological brain pulsation mechanisms driven by vasomotor, respiration, and cardiac rhythms in human brain increase during sleep, extending previous observations of their association with glymphatic brain clearance during sleep in rodents. The magnitudes of increased pulsations follow the rank order of vasomotor greater than respiratory greater than cardiac pulsations, with correspondingly declining spatial extents. Spectral entropy, previously known as vigilance and as an anesthesia metric, decreased during NREM sleep compared with the awake state in very low and respiratory frequencies, indicating reduced signal complexity. An EEG slow oscillation power increase occurring in the early sleep phase (NREM 1-2) spatially overlapped with pulsation changes, indicating reciprocal mechanisms between those measures.

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BACKGROUND: Patients with schizophrenia spectrum disorder have increased risk of coronary artery disease. AIMS: To investigate long-term outcomes of patients with schizophrenia spectrum disorder and coronary artery disease after coronary artery bypass grafting surgery (CABG). METHOD: Data from patients with schizophrenia spectrum disorder (n = 126) were retrospectively compared with propensity-matched (1:20) control patients without schizophrenia spectrum disorder (n = 2520) in a multicentre study in Finland. All patients were treated with CABG. The median follow-up was 7.1 years. The primary outcome was all-cause mortality. RESULTS: Patients with diagnosed schizophrenia spectrum disorder had an elevated risk of 10-year mortality after CABG, compared with control patients (42.7 v. 30.3%; hazard ratio 1.56; 95% CI 1.13-2.17; P = 0.008). Schizophrenia spectrum diagnosis was associated with a higher risk of major adverse cardiovascular events during follow-up (49.9 v. 32.6%, subdistribution hazard ratio 1.59; 95% CI 1.18-2.15; P = 0.003). Myocardial infarction (subdistribution hazard ratio 1.86; P = 0.003) and cardiovascular mortality (subdistribution hazard ratio 1.65; P = 0.017) were more frequent in patients with versus those without schizophrenia spectrum disorder, but there was no difference for stroke. Psychiatric ward admission, antipsychotic medication, antidepressant use and benzodiazepine use before CABG were not associated with outcome differences. After CABG, patients with schizophrenia spectrum disorder received statin therapy less often and had lower doses; the use of other cardiovascular medications was similar between schizophrenia spectrum and control groups. CONCLUSIONS: Patients with schizophrenia spectrum disorder have higher long-term risks of death and major adverse cardiovascular events after CABG. The results underline the vulnerability of these patients and highlight the importance of intensive secondary prevention and risk factor optimisation.

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OBJECTIVES: Paraplegia is a devastating complication in aortic aneurysm surgery. Modifying the spinal cord vasculature is a promising method in spinal cord protection. The aim of this study was to assess whether the spinal cord can be primed by occluding thoracic segmental arteries before simulated aneurysm repair in a porcine model. METHODS: Twelve piglets were randomly assigned to the priming group (6) and the control group (6). Eight uppermost thoracic segmental arteries were occluded at 5-minute intervals in the priming group before a 25-minute aortic crossclamp. In the control group, the aorta was crossclamped for 25 minutes. During the first 5 minutes, 8 segmental arteries were occluded. After the aortic crossclamping, piglets were observed under anesthesia for 5 hours and followed up 5 days postoperatively. Near-infrared spectroscopy, motor-evoked potentials, blood samples, neurology with the modified Tarlov score, and histopathology of the spinal cord were assessed. RESULTS: The median Tarlov score during the first postoperative day was higher in the priming group than in the control group (P = .001). At the end, 50% of the control animals had paraplegia compared with 0% of paraplegia in the priming group. The mean regional histopathologic score differed between the priming group and the control group (P = .02). The priming group had higher motor-evoked potentials during the operation at separate time points. The lactate levels were lower in the priming group compared with the control group (Pg = .001, Pg×t = .18). CONCLUSIONS: Acute priming protects the spinal cord from ischemic injury in an experimental aortic crossclamp model.

