Surface Of Cord Research Articles

Preoperative demonstration of the Adamkiewicz artery by magnetic resonance angiography in patients with descending or thoracoabdominal aortic aneurysms.

Investigating the possibility of magnetic resonance angiography (MRA) to visualize the Adamkiewicz artery of as a preoperative study of thoracic aortic aneurysms. From February 1998 to March 1999, 26 consecutive patients who had aneurysms of the thoracoabdominal or descending aorta underwent preoperative MRA to visualize the Adamkiewicz artery. Mean age was 60.5+/-11.5 years. Fifteen patients had non-dissecting aneurysm and 11 had aortic dissections. Nineteen patients underwent replacement of the aneurysms, four patients underwent endovascular stent-graft repair, and three patients were discharged without treatment of aneurysm. MRA was performed on a 1.5-T system (Magnetom, Siemens) and data acquisition was repeated two times following injection of gadolinium-DTPA. Source images were reconstructed with multiplanar reconstruction and maximum intensity projection. Criteria for the Adamkiewicz artery of were that the artery ascends from the dorsal branch of the intercostal or lumbar artery to the anterior mid-sagital surface of the spinal cord in the early phase. The Adamkiewicz arteries were demonstrated in 18 patients (69%). These arteries were originated from the left intercostal or lumbar arteries in 13 (72.2%) patients and from the right in 5 (27.8%) and from the Th8 branch in three, Th9 in seven, Th10 in two, Th11 in four, and L1 in two. All patients had graft replacement of the aorta using a partial bypass. All intercostal or lumber arteries, which were visualized as the origin of the Adamkiewicz artery, were reattached to the grafts. No spinal cord injury occurred. Preoperative detection the Adamkiewicz artery was possible by MRA and was very useful to reduce the incidence of ischemic injury of the spinal cord during surgery of the thoracoabdominal or descending aorta.

Effect of akatinol (memantine) in central spinal pain syndrome.

On the model of central spinal pain syndrome in rats induced by application of penicillin to the dorsal surface of the lumbar spinal cord, akatinol injected intraperitoneally at the peak of syndrome or applied locally simultaneously with penicillin produced a dose-dependent analgesic effect. Intraperitoneal injection of akatinol at the peak of pain syndrome inhibited neuronal activity in spinal dorsal horn: the amplitude of total evoked neuronal response significantly decreased and the duration of action potentials returned to normal. It is concluded that activation of NDMA receptors plays a significant role in the development of central spinal pain syndrome, in particular spontaneous pain attacks, hyperalgesia, and tactile allodynia. Akatinol can be an essential component of the complex pathogenetic therapy of central pains.

Serotonergic systems in the spinal cord of the amphibian urodelePleurodeles waltl

The role of the monoamine serotonin (5-HT) in modulating the neural networks underlying axial locomotor movements was studied in an adult amphibian urodele, Pleurodeles waltl. 5-HT was applied to an in vitro brainstem-spinal cord preparation of P. waltl, which displayed fictive axial locomotor patterns following bath application of N-methyl-D-aspartate (5 microM) with D-serine (10 microM). Our results showed that 5-HT (1-25 microM) produces a reversible increase in the cycle duration and the duration of rhythmic bursting activity recorded extracellularly from ventral roots innervating the axial musculature. When applied alone, 5-HT does not trigger axial locomotor activity. The distribution pattern of 5-HT immunoreactive (5-HT-ir) cells along the spinal cord was investigated both in intact and in chronic spinal animals. The number of 5-HT-ir cell bodies is higher at brachial levels and decreases through crural levels. Sparse oval or fusiform 5-HT-ir somata are present within the gray matter, just ventrolateral to the central canal. Longitudinal fibers were detected throughout the entire white matter, except in the medial part of the dorsal funiculi. Two columns of intensely labeled and profusely branching thick and thin fibers associated with numerous varicosities run continuously along the ventrolateral surface of the spinal cord. Three weeks following full spinal cord transection at the level of the second spinal root, all longitudinal processes had disappeared, indicating their supraspinal origin, whereas the ventrolateral plexes remained, suggesting that they originated from intraspinal 5-HT-ir cell bodies. Our data showing that spinal 5-HT is organized according to a rostrocaudal gradient suggest that the 5-HT systems of P. waltl are not related to the presence of limb motor pools but more likely are related to axial central pattern generators (CPGs) networks down the length of the spinal cord. The possible involvement of these two sources (descending vs. intraspinal) of 5-HT innervation in the modulation of the axial CPGs is discussed.

