Functional consequences of lumbar spinal cord contusion injuries in the adult rat

Our understanding of the substrates of locomotion, and hence our understanding of the causes of deficits following spinal cord injury, is still incomplete. While severe locomotor deficits can be induced by either contusion or laceration injuries or demyelination of thoracic spinal cord ventral and ventrolateral white matter, loss of mid-thoracic gray matter (intraspinal kainic acid injection) has no impact on locomotion. In contrast, loss of gray matter from the rostral lumbar segments induces severe locomotor deficits. This study examines the histological and locomotor outcomes following contusion injuries involving the rostral segments of the lumbar enlargement in the adult rat. Adult Sprague-Dawley rats received contusion injuries centered on the T13/L1, L2, or L3/4 spinal cord segments. Moderately severe injuries centered on the T13/L1 and L2 spinal cord segments induced more severe locomotor deficits than those centered on the L3/4 segments, despite a significantly smaller total gray matter volume loss (1.7 vs. 2.7 mm3). Moderately-severe injuries at T13/L1, L2, and L3/4 showed 21%, 31%, and 39% white matter sparing, respectively, with 6-week BBB scores of 10, 10, and 15.7, respectively. These data suggest that moderately-severe contusion injuries centered on the rostral segments of the lumbar enlargement induce more severe locomotor deficits than would be predicted by the histological outcome (spared white matter), suggesting that gray matter loss may play a role in functional deficits following some lumbar contusion injuries.     

Disturbances of cerebrospinal fluid flow attributable to arachnoid scarring cause interstitial edema of the cat spinal cord

OBJECTIVE: Spinal arachnoid scarring may be caused by trauma, inflammation, surgery, spinal instability, degenerative diseases, or malformations and may lead to progressive neurological deficits and syringomyelia. We wanted to investigate the effects of focal arachnoid scarring in the cervical spinal canal of cats on pressures in the subarachnoid space and spinal cord tissue, as well as on spinal cord histological features. METHODS: Twenty-nine adult cats were used for this study. Nine animals served as control animals, whereas 20 animals received a focal arachnoid scar at C1-C2, which was produced by placement of a kaolin-soaked fibrin sponge on the posterior surface of the spinal cord. After 4 months, pressure recordings above and below the scar, in the subarachnoid space and spinal cord, were performed. Elasticity measurements were performed with small bolus injections. Morphometric analyses of brain and ventricle volumes, sizes of the central canal, and sizes of the perivascular spaces in gray and white matter were also performed. RESULTS: No animal developed clinical or neurophysiological evidence of neurological symptoms at any time. In the kaolin-treated group, pressure recordings revealed a significant increase in the subarachnoid pressure at C1, because of the cerebrospinal fluid flow obstruction. Pressure gradients tended to increase at all measuring points. A significant difference was detected between the spinal cord and subarachnoid space at C2, where the intramedullary pressure exceeded the subarachnoid pressure. Elasticity was significantly increased in the spinal cord at C2. Intracranially, no evidence of hydrocephalus was observed. In the spinal cord, perivascular spaces were significantly enlarged in the posterior white matter above the arachnoid scar and in the central gray matter below the area of scarring in the cervical cord. CONCLUSION: Arachnoid scarring at C1-C2 produces an interstitial type of edema in the central gray matter below the area of scarring in the cat cervical cord, because of altered cerebrospinal fluid and extracellular fluid flow dynamics. These changes may be interpreted as the initial stage in the development of syringomyelic cavities.     

