Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “FLASH”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,171 records · Page 65Linked to original sources

The scotopic electroretinogram to blue flashes and pattern reversal visual evoked potentials in insulin dependent diabetes.

Pattern reversal visual evoked responses (PR-VEPs), the electroretinogram (ERG) to blue flashes of light in dark adaptation, the steady state ERG to 40 Hz flicker, and alterations in pupil diameter following dark adaptation were studied in 56 juvenile onset diabetics, 34 of whom had no ophthalmoscopic or photographic evidence of diabetic retinopathy (DR-group). The remaining 22 had mild background retinopathy (DR+group). Normal data was obtained from 24 subjects matched for age and sex with diabetics. Skin electrodes were used for all recordings. The scotopic 'b' wave of the ERG was significantly lower in amplitude in the DR- diabetics and it was even more reduced in the DR+group. The PR-VEP was significantly delayed in diabetics but there was no difference between the two groups. The steady state ERG was not significantly different between normals and diabetics. These findings indicate that retinal and more central abnormalities develop early in diabetics. Detection of objective electrophysiological abnormalities may be used to identify persons at risk of developing retinopathy and to monitor the effects of treatment.

Adolescent↗

Models for transmitter activation process in retinal rod outer segments to flash stimuli.

It has been generally accepted that transmitter molecules, which participated in the visual transduction process in retinal rod outer segments, are activated by bleached rhodopsin molecules serially one by one (serial activation model). This serial activation model accounts for some experimental observations, but not the quick and amplified activation of transmitter molecules. In this study, two models are proposed and solutions from the differential equations of the models are compared quantitatively with experimental observations. The two models proposed in this study are the serial-parallel activation model and the parallel-parallel activation model. In the serial-parallel activation model, rhodopsin molecules are activated by bleached rhodopsin molecules. Transmitter molecules are activated both by bleached and activated rhodopsin molecules. In the parallel-parallel activation model, both rhodopsin and transmitter molecules are activated by bleached and activated rhodopsin molecules. The time taken to activate 90% of transmitter molecules after flash stimuli, which bleaches 10(-4)% of rhodopsin, is 5.94 s, 3.91 ms and 23.7 microseconds for the serial, serial-parallel and parallel-parallel activation models, respectively. As contrasted to the serial activation model in which transmitter activation proceeds too slow, the present serial-parallel and parallel-parallel activation models can reproduce transmitter activation quick enough to account for the experimental observations.

Animals↗

Transduction steps which characterize retinal cone current responses to flash stimuli.

There are three prominent characteristics in current responses of retinal cones to flash stimuli when compared with those of rods. First, the time-to-peak of the photocurrent is two to four times faster than for the rod. Second, the photosensitivity of the cone is more than one order of magnitude lower than that of the rod. Third, current responses of cones resemble characteristic under-shoot in the recovery phase. At present, however, it is not known what kinds of mechanisms underlie these characteristics. In the present study, critical steps which characterize cone responses have been investigated by changing rate constants in the model for the signal transduction scheme of cone outer segments under the assumption that the scheme is basically the same as for rods. The computer simulations have shown that rate constants were divided into three categories: those which do not appreciably change photocurrent, those which change only photosensitivity, and those which change both sensitivity and speed. Furthermore, rate constants which characterize undershoot were identified. From these simulations it has been revealed that characteristics of the cone response could be reproduced by changing the rate constants. The critical ones are rate of rhodopsin deactivation, rate of GTP hydrolysis, and deactivation rate of activated phosphodiesterase. These results suggest possibilities that the signal transduction mechanisms in cones are basically the same as those for rods, while rate constants are different.

Animals↗

Intracortical generators of the flash VEP in monkeys.

Flash visual evoked potentials (VEPs) in unanesthetized monkeys were recorded from the cortical surface and from closely spaced intracortical sites together with associated multiple unit activity (MUA). The VEP depth profiles were subjected to current source density (CSD) analysis to delineate the laminar pattern of transmembrane current flows manifested by extracellular source and sinks. The initial surface recorded components (P15 and P18) were generated subcortically within the thalamocortical radiations. The distribution of current sources and sinks associated with two subsequent surface negative components. N24 and N40. demonstrates their generation within laminae IVA and IVCb respectively, both parvocellular thalamorecipient layers. Oscillatory potentials resembling those seen in human VEPs are observed riding on N40; analysis of MUA in conjunction with sources and sinks coincident with these wavelets provides evidence that they derive from both thalamocortical and cortical activity. MUA in the 20-60 msec range shows phasic increases throughout lamina IV, which are maximum in amplitude within lamina IVA. This increased firing is concurrent with the sinks observed within the parvocellular thalamorecipient sublaminae IVCb and IVA. A subsequent component, P65, coincident with a decrease in MUA to below the spontaneous level co-located with a lamina IVCb current source, probably arises from intracortically generated inhibitory activity within IVCb. The next VEP component, a surface negative potential at 95 msec, is coincident with current sources and sinks in lamina III, and is consistent with stellate cell input to supragranular elements. VEP components after N95 are not associated with either MUA or CSD activity and are probably generated in extrastriate cortex. Human counterparts of the simian VEP are proposed.