Surface Modification of Textile Tire Cords by Plasma Polymerization for Improvement of Rubber Adhesion

Abstract Aramid cords and fibers and polyester tire cords were treated by means of plasma polymerization techniques. Coatings of plasma-polymerized pyrrole or acetylene were deposited on the surface of cords and fibers in a custom-built semi-continuous reactor operated on a pulsed DC glow discharge. The deposition conditions of the plasma-polymer coatings were varied within wide limits. The cords were tested for adhesion in rubber in a industrial pull-out test. It was found that the plasma polymer coating can significantly increase pull-out forces. Coatings deposited under low power and high pressure conditions performed better than the coatings prepared under high power and low pressure conditions. The plasma-polymerized coatings were characterized by a range of analytical techniques and the performance results are explained in a tentative model based on the molecular structure of the films. The structure was found to be strongly dependent on the deposition conditions.

Mucociliary Transport Pathway on Laryngotracheal Tract and Stented Glottis in Guinea Pigs

We investigated the laryngotracheal mucociliary transport pathway of guinea pigs in vivo and immediately postmortem. Only intraperitoneal anesthesia was used during the procedure to avoid the disturbance of mucociliary function. Resin particles were used as the marking substance. A microcolpohysteroscope was placed at different levels in the laryngotracheal region for observing the marking particles and recording the transport pattern. The tracheal mucociliary transport flow primarily moved along the posterior wall and both lateral walls in a zigzag trace. Upon reaching the subglottis, the resin particles stayed underneath the vocal cords, and a whirlpool phenomenon developed. The majority of the particles were shifted and directed onto the posterior glottic area. With a short delay, some resin particles crossed over the free edge of the vocal cords and turned posteriorly along the medial upper cordal margin. No mucociliary transport could be observed on the entire upper surface of the true vocal cords, which is covered by squamous epithelium. Occasionally, a few resin particles in the vicinity of the epiglottic root traveled along the aryepiglottic folds toward the posterior commissure. All streams of mucociliary transport finally joined together in the interarytenoid area. After leaving the glottis, the resin particles traveled to the hypopharynx and entered the esophagus through the motion of deglutition. The pattern of mucociliary clearance in the laryngotracheal region was not delayed by stenting.

Responses of reticulospinal neurons in intact lamprey to vestibular and visual inputs.

A lamprey maintains the dorsal-side-up orientation due to the activity of postural control system driven by vestibular input. Visual input can affect the body orientation: illumination of one eye evokes ipsilateral roll tilt. An important element of the postural network is the reticulospinal (RS) neurons transmitting commands from the brain stem to the spinal cord. Here we describe responses to vestibular and visual stimuli in RS neurons of the intact lamprey. We recorded activity from the axons of larger RS neurons with six extracellular electrodes chronically implanted on the surface of the spinal cord. From these multielectrode recordings of mass activity, discharges in individual axons were extracted by means of a spike-sorting program, and the axon position in the spinal cord and its conduction velocity were determined. Vestibular stimulation was performed by rotating the animal around its longitudinal axis in steps of 45 degrees through 360 degrees. Nonpatterned visual stimulation was performed by unilateral eye illumination. All RS neurons were classified into two groups depending on their pattern of response to vestibular and visual stimuli; the groups also differed in the axon position in the spinal cord and its conduction velocity. Each group consisted of two symmetrical, left and right, subgroups. In group 1 neurons, rotation of the animal evoked both dynamic and static responses; these responses were much larger when rotation was directed toward the contralateral labyrinth, and the dynamic responses to stepwise rotation occurred at any initial orientation of the animal, but they were more pronounced within the angular zone of 0-135 degrees. The zone of static responses approximately coincided with the zone of pronounced dynamic responses. The group 1 neurons received excitatory input from the ipsilateral eye and inhibitory input from the contralateral eye. When vestibular stimulation was combined with illumination of the ipsilateral eye, both dynamic and static vestibular responses were augmented. Contralateral eye illumination caused a decrease of both types of responses. Group 2 neurons responded dynamically to rotation in both directions throughout 360 degrees. They received excitatory inputs from both eyes. Axons of the group 2 neurons had higher conduction velocity and were located more medially in the spinal cord as compared with the group 1 neurons. We suggest that the reticulospinal neurons of group 1 constitute an essential part of the postural network in the lamprey. They transmit orientation-dependent command signals to the spinal cord causing postural corrections. The role of these neurons is discussed in relation to the model of the roll control system formulated in our previous studies.

