Initial Negative Deflection Research Articles

A Method for Analysis of the Local Atrial Evoked Response for Determination of Atrial Capture in Permanent Pacing Systems

We developed a method for detection and analysis of the local atrial evoked response. Eleven patients undergoing permanent dual chamber pacemaker implantations for standard clinical indications were included in the study. Using a pacing system emulator, charge balancing using a variable triphasic stimulus waveform to reduce polarization artifact amplitude was performed first. This could not be completed in one patient because of a poor signal-to-noise ratio. Subsequent analysis of the local atrial evoked response in the remaining ten patients showed the typical signal to be a biphasic waveform with an initial negative deflection followed by a positive deflection nearly equal in amplitude. The mean amplitude of the atrial evoked response was 3.1 +/- 1.4 mV, while the intrinsic P wave amplitude in these same patients averaged 5.6 +/- 3.0 mV. The summed evoked response, a parameter that is directly proportional to the area of the signal, was used to determine atrial pacing threshold. The median atrial pacing threshold determined by the algorithm was 1.00 V. There was no instance of failure to detect loss of capture, nor was loss of capture inaccurately determined when there was still successful atrial pacing. Atrial capture in permanent pacing systems can thus be determined using an algorithm to record and analyze the local atrial evoked response. This method could potentially be useful in the automatic determination of atrial pacing threshold.

The magnitude of long-term potentiation of field potentials induced monosynaptically in region CA3 of guinea pig hippocampus

The magnitude of long-term potentiation (LTP) was re-examined for monosynaptic transmission between mossy fibers and CA3 neurons in thin sections of the hippocampus of the guinea pig. Although an initial negative deflection in the field potential showed apparent short-term potentiation, this deflection was concluded to reflect non-synaptic activation of CA3 neurons. Accordingly, the magnitude of LTP of monosynaptic transmission was re-calculated at 3.4 ± 0.9.

Variability in the characteristics of pontogeniculooccipital spikes during paradoxical sleep

An important criterion for identifying paradoxical sleep is the presence of a peculiar waveform recorded in the pons, lateral geniculate body, and visual cortex during that sleep state. These waveforms, termed PGO waves, have long been viewed as having large and constant amplitudes, an initial negative deflection in the visual cortex, and not being dependent on the levels of background illumination. Waveforms recorded during wakefulness have different characteristics, and these have been used to differentiate the waking state from paradoxical sleep. The present study demonstrated that most PGO waves have highly variable amplitudes during paradoxical sleep and that only a small fraction conform to the stereotypic wave characteristics of constant and large amplitudes and the presence of initial negative deflections. These findings argue against the criteria commonly used to differentiate PGO waves during paradoxical sleep from the eye movement potentials recorded in wakefulness.

The projection of muscle afferents from the hand to cerebral cortex in man.

This study provides direct evidence that muscle afferents from the human hand project to the cerebral cortex. Electrical stimulation within a purely muscle fascicle of the median nerve at the wrist produced a cerebral potential, the latency of which (to the initial negative deflection, N1) was the same as, or shorter than, the latency with stimulation of cutaneous fascicles. The average latencies to N1 for muscle afferent and cutaneous afferent inputs were 19.0 and 20.3 ms, respectively. This difference could not be accounted for by differences in peripheral conduction velocity. The site of the maximal initial negative deflection of the cerebral potential for muscle afferents was posterior to that for cutaneous afferents. This locus for muscle afferents corresponded to that for mixed afferent inputs. Muscle afferents contribute to, and may dominate, the cerebral potential produced by stimulation of the mixed median nerve at the wrist.

Change in somatosensory evoked potential in the rat recorded at the hemisphere with iron-induced epileptic focus.

In rats, microinjection of FeCl3 solution into the left sensorimotor cortex was performed to induce a chronic epileptic focus. One month or more after the microinjection, electrocutaneous stimuli were applied to part of the wrist joint and 50 consecutive somatosensory evoked potentials (SEPs) were averaged. SEP from the left cortex showed only an initial negative monophasic deflection while SEP from the contralateral cortex showed a normal configuration with initial positive-negative biphasic deflection in the majority of experimental animals.

