<?xml version="1.0" encoding="UTF-8"?>
<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns="http://purl.org/rss/1.0/"><channel rdf:about="http://www.clinph-journal.com/?rss=yes"><title>Clinical Neurophysiology</title><description>Clinical Neurophysiology RSS feed: Current Issue. As of January 1999, The journal  Electroencephalography and Clinical Neurophysiology , and its two sections  Electromyography and 
Motor Control  and  Evoked Potentials  have amalgamated to become this journal -  Clinical Neurophysiology 
 
 Clinical 
Neurophysiology is the official journal of the   International Federation of 
Clinical Neurophysiology ,  Italian Clinical Neurophysiology Society ,   The 
Japanese Society of Clinical Neurophysiology . It is dedicated to fostering research and disseminating information on all 
aspects of Clinical Neurophysiology, both normal and abnormal. The journal aims at publishing scholarly reports on human physiology and 
pathophysiology of both the central and the peripheral nervous system. The journal is interested in manuscripts reporting data on integrated 
neuroimaging of central nervous functions including, but not limited to, functional MRI, MEG, EEG, PET and other aspects of neuroimaging. 
Electromyography, motor control and somatosensory physiopathology are covered by the journal, as well as evoked potentials with special 
emphasis on studies of cognitive functions. Studies on animals and technical notes must have clear relevance and applicability to humans. 

 
 
 Electronic usage: 
 
 
An increasing number of readers access the journal online via ScienceDirect, one of the world's most 
advanced web delivery systems for scientific, technical and medical information. 
 
 Average monthly article downloads for this journal:  39,498* 
 

 * Figure is an average based on full text articles downloaded monthly via ScienceDirect between July 2007 and 
June 2008. 
</description><link>http://www.clinph-journal.com/?rss=yes</link><dc:publisher>Elsevier Inc.</dc:publisher><dc:language>en</dc:language><dc:rights> © 2010 Published by Elsevier Inc. All rights reserved. </dc:rights><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:issn>1388-2457</prism:issn><prism:volume>121</prism:volume><prism:number>10</prism:number><prism:publicationDate>October 2010</prism:publicationDate><prism:copyright> © 2010 Published by Elsevier Inc. All rights reserved. </prism:copyright><prism:rightsAgent>healthpermissions@elsevier.com</prism:rightsAgent><items><rdf:Seq><rdf:li rdf:resource="http://www.clinph-journal.com/article/PIIS1388245710006346/abstract?rss=yes"/><rdf:li rdf:resource="http://www.clinph-journal.com/article/PIIS138824571000636X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.clinph-journal.com/article/PIIS1388245710006401/abstract?rss=yes"/><rdf:li rdf:resource="http://www.clinph-journal.com/article/PIIS1388245710006413/abstract?rss=yes"/><rdf:li rdf:resource="http://www.clinph-journal.com/article/PIIS138824571000372X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.clinph-journal.com/article/PIIS138824571000338X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.clinph-journal.com/article/PIIS1388245710003457/abstract?rss=yes"/><rdf:li rdf:resource="http://www.clinph-journal.com/article/PIIS1388245710003445/abstract?rss=yes"/><rdf:li 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rdf:resource="http://www.clinph-journal.com/article/PIIS1388245710006127/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245710006346/abstract?rss=yes"><title>Contents</title><link>http://www.clinph-journal.com/article/PIIS1388245710006346/abstract?rss=yes</link><description></description><dc:title>Contents</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1388-2457(10)00634-6</dc:identifier><dc:source>Clinical Neurophysiology 121, 10 (2010)</dc:source><dc:date>2010-10-01</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2010-10-01</prism:publicationDate><prism:volume>121</prism:volume><prism:number>10</prism:number><prism:issueIdentifier>S1388-2457(10)X0010-4</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>i</prism:startingPage><prism:endingPage>i</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS138824571000636X/abstract?rss=yes"><title>Editorial Board</title><link>http://www.clinph-journal.com/article/PIIS138824571000636X/abstract?rss=yes</link><description></description><dc:title>Editorial Board</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1388-2457(10)00636-X</dc:identifier><dc:source>Clinical Neurophysiology 121, 10 (2010)</dc:source><dc:date>2010-10-01</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2010-10-01</prism:publicationDate><prism:volume>121</prism:volume><prism:number>10</prism:number><prism:issueIdentifier>S1388-2457(10)X0010-4</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>iii</prism:startingPage><prism:endingPage>iii</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245710006401/abstract?rss=yes"><title>Call for Abstracts</title><link>http://www.clinph-journal.com/article/PIIS1388245710006401/abstract?rss=yes</link><description></description><dc:title>Call for Abstracts</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1388-2457(10)00640-1</dc:identifier><dc:source>Clinical Neurophysiology 121, 10 (2010)</dc:source><dc:date>2010-10-01</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2010-10-01</prism:publicationDate><prism:volume>121</prism:volume><prism:number>10</prism:number><prism:issueIdentifier>S1388-2457(10)X0010-4</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>vii</prism:startingPage><prism:endingPage>vii</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245710006413/abstract?rss=yes"><title>Two scientific awards in Clinical Neurophysiology</title><link>http://www.clinph-journal.com/article/PIIS1388245710006413/abstract?rss=yes</link><description></description><dc:title>Two scientific awards in Clinical Neurophysiology</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1388-2457(10)00641-3</dc:identifier><dc:source>Clinical Neurophysiology 121, 10 (2010)</dc:source><dc:date>2010-10-01</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2010-10-01</prism:publicationDate><prism:volume>121</prism:volume><prism:number>10</prism:number><prism:issueIdentifier>S1388-2457(10)X0010-4</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>viii</prism:startingPage><prism:endingPage>viii</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS138824571000372X/abstract?rss=yes"><title>Reflexes as tools to study human neuromuscular system</title><link>http://www.clinph-journal.com/article/PIIS138824571000372X/abstract?rss=yes</link><description>Knowledge of the synaptic connections between neurons is a key prerequisite to understanding of the operation of the nervous system. While the anatomy of these connections (‘wirings’) can be obtained by histochemical methods, their functional connections can only be determined using electrophysiological recordings. The functional connection of selected afferent inputs or corticospinal fibres to motoneurons can be studied directly in animal preparations. Compared with the studies on human subjects, experiments on animals have advantages as precise stimulation of selected nerve fibres/neurons and intracellular recordings from accurate sites are possible. Therefore, interpretations of the connections of the stimulated fibres and neurons are straight forward and easy in animal experiments.