A microstructural study of spinal cord edema.

The experimental spinal cord edema was produced in a cat by the infusion method of Marmarou. Horseradish peroxidase (HRP) dissolved in autoserum of a cat was used as a tracer. After laminectomy, a 30-gauge needle was inserted into the intumescentia cervicalis. A total amount of 20 microliters of a tracer was infused at a rate of 10 microliters/hr. The structural features were studied immediately and 3 days after infusion. Immediately after infusion, HRP was noted in the infused white and gray matters. Though the perivascular space in the white matter at the infused site was widely distended and filled with HRP, the space in the gray matter was not distended but filled with HRP. HRP which was observed along vessels led to the surface of the spinal cord. Swelling of astrocyte was not observed. Three days after infusion, the extracellular space and the perivascular space in the infused white matter were still expanded but were not filled with HRP. The fine structural features were similar to the findings as seen in Marmarou's infusion type of brain edema. Using this model, it seems to be feasible to study the resolution process of spinal cord edema.

Therapeutic Window after Spinal Cord Trauma Is Longer than after Spinal Cord Ischemia

Department of Anesthesiology University of California, San Diego La Jolla, California 92093-0818mmarsala@ucsd.eduIn Reply:—We read carefully the comments of Drs. Albin and White on our recent article. 1As indicated by these authors, induction of spinal cord hypothermia (10°C) after traumatic spinal injury is still effective in providing protection if initiated 4 h after injury. 2,3In contrast, in our study, we observed a significant protection only if spinal hypothermia (27°C) was initiated immediately (5 min) after ischemia. Although the differences between the therapeutic efficacy of spinal hypothermia after spinal trauma and spinal ischemia are not clear, there are several points that need to be addressed.After injurious intervals of spinal ischemia, the development of irreversible neuronal degeneration shows very rapid onset. Using Nauta silver impregnation technique in rat, rabbit, or dog spinal ischemia models, we have found that irreversible neuronal degeneration is clearly developed as soon as 60–120 min after reflow following injurious intervals of ischemia. 4–7These data indicate that the process of irreversible neuronal degeneration is likely initiated during the early period (0–30 min) of reflow. Importantly, based on the data from our study, this process shows high temperature sensitivity. The lack of hypothermic protection after a longer period of normothermic reflow thus likely reflects the fact that the process of irreversible degeneration was already initiated or completed.In our study, intrathecal temperature was measured during and after a period of subcutaneous cooling. It is possible that the magnitude of the decrease in spinal parenchymal temperature does not completely reflect measured intrathecal temperature. However, in our previous methodologic study 8describing this cooling technique, we showed that there is a 2–3°C temperature gradient if measured on dorsal versus ventral spinal cord surface. Based on these data, we believe that spinal temperature is in the range of temperatures measured between dorsal and ventral spinal cord surface. Accordingly, measurement of spinal somatosensory evoked potentials showed a temperature-dependent increase in the N3 (postsynaptic) component during the period of cooling and a return to baseline after rewarming.Based on our previous data describing a very rapid onset of irreversible neuronal degeneration after spinal ischemia, the possibility that the therapeutic window could be enlarged if intrinsic spinal cord temperature were reduced to lower levels is uncertain. However, it is possible that the fraction of neurons undergo prolonged or delayed degeneration and that rescue of these neurons will eventually improve outcome. In this case, it is possible that deeper hypothermia (10–20°C) will be more effective in protecting this neuronal pool than temperatures (27°C) tested in our study. Accordingly, it would be important, using localized epidural or intrathecal cooling techniques 2,3,6,9(which are required to achieve deep spinal hypothermia), to determine the efficacy of such hypothermic treatment.

Responsiveness of rat substantia gelatinosa neurones to mechanical but not thermal stimuli revealed by in vivo patch-clamp recording.

