Voltage Attenuation Research Articles

Link between Pericardial Effusion and Attenuation of QRS Voltage in Patients with Hypothyroidism

Objectives: To determine the clinical correlates of peri- cardial effusion (PE) and a low-voltage electrocardiogram (ECG) in patients with primary hypothyroidism. Methods: ECG, echocardiography and blood tests, including thyroid function tests, were performed in 64 consecutive patients with primary hypothyroidism. Results: Twenty-four patients (38%) had PE and 16 patients (25%) had low voltage. To determine the important variables present in patients with hypothyroidism that may be related to PE, 3 variables (free T4, pulmonary artery systolic pressure and serum albumin) were used in the multivariate analysis. From the analysis, free T4 (odds ratio = 0.032) and pulmonary artery systolic pressure (odds ratio = 1.085) emerged as significant variables related to PE, whereas when 4 variables (free T4, serum albumin, pulmonary artery systolic pressure and PE) were used to determine the important variables related to low voltage, free T4 (odds ratio = 0.029) and serum albumin (odds ratio = 0.255) were the significant variables, but PE had no significant relation with low voltage (p = 0.424). Conclusions: In addition to its association with more severe thyroid hormone deficiency, the presence of PE was also associated with an increase in pulmonary artery pressure, whereas attenuation of QRS voltage was associated with lower colloid osmotic pressure in patients with hypothyroidism.

Thermal noise due to surface-charge effects within the Debye layer of endogenous structures in dendrites

An assumption commonly used in cable theory is revised by taking into account electrical amplification due to intracellular capacitive effects in passive dendritic cables. A generalized cable equation for a cylindrical volume representation of a dendritic segment is derived from Maxwell's equations under assumptions: (i) the electric-field polarization is restricted longitudinally along the cable length; (ii) extracellular isopotentiality; (iii) quasielectrostatic conditions; and (iv) homogeneous medium with constant conductivity and permittivity. The generalized cable equation is identical to Barenblatt's equation arising in the theory of infiltration in fissured strata with a known analytical solution expressed in terms of a definite integral involving a modified Bessel function and the solution to a linear one-dimensional classical cable equation. Its solution is used to determine the impact of thermal noise on voltage attenuation with distance at any particular time. A regular perturbation expansion for the membrane potential about the linear one-dimensional classical cable equation solution is derived in terms of a Green's function in order to describe the dynamics of free charge within the Debye layer of endogenous structures in passive dendritic cables. The asymptotic value of the first perturbative term is explicitly evaluated for small values of time to predict how the slowly fluctuating (in submillisecond range) electric field attributed to intracellular capacitive effects alters the amplitude of the membrane potential. It was found that capacitive effects are almost negligible for cables with electrotonic lengths L>0.5 , contributes up to 10% of the signal for cables with electrotonic lengths in the range between 0.25<L<0.5 , and dominates the membrane potential for electrotonically short cables (L<0.2) . These results show that electrotonically short dendritic cables with both ends sealed are prone to significant neurobiological thermal noise due to intracellular capacitive effects. The presence of significant thermal noise weakens the assumption of intracellular isopotentiality when approximating dendrites with compartments.

Circumferential pulmonary vein ablation for atrial fibrillation: back to the future?

antrum within the encircling lesions, elimination of anchor points of high frequency drivers, atrial debulking, and possibly ablation of ganglionated plexi within the targeted encircling lesions. As the role of PV antrum in AF is better understood, antral PV isolation has been widely performed as an effective ablation strategy to eliminate AF. It is within this context that we should evaluate the contribution by Arya et al. 7 in the current issue of the Journal. The authors report their experience in 674 consecutive patients, 85% of whom had paroxysmal AF, undergoing CPVA using a steerable sheath during 2005‐2007. An irrigated-tip ablation catheter was used with a maximum power of 25 W near the oesophagus and 40‐50 W elsewhere in the left atrium. The sole procedural endpoint was voltage attenuation along the circumferential lines around each set of PVs in patients with paroxysmal AF. Pulmonary vein isolation was not an endpoint of the procedure, but was achieved in 38% of patients. In a minority of patients with persistent AF, linear ablation along the roof and mitral isthmus was performed without confirmation of conduction block. Antiarrhythmic agents (flecainide or amiodarone) were used in 45% and 21% of patients for the first 3 and 6 months, respectively, and were discontinued after 6 months in all patients. Clinical outcome was based on symptoms or the presence of AF or AT on serial 7-day Holter recordings performed at 3, 6, and 12 months after the ablation procedure. The procedure and fluoroscopic times were approximately, 3 h, and 24 min, respectively. After a single-ablation procedure using a steerable sheath, 76% of patients were free from atrial arrhythmias during a 7-day monitoring period at 12 months. Approximately 50% of patients experienced early recurrence, which was due solely due to AT in about one-third of the patients. Early recurrence and a LA diameter .5 cm were associated with arrhythmia recurrence during follow-up. The clinical efficacy was similar among patients with paroxysmal or persistent AF. Six patients experienced pericardial tamponade, one of whom required surgery.