</description><dc:title>Reflexes as tools to study human neuromuscular system</dc:title><dc:creator>Kemal S. Türker</dc:creator><dc:identifier>10.1016/j.clinph.2010.04.019</dc:identifier><dc:source>Clinical Neurophysiology 121, 10 (2010)</dc:source><dc:date>2010-10-01</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2010-10-01</prism:publicationDate><prism:volume>121</prism:volume><prism:number>10</prism:number><prism:issueIdentifier>S1388-2457(10)X0010-4</prism:issueIdentifier><prism:section>Special Section on Motor Control</prism:section><prism:startingPage>1599</prism:startingPage><prism:endingPage>1601</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS138824571000338X/abstract?rss=yes"><title>High-yield decomposition of surface EMG signals</title><link>http://www.clinph-journal.com/article/PIIS138824571000338X/abstract?rss=yes</link><description>Abstract: Objective: Automatic decomposition of surface electromyographic (sEMG) signals into their constituent motor unit action potential trains (MUAPTs).Methods: A small five-pin sensor provides four channels of sEMG signals that are in turn processed by an enhanced artificial intelligence algorithm evolved from a previous proof-of-principle. We tested the technology on sEMG signals from five muscles contracting isometrically at force levels ranging up to 100% of their maximal level, including those that were covered with more than 1.5cm of adipose tissue. Decomposition accuracy was measured by a new method wherein a signal is first decomposed and then reconstructed and the accuracy is measured by comparison. Results were confirmed by the more established two-source method.Results: The number of MUAPTs decomposed varied among muscles and force levels and mostly ranged from 20 to 30, and occasionally up to 40. The accuracy of all the firings of the MUAPTs was on average 92.5%, at times reaching 97%.Conclusions: Reported technology can reliably perform high-yield decomposition of sEMG signals for isometric contractions up to maximal force levels.Significance: The small sensor size and the high yield and accuracy of the decomposition should render this technology useful for motor control studies and clinical investigations.</description><dc:title>High-yield decomposition of surface EMG signals</dc:title><dc:creator>S. Hamid Nawab, Shey-Sheen Chang, Carlo J. De Luca</dc:creator><dc:identifier>10.1016/j.clinph.2009.11.092</dc:identifier><dc:source>Clinical Neurophysiology 121, 10 (2010)</dc:source><dc:date>2010-10-01</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2010-10-01</prism:publicationDate><prism:volume>121</prism:volume><prism:number>10</prism:number><prism:issueIdentifier>S1388-2457(10)X0010-4</prism:issueIdentifier><prism:section>Special Section on Motor Control</prism:section><prism:startingPage>1602</prism:startingPage><prism:endingPage>1615</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245710003457/abstract?rss=yes"><title>Decoding the neural drive to muscles from the surface electromyogram</title><link>http://www.clinph-journal.com/article/PIIS1388245710003457/abstract?rss=yes</link><description>Abstract: This brief review discusses the methods used to estimate the neural drive to muscles from the surface electromyogram (EMG). Surface EMG has been classically used to infer the neural activation of muscle by associating its amplitude with the number of action potentials discharged by a population of motor neurons. Although this approach is valuable in some applications, the amplitude of the surface EMG is only a crude indicator of the neural drive to muscle. More advanced methods are now available to estimate the neural drive to muscle from the surface EMG. These approaches identify the discharge times of a few motor units by decomposing the EMG signal to determine the relative changes in neural activation. This approach is reliable in several conditions and muscles for isometric contractions of moderate force, but is limited to the few superficial units that can be identified in the recordings.</description><dc:title>Decoding the neural drive to muscles from the surface electromyogram</dc:title><dc:creator>Dario Farina, Aleš Holobar, Roberto Merletti, Roger M. Enoka</dc:creator><dc:identifier>10.1016/j.clinph.2009.10.040</dc:identifier><dc:source>Clinical Neurophysiology 121, 10 (2010)</dc:source><dc:date>2010-10-01</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2010-10-01</prism:publicationDate><prism:volume>121</prism:volume><prism:number>10</prism:number><prism:issueIdentifier>S1388-2457(10)X0010-4</prism:issueIdentifier><prism:section>Special Section on Motor Control</prism:section><prism:startingPage>1616</prism:startingPage><prism:endingPage>1623</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245710003445/abstract?rss=yes"><title>Influence of contraction strength on single motor unit synchronous activity</title><link>http://www.clinph-journal.com/article/PIIS1388245710003445/abstract?rss=yes</link><description>Abstract: Objective: The influence of contraction strength on motoneurone (MN) synchrony is poorly documented. With stronger contraction, more common and/or synchronized inputs might contribute to greater MN drive and generate more synchronous firings. This effect might be counterbalanced, however, by a negative impact of MN faster firing rates on synaptic effectiveness.Methods: Pairs of motor units (MUs) were tested at various force levels, in 2-s sequences. MN synchrony was assessed using the index k′, the synchronous impulse probability (SIP), and the synchronous impulse frequency (SIF) in cross-correlograms. MU inter-spike interval duration and variability, surface EMG activity and force output were evaluated concurrently.Results: Both SIP and SIF increased with contraction strength, whereas k′ remained unaffected. Faster firing rates and stronger contraction had the greatest effects on SIF.Conclusions: By testing the same MUs at different force levels, we showed that contraction strength does influence MN synchrony. The enhancement of MU synchrony with stronger contraction suggests an efficient contribution of more common and/or synchronized inputs.Significance: Force output must be controlled when assessing MN synchrony. Normalizing MU synchronous activity per reference spike is preferable to minimize the influence of firing rate. This is particularly relevant for clinical research, in conditions of poorer neuromuscular control.