Animals↗

Developmental wave form analysis of the neonatal flash evoked potential.

A multiple regression technique was used to describe the wave form of the flash evoked potential (VEP) in 64 neonates born between 28 and 39 weeks of gestation. The successive appearance of new features in the VEP with increasing gestational age at birth was used to define 5 components, of which specimens were obtained by averaging VEPs of 18 selected infants. The VEPs of the other 46 infants were expressed as linear sums of the components, each multiplied by a weighting coefficient. The method accounted for 74 +/- 11% (mean +/- 1 S.D.) of the rms power of the observed VEPs and was used to demonstrate significant effects on wave form maturation from fetal growth retardation and maternal smoking in pregnancy.

Electrophysiology↗

Subcortical contributions to the surface-recorded flash-VEP in the awake macaque.

Epidural mapping of flash-VEP in awake monkeys revealed a reliable, short latency negativity, N25 (onset: 18-22 msec; peak: 23-27 msec; duration: 15-20 msec), with a broad frontal surface distribution (frontolateral maximum). N25 was dissociable from the electroretinogram (ERG), from cortical VEP and from the high frequency oscillations (wavelets) coextensive with the ERG and with cortical VEP. Depth recordings traced N25 from its surface maximum down to the lateral geniculate nucleus (LGN). Concomitant VEP, current source density (CSD) and multiunit activity (MUA) profiles obtained with multicontact electrodes showed that the peak and later portion of N25 arise primarily from current sinks (associated with MUA increases) that reflect transmembrane current flow attending depolarization of cells in lamina 6, the uppermost lamina, but may also receive contributions from the more ventral LGN laminae. The initial portion of N25 arises from similar processes near the lamina 3/2 border. Wavelets, in contrast, are prominent in VEP, CSD and MUA within LGN, but attenuate rapidly above LGN. LGN laminar and cellular morphology predict volume conduction of N25 over a wide arc lateral and anterior to LGN and roughly horizontal isopotential planes medial and posterior to LGN. Recordings on the brain surface, within LGN, and in the regions surrounding LGN are consistent with these predictions. Possible contributions from other structures and how these results fit with data obtained in humans are considered.

Animals↗

Eye closure affects flash VEP latency in dementia.

In a group of 27 demented patients (21 with DAT and 6 with MID) with normal pattern VEP (PVEP), the latencies of the main flash VEP (FVEP) components (P1, N2, P2 and N3) were assessed both with open and closed eyes. At variance from controls, demented patients showed that both P2 and N3 components are significantly delayed with closed eyes while neither P1 nor N2 timings are affected. Control studies ruled out the possibility that such an outcome might depend on a defective pupillary responsiveness and/or an impaired sensitivity to luminance changes. On these grounds it is suggested that the effect of mode of stimulation on FVEP latency in demented patients is more likely to depend on "central" than on "peripheral" mechanisms. The dependence of latency changes on closure of the eyes seems to negate the direct effect of lesions upon visual structures and suggests an impairment of the modulatory action of non-visual afferents upon the activity of the visual cortex.

Aged↗

Establishment of normal values for flash visual evoked potentials (VEPs) in preterm infants: a longitudinal study with special reference to two components of the N1 wave.

To establish normal values for flash visual evoked potentials (VEPs) in the preterm period, we analyzed 356 records from 63 neurologically normal infants (26-35 weeks gestation) followed longitudinally. Using both sleep and drowsy state recording within the same session and a mean of 5.7 weekly recording sessions per infant, we hypothesized that the prominent negative wave (N1) consisted of 2 negative components, N1a (early) and N1b (late). This hypothesis could explain the previously reported variability in VEP indices. With a precise definition of the N1a peak, we were able to establish reference ranges for N1a peak latencies at various postmenstrual ages (PMA) which, unlike those previously reported, are narrow enough to be clinically useful. From a cross-sectional analysis we found that the N1a peak latency decreased with maturation at about 4.6 msec/week between 30 and 40 weeks PMA (P < 0.001). We also analyzed the N1 wave form and demonstrated its developmental maturation during this period. There were significant decreases in the amplitudes of both the N1a and N1b peaks with maturation (P < 0.001), but the decrease of the N1a amplitude was steeper than that of N1b. The N1 wave form changed from a wave in which the early peak (N1a) was higher than the late peak (N1b) into the reverse with N1b higher than N1a. This wave change may be related to developmental processes in the visual system. Longitudinal follow-up revealed that extra-uterine life may accelerate the maturation of the N1 wave form but has no effect on the decrease of the absolute values of peak latencies.