1. Synaptic responses of 46 substantia gelatinosa (SG) neurones in the spinal dorsal horn to cutaneous mechanical and/or thermal stimuli were investigated in an in vivo rat preparation with whole-cell patch-clamp recordings. The clamped neurones were identified as being in the SG based on either their morphological features by intrasomatic injection of biocytin or the depth of the neurones from the surface of the spinal cord. 2. In all SG neurones examined where spontaneous EPSCs occurred, pinch (noxious) and air (innocuous) stimuli applied to the ipsilateral hindlimb elicited a barrage of EPSCs (some of which initiated an action potential under current-clamp conditions), which subsided just after cessation of the stimuli without any residual slow current (or after-discharge). The spontaneous and evoked EPSCs were reversibly abolished by a non-N-methyl-D-aspartate (non-NMDA) receptor antagonist, CNQX (20 microM). 3. Noxious (>= 45 C) or innocuous (<= 40 C) thermal stimuli did not elicit any synaptic responses in all 18 SG neurones tested which were sensitive to mechanical stimuli. Noxious cold stimulation (<= 10 C) also failed to produce any responses (n = 6). 4. It is concluded that both noxious and innocuous mechanical information to SG neurones are transmitted primarily by activation of non-NMDA receptors, probably without any involvement of slow synaptic transmission, and that thermal information is conveyed to areas of the dorsal horn other than SG.

Intrathecal drug therapy for chronic pain: from basic science to clinical practice.

Intrathecal drug therapy for chronic pain: from basic science to clinical practice.

Responses to spinal microstimulation in the chronically spinalized rat and their relationship to spinal systems activated by low threshold cutaneous stimulation.

We describe the responses evoked by microstimulation of interneuronal regions of the spinal cord in unanesthetized rats chronically spinalized at T10-T12. One to three weeks after spinalization, sites in the lumbar spinal cord were stimulated using trains of low current microstimulation. The isometric force produced by stimulation of a spinal site was measured at the ankle. Responses were reliably observed from stimulation of a region within the first 1250 microm from the dorsal surface of the spinal cord. These responses were clearly not due to direct motoneuronal activation and were maintained after chronic deafferentation. The force evoked by microstimulation and measured at the ankle varied smoothly across the workspace. Simultaneous stimulation of two sites in the spinal cord produced a response that was a simple linear summation of the responses evoked from each of the sites alone. Microstimulation generally produced a highly non-uniform distribution of response directions, biased toward responses which pulled the limb toward the body. Within these distributions there appeared to be two main types of responses. These different types of responses were preferentially evoked by microstimulation of different rostrocaudal regions of the spinal cord. This anatomical organization paralleled the spinal cutaneous somatotopy, as assessed by recording cutaneous receptive fields of neurons at sites to which the microstimulation was applied. This relationship was maintained after chronic deafferentation. The findings described here in the rat spinal cord in large part replicate those previously described in the frog.

Endoscopy of spinal cord and posterior fossa by a lumbar percutaneous approach: endoscopic anatomy in cadavers.

Endoscopy has a long history and is used extensively today following recent technical improvements. Endoscopy has been used in neurosurgery to examine ventricles, cisterns, and intra-arteries. In this study, we evaluated the possibility of endoscopic examination and treatment in the narrow confines of the subarachnoid space of the spine and the posterior fossa. Endoscopes with external diameters of 0.5, 1.4, and 2.2 mm were used. While the first two endoscopes had rigid tips, the 2.2-mm endoscope had a directable tip. Each endoscope was inserted percutaneously in the lumbar region in five cadavers and was advanced cranially into the posterior fossa under endoscopic monitoring. Arteries, veins and nerve roots upon the surface of the spinal cord could be distinguished readily with all endoscopes. All endoscopes could be inserted under direct observation, avoiding these vessels and nerve roots. Further rostral advancement of the endoscope permitted visualization of the upper spinal cord, cisterna magna at the foramen magnum, and the fourth ventricle. The lower aspect of the cerebellum, the foramen of Magendie, and the cerebral aqueduct could be observed from below. When the endoscope was advanced ventrolaterally, the vertebral artery and lower cranial nerves were observed. From this preliminary cadaver study, endoscopy via lumbar puncture appeared useful for inspection of structures surrounding the spinal cord and posterior fossa, and for some simple treatments.

Effects of omega-agatoxin IVA, a P-type calcium channel antagonist, on the development of spinal neuronal hyperexcitability caused by knee inflammation in rats.