</description><dc:title>Influence of contraction strength on single motor unit synchronous activity</dc:title><dc:creator>Annie Schmied, Martin Descarreaux</dc:creator><dc:identifier>10.1016/j.clinph.2010.02.165</dc:identifier><dc:source>Clinical Neurophysiology 121, 10 (2010)</dc:source><dc:date>2010-10-01</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2010-10-01</prism:publicationDate><prism:volume>121</prism:volume><prism:number>10</prism:number><prism:issueIdentifier>S1388-2457(10)X0010-4</prism:issueIdentifier><prism:section>Special Section on Motor Control</prism:section><prism:startingPage>1624</prism:startingPage><prism:endingPage>1632</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245710003470/abstract?rss=yes"><title>The α-motoneuron pool as transmitter of rhythmicities in cortical motor drive</title><link>http://www.clinph-journal.com/article/PIIS1388245710003470/abstract?rss=yes</link><description>Abstract: Objective: Investigate the effectiveness and frequency dependence of central drive transmission via the α-motoneuron pool to the muscle.Methods: We describe a model for the simulation of α-motoneuron firing and the EMG signal as response to central drive input. The transfer in the frequency domain is investigated. Coherence between stochastical central input and EMG is also evaluated.Results: The transmission of central rhythmicities to the EMG signal relates to the spectral content of the latter. Coherence between central input to the α-motoneuron pool and the EMG signal is significant whereby the coupling strength hardly depends on the frequency in a range from 1 to 100Hz. Common central input to pairs of α-motoneurons strongly increases the coherence levels. The often-used rectification of the EMG signal introduces a clear frequency dependence.Conclusions: Oscillatory phenomena are strongly transmitted via the α-motoneuron pool. The motoneuron firing frequencies do play a role in the transmission gain, but do not influence the coherence levels. Rectification of the EMG signal enhances the transmission gain, but lowers coherence and introduces a strong frequency dependency. We think that it should be avoided.Significance: Our findings show that rhythmicities are translated into α-motoneuron activity without strong non-linearities.</description><dc:title>The α-motoneuron pool as transmitter of rhythmicities in cortical motor drive</dc:title><dc:creator>Dick F. Stegeman, Wendy J.M. van de Ven, Gijs A. van Elswijk, Robert Oostenveld, Bert U. Kleine</dc:creator><dc:identifier>10.1016/j.clinph.2010.03.052</dc:identifier><dc:source>Clinical Neurophysiology 121, 10 (2010)</dc:source><dc:date>2010-10-01</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2010-10-01</prism:publicationDate><prism:volume>121</prism:volume><prism:number>10</prism:number><prism:issueIdentifier>S1388-2457(10)X0010-4</prism:issueIdentifier><prism:section>Special Section on Motor Control</prism:section><prism:startingPage>1633</prism:startingPage><prism:endingPage>1642</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245710003469/abstract?rss=yes"><title>Deciphering the contribution of intrinsic and synaptic currents to the effects of transient synaptic inputs on human motor unit discharge</title><link>http://www.clinph-journal.com/article/PIIS1388245710003469/abstract?rss=yes</link><description>Abstract: The amplitude and time course of synaptic potentials in human motoneurons can be estimated in tonically discharging motor units by measuring stimulus-evoked changes in the rate and probability of motor unit action potentials. However, in spite of the fact that some of these techniques have been used for over 30 years, there is still no consensus on the best way to estimate the characteristics of synaptic potentials or on the accuracy of these estimates. In this review, we compare different techniques for estimating synaptic potentials from human motor unit discharge and also discuss relevant animal models in which estimated synaptic potentials can be compared to those directly measured from intracellular recordings. We also review the experimental evidence on how synaptic noise and intrinsic motoneuron properties influence their responses to synaptic inputs. Finally, we consider to what extent recordings of single motor unit discharge in humans can be used to distinguish the contribution of changes in synaptic inputs versus changes in intrinsic motoneuron properties to altered motoneuron responses following CNS injury.</description><dc:title>Deciphering the contribution of intrinsic and synaptic currents to the effects of transient synaptic inputs on human motor unit discharge</dc:title><dc:creator>Randall K. Powers, Kemal S. Türker</dc:creator><dc:identifier>10.1016/j.clinph.2009.10.041</dc:identifier><dc:source>Clinical Neurophysiology 121, 10 (2010)</dc:source><dc:date>2010-10-01</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2010-10-01</prism:publicationDate><prism:volume>121</prism:volume><prism:number>10</prism:number><prism:issueIdentifier>S1388-2457(10)X0010-4</prism:issueIdentifier><prism:section>Special Section on Motor Control</prism:section><prism:startingPage>1643</prism:startingPage><prism:endingPage>1654</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS138824571000341X/abstract?rss=yes"><title>Neural control of locomotion and training-induced plasticity after spinal and cerebral lesions</title><link>http://www.clinph-journal.com/article/PIIS138824571000341X/abstract?rss=yes</link><description>Abstract: Standing and walking require a plethora of sensorimotor interactions that occur throughout the nervous system. Sensory afferent feedback plays a crucial role in the rhythmical muscle activation pattern, as it affects through spinal reflex circuits the spinal neuronal networks responsible for inducing and maintaining rhythmicity, drives short-term and long-term re-organization of the brain and spinal cord circuits, and contributes to recovery of walking after locomotor training. Therefore, spinal circuits integrating sensory signals are adjustable networks with learning capabilities. In this review, I will synthesize the mechanisms underlying phase-dependent modulation of spinal reflexes in healthy humans as well as those with spinal or cerebral lesions along with findings on afferent regulation of spinal reflexes and central pattern generator in reduced animal preparations. Recovery of walking after locomotor training has been documented in numerous studies but the re-organization of spinal interneuronal and cortical circuits need to be further explored at cellular and physiological levels. For maximizing sensorimotor recovery in people with spinal or cerebral lesions, a multidisciplinary approach (rehabilitation, pharmacology, and electrical stimulation) delivered during various sensorimotor constraints is needed.</description><dc:title>Neural control of locomotion and training-induced plasticity after spinal and cerebral lesions</dc:title><dc:creator>Maria Knikou</dc:creator><dc:identifier>10.1016/j.clinph.2010.01.039</dc:identifier><dc:source>Clinical Neurophysiology 121, 10 (2010)</dc:source><dc:date>2010-10-01</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2010-10-01</prism:publicationDate><prism:volume>121</prism:volume><prism:number>10</prism:number><prism:issueIdentifier>S1388-2457(10)X0010-4</prism:issueIdentifier><prism:section>Special Section on Motor Control</prism:section><prism:startingPage>1655</prism:startingPage><prism:endingPage>1668</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245710003500/abstract?rss=yes"><title>Persistent inward currents in spinal motoneurons: Important for normal function but potentially harmful after spinal cord injury and in amyotrophic lateral sclerosis</title><link>http://www.clinph-journal.com/article/PIIS1388245710003500/abstract?rss=yes</link><description>Abstract: Meaningful body movements depend on the interplay between synaptic inputs to motoneurons and their intrinsic properties. Injury and disease often alter either or both of these factors and cause motoneuron and movement dysfunction. The ability of the motoneuronal membrane to generate persistent inward currents (PICs) is especially potent in setting the intrinsic excitability of motoneurons and can drastically change the motoneuron output to a given input. In this article, we review the role of PICs in modulating the excitability of spinal motoneurons during health, and their contribution to motoneuron excitability after spinal cord injury (SCI) and in amyotrophic lateral sclerosis (ALS) leading to exaggerated long-lasting reflexes and muscle spasms, and contributing to neuronal degeneration, respectively.