Electroencephalography↗

Flash P2 delay in primary degenerative dementia of the Alzheimer type.

1. Flash visual evoked responses of 31 patients meeting DSM-III-R criteria for primary degenerative dementia of the Alzheimer type were compared with 31 healthy controls. 2. P1 latency was normal (75 +/- 6 msec Alzheimer's; 75 +/- 6 msec controls). 3. P2 was significantly delayed (162 +/- 32 msec, 147 +/- 20 msec, p < 0.03) among patients. 4. P1-P2 interpeak latency was significantly increased (87 +/- 32 msec, 71 +/- 21 msec, p < 0.03) among patients.

Aged↗

Comparison of flash-induced light-scattering transients and proton efflux from auxinic-herbicide resistant and susceptible wild mustard protoplasts: a possible role for calcium in mediating auxinic herbicide resistance.

Comparison of flash-induced light-scattering signals from protoplasts of auxinic herbicide-resistant ('R') and -susceptible ('S') wild mustard biotypes suggest that ATP-dependent activity manifested as a conformational change differs between the biotypes. The signal obtained from R protoplasts is unaffected by 50 microM picloram, an auxin analogue. In comparison, the signal amplitude from the S protoplasts decreases 40% in 20 microM picloram and is abolished in 50 microM picloram. Signal amplitude from the R protoplasts can be decreased by simultaneous incubation with 50 microM picloram and 50 microM verapamil, a calcium channel blocker. Incubation of the S protoplasts with the calcium ionophore A23187 in the presence of 0.5 mM calcium reduced the inhibitory effect of picloram. Absorbance spectrophotometry using acridine orange as a pH indicator suggests that picloram affects the proton flux in the S biotype only. Based on these results, we hypothesize that picloram affects the calcium and hydrogen dynamics in the S biotype. Because the scattering characteristics of S protoplasts incubated with picloram can be nearly reproduced in the R protoplasts by simultaneous incubation with picloram and verapamil, calcium may have a significant role in modulating auxinic herbicide resistance. To our knowledge, this is the first report to implicate such a role for calcium.

Acridine Orange↗

Flash burns to the face.

A characteristic 'crow's foot' pattern is seen around the eye in many flash burns. The protective blink reflex underlies this, and the injury is due to convected rather than radiant energy.

Adult↗

Quantitative electrophysiological studies of regenerating visuotopic maps in goldfish--II. Delayed recovery of sensitivity to small light flashes.

The regenerating retinotectal projection of goldfish was mapped with punctate flashes of light produced by red light-emitting diodes. The characteristics of multiunit receptive fields were studied in fish kept at 25 degrees C at different times after unilateral optic nerve crush. From about 20 days, when the first visually-evoked responses to black-on-white stimuli appeared, until about 40 days, no consistent responses to light-emitting diodes could be obtained, although high-contrast, long-duration light-emitting diode stimuli elicited weak off-responding. At around 40 days, responses to light-emitting diodes reappeared as the amplitude of evoked multiunit activity increased sharply. At their emergence, light-emitting diode-sensitive multiunit receptive fields were irregular and only slightly enlarged, but quickly regained normal shape and size. Conformity to a linear and uniform visuotopography recovered more slowly and, in some individuals, incompletely. The results suggest that "on" and "off" optic fiber systems, probably with small terminal arbors, are functionally expressed at a later time in regeneration than the predominantly "off" system manifested earlier. The different time courses of recovery in these systems explain several aspects of the recovery of visual behavior during optic nerve regeneration.

Action Potentials↗

Hypothermia and chloropent anesthesia differentially affect the flash evoked potentials of hooded rats.