Electrophysiological changes during EMDR treatment in pateints with combat-related PTSD

Results Before the treatment, EEG recorded basic activity of low voltage (attenuation) of 20 μV, frequency of beta range (17-26 Hz), bioccipital, with no pathologic activity. Patient had prominent vegetative symptoms (anxiety, heart rate 100/min). Background activity immediately after the treatment records the amplitude values of around 50 μV, frequency of around 11-12 Hz. After the end of the treatment background activity possesses the amplitude value of about 37 μV, holding the persistence in frequency.

Mechanism of attenuation of the QRS voltage in heart failure: a hypothesis

Attenuation of the QRS voltage (QRSV) in patients with decompensated heart failure (HF) has been known for a long time, but its mechanism has been elusive. In a canine model of HF, QRSV was seen in intracardiac and epicardial electrograms (ECGs), but no surface ECGs were recorded in that study to evaluate the ECG expression of an equivalent standard ECG. 'Quasi-intracardial' ECGs in patients with peripheral oedema (PERED) of non-cardiac aetiology and no HF did not show changes while the simultaneously recorded standard surface ECGs showed QRSV. Therefore, a synthesis of the above two observations is implemented to propose the hypothesis that QRSV in patients with decompensated HF is because of a combination of heart-based influences, and the impact of the PERED, with different proportions of these two influences in different patients depending on the extent of changes in the heart (pressure, volume, ischaemia changes) and the passive body volume conductor (PERED).

TRIP8b Splice Variants Form a Family of Auxiliary Subunits that Regulate Gating and Trafficking of HCN Channels in the Brain

Hyperpolarization-activated cyclic nucleotide-regulated (HCN) channels, which generate the I(h) current, mediate a number of important brain functions. The HCN1 isoform regulates dendritic integration in cortical pyramidal neurons and provides an inhibitory constraint on both working memory in prefrontal cortex and spatial learning and memory in the hippocampus. Altered expression of HCN1 following seizures may contribute to the development of temporal lobe epilepsy. Yet the regulatory networks and pathways governing HCN channel expression and function in the brain are largely unknown. Here, we report the presence of nine alternative N-terminal splice forms of the brain-specific cytoplasmic protein TRIP8b and demonstrate the differential effects of six isoforms to downregulate or upregulate HCN1 surface expression. Furthermore, we find that all TRIP8b isoforms inhibit channel opening by shifting activation to more negative potentials. TRIP8b thus functions as an auxiliary subunit that provides a mechanism for the dynamic regulation of HCN1 channel expression and function.

Startle epilepsy associated with gait‐induced seizures: Pathomechanism analysis using EEG, MEG, and PET studies

We describe herein a girl who has had startle-induced seizures since she was 3 years old. These seizures were refractory to antiepileptic medications and worsened when the patient was 9 years old, following termination of phenytoin administration because of adverse effects. During this period she could walk only a few steps with support, and sudden drop attacks inevitably occurred. Interictal electroencephalography (EEG) revealed abundant spike-wave activity at the centroparietal midline areas, and ictal EEG of poststartle and gait-induced seizures revealed initial voltage attenuation followed by recruitment of vertex activity, which preceded a tonic or myoclonic-atonic phase. Magnetic resonance imaging (MRI) results were unremarkable, but magnetoencephalography (MEG) and positron emission tomography (PET) suggested the presence of an extensive epileptogenic zone in the bilateral pericentral gyri, and the bilateral paracentral and left precuneus lobules, including the primary motor, supplementary motor, and supplementary sensory areas. The pathophysiologic significance of these structures is discussed.