</description><dc:title>Persistent inward currents in spinal motoneurons: Important for normal function but potentially harmful after spinal cord injury and in amyotrophic lateral sclerosis</dc:title><dc:creator>S.M. ElBasiouny, J.E. Schuster, C.J. Heckman</dc:creator><dc:identifier>10.1016/j.clinph.2009.12.041</dc:identifier><dc:source>Clinical Neurophysiology 121, 10 (2010)</dc:source><dc:date>2010-10-01</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2010-10-01</prism:publicationDate><prism:volume>121</prism:volume><prism:number>10</prism:number><prism:issueIdentifier>S1388-2457(10)X0010-4</prism:issueIdentifier><prism:section>Special Section on Motor Control</prism:section><prism:startingPage>1669</prism:startingPage><prism:endingPage>1679</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245710003494/abstract?rss=yes"><title>Stretch sensitive reflexes as an adaptive mechanism for maintaining limb stability</title><link>http://www.clinph-journal.com/article/PIIS1388245710003494/abstract?rss=yes</link><description>Abstract: The often studied stretch reflex is fundamental to the involuntary control of posture and movement. Nevertheless, there remains controversy regarding its functional role. Many studies have demonstrated that stretch reflexes can be modulated in a task appropriate manner. This review focuses on modulation of the long-latency stretch reflex, thought to be mediated, at least in part, by supraspinal pathways. For example, this component of the stretch reflex increases in magnitude during interactions with compliant environments, relative to its sensitivity during interactions with rigid environments. This suggests that reflex sensitivity increases to augment limb stability when that stability is not provided by the environment. However, not all results support the stabilizing role of stretch reflexes. Some studies have demonstrated that involuntary responses within the time period corresponding to the long-latency reflex can destabilize limb posture. We propose that this debate stems from the fact that multiple perturbation-sensitive pathways can contribute to the long-latency stretch reflex and that these pathways have separate functional roles. The presented studies suggest that neural activity occurring within the period normally ascribed to the long-latency stretch reflex is highly adaptable to current task demands and possibly should be considered more intelligent than “reflexive”.</description><dc:title>Stretch sensitive reflexes as an adaptive mechanism for maintaining limb stability</dc:title><dc:creator>Jonathan Shemmell, Matthew A. Krutky, Eric J. Perreault</dc:creator><dc:identifier>10.1016/j.clinph.2010.02.166</dc:identifier><dc:source>Clinical Neurophysiology 121, 10 (2010)</dc:source><dc:date>2010-10-01</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2010-10-01</prism:publicationDate><prism:volume>121</prism:volume><prism:number>10</prism:number><prism:issueIdentifier>S1388-2457(10)X0010-4</prism:issueIdentifier><prism:section>Special Section on Motor Control</prism:section><prism:startingPage>1680</prism:startingPage><prism:endingPage>1689</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245710003482/abstract?rss=yes"><title>Reflex responses of masseter muscles to sound</title><link>http://www.clinph-journal.com/article/PIIS1388245710003482/abstract?rss=yes</link><description>Abstract: Acoustic stimuli can evoke reflex EMG responses (acoustic jaw reflex) in the masseter muscle. Although these were previously ascribed to activation of cochlear receptors, high intensity sound can also activate vestibular receptors. Since anatomical and physiological studies, both in animals and humans, have shown that masseter muscles are a target for vestibular inputs we have recently reassessed the vestibular contribution to masseter reflexes. We found that high intensity sound evokes two bilateral and symmetrical short-latency responses in active unrectified masseter EMG of healthy subjects: a high threshold, early p11/n15 wave and a lower threshold, later p16/n21 wave. Both of these reflexes are inhibitory but differ in their threshold, latency and appearance in the rectified EMG average. Experiments in healthy subjects and in patients with selective lesions showed that vestibular receptors were responsible for the p11/n15 wave (vestibulo-masseteric reflex) whereas cochlear receptors were responsible for the p16/n21 wave (acoustic masseteric reflex). The possible functional significance of the double vestibular control over masseter muscles is discussed.</description><dc:title>Reflex responses of masseter muscles to sound</dc:title><dc:creator>Franca Deriu, Elena Giaconi, John C. Rothwell, Eusebio Tolu</dc:creator><dc:identifier>10.1016/j.clinph.2009.11.093</dc:identifier><dc:source>Clinical Neurophysiology 121, 10 (2010)</dc:source><dc:date>2010-10-01</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2010-10-01</prism:publicationDate><prism:volume>121</prism:volume><prism:number>10</prism:number><prism:issueIdentifier>S1388-2457(10)X0010-4</prism:issueIdentifier><prism:section>Special Section on Motor Control</prism:section><prism:startingPage>1690</prism:startingPage><prism:endingPage>1699</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245710003408/abstract?rss=yes"><title>Effect of gender, age, fatigue and contraction level on electromechanical delay</title><link>http://www.clinph-journal.com/article/PIIS1388245710003408/abstract?rss=yes</link><description>Abstract: Objective: The aim of this study was to determine electromechanical delay (EMD) using supramaximal stimuli and to investigate its variation with gender, age, contraction level and fatigue.Methods: Fifteen male and 15 female healthy subjects (aged between 18 and 60) participated in our study. Electromyogram (EMG) recordings were taken from triceps surae muscle. While subjects contracted their muscles voluntarily at specified percentages of maximum voluntary contraction, 10 supramaximal stimuli were applied to the tibial nerve. The time lag between the onset of the EMG response (M-wave) and the onset of force generation was calculated as EMD.Results: EMD was found to be 8.5±1.3ms (at rest condition), which is much shorter than those reported in previous studies. Although EMD did not significantly vary with gender (P&gt;0.05), it decreased significantly with escalating muscle contraction level (P&lt;0.05) and increased significantly with advancing age and with fatigue (P&lt;0.05).Conclusions: EMD was found to be considerably shorter than those reported in previous studies, and hence we discuss the possible reasons underlying this difference. We suggest that supramaximal nerve stimulation and high resolution EMG and force recording may have generated this difference.Significance: Current findings suggest that EMD is very sensitive to the method used to determine it. We discuss the reasons for the short EMD value that we have found in the present study.