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T G Yuen

Publications and source records attributed to T G Yuen.

At least 19 recordsLinked to original sources
PubMed1992

Damage in peripheral nerve from continuous electrical stimulation: comparison of two stimulus waveforms.

The propensity for two types of charge-balanced stimulus waveforms to induce injury during eight hours of continuous electrical stimulation of the cat sciatic nerve was investigated. One waveform was a biphasic, controlled-current pulse pair, each phase 50 microseconds in duration, with no delay between the phases ('short pulse', selected to excite primarily large axons), whereas in the second type each phase was 100 microseconds in duration, with a 400 microsecond delay between the phases (selected to excite axons of a broader spectrum of diameters). The sciatic nerve was examined for early axonal degeneration (EAD) seven days after the session of continuous stimulation. With both waveforms, the threshold stimulus current for axonal injury was greater than the current required to excite all of the nerve's large axons. The correlation between simple stimulus parameters and the amount of EAD was poor, especially with the 'short pulse' waveform, probably due to variability between animals. When the stimulus was normalised with respect to the current required to fully recruit the large axons, a good association between damage and stimulus amplitude emerged. The damage threshold was higher for the 'short pulse' waveform. The implications for clinical protocols are discussed.

Animals↗
PubMed1992

Stimulation with chronically implanted microelectrodes in the cochlear nucleus of the cat: histologic and physiologic effects.

The effects of several hours of continuous electrical stimulation in the cats' cochlear nucleus with chronically implanted activated iridium microelectrodes was investigated from the changes in the evoked response near the inferior colliculus and also by histologic evaluation of the stimulated tissue. The stimulating microelectrodes had geometric surface areas of 75-500 microns2. They were pulsed continuously for 4 h, at a pulse repetition rate of 200 Hz, using charge-balanced pulse pairs. The charge per phase was 1.8 or 3.6 nC/ph. The animals were sacrificed for histologic evaluation 2 h, or several days later. The only remarkable histologic change resulting from the 4 h of stimulation was some aggregation of lymphocytes at the site of stimulation. However, depression of the electrical excitability of neurons near the sites often persisted for several days after 4 h of stimulation at 3.6 nC/phase. The charge per phase of the stimulus pulse pair was correlated strongly with the depression of excitability, and there was a weaker correlation between the depression and the amplitude of the first phase of voltage transient induced across the electrode-tissue interface. The charge density, calculated from the geometric surface area of the stimulating electrodes, was poorly correlated with the severity of the depression. The findings suggest a means of detecting impending stimulation-induced neural damage while it is still reversible.

Animals↗
PubMed1990

Local anaesthetic block protects against electrically-induced damage in peripheral nerve.

This study is one of a series addressing the mechanisms involved in the production of neural damage caused by continuous, prolonged electrical stimulation of peripheral nerve. It has been previously shown that sustained, high frequency electrical stimulation of the cat's peroneal nerve may cause irreversible neural damage in the form of axonal degeneration of the large myelinated fibres. In this study we demonstrate that blocking the action potentials on most of the nerve fibres with local anaesthetics (10% procaine or 2% lidocaine) almost completely prevents the axonal degeneration. The abolition of axonal injury by local anaesthetic block strongly suggests that the electrically-induced damage is due to prolonged electrical excitation of axons. Furthermore, since less than complete suppression of the induced neural activity by local anaesthetic engenders essentially complete sparing of all axons, our results suggest that the damage to individual axons derives, at least in part, from stimulation-induced global changes in the nerve.

Action Potentials↗
PubMed1990

Partial pressure of oxygen in brain and peripheral nerve during damaging electrical stimulation.

The studies were performed to elucidate the mechanism underlying the neural damage which may occur during prolonged electrical stimulation of either brain tissue or peripheral nerve. The partial pressure of oxygen (pO2) was measured in the sciatic nerve and the cerebral cortex of adult cats before and during direct, local electrical stimulation of these neural tissues, using stimulus parameters capable of inducing neural injury. pO2 was monitored by the polarographic method, employing a platinum microelectrode inserted into the tissue adjacent to or beneath the stimulating electrode. In the sciatic nerve there was no marked change in intrafascicular pO2 in three cats upon initiation of the electrical stimulation. In a fourth animal intraneural pO2 increased briefly upon initiation of the stimulation. In no case did the intrafascicular compartment of nerves become significantly hypoxic. In the cerebral cortex, the start of stimulation was accompanied by a significant increase (approximately 12-15 Torr) in intracortical pO2 beneath the stimulating electrode, and pO2 remained at or above the pre-stimulus value for the duration of the stimulation. These results show that extracellular hypoxia is unlikely to be a significant factor in the neural injury induced in brain or peripheral nerve by prolonged electrical stimulation.