Natural history of electrical interventricular septal force in the course of left ventricular hypertrophy in man

Initial electrical forces emanating from interventricular septal depolarization, being directed to the right and anteriorly, normally produce an initial negative deflection or Q wave in leads I, aVL and V6 and an initial positive deflection or R wave in leads V1 and V2. The observations of hypertrophied interventricular septum, an integral part of the left ventricle, in patients with left ventricular hypertrophy would predict an increase in these septal electrical forces similar to the total left ventricular (QRS) forces in these subjects. Contrary to this expectation, several studies document an actual decrease or absence of the normally oriented initial forces in ECGs of patients with the criteria of left ventricular hypertrophy. In order to clarify the nature of this paradox, this study was initiated. Our observations suggest that the normal initial septal forces indeed increase as expected, during the initial four to six years, and subsequently show a progressive decline in patients with left ventricular hypertrophy. Although the precise mechanism for the bimodal change in the septal forces during the period of the constancy of the total QRS forces is not clear, a hypothesis based on the current knowledge is advanced to explain these observations.

THE SPINAL EVOKED POTENTIALS CONDUCTED FROM THE SPINOUS PROCESSES

1) The spinal evoked potentials (S. E. P.) obtained from the spinous processes are very much similar with the potential which are obtained from the epidural space.2) The initial negative deflection corresponding to the action potentials of the dorsolateral tracts of spinal cord, and the second to those of the dorsal tracts was confirmed by the animal experiments.3) The relationship between intensity and duration of the cord distraction trauma was explored in cats. The etiology of cord damage by distraction is probably due to ischemia.4) In one patient who had an incomplete spinal cord injury, the S. E. P. has disappeared during correction of the kyphoscoliosis with a Harrington Distraction Rod, however with the partial release of distraction, it recovered immediately.In another patient with supposedly complete injury at C5 level incompleteness was actually proved with the examination of the spinal evoked potentials.In two incomplete cord injuries at C4 and C6 injuries respectively, a nearly normal S. E. P. was recorded.In the case of complete quadriplegic patients, the S. E. P. was not recorded at all the level above lesion.5) As the results of our study, we are certain that the S. E. P. which is obtained from K-wire inserted into the spinous processes can be safely and easily used for the examination of spinal cord function in various clinical situation. The gained data was also highly reliable.

Electrophysiological characterization ofDrosophila ocelli

Drosophila have 3 simple eyes, ocelli, located on the vertex of the head, in addition to 2 compound eyes. We determined ocellar function using the electroretinogram (ERG) and vision mutants. The ERG waveform in response to a 1 s stimulus was a slow negative (receptor depolarizing) potential followed by a return to baseline at light-off (Fig. 1). During long stimuli there was an exponential decay to baseline after the initial negative deflection. At light-off there was a positive overshoot and return to baseline (Fig. 2). During a long stimulus the ERG reflected stepwise changes in intensity, with a negative response to an increase in intensity and positive polarization to a decrease (Fig. 3). The ERG thus reflects extraction of intensity change information. The ocellar ERG waveforms (Fig. 4) and intensity-response functions (Fig. 5) were similar across wavelengths ranging from 370 to 520 nm. The ocellar spectral sensitivity peaks around 350–370 nm (ultraviolet) and 445 nm (blue) (Fig. 6). Chromatic adaptation with intense 370 or 445 nm did not selectively reduce 370 or 445 nm peak sensitivities (Fig. 7). These findings offer no support for more than one ocellar receptor type. In additional experiments, bright 570 nm adaptation was found to increase responsivity relative to bright short wavelength adaptation. These wavelength-specific effects were elicited even during anoxia suggesting wavelength-dependent photopigment interconversions (Fig. 8). Spectral adaptation data were obtained suggesting that ocelli have a stable (non-bleaching) metarhodopsin. Spectral adaptation and sensitivity data allowed an approximation of the metarhodopsin spectrum which has long wavelength and ultraviolet maxima (Fig. 7). Comparisons between the ERG waveforms and spectral sensitivities of normal and visual mutantDrosophila suggest that the absence of compound eye receptor types has no effect on the ocellar ERG. Also, strains with or without screening pigments do not show significant differences. However, 2 mutants with abnormal compound eye receptor potentials had ocellar abnormalities.