</description><dc:title>Effect of gender, age, fatigue and contraction level on electromechanical delay</dc:title><dc:creator>Ş. Utku Yavuz, Aylin Şendemir-Ürkmez, Kemal S. Türker</dc:creator><dc:identifier>10.1016/j.clinph.2009.10.039</dc:identifier><dc:source>Clinical Neurophysiology 121, 10 (2010)</dc:source><dc:date>2010-10-01</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2010-10-01</prism:publicationDate><prism:volume>121</prism:volume><prism:number>10</prism:number><prism:issueIdentifier>S1388-2457(10)X0010-4</prism:issueIdentifier><prism:section>Special Section on Motor Control</prism:section><prism:startingPage>1700</prism:startingPage><prism:endingPage>1706</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS138824571000060X/abstract?rss=yes"><title>Quantitative EEG and cerebral ischemia</title><link>http://www.clinph-journal.com/article/PIIS138824571000060X/abstract?rss=yes</link><description>In recent years there has been renewed interest in using EEG for the detection of cerebral ischemia. There is coupling between neuronal activity and cerebral blood flow (CBF) and EEG changes occur within seconds of reduction in CBF (). This forms the basis for intraoperative EEG monitoring for patients undergoing surgeries with a high risk for cerebral ischemia, such as carotid endarterectomy (). As CBF falls below 25–30mL/100g/min faster frequencies are progressively lost and prominent slowing of EEG background activity appears. When CBF falls below 8–10mL/100g/min, low enough to cause irreversible cell death, all EEG frequencies are suppressed (). Therefore, it is theoretically possible to distinguish reversible ischemia from infarction by EEG and use this tool to identify a window of opportunity during which the progression from reversible to permanent damage can be stopped.</description><dc:title>Quantitative EEG and cerebral ischemia</dc:title><dc:creator>Daniel Friedman, Jan Claassen</dc:creator><dc:identifier>10.1016/j.clinph.2010.01.018</dc:identifier><dc:source>Clinical Neurophysiology 121, 10 (2010)</dc:source><dc:date>2010-10-01</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2010-10-01</prism:publicationDate><prism:volume>121</prism:volume><prism:number>10</prism:number><prism:issueIdentifier>S1388-2457(10)X0010-4</prism:issueIdentifier><prism:section>Editorials</prism:section><prism:startingPage>1707</prism:startingPage><prism:endingPage>1708</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245710002695/abstract?rss=yes"><title>The onset of ALS?</title><link>http://www.clinph-journal.com/article/PIIS1388245710002695/abstract?rss=yes</link><description>The onset of amyotrophic lateral sclerosis (ALS) is undefined, but it is widely believed that neurodegeneration, whether in the motor cortex or in the lower motor neurons, begins long before the onset of symptomatic weakness (). However, studies of lower motor neuron (LMN) function suggest that both in sporadic ALS () and in familial SOD-1 ALS () weakness is detectable only several months after the commencement of progressive LMN dysfunction.  applied the threshold tracking transcranial magnetic stimulation technique (TTTMS) and found markers of cortical hyperexcitability in ALS patients, including both sporadic and SOD-1 mutation familial ALS. In this earlier study, in two pre-symptomatic SOD-1 mutation carriers, who developed clinical features of the disease within 3-months after assessment of cortical excitability, the short-inhibitory cortical interval (SICI) was abnormal. An additional pre-symptomatic SOD-1 mutation carrier showed reduced SICI in the motor cortex contralateral to the side of onset of muscle weakness, 8months before clinical onset. This result suggested that upper motor neuron (UMN) dysfunction antedates clinical weakness in ALS, but that it does not necessarily occur before LMN degeneration.</description><dc:title>The onset of ALS?</dc:title><dc:creator>Mamede de Carvalho, Michael Swash</dc:creator><dc:identifier>10.1016/j.clinph.2010.03.002</dc:identifier><dc:source>Clinical Neurophysiology 121, 10 (2010)</dc:source><dc:date>2010-10-01</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2010-10-01</prism:publicationDate><prism:volume>121</prism:volume><prism:number>10</prism:number><prism:issueIdentifier>S1388-2457(10)X0010-4</prism:issueIdentifier><prism:section>Editorials</prism:section><prism:startingPage>1709</prism:startingPage><prism:endingPage>1710</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245710003159/abstract?rss=yes"><title>Lateralised EEG power and phase dynamics related to motor response execution</title><link>http://www.clinph-journal.com/article/PIIS1388245710003159/abstract?rss=yes</link><description>Abstract: Objective: This study aimed to determine the underlying bases of single-trial electroencephalographic (EEG) activities of movement-related potential (MRP) and α-band event-related desynchronisation (α-ERD), both of which are cortical activities related to motor response execution because of their dependence on response time and laterality.Methods: We compared stimulus- and response-triggered EEG power and phase dynamics ipsilateral and contralateral to the response hand in Go trials during visual Go/NoGo reaction time tasks.Results: Two lateralised EEG power and phase dynamics were observed: transient power decreases in α-band EEG (corresponding to α-ERD) and consistent contralateral phase lags of θ-band EEG.Conclusions: α-ERD around the response onset is not substantially reflected in the MRP waveforms mainly because of phase inconsistency. Lateralised MRP waveforms around the response onset are mainly attributed to consistent contralateral phase lags in θ-band additive EEG deflections.Significance: Our results indicate that while both α-ERD and lateralised MRP are related to motor response execution, they reflect separate cortical activities. Analysis of EEG power and phase dynamics can help in elucidating the detailed underlying bases of cortical activities.</description><dc:title>Lateralised EEG power and phase dynamics related to motor response execution</dc:title><dc:creator>Kentaro Yamanaka, Yoshiharu Yamamoto</dc:creator><dc:identifier>10.1016/j.clinph.2010.03.027</dc:identifier><dc:source>Clinical Neurophysiology 121, 10 (2010)</dc:source><dc:date>2010-10-01</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2010-10-01</prism:publicationDate><prism:volume>121</prism:volume><prism:number>10</prism:number><prism:issueIdentifier>S1388-2457(10)X0010-4</prism:issueIdentifier><prism:section>Original Research Articles</prism:section><prism:startingPage>1711</prism:startingPage><prism:endingPage>1718</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245710000593/abstract?rss=yes"><title>Additional value of quantitative EEG in acute anterior circulation syndrome of presumed ischemic origin</title><link>http://www.clinph-journal.com/article/PIIS1388245710000593/abstract?rss=yes</link><description>Abstract: Objective: The clinical course of acute stroke can be highly variable and for effective management outcome prediction needs to be refined. We investigated whether EEG parameters are of additional diagnostic and prognostic value in the early phase of acute ischemic anterior circulation stroke.Methods: Ninety-four patients presenting with acute anterior circulation syndrome (ACS) of presumed ischemic origin were incrementally included. Clinical characteristics were correlated with volume of ischemia and EEG parameters. Predictive values for definite stroke, early neurological deterioration, spontaneous early neurological improvement and death within 1week after ACS were calculated using ROC curves and logistic regression modelling.Results: In patients with normal or near normal NIHSS score of 0 or 1, the pairwise derived brain symmetry index (pdBSI) was an independent predictor for definite stroke displaying an overall accuracy of 80%. Early neurological deterioration was independently predicted by pdBSI with a correct classification rate of 95%. In ROC analysis, death was predicted by pdBSI with overall accuracy of 97%. Spontaneous neurological improvement was independently predicted by the delta+theta/alpha+beta – ratio with overall accuracy of 75%. Small-vessel stroke was independently predicted by pdBSI with a correct classification rate of 92%.Conclusions: EEG may be of prognostic value for spontaneous neurological improvement, early neurological deterioration and death in the acute setting of acute anterior circulation syndrome of presumed ischemic origin.Significance: These findings may have an impact on stroke care.