Both N- and P-type high-threshold calcium channels are located presynaptically in the CNS and are involved in the release of transmitters. To investigate the importance of P-type calcium channels in the generation of inflammation-evoked hyperexcitability of spinal cord neurons, electrophysiological recordings were made from wide-dynamic-range neurons with input from the knee joint in the anesthetized rat. The responses of each neuron to innocuous and noxious pressure onto the knee and the ankle were continuously assessed before and during the development of an inflammation in the knee joint induced by the injections of K/C into the joint cavity. The specific antagonist at P-type calcium channels omega-agatoxin was administered into a 30-microl trough on the spinal cord surface above the recorded neuron. In most neurons the application of omega-agatoxin before induction of inflammation slightly enhanced the responses to pressure onto the knee and ankle or left them unchanged. Two different protocols were then followed. In the control group (13 rats) only Tyrode was administered to the spinal cord during and after induction of inflammation. In these neurons the responses to mechanical stimuli applied to both the inflamed knee and to the noninflamed ankle showed a significant increase over 4 h. In the experimental group (12 rats) omega-agatoxin was applied during knee injection and in five 15-min periods up to 180 min after kaolin. This prevented the increase of the neuronal responses to innocuous pressure onto the knee and to innocuous and noxious pressure onto the ankle; only the responses to noxious pressure onto the knee were significantly enhanced during development of inflammation. Thus the development of inflammation-evoked hyperexcitability was attenuated by omega-agatoxin, and this suggests that P-type calcium channels in the spinal cord are involved in the generation of inflammation-evoked hyperexcitability of spinal cord neurons. Finally, when omega-agatoxin was administered to the spinal cord 4 h after the kaolin injection, i.e., when inflammation-evoked hyperexcitability was fully established, the responses to innocuous and noxious pressure onto the knee were reduced by 20-30% on average. The shift in the effect of omega-agatoxin, from slight facilitation or no change of the responses before inflammation to inhibition in the state of hyperexcitability, indicates that P-type calcium channels are important for excitatory synaptic transmission involved in the maintenance of inflammation-evoked hyperexcitability.

Modulation of fibronectin expression in the central nervous system of Lewis rats with experimental autoimmune encephalomyelitis.

Fibronectin (FN), a large family of plasma and extracellular matrix (ECM) glycoproteins, plays an important role in leukocyte migration. In normal central nervous system (CNS), a fine and delicate mesh of FN is virtually restricted to the basal membrane of cerebral blood vessels and to the glial limitans externa. Experimental autoimmune encephalomyelitis (EAE), an inflammatory CNS demyelinating disease, was induced in Lewis rats with a spinal cord homogenate. During the preclinical phase and the onset of the disease, marked immunolabelling was observed on the endothelial luminal surface and basal lamina of spinal cord and brainstem microvasculature. In the paralytic phase, a discrete labelling was evident in blood vessels of spinal cord and brainstem associated or not with an inflammatory infiltrate. Conversely, intense immunolabelling was present in cerebral and cerebellar blood vessels, which were still free from inflammatory cuffs. Shortly after clinical recovery minimal labelling was observed in a few blood vessels. Brainstem and spinal cord returned to normal, but numerous inflammatory foci and demyelination were still evident near the ventricle walls, in the cerebral cortex and in the cerebellum. Intense expression of FN in brain vessels ascending from the spinal cord towards the encephalon preceded the appearance of inflammatory cells but faded away after the establishment of the inflammatory cuff. These results indicate an important role for FN in the pathogenesis of CNS inflammatory demyelinating events occurring during EAF.

Intramedullary cavernous haemangiomas: clinical features, imaging diagnosis, surgical resection and outcome

The diagnosis, surgical treatment and outcome of seven patients with histologically verified intramedullary cavernous haemangiomas are reported. Five males and two females, with progressive myelopathy were observed. The patients were aged between 7 and 61 years. The duration of their symptoms and signs before diagnosis varied from one month to 5 years. Magnetic resonance (MR) imaging was performed in all patients and spinal angiography was performed in five. All the patients underwent microsurgical resection of the cavernous haemangiomas. MR imaging diagnosed cavernous haemangiomas in all seven patients. T1-weighted images with or without contrast enhancement best defined the margins and size of the lesions. They also illustrated the exophytic components and the change in spinal cord surface well, and were important to surgical planning. T2-weighted images may be suboptimal due to their magnetic susceptibility artifacts. In all lesions, total removal was achieved. Postoperative neurological function improved in all patients in long term follow-up. With the advantages of MR examinations and more understanding about the pathological characteristics of intramedullary cavernous haemangiomas, total removal of the mass lesion should be attempted and the outcome is generally good.

