Ascending and Long Spinal Pathways: Dorsal Columns, Spinocervical Tract and Spinothalamic Tract

1973 ◽  
pp. 315-338 ◽  
Author(s):  
A. G. Brown
Keyword(s):  
Spinothalamic Tract ◽  
Spinal Pathways ◽  
Dorsal Columns

Thalamic nociceptive systems

1985 ◽  
Vol 308 (1136) ◽  
pp. 339-345 ◽  
Keyword(s):  
Clinical Data ◽  
Experimental Pain ◽  
Turn Of The Century ◽  
Spinothalamic Tract ◽  
Spinal Pathways ◽  
Electrophysiological Data ◽  
Electrophysiological Recordings ◽  
Pain Centre ◽  
Made In

A role for thalamic structures in the processing of signals of nociception and pain has been suggested on the basis of clinical data since the turn of the century. Searches for a ‘pain centre’ by lesion or stimulation were often disappointing and the electrophysiological data were rare and usually contradictory. However, recent electrophysiological anatomical and neuropharmacological studies, made in various species (mainly rat and monkey) appear now progressively to give some clues in the understanding of pain process at the thalamic level. These studies have been mainly concerned with the areas receiving projections from ascending spinal pathways conveying noxious inputs, either directly by the spinothalamic tract or indirectly by the spinoreticulothalamic pathway. The eventual respective roles of these thalamic structures are considered. Electrophysiological recordings from thalamic structures in a model of experimental pain, arthritic rats, are also presented.

Intraspinal Localization of the Somatosensory Evoked Potential

Neurosurgery ◽  
1981 ◽  
Vol 9 (2) ◽  
pp. 157-162 ◽  
Author(s):  
Alan R. Cohen ◽  
Wise Young ◽  
Joseph Ransohoff
Keyword(s):  
Spinal Injury ◽  
Dorsal Column ◽  
Wave Form ◽  
Onset Latency ◽  
Spinal Pathways ◽  
Cavitron Ultrasonic Surgical Aspirator ◽  
Dorsal Columns ◽  
Dorsal Column Lesion ◽  
Sciatic Nerve Stimulation ◽  
Necessary And Sufficient

Abstract Somatosensory evoked potentials (SEPs) are used widely for monitoring neurophysiological function in experimental spinal injury. Yet the spinal pathways for SEP conduction remain unclear. Consequently, we sought to define specific changes in the SEP after interruption of selected spinal pathways. We activated cortical SEPs with sciatic nerve stimulation in 11 anesthetized (25 mg of pentobarbital per kg) cats after a multilevel thoracic laminectomy. The most consistent wave form component was an initial positivity (IP) at a 17- to 19-ms onset latency. We then used a Cavitron ultrasonic surgical aspirator to interrupt specific spinal pathways. A unilateral dorsal column lesion abolished the ipsilateral IP, but did not affect conduction in the contralateral column. Bilateral dorsal column lesions obliterated the IP, but sometimes left some longer latency components. Interruption of all but the ventral columns abolished the SEPs. When we interrupted all spinal pathways but the dorsal columns, an intact IP remained. In fact, a distinct IP was conducted through a single dorsal column after the division of all other spinal cord pathways. We conclude that, in the barbiturate-anesthetized cat: (a) the most consistent SEP wave form is an initial positivity at a 17- to 19-ms onset latency, (b) the integrity of the dorsal columns is both necessary and sufficient to conduct a normal-appearing IP component of the SEP. (c) the lateral columns may carry some longer latency component of the SEP. (d) the ventral columns carry no component of the SEP, and (e) bilateral recording may be useful for detecting asymmetry of injury.

Histopathology of experimental hematomyelia

1991 ◽  
Vol 75 (6) ◽  
pp. 911-915 ◽  
Author(s):  
Thomas H. Milhorat ◽  
David E. Adler ◽  
Ian M. Heger ◽  
John I. Miller ◽  
Joanna R. Hollenberg-Sher
Keyword(s):  
Spinal Cord ◽  
Tissue Injury ◽  
Central Canal ◽  
Microglial Cells ◽  
Neurological Deficits ◽  
Thoracic Spinal Cord ◽  
Content Type ◽  
Thoracic Spinal ◽  
Cellular Debris ◽  
Dorsal Columns