Animals↗
PubMed1990

Charge density and charge per phase as cofactors in neural injury induced by electrical stimulation.

The possibility of neural injury during prolonged electrical stimulation of the brain imposes some constraints on the use of this technique for therapeutic and experimental applications. Stimulating electrodes of various sizes were used to investigate the interactions of two stimulus parameters, charge density and charge per phase, in determining the threshold of neural injury induced by electrical stimulation. Platinum electrodes ranging in size from 0.002 to 0.5 cm2 were implanted over the parietal cortex of adult cats. Penetrating microelectrodes fabricated from iridium, with surface areas of 65 +/- 3 x 10(-6) cm2 were inserted into the parietal cortex. Ten days after implantation, the electrodes were pulsed continuously for 7h using charge balanced, current regulated, symmetric pulse pairs, 400 microseconds per phase in duration, at a repetition rate of 50 Hz. The animals were perfused immediately after the stimulation for histologic evaluation of the brain tissue subjacent to the electrode sites. The results show that charge density (as measured at the surface of the stimulating electrode), and charge per phase, interact in a synergistic manner to determine the threshold of stimulation-induced neural injury. This interaction occurs over a wide range of both parameters; for charge density from at least 10 to 800 microC/cm2 and, for charge per phase, from at least 0.05 to 5.0 microC per phase. The significance of these findings in elucidating the mechanisms underlying stimulation-induced injury is discussed.

Animals↗
PubMed1989

Histologic and physiologic evaluation of electrically stimulated peripheral nerve: considerations for the selection of parameters.

Helical electrodes were implanted around the left and right common peroneal nerves of cats. Three weeks after implantation one nerve was stimulated for 4-16 hours using charge-balanced, biphasic, constant current pulses. Compound action potentials (CAP) evoked by the stimulus were recorded from over the cauda equina before, during and after the stimulation. Light and electron microscopy evaluations were conducted at various times following the stimulation. The mere presence of the electrode invariably resulted in thickened epineurium and in some cases increased peripheral endoneurial connective tissue beneath the electrodes. Physiologic changes during stimulation included elevation of the electrical threshold of the large axons in the nerve. This was reversed within one week after stimulation at a frequency of 20 Hz, but often was not reversed following stimulation at 50-100 Hz. Continuous stimulation at 50 Hz for 8-16 hours at 400 microA or more resulted in neural damage characterized by endoneurial edema beginning within 48 hours after stimulation, and early axonal degeneration (EAD) of the large myelinated fibers, beginning by 1 week after stimulation. Neural damage due to electrical stimulation was decreased or abolished by reduction of the duration of stimulation, by stimulating at 20 Hz (vs. 50 Hz) or by use of an intermittent duty cycle. These results demonstrate that axons in peripheral nerves can be irreversely damaged by 8-16 hours of continuous stimulation at 50 Hz. However, the extent to which these axons may subsequently regenerate is uncertain. Therefore, protocols for functional electrical stimulation in human patients probably should be evaluated individually in animal studies.

Animals↗
PubMed1988

Comparison of neural damage induced by electrical stimulation with faradaic and capacitor electrodes.

Arrays of platinum (faradaic) and anodized, sintered tantalum pentoxide (capacitor) electrodes were implanted bilaterally in the subdural space of the parietal cortex of the cat. Two weeks after implantation both types of electrodes were pulsed for seven hours with identical waveforms consisting of controlled-current, charge-balanced, symmetric, anodic-first pulse pairs, 400 microseconds/phase and a charge density of 80-100 microC/cm2 (microcoulombs per square cm) at 50 pps (pulses per second). One group of animals was sacrificed immediately following stimulation and a second smaller group one week after stimulation. Tissues beneath both types of pulsed electrodes were damaged, but the difference in damage for the two electrode types was not statistically significant. Tissue beneath unpulsed electrodes was normal. At the ultrastructural level, in animals killed immediately after stimulation, shrunken and hyperchromic neurons were intermixed with neurons showing early intracellular edema. Glial cells appeared essentially normal. In animals killed one week after stimulation most of the damaged neurons had recovered, but the presence of shrunken, vacuolated and degenerating neurons showed that some of the cells were damaged irreversibly. It is concluded that most of the neural damage from stimulations of the brain surface at the level used in this study derives from processes associated with passage of the stimulus current through tissue, such as neuronal hyperactivity rather than electrochemical reactions associated with current injection across the electrode-tissue interface, since such reactions occur only with the faradaic electrodes.

