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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Central projections of messages evoked by dental pulp stimulation have been searched for in awake cats and recorded at unitary level. A head-top frame screwed to the skull served to fix the animal in the stereotaxic instrument precisely and in the usual orientation. 2. Three types of responses could be distinguished, each with characteristic thalamic localization: --one was of the specific type: it occurred at short latency, followed rapid rates of stimulation, and was localized in VPM and SG; --a second type had longer latency, did not follow rapid rates of stimulation, was frequently bilateral, and was localized in VPM, CM-Pf and Posterior Group; --the third type was a complex response, exhibiting inhibitory and excitatory phases; extremely labile, it disappeared during wakefulness; it was found in LP and CM-Pf. 3. The responses elicited by dental pulp stimulation and recorded in the periaqueductal grey matter mostly originated from face muscle messages provoked by the jaw opening reflex. 4. The possible contributions to pain perception made by each of the different thalamic responses is discussed, as well as the adequacy of dental pulp stimulation for producing a purely nociceptive signal.
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PMID:Thalamic and mid-brain responses to dental pulp afferent messages in awake cats. 92 32

(1) A similar proportion of cells in the VPM (24.7%), MGmc (24%), CM (26.8%) and CL (28.6%) is activated by electrical stimulation of the cat's dental pulp. However the thresholds are very different, cells belonging to the first group of the VPM being often activated by stimulation below 0.1 V. (2) Pain seems to be the unique sensation evoked by pulpal stimulation. A first group of cells somatotopically localized in the VPM displays a primary type of response. These cells can also be activated from an oral or perioral field. This fact is reminiscent of referred pain phenomenon often encountered in the clinic. (3) A second group of cells scattered in the VPM and activated by pulpal stimulation displays a non-primary type of response. (4) Strong pinching of the skin activates some MGmc cells tonically. Response characteristics of the MGmc cells after pulpal stimulation are heterogeneojs. (5) CM cells activated by pulpal stimulation display long latency responses whose properties are similar to those obtained after somatic stimulation. However, the latency of responses are shorter after limb stimulation than after pulpal stimulation.
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PMID:[A microphysiologic study of thalamic projection of the cat's dental pulp (author's transl)]. 114 47

It was aimed to assess if intrathecal (i.t.) injections of acetylsalicylic acid and salicylic acid depress C fibre-evoked activity in the sensory part of the nociceptive system. In rats under urethane anaesthesia, activity was elicited in single neurones in the dorsomedial part of the ventral nucleus (VDM) of the thalamus and in ascending axons of the spinal cord by supramaximal electrical stimulation of the sural nerve. Acetylsalicylic acid and salicylic acid injected i.t. significantly reduced the activity evoked in thalamic neurones. The maximum depression amounted to about 50% of the activity evoked in the controls and was produced by acetylsalicylic acid at a dose of 50 micrograms (0.28 mumol)/rat and by salicylic acid at a dose of 37.5 micrograms (0.27 mumol)/rat. Indomethacin injected i.t. also reduced C fibre-evoked activity in the thalamus in a dose-dependent fashion, 100 micrograms producing a 50% depression. Salicylic acid (37.5 micrograms/rat, i.e.) depressed C fibre-evoked activity in ascending axons but had no effect on A beta fibre-evoked activity. It is concluded that i.t. injection of acetylsalicylic acid selectively inhibits nociceptive impulse transmission in the spinal cord by an action of the salicylic acid moiety. It is possible that prostaglandins are involved in the central action of salicylic acid.
Pain 1992 May
PMID:Intrathecal injection of acetylsalicylic acid, salicylic acid and indomethacin depresses C fibre-evoked activity in the rat thalamus and spinal cord. 1183 30

In current clinical practice, two brain structures are stimulated for the relief of chronic pain, namely the somatosensory thalamic nuclei (VPL-VPM) and the periventricular and periaqueductal gray matter (PVG-PAG). Whereas stimulation of the VPL-VPM is almost exclusively used for the treatment of deafferentation pain, stimulation of the PVG-PAG is mostly used in cases of nociceptive pain. We present our results of VPL-VPM stimulation in 36 patients with deafferentation pain. Initial pain relief was obtained in 61% of patients. To-day, after a mean follow-up of more than 4 years, 30% are still pain free. This success rate was found to be lower than the mean reported success rate of 57%, based on a survey of the world literature. Upon reviewing the literature, it was apparent that the reported success rates vary considerably between different authors. Some tentative explanations are given for this large discrepancy in success rate. The mechanisms by which electrical stimulation of the VPL-VPM suppresses deafferentation pain remain to be elucidated. Recent clinical and experimental findings suggest that a dopaminergic mechanism might be involved.
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PMID:Deep brain stimulation in the treatment of chronic pain in man: where and why? 209 2

