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T J Ness

Publications and source records attributed to T J Ness.

43 records · Page 3Linked to original sources
PubMed1987

Contribution of the site of heating to variability in the latency of the rat tail flick reflex.

The rat tail flick reflex is a commonly used assay of thermal nociception. Variability in the latency to respond due to the locus of tail heating was examined in spinalized (midthoracic) rats and evaluated retrospectively using data from two previously published studies. In all 3 sets of data, a significant relation was found between the proximal-distal site of heating on the tail and the latency of the tail flick reflex. Heating of the most distal sites resulted in shortest response latencies.

Animals↗
PubMed1987

A distension control device useful for quantitative studies of hollow organ sensation.

Quantitative studies of visceral nociception have been limited due to the lack of an easily controlled, reproducible stimulus. Distension of hollow viscera is painful in humans. The device described here allows control over a phasic distending stimulus satisfactory for quantitative neurophysiologic, behavioral or pharmacologic studies.

Air Pressure↗
PubMed1987

Characterization of neuronal responses to noxious visceral and somatic stimuli in the medial lumbosacral spinal cord of the rat.

The cutaneous receptive fields, long ascending projections, and responses to colorectal distension (20-100 mmHg) and tail movement of 252 neurons in spinal segments L6-S1 were characterized in pentobarbital- or halothane-N2O anesthetized, physiologically intact male rats. Seventeen additional neurons were studied in spinalized rats. Neurons studied were located within 0.5 mm of the midline at depths 0.2-1.4 mm from the spinal cord dorsum and included the area immediately dorsal and lateral to the central canal. Colorectal distension and/or antidromic invasion from the contralateral ventral quadrant of the cervical spinal cord were used as search stimuli. One hundred seventeen neurons responded to noxious colorectal distension; many had long ascending projections and convergent somatic input from deep joint receptors, ipsilateral perianal/scrotal cutaneous receptive fields, or both. Stimulus-response functions (SRFs) of 45 neurons to graded colorectal distension were linear, allowing extrapolation of threshold distending pressures to neuronal response. Neurons responsive to colorectal distension were subdivided into four classes based on their initial response colorectal distension (75-80 mmHg, 20 s). Short-latency abrupt (SL-A) neurons were excited at short latency by colorectal distension; activity abruptly returned to base line following termination of distension. Most SL-A neurons had long ascending projections, convergent somatic receptive fields, and 4/6 tested were excited by bradykinin administered intraarterially. The threshold distending pressure, estimated from the SRFs of 19 SL-A neurons, extrapolated to 2.7 mmHg. Short-latency sustained (SL-S) neurons were also excited at short latency by colorectal distension, but responses were sustained for 4-120 s following termination of distension. Most SL-S neurons had long ascending projections, convergent somatic receptive fields, and 18/20 tested were excited by intraarterial bradykinin. The threshold distending pressure, estimated from the SRFs of 20 SL-A neurons, extrapolated to 17.0 mmHg. Long-latency (LL) neurons were excited by colorectal distension at long latency following the onset of distension. No LL neurons had demonstrable long ascending projections, and few had convergent excitatory somatic fields. Three of five LL neurons were excited by intraarterial bradykinin. The threshold distending pressure, estimated from the SRFs of six LL neurons, extrapolated to 9.8 mmHg. Inhibited (INHIB) neurons were spontaneously active and were inhibited by colorectal distension.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1987

Quantitative comparison of inhibition of visceral and cutaneous spinal nociceptive transmission from the midbrain and medulla in the rat.