</description><dc:title>Additional value of quantitative EEG in acute anterior circulation syndrome of presumed ischemic origin</dc:title><dc:creator>Rishi V.A. Sheorajpanday, Guy Nagels, Arie J.T.M. Weeren, Didier De Surgeloose, Peter P. De Deyn</dc:creator><dc:identifier>10.1016/j.clinph.2009.10.037</dc:identifier><dc:source>Clinical Neurophysiology 121, 10 (2010)</dc:source><dc:date>2010-10-01</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2010-10-01</prism:publicationDate><prism:volume>121</prism:volume><prism:number>10</prism:number><prism:issueIdentifier>S1388-2457(10)X0010-4</prism:issueIdentifier><prism:section>Original Research Articles</prism:section><prism:startingPage>1719</prism:startingPage><prism:endingPage>1725</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245710003512/abstract?rss=yes"><title>Clinical utility of distributed source modelling of interictal scalp EEG in focal epilepsy</title><link>http://www.clinph-journal.com/article/PIIS1388245710003512/abstract?rss=yes</link><description>Abstract: Objective: Assess the clinical utility of non-invasive distributed EEG source modelling in focal epilepsy.Methods: Interictal epileptiform discharges were recorded from eight patients – benign focal epilepsy of childhood (BFEC), four; mesial temporal lobe epilepsy (MTLE), four. EEG source localization (ESL) applied 48 forward–inverse–subspace set-ups: forward – standardized, leadfield-interpolated boundary element methods (BEMs, BEMi), finite element method (FEMi); inverse – minimum norm (MNLS), L1 norm (L1), low resolution electromagnetic tomography (LORETA), standardized LORETA (sLORETA); subspace – whole volume (3D), cortex with rotating sources (CxR), cortex with fixed sources (CxN), cortex with fixed extended sources (patch). Current density reconstruction (CDR) maxima defined ‘best-fit’.Results: From 19,200 CDR parameter results and 2304 CDR maps, the dominant variables on best-fit were inverse model and subspace constraint. The most clinically meaningful and statistically robust results came with sLORETA–CxR/patch (lower Rolandic in BFEC, basal temporal lobe in MTLE). Computation time was inverse model dependent: sub-second (MNLS, sLORETA), seconds (L1), minutes (LORETA).Conclusions: From the largest number of distributed ESL approaches compared in a clinical setting, an optimum modelling set-up for BFEC and MTLE incorporated sLORETA (inverse), CxR or patch (subspace), and either BEM or FEMi (forward). Computation is efficient and CDR results are reproducible.Significance: Distributed source modelling demonstrates clinical utility for the routine work-up of unilateral BFEC of the typical Rolandic variety, and unilateral MTLE secondary to hippocampal sclerosis.</description><dc:title>Clinical utility of distributed source modelling of interictal scalp EEG in focal epilepsy</dc:title><dc:creator>C. Plummer, M. Wagner, M. Fuchs, S. Vogrin, L. Litewka, S. Farish, C. Bailey, A.S. Harvey, M.J. Cook</dc:creator><dc:identifier>10.1016/j.clinph.2010.04.002</dc:identifier><dc:source>Clinical Neurophysiology 121, 10 (2010)</dc:source><dc:date>2010-10-01</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2010-10-01</prism:publicationDate><prism:volume>121</prism:volume><prism:number>10</prism:number><prism:issueIdentifier>S1388-2457(10)X0010-4</prism:issueIdentifier><prism:section>Original Research Articles</prism:section><prism:startingPage>1726</prism:startingPage><prism:endingPage>1739</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245710003391/abstract?rss=yes"><title>Rolandic discharges: Clinico-neurophysiological correlation</title><link>http://www.clinph-journal.com/article/PIIS1388245710003391/abstract?rss=yes</link><description>Abstract: Objective: The aim of this study was to analyze neurophysiologic aspects of rolandic discharges.Methods: We reviewed 45 electroencephalograms of patients divided into two groups: those with benign childhood epilepsy with centrotemporal spikes (BCECTS) and symptomatic partial epilepsy (SPE), following ILAE criteria (1989). The EEG data analyzed were: horizontal dipole discharges, double spike phenomenon, the extension of epileptiform discharges and background activity.Results: There was a predominance of horizontal dipole between patients with BCECTS compared with patients with SPE; however, this difference was not statistically significant. There was also no statistically significant difference between the two groups when the double spike phenomenon and the extension of discharges beyond the rolandic area were considered. The slower background activity in the SPE group was the only variable with statistical significance.Conclusions: This study revealed similarities between rolandic discharges of two different epilepsy groups. The only reliable parameter to differentiate the groups was the background activity.Significance: Our findings suggest that most EEG rolandic features are not pathognomonic of BCECTS, as they are related to the area of the discharges and not to the epileptic syndrome itself.</description><dc:title>Rolandic discharges: Clinico-neurophysiological correlation</dc:title><dc:creator>L.L. Medeiros, C. Yasuda, K.M.R. Schmutzler, M.M. Guerreiro</dc:creator><dc:identifier>10.1016/j.clinph.2010.03.050</dc:identifier><dc:source>Clinical Neurophysiology 121, 10 (2010)</dc:source><dc:date>2010-10-01</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2010-10-01</prism:publicationDate><prism:volume>121</prism:volume><prism:number>10</prism:number><prism:issueIdentifier>S1388-2457(10)X0010-4</prism:issueIdentifier><prism:section>Original Research Articles</prism:section><prism:startingPage>1740</prism:startingPage><prism:endingPage>1743</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245710003536/abstract?rss=yes"><title>Memory-based mismatch response to changes in duration of auditory stimuli: An MEG study</title><link>http://www.clinph-journal.com/article/PIIS1388245710003536/abstract?rss=yes</link><description>Abstract: Objective: Differences in physical features and occurrence probability between standards and deviants in oddball paradigms provide contributions to magnetic mismatch negativity (MMNm). We aimed to reduce these influential factors and extract memory-based MMNm by adding a control paradigm.Methods: Magnetoencephalographic responses were recorded in 13 healthy adults with an oddball paradigm (125-ms standard and 50-ms deviant tones) and an equiprobable control paradigm (50-ms control and four other duration-varying tones). The stimulus onset asynchrony was 500ms. Controlled MMNm was obtained by subtracting control-evoked responses from deviant-evoked responses.Results: With respect to the onset of stimulus difference, the peak latency of controlled MMNm was compatible with previous intracranial MMN recordings. Both controlled and traditional MMNm were generated around the superior temporal cortex, whereas the controlled MMNm amplitude was about 70% of traditional MMNm amplitude. Right-hemispheric dominance was observed in traditional MMNm but not in controlled MMNm. N100m amplitude was smaller in standard-evoked than in deviant- or control-evoked responses.Conclusions: Controlled MMNm reflects memory-based processing of duration changes, whereas traditional MMNm additionally involves non-memory activations related to differential refractoriness states and physical properties between standard and deviant stimuli.Significance: The memory-based processing of auditory deviants may be preferentially extracted by adding a control paradigm.