Electrical stimulation in the PAG has been shown to elicit profound analgesia in experimental animals that is at least in part due to the release of endogenous opioid substances. Electrical stimulation in the thalamic nuclei VPL and VPM inhibits the activation of spinal dorsal horn neurons by noxious stimuli. Acute electrical stimulation in these two targets relieves chronic pain in about 80% of patients. Chronic electrical stimulation by permanently implanted electrodes relieves pain in about 70% of patients with pain of peripheral or nociceptive origin but in only about 50% of patients with central pain resulting from deafferentation. Stimulating electrodes are implanted stereotactically by a burr hole under local anesthesia. Transient complications occur in 15% to 25% of patients and include infections, malfunctions of the stimulating hardware, pain at the implant sites, and mild temporary neurologic deficits. Permanent complications, including hemiparesis, intracranial hemorrhage, and death, occur in 1% to 2% of patients. Brain stimulation is recommended for the treatment of chronic pain in patients in whom other forms of treatment have failed. The technique is reasonably safe and provides pain relief for a group of patients who have exhausted all other therapeutic modalities. Unfortunately, not all patients receive effective pain relief with brain stimulation. Other stimulation targets such as the K-F nucleus in the parabrachial region of the brain stem are currently being explored in an attempt to provide pain relief to a greater proportion of patients. In addition, improvements in stimulation hardware have made the technique easier and more effective.
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PMID:Brain stimulation. 213 74

This study aimed to investigate if the non-steroid anti-inflammatory agents, indomethacin, ibuprofen, and diclofenac, are capable of depressing sensory responses of the nociceptive system by a central action. For this purpose, experiments were carried out on rats under urethane anaesthesia in which activity was elicited by electrical stimulation of afferent C fibres in the sural nerve. Recordings were made ipsi- or contralaterally from single neurones in the dorsomedial part of the ventral nucleus (VDM) of the thalamus. The 3 drugs produced a dose-dependent depression of the evoked activity which amounted to about 60% of the controls at the highest doses employed and lasted longer than 60 min. Their potency ranking, according to the ED50 values (in brackets), is: indomethacin (5 mg/kg) greater than diclofenac (10.9 mg/kg) greater than ibuprofen (15.6 mg/kg). The results suggest that a central action might contribute to the analgesia produced by these non-steroid anti-inflammatory agents.
Pain 1990 Apr
PMID:Central effect of the non-steroid anti-inflammatory agents, indomethacin, ibuprofen, and diclofenac, determined in C fibre-evoked activity in single neurones of the rat thalamus. 1183 30

In both cats and Japanese macaques, there are nociceptive specific (NS) and wide dynamic range (WDR) neurons in the shell region of the caudal ventrobasal (VB) complex of the thalamus. This comprises both the nucleus ventralis posteromedialis proper (VPM proper), and the nucleus ventralis posterolateralis (VPL). These two classes of nociceptive neurons are spatially segregated, WDR neurons being located both more anteriorly and in a narrow belt around the VB complex. Both NS and WDR neurons are somatotopically organized. These two classes of nociceptive neurons may constitute a thalamic link in the pain pathway from both the dorsal horn of the spinal cord and its trigeminal homologue, to the primary somatosensory cortex. Visceral sympathetic afferent inputs also project to the VPL part of the shell region of the caudal VB complex, there being viscerosomatic convergence onto both NS and WDR neurons. Visceral and cutaneous pain pathways thus appear to share a common projection locus in the shell region of the caudal VB complex.
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PMID:Thalamic mechanism of pain: shell theory of thalamic nociception. 250 13