Derivation of cable parameters for a reduced model that retains asymmetric voltage attenuation of reconstructed spinal motor neuron dendrites

Spinal motor neurons have voltage gated ion channels localized in their dendrites that generate plateau potentials. The physical separation of ion channels for spiking from plateau generating channels can result in nonlinear bistable firing patterns. The physical separation and geometry of the dendrites results in asymmetric coupling between dendrites and soma that has not been addressed in reduced models of nonlinear phenomena in motor neurons. We measured voltage attenuation properties of six anatomically reconstructed and type-identified cat spinal motor neurons to characterize asymmetric coupling between the dendrites and soma. We showed that the voltage attenuation at any distance from the soma was direction-dependent and could be described as a function of the input resistance at the soma. An analytical solution for the lumped cable parameters in a two-compartment model was derived based on this finding. This is the first two-compartment modeling approach that directly derived lumped cable parameters from the geometrical and passive electrical properties of anatomically reconstructed neurons.

Fractional cable equation models for anomalous electrodiffusion in nerve cells: infinite domain solutions

We introduce fractional Nernst-Planck equations and derive fractional cable equations as macroscopic models for electrodiffusion of ions in nerve cells when molecular diffusion is anomalous subdiffusion due to binding, crowding or trapping. The anomalous subdiffusion is modelled by replacing diffusion constants with time dependent operators parameterized by fractional order exponents. Solutions are obtained as functions of the scaling parameters for infinite cables and semi-infinite cables with instantaneous current injections. Voltage attenuation along dendrites in response to alpha function synaptic inputs is computed. Action potential firing rates are also derived based on simple integrate and fire versions of the models. Our results show that electrotonic properties and firing rates of nerve cells are altered by anomalous subdiffusion in these models. We have suggested electrophysiological experiments to calibrate and validate the models.

Passive membrane properties and electrotonic signal processing in retinal rod bipolar cells

Rod bipolar cells transmit visual signals from their dendrites, where they receive input from rod photoreceptors, to their axon terminals, where they synapse onto amacrine cells. Little is known, however, about the transmission and possible transformation of these signals. We have combined axon terminal recording in retinal slices, quantitative, light-microscopic morphological reconstruction and computer modelling to obtain detailed compartmental models of rat rod bipolar cells. Passive cable properties were estimated by directly fitting the current responses of the models evoked by voltage pulses to the physiologically recorded responses. At a holding potential of -60 mV, the average best-fit parameters were 1.1 microF cm(-2) for specific membrane capacitance (C(m)), 130 Omega cm for cytoplasmic resistivity (R(i)), and 24 kOmega cm(2) for specific membrane resistance (R(m)). The passive integration of excitatory and inhibitory synaptic inputs was examined by computer modelling with physiologically realistic synaptic conductance waveforms. For both transient and steady-state synaptic inhibition, the inhibitory effect was relatively insensitive to the location of the inhibition. For transient synaptic inhibition, the time window of effective inhibition depended critically on the relative timing of inhibition and excitation. The passive signal transmission between soma and axon terminal was examined by the electrotonic transform and quantified as the frequency-dependent voltage attenuation of sinusoidal voltage waveforms. For the range of parameters explored (axon diameter and length, R(i)), the lowest cutoff frequency observed was approximately 300 Hz, suggesting that realistic scotopic visual signals will be faithfully transmitted from soma to axon terminal, with minimal passive attenuation along the axon.

Stimulus-Induced Diffuse Voltage Attenuation (SIDVA): A Previously Undescribed EEG Pattern in a Critically Ill Child

We report the case of a 15-month-old critically ill child with stimulus-induced diffuse voltage attenuation, a previously unreported electroencephalogram pattern. No clinical evidence of seizure activity was associated with these EEG changes. The patient went on to have a full recovery. This case suggests that critically ill children have distinct stimulus induced electrographic patterns from those seen in adults. Additional research is needed to define the significance of these patterns.

The Electrotonic Structure of Pyramidal Neurons Contributing to Prefrontal Cortical Circuits in Macaque Monkeys Is Significantly Altered in Aging