Anesthetics and body temperature alterations are both known to alter parameters of sensory-evoked responses. However few studies have quantitatively assessed the contributions of hypothermia to anesthetic-induced changes. Two experiments were performed. In the first, chronically implanted rats were injected with either 0, 0.05, 0.10 or 0.20 ml Chloropent/100 g b.w., while body temperature was maintained. Flash evoked potentials recorded 30 min later showed increased latencies but only minor (not statistically significant) changes in amplitude. In the second experiment the same rats were anesthetized with 0.35 ml Chloropent/100 g b.w. and rectal temperature was systematically varied between 31 degrees C and 37 degrees C. Over the ranges of temperature and anesthetic employed, latencies increased more extensively with hypothermia than with anesthesia. P1N1 amplitude doubled when temperature was lowered to 31C, but P2N2 and N2P3 amplitudes declined over the same temperature range. Anesthetic-induced changes in peak-to-peak amplitude did not reach statistical significance when body temperature was constant. The findings suggest that previously reported alterations in evoked potentials following anesthesia may have been confounded with hypothermia.

Anesthetics↗

Superior colliculus lesions and flash evoked potentials from rat cortex.

It is generally assumed that the primary response of the rat flash evoked potential (FEP) is activated by a retino-geniculate path, and that the secondary response reflects input to the cortex by way of the superior colliculus (SC) or other brainstem structures. In the present study, male Long-Evans rats were implanted with monopolar screw electrodes placed over the left visual cortex, and a pair of twisted monopolar depth electrodes, which were used to produce electrolytic lesions, were placed in each SC. One half of the animals did not receive the electrolytic treatment (controls). FEP waveforms were obtained from all animals prior to treatment, and 2 and 5 days after treatment. Histological analysis was performed to verify electrode placement and determine lesion size. Electrolytic lesions resulting in massive destruction of the SC produced no decrement in any portion of the rat FEP but did produce an increase in amplitude of the N2P3 component. The data show that the secondary response is not generated by SC in rats, but that SC may modulate amplitude of the response.

Animals↗

Surface distribution of flash-evoked and pattern reversal-evoked potentials in hooded rats.

Simultaneous recording from 21 electrode sites in a 4 X 4 mm area over the posterior cortex was used to determine the surface distribution of all major peaks which constitute flash-evoked potentials (FEPs) and pattern reversal evoked-potentials (PREPs) in hooded rats. Topographical maps were constructed with respect to Bregma and midline reference points. The data indicate that not all of the peaks which constitute either evoked potential have their greatest amplitude within the classically defined primary visual cortex. Further, since the FEPs were produced by uniform stimulation, the data suggest that surface regions of the rat visual cortex differ in ways other than simply the portion of the visual field from which information is received.

Animals↗

Optimization of spoiler gradients in FLASH MRI.

The FLASH technique for fast magnetic resonance (MR) imaging often employs strong magnetic field gradients, called spoiler gradients, to dephase the transverse magnetization after it has been measured. Otherwise, image artifacts can develop. The effectiveness of spoiler gradients at suppressing these artifacts was evaluated experimentally on two-dimensional MR images of a uniform phantom and patients. It was informative to compare the magnetization immediately before the RF excitation in each phase encoding step. Only spoiler gradients in the slice selection direction were effective. Spoiler gradients that decreased steadily from a large amplitude in the first phase encoding step to zero in the last minimized the transverse magnetization and suppressed the image artifact, without changing the image contrast.

Humans↗

A multi-plane scout sequence using flash imaging.

A new pulse sequence is presented for multi-plane imaging which simultaneously acquires images in the axial, coronal, and sagittal planes. Combined with FLASH imaging or other similar techniques, T1- and T2-weighted images in all three planes can be acquired in approximately 12 and 30 seconds, respectively. The sequence is easily implemented by modifying a multi-slice sequence to provide a rotation of gradient assignments between slice excitations. This sequence has been used extensively as a rapid "scout" scan. Several clinical examples are included.

Arachnoid↗

Advances in cardiac applications of subsecond flash MRI.

Flow-suppressed, subsecond FLASH MR images of the normal human heart have been obtained from single cardiac cycles using a 2.0-T whole-body MRI/MRS system (Siemens Magnetom) equipped with conventional 10 mT m-1 gradients. The present results demonstrate further technical improvements as compared to a previous report on the same subject (Magn. Reson. Med. 13:150-157; 1990). Measuring times of 139 msec and 209 msec were achieved by reducing the repetition time to TR = 4.36 msec (TE = 2.8 msec) and the spatial resolution to 32 x 128 or 48 x 128 measured data points, respectively. The flip angle was optimized to 12 degrees. Spatial pre-saturation of 60 mm thick sections adjacent to the imaging plane resulted in a suppression of the blood signal and a clear delineation of the myocardium. Oblique rotation of the imaging slice provides convenient access to the anatomical long axis and short axis views of the heart. EKG-triggered images from separate heartbeats but at different cardiac phases demonstrate that the effective time resolution is considerably less than the actual imaging time.

Electrocardiography↗