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OBJECTIVE: To assess the inter-rater reliability of MScanFit MUNE using a "Round Robin" research design. METHODS: Twelve raters from different centres examined six healthy study participants over two days. Median, ulnar and common peroneal nerves were stimulated, and compound muscle action potential (CMAP)-scans were recorded from abductor pollicis brevis (APB), abductor digiti minimi (ADM) and anterior tibial (TA) muscles respectively. From this we calculated the Motor Unit Number Estimation (MUNE) and "A50", a motor unit size parameter. As statistical analysis we used the measures Limits of Agreement (LOA) and Coefficient of Variation (COV). Study participants scored their perception of pain from the examinations on a rating scale from 0 (no pain) to 10 (unbearable pain). RESULTS: Before this study, 41.6% of the raters had performed MScanFit less than five times. The mean MUNE-values were: 99.6 (APB), 131.4 (ADM) and 126.2 (TA), with LOA: 19.5 (APB), 29.8 (ADM) and 20.7 (TA), and COV: 13.4 (APB), 6.3 (ADM) and 5.6 (TA). MUNE-values correlated to CMAP max amplitudes (R2-values were: 0.463 (APB) (p<0.001), 0.421 (ADM) (p<0.001) and 0.645 (TA) (p<0.001)). The average perception of pain was 4. DISCUSSION: MScanFit indicates a high level of inter-rater reliability, even with only limited rater experience and is overall reasonably well tolerated by patients. These results may indicate MScanFit as a reliable MUNE method with potential as a biomarker in drug trials.

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BACKGROUND AND OBJECTIVES: Mutations in the ganglioside-induced differentiation-associated protein 1 (GDAP1) gene cause autosomal dominant or autosomal recessive forms of Charcot-Marie-Tooth disease (CMT). Our aim was to study the clinical phenotype of patients with CMT caused by heterozygous p.His123Arg in GDAP1. METHODS: Twenty-three Finnish patients were recruited from a population-based cohort and through family investigation. Each patient was examined clinically and electrophysiologically. The Neuropathy Symptom Score and the Neuropathy Disability Score (NDS) were used in clinical evaluation. RESULTS: The median age at onset of symptoms was 17 years among patients with p.His123Arg in GDAP1. Motor symptoms were markedly more common than sensory symptoms at onset. All patients had distal weakness in lower extremities, and 17 (74%) patients had proximal weakness. Muscle atrophy and pes cavus were also common. Nineteen (82%) patients had sensory symptoms such as numbness or pain. The disease progressed with age, and the NDS increased 8.5 points per decade. Electrodiagnostic testing revealed length-dependent, sensory and motor axonal polyneuropathy. EDx findings were asymmetrical in 14 patients. Genealogic study of the families suggested a founder effect. DISCUSSION: We found that CMT in patients with p.His123Arg in GDAP1 is relatively mild and slow in progression.

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AIM OF THE STUDY: EEG slow wave activity (SWA) has shown prognostic potential in post-resuscitation care. In this prospective study, we investigated the accuracy of continuously measured early SWA for prediction of the outcome in comatose cardiac arrest (CA) survivors. METHODS: We recorded EEG with a disposable self-adhesive frontal electrode and wireless device continuously starting from ICU admission until 48 h from return of spontaneous circulation (ROSC) in comatose CA survivors sedated with propofol. We determined SWA by offline calculation of C-Trend® Index describing SWA as a score ranging from 0 to 100. The functional outcome was defined based on Cerebral Performance Category (CPC) at 6 months after the CA to either good (CPC 1-2) or poor (CPC 3-5). RESULTS: Outcome at six months was good in 67 of the 93 patients. During the first 12 h after ROSC, the median C-Trend Index value was 38.8 (interquartile range 28.0-56.1) in patients with good outcome and 6.49 (3.01-18.2) in those with poor outcome showing significant difference (p < 0.001) at every hour between the groups. The index values of the first 12 h predicted poor outcome with an area under curve of 0.86 (95% CI 0.61-0.99). With a cutoff value of 20, the sensitivity was 83.3% (69.6%-92.3%) and specificity 94.7% (83.4%-99.7%) for categorization of outcome. CONCLUSION: EEG SWA measured with C-Trend Index during propofol sedation offers a promising practical approach for early bedside evaluation of recovery of brain function and prediction of outcome after CA.