Relation between cellular excitation and inhibition and averaged evoked potentials in the inferior colliculus of the rat

Single and multineuronal response patterns in the form of peri-stimulus-time histograms (PSTH) and simultaneously averaged evoked field potentials (AEP) were investigated for correlations between PSTH and AEP waveforms. Concomitant changes in both waveforms were also studied as a function of stimulus frequency and recording location. A short latency initial excitation exhibited by most neurons was temporally correlated with either the slope or peak of the initial negative deflection of the AEP. This was usually followed by a brief cellular inhibition and a transient positive deflection of the AEP. A sustained potential shift (+ or −) was often observed in the AEP and correlated with the duration, polarity, and location of local cellular excitation and inhibition. Intracellular data as reported in the literature indicate that the interpretation of field potentials as summated postsynaptic potentials is consistent with these results.

Inhibitory mechanisms in the rabbit olfactory bulb: dendrodendritic mechanisms

The unitary responses of mitral and granular layer cells and olfactory bulb field potentials following stimulation of the lateral olfactory tract (LOT), olfactory nerves and anterior limb of the anterior commissure (AAC) were analyzed. The hyperpolarization that followed antidromic invasion of mitral cells was shown to result from a synaptically evoked inhibitory potential. The analysis of the LOT evoked field potential indicated that the initial negative deflection represented antidromic invasion of mitral cell somata and dendrites. The results suggest that the second negative deflection fo the field potential represented a synaptically evoked depolarization of granule cell dendrites, while the succeeding positive deflection represented the synaptically evoked inhibition of mitral cell dendrites and somata. A conditioning LOT stimulus inhibited the intracellularly recorded hyperpolarization of mitral cells and abolished the field potential evoked by a test LOT stimulus. In addition, cells in the granular layer that responded to LOT stimulation were inhibited by conditioning stimuli supplied to the LOT, AAC or olfactory nerves. The results are consistent with and lend support to the dendrodendritic hypothesis advanced by Rall et al. and suggest that the cells in the granular layer which are activated by the dendrites of mitral cells are granule cells.

Spontaneous electrical activity of human muscle

The spontaneous electrical activity of human muscle was studied in 197 normals, 67 patients with peripheral nerve involvement and 29 patients with progressive muscular dystrophy. “Noise” was observed in the end-plate zones of normal muscle; after minute displacements of the electrode the noise could be seen to consist of randomly occurring purely negative discharges 0.5–2 msec in duration and up to 100 μV in amplitude. This activity probably represents extracellularly recorded miniature end-plate potentials. Outside the end-plate zones of normal muscle a single site was rarely encountered yielding a spontaneous discharge similar to the fibrillation potentials of denervated muscle. In normal muscle such a discharge may correspond to the propagated disphasic potentials superimposed on the “end-plate noise”. The fibrillation potentials in patients with lower motor neurone disease were found to have longer durations than usually stated (1–5 msec as compared with 0.5–2 msec), a significant proportion of triphasic potentials (30%) and voltages half of which were of the same order (100–300 μV) as those of motor unit potentials. The fibrillations found in 29 of 76 patients with progressive muscular dystrophy had the same average duration, amplitude and shape as in denervated muscles. The fibrillation potentials were initiated in the end-plate zone as evidenced by the initial negative deflection of the potential recorded there and the initial positive deflection outside the end-plate zone. The initiation of the fibrillation potentials cannot be ascribed to mechanical stimulation by the intramuscular needle electrode since fibrillation potentials could also be recorded subcutaneously. With the 50 μ diameter leads of a multi-electrode fibrillation potentials were recorded with peak-to-peak amplitudes as high as 8.5 mV. The decline in amplitude along the multi-lead electrode was the same for fibrillation potentials 1 mV or more in amplitude as for the spike components of motor unit potentials, the voltage falling to less than one-tenth of maximum within 0.45 mm. This suggests that “high voltage” fibrillation potentials represent the spontaneous discharge of a sub-unit. The amplitudes of 100–600 μV fibrillation potentials declined relatively less with distance, suggesting that they were recorded farther away from the generators (about 0.5 mm) than the high voltage potentials. The small amplitude and rapid attenuation of positive sharp waves suggest that they are derived from a single muscle fibre. Cross talk in our multi-lead electrodes was insignificant and cannot explain the discrepancy between our findings and those of other investigators with regard to the voltage decline of spike potentials. The cause of fibrillation potentials is discussed in the light of the present knowledge of the properties of the membrane of denervated muscle fibres.

The C-wave of the human ERG. Its intensity dependence and pupillociliary orgin.

