<?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 , 
the  Brazilian Society of Clinical Neurophysiology , the  Czech 
Society of Clinical Neurophysiology , and the  Italian Clinical Neurophysiology 
Society .


The journal is dedicated to fostering research and disseminating information on all aspects of both normal and 
abnormal functioning of the nervous system. The key aim of the publication is to disseminate scholarly reports on the pathophysiology 
underlying diseases of the central and peripheral nervous system of human patients. Clinical trials that use neurophysiological measures 
to document change are encouraged, as are manuscripts reporting data on integrated neuroimaging of central nervous function including, 
but not limited to, functional MRI, MEG, EEG, PET and other neuroimaging modalities. 
 The Journal has special emphases on epilepsy 
and on studies of cognitive function and cognitive disorders. Motor neurone and neuromuscular diseases, vestibular disorders, motor control 
and somatosensory physiopathology are also covered by the Journal. Studies on animals and technical notes must have clear relevance and 
applicability to human disease, and studies reporting normative data for specific tests must have clear novelty. Case Reports are not 
generally accepted as full length submissions but may be considered as peer-reviewed Letters. 
 
 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> © 2012 International Federation of Clinical Neurophysiology. Published by Elsevier Inc. All rights reserved. </dc:rights><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:issn>1388-2457</prism:issn><prism:volume>123</prism:volume><prism:number>5</prism:number><prism:publicationDate>May 2012</prism:publicationDate><prism:copyright> © 2012 International Federation of Clinical Neurophysiology. 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/PIIS1388245712002064/abstract?rss=yes"/><rdf:li rdf:resource="http://www.clinph-journal.com/article/PIIS1388245712002076/abstract?rss=yes"/><rdf:li rdf:resource="http://www.clinph-journal.com/article/PIIS1388245712002131/abstract?rss=yes"/><rdf:li rdf:resource="http://www.clinph-journal.com/article/PIIS1388245711007528/abstract?rss=yes"/><rdf:li rdf:resource="http://www.clinph-journal.com/article/PIIS138824571100681X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.clinph-journal.com/article/PIIS1388245711006730/abstract?rss=yes"/><rdf:li rdf:resource="http://www.clinph-journal.com/article/PIIS1388245711006729/abstract?rss=yes"/><rdf:li rdf:resource="http://www.clinph-journal.com/article/PIIS1388245711006304/abstract?rss=yes"/><rdf:li rdf:resource="http://www.clinph-journal.com/article/PIIS1388245711006262/abstract?rss=yes"/><rdf:li rdf:resource="http://www.clinph-journal.com/article/PIIS1388245712000569/abstract?rss=yes"/><rdf:li rdf:resource="http://www.clinph-journal.com/article/PIIS1388245711006778/abstract?rss=yes"/><rdf:li rdf:resource="http://www.clinph-journal.com/article/PIIS1388245711006869/abstract?rss=yes"/><rdf:li rdf:resource="http://www.clinph-journal.com/article/PIIS1388245711006754/abstract?rss=yes"/><rdf:li rdf:resource="http://www.clinph-journal.com/article/PIIS1388245711006316/abstract?rss=yes"/><rdf:li rdf:resource="http://www.clinph-journal.com/article/PIIS1388245711006249/abstract?rss=yes"/><rdf:li rdf:resource="http://www.clinph-journal.com/article/PIIS1388245711007887/abstract?rss=yes"/><rdf:li rdf:resource="http://www.clinph-journal.com/article/PIIS1388245711007875/abstract?rss=yes"/><rdf:li rdf:resource="http://www.clinph-journal.com/article/PIIS1388245711006833/abstract?rss=yes"/><rdf:li rdf:resource="http://www.clinph-journal.com/article/PIIS138824571100678X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.clinph-journal.com/article/PIIS1388245711006717/abstract?rss=yes"/><rdf:li rdf:resource="http://www.clinph-journal.com/article/PIIS1388245711006821/abstract?rss=yes"/><rdf:li rdf:resource="http://www.clinph-journal.com/article/PIIS1388245711007905/abstract?rss=yes"/><rdf:li rdf:resource="http://www.clinph-journal.com/article/PIIS1388245711006742/abstract?rss=yes"/><rdf:li rdf:resource="http://www.clinph-journal.com/article/PIIS1388245711006870/abstract?rss=yes"/><rdf:li rdf:resource="http://www.clinph-journal.com/article/PIIS1388245711006808/abstract?rss=yes"/><rdf:li rdf:resource="http://www.clinph-journal.com/article/PIIS1388245711006791/abstract?rss=yes"/><rdf:li rdf:resource="http://www.clinph-journal.com/article/PIIS1388245711006766/abstract?rss=yes"/><rdf:li rdf:resource="http://www.clinph-journal.com/article/PIIS138824571100633X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.clinph-journal.com/article/PIIS1388245711006250/abstract?rss=yes"/><rdf:li rdf:resource="http://www.clinph-journal.com/article/PIIS1388245711006894/abstract?rss=yes"/><rdf:li rdf:resource="http://www.clinph-journal.com/article/PIIS1388245711006705/abstract?rss=yes"/><rdf:li rdf:resource="http://www.clinph-journal.com/article/PIIS1388245711006699/abstract?rss=yes"/><rdf:li rdf:resource="http://www.clinph-journal.com/article/PIIS1388245711006675/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245712002064/abstract?rss=yes"><title>Contents</title><link>http://www.clinph-journal.com/article/PIIS1388245712002064/abstract?rss=yes</link><description></description><dc:title>Contents</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1388-2457(12)00206-4</dc:identifier><dc:source>Clinical Neurophysiology 123, 5 (2012)</dc:source><dc:date>2012-05-01</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2012-05-01</prism:publicationDate><prism:volume>123</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1388-2457(12)X0004-X</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>i</prism:startingPage><prism:endingPage>ii</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245712002076/abstract?rss=yes"><title>Editorial Board</title><link>http://www.clinph-journal.com/article/PIIS1388245712002076/abstract?rss=yes</link><description></description><dc:title>Editorial Board</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1388-2457(12)00207-6</dc:identifier><dc:source>Clinical Neurophysiology 123, 5 (2012)</dc:source><dc:date>2012-05-01</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2012-05-01</prism:publicationDate><prism:volume>123</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1388-2457(12)X0004-X</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/PIIS1388245712002131/abstract?rss=yes"><title>Preliminary Announcement</title><link>http://www.clinph-journal.com/article/PIIS1388245712002131/abstract?rss=yes</link><description></description><dc:title>Preliminary Announcement</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1388-2457(12)00213-1</dc:identifier><dc:source>Clinical Neurophysiology 123, 5 (2012)</dc:source><dc:date>2012-05-01</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2012-05-01</prism:publicationDate><prism:volume>123</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1388-2457(12)X0004-X</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>847</prism:startingPage><prism:endingPage>847</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245711007528/abstract?rss=yes"><title>Pain and attention – friends or foes?</title><link>http://www.clinph-journal.com/article/PIIS1388245711007528/abstract?rss=yes</link><description>There is a close biological association between pain and attention. Pain attracts attention which guides the affected individual to adopt protective behaviors such as withdrawal, flight, or taking care of the injured body. Thus, both phenomena form a good alliance that serves to prevent or overcome bodily harm. However, this alliance can also make patients suffer in prolonged and chronic pain states when there is no easy way to get rid of the cause of pain. In situations where the patient seeks to pursue behavioral goals outside the focus of pain he or she will be permanently interrupted by pain.</description><dc:title>Pain and attention – friends or foes?</dc:title><dc:creator>Michael Hauck, Jürgen Lorenz</dc:creator><dc:identifier>10.1016/j.clinph.2011.10.010</dc:identifier><dc:source>Clinical Neurophysiology 123, 5 (2012)</dc:source><dc:date>2011-11-17</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2011-11-17</prism:publicationDate><prism:volume>123</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1388-2457(12)X0004-X</prism:issueIdentifier><prism:section>Editorials</prism:section><prism:startingPage>848</prism:startingPage><prism:endingPage>849</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS138824571100681X/abstract?rss=yes"><title>Repetitive transcranial magnetic stimulation as a treatment for essential tremor?</title><link>http://www.clinph-journal.com/article/PIIS138824571100681X/abstract?rss=yes</link><description>Repetitive transcranial magnetic stimulation (rTMS) has been tested as a treatment for various neurological and psychiatric disorders. With rTMS delivered at regular rates, it was found that high frequency rTMS (&gt;1Hz, generally 5Hz or higher) increased cortical excitability () and this has been tested as a treatment for conditions such as depression, stroke (ipsilesional hemisphere) and Parkinson’s disease (PD). On the other hand, low frequency rTMS (1Hz or lower) reduced cortical excitability () and has been studied as a treatment for epilepsy, stroke (contralesional hemisphere), schizophrenia and levodopa-induced dyskinesias. rTMS is currently an approved treatment for medication resistant depression in several countries including the United States and Canada. However, there is considerable subject to subject variability in the effects of rTMS ().</description><dc:title>Repetitive transcranial magnetic stimulation as a treatment for essential tremor?