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

In this study cutaneous nociceptive messages are followed at different levels of the CNS, from the periphery to the cortex. A brief summary is given concerning the role of the fine myelinated and unmyelinated fibres which are specifically activated by noxious stimuli. A more extensive review considers the spinal mechanisms which sustain the transmission of nociceptive messages; the electrophysiological properties of interneurones located in laminae VIII, V, and I of the dorsal horn are described in detail. At the same time, the problem of the ascending projections of those cells activated by nociceptive stimuli is discussed. Particular attention is paid to the controls acting at the spinal level: segmental controls are described first and lead to discussion of the "gate control theory"; descending inhibitory controls are then discussed and their importance emphasized. The complexity of pain mechanisms at the supra-spinal level is underlined and a brief review considers the role of various bulbar, mesencephalic and thalamic structures involved in transmission of noxious messages. Among these structures, the PO group of nuclei seem to have a particular role in pain processes. Although the importance of the cortex for final integration of nociceptive messages is discussed, a brief summary is also given of investigations into the role of somatic area SII.
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PMID:[Neurophysiological data on transmission and integration of nociceptive messages (author's transl)]. 19 56

The sequential ordering of spikes emitted by single thalamic neurons which respond to noxious stimulation was studied using rats anesthetized with a mixture of alpha-chloralose and urethane. An electrical stimulus applied to the sciatic nerve contralateral to the thalamic recording site fired single thalamic SII neurons with a short latency spike burst and with long latency spikes which occurred at relatively fixed intervals. On repetition of stimulation, the short latency spike burst formed a high amplitude peak on sequential spike density histograms (I of Fig. 2B); the long latency spikes formed peaks of relatively low amplitude (M1, M2, M3 of Fig. 2B). Histograms of touch and light pressure relay neurons found within the thalamic SII differed conspicuously from that of Fig. 2B. Further experiments revealed that the I peak contained frequency coded information about the stimulus intensity, whereas the M peaks with their temporal relationship to the I peak coded information pertaining to a particular sensory modality. The M peaks are formed by timed firing in a positive feedback loop found between the thalamic SII and the nucleus centrum medianum-nucleus parafascicularis (CM-Pf) neurons. Consequently, the M peaks can be abolished without losing the I peak by a lesion placed in a portion of the CM-Pf complex or by the administration or morphine which is able to disorganize the timing mechanism of the feedback loop. Therefore, it is reasonably certain that the modality coded by the M peaks is pain.
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PMID:Thalamic mechanisms that process a temporal pulse code for pain. 125 35

We studied six patients who developed spontaneous hemibody pain following lesions of the parietal lobe. The pain was characterized as burning or icelike, and was associated with impairment of pin and temperature appreciation. Computed tomographic scanning showed that the common area of involvement in all cases was the white matter deep to both the caudal insula and the opercular region of the posterior parietal cortex. We suggest that disruption of the interconnections between these cerebral cortical areas (including the second somatosensory representation, SII) and the thalamus, particularly the intralaminar and ventroposterior nuclei, may be responsible for producing a thalamocortical disconnection syndrome with spontaneous pain as its clinical manifestation.
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PMID:Parietal pseudothalamic pain syndrome. Clinical features and anatomic correlates. 141 10

Experiments were performed to characterize cerebral cortical activity and pain behavior elicited by electrical stimulation of the tooth pulp in unanesthetized monkeys. Four monkeys were trained on two different operant paradigms: two on a simple escape task and two on an appetitive tolerance-escape task. All monkeys were implanted with bipolar stimulating electrodes in the right maxillary canine tooth and subdural recording electrodes over the left primary (SI) and/or secondary (SII) somatosensory cortices. Subdural tooth pulp-evoked potentials (TPEPs) recorded over the SII consisted of components P1 (27.5 ms), N1 (40.3 ms), P2 (84.0 ms), N2 (163.5 ms), P3 (295.3 ms), and N3 (468.0 ms). The long latency component (P3-N3) was found exclusively over the SII and was elicited by high intensity stimulation. The appearance of component P3-N3 required the recruitment of A delta nerve fibers into the maxillary nerve compound action potential and was correlated with high frequencies of escape. Administration of morphine sulfate (4 mg/kg, i.m.) caused a contemporaneous reduction in escape frequency and in the amplitude of P3-N3 recorded over the SII. The relationships between TPEP amplitude, escape behavior and A delta nerve fiber activity strongly suggest that the SII is involved with nociception and pain behavior.
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PMID:Cortical nociceptive responses and behavioral correlates in the monkey. 380 65

Our small experiences with electrical stimulation in the VPL and VPM for dysesthetic pain show that it provoked only paresthesia and induced some relief of pain. It does not increase the beta-endorphin level in CSF. To clarify the anatomical substrata in VPL stimulation, neuroanatomical studies were done about the inputs to VPL in man, monkey and cat by the Fink-Heimer method. The spinothalamic tract terminates in VPL in a patchy fashion in the monkey. The corticothalamic fibers from SI and SII cortex project to VPL and VPM in somatotopical organization in the cat. SI and SII cortices have reciprocal connections, in addition to projections to area 5 or SIII cortex. The corticofugal fibers to the magnocellular and gigantocellular tegmental fields are suggested in addition to the dorsal column nuclei, spinal trigeminal nuclei and spinal posterior horn in cat. The medial lemniscus input to VPL and the above neural circuits are thought to be associated with VPL stimulation.
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PMID:Clinicoanatomical study of thalamic stimulation for pain relief. 393 84

