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Biomedical subjects

H L Fields

Publications and source records attributed to H L Fields.

At least 127 records · Page 7Linked to original sources
PubMed1979

Role of pain in placebo analgesia.

The hypothesis that perceived pain intensity can influence placebo analgesia was tested. One hundred and seven subjects rated their pain from from 0 to 10 on a visual analog scale after a standard wisdom tooth extraction. The expected course of such postoperative pain in the absence of therapy or placebo is a steady increase; this was confirmed by blind administration of the placebo. When placebos were given intravenously in view of the patients, some (placebo nonresponders) reported that their pain increased, whereas others (placebo responders) reported that their pain either decreased or remained the same over the next 60 min. A placebo response was more likely to occur if the pain rating 5 min prior to placebo administration (initial pain) was greater than 2.6. Furthermore, placebo responders with initial pain above this 2.6 level reported significantly greater mean analgesia than those with lower initial pain. Indeed, responders with initial pain less than 2.6 reported no change in pain during the 60 min after administration of a placebo. When their initial pain level was greater than 2.6, they reported a steady decline in pain over this period. However, above the 2.6 level there was no obvious relationship between the magnitude of the placebo analgesia and the initial pain.

Analgesia↗
PubMed1979

Segmental and descending influences on intraspinal thresholds of single C-fibers.

1. The effect was studied of various conditioning stimuli on the threshold of single C-fibers near their spinal terminals. Spikes were recorded in L6 and L7 dorsal root ganglia of cats. A stimulating electrode in the superficial dorsal horn delivered periodic pulses whose widths were adjusted automatically to near threshold for antidromic spike production. Most units were classified according to their adequate cutaneous stimuli, as C-mechanoreceptors, high-threshold mechanoreceptors, or polymodal nociceptors. 2. Orthodromic activity in all units increased their threshold for up to several minutes; the maximum and rate of decay depended on the amount of activity. This phenomenon parallels the hyperpolarizing afterpotential of C-fibers in peripheral nerve and, we suggest, is probably due to the aftereffect of impulses. 3. Cutaneous conditioning stimuli were applied for 10-20 s near the receptive fields of tested units, but without activating them. During the brushing of skin hair, all threshold changes were decreases; during pinching most changes were increases; during noxious heating the numbers of increases and decreases were similar. It will be necessary to analyze the responses of postsynaptic cells in order to know the physiological significance of these threshold changes. 4. Stimulation in the nucleus raphe magnus caused in half the units higher intraspinal thresholds. If this result is causally related to the previously reported inhibition of neuronal responses in the dorsal horn by the nucleus raphe magnus (NRM), then increased thresholds could reflect either direct presynaptic inhibition or facilitation of inhibitory connections. 5. No correlation between receptive-field classification and the response of terminals to natural cutaneous stimulation or stimulation of the NRM could be discovered. However, the terminals of all kinds of C-fibers differ from A-fibers in their reaction to noxious cutaneous and NRM stimulation, suggesting they are subject to a different system of control.

Animals↗
PubMed1978

The mechanism of placebo analgesia.

The effect of naloxone on dental postoperative pain was studied to examine the hypothesis that endorphins mediate placebo analgesia. All patients had extraction of impacted mandibular third molars with diazepam, N2O, and local block with mepivacaine. 3 h and 4 h after surgery naloxone or a placebo was given under randomised, double-blind conditions. Pain was evaluated on a visual analogue scale. Patients given naloxone reported significantly greater pain than those given placebo. Patients given placebo as their first drug was either placebo responders, whose pain was reduced or unchanged, or nonresponders whose pain increased. Naloxone given as a second drug produced no additional increase in pain levels in nonresponders but did increase pain levels of placebo responders. Nonresponders had a final mean pain rating identical to that of responders who received naloxone as their second drug. Thus the enhancement of reported pain produced by naloxone can be entirely accounted for by its effect on placebo responders. These data are consistent with the hypothesis that endorphin release mediates placebo analgesia for dental postoperative pain.

Adolescent↗
PubMed1978

Endogenous pain control mechanisms: review and hypothesis.

The anatomy, physiology, and pharmacology of an intrinsic neural network that monitors and modulates the activity of pain-transmitting neurons is reviewed. This system can be activated by opiate administration or by electrical stimulation of discrete brainstem sites. Evidence is presented that its pain-suppressing action is mediated in part by endogenous opiatelike compounds (endorphins). This pain suppression system is organized at three levels of the neuraxis: midbrain, medulla, and spinal cord. Activation of neurons in the midbrain periaqueductal gray matter (by electrical stimulation, opiates, and possibly psychological factors) excites neurons of the rostral medulla, some of which contain serotonin. The medullary neurons, in turn, project to and specifically inhibit the firing of trigeminal and spinal pain-transmission neurons. As part of a negative feedback loop, the output of the pain transmission neurons, i.e., pain itself, is an important factor in activating the pain-suppression system. A neural model which incorporates the experimental findings is proposed, and the clinical implications of the model are discussed.

Analgesia↗
PubMed1978

Evidence that raphe-spinal neurons mediate opiate and midbrain stimulation-produced analgesias.

