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R D Foreman

Publications and source records attributed to R D Foreman.

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Effects of dorsal column stimulation on primate spinothalamic tract neurons.

The effect of dorsal column stimulation on spinothalamic tract cells was investigated in anesthetized monkeys. The dorsal column stimuli were applied at midthoracic or at cervical levels of the cord, while the responses of spinothalamic tract cells of the lumbosacral enlargement were examined. A dorsal column volley depressed the activity of spinothalamic tract cells for about 150 ms. A similar depression was observed whether the spinothalamic tract cell was classified as hair activated, low, or high threshold, based on its response properties to cutaneous stimulation. The hair-activated and low-threshold spinothalamic tract cells were initially excited by the dorsal column volley, but often it was possible to demonstrate that a depression could be produced by stimuli which were too weak to cause excitation of these cells. Depression was produced both of the responses of spinothalamic tract cells to electrical stimulation of peripheral nerves and to mechanical stimulation of cutaneous nociceptors. A similar depression was produced by electrical stimulation of large afferents in peripheral nerves. The pathway mediating the depression of spinothalamic tract cells was shown to involve antidromic invasion of collaterals of dorsal column fibers. The best points for stimulation of the cord to produce a depression were over the ipsilateral dorsal column. A lesion interrupting the dorsal column eliminated the depression of cells below the lesion, whereas a lesion of much of the lateral column had no effect. The mechanism of the depression is likely to be complex. Apart from interactions at an interneuronal level, dorsal column volleys can be presumed to collide with sensory input from afferents which project up the dorsal column; collision would interfere chiefly with the responses of hair-activated and low-threshold spinothalamic tract cells. In addition, dorsal column volleys were shown to evoke inhibitory postsynaptic potentials in some spinothalamic tract neurons, and they also produced primary afferent depolarization, at least of large cutaneous afferemts. The excitation of hair-activated and low-threshold spinothalamic tract cells argues against their participation in signaling pain, since dorsal column stimulation in humans does not produce pain at stimulus intensities and frequencies which should activate such neurons. Alternatively, an ascending volley in the dorsal column or in other pathways may interfere with pain transmission in the brain.

Animals↗

Conduction in descending spinal pathways initiated by somatosympathetic reflexes.

In anesthetized, paralyzed cats, the effects of stimulation at the dorsolateral sulcus (DLS) of the spinal cord at the C8 segment were recorded from the T2 white ramus. Stimulation of the DLS at the C8 segment produced evoked responses which had average conduction latencies of 13.3, 25.8, and 43.4 ms and were designated as the early, intermediate, and late response, respectively. Intermediate and late evoked responses were also recorded when the contralateral funiculus, the third or late evoked response was abolished or greatly attenuated, but the intermediate response was still observed although it was diminished in amplitude. The early evoked response was usually observed with stimulation at the ipsilateral C8 segment following placement of the lesion. These data suggest that afferent impulses, which ascend to supraspinal segments of the central nervous system, are transmitted to preganglionic neurons of the sympathetic nervous system through descending pathways in the dorsolateral funiculus of the spinal cord. Stimulation of afferent fibers on the ipsilateral or contralateral side of the spinal cord produces volleys which ascend unilaterally and descend bilaterally to preganglionic neurons. The pathways producing the intermediate evoked response, which was still observed after an ipsilateral lesion was made in the spinal cord, may include both the ascending pathway and other connections with the preganglionic neurons.

Animals↗

Responses of primate spinothalamic tract neurons to electrical stimulation of hindlimb peripheral nerves.

The responses of spinothalamic tract neurons were studied by extra- and intracellular recordings from the lumbosacral spinal cord in anesthetized rhesus monkeys (Macaca mulatta). The neurons were identified by antidromic activation from the contralateral diencephalon. They were then classified by the mildest form of mechanical stimulation applied to the ipsilateral hindlimb. The effects of electrical stimulation of the nerve(s) supplying the receptive field were investigated. Graded electrical stimulation revealed that the threshold responses of spinothalamic tract neurons excited by weak mechanical stimuli occurred when the largest afferent fibers were activated. On the other hand, neurons that required intense mechanical stimulation for their excitation tended to have higher thresholds to electrical stimulation. Some spinothalamic tract cells were shown to receive monosynaptic excitatory connections from peripheral nerve fibers, although polysynaptic connections may generally be more important. An input from unmyelinated afferent fibers was demonstrated. It is concluded the primate spinothalamic tract neurons receive a rich convergent input from a variety of cutaneous receptors. The experiments provide some evidence for the most likely types of receptors.

Animals↗

Organization and receptive fields of primate spinothalamic tract neurons.