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Surgical repair of thoracic aorta can compromise blood flow of the spinal cord. To mitigate spinal cord ischemia (SCI) additional protection methods are needed. In experimental studies remote ischemic preconditioning (RIPC) has proven to be an effective method of protecting organs from ischemia. The aim of the study was to assess efficacy of RIPC in spinal cord protection in a chronic porcine model. Sixteen piglets were assigned into the RIPC group (8) and the control group (8). RIPC was performed using blood pressure cuff in a 5-minute ischemia followed by a 5-minute reperfusion repeating cycles 4 times. The left subclavian artery and all segmental arteries above diaphragm were ligated at 5-minute intervals to accomplish SCI. The follow-up comprised a 4-hour intensive monitoring and a 7-day recovery phase. Blood samples were obtained, motor-evoked potentials and near-infrared spectroscopy (NIRS) of longitudinal back muscles were measured. Paraplegia was assessed every day postoperatively. Histopathological analysis of the spinal cord was performed after 7 days. NIRS values 4 hours after SCI were higher in the RIPC group, 45.5 (44.5-47.0), than in the control group, 41.5 (40.5-44.0) (P = 0.042). Nadir value of NIRS was 43.4 (39.3-46.0) in the RIPC group and 38.9 (38.-40.0) in the control group (P = 0.014). On the first postoperative day the RIPC group reached modified Tarlov score of 3 (2-3) vs 2 (1-2) in the control group (P = 0.024). RIPC hastens the recovery from SCI during the first postoperative day.

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OBJECTIVE: To assess relationship of non-melancholic and melancholic subtypes of depressive symptoms with all-cause mortality among cardiovascular risk persons. METHODS: A population-based prospective study of 2522 Finnish middle-aged persons with elevated cardiovascular risk was conducted. Depressive symptoms were assessed by the Beck's Depression Inventory. Data on mortality were obtained from The Official Statistics of Finland after 11-year follow-up. RESULTS: At baseline, the prevalence of non-melancholic and melancholic depressive symptoms was 14.9% and 5.2%, respectively. During the mean follow-up time of 11 years, 8.1% (n = 164) of those without, 13.9% (n = 52) of those with non-melancholic, and 10.7% (n = 14) of those with melancholic depressive symptoms died. Compared to non-depressive subjects, the hazard ratio for time to all-cause mortality was 1.67 (95% CI: 1.21-2.32, p = .002) in non-melancholically depressive and 1.01 (95% CI: 0.56-1.83, p = .97) in melancholically depressive subjects, when adjusted for age, gender, education, smoking, alcohol use, BMI, hypertension, dyslipidaemia, and glucose disorders. In comparison to the mortality rate in the general population throughout Finland over the same period, non-depressiveness was associated with a decreased standardized mortality rate. CONCLUSION: Non-melancholic depressive symptoms seem to be associated with excess all-cause mortality. In clinical settings, recognition of non-melancholic depressive symptoms should be emphasised.

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OBJECTIVE: Our goal was to discover attention- and inhibitory control-related differences in the main oscillations of the brain of children who stutter (CWS) compared to typically developed children (TDC). METHODS: We performed a time-frequency analysis using wavelets, fast Fourier transformation (FFT) and the Alpha/Theta power ratio of EEG data collected during a visual Go/Nogo task in 7-9 year old CWS and TDC, including also the time window between consecutive tasks. RESULTS: CWS showed significantly reduced occipital alpha power and Alpha/Theta ratio in the "resting" or preparatory period between visual stimuli especially in the Nogo condition. CONCLUSIONS: The CWS demonstrate reduced inhibition of the visual cortex and information processing in the absence of visual stimuli, which may be related to problems in attentional gating. SIGNIFICANCE: Occipital alpha oscillation is elementary in the control and inhibition of visual attention and the lack of occipital alpha modulation indicate fundamental differences in the regulation of visual information processing in CWS. Our findings support the view of stuttering as part of a wide-ranging brain dysfunction most likely involving also attentional and inhibitory networks.