</dc:title><dc:creator>Robert Chen</dc:creator><dc:identifier>10.1016/j.clinph.2011.09.015</dc:identifier><dc:source>Clinical Neurophysiology 123, 5 (2012)</dc:source><dc:date>2011-10-10</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2011-10-10</prism:publicationDate><prism:volume>123</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1388-2457(12)X0004-X</prism:issueIdentifier><prism:section>Editorials</prism:section><prism:startingPage>850</prism:startingPage><prism:endingPage>851</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245711006730/abstract?rss=yes"><title>Unraveling the brainstem mysteries in late-preterm infants</title><link>http://www.clinph-journal.com/article/PIIS1388245711006730/abstract?rss=yes</link><description>In this issue of “Clinical Neurophysiology”,  address an important issue: the functional integrity of the auditory brainstem in late-preterm infants. This group of infants is typically defined as 34–36weeks’ gestation, and their incidence is steadily increasing (20% from 1990 to 2006; comprising 70% of all singleton preterm births in the US, independently from increases in multiple gestations in the same time frame) (). Late preterm infants are traditionally perceived by clinicians as physiologically similar to full term infants and are often treated similarly, though different degrees of immaturity are evident in respiratory, metabolic, immunological and neurological functioning (). There is a substantial body of evidence in the literature demonstrating that very or extremely preterm infants are at major risk for brain damage resulting in diverse neurological impairment, with more than 50% of survivors exhibiting mainly cerebral palsy, but also later cognitive, learning and behavioral difficulties, including auditory dysfunction (). However, limited information is currently available for brain development and function in infants born late preterm. Quantitative MRI and neuropathological studies in preterms (including late preterm infants) support evidence for a so-called “rapid growth phase” of different regions and tissues of the brain, affecting both its macro- and microstructural organization (). This would make the immature brain particularly susceptible to neuronal injury, involving not only myelination and the white matter microstructure, but also the cortical gray matter, the cerebellum, the thalamus, the basal ganglia, the hippocampus and the brainstem to varying degrees ().</description><dc:title>Unraveling the brainstem mysteries in late-preterm infants</dc:title><dc:creator>Dimitrios I. Zafeiriou, Euthymia Vargiami</dc:creator><dc:identifier>10.1016/j.clinph.2011.09.009</dc:identifier><dc:source>Clinical Neurophysiology 123, 5 (2012)</dc:source><dc:date>2011-10-05</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2011-10-05</prism:publicationDate><prism:volume>123</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1388-2457(12)X0004-X</prism:issueIdentifier><prism:section>Editorials</prism:section><prism:startingPage>852</prism:startingPage><prism:endingPage>853</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245711006729/abstract?rss=yes"><title>Widespread spread: Another pitfall for ulnar sensory conduction study</title><link>http://www.clinph-journal.com/article/PIIS1388245711006729/abstract?rss=yes</link><description>The antidromic ulnar sensory conduction study (AUSCS) recording from digit 5 is routinely used in the evaluation of neuromuscular disorders (). Although generally straightforward, AUSCS has technical pitfalls, a motor artifact being the most frequently encountered. The source of the artifact is a volume-conducted motor response () that may be significantly influenced by a limb position (). Rutkove reported that placement of recording electrodes distally around digit 5 and an extended and abducted finger position can minimize the motor artifact ().</description><dc:title>Widespread spread: Another pitfall for ulnar sensory conduction study</dc:title><dc:creator>Hiroyuki Nodera</dc:creator><dc:identifier>10.1016/j.clinph.2011.09.008</dc:identifier><dc:source>Clinical Neurophysiology 123, 5 (2012)</dc:source><dc:date>2011-09-30</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2011-09-30</prism:publicationDate><prism:volume>123</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1388-2457(12)X0004-X</prism:issueIdentifier><prism:section>Editorials</prism:section><prism:startingPage>854</prism:startingPage><prism:endingPage>854</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245711006304/abstract?rss=yes"><title>EEG in the emergency department: Speeding the patients toward the right treatment plans</title><link>http://www.clinph-journal.com/article/PIIS1388245711006304/abstract?rss=yes</link><description>Health care is moving toward more quickly resolving medical diagnostic problems so as to initiate proper treatment plans promptly. The internet has speeded this process. The cultural desire to obtain results right away is gradually replacing the professional patience of past years. Neurodiagnostic testing is well suited to this evolution to immediate answers. Continuous ICU EEG is a good example of getting the right information to the right physicians in time to make the right care choices quickly, speeding the recovery, reducing the chances for complications, and reducing the overall cost of care.</description><dc:title>EEG in the emergency department: Speeding the patients toward the right treatment plans</dc:title><dc:creator>Marc R. Nuwer</dc:creator><dc:identifier>10.1016/j.clinph.2011.09.004</dc:identifier><dc:source>Clinical Neurophysiology 123, 5 (2012)</dc:source><dc:date>2011-09-28</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2011-09-28</prism:publicationDate><prism:volume>123</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1388-2457(12)X0004-X</prism:issueIdentifier><prism:section>Editorials</prism:section><prism:startingPage>855</prism:startingPage><prism:endingPage>855</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245711006262/abstract?rss=yes"><title>Cycling thalamic stimulation, neuronal entropy, and tremor</title><link>http://www.clinph-journal.com/article/PIIS1388245711006262/abstract?rss=yes</link><description>Deep brain stimulation (DBS) is a procedure involving the implantation of a neurostimulator that sends electrical impulses to specific parts of the brain. It has been demonstrated effective in relieving symptoms of patients with Parkinson’s disease as well as other conditions. The underlying principles and the mechanisms by which DBS affects brain activity and leads to the symptomatic benefit are still not clear (). The history of modern times DBS as a therapeutic option re-commenced some 20years ago, with significant scientific contributions on technical improvements from many authors in the field.</description><dc:title>Cycling thalamic stimulation, neuronal entropy, and tremor</dc:title><dc:creator>Francesc Valldeoriola, Josep Valls-Sole</dc:creator><dc:identifier>10.1016/j.clinph.2011.08.026</dc:identifier><dc:source>Clinical Neurophysiology 123, 5 (2012)</dc:source><dc:date>2011-09-28</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2011-09-28</prism:publicationDate><prism:volume>123</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1388-2457(12)X0004-X</prism:issueIdentifier><prism:section>Editorials</prism:section><prism:startingPage>856</prism:startingPage><prism:endingPage>857</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245712000569/abstract?rss=yes"><title>A practical guide to diagnostic transcranial magnetic stimulation: Report of an IFCN committee</title><link>http://www.clinph-journal.com/article/PIIS1388245712000569/abstract?rss=yes</link><description>Highlights: ► This guideline paper provides an up-date on the clinical use of transcranial magnetic stimulation (TMS). ► The clinically relevant technical and physiological principles of TMS are outlined. ► A detailed description how to examine corticomotor conduction to the hand, leg, trunk and facial muscles is presented.Abstract: Transcranial magnetic stimulation (TMS) is an established neurophysiological tool to examine the integrity of the fast-conducting corticomotor pathways in a wide range of diseases associated with motor dysfunction. This includes but is not limited to patients with multiple sclerosis, amyotrophic lateral sclerosis, stroke, movement disorders, disorders affecting the spinal cord, facial and other cranial nerves. These guidelines cover practical aspects of TMS in a clinical setting. We first discuss the technical and physiological aspects of TMS that are relevant for the diagnostic use of TMS. We then lay out the general principles that apply to a standardized clinical examination of the fast-conducting corticomotor pathways with single-pulse TMS. This is followed by a detailed description of how to examine corticomotor conduction to the hand, leg, trunk and facial muscles in patients. Additional sections cover safety issues, the triple stimulation technique, and neuropediatric aspects of TMS.</description><dc:title>A practical guide to diagnostic transcranial magnetic stimulation: Report of an IFCN committee</dc:title><dc:creator>S. Groppa, A. Oliviero, A. Eisen, A. Quartarone, L.G. Cohen, V. Mall, A. Kaelin-Lang, T. Mima, S. Rossi, G.W. Thickbroom, P.M. Rossini, U. Ziemann, J. Valls-Solé, H.R. Siebner</dc:creator><dc:identifier>10.1016/j.clinph.2012.01.010</dc:identifier><dc:source>Clinical Neurophysiology 123, 5 (2012)</dc:source><dc:date>2012-02-20</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2012-02-20</prism:publicationDate><prism:volume>123</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1388-2457(12)X0004-X</prism:issueIdentifier><prism:section>Guidelines</prism:section><prism:startingPage>858</prism:startingPage><prism:endingPage>882</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245711006778/abstract?rss=yes"><title>Effect of levetiracetam monotherapy on background EEG activity and cognition in drug-naïve epilepsy patients</title><link>http://www.clinph-journal.com/article/PIIS1388245711006778/abstract?rss=yes</link><description>Highlights: ► We evaluated the effect of LEV on background EEG and cognition in epilepsy patients. ► LEV decreases slow frequency power and increases fast frequency power. ► LEV causes improvement in diverse neuropsychological tests. ► Some EEG changes across LEV therapy were correlated with change in cognitive tests.Abstract: Objective: To investigate the cognitive effect of levetiracetam (LEV) monotherapy with quantitative electroencephalogram (EEG) analysis and neuropsychological (NP) tests.Methods: Twenty-two drug-naïve epilepsy patients were enrolled. EEG recordings were performed before and after LEV therapy. Relative power of discrete frequency bands was computed, as well as alpha peak frequency (APF) at occipital electrodes. Eighteen patients performed a battery of NP tests twice across LEV treatment.Results: LEV therapy decreased the power of delta (1–3Hz, p&lt;0.01) and theta (3–7Hz, p&lt;0.05) bands and increased that of alpha-2 (10–13Hz, p&lt;0.05) and beta-2 (19–24Hz, p&lt;0.05) bands. Region-specific spectral change was observed: delta power change was significant in fronto-polar region, theta in anterior region, alpha-2 in broad region, and beta-2 in left fronto-central region. APF change was not significant. Improvement in diverse NP tests requiring attention, working memory, language and executive function was observed. Change in theta, alpha-2, and beta-2 power was correlated with improvement in several NP tests.Conclusions: Our data suggest LEV is associated with acceleration of background EEG frequencies and improved cognitive function. Change in frequency band power could predict improvement in several cognitive domains across LEV therapy.Significance: Combined study of quantitative EEG analysis and NP tests can be useful in identifying cognitive effect of antiepileptic drugs.