Animals↗
PubMed1987

Tissue response to potential neuroprosthetic materials implanted subdurally.

A histologic study was made of the response of the leptomeninges and underlying cerebral cortex of the cat to subdural implantation of 3 insulating materials (HR605-P, Parylene-C and PI-2555) and a polymeric electrode component (MMA/MAPTAC) for periods of 8 and 16 wk. The tissue reactions were compared with those elicited by the arrays of Dacron mesh matrices, pure platinum controls and by positive controls (Ag-AgCl) known to cause reactions in the brain. Sites beneath the Dacron mesh matrix, pure platinum control implants and beneath all insulating materials implanted for 8 and 16 wk appeared indistinguishable, exhibiting little tissue reaction. All neurons appeared normal. The leptomeninges and cortex beneath the Ag-AgCl implants showed a chronic inflammatory reaction after 8 and 16 wk. Despite varying amounts of oedema, gliosis and ingrowth of connective tissue in the molecular layer, virtually all underlying neurons appeared normal.

Animals↗
PubMed1987

Characterization of electrode dissolution products on the high-voltage electron microscope.

Deposits left by electrodes and biocompatibility test specimens implanted in brain or peripheral nerve were characterized by X-ray microprobe analysis, electron diffraction and stereoscopic imaging using a high-voltage electron microscope. Examination of thick (1-micron) sections of neural tissue confirmed that the electron-dense bodies found adjacent to electrode positions consist of elements originating in the implant material (with the exceptions of the S and Se found in association with Ag). These elements have no long-range order, suggesting they are complexed with biological molecules. In some cases the deposits appear to be caused by pulsing the electrode with current, while in other cases the deposits are corroded or abraded from the electrode or are otherwise not associated with the neuroprosthetic functioning of the implant.

Animals↗
PubMed1986

Histopathologic evaluation of prolonged intracortical electrical stimulation.

Chronic stimulating microelectrodes fabricated from platinum-30% iridium (Pt-30%Ir) or activated iridium were implanted in assemblies of three in the left sensorimotor cortex of the cat and pulsed continuously at currents of 10 to 320 microA (100 to 3200 microC/cm2 X ph, 2 to 64 nC/ph) for periods of 24 h or for 23 h/day for 7 days. The microelectrodes had beveled tips with uninsulated geometric surface areas of 20 X 10(-6) cm2. Neuronal activity evoked by the focal stimulation was monitored by recording compound action potentials from the ipsilateral pyramidal tract. By this criterion neuronal activation thresholds were 5 to 15 microA (50 to 150 microC/cm2 X ph, 1 to 3 nC/ph) for both types of electrodes. Histologic evaluations of tissue surrounding the electrode tips were carried out by either light or electron microscopy. No neural damage was induced by 24 or 161 h of pulsing using either type of electrode at currents of 10 to 80 microA. Neural damage attributable to electrical stimulation per se was observed in a few sites pulsed with 320 microA (3200 microC/cm2 X ph, 64 nC/ph, 16 A/cm2) with Pt-30%Ir but not activated iridium electrodes of the same size. Electrode dissolution appears to be best correlated with charge density and current density. Dissolution of the Pt-30%Ir microelectrode tip was observed by scanning electron microscopy at charge densities as low as 200 microC/cm2 X ph (1 A/cm2), whereas erosion of activated iridium microelectrodes occurred only at the highest charge and current densities (3200 microC/cm2 X ph, 16 A/cm2). Thus, the activated iridium electrode is superior to Pt-30%Ir for chronic stimulations, from the standpoint of electrode tip stability, because with the former, in contrast to the alloy, detectable erosion occurred only at an intensity well above that required for activation of nearby neurons.

Animals↗
PubMed1979

Intracellular calcium deposition in brain following electrical stimulation.