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Collagen XIII occurs as both a transmembrane-bound and a shed extracellular protein and is able to regulate the formation and function of neuromuscular synapses. Its absence results in myasthenia: presynaptic and postsynaptic defects at the neuromuscular junction (NMJ), leading to destabilization of the motor nerves, muscle regeneration and atrophy. Mutations in COL13A1 have recently been found to cause congenital myasthenic syndrome, characterized by fatigue and chronic muscle weakness, which may be lethal. We show here that muscle defects in collagen XIII-deficient mice stabilize in adulthood, so that the disease is not progressive until very late. Sciatic nerve crush was performed to examine how the lack of collagen XIII or forced expression of its transmembrane form affects the neuromuscular synapse regeneration and functional recovery following injury. We show that collagen XIII-deficient male mice are unable to achieve complete NMJ regeneration and functional recovery. This is mainly attributable to presynaptic defects that already existed in the absence of collagen XIII before injury. Shedding of the ectodomain is not required, as the transmembrane form of collagen XIII alone fully rescues the phenotype. Thus, collagen XIII could serve as a therapeutic agent in cases of injury-induced PNS regeneration and functional recovery. We conclude that intrinsic alterations at the NMJ in Col13a1-/- mice contribute to impaired and incomplete NMJ regeneration and functional recovery after peripheral nerve injury. However, such alterations do not progress once they have stabilized in early adulthood, emphasizing the role of collagen XIII in NMJ maturation.SIGNIFICANCE STATEMENT Collagen XIII is required for gaining and maintaining the normal size, complexity, and functional capacity of neuromuscular synapses. Loss-of-function mutations in COL13A1 cause congenital myasthenic syndrome 19, characterized by postnatally progressive muscle fatigue, which compromises patients' functional capacity. We show here in collagen XIII-deficient mice that the disease stabilizes in adulthood once the NMJs have matured. This study also describes a relevant contribution of the altered NMJ morphology and function to neuromuscular synapses, and PNS regeneration and functional recovery in collagen XIII-deficient mice after peripheral nerve injury. Correlating the animal model data on collagen XIII-associated congenital myasthenic syndrome, it can be speculated that neuromuscular connections in congenital myasthenic syndrome patients are not able to fully regenerate and restore normal functionality if exposed to peripheral nerve injury.

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PURPOSE: The purpose of this prospective 3-year follow-up was to investigate the association of glucose, insulin, and cholesterol levels with peripheral nervous system function in overweight and obese subjects. METHODS: Forty nondiabetic overweight and obese adults were enrolled, of whom 29 completed the follow-up. Peripheral nervous system function was measured and defined by conduction studies of the peroneal motor nerve and the radial, sural, and medial plantar sensory nerves. Serum insulin and glucose levels were determined with an oral glucose tolerance test, and cholesterol levels were measured. The measurements were performed at baseline and after 3 years. RESULTS: The change in serum insulin level at 120 minutes after an oral glucose tolerance test was positively associated with changes in peroneal nerve conduction velocities and F-wave mean, sural nerve conduction and medial plantar nerve conduction velocities. Action potential amplitudes decreased consistently and significantly in all sensory nerves. CONCLUSIONS: The change in serum insulin level at 120 minutes appears to be positively associated with changes in nerve conduction velocities more than 3 years but not with nerve action potential amplitudes. Significant decreases in the action potential amplitudes of all sensory nerves suggest that such changes might be the earliest detectable sign of damage to the peripheral nervous system in overweight and obese people without type 2 diabetes.

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BACKGROUND: Charcot-Marie-Tooth (CMT) disease is the most common hereditary neuromuscular disorder with a population prevalence of 9.7-82.3/100,000. In this study, we have estimated the prevalence of CMT and its subtypes in Finland and examined the frequency of molecular etiologies. METHODS: A population-based survey included adult patients with peripheral neuropathy from the province of Northern Ostrobothnia, Finland. Secondary causes of peripheral polyneuropathy were excluded and patients with clinical and neurophysiological features pertinent with CMT were included. Molecular diagnostics was carried out when DNA was available. RESULTS: We found 107 subjects with CMT yielding a prevalence 34.6/100,000 in Northern Ostrobothnia. The heterozygous point mutation p.His123Arg in ganglioside induced differentiation associated protein 1 (GDAP1) was found in 31.5% and peripheral myelin protein 22 (PMP22) duplication in 16.9% of the affected. Point mutations in myelin protein zero, mitofusin 2, and gap junction protein beta 1 accounted for 6.7% of the cases. In addition, 18 persons had hereditary neuropathy with liability to pressure palsies and 15 of them carried the PMP22 deletion. CONCLUSIONS: The prevalence of CMT in Northern Ostrobothnia, Finland, seems to be slightly higher than those in previous studies in European populations. Founder mutation in the GDAP1 gene accounts for a large part of the genetically defined CMT2 in Finland.