Whereas neuronal numbers are largely preserved in normal aging, subtle morphological changes occur in dendrites and spines, whose electrotonic consequences remain unexplored. We examined age-related morphological alterations in 2 types of pyramidal neurons contributing to working memory circuits in the macaque prefrontal cortex (PFC): neurons in the superior temporal cortex forming "long" projections to the PFC and "local" projection neurons within the PFC. Global dendritic mass homeostasis, measured by 3-dimensional scaling analysis, was conserved with aging in both neuron types. Spine densities, dendrite diameters, lengths, and branching complexity were all significantly reduced in apical dendrites of long projection neurons with aging, but only spine parameters were altered in local projection neurons. Despite these differences, voltage attenuation due to passive electrotonic structure, assuming equivalent cable parameters, was significantly reduced with aging in the apical dendrites of both neuron classes. Confirming the electrotonic analysis, simulated passive backpropagating action potential efficacy was significantly higher in apical but not basal dendrites of old neurons. Unless compensated by changes in passive cable parameters, active membrane properties, or altered synaptic properties, these effects will increase the excitability of pyramidal neurons, compromising the precisely tuned activity required for working memory, ultimately resulting in age-related PFC dysfunction.

Ipsilateral hemispheric ischaemic hypoxic changes during central line placement: a video-electroencephalogram correlate

When venous access is needed for intravenous fluids or antibiotics and a peripheral site is unavailable or not suitable, a central line is placed either in the neck or the...

Voltage attenuation in reconstructed type-identified motor neurons as a constraint for reduced models

The morphologies of six type-identified cat spinal motorneurons were downloaded from a public database [2] andimported into the NEURON simulation environment.Passive parameters were set to experimentally determinedvalues from these same cells [3]. DDVA was characterizedby calculating the voltage attenuation between the somaand all sites on the dendrites in both directions.

Functional Structure of the Mitral Cell Dendritic Tuft in the Rat Olfactory Bulb

The input-output transform performed by mitral cells, the principal projection neurons of the olfactory bulb, is one of the key factors in understanding olfaction. We used combined calcium and voltage imaging from the same neuron and computer modeling to investigate signal processing in the mitral cells, focusing on the glomerular dendritic tuft. The main finding was that the dendritic tuft functions as a single electrical compartment for subthreshold signals within the range of amplitudes detectable by voltage-sensitive dye recording. These evoked EPSPs had uniform characteristics throughout the glomerular tuft. The Ca(2+) transients associated with spatially uniform subthreshold synaptic potentials were comparable but not equal in amplitude in all regions. The average range of normalized amplitudes of the EPSP-driven Ca(2+) signals from different locations on dendritic branches in the glomerular tuft was relatively narrow and appeared to be independent of the dendritic surface-to-volume ratio. The computer simulations constrained by the imaging data indicated that a synchronized activation of approximately 100 synapses randomly distributed on tuft branches was sufficient to generate spatially homogenous EPSPs. This number of activated synapses is consistent with the data from anatomical studies. Furthermore, voltage attenuation of the EPSP along the primary dendrite at physiological temperature was weak compared with other cell types. In the model, weak attenuation of the EPSP along the primary dendrite could be accounted for by passive electrical properties of the mitral cell.

A Modified Cable Formalism for Modeling Neuronal Membranes at High Frequencies

Intracellular recordings of cortical neurons in vivo display intense subthreshold membrane potential ( V m) activity. The power spectral density of the V m displays a power-law structure at high frequencies (>50 Hz) with a slope of ∼−2.5. This type of frequency scaling cannot be accounted for by traditional models, as either single-compartment models or models based on reconstructed cell morphologies display a frequency scaling with a slope close to −4. This slope is due to the fact that the membrane resistance is short-circuited by the capacitance for high frequencies, a situation which may not be realistic. Here, we integrate nonideal capacitors in cable equations to reflect the fact that the capacitance cannot be charged instantaneously. We show that the resulting nonideal cable model can be solved analytically using Fourier transforms. Numerical simulations using a ball-and-stick model yield membrane potential activity with similar frequency scaling as in the experiments. We also discuss the consequences of using nonideal capacitors on other cellular properties such as the transmission of high frequencies, which is boosted in nonideal cables, or voltage attenuation in dendrites. These results suggest that cable equations based on nonideal capacitors should be used to capture the behavior of neuronal membranes at high frequencies.

ECG Changes and Voltage Attenuation in Congestive Heart Failure

The electrocardiogram (ECG) is invaluable in providing diagnosis, prognosis, and information for decision making in the management of patients with congestive heart failure (CHF). In addition to the traditional applications of the ECG, which are of importance in the management of patients with CHF, and include indeed the bulk of ECG derived information, a recently described association of peripheral edema with attenuated ECG voltage, provides an expanded dimension in diagnostics. These attenuations result in decreased amplitude of QRS complexes, P-waves, and shortened duration of QRS complexes and QT intervals, with significant diagnostic implications. Alleviation of peripheral edema in response to diuresis in patients with CHF reverses all above alterations.