Effect of ZnO contents at the surface of brass-plated steel cord on the adhesion property to rubber compound

An effect of ZnO concentration at the surface of brass-plated steel cord on the adhesion property between a rubber compound and a brass-plated steel cord was investigated. Cord composition was determined by an Auger microscope with Ar ion sputtering. Two different steel cords were prepared; one (cord A) had higher ZnO concentration at the cord surface compared to the other (cord B). Pull-out force of unaged adhesion sample of cord A was lower than that of cord B. But the adhesion durability of the humidity-aged adhesion sample of cord A was better than the latter. Rubber coverage of the pull out cord for the unaged adhesion samples of cord A was poor, indicating insufficient formation of an adhesion layer. Pull-out force of the thermal-aged adhesion samples decreased with increasing aging time and that of cord A was lower than that of cord B. The enhancement of rubber coverage during initial aging period could be explained by an additional formation of copper sulfide at the adhesion interphase and an increase of modulus of rubber compound adjacent to the adhesion layer. With further increases of aging time, adhesion interphase grew excessively and the physical property of rubber compound deteriorated significantly, such that rubber coverage of adhesion samples decreased markedly with increasing aging time.

Peculiarities of extraspinally recorded field spinal potentials

It is demonstrated that field potentials generated in the lumbosacral spinal cord and usually recorded as a dorsal surface potential spread to the tissues of the back body surface. The component composition of these extraspinally recorded responses somewhat differs from that of the potential recorded from the spinal cord surface. The reasons for such a difference and possible approaches providing higher informative value of non-invasive studies of spinal cord potentials are discussed.

Mu- and delta-opioid receptor mRNAs are expressed in spinally projecting serotonergic and nonserotonergic neurons of the rostral ventromedial medulla.

The rostral ventromedial medulla (RVM) is an important mediator of the supraspinal component of opioid antinociception. Previous studies have suggested that activation of the cloned mu- and delta-opioid receptors (MOR1 and DOR1 respectively) in the RVM produces the antinociception mediated by spinally projecting neurons. In the present study, we investigated the expression of mRNA encoding either MOR1 or DOR1 in the RVM of rats. In addition, we examined quantitatively the expression of MOR1 and DOR1 mRNAs in spinally projecting RVM neurons including serotonergic (5HT) cells by using in situ hybridization, immunocytochemistry, retrograde tract-tracing, and the physical disector. Brainstem neurons were labeled in 14 male Sprague-Dawley rats by applying Fluoro-Gold (FG) topically to the dorsal surface of the lumbosacral spinal cord. Five-micrometer-thick cryostat sections were cut and in situ hybridization was performed by using full-length cRNA probes labeled with 35S-UTP. We found that 43% of RVM projection neurons expressed MOR1 mRNA and 83% of RVM projection neurons expressed DOR1 mRNA. Of 192 retrogradely labeled cells in the RVM, 51 cells (27%) were immunoreactive for 5HT. Of this population, half appeared to be labeled for the mRNA encoding MOR1 and over three-fourths appeared to be labeled for the mRNA encoding DOR1. Thus, we conclude that bulbospinal neurons express MOR1 and DOR1; moreover, MOR1 and DOR1 are expressed by significant proportions of 5HT neurons projecting to or through the dorsal spinal cord.

Effect of L-arginine in central spinal pain syndrome

When applied in combination with penicillin (2000 U) to the dorsal surface of the spinal cord, L-arginine in a low concentration of 100 nmol had a pronociceptive effect, while being applied in concentrations of 65–130 μmol with penicillin or injected intramuscularly before penicillin (15,000 U) L-arginine exhibited an analgesic effect. The opposite effects of L-arginine as the precursor of NO and of opioid dipeptide kyotorphin are demonstrated.

Spinal integration of antidromic mediated cutaneous vasodilation during dorsal spinal cord stimulation in the rat

The purpose of this study was to determine the involvement of supraspinal centers and spinal synaptic integration in cutaneous vasodilation mediated by dorsal spinal cord stimulation (DCS). Laser Doppler flowmetry was used to assess cutaneous blood flow changes in the rat hindpaw during DCS with a unipolar ball electrode placed at the L2-L3 spinal level. Results demonstrated that transecting the spinal cord at the T10 spinal segment did not alter the DCS response while T13 spinal transection abolished the DCS-induced vasodilation. Inhibition of synaptic activity with topical application of muscimol (0.2 mM) on the dorsal surface of the spinal cord markedly attenuated the DCS response. In conclusion DCS-induced vasodilation involved synaptic integration but did not require input from rostral spinal sites or supraspinal areas.