The multiphasic character of the vertabrate ERG is a well-recognized and generally accepted concept. By convention the initial negative deflection from the resting potential is called the a-wave, the second, corneal positive deflection, the b-wave; another slow positive deflection, the c-wave; and finally, a variably present, negative deflection, the d-wave, associated with the offeffect. The principal portion of the ERG, comprising the a- and b-waves, has been the subject of extensive investigation for many years. The c-wave, especially as it is present in the human, has received considerably less attention. This may be due, in part, to the fact that no associated potential exists in the optic nerve. In the absence of such a potential, the c-wave is thought to be unrelated to the act of vision. The literature concerning the nature and origin of the c-wave is confusing. Hartline 1 suggested that the c-wave of the human ERG might

Electrical signs of impulse conduction in spinal motoneurons.

An analysis has been made of the electrical responses recorded on the surface and within the substance of the first sacral spinal segment when the contained motoneurons are excited by single and repeated antidromic ventral root volleys. A succession of negative deflections, designated in order of increasing latency m, i, b, d, has been found. Each of those deflections possesses some physiological property or properties to distinguish it from the remainder. Indicated by that fact is the conclusion that the successive deflections represent impulse conduction through successive parts of the motoneurons that differ in behavior, each from the others. Since the spinal cord constitutes a volume conductor the negative deflections are anteceded by a positive deflection at all points except that at which the axonal impulses first enter from the ventral root into the spinal cord. Frequently two or more negative deflections are recorded together in overlapping sequence, but for each deflection a region can be found in which the onset of that deflection marks the transition from prodromal positivity to negativity. Deflection m is characteristic of axonal spikes. Latent period is in keeping with known axonal conduction velocity. Refractory period is brief. The response represented by m is highly resistant to asphyxia. Maximal along the line of ventral root attachment and attenuating sharply therefrom, deflection m can be attributed only to axonal impulse conduction. Deflection i is encountered only within the cord, and is always associated with a deflection b. The i,b complex is recordable at loci immediately dorsal to regions from which m is recorded, and immediately ventral to points from which b is recorded in isolation from i. Except for its great sensitivity to asphyxia, deflection i has properties in common with those of m, but very different from those of b or d. To judge by properties i represents continuing axonal impulse conduction into a region, however, that is readily depolarized by asphyxia. Deflection b possesses a unique configuration in that the ascending limb is sloped progressively to the right indicating a sharp decrease in velocity of the antidromic impulses penetrating the b segment. A second antidromic volley will not conduct from i segment to b segment of the motoneurons unless separated from the first by nearly 1 msec. longer than is necessary for restimulation of axons. This value accords with somatic refractoriness determined by other means. Together with spatial considerations, the fact suggests that b represents antidromic invasion of cell bodies. Deflection d is ubiquitous, but in recordings from regions dorsal and lateral to the ventral horn, wherein an electrode is close to dendrites, but remote from other segments of motoneurons, d is the initial negative deflection. In latency d is variable to a degree that demands that it represent slow conduction through rather elongated structures. When associated with deflection b, deflection d may arise from the peak of b with the only notable discontinuity provided by the characteristically sloped rising phase of b. Deflection d records the occupation by antidromic impulses of the dendrites. Once dendrites have conducted a volley they will not again do so fully for some 120 msec. Embracing the several deflections, recorded impulse negativity in the motoneurons may endure for nearly 5 msec. When the axonal deflection m is recorded with minimal interference from somatic currents, it is followed by a reversal of sign to positivity that endures as long as impulse negativity can be traced elsewhere, demonstrating the existence of current flow from axons to somata as the latter are occupied by impulses. Note is taken of the fact that impulse conduction through motoneurons is followed by an interval, measurable to some 120 msec., during which after-currents flow. These currents denote the existence in parts of the intramedullary motoneurons of after-potentials the courses of which must differ in different parts of the neurons, otherwise nothing would be recorded. The location of sources and sinks is such as to indicate that a major fraction of the current flows between axons and somata. For approximately 45 msec. the direction of flow is from dendrites to axons. Thereafter, and for the remaining measurable duration, flow is from axons to dendrites.