✓ The pathology of hematomyelia was examined in 35 rats following the stereotactic injection of 2 µl blood into the dorsal columns of the thoracic spinal cord. This experimental model produced a small ball-hemorrhage without associated neurological deficits or significant tissue injury. Histological sections of the whole spinal cord were studied at intervals ranging from 2 hours to 4 months after injection. In acute experiments (2 to 6 hours postinjection), blood was sometimes seen within the lumen of the central canal extending rostrally to the level of the fourth ventricle. Between 24 hours and 3 days, the parenchymal hematoma became consolidated and there was an intense proliferation of microglial cells at the perimeter of the lesion. The cells invaded the hematoma, infiltrated its core, and removed erythrocytes by phagocytosis. Rostral to the lesion, the lumen of the central canal was found to contain varying amounts of fibrin, proteinaceous material, and cellular debris for up to 15 days. These findings were much less prominent in the segments of the canal caudal to the lesion. Healing of the parenchymal hematoma was usually complete within 4 to 6 weeks except for residual hemosiderin-laden microglial cells and focal gliosis at the lesion site. It is concluded that the clearance of atraumatic hematomyelia probably involves two primary mechanisms: 1) phagocytosis of the focal hemorrhage by microglial cells; and 2) drainage of blood products in a rostral direction through the central canal of the spinal cord.

Inhibition of primate spinothalamic tract neurons by stimulation in the region of the nucleus raphe magnus

1976 ◽  
Vol 114 (2) ◽  
pp. 328-333 ◽  
Author(s):  
J.E. Beall ◽  
R.F. Martin ◽  
A.E. Applebaum ◽  
W.D. Willis
Keyword(s):  
Spinothalamic Tract ◽  
Nucleus Raphe Magnus ◽  
Raphe Magnus

Control of torque direction by spinal pathways at the cat ankle joint

1993 ◽  
Vol 97 (2) ◽  
pp. 366-371 ◽  
Author(s):  
T. Richard Nichols ◽  
John H. Lawrence ◽  
Stephen J. Bonasera
Keyword(s):  
Ankle Joint ◽  
Spinal Pathways

The effect of a kainate GluR5 receptor antagonist on responses of spinothalamic tract neurons in a model of peripheral neuropathy in primates

Pain ◽  
2004 ◽  
Vol 111 (1) ◽  
pp. 151-161 ◽  
Author(s):  
J. Palecek ◽  
V. Neugebauer ◽  
S. M. Carlton ◽  
S. Iyengar ◽  
W. D. Willis
Keyword(s):  
Peripheral Neuropathy ◽  
Receptor Antagonist ◽  
Spinothalamic Tract

Spatial summation of heat-induced pain: influence of stimulus area and spatial separation of stimuli on perceived pain sensation intensity and unpleasantness

1989 ◽  
Vol 62 (6) ◽  
pp. 1270-1279 ◽  
Author(s):  
D. D. Price ◽  
J. G. McHaffie ◽  
M. A. Larson
Keyword(s):  
Spatial Summation ◽  
Stimulus Size ◽  
Experimental Series ◽  
Pain Sensation ◽  
Thermal Probe ◽  
Spinothalamic Tract ◽  
Nociceptive Neurons ◽  
Thermal Probes ◽  
Perceived Pain ◽  
Thermal Stimuli

1. Psychophysical experiments were initiated to determine the possible influence of increasing stimulus size on perceived pain intensity. Six trained human subjects (5 male, 1 female) made visual analogue scale (VAS) ratings for pain-sensation intensity and unpleasantness in response to nociceptive thermal stimuli. Test stimuli consisted of 5-s duration heat pulses (45-50 degrees C in 1 degrees increments) delivered by one, two, or three contact thermal probes (1 cm2 each) applied to the medial aspect of the anterior forearm. 2. The area of skin receiving noxious thermal stimuli was changed by randomly varying the number of thermodes activated. The effects of varying the distance between the thermal probes also were evaluated. In the first series of experiments, thermal-probe separation was kept close to 0; in subsequent experimental series, the thermodes were separated by either 5 or 10 cm. 3. In each experimental series, considerable spatial summation occurred in both pain-sensation intensity and unpleasantness dimensions of pain. This summation occurred throughout the nociceptive thermal range of 45-50 degrees C and was larger at suprathreshold temperatures (greater than or equal to 47 degrees C) than those near threshold (less than or equal to 46 degrees C). Unlike spatial summation of perceived warmth, that of pain was not characterized by systematic changes in power-function exponents but as approximately upward parallel displacements in double-logarithmic coordinates. 4. Thermal-probe separation over a range of 0-10 cm had no effects on spatial summation of pain-sensation intensity or pain unpleasantness. In contrast, increasing thermal-probe separation increased the subjects' ability to discriminate differences in stimulus size and their ability to detect correctly the number of thermal probes activated. 5. Because affective VAS ratings of unpleasantness were linearly related to, but distinctly and systematically less than, VAS ratings of pain-sensation intensity, it was clear that subjects responded quite differently to these two pain dimensions. Affective judgements were not additionally influenced by thermal probe separation and hence by the ability to perceive stimulus size or number of thermal probes activated. 6. The results indicate that powerful spatial-summation mechanisms exist for heat-induced pain. Spatial summation of pain is likely to be subserved both by local integration mechanisms at the level of single spinothalamic-tract neurons and by recruitment of central nociceptive neurons, because spatial summation of pain occurred to approximately equal extents under conditions of thermode separations over a distance of at least 20 cm.