ECG changes following cardioversion and defibrillation.

changes of the QRS amplitude following defibrillation or cardioversion have never been reported in humans. prospective analysis of patients externally cardioverted or defibrillated for ventricular and supraventricular tachyarrhythmias. Patients with coronary artery disease (CAD) and acute coronary syndrome (ACS) formed group A and patients without CAD but with external cardioversion/defibrillation formed group B. Patients in the control group (group C) experienced a shock by an Internal Cardioverter Defibrillator (ICD). All patients underwent the same study protocol: serial ECG's were recorded and sums (Sigma) of the QRS amplitude created separately for the precordial and peripheral leads. Sigma were then compared with baseline values and changes indicated as percentage (%). We included a total of 45 patients in our study: 21 patients (47%) in group A, 11 patients (24%) in group B and 13 patients (29%) in group C. Median age was 66 years in group A, 55 in group B and 52 in group C. In group A mean change of the R amplitude was -35% in precordial and -16% in the peripheral leads. In group B mean change of the R amplitude was -16% in the precordial and -2% in the peripheral leads. The QRS amplitude changed -23% in the precordial leads in group A and -14% in group B. 13 patients with external defibrillation or cardioversion of group A + B and all patients of the control group (n = 13) showed no voltage changes. The most pronounced R and QRS attenuation was seen in patients with acute coronary syndrome, CAD and those in whom manual chest compressions had been necessary. Changes appeared after a mean period of 23 hours and returned to normal after a mean of 62 hours. we report the phenomenon of reversible voltage loss after external defibrillation or cardioversion. A possible explanation for this phenomenon might be tissue oedema in the chest area after electrical and traumatic injury. An alternative reason might be myocardial stunning. The exact pathophysiological mechanism leading to reversible voltage attenuation remains unclear and needs further exploration in studies with a larger sample of patients.

ECG changes following cardioversion and defibrillation.

changes of the QRS amplitude following defibrillation or cardioversion have never been reported in humans. prospective analysis of patients externally cardioverted or defibrillated for ventricular and supraventricular tachyarrhythmias. Patients with coronary artery disease (CAD) and acute coronary syndrome (ACS) formed group A and patients without CAD but with external cardioversion/defibrillation formed group B. Patients in the control group (group C) experienced a shock by an Internal Cardioverter Defibrillator (ICD). All patients underwent the same study protocol: serial ECG's were recorded and sums (Sigma) of the QRS amplitude created separately for the precordial and peripheral leads. Sigma were then compared with baseline values and changes indicated as percentage (%). We included a total of 45 patients in our study: 21 patients (47%) in group A, 11 patients (24%) in group B and 13 patients (29%) in group C. Median age was 66 years in group A, 55 in group B and 52 in group C. In group A mean change of the R amplitude was -35% in precordial and -16% in the peripheral leads. In group B mean change of the R amplitude was -16% in the precordial and -2% in the peripheral leads. The QRS amplitude changed -23% in the precordial leads in group A and -14% in group B. 13 patients with external defibrillation or cardioversion of group A + B and all patients of the control group (n = 13) showed no voltage changes. The most pronounced R and QRS attenuation was seen in patients with acute coronary syndrome, CAD and those in whom manual chest compressions had been necessary. Changes appeared after a mean period of 23 hours and returned to normal after a mean of 62 hours. we report the phenomenon of reversible voltage loss after external defibrillation or cardioversion. A possible explanation for this phenomenon might be tissue oedema in the chest area after electrical and traumatic injury. An alternative reason might be myocardial stunning. The exact pathophysiological mechanism leading to reversible voltage attenuation remains unclear and needs further exploration in studies with a larger sample of patients.

Cellular Mechanisms for Direction Selectivity in the Retina

Direction selectivity represents a fundamental computation found across multiple sensory systems. In the mammalian visual system, direction selectivity appears first in the retina, where excitatory and inhibitory interneurons release neurotransmitter most rapidly during movement in a preferred direction. Two parallel sets of interneuron signals are integrated by a direction-selective ganglion cell, which creates a direction preference for both bright and dark moving objects. Direction selectivity of synaptic input becomes amplified by action potentials in the ganglion cell dendrites. Recent work has elucidated direction-selective mechanisms in inhibitory circuitry, but mechanisms in excitatory circuitry remain unexplained.