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BACKGROUND: Paraplegia is one of the most severe complications occurring after the repair of thoracic and thoracoabdominal aortic aneurysms. Remote ischemic preconditioning (RIPC) has been shown to mitigate neurologic damage, and this study assessed its efficacy in preventing spinal cord ischemia. METHODS: The study randomized 16 female pigs into an RIPC group (n = 8) and a control group (n = 8). The RIPC group underwent four cycles of 5-minute ischemia-reperfusion episodes by intermittent occlusion of the left iliac artery. All animals underwent systematic closure of the left subclavian artery and segmental arteries of the descending thoracic aorta to the level of diaphragm. Motor-evoked potential monitoring was performed in both hind limbs. Continuous electrocardiogram and hemodynamics were monitored, and pulmonary artery blood samples were collected. A neurologic assessment was performed 6 hours after the procedure. The thoracic and lumbar portions of the spinal cord were collected for histologic and immunohistochemical analysis. RESULTS: The bilateral motor-evoked potential amplitude responses were higher in the RIPC group (p < 0.05) than in the control group; the difference was detected already before spinal cord ischemia. Paraplegia occurred in 1 control animal. Immunohistochemical total scores of antioxidant response regulator nuclear factor erythroid 2-related factor 2 were better in the RIPC group (11.0; range, 8.5 to 14.0) than in the control group (5.2; range, 1.0 to 9.0; p = 0.023). CONCLUSIONS: RIPC induces electrophysiologic changes in the central nervous system that may confer spinal cord protection extending the resistance to ischemia. The significantly higher nuclear factor erythroid 2-related factor 2 scores suggest better neuronal cell protection against oxidative stress in the RIPC group.

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OBJECTIVE: The aim of the study was to investigate inhibitory control by evaluating possible differences in the strength and distribution of the brain activity in a visual Go/Nogo task in children who stutter (CWS) compared to typically developing children (TDC). METHODS: Eleven CWS and 19 TDC participated. Event related potentials (ERP) were recorded using a 64-channel EEG-cap during an equiprobable visual Go/Nogo task. The global field power (GFP) as well as the mean amplitudes in the P3 time frame were compared between groups. Additionally, the potential maps of the groups were investigated visually in the N2 and P3 time windows. RESULTS: The groups differed significantly in the right frontal area especially in the Nogo condition (p<0.001) with CWS showing smaller (less positive) mean amplitudes, most likely due to a prolonged and asymmetrical N2 component. Also the fronto-central Nogo P3 component was rather indistinct in CWS, but easily recognizable in TDC in the potential maps. CONCLUSIONS: The CWS show atypical brain activation compared to the TDC in a Go/Nogo task as indexed by the excessive N2-related activity in both conditions and reduced P3-related activity in Nogo condition. SIGNIFICANCE: These findings indicate atypical stimulus evaluation and response inhibition processes in CWS.

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PURPOSE OF THE STUDY: The main aim of the study was to investigate the attentional and inhibitory abilities and their underlying processes of children who stutter by using behavioural measurement and event-related potentials (ERP) in a visual Go/Nogo paradigm. METHODS: Participants were 11 children who stutter (CWS; mean age 8.1, age range 6.3-9.5 years) and 19 typically developed children (TDC; mean age 8.1, age range 5.8-9.6 years). They performed a visual Go/Nogo task with simultaneous EEG recording to obtain ERP responses. RESULTS: Results showed that CWS had longer N2 and P3 latencies in the Go condition compared to the TDC. In contrast, the groups did not differ significantly in the Nogo condition or behavioural measures. CONCLUSIONS: Our findings did not confirm less efficient inhibitory control in CWS but suggest atypical attentional processing such as stimulus evaluation and response selection. EDUCATIONAL OBJECTIVES: The reader will be able to (a) describe recent findings on attention and inhibitory control in children who stutter, (b) describe the measurement of attentional processing, including inhibitory control, and (c) describe the findings on attentional processing in children who stutter as indexed by the event-related potentials in a visual Go/Nogo paradigm.

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