The distribution of tooth pulp-evoked potentials (TPEPs) was characterized in the primary motor (MI), primary somatosensory (SI) and secondary somatosensory (SII) cortices of the monkey. Bipolar electrical tooth pulp stimulation elicited TPEP components P23 and N44 over SI, P26 and N72 over MI, and P72, N161, P280, N420, P561 and N662 over SII. Muscular artifacts and extradental input did not affect the TPEP as demonstrated by experiments using a neuromuscular blocking agent and removal of the pulp, respectively. The short latency TPEPs recorded over SI and MI were evoked by low stimulus intensities and activation of A beta nerve fibers, whereas the long latency TPEPs recorded over SII required higher stimulus intensities and the additional recruitment of A delta nerve fibers. Intracortical recordings revealed polarity reversals of components P23 and N44 in area 3b, P26 and N72 in area 4, and P72, N161, P280, N420, P561 and N662 in the upper bank of the lateral sulcus (SII). Evidence presented in this study suggests that TPEPs recorded from SI and MI relate to non-nociceptive mechanisms while TPEPs recorded from SII relate to nociceptive mechanisms.
Pain 1985 Jul
PMID:Tooth pulp-evoked potentials in the monkey: cortical surface and intracortical distribution. 403 22

Since our previous study of pain somatosensory evoked potentials (SEPs) following CO2 laser stimulation of the hand dorsum could not clarify whether the early cortical component N1 was generated from the primary somatosensory cortex (SI) or the secondary somatosensory cortex (SII) or both, the scalp topography of SEPs following CO2 laser stimulation of the foot dorsum was studied in 10 normal subjects and was compared with that of the hand pain SEPs and the conventional SEPs following electrical stimulation of the posterior tibial nerve recorded in 8 and 6 of the 10 subjects, respectively. Three components (N1, N2 and P2) were recorded for both foot and hand pain SEPs. N1 of the foot pain SEPs was maximal at the midline electrodes (Cz or CPz) in all data where that potential was recognized, but the potential field distribution was variable among subjects and even between two sides within the same subject. N1 of the hand pain SEPs was maximal at the contralateral central or midtemporal electrode. The scalp distribution of N2 and P2, however, was not different between the foot and hand pain SEPs. The mean peak latency of N1 following stimulation of foot and hand was found to be 191 msec and 150 msec, respectively, but there was no significant difference in the interpeak latency of N1-N2 between foot and hand stimulation. It is therefore concluded that N1 of the foot pain SEPs is generated mainly from the foot area of SI. The variable scalp distribution of the N1 component of the foot pain SEPs is likely due to an anatomical variability among subjects and even between sides.
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PMID:Pain-related somatosensory evoked potentials following CO2 laser stimulation of foot in man. 753 Jan 85

Painful intracutaneous electric finger shock was delivered to the fifth digit of the non-dominant hand of five healthy volunteers. Whole head evoked magnetic field maps were collected and cortical localizations were calculated using local sphere equivalent current dipole fits. MRI scans were used to identify the anatomical structures where magnetic field sources were located. Anatomically, sources were identified bilaterally in the primary somatosensory region and SII-Insula regions. Additionally, frontal operculum sources were observed contralaterally in two subjects. Temporally, an initial contralateral SI activation at 40-60 ms was followed by several SII-Insula responses over the next several hundred milliseconds (ms). These SII-Insula responses were often interspersed with additional activations of the SI region. These later responses were observed in both hemispheres.
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PMID:Whole head mapping of magnetic fields following painful electric finger shock. 758 Mar 98

The initial somatosensory evoked magnetic fields following painful heat stimulation by CO2 laser beam applied to the upper and lower limb were investigated in normal subjects. The main deflections, 'Pain MA' and 'Pain ML' following the arm and leg stimulation, respectively, were identified in the bilateral second sensory cortices (SII). The onset latencies of Pain MA and Pain ML were approximately 150 and 200 ms, respectively. No consistent equivalent current dipole was found in other areas including the primary sensory cortex in each hemisphere. Therefore, we consider that neurons in the bilateral SII are initially activated following painful heat stimulation.
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PMID:Pain-related magnetic fields following painful CO2 laser stimulation in man. 767 7

Pain is a diverse sensory and emotional experience that likely involves activation of numerous regions of the brain. Yet, many of these areas are also implicated in the processing of nonpainful somatosensory information. In order to better characterize the processing of pain within the human brain, activation produced by noxious stimuli was compared with that produced by robust innocuous stimuli. Painful heat (47-48 degrees C), nonpainful vibratory (110 Hz), and neutral control (34 degrees C) stimuli were applied to the left forearm of right-handed male subjects. Activation of regions within the diencephalon and telencephalon was evaluated by measuring regional cerebral blood flow using positron emission tomography (15O-water-bolus method). Painful stimulation produced contralateral activation in primary and secondary somatosensory cortices (SI and SII), anterior cingulate cortex, anterior insula, the supplemental motor area of the frontal cortex, and thalamus. Vibrotactile stimulation produced activation in contralateral SI, and bilaterally in SII and posterior insular cortices. A direct comparison of pain and vibrotactile stimulation revealed that both stimuli produced activation in similar regions of SI and SII, regions long thought to be involved in basic somatosensory processing. In contrast, painful stimuli were significantly more effective in activating the anterior insula, a region heavily linked with both somatosensory and limbic systems. Such connections may provide one route through which nociceptive input may be integrated with memory in order to allow a full appreciation of the meaning and dangers of painful stimuli. These data reveal that pain-related activation, although predominantly contralateral in distribution, is more widely dispersed across both cortical and thalamic regions than that produced during innocuous vibrotactile stimulation. This distributed cerebral activation reflects the complex nature of pain, involving discriminative, affective, autonomic, and motoric components. Furthermore, the high degree of interconnectivity among activated regions may account for the difficulty of eliminating pathological pain with discrete CNS lesions.
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PMID:Distributed processing of pain and vibration by the human brain. 802 64


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