</description><dc:title>Effect of levetiracetam monotherapy on background EEG activity and cognition in drug-naïve epilepsy patients</dc:title><dc:creator>Jounhong Ryan Cho, Dae Lim Koo, Eun Yeon Joo, So Mi Yoon, Eunji Ju, James Lee, Dae Young Kim, Seung Bong Hong</dc:creator><dc:identifier>10.1016/j.clinph.2011.09.012</dc:identifier><dc:source>Clinical Neurophysiology 123, 5 (2012)</dc:source><dc:date>2011-10-14</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2011-10-14</prism:publicationDate><prism:volume>123</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1388-2457(12)X0004-X</prism:issueIdentifier><prism:section>Epilepsy</prism:section><prism:startingPage>883</prism:startingPage><prism:endingPage>891</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245711006869/abstract?rss=yes"><title>Cerebral effects of binge drinking: Respective influences of global alcohol intake and consumption pattern</title><link>http://www.clinph-journal.com/article/PIIS1388245711006869/abstract?rss=yes</link><description>Highlights: ► Binge drinking leads to striking cerebral alterations, as indexed by event-related potentials. ► Young binge drinkers present early and global electrophysiological impairments, affecting low-level (perception and attention) as well as high-level (decision) cognitive stages. ► The specific consumption pattern observed in binge drinking (i.e., alternating intense intoxications and withdrawal episodes) is particularly deleterious for the brain.Abstract: Objective: Binge drinking is a major health concern, but its cerebral correlates are still largely unexplored. We aimed at exploring (1) the cognitive step at which these deficits appear and (2) the respective influence of global alcohol intake and specific binge-drinking consumption pattern on this deficit.Methods: On the basis of a screening phase (593 students), 80 participants were selected and distributed in four groups (control non-drinkers, daily drinkers, low and high binge drinkers). Event-related potentials (ERPs) were recorded while performing a simple visual oddball task.Results: Binge drinking was associated with massive ERP impairments, starting at the perceptive level (P100/N100 and N170/P2) and spreading through the attentional (N2b/P3a) and decisional (P3b) ones. Moreover, these deficits were linked with global alcohol intake and also with the specific binge-drinking consumption pattern.Conclusions: Binge drinkers presented early and global ERP deficits, affecting basic and high-level cognitive stages. Moreover, we showed that binge drinking is deleterious for the brain because of alcohol consumption per se, and also because of its specific consumption pattern.Significance: The present results show that binge-drinking habits lead to striking brain consequences, particularly because of the repeated alternation between intense intoxications and withdrawal episodes.</description><dc:title>Cerebral effects of binge drinking: Respective influences of global alcohol intake and consumption pattern</dc:title><dc:creator>P. Maurage, F. Joassin, A. Speth, J. Modave, P. Philippot, S. Campanella</dc:creator><dc:identifier>10.1016/j.clinph.2011.09.018</dc:identifier><dc:source>Clinical Neurophysiology 123, 5 (2012)</dc:source><dc:date>2011-11-07</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2011-11-07</prism:publicationDate><prism:volume>123</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1388-2457(12)X0004-X</prism:issueIdentifier><prism:section>Cerebral Function and its Development</prism:section><prism:startingPage>892</prism:startingPage><prism:endingPage>901</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245711006754/abstract?rss=yes"><title>Chronic treatment with rivastigmine in patients with Alzheimer’s disease: A study on primary motor cortex excitability tested by 5Hz-repetitive transcranial magnetic stimulation</title><link>http://www.clinph-journal.com/article/PIIS1388245711006754/abstract?rss=yes</link><description>Highlights: ► Abnormal 5 Hz-rTMS responses in AD patients, indicate altered synaptic plasticity. ► These responses remain abnormal even after chronic treatment with rivastigmine. ► Our results might explain why rivastigmine yields a poor clinical benefit in AD. ► AD patients might fare better with drugs improving cortical plasticity.Abstract: Objective: To investigate changes in cortical excitability and short-term synaptic plasticity we delivered 5Hz repetitive transcranial magnetic stimulation (rTMS) over the primary motor cortex in 11 patients with mild-to-moderate Alzheimer’s disease (AD) before and after chronic therapy with rivastigmine.Methods: Resting motor threshold (RMT), motor evoked potential (MEP), cortical silent period (CSP) after single stimulus and MEP facilitation during rTMS trains were tested three times during treatment. All patients underwent neuropsychological tests before and after receiving rivastigmine. rTMS data in patients were compared with those from age-matched healthy controls.Results: At baseline, RMT was significantly lower in patients than in controls whereas CSP duration and single MEP amplitude were similar in both groups. In patients, rTMS failed to induce the normal MEP facilitation during the trains. Chronic rivastigmine intake significantly increased MEP amplitude after a single stimulus, whereas it left the other neurophysiological variables studied unchanged. No significant correlation was found between patients’ neuropsychological test scores and TMS measures.Conclusions: Chronic treatment with rivastigmine has no influence on altered cortical excitability and short-term synaptic plasticity as tested by 5Hz-rTMS.Significance: The limited clinical benefits related to cholinesterase inhibitor therapy in patients with AD depend on factors other than improved plasticity within the cortical glutamatergic circuits.</description><dc:title>Chronic treatment with rivastigmine in patients with Alzheimer’s disease: A study on primary motor cortex excitability tested by 5Hz-repetitive transcranial magnetic stimulation</dc:title><dc:creator>A. Trebbastoni, F. Gilio, F. D’Antonio, C. Cambieri, M. Ceccanti, C. de Lena, M. Inghilleri</dc:creator><dc:identifier>10.1016/j.clinph.2011.09.010</dc:identifier><dc:source>Clinical Neurophysiology 123, 5 (2012)</dc:source><dc:date>2011-10-13</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2011-10-13</prism:publicationDate><prism:volume>123</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1388-2457(12)X0004-X</prism:issueIdentifier><prism:section>Alzheimer's Disease, Dementia and other Cognitive Disorders</prism:section><prism:startingPage>902</prism:startingPage><prism:endingPage>909</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245711006316/abstract?rss=yes"><title>Emergent EEG in the emergency department in patients with altered mental states</title><link>http://www.clinph-journal.com/article/PIIS1388245711006316/abstract?rss=yes</link><description>Highlights: ► Availability of a rapid, standard full montage EEG in the emergency department is a feasible goal. ► Specific presentations of altered mental status offer the best diagnostic benefit of EEG in the emergency department. ► Abbreviated 5min full-montage EEG presents adequate reliability which should improve acceptance and use of EEG in the emergency department.Abstract: Objective: To evaluate whether EEG performed within 30min of referral by an ED physician helps establish diagnosis and/or changes management and in which clinical setting.Methods: Single-center prospective cohort intervention study 1day/week, of sequentially referred adult patients with clinical seizures or altered mental status (AMS). Standard EEGs were performed by an EEG technician using a commercially available cap, interpreted by an epileptologist, immediately reported to the ED physician and a utility survey completed. Quality and interpretation of 20min EEGs was compared to pre-specified 5min segments of each EEG using the kappa coefficient.Results: Over 1year, 82 patients underwent ED EEG. Tonic clonic seizure activity had occurred in 33%. Mean time for EEG setup was 13.1±6.2min. EEG assisted the diagnosis in 51%, changed ED management in 4% and would be ordered again if EEG was available in 46%. Positive utility of EEG was significantly associated with toxicologic, psychiatric and endocrine/metabolic causes of AMS vs. other causes (p&lt;0.001) and sudden onset AMS (p=0.007). Independent predictors of whether ED EEG would be ordered if available were witnessed seizures (p=0.01), no prior head trauma (p=0.001) and survey respondent being a physician assistant (vs. MD) (p=0.02). The 5 (vs. 20) min EEG presented good agreement on waveform shape/amplitude (kappa=0.78), artifact (kappa=0.75) and interpretation categories (all kappa levels ⩾0.70).Conclusions: Rapid availability of standard full-montage EEG in the ED is feasible and helps establish a diagnosis in about half of AMS patients, but rarely changes management. An abbreviated 5min full-montage EEG presents adequate reliability which may improve use in the ED.Significance: Specific presentations of AMS offer the best diagnostic benefit for EEG in the ED.