</description><dc:title>Memory-based mismatch response to changes in duration of auditory stimuli: An MEG study</dc:title><dc:creator>Wan-Yu Hsu, Chia-Hsiung Cheng, Hsuan-Chun Lin, Kwong-Kum Liao, Zin-An Wu, Low-Tone Ho, Yung-Yang Lin</dc:creator><dc:identifier>10.1016/j.clinph.2010.04.003</dc:identifier><dc:source>Clinical Neurophysiology 121, 10 (2010)</dc:source><dc:date>2010-10-01</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2010-10-01</prism:publicationDate><prism:volume>121</prism:volume><prism:number>10</prism:number><prism:issueIdentifier>S1388-2457(10)X0010-4</prism:issueIdentifier><prism:section>Original Research Articles</prism:section><prism:startingPage>1744</prism:startingPage><prism:endingPage>1750</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245710003524/abstract?rss=yes"><title>Mismatch negativity: A tool for studying morphosyntactic processing?</title><link>http://www.clinph-journal.com/article/PIIS1388245710003524/abstract?rss=yes</link><description>Abstract: Objective: Mismatch negativity (MMN) was originally shown in a passive auditory oddball paradigm to be generated by any acoustical change. More recently, it has been applied to the study of higher order linguistic levels including the morphosyntactic level in spoken language comprehension. In this study, we present two MMN experiments to determine whether morphosyntactic features are involved in the representations underlying the morphosyntactic processing.Methods: We reported two MMN experiments in passive auditory oddball paradigm with pairs of French words, a pronoun and a verb, differing in agreement grammaticality. These two experiments differed in the number of morphosyntactic features producing agreement violations, i.e. either of person and number features or of person feature.Results: We observed no effect of grammaticality on the MMN response for these two experiments.Conclusions: Our studies highlight the difficulties encountered in studying morphosyntactic level with the passive auditory oddball paradigm.Significance: The reasons for our inability to replicate previous studies are presented, and methodological changes in the passive auditory oddball paradigm are proposed to better tap into the morphosyntactic level.</description><dc:title>Mismatch negativity: A tool for studying morphosyntactic processing?</dc:title><dc:creator>Angèle Brunellière, Ulrich H. Frauenfelder</dc:creator><dc:identifier>10.1016/j.clinph.2010.03.053</dc:identifier><dc:source>Clinical Neurophysiology 121, 10 (2010)</dc:source><dc:date>2010-10-01</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2010-10-01</prism:publicationDate><prism:volume>121</prism:volume><prism:number>10</prism:number><prism:issueIdentifier>S1388-2457(10)X0010-4</prism:issueIdentifier><prism:section>Original Research Articles</prism:section><prism:startingPage>1751</prism:startingPage><prism:endingPage>1759</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245710003378/abstract?rss=yes"><title>Time and frequency domain event-related electrical activity associated with response control in schizophrenia</title><link>http://www.clinph-journal.com/article/PIIS1388245710003378/abstract?rss=yes</link><description>Abstract: Objective: To confirm previously reported abnormalities in time domain EEG components during a go/no-go task in schizophrenia, and to test the hypothesis that patients exhibit abnormalities in frequency domain components reflecting indices of behavioural impairment.Methods: EEG data were recorded from 17 male schizophrenia patients in a stable phase of illness and 17 healthy controls.Results: As compared with controls, patients displayed smaller N200 amplitudes and less evoked theta for correct hit trials; and smaller N200 and P300 amplitudes and less evoked delta and theta for correct reject trials. Effect sizes were largest for evoked delta. Source localisation revealed reduced activation in schizophrenia patients during the N200 and P300 time windows in anterior and posterior cingulate, medial frontal gyrus and precuneus. Evoked delta and theta oscillations were significantly correlated with the variability of reaction times and the performance level statistic d-prime.Conclusions: The results demonstrate impairment of frontal and parietal brain areas involved in response control in schizophrenia. They also suggest that the timing of oscillations in patients is less precise leading to smaller evoked amplitudes and more variable reaction times.Significance: These findings add to the evidence that abnormal EEG oscillations contribute to impaired behavioural control in schizophrenia.</description><dc:title>Time and frequency domain event-related electrical activity associated with response control in schizophrenia</dc:title><dc:creator>Kathrin Doege, Mahendra Kumar, Alan Thomas Bates, Debasis Das, Marco Paul Maria Boks, Peter Francis Liddle</dc:creator><dc:identifier>10.1016/j.clinph.2010.03.049</dc:identifier><dc:source>Clinical Neurophysiology 121, 10 (2010)</dc:source><dc:date>2010-10-01</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2010-10-01</prism:publicationDate><prism:volume>121</prism:volume><prism:number>10</prism:number><prism:issueIdentifier>S1388-2457(10)X0010-4</prism:issueIdentifier><prism:section>Original Research Articles</prism:section><prism:startingPage>1760</prism:startingPage><prism:endingPage>1771</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245710003366/abstract?rss=yes"><title>Size does matter: The influence of motor unit potential size on statistical motor unit number estimates in healthy subjects</title><link>http://www.clinph-journal.com/article/PIIS1388245710003366/abstract?rss=yes</link><description>Abstract: Objective: The statistical method of motor unit number estimation (MUNE) assumes that all motor unit potentials (MUPs) have the same size. The present study aims to evaluate the consequences of this assumption as well as its implications for the validity of statistical MUNEs.Methods: We performed statistical and multiple point stimulation (MPS) MUNE with an array of 120 electrodes on the thenar muscles of 15 healthy subjects. These recordings allow isolation and quantification of the effect of non-uniform MUP size on MUNE, because the differences in submaximal CMAP size (and, hence, in MUNE) between electrodes are due almost entirely to differences in (summed) MUP size.Results: We found no correlation between statistical and MPS MUNEs. Statistical MUNEs proved very sensitive to small variations in the “bandwidth” (variance) of the response series; MUNEs from electrodes only 8mm apart could deviate by as much as 60%. This variation in bandwidth resulted from spatial (and, hence, size) differences between the contributing MUPs.Conclusions: Statistical MUNEs are very sensitive to violation of the uniform MUP-size assumption, to an extent that blurs any correlation with MPS MUNE in healthy subjects.Significance: Statistical MUNE cannot be used to detect mild to moderate motor unit losses.