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The biomedical sciences have recently undergone revolutionary change, due to the ability to digitize and store large data sets. In neuroscience, the data sources include measurements of neural activity measured using electrode arrays, EEG and MEG, brain imaging data from PET, fMRI, and optical imaging methods. Analysis, visualization, and management of these time series data sets is a growing field of research that has become increasingly important both for experimentalists and theorists interested in brain function. The first part of the book contains a set of chapters which provide non-technical conceptual background to the subject. Salient features include the adoption of an active perspective of the nervous system, an emphasis on function, and a brief survey of different theoretical accounts in neuroscience. The second part is the longest in the book, and contains a refresher course in mathematics and statistics leading up to time series analysis techniques. The third part contains applications of data analysis techniques to the range of data sources indicated above, and the fourth part contains special topics.

Background and purpose Various electrodiagnostic criteria have been developed in Guillain–Barré syndrome (GBS). Their performance in a broad representation of GBS patients has not been evaluated. Motor conduction data from the International GBS Outcome Study (IGOS) cohort were used to compare two widely used criterion sets and relate these to diagnostic amyotrophic lateral sclerosis criteria. Methods From the first 1500 patients in IGOS, nerve conduction studies from 1137 (75.8%) were available for the current study. These patients were classified according to nerve conduction studies criteria proposed by Hadden and Rajabally. Results Of the 1137 studies, 68.3% (N = 777) were classified identically according to criteria by Hadden and Rajabally: 111 (9.8%) axonal, 366 (32.2%) demyelinating, 195 (17.2%) equivocal, 35 (3.1%) inexcitable and 70 (6.2%) normal. Thus, 360 studies (31.7%) were classified differently. The areas of differences were as follows: 155 studies (13.6%) classified as demyelinating by Hadden and axonal by Rajabally; 122 studies (10.7%) classified as demyelinating by Hadden and equivocal by Rajabally; and 75 studies (6.6%) classified as equivocal by Hadden and axonal by Rajabally. Due to more strictly defined cutoffs fewer patients fulfilled demyelinating criteria by Rajabally than by Hadden, making more patients eligible for axonal or equivocal classification by Rajabally. In 234 (68.6%) axonal studies by Rajabally the revised El Escorial (amyotrophic lateral sclerosis) criteria were fulfilled; in axonal cases by Hadden this was 1.8%. Conclusions and discussion This study shows that electrodiagnosis in GBS is dependent on the criterion set utilized, both of which are based on expert opinion. Reappraisal of electrodiagnostic subtyping in GBS is warranted.

Atlas of Nerve Conduction Studies and Electromyography is the perfect anatomical guide for neurologists, specialists in physical medicine and rehabilitation, and electrodiagnostic medicine consultants, while also providing support for individuals in residency training programs, critical care medicine, neurological surgery, and family practice.

Background Subclinical left ventricular (LV) longitudinal myocardial systolic dysfunction occurs in patients with diabetes mellitus (DM) and preserved LV ejection fraction (LVEF), and is closely related to DM-related complications. However, the association of diabetic neuropathy (DN) with subclinical LV systolic longitudinal dysfunction in such patients has not been fully clarified. Methods The subjects of this study were 112 consecutive DM patients with preserved LVEF (all ≥50%) without coronary artery disease and overt heart failure (aged 59 ± 14 years; 60 women, 52 men). Global longitudinal strain (GLS) was determined as the average peak strain of 18 segments from the three standard apical views, and was expressed as an absolute value. DN was diagnosed by experienced diabetologists. Median, ulnar, and sural nerves were subjected to motor and sensory nerve conduction studies. F-wave latency was defined as the minimum F-wave latency after a total of 16 stimulations of the tibial nerve. Results Forty-one (37%) patients were clinically diagnosed with DN. LV functions of DM patients with and without DN were similar except for GLS being significantly smaller in patients with than in patients without DN (18 ± 2% vs. 20 ± 2%, p < 0.001). It was noteworthy that, of the parameters for the nerve conduction study, only F-wave latency correlated with GLS (r = −0.34, p < 0.001), and also was identified as an independent determinative value of GLS in a multivariate linear regression model (β = −0.25, p = 0.001) even after adjustment for other closely related GLS factors. Conclusions Monitoring of F-wave latency may aid early detection of not only DN but also subclinical LV dysfunction. Joint planning of assessment by diabetologists and cardiologists is therefore advisable for better management of DM patients.