</description><dc:title>Emergent EEG in the emergency department in patients with altered mental states</dc:title><dc:creator>Wendy C. Ziai, Dan Schlattman, Rafael Llinas, Santosh Venkatesha, Melvin Truesdale, Anastasia Schevchenko, Peter W. Kaplan</dc:creator><dc:identifier>10.1016/j.clinph.2011.07.053</dc:identifier><dc:source>Clinical Neurophysiology 123, 5 (2012)</dc:source><dc:date>2011-10-05</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2011-10-05</prism:publicationDate><prism:volume>123</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1388-2457(12)X0004-X</prism:issueIdentifier><prism:section>Alzheimer's Disease, Dementia and other Cognitive Disorders</prism:section><prism:startingPage>910</prism:startingPage><prism:endingPage>917</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245711006249/abstract?rss=yes"><title>Adiposity measures predict olfactory processing speed in older adult carriers of the apolipoprotein E ε4 allele</title><link>http://www.clinph-journal.com/article/PIIS1388245711006249/abstract?rss=yes</link><description>Highlights: ► Positive correlations for P3 latency with both BMI and waist circumference were observed in older adults at risk for Alzheimer’s disease (AD). ► As BMI and waist circumference increased, P3 latencies also increased. ► Olfactory processing speed may be useful in detecting effects of adiposity on brain integrity and function in e4+ persons. ► Olfactory processing speed may be useful in monitoring effects of adiposity on brain integrity and function in e4+ persons.Abstract: Objective: The current study investigated the relationship between adiposity and P3 latency.Methods: Fifty-one adults in two age groups (18–25 and 65+) participated. Odor stimuli were delivered via olfactometer as participants focused on a computer screen. Each stimulus was followed by presentation on the screen of four odor identification choices. Participants attempted identification by button press. Olfactory event-related potentials (OERPs) were recorded. BMI and waist circumference were measured as indicators of adiposity.Results: In bivariate analyses with all participants included, positive correlations for P3 latency with both BMI and waist circumference were observed, indicating that as adiposity increased latencies also increased. When each age group was separately examined, correlations between adiposity measures and latency remained statistically significant for older adults. Furthermore, ApoE ε4 allele status was examined. Latencies remained positively correlated with adiposity in older adult ε4 carriers; but not in non-carriers.Conclusions: This study indicates that adiposity predicts olfactory processing speed in older adults, specifically in ε4 carriers.Significance: The results suggest that olfactory processing speed may be a useful measure for detecting and following the effects of adiposity on brain integrity and cognitive function in those at genetic risk for AD.</description><dc:title>Adiposity measures predict olfactory processing speed in older adult carriers of the apolipoprotein E ε4 allele</dc:title><dc:creator>R. Zamora, J. Bartholow, E. Green, C.D. Morgan, C. Murphy</dc:creator><dc:identifier>10.1016/j.clinph.2011.09.001</dc:identifier><dc:source>Clinical Neurophysiology 123, 5 (2012)</dc:source><dc:date>2011-11-07</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2011-11-07</prism:publicationDate><prism:volume>123</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1388-2457(12)X0004-X</prism:issueIdentifier><prism:section>Alzheimer's Disease, Dementia and other Cognitive Disorders</prism:section><prism:startingPage>918</prism:startingPage><prism:endingPage>924</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245711007887/abstract?rss=yes"><title>Early attentional modulation by alcohol-related cues in young binge drinkers: An event-related potentials study</title><link>http://www.clinph-journal.com/article/PIIS1388245711007887/abstract?rss=yes</link><description>Highlights: ► ERP data showed that significantly larger P100 amplitudes are elicited by alcohol-related pictures in binge drinkers than in control students. ► All students had significantly faster responses to alcohol-related stimuli compared to non alcohol-related ones. ► The valence of the cues did not influence the observed heightened electrophysiological or behavioural reactivity elicited by alcohol cues.Abstract: Objective: Episodic excessive alcohol consumption (i.e., binge drinking) is now considered to be a major concern in our society. Previous studies have shown that alcohol cues can capture attentional resources in chronic alcoholic populations and that the phenomenon is associated with the development and maintenance of alcoholism. Using event-related potentials (ERPs), we investigated the responses of binge drinkers to alcohol-related pictures.Methods: Two groups of college students (n=18 in each group) were recruited for the study. One group was composed of binge drinkers and the other of controls. Each student completed a simple visual oddball paradigm in which alcohol-related and non-alcohol-related pictures (positive, neutral or negative) were presented. ERPs were recorded to explore the electrophysiological activity associated with the processing of each cue during the different cognitive steps.Results: Although there were no behavioural differences between the two groups after detection of alcohol- and non-alcohol-related cues, the ERP data indicated that processing of alcohol-related stimuli was modulated by binge drinking: in the binge drinkers, the P100 amplitudes elicited by the alcohol-related pictures were significantly larger than those elicited by the non-alcohol pictures.Conclusions: The present study provides evidence for an early processing enhancement, indexed by increased P100 amplitude, in binge drinkers when confronted with alcohol cues.Significance: These findings suggest that higher reactivity to alcohol cues is not a phenomenon limited to adult alcoholics, but that young binge drinkers exhibit signs of prioritizing processing related to alcohol. Prevention intervention for alcohol misuse in young people should consider approaches that address this automatic cue reactivity.</description><dc:title>Early attentional modulation by alcohol-related cues in young binge drinkers: An event-related potentials study</dc:title><dc:creator>Géraldine Petit, Charles Kornreich, Pierre Maurage, Xavier Noël, Clément Letesson, Paul Verbanck, Salvatore Campanella</dc:creator><dc:identifier>10.1016/j.clinph.2011.10.042</dc:identifier><dc:source>Clinical Neurophysiology 123, 5 (2012)</dc:source><dc:date>2011-11-28</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2011-11-28</prism:publicationDate><prism:volume>123</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1388-2457(12)X0004-X</prism:issueIdentifier><prism:section>Psychophysiology and Psychopathology</prism:section><prism:startingPage>925</prism:startingPage><prism:endingPage>936</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245711007875/abstract?rss=yes"><title>Greater sensitivity of the P300 component to bimodal stimulation in an event-related potentials oddball task</title><link>http://www.clinph-journal.com/article/PIIS1388245711007875/abstract?rss=yes</link><description>Abstract: Objective: Studies that explore neurophysiological correlates of psychiatric disorders have commonly used event-related potentials during a visual or an auditory oddball task with the main results being changes in the P300 component. In the present study, a bimodal oddball design with synchronized pairs of audio–visual stimuli was used to further improve the clinical sensitivity of the P300.Methods: Two groups of healthy participants, one consisting of students displaying anxious–depressive tendencies and the other of control students, completed visual, auditory and two kinds of audio–visual oddball task (one using emotional stimuli and the other using geometrical figures and simple sounds), in which they had to detect deviant rare stimuli among more frequently presented standard stimuli as quickly as possible. Behavioral performance and P300 data were analyzed.Results: The subjects with anxious and depressive tendencies had lower P300 amplitudes than controls, but only in the bimodal tasks.Conclusions: Although the two groups differed in their levels of anxiety and depression, only the bimodal tasks were able to identify these differences.Significances: These results suggest that a bimodal oddball design should be used in future studies to increase the sensitivity of P300 differences for differentiating between healthy participants and those with clinical symptoms.