Endocardiac electrocardiogram obtained by heart catheterization in the man

The electrocardiographic variations registered by endocardiac catheterization in man are described on the basis of twenty-three cases studied. The tracings show mainly the variations of potential of the heart, detected at the endocardiac surface. Endocardiac leads can be considered to be direct leads. The tracings are endocardiac electrograms. The auricular endocardiac electrogram (endocardiac P wave) consist normally of a series of rapid deflections (S, e, i, o waves) joined to a final slow deflection (Ta wave) by means of the o− u segment. The shape of the auricular electroendogram undergoes modifications according to the position of the electrode inside the auricle. Rapid deflections represent the process of depolarization of the auricles. Repolarization is represented by the final slow portion, as in the ventricular complex. The initial negative deflection (S wave) of the auricular complex is regarded as an exponent of the activity of the sino-auricular node. The endocardiac ventricular electrogram undergoes modifications in shape, depending upon whether the electrode is placed in the right ventricle or right auricle. The electroendogram obtained from the ventricle (type I) shows an initial positive deviation (R wave) produced by the excitation of the interventricular septum which is followed by a negative deflection of large amplitude (S wave) and a large negative T wave. The waves of depolarization and of repolarization of the ventricular wall (R waves and T waves) have, then, the same direction. The positive deviation of the S-T segment is greater as the catheter approaches nearer the septum. The ventricular electroendogram recorded from inside the auricle (type II) traces the negative potentials of the ventricular activity during the spreading of the excitation wave. It begins with a negative deflection (Q or QS wave) followed by a positive deviation, an inconstant element, and ends in a T wave which is usually negative, sharply pointed, and deep. The ventricular complex of this type of tracing is similar to the ventricular complex of the esophageal electrocardiogram obtained when the catheter is at the level of the auricle. The variations of endocardiac potential in bundle branch block, in one case of auricular extrasystoles, in one case of auricular asynchronism, and in cases of premature contractions of the right and left ventricles are described. The electrocardiographic curves registered with the catheter placed in the superior and inferior venae cavae and at different sites in the venous system are described. In bundle branch block of the common type, the endocardiac electrogram taken from inside the ventricle shows the absence of the initial positive (R) wave as a result of the abnormal excitation of the interventricular septum which is accomplished from right to left. The right ventricular cavity remains negative during the inscription of QRS complex. In bundle branch block of the uncommon type the right ventricular cavity is initially positive. In the cases of bundle branch block which were studied the endocardiac electrogram shows the same characteristics that have been observed in experimental bundle branch block in the dog.

The significance of an absent or a small initial positive deflection in the precordial lead

1. 1. The initial positive deflection in the precordial lead (Q-wave of old, R-wave of new technique) was absent in 2.7 per cent of 4,500 consecutive hospital patients and was small (2 mm. or less) in 3.9 per cent. 2. 2. In two-thirds of the patients, absence of this deflection was associated with recent or old coronary thrombosis and anterior wall infarction, and in one-fifth, with coronary artery disease alone, with or without hypertension. 3. 3. The initial positive deflection was also absent in 14 cases diagnosed as acute and chronic glomerulonephritis, rheumatic and syphilitic valvular disease, pneumothorax, Graves' disease, and acute myocarditis. There was no evidence of myocardial infarction in these cases. 4. 4. In patients with an M or W-shaped QRS complex precordial leads obtained from other positions on the chest wall usually demonstrated absence of the initial positive deflection. This holds frequently when a large initial negative deflection precedes a large positive deflection. 5. 5. Absence of this deflection was permanent in the majority of cases even when an abnormal T 4 and abnormal standard leads returned to normal. 6. 6. Absence of the initial positive deflection was accompanied by an abnormal T 4 in 54 per cent of cases. 7. 7. Of the patients with a small initial positive deflection 7.5 per cent had no clinical evidence of cardiovascular disease. The remainder suffered from coronary thrombosis (29 per cent), coronary artery disease with or without hypertension (37 per cent), rheumatic valvular disease (17 per cent), miscellaneous heart involvement (12 per cent). These included cases of intraventricular or bundle-branch block. 8. 8. In only one-fifth of these patients was there an associated abnormal T-wave in the precordial lead. A small initial positive deflection was significant when followed by an intrinsic deflection of at least 10 mm. 9. 9. In a large group of cases with anterior wall infarction, diagnosed electrocardiographically or at autopsy, the initial positive deflection was absent in more than one-half, small in one-sixth, and normal in one-third. In posterior wall infarction this deflection was rarely absent but was frequently small. 10. 10. In 26 patients with a small initial positive deflection, myocardial infarction was found 15 times. Only one case showed normal heart muscle. 11. 11. Comparison of the ordinary method of recording the precordial lead with the “zero potential” method of Wilson revealed no practical advantage of the latter as far as diagnosis was concerned.