Electrical stimulation, given daily with a short pulsed, asymmetric biphasic waveform, was effective for enhancement of healing rates for patients with diabetes and open ulcers.

Various electrical stimulation waveforms have been used to enhance wound healing, with little consideration for potential differences in their physiologic effect. The present study evaluated the effect of stimulation waveform and electrode placement on wound healing. Eighty patients with spinal cord injury and one or more pressure ulcers were treated. A total of 185 ulcers received 45 minutes of stimulation daily. Each ulcer was subjected to one of four treatment protocols: asymmetric biphasic waveform, symmetric biphasic waveform, microcurrent stim-ulation, or a sham control protocol. Electrodes were placed outside the wounds, over intact skin and surrounding the area of the ulcer. Data were categorized by ulcers which healed during the protocol and those which did not. Analysis of the "good response" ulcers (n = 104) showed significantly better healing rates for those receiving stimulation with the asymmetric biphasic waveform, compared with the control and microcurrent groups. Mean healing rates from the present study were similar to previously reported measures. The waveforms studied possessed minimal polar capabilities, and the electrodes were placed outside the wound. These data show that electrical stimulation clearly enhanced healing of pressure ulcers in a significant number of individuals with spinal cord injury; the physiologic implications of these findings relative to the mechanism(s) by which electrical stimulation enhances wound healing are discussed. However, extrapolation of these results to patients with other types of wounds must await further study.

1. The influence of age on striatal neuron Ca2+ physiology was studied through an analysis of intracellularly recorded Ca(2+)-mediated plateau potentials. In vitro brain slices from young and aged rats were treated with the K+ channel blocker tetraethylammonium (30 mM) to facilitate the expression of plateau potentials. A sample of neurons was also filled with biocytin and post hoc correlations were performed between morphology and physiology. 2. Testing of sampling parameters in neurons from young rats revealed that tetrodotoxin did not affect the amplitude or duration of plateau potentials. The membrane potential induced during plateau testing and the rate of plateau potential generation, however, had to be held constant because these variables affected plateau potential duration. 3. A significant age-related decrease was found in the duration of Ca(2+)-mediated plateau potentials that could not be explained by alterations in the activation or inactivation properties of the plateau potential. Investigation into relationships between cell morphology and plateau potential duration revealed a number of correlations. Soma size and dendritic length were correlated with plateau potential duration, independent of age (hierarchical regression), and an age-related decrease in dendritic length but not in soma size was found. Spine density and plateau potential duration were also correlated, but the significance depended on the variance associated with age. These data indicate that the extent of somadendritic membrane (including spines) affects plateau potential duration in striatal neurons and that dendrite and spine loss in aged animals may contribute to age-related decreases in plateau potential duration. 4. The response to replacement of Ca2+ with Ba2+ was age dependent, with Ba2+ causing a greater increase in the duration of plateau potentials in young neurons. These data rule out an increase in Ca(2+)-mediated inactivation of Ca2+ channels as a primary cause for the shortening of plateau potentials in aged neurons. Our morphological findings suggest that dendritic regression in aged neurons may have reduced the number of Ca2+ channels participating in plateau potential generation, but other mechanisms related to changes in the type of Ca2+ channel expressed and possible differences in their inactivation kinetics may also contribute to the age-related change in plateau potential duration.

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