</description><dc:title>Size does matter: The influence of motor unit potential size on statistical motor unit number estimates in healthy subjects</dc:title><dc:creator>J.H. Blok, J.P. van Dijk, J. Drenthen, E.M. Maathuis, D.F. Stegeman</dc:creator><dc:identifier>10.1016/j.clinph.2010.03.048</dc:identifier><dc:source>Clinical Neurophysiology 121, 10 (2010)</dc:source><dc:date>2010-10-01</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2010-10-01</prism:publicationDate><prism:volume>121</prism:volume><prism:number>10</prism:number><prism:issueIdentifier>S1388-2457(10)X0010-4</prism:issueIdentifier><prism:section>Original Research Articles</prism:section><prism:startingPage>1772</prism:startingPage><prism:endingPage>1780</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245710002701/abstract?rss=yes"><title>Corticomotoneuronal function in asymptomatic SOD-1 mutation carriers</title><link>http://www.clinph-journal.com/article/PIIS1388245710002701/abstract?rss=yes</link><description>Abstract: Objective: Diffusion tensor imaging (DTI) recently identified structural abnormalities of corticomotoneurons in asymptomatic copper/zinc superoxide-dismutase-1 (SOD-1) gene mutation carriers. The potential existence of longstanding corticomotoneuronal dysfunction would clearly have consequences for the medical management of asymptomatic SOD-1 mutation carriers. To clarify this unexpected finding, DTI techniques were combined with threshold tracking transcranial magnetic stimulation (TMS) to assess the anatomical and functional integrity of corticomotoneurons in asymptomatic SOD-1 mutation carriers.Methods: TMS studies were undertaken using a 90mm circular coil on seven asymptomatic SOD-1 mutation carriers and results were compared to 62 healthy controls. DTI studies were carried out using a 3T magnetic resonance device in the same asymptomatic SOD-1 mutation carriers. Results were compared to age-matched healthy controls.Results: In contrast to previous findings, there were no significant differences in fractional anisotropy (SOD-1 mutation carriers, 0.62±0.01; controls, 0.61±0.02, P=0.2) and trace apparent diffusion coefficient (SOD-1 mutation carriers, 0.003±0.0001; controls, 0.003±0.0001) in asymptomatic SOD-1 mutation carriers. Of further relevance, there were no significant differences in short-interval intracortical inhibition (SOD-1 mutation carriers, 7.9±3.4%; controls, 8.5±1.1%, P=0.26), intracortical facilitation (P=0.5), MEP amplitude (P=0.44), resting motor threshold (P=0.36) and cortical silent period duration (P=0.29).Conclusions: Combined anatomical and functional modalities established normal integrity of corticomotoneurons in asymptomatic SOD-1 mutation carrier subjects.Significance: Additional factors other than simply SOD-1 mutation expression are required to trigger cortical hyperexcitability and neurodegeneration in FALS.</description><dc:title>Corticomotoneuronal function in asymptomatic SOD-1 mutation carriers</dc:title><dc:creator>Steve Vucic, Jennica M.C. Winhammar, Dominic B. Rowe, Matthew C. Kiernan</dc:creator><dc:identifier>10.1016/j.clinph.2010.02.164</dc:identifier><dc:source>Clinical Neurophysiology 121, 10 (2010)</dc:source><dc:date>2010-10-01</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2010-10-01</prism:publicationDate><prism:volume>121</prism:volume><prism:number>10</prism:number><prism:issueIdentifier>S1388-2457(10)X0010-4</prism:issueIdentifier><prism:section>Original Research Articles</prism:section><prism:startingPage>1781</prism:startingPage><prism:endingPage>1785</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245710003433/abstract?rss=yes"><title>Overestimation of saccadic peak velocity recorded by electro-oculography compared to video-oculography and scleral search coil</title><link>http://www.clinph-journal.com/article/PIIS1388245710003433/abstract?rss=yes</link><description>Peak velocity of saccadic eye movements is a crucial motor parameter in clinical neurology and oculomotor research. It may help to assign patients’ lesions to even very small brain regions which are not (yet) recognizable with magnetic resonance imaging (MRI). Horizontal slowing of saccades is associated with pontine lesions of the paramedian pontine reticular formation while saccades in cerebellar or cortical lesions are usually not slowed (). Accordingly, saccade velocity helps to classify and distinguish neurodegenerative and genetic movement disorders, e.g. Parkinson’s disease or spinocerebellar ataxias. However, related studies are often not easily comparable as different recording techniques (e.g. electro-oculography, video-oculography, and scleral search coil) and different paradigms (e.g., reflexive, self-paced saccades) are used irrespective of their influence on saccade velocity. Therefore, we intraindividually compared saccadic peak velocities using electro-oculography (EOG), video-oculography (VOG) and scleral search coil (SSC) in a variety of saccade types and conditions to assess the comparability of these methods.</description><dc:title>Overestimation of saccadic peak velocity recorded by electro-oculography compared to video-oculography and scleral search coil</dc:title><dc:creator>Maren Lappe-Osthege, Silke Talamo, Christoph Helmchen, Andreas Sprenger</dc:creator><dc:identifier>10.1016/j.clinph.2010.03.051</dc:identifier><dc:source>Clinical Neurophysiology 121, 10 (2010)</dc:source><dc:date>2010-10-01</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2010-10-01</prism:publicationDate><prism:volume>121</prism:volume><prism:number>10</prism:number><prism:issueIdentifier>S1388-2457(10)X0010-4</prism:issueIdentifier><prism:section>Letter to the Editor</prism:section><prism:startingPage>1786</prism:startingPage><prism:endingPage>1787</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245710006127/abstract?rss=yes"><title>Corrigendum to “Editorial: Whither needle EMG? by David Burke” [Clinical Neurophysiology 121 (9) (2010) 1373–1375]</title><link>http://www.clinph-journal.com/article/PIIS1388245710006127/abstract?rss=yes</link><description>The text states “The recording surface should be small and the bandpass restricted (say 1–5kΩ)”. This should read “The recording surface should be small and the bandpass restricted (say 1–5kHz)’</description><dc:title>Corrigendum to “Editorial: Whither needle EMG? by David Burke” [Clinical Neurophysiology 121 (9) (2010) 1373–1375]</dc:title><dc:creator>David Burke</dc:creator><dc:identifier>10.1016/j.clinph.2010.08.001</dc:identifier><dc:source>Clinical Neurophysiology 121, 10 (2010)</dc:source><dc:date>2010-10-01</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2010-10-01</prism:publicationDate><prism:volume>121</prism:volume><prism:number>10</prism:number><prism:issueIdentifier>S1388-2457(10)X0010-4</prism:issueIdentifier><prism:section>Corrigendum</prism:section><prism:startingPage>1788</prism:startingPage><prism:endingPage>1788</prism:endingPage></item></rdf:RDF>