</description><dc:title>Greater sensitivity of the P300 component to bimodal stimulation in an event-related potentials oddball task</dc:title><dc:creator>Salvatore Campanella, Dyna Delle-Vigne, Charles Kornreich, Paul Verbanck</dc:creator><dc:identifier>10.1016/j.clinph.2011.10.041</dc:identifier><dc:source>Clinical Neurophysiology 123, 5 (2012)</dc:source><dc:date>2011-11-28</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2011-11-28</prism:publicationDate><prism:volume>123</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1388-2457(12)X0004-X</prism:issueIdentifier><prism:section>Psychophysiology and Psychopathology</prism:section><prism:startingPage>937</prism:startingPage><prism:endingPage>946</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245711006833/abstract?rss=yes"><title>The influence of transient spatial attention on the processing of intracutaneous electrical stimuli examined with ERPs</title><link>http://www.clinph-journal.com/article/PIIS1388245711006833/abstract?rss=yes</link><description>Highlights: ► Transient spatial attention affects early ERP components elicited by intracutaneous electrical stimuli. ► Unattended intracutaneous electrical stimuli seem to induce a “call for attention”. ► Source analyses suggest that attentional modulation takes place within secondary somatosensory areas and the anterior cingulate cortex.Abstract: Objective: Determine the influence of transient spatial attention on the processing of intracutaneous electrical stimuli.Methods: Electrical stimuli, a single pulse or five pulses, were presented at the index fingers of the left or right hand. The to-be-attended hand and stimulated finger varied randomly from trial to trial. Participants had to press a foot pedal only when the relevant stimulus, varied between participants, occurred at the attended hand. EEG was measured to extract relevant ERP components.Results: The N100 and N150 were enhanced for attended as compared to unattended stimuli. The N100, N150, P260, and the P500 were enlarged for five pulse as compared to single pulse stimuli. The P260, which is thought to reflect a call for attention, was enhanced for unattended as compared to attended stimuli. Source analyses indicate that attentional effects on the N100, N150, and P260 may be related to changes in activity in secondary somatosensory areas and the anterior cingulate cortex.Conclusions: A transient manipulation of spatial attention increases cortical activity induced by attended relative to unattended intracutaneous electrical stimuli, but initially unattended stimuli appear to induce an enhanced orienting effect.Significance: Initially unattended intracutaneous electrical stimuli seem to induce a call for attention.</description><dc:title>The influence of transient spatial attention on the processing of intracutaneous electrical stimuli examined with ERPs</dc:title><dc:creator>Rob H.J. Van der Lubbe, Jan R. Buitenweg, Maria Boschker, Bernard Gerdes, Marijtje L.A. Jongsma</dc:creator><dc:identifier>10.1016/j.clinph.2011.08.034</dc:identifier><dc:source>Clinical Neurophysiology 123, 5 (2012)</dc:source><dc:date>2011-10-13</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2011-10-13</prism:publicationDate><prism:volume>123</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1388-2457(12)X0004-X</prism:issueIdentifier><prism:section>Psychophysiology and Psychopathology</prism:section><prism:startingPage>947</prism:startingPage><prism:endingPage>959</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS138824571100678X/abstract?rss=yes"><title>Do age-related changes contribute to the flanker effect?</title><link>http://www.clinph-journal.com/article/PIIS138824571100678X/abstract?rss=yes</link><description>Highlights: ► This study aimed to examine age-related changes in flanker interference. ► This study examined if age interacts with different sources of flanker interference. ► The results show that aging did not increase flanker interference.Abstract: Objectives: The present study examined age-related changes in the flanker effect and the extent to which age interacts with flanker-induced differences in perceptual processing, which contribute to the flanker effect.Methods: We adopted a modified flanker-task paradigm that incorporates PRO (i.e., hand responses correspond to target arrows) and ANTI (i.e., hand responses do not correspond to target arrows) conditions. Participants from two age groups searched for a centrally presented target flanked on each side by stimuli that were associated with either the same response as the target (congruent), the opposite response (incongruent), or neither response (neutral). Event-related potentials (ERPs), lateralized readiness potentials (LRPs), and behavioral performance were measured.Results: The behavioral-data results showed that a typical flanker effect was present in both age groups in PRO and ANTI conditions, suggesting that flanker-induced differences in perceptual processing contributed to the flanker effect in a similar manner for both age groups. Furthermore, no increase in flanker interference was observed in older adults. LRP profiles also provided convergent evidence showing that perceptually based flanker effects were similar for both age groups.Conclusions: The present study suggests that aging does not increase flanker interference, nor does it alter perceptually based flanker interference.Significance: The present study found that older adults could be just as capable as younger adults in resolving flanker interference by adopting different strategies to compensate for their deficiencies.</description><dc:title>Do age-related changes contribute to the flanker effect?</dc:title><dc:creator>Shulan Hsieh, Yu-Chi Liang, Yu-Che Tsai</dc:creator><dc:identifier>10.1016/j.clinph.2011.09.013</dc:identifier><dc:source>Clinical Neurophysiology 123, 5 (2012)</dc:source><dc:date>2011-10-05</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2011-10-05</prism:publicationDate><prism:volume>123</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1388-2457(12)X0004-X</prism:issueIdentifier><prism:section>Psychophysiology and Psychopathology</prism:section><prism:startingPage>960</prism:startingPage><prism:endingPage>972</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245711006717/abstract?rss=yes"><title>Spread to the dorsal ulnar cutaneous branch: A pitfall during the routine antidromic sensory nerve conduction study of the ulnar nerve</title><link>http://www.clinph-journal.com/article/PIIS1388245711006717/abstract?rss=yes</link><description>Highlights: ► A pitfall of the antidromic ulnar sensory nerve conduction study has been described. ► Wrist stimulation may easily spread to the dorsal ulnar cutaneous (DUC) branch. ► The spread would not be recognized without monitoring the DUC response. ► This spread may increase the routine antidromic SNAP amplitude up to 87%.Abstract: Objective: To document the incidence and effects of a previously unreported pitfall during routine antidromic sensory nerve conduction study (SCS) of the ulnar nerve: the spread of the wrist stimulation to the dorsal ulnar cutaneous (DUC) branch.Methods: The subjects consisted of 20 healthy volunteers. An antidromic sensory nerve action potential (SNAP) was recorded over the proximal interphalangeal joint of the little finger, and the DUC response was monitored over the dorsum of hand to check for the occurrence of this spread.Results: The spread occurred in all subjects, which caused a 4–87% increase in the SNAP amplitude. The likelihood that this spread may occur during routine SCS varied among the subjects, and also within an individual subject depending on minute shifts of the stimulating site. Selective stimulation of the ulnar main trunk up to maximal intensity without spread to the DUC was not achieved despite every effort in two subjects.Conclusions: This spread phenomenon may occur frequently during routine antidromic SCS, but would not be recognized without monitoring the DUC response.Significance: This pitfall may interfere with the reproducibility of the SNAP amplitude, and also with the diagnosis of ulnar neuropathy at the wrist.</description><dc:title>Spread to the dorsal ulnar cutaneous branch: A pitfall during the routine antidromic sensory nerve conduction study of the ulnar nerve</dc:title><dc:creator>Hideharu Murashima, Masahiro Sonoo, Hiroshi Tsukamoto, Shingo Kawakami, Yasuomi Kawamura, Keiichi Hokkoku, Yuki Hatanaka, Teruo Shimizu</dc:creator><dc:identifier>10.1016/j.clinph.2011.08.031</dc:identifier><dc:source>Clinical Neurophysiology 123, 5 (2012)</dc:source><dc:date>2011-10-17</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2011-10-17</prism:publicationDate><prism:volume>123</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1388-2457(12)X0004-X</prism:issueIdentifier><prism:section>Motor Neurone and Neuromuscular Diseases</prism:section><prism:startingPage>973</prism:startingPage><prism:endingPage>978</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245711006821/abstract?rss=yes"><title>Modulating oscillatory brain activity correlates of behavioral inhibition using transcranial direct current stimulation</title><link>http://www.clinph-journal.com/article/PIIS1388245711006821/abstract?rss=yes</link><description>Highlights: ► EEG recordings were compared following anodal and sham right inferior frontal gyrus-tDCS. ► A significant and selective diminution of theta band was evident in the rIFG area. ► rIFG stimulation improved behavioral inhibition as well as its electrophysiological correlates.Abstract: Objective: Studies have mainly documented behavioral changes induced by transcranial direct current stimulation (tDCS), but recently cortical modulations of tDCS have also been investigated. Our previous work revealed behavioral inhibition modulation by anodal tDCS over the right inferior frontal gyrus (rIFG); however, the electrophysiological correlates underlying this stimulation montage have yet to be established. The current work aimed to evaluate the distribution of neuronal oscillations changes following anodal tDCS over rIFG coupled with cathodal tDCS over left orbitofrontal cortex (lOFC) using spectral power analysis.Methods: Healthy subjects underwent sham and real tDCS (15min, 1.5mA, anodal rIFG; cathodal lOFC) stimulation conditions in a single-blind, placebo-controlled cross-over trial. Following tDCS session, resting EEG recordings were collected during 15min.Results: Analysis showed a significant and selective diminution of the power of theta band. The theta diminution was observed in the rIFG area (represented the anode electrode), and was not found in the lOFC area (represented the cathode electrode). A significant effect was observed only in the theta but not in other bands.Conclusions: These results are the first demonstration of modulating oscillatory activity as measured by EEG with tDCS over rIFG in general, and documenting theta band reduction with this montage in particular.Significance: Our results may explain the improvement in behavioral inhibition reported in our previous work, and although this study was conducted with healthy subjects, the findings suggest that tDCS may also modulate electrophysiological changes among ADHD patients, where decreasing theta activity is the target of neuro-feedback methods aimed to improve cognitive control.