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W K Dong

Publications and source records attributed to W K Dong.

30 records · Page 2Linked to original sources

Peak latency differences in evoked potentials elicited by painful dental and cutaneous stimulation.

Long-latency evoked potentials (EPs) (50-400 msec) have been obtained from humans during both noxious stimulation of tooth and cutaneous sites in studies of pain and analgesic states. This study investigated whether EPs elicited by tooth and lip stimulation differed in peak latency and whether EPs obtained during painful cutaneous stimulation showed increasing peak latency values with increased conduction distance. Twelve volunteers received painful electrical stimulation at four sites: tooth, lip, thumb, and toe in counterbalanced orders. Evoked potentials recorded at vertex were summation averaged over 128 trials. Multivariate stepwise discriminate analysis was used to determine whether any of the peak latencies of the event-related potentials differed across stimulation sites. No significant latency differences were observed across lip, thumb or toe at any of the major peaks. Since peaks of these EPs did not vary in latency with conduction distance, they appear to reflect processing at higher levels rather than sensory transmission. The negative 140 msec peak of the dental waveform occurred significantly later than the same peak at cutaneous sites.

Adult↗

Origins of tooth pulp-evoked far-field and early near-field potentials in the cat.

Electrical stimulation of the mandibular canine tooth pulp in barbiturate-anesthetized cats activated myelinated A-beta-fibers in the inferior alveolar (dental) nerve and evoked a complex pattern of short-latency potentials that were recorded epidurally from the cortex. Three far-field components ( FFPs designated I, IIa,b, and IIIa,b) and two early near-field components ( ENFPs designated P1 and N1) were identified from computer-averaged potentials recorded over the contralateral lateral sigmoid gyrus or ipsilateral presylvian /anterior coronal gyri. Several corroborative lines of evidence indicated that tooth pulp-evoked FFPs and ENFPs originate from the following generator sources: I, inferior alveolar (dental) nerve/semilunar (gasserian) ganglion; IIa,b, trigeminal lemniscal fibers from the principal (main) sensory nucleus; IIIa,b, thalamocortical fibers from the thalamic ventral posteromedial nucleus; P1, N1, cytoarchitectural area 3 on the banks of the coronal or orbital sulcus. The latencies and waveforms of volume-conducted, surface-recorded potentials were not significantly different from those recorded at putative generator sites along the trigeminal lemniscal projection system. The short latencies and distribution of surface- and depth-recorded tooth pulp-evoked potentials suggested bilateral, trisynaptic paths from peripheral nerve to cortical neurons. Amplitude measurements of FFPs and ENFPs recorded at the cortical, epidural surface were compared to calculated values based on a mathematical model of two concentric spheres of inhomogeneous media in which a single equivalent dipole is radially oriented at some distance from the center. The morphology and distribution of FFPs and ENFPs are discussed in relationship to source geometry. Surface- and depth-recorded tooth pulp-evoked potentials had recovery functions that were covariant with rates of stimulation. In addition, stimulation of putative generator sites along the trigeminal lemniscal system reproduced portions of the tooth pulp-evoked surface-recorded potentials. Selective ablation of trigeminal cortical area 3 abolished ENFPs and lesions of lemniscal brain stem sites abolished FFPs . Disruption of extralemniscal brain stem sites had no effect on the surface-recorded evoked potentials examined. These findings and other supporting evidence from previous studies imply that the projection of fast-conducting tooth pulp input to the cortex may subserve a nonnociceptive modality and participate in sensorimotor integration.

Afferent Pathways↗

Autoradiographic location of sensory nerve endings in dentin of monkey teeth.

We have used the autoradiographic method to locate trigeminal nerve endings in monkey teeth. The nerve endings were labeled in two adult female Macaca fascicularis by 20 hours of axonal transport of radioactive protein (3H-L-proline). We found a few labeled axons in contralateral mandibular central incisors and one mandibular canine. In ipsilateral teeth, numerous myelinated and unmyelinated axons were labeled; they formed a few terminal branches in the roots but primarily branched in the crown to form the peripheral plexus of Raschkow and to terminate as free endings in the odontoblast layer, predentin, and as far as 120 micrometers into dentinal tubules. Electron microscopic autoradiography showed that the radioactive axonally transported protein was confined to sensory axons and endings; odontoblasts and dentin matrix were not significantly labeled. Labeled free nerve endings were closely apposed to odontoblasts in dentin but did not form distinctive junctions with them. Nerve endings were most numerous in the regular tubular dentin of the crown adjacent to the tip of the pulp horn, occurring in at least half of the dentinal tubules there. Reparative dentin was poorly innervated, even near the tip of the crown, and it had a different tubular structure and adjacent pulpal structure from the innervated dentin. Radicular dentin was not innervated in most areas but did contain a few labeled axons where the predentin was wide and the odontoblasts were columnar, as at the buccal and lingual poles of some roots. Our results show tha dentinal sensory nerve endings in primate teeth can be profuse, sparse, or absent depending on the location and structure of dentin and its adjacent pulp. When dentin was innervated, the tubules were straight and contained odontoblast processes, the predentin was wide, the odontoblast cell bodies were relatively columnar, and there was an adjacent cell-free zone and pulpal nerve plexus.