1. The descending inhibition of neuronal responses by focal electrical stimulation or glutamate microinjections in the periaqueductal gray (PAG) or rostral ventromedial medulla (RVM) was quantitatively studied on 61 spinal neurons in halothane-N2O-anesthetized paralyzed rats. Thirty-six neurons were located in the medial L6-S1 spinal cord and were consistently and reproducibly excited by distension of the descending colon and rectum (75 mmHg). Twenty-five other neurons were located in the dorsal horn of spinal segments L3-L5 and were consistently and reproducibly excited by radiant heating (50 degrees C) of the glabrous skin of the plantar surface of the left (ipsilateral) hind foot. 2. The inhibition of neuronal responses to colorectal distension by stimulation in the PAG or RVM differed quantitatively when examined on the same spinal neurons. Inhibition of neuronal responses to distension occurred at a lower mean threshold of stimulation in the RVM than in the PAG. The mean intensity of stimulation in the RVM producing an attenuation to 50% of the control response to colorectal distension (75 mmHg, 20 s) was significantly lower than the mean intensity of stimulation in the PAG producing a 50% attenuation of the same spinal units. The mean magnitude of inhibition produced by stimulation in the RVM was significantly greater than that produced on the same spinal units by the same intensity of stimulation in the PAG. However, stimulation in the RVM and PAG produced the same mean percent change in inhibition per 25-microA increase in the intensity of stimulation. Thus the slopes of the lines of recruitment of descending inhibition from the PAG and RVM as a function of increasing intensities of stimulation are the same; the lines of recruitment of inhibition are parallel. These findings are virtually identical to those found by others in studies of modulation of neuronal responses to noxious heating of the skin. 3. Neuronal intensity coding to both graded heating of the hindfoot and graded colorectal distension was montonus and accelerating and could be expressed as linear stimulus-response functions (SRFs) in the temperature and pressure ranges studied (46-52 degrees C, 25-100 mmHg). Stimulation in the PAG modulated the SRFs differently than did stimulation in the RVM. Stimulation in the PAG decreased the slope of the SRFs without affecting the units' thresholds of response, thus influencing the gain control of both cutaneous and visceral nociception in the spinal cord.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1986

Centrifugal modulation of the rat tail flick reflex evoked by graded noxious heating of the tail.

Centrifugal modulation from the midbrain, pons and medulla of the spinal nociceptive tail flick (TF) reflex evoked by graded noxious heating of the tail was studied in lightly pentobarbital-anaesthetized rats. In initial experiments, the relationship between the intensity of the noxious thermal stimulus and the TF latency was characterized. The thermal stimulus was provided by a lamp focused on the ventral surface of a rat's tail. Five different rates of heating of the tail were varied systematically by altering the voltage supplied to the lamp and were characterized using a thermocouple to measure the temperature of tissue exposed to the radiant heat. A linear stimulus-response function relating the inverse of the latency of the TF to the rate of heating of the tail was established. However, the mean cutaneous tissue temperature of the exposed tail at the time of the TF was found to be invariant and independent of the rate of heating. Focal electrical stimulation in the midbrain, pons and medulla modulated the TF reflex in two different ways, analogous to modulations of stimulus-response functions of single-cell recordings of spinal dorsal horn neurons. A Type I modulation, analogous to the parallel shift in response threshold seen in spinal dorsal horn neurons, was an absolute increase in the thermal threshold of the TF reflex. A Type II modulation, analogous to a change in slope or gain seen in spinal dorsal horn neurons, was a linear increase in the thermal threshold of the TF reflex as a function of the rate of heating. Type I modulations were produced by electrical stimulation in the ventromedial medulla (n. raphe magnus and n. reticularis gigantocellularis) and lateral periaqueductal gray of the midbrain. Type II modulations were produced by electrical stimulation in the dorsolateral pons, locus coeruleus-subcoeruleus and in the medial periaqueductal gray. This experimental approach has shown itself to be useful in the characterization of descending inhibition of nociception. Much simpler and less invasive than analogous spinal dorsal horn single cell electrophysiologic studies, it can be used to study the mechanisms of centrifugal modulation of nociceptive flexion reflexes and further establishes the utility of the lightly anaesthetized rat preparation for studies of nociception-antinociception.

Animals↗
PubMedDate not supplied

Long-term use of gabapentin for treatment of pain after traumatic spinal cord injury.

OBJECTIVE: To determine the long-term efficacy of gabapentin as a treatment of pain after spinal cord injury. DESIGN: All patients with traumatic-onset spinal cord injury treated with gabapentin were identified and followed up using a longitudinal observational design with two contact points (6 and 36 months after the trial) using a semi-structured interview. The first follow-up interview attempted to capture all 31 patients placed on therapeutic trial. The second follow-up interview attempted to capture those reporting a favorable response (n = 14) to the therapeutic trial at the first follow-up. RESULTS: Of the 27 patients contacted at the first follow-up (87% response rate), 6 (22%) discontinued the trial secondary to intolerable side effects; therefore, the pain analgesic effects of gabapentin in these patients could not be determined. Of the remaining 21 patients, 14 (67%) reported a favorable response (i.e., a 2 or greater point reduction on a 0-10 pain-rating scale). The second follow-up interview captured 11 (79% response rate) of the 14 patients reporting a favorable response at the first interview, and 91% (10 of 11 patients) continued to report that gabapentin was an effective analgesic. There was no evidence to suggest dosing difficulties due to tolerance over the 3-year period. Sedation, dizziness, and forgetfulness were the most common side effects. CONCLUSIONS: Gabapentin may be an effective treatment of pain after spinal cord injury among those able to tolerate initial and long-term side effects.

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