Intended for clinicians who perform electrodiagnostic procedures as an extension of their clinical examination, and for neurologists and physiatrists who are interested in neuromuscular disorders and noninvasive electrodiagnostic methods, particularly those practicing electromyography (EMG), Electrodiagnosis in Diseases of Nerve and Muscle: Principles and Practice provides a comprehensive review of most peripheral nerve and muscle diseases, including specific techniques and locations for performing each test.

Phase-synchronization is a manifestation of interaction between neuronal groups measurable from LFP, EEG or MEG signals, however, volume conduction can cause the coherence and the phase locking value to spuriously increase. It has been shown that the imaginary component of the coherency (ImC) cannot be spuriously increased by volume-conduction of independent sources. Recently, it was proposed that the phase lag index (PLI), which estimates to what extent the phase leads and lags between signals from two sensors are nonequiprobable, improves on the ImC. Compared to ImC, PLI has the advantage of being less influenced by phase delays. However, sensitivity to volume-conduction and noise, and capacity to detect changes in phase-synchronization, is hindered by the discontinuity of the PLI, as small perturbations turn phase lags into leads and vice versa. To solve this problem, we introduce a related index, namely the weighted phase lag index (WPLI). Differently from PLI, in WPLI the contribution of the observed phase leads and lags is weighted by the magnitude of the imaginary component of the cross-spectrum. We demonstrate two advantages of the WPLI over the PLI, in terms of reduced sensitivity to additional, uncorrelated noise sources and increased statistical power to detect changes in phase-synchronization. Another factor that can affect phase-synchronization indices is sample-size bias. We show that, when directly estimated, both PLI and the magnitude of the ImC have typically positively biased estimators. To solve this problem, we develop an unbiased estimator of the squared PLI, and a debiased estimator of the squared WPLI. ►New measure of phase‐synchronization, the Weighted Phase-Lag-Index. ►Reduced sensitivity to addition of uncorrelated sources. ►Increased sensitivity to detect differences in phase‐synchronization. ►New, unbiased estimator procedure for Phase-Lag‐Index. ►Debiased estimator for Weighted Phase‐Lag‐Index.

The speed of impulse transmission is critical for optimal neural circuit function, but it is unclear how the appropriate conduction velocity is established in individual axons. The velocity of impulse transmission is influenced by the thickness of the myelin sheath and the morphology of electrogenic nodes of Ranvier along axons. Here we show that myelin thickness and nodal gap length are reversibly altered by astrocytes, glial cells that contact nodes of Ranvier. Thrombin-dependent proteolysis of a cell adhesion molecule that attaches myelin to the axon (neurofascin 155) is inhibited by vesicular release of thrombin protease inhibitors from perinodal astrocytes. Transgenic mice expressing a dominant-negative fragment of VAMP2 in astrocytes, to reduce exocytosis by 50%, exhibited detachment of adjacent paranodal loops of myelin from the axon, increased nodal gap length, and thinning of the myelin sheath in the optic nerve. These morphological changes alter the passive cable properties of axons to reduce conduction velocity and spike-time arrival in the CNS in parallel with a decrease in visual acuity. All effects were reversed by the thrombin inhibitor Fondaparinux. Similar results were obtained by viral transfection of tetanus toxin into astrocytes of rat corpus callosum. Previously, it was unknown how the myelin sheath could be thinned and the functions of perinodal astrocytes were not well understood. These findings describe a form of nervous system plasticity in which myelin structure and conduction velocity are adjusted by astrocytes. The thrombin-dependent cleavage of neurofascin 155 may also have relevance to myelin disruption and repair.