A technique is described for recording from axons belonging to the spinothalamic tract of the monkey. The axons arose from cell bodies located within the spinal cord since the latency of orthodromic activation by afferents within the dorsal funiculus was short. The axons were antidromically activated from the ipsilateral diencephalon. The spectrum of conduction velocities indicates that the recordings favored large-diamter axons. However, all of the classes of spinothalamic tract units described from soma-dendritic recordings were represented in the sample. When the locations of the axons in the ventrolateral white matter were mapped, there was virtually complete overlap in the distributions of hair-activated, low-, and high-threshold spinothalamic tract axons, suggesting that the "lateral spinothalamic tract" conveys tactile, as well as pain and temperature, information. The only segregated population of axons were those belonging to units activated by receptors in deep tissues, including muscle. These were in a band along the ventral surface of the cord. The stimulus points for antidromically activating spinothalamic cells of axons were in the known diencephalic course of the spinothalamic tract, including the ventral posterior lateral nucleus. Stimulus point locations were similar for high-threshold and other categories of units. Receptive-field sizes were smaller for high-threshold spinothalamic cells or axons than for hair-activated or low-threshold units. Receptive-field size was correlated with position on the hindlimb. The smallest fields belonged to cells in lamina I, with progressively larger sizes for cells in laminae IV and V. Receptive-field shape was evaluated by the length/width ratio, which was smallest for high-threshold units and progressively larger for low-threshold and hair-activated units. The receptive-field positions of spinothalamic tract axons were related to the locations of the axons. There was a rough somatotopic representation in the tract, with the most caudal dermatomes represented dorsolaterally, and the most rostral ventromedially.

Animals↗

Static and dynamic responses of spinothalamic tract neurons to mechanical stimuli.

The activity of primate spinothalamic tract neurons was investigated. Units were identified by antidromic activation from the diencephalon. Most had a spontaneous discharge. The fastest spontaneous discharge rates were from neurons activated by receptors in muscles or joints. However, such activity could be decreased by repositioning the hindlimb. Spontaneous activity was also altered by changes in anesthetic level. Time-interval histograms demonstrated the patterns of spontaneous discharge. Many units could be excited by noxious stimulation. Graded step displacements of the skin often evoked a slowly adapting discharge which was a function of pressure (or displacements above a threshold of some hundreds of microns). Responses continued to increase as pressures became noxious. Rapidly adapting responses of hair-activated and low-threshold spinothalamic tract neurons were tested with ramp stimuli and found to signal acceleration (or a higher derivative of position), velocity, or a combination of these. Responses to stimulus acceleration were prominent when hairs were displaced, while responses to stimulus velocity were seen with displacement of the skin. Possible receptor types which might account for the observations are discussed.

Action Potentials↗

Heart rate--QT relationships during baroreceptor stimulation with diminished autonomic influence on the ventricles. Ventricular autonomic tone and QT interval.

The shortening of the QT interval of the electrocardiogram coincident with acceleration of heart rate and vice versa has been accepted for many years as evidence that the action potential duration and hence QT are necessarily dependent on heart rate. Exceptions to this rule have been attributed to the intervention of counteracting autonomic effects. In order to test this assumption, 26 conscious dogs divided into three groups were tested during baroreceptor stimulation by a bolus injection of phenylephrine. Seventeen dogs had been used in earlier studies in which they had undergone an experimental anterior myocardial infarction with apparent full recovery. A group of those dogs underwent beta-adrenergic blockade by intravenous atenolol 30 min prior to the baroreceptor activation. To test the intactness of the baroreceptor responses in the previously infarcted dogs, a third group of nine dogs that had had no prior myocardial infarction was included. All dogs were adapted to the laboratory environment and were not sedated during experiments. Simultaneous recordings of RR, QT interval, and phasic arterial pressure were made in all dogs before and during baroreceptor stimulation. In the normal group, and the previously infarcted group that received no atenolol, baroreceptor stimulation elicited a small (8/msec), but significant prolongation of the QT associated with a nearly 50% reduction in heart rate. The QT interval of the atenolol-treated dogs, although significantly more prolonged before stimulation, remained unchanged during the reflex. The data indicate that withdrawal of ventricular sympathetic tone may prolong the QT interval, thereby confirming the role of sympathetic innervation in the control of QT.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Emerging clinical applications of electrical stimulation: opportunities for restoration of function.

Emerging clinical application of electrical stimulation in three systems is reviewed. In the bladder, stimulation of sacral posterior roots reduces reflex incontinence and significantly improves bladder capacity. With the combination of anterior and posterior root stimulation, bladder control can be achieved without the need for rhizotomy. Preliminary research demonstrates that bladder contractions may also be generated by stimulation of the urethral sensory branch of the pudendal nerve, even after acute spinal cord transection, while inhibition of the bladder and control of urge incontinence can be achieved by stimulation of the whole pudendal nerve. Spinal cord stimulation can modulate the activity of the intrinsic cardiac nervous system involved in the regulation of regional cardiac function and significantly reduce the pain associated with angina pectoris. Finally in the area of upper airway disorders, functional electrical stimulation has great potential for increasing life support as well as for quality of life in chronic ailments, particularly obstructive sleep apnea and dysphagia.

Angina Pectoris↗