</description><dc:title>Modulating oscillatory brain activity correlates of behavioral inhibition using transcranial direct current stimulation</dc:title><dc:creator>Liron Jacobson, Adi Ezra, Uri Berger, Michal Lavidor</dc:creator><dc:identifier>10.1016/j.clinph.2011.09.016</dc:identifier><dc:source>Clinical Neurophysiology 123, 5 (2012)</dc:source><dc:date>2011-10-13</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2011-10-13</prism:publicationDate><prism:volume>123</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1388-2457(12)X0004-X</prism:issueIdentifier><prism:section>Neural Plasticity, Functional Adaptation and Recovery</prism:section><prism:startingPage>979</prism:startingPage><prism:endingPage>984</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245711007905/abstract?rss=yes"><title>Auditory evoked magnetic fields in patients with absent brainstem responses due to auditory neuropathy with optic atrophy</title><link>http://www.clinph-journal.com/article/PIIS1388245711007905/abstract?rss=yes</link><description>Highlights: ► Auditory evoked fields were measured in three patients with auditory neuropathy and optic atrophy showing absence of auditory brainstem responses. ► Bihemispherical AEF responses were clearly recorded in all patients for either left or right ear stimulus. ► Presence and abnormality of auditory cortical responses can be evaluated by AEFs in patients with auditory neuropathy even in the absence of ABRs.Abstract: Objective: To examine whether auditory evoked fields (AEFs) can be used to objectively evaluate hearing in patients with absent auditory brainstem responses (ABRs) due to auditory neuropathy.Methods: Subjects were 3 patients with auditory neuropathy, 1 male aged 29years and 2 females aged 18 and 27years, with absence of click evoked ABRs for bilateral ear stimuli at a level of 105dB nHL. All patients also had optic atrophy. AEFs were measured with a helmet-shaped magnetoencephalography system for 2.0kHz tone bursts of 60ms duration to the unilateral ear.Results: Bihemispherical AEF responses were clearly recorded in all three patients for either left or right ear stimulus. Although the latencies of N100m were severely prolonged and amplitudes were considerably decreased compared to the normal range of N100m responses in our facilities, N100m latency of AEF was shorter in the contralateral hemisphere to the stimulated ear, as usually found in normal subjects, despite the abnormal delay in N100m latency in all conditions.Conclusions: Presence and abnormality of auditory cortical responses can be evaluated by AEFs in patients with auditory neuropathy even under null responses in ABRs.Significance: AEFs are useful to evaluate residual hearing in patients with auditory neuropathy.</description><dc:title>Auditory evoked magnetic fields in patients with absent brainstem responses due to auditory neuropathy with optic atrophy</dc:title><dc:creator>Yusuke Takata, Tetsuaki Kawase, Nobukazu Nakasato, Akitake Kanno, Toshimitsu Kobayashi</dc:creator><dc:identifier>10.1016/j.clinph.2011.10.044</dc:identifier><dc:source>Clinical Neurophysiology 123, 5 (2012)</dc:source><dc:date>2011-11-28</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2011-11-28</prism:publicationDate><prism:volume>123</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1388-2457(12)X0004-X</prism:issueIdentifier><prism:section>Sensation, Central Sensory Pathways and their Disorders</prism:section><prism:startingPage>985</prism:startingPage><prism:endingPage>992</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245711006742/abstract?rss=yes"><title>Functional abnormality of the auditory brainstem in high-risk late preterm infants</title><link>http://www.clinph-journal.com/article/PIIS1388245711006742/abstract?rss=yes</link><description>Highlights: ► Little is known bout whether high-risk late preterm infants has brainstem impairment. ► Maximum length sequence brainstem auditory evoked response was found to be abnormal in these infants. ► This suggests that more central regions of the auditory brainstem are impaired in high-risk late preterm infants.Abstract: Objective: To examine whether late preterm infants with perinatal problems are at risk of brainstem auditory impairment.Methods: 68 high-risk late preterm infants (gestation 33–36weeks) with perinatal problems or conditions were studied at term using maximum length sequence brainstem auditory evoked response. The controls were 41 normal term infants and 37 low-risk late preterm infants.Results: Compared with normal term infants, the high-risk late preterm infants demonstrated a significant abnormal increase in MLS BAER variables that mainly reflect more central function of the brainstem auditory pathway, including wave V latency, III–V and I–V interpeak intervals, and III–V/I–III interval ratio. The abnormalities were more significant at higher than at lower click rates. The slopes of MLS BAER-rate function for these variables were increased. Compared with low-risk late preterm infants, the high-risk infants showed similar, though slightly less significant, abnormalities, mainly a significant increase in III–V and I–V intervals.Conclusions: Maximum length sequence brainstem auditory evoked response components that mainly reflect central function of the auditory brainstem were abnormal at term in high-risk late preterm infants.Significance: More central regions of the auditory brainstem are impaired in high-risk late preterm infants, which is mainly caused by associated perinatal problems or conditions.</description><dc:title>Functional abnormality of the auditory brainstem in high-risk late preterm infants</dc:title><dc:creator>Ze D. Jiang, Li L. Ping, Andrew R. Wilkinson</dc:creator><dc:identifier>10.1016/j.clinph.2011.08.032</dc:identifier><dc:source>Clinical Neurophysiology 123, 5 (2012)</dc:source><dc:date>2011-10-05</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2011-10-05</prism:publicationDate><prism:volume>123</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1388-2457(12)X0004-X</prism:issueIdentifier><prism:section>Sensation, Central Sensory Pathways and their Disorders</prism:section><prism:startingPage>993</prism:startingPage><prism:endingPage>1001</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245711006870/abstract?rss=yes"><title>Transcranial magnetic stimulation and peristimulus frequencygram</title><link>http://www.clinph-journal.com/article/PIIS1388245711006870/abstract?rss=yes</link><description>Highlights: ► We have used a combination of probability and frequency-based analysis techniques to characterise the silent period observed following subthreshold, threshold and suprathreshold TMS during a weak contraction of the human FDI muscle. ► Using this approach we have shown that the duration of the silent period is longer than previously reported. ► The results highlight the importance of using both probability and frequency-based analysis for determining the duration of inhibitory events in peripheral recordings.Abstract: Objective: The aim of our study was to use peristimulus frequencygram (PSF) constructed from single motor unit recordings to further characterise the responses evoked by low intensity TMS.Methods: Twelve healthy subjects (age 32±11 years) received single-pulse TMS over the first dorsal interosseus (FDI) motor area during weak isometric index finger abduction. Several hundred stimuli were delivered at a frequency of ∼0.3Hz and at an intensity of 79–110% of active motor threshold. FDI electromyogram (EMG) was recorded with surface and intramuscular fine wire electrodes. For single motor units, data analysis involved construction of a peristimulus time histogram (PSTH) and PSF. Surface EMG analysis involved signal averaging. Cumulative sums (CUSUMs) were calculated for SEMG, PSTH, and PSF data.Results: Forty-five single motor units were identified. The average number of stimuli per unit was 201±112. Characterisation of the response evoked by TMS differed with the use of SEMG, PSTH, and PSF CUSUMs.Conclusions: The duration of the EMG silence that follows the MEP during voluntary contraction was longer in the PSF than SEMG and PSTH.Significance: These findings highlight the importance of using both probability and frequency-based analysis when determining the duration of inhibitory events in peripheral recordings.</description><dc:title>Transcranial magnetic stimulation and peristimulus frequencygram</dc:title><dc:creator>Gabrielle Todd, Nigel C. Rogasch, Kemal S. Türker</dc:creator><dc:identifier>10.1016/j.clinph.2011.09.019</dc:identifier><dc:source>Clinical Neurophysiology 123, 5 (2012)</dc:source><dc:date>2011-10-24</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2011-10-24</prism:publicationDate><prism:volume>123</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1388-2457(12)X0004-X</prism:issueIdentifier><prism:section>Movement, Motor Control and Movement Disorders</prism:section><prism:startingPage>1002</prism:startingPage><prism:endingPage>1009</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245711006808/abstract?rss=yes"><title>Continuous theta-burst stimulation of the primary motor cortex in essential tremor</title><link>http://www.clinph-journal.com/article/PIIS1388245711006808/abstract?rss=yes</link><description>Highlights: ► This study examined the effect of neocortical rTMS on essential tremor. ► We show a consistent reduction of tremor amplitude after continuous theta burst stimulation of the primary motor cortex. ► Modified transcranial stimulation protocols may be a therapeutic option in the treatment of essential tremor.Abstract: Objective: We investigated whether essential tremor (ET) can be altered by suppressing the corticospinal excitability in the primary motor cortex (M1) with transcranial magnetic stimulation.Methods: 10 Patients with ET and 10 healthy controls underwent transcranial continuous theta-burst stimulation (cTBS) of the left primary motor hand area at 80% (real cTBS) and 30% (control cTBS) of active motor threshold in two separate sessions at least one week apart. Postural tremor was rated clinically and measured accelerometrically before and after cTBS. Corticospinal excitability was assessed by recording the motor evoked potentials (MEP) from the first dorsal interosseous muscle.Results: Real cTBS but not control cTBS reduced the tremor total power assessed with accelerometry. This beneficial effect was subclinical as there were no significant changes in clinical tremor rating after real cTBS. Relative to control cTBS, real cTBS reduced corticospinal excitability in the stimulated primary motor cortex only in healthy controls but not in ET patients.Conclusion: Real cTBS has a beneficial effect on ET. Since cTBS did not induce a parallel reduction in corticospinal excitability, this effect was not mediated by a suppression of the corticospinal motor output.Significance: “Inhibitory” cTBS of M1 leads to a consistent but subclinical reduction in tremor amplitude.