Animals↗

Profound arterial hypotension in dogs: brain electrical activity and organ integrity.

To determine whether non-invasive measurement of brain electrical activity can predict ischemic brain damage, we recorded the electroencephalogram (EEG) and somatosensory- (SEP) and auditory- (AEP) evoked potentials before, during, and after trimethaphan-induced profound arterial hypotension in dogs. The authors set out to compare the change in electrical activity with the degree of brain damage, as determined by microscopic examination. Dogs were anesthetized with halothane (1.4 vol % inspired), maintained horizontal (head at the level of the heart), and ventilated mechanically (FIO2 0.50); deviations from normal acid-base status were corrected. Twenty animals received a 1.5-mg/kg intravenous bolus of trimethaphan. Three animals were resistant to the drug. The remaining animals had profound hypotension [mean arterial blood pressure (MABP) at some steady level between 12 and 25 mmHg] for 1 h. Eight of these animals died during or soon after the hypotensive period as a consequence of cardiac arrest (three), intestinal bleeding (three) or unknown causes (two). In all survivors, EEG intensity and the amplitude of the SEP decreased during hypotension; both variables recovered with restoration of MABP. All nine animals surviving hypotension had no apparent neurologic or behavioral deficit nor any histologic evidence of ischemic brain cell injury. We were thus unable to find a MABP threshold for brain with minimal brain injury. Our findings suggest, under the conditions of our experiments, a great margin of tolerance for profound hypotension by the brain in this species. Other organ systems--the heart, gastrointestinal tract, and liver--proved to be more susceptible to ischemic damage. Eight of the nine surviving animals had elevations in serum alanine transaminase (SGPT), aspartate transaminase (SGOT), and alkaline phosphatase. Animals with the greatest increases in these enzymes showed centrilobular hepatocyte degeneration.

Animals↗

Trigeminal evoked potentials: origins in the cat.

Short latency brain stem (far-field) and cortical (early-field) potentials were evoked by stimulation of the main nerve epidurally over the primary sensorimotor cortex. The specific generators of these volume conducted potentials were identified from both lesion and recording studies in the trigeminal lemniscal system. Far-field components I, II and III, respectively, originate from the semilunar ganglion, trigeminal lemniscus and thalamocortical radiation; whereas early near-field components P1 and N1 originate from the cortical cell layers.

Action Potentials↗

Origins of cat somatosensory far-field and early near-field evoked potentials.

A complex pattern of potentials evoked by forelimb cutaneous nerve stimulation was recorded from the skull surface of barbiturate anesthetized cats and was resolved by computer averaging. Seven far-field components (designated I-VII) and several larger early near-field components (designated P1, N1, P2, N2 and P3) have been identified from averaged potentials. All far- and early near-field components were elicited by activation of myelinated nerve fibers. Their latency and amplitude depended entirely on the number of large myelinated nerve fibers recruited into the nerve volley. Spinal lesions showed that peripherally evoked far- and early near-field potentials were generated from both lemniscal and extralemniscal sources. Far-field and early near-field potentials were evoked either from the lemniscal system by dorsal column stimulation or from the extralemniscal system by cutaneous nerve stimulation after dorsal column lesions. These potentials were similar in configuration to those evoked by cutaneous nerve stimulation in the intact cat. Sequential rostral to caudal ablations and lesions within the lemniscal or extralemniscal system eliminated the potentials selectively. The following sites of origin were proposed: I--peripheral nerve; II (IIa)--dorsal columns; IIb--spinothalamic tract; III--dorsal column nuclei or medial lemniscus; III, IV--spinocerebellar and spinoreticular tracts; V--lateral reticular nucleus or reticulocerebellar tract; VI, VII--cerebellum; P1--lateral and medial thalamic nuclei or thalamocortical projections; N1, P2--sensorimotor cortical areas; N2, P3--association cortical areas. Lemniscal and extralemniscal far- and early near-field potentials were generated from common as well as separate sites. The latencies of somatosensory far- and early near-field potentials recorded extracranially in this study closely correlated with the latencies of local potentials recorded by others at the proposed lemniscal and extralemniscal sites of origin. The contribution of extralemniscal sources to far- and early near-field potentials and their importance to clinical measurement of somatosensory evoked potentials and diagnosis of neurological disorders are discussed.