The effects of electrical stimulation of the cat cerebral cortex have been evaluated by light and electron microscopy following a wide variety of stimulation parameters (QD/ph of 10 - 300 muC/cm2/ph). Platinum or rhodium disc electrode arrays were bilaterally implanted subdurally on the parietal cortex and subjected to 36-hour stimulations (9 hrs./day for 4 days). Prominent among the degenerative changes shown by electron microscopy were dense crystalline inclusions that were identified as calcium hydroxyapatite (CHA) crystals by electron diffraction and energy dispersive X-ray analysis. The appearance of intracellular calcification generally paralleled the onset of other degenerative changes in stimulated tissue, including gliosis, mitochondrial swelling, lipid inclusions, degenerating cells, neuronal loss, and phagocytic activity. A preferential deposition of calcium was noted in mitochondria of several cell types and in postsynaptic dendrites. The mechanism of the apparently electroresponsive calcium deposition is obscure; however, a plausible explanation is that increased cyclic AMP levels, known to occur with electrical stimulation of nervous tissue, result in enhanced calcium plasmalemmal permeability.

Animals↗
PubMed1979

Evaluation of electrode array material for neural prostheses.

Matrix support materials for brain surface electrodes used in neuroprosthetic applications were evaluated after chronic subdural implantation over the parietal cortex of the cat. Four types of array fabricated with Silastic, Dacron mesh, or platinum wire annuli were implanted for periods ranging from 5 weeks to 1 year. We evaluated the arrays by access resistance measurements and gross and histological observations of the tissue beneath both nonstimulated and stimulated electrodes. A porous type matrix constructed of Dacron mesh proved to be the superior design because of its minimal compression of the cortical surface, facility of handling during implantation and autopsy, and satisfactory electrical characteristics provided by a good electrode-brain interface. (Neurosurgery, 5: 681--686, 1979).

Animals↗
PubMed1977

Neuropathological effects of intracerebral platinum salt injections.

Multiple intracerebral injections of a mixture of platinum salts were made in 9 adult cats and the brains studied by light and electron microscopy at 5-12 days post injection. At the center of the lesions normal cortical architecture was completely replaced by edematous areas containing lipid-laden macrophages and cellular debris. The lesion periphery was characterized by perivascular edema and degenerative changes including cytoplasmic lipid inclusions and vacuolations with selective vulnerability of neurons. Membranous cytoplasmic bodies (MCB), zebra bodies and multiple nucleoli were observed in several cell types. This ultrastructural pattern, mimicked to some extent, that observed following electrical stimulation of brain following chronically implanted platinum and rhodium electrodes. The induction of zebra bodies and MCB, both of which are morphologic features of human neurolipidoses associated with congenital enzyme deficiencies, suggests an inhibitory effect of platinum on brain enzymes. Functional electrical stimulation of brain and other organs is currently being employed in a wide variety of clinical applications (14, 15). A mandatory consideration is that of the long-term effects of the stimuli as well as the electrodes themselves on the tissues involved. The histological effects and mechanisms of tissue damage following chronic application of electrical stimuli to brain have been the subject of several investigations in this laboratory (1, 14-18). Factors contributing to neural damage induced by electrical stimulation include noxious products resulting from electrode dissolution. In vitro studies employing electrochemical (3,9) and scanning electron microscopy (6) techniques have established that erosion of noble metal electrodes occurs, even when passing relatively small stimulation currents. Such electrode dissolution is of particular importance in long term applications of neural prostheses. The present study was initiated to assess the contribution of platinum electrode erosion products to neurla damage following electrical stimulation of brain, specifically to distinguish morphological changes resulting directly from electrode solubilization as opposed to electrical factors. Accordingly, intracerebral injections of graded volumes of platinum salts were made in an attempt to stimulate the presence of platinum electrode dissolution products.

Animals↗
PubMed1975

Electrical stimulation of the brain. IV. Ultrastructural studies.

The ultrastructural response of tissues of the cat's central nervous system to chronic electrical stimulation with various parameters has been evaluated at four and a half days post stimulation. Cellular alterations included widespread cytoplasmic vacuolations, architectural derangement and disruption of plasmalemma and other membranes. Lipid inclusions and dense crystalline bodies were prominent in astrocyte-like phagocytic cells in the more severe lesions. Despite endothelial damage in brain parenchymal capillaries, significant extravasation of horseradish peroxidase was not observed. The ultrastructural damage observed following electrical stimulation varied from mild to severe. Although none of the parameters tested was found to be "safe" for clinical applications, it should be emphasized that the stimulations delivered in the present study were essentially continuous.

Animals↗