</description><dc:title>Continuous theta-burst stimulation of the primary motor cortex in essential tremor</dc:title><dc:creator>Helge Hellriegel, Eva M. Schulz, Hartwig R. Siebner, Günther Deuschl, Jan H. Raethjen</dc:creator><dc:identifier>10.1016/j.clinph.2011.08.033</dc:identifier><dc:source>Clinical Neurophysiology 123, 5 (2012)</dc:source><dc:date>2011-10-10</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2011-10-10</prism:publicationDate><prism:volume>123</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1388-2457(12)X0004-X</prism:issueIdentifier><prism:section>Movement, Motor Control and Movement Disorders</prism:section><prism:startingPage>1010</prism:startingPage><prism:endingPage>1015</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245711006791/abstract?rss=yes"><title>Early and late components of feed-forward postural adjustments to predictable perturbations</title><link>http://www.clinph-journal.com/article/PIIS1388245711006791/abstract?rss=yes</link><description>Highlights: ► Two components of feed-forward postural adjustments are demonstrated. ► The sequence of the two components was preserved with changes in body position; each component was preceded by anticipatory synergy adjustments. ► The results fit the referent body configuration hypothesis.Abstract: Objectives: The purpose was to investigate two types of feed-forward postural adjustments associated with preparation to predictable external perturbations.Methods: Nine subjects stood on a wedge, toes-up or toes-down while a pendulum impacted their shoulders. EMGs of leg and trunk muscles were analyzed within the framework of the uncontrolled manifold hypothesis.Results: Early postural adjustments (EPAs) were seen 400–500ms and anticipatory postural adjustments (APAs), 100–150ms prior to the impact. EPAs and APAs were also seen in the time profiles of muscle modes representing muscle groups with linear scaling of the activation levels. Center of pressure shifts were stabilized by co-varied adjustments in muscle mode magnitudes across trials. The index of these multi-muscle synergies showed two drops (anticipatory synergy adjustments, ASAs), prior to EPA and APA in each subject. The findings were consistent between the two conditions.Conclusions: The results show that feed-forward postural adjustments represent a sequence of two phenomena, EPAs and APAs. Each of those is preceded by ASAs that reduce stability of a variable that is to be adjusted during the EPAs and APAs. The findings fit a hierarchical scheme with synergic few-to-many mappings at each level of the hierarchy based on the referent body configuration hypothesis.Significance: The results show the complexity of the postural preparation to action. Potentially, they have implications for the current strategies of rehabilitation of patients with neuro-motor disorders characterized by impaired postural control.</description><dc:title>Early and late components of feed-forward postural adjustments to predictable perturbations</dc:title><dc:creator>Vennila Krishnan, Mark L. Latash, Alexander S. Aruin</dc:creator><dc:identifier>10.1016/j.clinph.2011.09.014</dc:identifier><dc:source>Clinical Neurophysiology 123, 5 (2012)</dc:source><dc:date>2011-10-10</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2011-10-10</prism:publicationDate><prism:volume>123</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1388-2457(12)X0004-X</prism:issueIdentifier><prism:section>Movement, Motor Control and Movement Disorders</prism:section><prism:startingPage>1016</prism:startingPage><prism:endingPage>1026</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245711006766/abstract?rss=yes"><title>Effects of anodal tDCS on lumbar propriospinal system in healthy subjects</title><link>http://www.clinph-journal.com/article/PIIS1388245711006766/abstract?rss=yes</link><description>Highlights: ► Anodal tDCS decreases lumbar propriospinal system excitability in healthy subjects. ► For the first time, the results of this series of experiments show that anodal tDCS induces post effects on spinal networks. ► These results suggest that anodal tDCS could be of interest in neuro-rehabilitation in order to improve locomotion in patients with central nervous system lesions.Abstract: Objective: It has recently been shown that transcranial direct current stimulation (tDCS) (1) can modify lumbar spinal network excitability and (2) decreases cervical propriospinal system excitability. Thus the purpose of this series of experiments was to determine if anodal tDCS applied over the leg motor cortex area induces changes in lumbar propriospinal system excitability. To that end, the effects of anodal tDCS and sham tDCS on group I and group II propriospinal facilitation of quadriceps motoneurones were studied in healthy subjects.Methods: Common peroneal nerve group I and group II quadriceps H-reflex facilitation was assessed in 15 healthy subjects in two randomised conditions: anodal tDCS condition and sham tDCS condition. Recordings were performed before, during and after the end of the cortical stimulation.Results: Compared to sham, anodal tDCS decreases significantly CPN-induced group I and II quadriceps H-reflex facilitation during and also after the end of the cortical stimulation.Conclusions: Anodal tDCS induces (1) modulation of lumbar propriospinal system excitability (2) post-effects on spinal network.Significance: These results open a new vista to regulate propriospinal lumbar system excitability in patients and suggest that anodal tDCS would be interesting for neuro-rehabilitation of patients with central nervous system lesions.</description><dc:title>Effects of anodal tDCS on lumbar propriospinal system in healthy subjects</dc:title><dc:creator>N. Roche, A. Lackmy, V. Achache, B. Bussel, R. Katz</dc:creator><dc:identifier>10.1016/j.clinph.2011.09.011</dc:identifier><dc:source>Clinical Neurophysiology 123, 5 (2012)</dc:source><dc:date>2011-10-20</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2011-10-20</prism:publicationDate><prism:volume>123</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1388-2457(12)X0004-X</prism:issueIdentifier><prism:section>Movement, Motor Control and Movement Disorders</prism:section><prism:startingPage>1027</prism:startingPage><prism:endingPage>1034</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS138824571100633X/abstract?rss=yes"><title>Modulating effects of bodyweight unloading on the lower limb nociceptive withdrawal reflex during symmetrical stance</title><link>http://www.clinph-journal.com/article/PIIS138824571100633X/abstract?rss=yes</link><description>Highlights: ► Bodyweight unloading enhances the spinal nociceptive reflex excitability without changing the organisation of its receptive fields. ► The current study shows that unloading bodyweight enhances withdrawal reflex excitability creating the optimal withdrawal strategy of the ipsilateral limb while preserving balance by the contralateral limb. ► The present study shows that unloading the bodyweight determines a general increase of the withdrawal reflex excitability to prepare the limb in taking the first walking step.Abstract: Objective: To investigate the effects of bodyweight unloading on the excitability of the nociceptive withdrawal reflex (NWR) and of its receptive fields organisation during quiet stance in humans.Methods: The NWR was elicited in 14 volunteers by electrical stimulation of the sole of the foot at mid-forefoot, arch, and heel points. Participants stood upright and wore a whole-body harness connected via a rope to a pulley. Data were recorded at 0%, 10%, 25% and 40% of the bodyweight unloading. The root mean square of the EMG activity was measured bilaterally from several lower limb muscles. Kinematics of ankle, knee, and hip were measured bilaterally using goniometers.Results: Two-way ANOVA for repeated measures revealed higher reflex sizes at higher degrees of unloading in the tibialis anterior, soleus, and biceps femoris muscles and in the kinematics of the knee joint of the ipsilateral limb. No interaction between stimulation site and unloading was revealed.Conclusions: Unloading induced a generalised enhancement of NWR excitability without modifying the reflex receptive field organisation.Significance: Our study indicates that bodyweight unloading in general enhances the NWR excitability and suggests that only load-related afferent inputs in concert with joint movements may modify the modular organisation of the NWR.