Key Points All currents in the brain superimpose to yield an 'electric field' at any given point in space. The current sources and sinks form dipoles or higher-order n-poles. Extracellular currents arise from many sources, including synaptic currents, fast action potentials and their afterpotentials, calcium spikes and voltage-dependent intrinsic currents. The magnitude of extracellular currents depends critically on two factors: the cytoarchitectural organization of a network and the temporal synchrony of the various current sinks and sources. Depending on the recording method, neuroscientists distinguish between electroencephalogram (EEG), electrocorticogram (ECoG) and local field potential (LFP; also known as micro-, depth or intracranial EEG), although all of these measures refer to the same biophysical process. The electric field is the force 'felt' by an electric charge, and can be transmitted through brain volume. The extent of volume conduction depends on the relationships between the current dipole and the features of the conductive medium. High-density sampling of the extracellular field with contemporary methods enables the calculation of current source density, and therefore the localization of current sinks and sources. The voltage gradients generated by highly synchronous activity of neuronal groups can affect the transmembrane potential of the member neurons and alter their excitability through ephaptic coupling. Synchronous spiking of nearby neurons is the main source of the high-frequency components of the local field. There is a discernable relationship between the temporal evolution of cell assemblies and the time-dependent changes of the spatially distributed currents. High-density, wide-band recordings of the local field can therefore provide access to both afferent inputs and the spiking output of neurons. Neuronal activity in the brain gives rise to transmembrane and extracellular electromagnetic fields that can be measured in the extracellular medium using several approaches. In this Review, Buzsáki and colleagues provide an overview of the mechanisms that underlie the generation of extracellular currents and fields. Neuronal activity in the brain gives rise to transmembrane currents that can be measured in the extracellular medium. Although the major contributor of the extracellular signal is the synaptic transmembrane current, other sources — including Na + and Ca 2+ spikes, ionic fluxes through voltage- and ligand-gated channels, and intrinsic membrane oscillations — can substantially shape the extracellular field. High-density recordings of field activity in animals and subdural grid recordings in humans, combined with recently developed data processing tools and computational modelling, can provide insight into the cooperative behaviour of neurons, their average synaptic input and their spiking output, and can increase our understanding of how these processes contribute to the extracellular signal.

Based on related measurements by others, an earlier publication suggested increased nerve conduction velocity (NCV) with stretch in myelinated fibers, an anomaly based on existing knowledge, and hypothesized that widening of narrow zigzag gaps between structures of interdigitated Schwann cell processes at the node affected saltatory conduction to produce this increased NCV. A new nodal resistance R ne between the axonal membrane and extracellular fluid was introduced into the century old cable theory. Later, a direct and careful measurement of ulnar NCV across a 10 cm segment around the elbow by another publication appeared to support the suggestion of increased NCV with stretch. However, in order to eliminate the possibility of slacks of ulnar nerve in the upper arm affecting the measurements, the present work was taken up on a shorter 5 cm segment which again supported the suggestion, increasing confidence in the R ne hypothesis. Furthermore, wrist flexion or extension was also observed to affect the ulnar NCV at the elbow to some extent, revealing a new phenomenon. While attempting to formulate an analytical treatment of R ne , the earlier work found it very challenging as the physical structure was extremely complex. Proposing an alternative physical model to simulate the variation in R ne suggested earlier, the current study presents an analytical treatment that relates R ne and a corresponding effective resistivity value to increases in stretch, and relates these quantitatively to stretch values based on the measured values of NCV. This then provided the basis of a quantitative analysis which could be useful for future research. While appreciating that other microstructures in the node at or near the axonal membrane may also contribute to the observed anomaly, but lack of direct experimental evidence related to nerve stretch tends to weigh more on the R ne hypothesis in explaining the anomaly.

Action potential timing is fundamental to information processing; however, its determinants are not fully understood. Here we report unexpected structural specializations in the Ranvier nodes and internodes of auditory brainstem axons involved in sound localization. Myelination properties deviated significantly from the traditionally assumed structure. Axons responding best to low-frequency sounds had a larger diameter than high-frequency axons but, surprisingly, shorter internodes. Simulations predicted that this geometry helps to adjust the conduction velocity and timing of action potentials within the circuit. Electrophysiological recordings in vitro and in vivo confirmed higher conduction velocities in low-frequency axons. Moreover, internode length decreased and Ranvier node diameter increased progressively along the distal axon segments, which simulations show was essential to ensure precisely timed depolarization of the giant calyx of Held presynaptic terminal. Thus, individual anatomical parameters of myelinated axons can be tuned to optimize pathways involved in temporal processing. Action potential timing is fundamental to information processing, but its determinants are not fully understood. Here the authors demonstrate unexpected structural specializations of myelinated axons in the auditory brainstem that help to adjust action potential arrival time for sound localization.