The present experiments were undertaken to assess the role of neurons in the nucleus raphe magnus (NRM) in mediating opiate and stimulation-produced analgesias. A cannode for both electric stimulation and local opiate microinjection was placed in the midbrain preiaqueductal gray region of decerebrate or chloralose-urethane anesthetized cats. Microelectrodes recorded the responses of medullary NRM neurons. Raphe-spinal neurons were identified by antidromic activation from the cerevical spinal cord. Fifteen of 20 raphe-spinal cells tested were excited by electrical stimulation of the midbrain. Of 49 NRM neurons tested, 26 were excited by either systemic or midbrain injection of opiate agonist. Twelve of 33 NRM cells tested by midbrain microinjection were excited. In 10 the effect was reversed by naloxone. Seventeen raphe-spinal neurons were tested; 5 showed naloxone-reversible excitation to either midbrain or intravenous injection of opiates. NRM neurons respond to auditory and somatic stimuli; at least half respond maximally to somatic stimuli of noxious intensity. These findings are consistent with the hypothesis that the raphe-spinal projection mediates opiate and electrical stimulation-produced effects from midbrain sites. The properties of raphe-spinal neurons suggest that they are part of a negative feedback system which monitors and limits the output of spinal dorsal horn pain-transmission neurons.

Action Potentials↗
PubMed1977

Nucleus raphe magnus inhibition of spinal cord dorsal horn neurons.

In decerebrate cats, electrical stimulation of nucleus raphe magnus (NRM) of the medulla produced marked inhibition of spinal neurons in lumbosacral dorsal horn. Only neurons with high threshold inputs were inhibited. These cells were located in lamina I and in or near laminae V and VI. The duration of inhibition produced was related to the stimulus train length. An ipsilateral lesion of the dorsolateral funiculus at L1 markedly reduced the inhibition of neurons caudal to the lesion. Although NRM stimulation was the most effective, inhibition from more lateral sites could be obtained at higher stimulus intensities. NRM induced inhibition is probably mediated by a direct projection via the dorsolateral funiculus to spinal dorsal horn laminae I, II, V and VI. The results are discussed in relation to proposed mechanisms underlying the analgesia produced by NRM stimulation.

Animals↗
PubMed1977

Somatosensory properties of spinoreticular neurons in the cat.

(1) Spinal cord neurons projecting to the brain stem were studied in cats prepared by decerebration or anesthetized with barbiturate or nitrous oxide and halothane. Antidromic stimulation from the medial pontomedullary reticular formation (MDRF) and midbrain (MB) was used to identify the site of projection. (2) Receptive fields were mapped using adequate stimuli. A variety of noxious stimuli was employed to establish the capacity of these neurons to transmit nociceptive input. (3) Neurons were found to project bilaterally to the MPRF. Of 46 units tested for a more rostral projection, only 13 were activated from the MB electrode. (4) Neurons fall into three categories based on receptive fields: cutaneous, restricted (SR); deep, restricted (DR); and complex, extensive (CE). All 16 SR neurons were located in the dorsal horn and had low thresholds to mechanical stimulation of the skin. Seven discharged maximally to nociceptive inputs. The 34 DR neurons were widely distributed in the spinal gray and responded to pressure upon subcutaneous structures. Although 13 neurons increased their firing rate as the stimulus intensity was increased into the noxious range, nociceptive input could only be established with confidence in 4 neurons. The 38 CE neurons were located ventrally in the spinal gray and had highly convergent inputs from cutaneous and deep receptors. Ten responded maximally to noxious stimulation.

Afferent Pathways↗
PubMed1976

Opiate and stimulus-produced analgesia: functional anatomy of a medullospinal pathway.

Neurons in ventromedial medulla, including the nucleus raphe magnus, project to trigeminal nucleus caudalis and, via the dorsolateral funiculus, to spinal dorsal horn. The terminals of this descending system are in loci containing cells responsive to noxious stimuli. Electrical stimulation of nucleus raphe magnus selectively inhibits spinal dorsal horn neurons that respond to noxious stimuli. These neurons are located near the anatomically demonstrated terminals of this descending system. Dorsolateral funiculus lesions block this descending inhibition of spinal neurons as well as the analgesic action of morphine. This evidence supports the hypothesis that this neuron population mediates the analgesia produced by opiates and electrical stimulation of certain diencephalic and brainstem sites.

Analgesia↗
PubMed1976

Observations on the analgesic effects of needle puncture (acupuncture).

The present study was undertaken in order to investigate the analgesic effect of needle puncture in a small self-selected group of patients with chronic or acute pain, and to examine the factors which determine success or failure of this treatment modality. We have found that in chronic painful conditions, needle puncture may be very effective in producing at least transient analgesia. It also can produce permanent relief of acute (self-limited) pains. Needle puncture was not helpful in the management of pain resulting from nerve damage. High score on psychometric indicators of anxiety and depression is a significant predictor os successful needle puncture analgesia in patients with chronic pain. Comparison of our results to studies of counterirritation indicate that the analgesia produced by needle puncture involves a mechanism similar to that of counterirritation-induced analgesia.

Acupuncture Therapy↗