</description><dc:title>Modulating effects of bodyweight unloading on the lower limb nociceptive withdrawal reflex during symmetrical stance</dc:title><dc:creator>Mariano Serrao, Erika G. Spaich, Ole Kæseler Andersen</dc:creator><dc:identifier>10.1016/j.clinph.2011.09.006</dc:identifier><dc:source>Clinical Neurophysiology 123, 5 (2012)</dc:source><dc:date>2011-10-03</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2011-10-03</prism:publicationDate><prism:volume>123</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1388-2457(12)X0004-X</prism:issueIdentifier><prism:section>Movement, Motor Control and Movement Disorders</prism:section><prism:startingPage>1035</prism:startingPage><prism:endingPage>1043</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245711006250/abstract?rss=yes"><title>Tremor reduction and modeled neural activity during cycling thalamic deep brain stimulation</title><link>http://www.clinph-journal.com/article/PIIS1388245711006250/abstract?rss=yes</link><description>Highlights: ► Tremor and firing pattern entropy of model neurons decreased from baseline levels with cycling stimulation. ► Cycling with stimulation on for at least 60% of the time was as effective as continuous 125Hz stimulation at reducing tremor. ► Cycling stimulation decreased the firing pattern entropy of model neurons by regularizing pathological bursting, while pauses in stimulation generated rebound bursts and allowed transmission of pathological bursts.Abstract: Objective: The effectiveness of deep brain stimulation (DBS) depends on both the frequency and the temporal pattern of stimulation. We quantified responses to cycling DBS with constant frequency to determine if there was a critical on and/or off time for alleviating tremor.Methods: We measured postural tremor in 10 subjects with thalamic DBS and quantified neuronal entropy in a network model of Vim thalamic DBS. We tested 12 combinations of cycling on/off times that maintained the same average frequency of 125Hz, four constant frequency settings, and baseline.Results: Tremor and neural firing pattern entropy decreased as the percent on time increased from 50% to 100%. Cycling with stimulation on for at least 60% of the time was as effective as regular stimulation. All cycling settings reduced the firing pattern entropy of model neurons from the no stimulation condition by regularizing pathological firing patterns, either through synaptically-mediated inhibition or axon excitation.Conclusions: These results indicate that pauses present in cycling stimulation decreased its effectiveness in suppressing tremor, and that changes in the amount of tremor suppression were strongly correlated with changes in the firing pattern entropy of model neurons.Significance: Cycling stimulation may reduce power consumption during clinical DBS, and thereby increase the battery life of the implanted pulse generator.</description><dc:title>Tremor reduction and modeled neural activity during cycling thalamic deep brain stimulation</dc:title><dc:creator>Alexis M. Kuncel, Merrill J. Birdno, Brandon D. Swan, Warren M. Grill</dc:creator><dc:identifier>10.1016/j.clinph.2011.07.052</dc:identifier><dc:source>Clinical Neurophysiology 123, 5 (2012)</dc:source><dc:date>2011-10-05</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2011-10-05</prism:publicationDate><prism:volume>123</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1388-2457(12)X0004-X</prism:issueIdentifier><prism:section>Movement, Motor Control and Movement Disorders</prism:section><prism:startingPage>1044</prism:startingPage><prism:endingPage>1052</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245711006894/abstract?rss=yes"><title>Repeatability of vibration thresholds measured with the Neurothesiometer: Is it a valid and reliable research tool?</title><link>http://www.clinph-journal.com/article/PIIS1388245711006894/abstract?rss=yes</link><description>The Neurothesiometer is one of the most commonly used devices for the assessment of vibration sensitivity, being used for clinical research with healthy subjects () as well as for screening of polyneuropathic diseases (). Thresholds assessed with the Neurothesiometer can be expressed either as the applied voltage shown by equipment or as the indentation of the vibrating probe in the skin (μm), whereby the latter is preferred for scientific purposes. In order to convert voltage readings into indentation amplitudes, a calibration equation is needed, which may be provided by the manufacturer and can also be obtained by using other systems as reference, e.g. laser measuring systems. In both cases, the relation between the applied voltage and the resultant indentation seems to be nonlinear ().</description><dc:title>Repeatability of vibration thresholds measured with the Neurothesiometer: Is it a valid and reliable research tool?</dc:title><dc:creator>Günther Schlee, Marlen Schleusener, Thomas L. Milani</dc:creator><dc:identifier>10.1016/j.clinph.2011.09.021</dc:identifier><dc:source>Clinical Neurophysiology 123, 5 (2012)</dc:source><dc:date>2011-10-24</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2011-10-24</prism:publicationDate><prism:volume>123</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1388-2457(12)X0004-X</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>1053</prism:startingPage><prism:endingPage>1054</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245711006705/abstract?rss=yes"><title>Ocular vestibular evoked myogenic potential (oVEMP) responses in acute vestibular neuritis</title><link>http://www.clinph-journal.com/article/PIIS1388245711006705/abstract?rss=yes</link><description>The vestibular afferents which mediate ocular vestibular myogenic potentials (oVEMPs) produced by air-conduced (AC) and bone-conducted (BC) stimuli remain controversial, although these are likely to consist of irregularly discharging afferents arising from the otolith organs ().  have recently reported the changes occurring for oVEMPs and cervical vestibular evoked myogenic potentials (cVEMPs) in response to AC sound in patients with vestibular neuritis (VN). The cases of VN were classified as having involvement of the superior, inferior or both divisions of the vestibular nerve.  found that oVEMPs were affected in superior VN while cVEMPS were apparently normal, while the converse held for inferior VN. They proposed that this indicated that oVEMPs were the result of utricular activation.</description><dc:title>Ocular vestibular evoked myogenic potential (oVEMP) responses in acute vestibular neuritis</dc:title><dc:creator>Sendhil Govender, James G. Colebatch</dc:creator><dc:identifier>10.1016/j.clinph.2011.08.030</dc:identifier><dc:source>Clinical Neurophysiology 123, 5 (2012)</dc:source><dc:date>2011-10-05</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2011-10-05</prism:publicationDate><prism:volume>123</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1388-2457(12)X0004-X</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>1054</prism:startingPage><prism:endingPage>1055</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245711006699/abstract?rss=yes"><title>Controversy on the sensory origin of oVEMP to air-conducted sound: A reply to “Ocular vestibular evoked myogenic potential (oVEMP) responses in acute vestibular neuritis”</title><link>http://www.clinph-journal.com/article/PIIS1388245711006699/abstract?rss=yes</link><description>We thank Drs.  for their interest in our article () and for raising issues about the origin of ocular and cervical vestibular evoked myogenic potentials (VEMP) in response to air-conducted sound (ACS) or bone-conducted vibration (BCV). As they mention, there has been debate about the origin of the VEMP, especially the ocular VEMP (oVEMP) activated by ACS (). In our study, we found that patients with superior vestibular neuritis had an abnormal oVEMP and normal cervical VEMP (cVEMP), while patients with inferior vestibular neuritis exhibited a normal oVEMP and abnormal cVEMP in response to ACS. We agree with the view of Drs. Govender and Colebatch that these findings do not necessarily indicate that oVEMP induced by ACS originates only in the utricle. That is why we just raised the possibility of an oVEMP in response to ACS from activation of the utricle (). We believe that further electrophysiological studies and observations in other vestibular disorders would settle this issue in the near future.</description><dc:title>Controversy on the sensory origin of oVEMP to air-conducted sound: A reply to “Ocular vestibular evoked myogenic potential (oVEMP) responses in acute vestibular neuritis”</dc:title><dc:creator>Sun-Young Oh, Ji Soo Kim</dc:creator><dc:identifier>10.1016/j.clinph.2011.09.007</dc:identifier><dc:source>Clinical Neurophysiology 123, 5 (2012)</dc:source><dc:date>2011-10-05</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2011-10-05</prism:publicationDate><prism:volume>123</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1388-2457(12)X0004-X</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>1055</prism:startingPage><prism:endingPage>1056</prism:endingPage></item><item rdf:about="http://www.clinph-journal.com/article/PIIS1388245711006675/abstract?rss=yes"><title>Reply to correspondence “Ocular vestibular evoked myogenic potential (oVEMP) responses in acute vestibular neuritis”</title><link>http://www.clinph-journal.com/article/PIIS1388245711006675/abstract?rss=yes</link><description>We read with great interest the above correspondence written by  in relation to the otolith afferent origin (saccule or utricle, or both) of ocular vestibular evoked myogenic potentials (oVEMPs) (). This correspondence was written in relation to the recently published work by , which demonstrated the predominant involvement of oVEMPs in patients with acute vestibular neuritis involving the superior vestibular nerve. As commented by us in a related editorial (), involvement of the superior vestibular nerve alone does not imply utricular involvement in the absence of saccular involvement.</description><dc:title>Reply to correspondence “Ocular vestibular evoked myogenic potential (oVEMP) responses in acute vestibular neuritis”</dc:title><dc:creator>Eleftherios S. Papathanasiou</dc:creator><dc:identifier>10.1016/j.clinph.2011.08.028</dc:identifier><dc:source>Clinical Neurophysiology 123, 5 (2012)</dc:source><dc:date>2011-10-10</dc:date><prism:publicationName>Clinical Neurophysiology</prism:publicationName><prism:publicationDate>2011-10-10</prism:publicationDate><prism:volume>123</prism:volume><prism:number>5</prism:number><prism:issueIdentifier>S1388-2457(12)X0004-X</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>1056</prism:startingPage><prism:endingPage>1057</prism:endingPage></item></rdf:RDF>