Animal models designed to test the effectiveness of analgesic agents against viceral pain typically rely on a noxious chemical irritation of the peritoneum, e.g., acetic acid and phenylquinone writhing tests. While useful, this type of assay depends upon an acute inflammation and the release of local alogens. Further, ethical and scientific constraints prevent repeated assessments in a single animal, thereby compounding the difficulty of assessing tolerance development to analgesic agents. To overcome these constraints we developed a model for mechanical visceral pain (VPM) based on a repeatable and reversible duodenal distention in the rat. A chronic indwelling intraduodenal balloon catheter is well tolerated and upon inflation produces a writhing response graded in proportion to distention. This response is inhibited by morphine in a dose dependent manner.
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PMID:Mechanical visceral pain model: chronic intermittent intestinal distention in the rat. 272 33

Pyrazolone and salicylic acid derivatives and the aniline derivative, paracetamol, are often classified as peripherally acting analgesic agents, while morphine is a centrally acting analgesic agent. Since indications exist that the non-opioid analgesic agents can also produce central effects, experiments were carried out on rats under urethane anaesthesia in which activity was recorded from single neurones in the dorsomedial part of the ventral nucleus (VDM) of the thalamus that was elicited by supramaximal electrical stimulation of nociceptive afferents in the sural nerve. In addition, activity was recorded in ascending axons of the spinal cord which was evoked by electrical stimulation of nociceptive afferents in the sural nerve. The substances studied were morphine, the pyrazolone derivatives, metamizol (dipyrone) and aminophenazone ('Pyramidon'), lysine acetylsalicylate, and paracetamol. All drugs were found to depress dose-dependently evoked activity in VDM neurones after intravenous (i.v.) injection. The ED50 of morphine in depressing evoked activity in VDM neurones is 0.05 mg/kg. Morphine also dose-dependently reduced activity in ascending axons of the spinal cord, the ED50 being 1.7 mg/kg. The ED50 of metamizol in depressing evoked activity in VDM neurones is 120 mg/kg, and that of aminophenazone is 22.7 mg/kg. The 2 ED50 values differ significantly. It has been found previously that metamizol increased nociceptive activity in some ascending axons and aminophenazone increased this activity in all ascending axons tested. The ED50 of lysine acetylsalicylate in depressing evoked activity in VDM neurones is 74 mg/kg. The drug did not reduce nociceptive activity in ascending axons of the spinal cord. The ED50 of paracetamol in depressing evoked activity in VDM neurones is 19.0 mg/kg. Paracetamol did not depress nociceptive activity in ascending axons of the spinal cord at a dose as high as 150 mg/kg administered by intraperitoneal injection. Naloxone (0.2 mg/kg i.v.) abolished the depressant effects of morphine but failed to reduce those of the non-opioid analgesic agents even at a high dose (1 mg/kg i.v.). Unlike morphine, the non-opioid analgesic agents did not completely block evoked activity in VDM neurones but only partially blocked their activation. The results suggest that the non-opioid analgesic agents tested can produce a central analgesic effect which, however, is weaker than that of morphine.
Pain 1988 Mar
PMID:Depression by morphine and the non-opioid analgesic agents, metamizol (dipyrone), lysine acetylsalicylate, and paracetamol, of activity in rat thalamus neurones evoked by electrical stimulation of nociceptive afferents. 312 87

The opiate antagonist naloxone has been reported to cause pain relief. Therefore, the effect was determined of naloxone, injected intravenously, on the activity in single neurones of the dorsomedial part of the ventral nucleus (VDM) in the thalamus of rats under urethane anaesthesia elicited by electrical stimulation of nociceptive afferents in the sural nerve. Naloxone inhibited evoked nociceptive activity in a dose-dependent manner. High doses (5 mg/kg and 1 mg/kg) either increased or reduced the activity, inhibition prevailing at the lower dose. At lower doses (0.5 mg/kg, 0.2 mg/kg and 0.1 mg/kg), naloxone caused only inhibition, the ED50 being 0.36 mg/kg. The (+)-isomer of naloxone (0.2 mg/kg and 2 mg/kg) was ineffective, indicating that the effects of naloxone, which is the (-)-isomer, are stereospecific. The opposing effects exerted by naloxone at high and low doses may be due to the processing of nociceptive messages delivered to the thalamus by multiple endogenous opioid systems with differing susceptibility to naloxone. The results present evidence that naloxone at low doses may cause relief in particular conditions of pain.
Pain 1988 Dec
PMID:Dose-dependent inhibition by naloxone of nociceptive activity evoked in the rat thalamus. 322 60


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