Spatiotemporal CCR1, CCL3(MIP-1α), CXCR4, CXCL12(SDF-1α) expression patterns in a rat spinal cord injury model of posttraumatic neuropathic pain

2011 ◽  
Vol 14 (5) ◽  
pp. 583-597 ◽  
Author(s):  
Friederike Knerlich-Lukoschus ◽  
Beata von der Ropp-Brenner ◽  
Ralph Lucius ◽  
Hubertus Maximilian Mehdorn ◽  
Janka Held-Feindt
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Neuropathic Pain ◽  
Substance P ◽  
Time Course ◽  
Behavioral Testing ◽  
Dorsal Horns ◽  
Cord Injury ◽  
Dorsal Columns ◽  
Spinal Cord Contusion

Object Central neuropathic pain is a frequent challenging complication after spinal cord injury (SCI), and specific therapeutic approaches remain elusive. The purpose of the present investigations was to identify potential key mediators of these pain syndromes by analyzing detailed expression profiles of important chemokines in an experimental SCI paradigm of posttraumatic neuropathic pain in rats. Methods Expression of CCR1, CCL3(MIP-1α), CXCR4, and CXCL12(SDF-1α) was investigated in parallel with behavioral testing for mechanical and thermal nociceptive thresholds after standardized SCI; 100-kdyn (moderate injury) and 200-kdyn (severe injury) force-defined thoracic spinal cord contusion lesions were applied via an Infinite Horizon Impactor at the T-9 level. Sham controls received laminectomies. Hindlimb locomotor function as well as mechanical and thermal sensitivities were monitored weekly by standardized behavioral testing after SCI. Chemokine expression was analyzed by real-time reverse transcriptase polymerase chain reaction in the early (7 days postoperatively) and late (42 days postoperatively) time courses after SCI, and immunohistochemical analysis (anatomical and quantitative) was performed 2, 7, 14, and 42 days after lesioning. Double staining with cellular markers and pain-related peptides (substance P and CGRP) or receptors (TRPV-1, TRPV-2, VRL-1, and TLR-4) was performed. Based on data obtained from behavioral testing, quantified immunohistochemical chemokine expressions in individual animals were correlated with the respective mechanical and thermal sensitivity thresholds 6 weeks after SCI. Results After 200-kdyn lesions, the animals exhibited prolonged reduction in their nociceptive thresholds, while 100-kdyn groups showed pain-related behaviors only in the early time course after SCI. Investigated chemokines were widely induced after SCI, involving cervical, thoracic, and lumbar spinal cord levels far beyond the lesion core. CCR1 and CCL3 were induced significantly in the dorsal horns 2 days after lesioning and remained at high levels after SCI with significantly higher intensities after 200-kdyn than 100-kdyn contusions. CXCR4 and CXCL12 levels continuously increased from 2 to 42 days after moderate and severe lesions. Additionally, chemokines were induced significantly in dorsal columns, with highest density levels 42 days after 200-kdyn lesions. In dorsal horns, CCR1 was coexpressed with TRPV-1 while CXCR4 and CXCL12 were partially coexpressed with substance P and CGRP. In dorsal columns, CCL3/CCR1 colabeled with GFAP, TRPV-2, TRPV-1, TLR-4; CXCR4/CXCL12 coexpressed with GFAP, CD68/ED1, and TLR4. Chemokine immunoreactivity density levels, especially CCL3 and its receptor, correlated in part significantly with nociceptive thresholds. Conclusions The authors report lesion grade–dependent upregulation of different chemokines/chemokine receptors after spinal cord contusion lesions in pain-processing spinal cord regions in a clinically relevant model of traumatic SCI in rats. Prolonged chemokine induction further correlated with below-level pain development in the delayed time course after severe SCI and was coexpressed with pain-associated peptides and receptors, suggesting that chemokines play a crucial role in chronic central pain mechanisms after SCI.

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