Correction to: Is the new ASNM intraoperative neuromonitoring supervision "guideline" a trustworthy guideline? A commentary.

The article Is the new ASNM intraoperative neuromonitoring supervision "guideline" a trustworthy guideline? A commentary, written by Stanley A. Skinner, Elif Ilgaz Aydinlar, Lawrence F. Borges, Bob S. Carter, Bradford L. Currier, Vedran Deletis, Charles Dong, John Paul Dormans, Gea Drost, Isabel Fernandez­Conejero, E. Matthew Hoffman, Robert N. Holdefer, Paulo Andre Teixeira Kimaid, Antoun Koht, Karl F. Kothbauer, David B. MacDonald, John J. McAuliffe III, David E. Morledge, Susan H. Morris, Jonathan Norton, Klaus Novak, Kyung Seok Park, Joseph H. Perra, Julian Prell, David M. Rippe, Francesco Sala, Daniel M. Schwartz, Martín J. Segura, Kathleen Seidel, Christoph Seubert, Mirela V. Simon, Francisco Soto, Jeffrey A. Strommen, Andrea Szelenyi, Armando Tello, Sedat Ulkatan, Javier Urriza and Marshall Wilkinson, was originally published electronically on the publisher's internet portal (currently SpringerLink) on 05 January 2019 without open access. With the author(s)' decision to opt for Open Choice the copyright of the article changed on 30 January 2019 to © The Author(s) 2019 and the article is forthwith distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits use, duplication, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license and indicate if changes were made. The original article has been corrected.

The crossroads of anxiety: distinct neurophysiological maps for different symptomatic groups.

BACKGROUND: Despite the devastating impact of anxiety disorders (ADs) worldwide, long-lasting debates on causes and remedies have not solved the clinician's puzzle: who should be treated and how? Psychiatric classifications conceptualize ADs as distinct entities, with strong support from neuroscience fields. Yet, comorbidity and pharmacological response suggest a single "serotonin dysfunction" dimension. Whether AD is one or several disorders goes beyond academic quarrels, and the distinction has therapeutic relevance. Addressing the underlying dysfunctions should improve treatment response. By its own nature, neurophysiology can be the best tool to address dysfunctional processes. PURPOSE: To search for neurophysiological dysfunctions and differences among panic disorder (PD), agoraphobia-social-specific phobia, obsessive-compulsive disorder (OCD) and generalized anxiety disorder. METHODS: A sample population of 192 unmedicated patients and 30 aged-matched controls partook in this study. Hypothesis-related neurophysiological variables were combined into ten independent factors: 1) dysrhythmic patterns, 2) delta, 3) theta, 4) alpha, 5) beta (whole-head absolute power z-scores), 6) event-related potential (ERP) combined latency, 7) ERP combined amplitude (z-scores), 8) magnitude, 9) site, and 10) site of hyperactive networks. Combining single variables into representative factors was necessary because, as in all real-life phenomena, the complexity of interactive processes cannot be addressed through single variables and the multiplicity of potentially implicated variables would demand an extremely large sample size for statistical analysis. RESULTS: The nonparametric analysis correctly classified 81% of the sample. Dysrhythmic patterns, decreased delta, and increased beta differentiated AD from controls. Shorter ERP latencies were found in several individual patients, mostly from the OCD group. Hyperactivities were found at the right frontorbital-striatal network in OCD and at the panic circuit in PD. CONCLUSIONS: Our findings support diffuse cortical instability in AD in general, with individual differences in information processing deficits and regional hyperactivities in OCD and PD. Study limitations and the rationale behind the variable selection and combination strategy will be discussed before addressing the therapeutic implications of our findings.

Auditory brainstem responses as a clinical evaluation tool in children after perinatal encephalopathy.

UNLABELLED: Auditory brainstem responses (ABR) reveals the neurophysiological status of the neural axis. In this study we compared the ABR of healthy children, under 1-year-old, with children who suffered from perinatal encephalopathy (PE). OBJECTIVE: The purpose of this study was to characterize the ABR differences between children with PE and healthy children in order to identify groups with specific neurophysiological profiles, associated with their neurological condition. METHODS: Thirty-six children with perinatal encephalopathy (PE) and 36 healthy children, ages 1-12 months, were studied. The variables considered were: latencies of waves I, II, N1, III, V, and N2; interpeak latency interval (IPL) of waves I-III, III-V, and I-V; as well as amplitudes of waves I, III, and V. The results were analyzed using ANOVA, as well as Ji(2), and Ward's cluster analysis. RESULTS: The absolute latencies of the ABR showed an inverse correlation with the children's age. Latencies of waves I, II, N1, V, and N2, IPL III-V, and amplitude of waves III and V show significant differences (p<0.05) between healthy and PE children. Children with PE showed greater absolute latencies and larger wave amplitudes than the control group. Ward's cluster analysis, used to define the groups with similar functional characteristics, revealed three groups: fast, intermediate, and slow-responders, depending on their wave latencies and IPL wave amplitudes. These groups were gender- (p<0.03), age- (p<0.0001), and neurological damage- (p<0.01) related. CONCLUSIONS: Our data clearly show that the ABR obtained from PE children differ from ABR obtained from healthy children. PE infants showed larger wave latencies, intervals amplitudes than the control group. Three functional profiles resulted from the groups established using the Ward's method, and these indicate their neurological functional condition.