Afferent Pathways↗

Nociceptive responses of neurons in medial thalamus and their relationship to spinothalamic pathways.

1. An extracellular study of the cat medial thalamus has revealed four types of somatosensory neurons. These were located primarily in the n. parafascicularis, n. subparafascicularis, and n. centralis lateralis; none were found in the n. centrum medianum. There was no functional segregation of neurons within each nucleus or between nuclei. Each type of neuron had large and often bilateral receptive areas. No somatotopic organization of neurons was found within the medial thalamus. 2. Noxious (N) and noxious-tap (NT) neurons comprising 72% of the sample (78 of 109 total) were considered to be nociceptive. N cells responded exclusively to noxious mechanical stimulation of skin, muscle fascia, tendons, and joints, and to direct stimulation of A-delta- and C-fiber groups in cutaneous, articular, and muscle nerves. NT cells responded to noxious and tap stimulation in a differential manner and to stimulation of the entire spectrum of A- and C-fibers. N and NT cells accurately signaled the duration of noxious mechanical stimulation. Their nociceptive responses were also graded as a function of both noxious stimulus intensity and the number of activated A-delta- and C-fibers. Stimulation of A- and C-fibers evoked, respectively, an inital burst and a late burst of discharges. A brief period of inhibition intervened between the initial and late bursts of NT cells. Prolonged afterdischarge was often observed following noxious natural stimulation or stimulation of A-delta- and C-fibers. The phenomenon of discharge "windup" was observed during iterative stimulation of C-fibers. 3. Tap (T) neurons (10%) responded only to brisk but innocuous taps applied to skin or underlying tissue. These cells were driven only by activation of A-alpha- and A-beta-fibers. The response to such stimulation was seen as an initial burst of discharges followed by an inhibitory period. 4. Inhibited (I) neurons (18%) had resting discharges that were inhibited by noxious stimuli and stimulation of A-beta- and C-fiber groups. 5. The results obtained from monitoring the peripherally evoked responses of nociceptive N and NT neurons before and after selective lesions of the spinal cord strongly suggested that the spinothalamic tracts were the only spinal projections mediating A- and C-fiber input to these cells. Each spinothalamic tract apparently carried information originating from both sides of the body.

Animals↗

Nociceptive responses of neurons in the posterior group of nuclei and medial thalamus.

Anatomical studies have shown that fibers of the spinothalamic tract terminate in both the posterior group of nuclei (PO) and the nuclei of the medial thalamus. Only the PO receives fiber terminations from the spinocervicothalamic and dorsal column-medial lemniscal projections. This difference in connectively is reflected in the functional differences between the neurons in the PO and those in the medial thalamus. Although both PO and medial thalamus contain a large proportion of nociceptive neurons, only the PO contains neurons that have "lemniscal" response properties. Lesion studies have demonstrated the importance of the spinothalamic tract in mediating A and C fiber input to nociceptive neurons in the PO and medial thalamus. These studies showed that the nociceptive neurons in PO also receive A fiber input from the dorsal column-medial lemniscal projection and A and C fiber input from the spinocervicothalamic projection.

Afferent Pathways↗

Possible physiological bases for acupuncture analgesia.

Neurophysiological studies of electrical responses of single cells at various levels of the nervous system to noxious and non-noxious stimulation may give clues regarding acupuncture analgesia. Many cells show convergent properties receiving input from both low and high threshold cutaneous and peripheral nerve stimulation. Often the former may inhibit the latter. Our studies illustrate three examples of inhibition mechanisms which may play a role in attenuation of noxiously induced impulses, especially the prolonged discharge. Discussed briefly are othe suggested CNS mechanisms that may be involved in processing and attenuating noxious information, including those in brainstem and intralaminar nuclei.

Acupuncture Therapy↗