Experimental spinal epidural abscess: a pathophysiological model in the rabbit

To define the pathophysiology of spinal cord dysfunction associated with spinal epidural abscess formation, we developed an experimental model. Spinal epidural abscesses were produced in rabbits by injecting Staphylococcus aureus into the posterior thoracolumbar epidural space under direct vision. Progressive neurological deficits were detected in 18 of 20 animals; severe paraparesis or paraplegia occurred in 75%, and sphincter dysfunction occurred in 55%. Clinical data, including the results of plain spine roentgenography, myelography, and biochemical and bacteriological examination of the cerebrospinal fluid, were recorded. Epidural abscesses with varying degrees of spinal cord compression were confirmed pathologically in 95% of the experimental group. Spinal cord white matter changes included vacuolization, loss of myelin, and axonal swelling. The gray matter of the spinal cords was relatively preserved. There was no microscopic evidence of thrombosis or vasculitis in the major blood vessels supplying the spinal cords. Histopathological changes detected in the spinal cords were more consistent with direct compression of neural tissue than with infarction. The progressive clinical course and the histopathological changes in the spinal cord after compression by abscess closely resembled those of experimental compression of the spinal cord by epidural neoplasm.     

Motor control in the human spinal cord

Features of the human spinal cord motor control are described using two spinal cord injury models: (i) the spinal cord completely separated from brain motor structures by accidental injury; (ii) the spinal cord receiving reduced and altered supraspinal input due to an incomplete lesion. Systematic studies using surface electrode polyelectromyography were carried out to assess skeletal muscle reflex responses to single and repetitve stimulation in a large number of subjects. In complete spinal cord injured subjects the functional integrity of three different neuronal circuits below the lesion level is demonstrated: first, simple mono- and oligosynaptic reflex arcs and polysynaptic pathways; second, propriospinal interneuron system with their cell in the gray matter and the axons in the white matter of the spinal cord conducting activity between different spinal cord segments; and third, internuncial gray matter neurons with short axons and dense neuron contact within the spinal gray matter. All of these three systems participate continuously in the generation of spinal cord reflex output activating muscles. The integration of these systems and their relative degree of excitation and set-up produces characteristic functions of motor control. In incomplete spinal cord injured patients, the implementation of brain motor control depends on the profile of residual brain descending input and its integration with the functional neuronal circuits below the lesion. Locomotor patterns result from the establishment of a new structural relationship between brain and spinal cord. The functions of this new structural relationship are expressed as an alternative, but characteristic and consistent neurocontrol. The more we know about how the brain governs spinal cord networks, the better we can describe human motor control. On the other hand such knowledge is essential for the restoration of residual functions and for the construction of new cord circuitry to expand the functions of the injured spinal cord.     

Clinical and experimental studies on permeability of tracers in normal spinal cord and syringomyelia

Delayed CT Myelography (CTM) demonstrated intramedullary cavities in 18 patients, most of which appeared on the 6-hour scan. The attenuation values of the normal spinal cord increased progressively with time, and recorded a peak at 6 hours. The CT numbers of the gray matter of metrizamide were significantly high, as compared with those of iotrol. In the tracer study reported, lanthanum penetrated through the marginal glia to the normal and pathologic spinal cord. Reaction products of horseradish peroxidase (HRP) were mainly in the extracellular space of the normal spinal cord. The pathologic spinal cord, however, allowed the passage of HRP into the parenchyma through the extracellular space of the marginal glia. Consequently, the extracellular space of the spinal cord surface constitutes a pathway for cerebrospinal fluid solutes. Either metrizamide or iotrol thus diffuses into the spinal cord from the subarachnoid space.     

The importance of fluid-structure interaction in spinal trauma models

While recent studies have demonstrated the importance of the initial mechanical insult in the severity of spinal cord injury, there is a lack of information on the detailed cord-column interaction during such events. In vitro models have demonstrated the protective properties of the cerebrospinal fluid, but visualization of the impact is difficult. In this study a computational model was developed in order to clarify the role of the cerebrospinal fluid and provide a more detailed picture of the cord-column interaction. The study was validated against a parallel in vitro study on bovine tissue. Previous assumptions about complete subdural collapse before any cord deformation were found to be incorrect. Both the presence of the dura mater and the cerebrospinal fluid led to a reduction in the longitudinal strains within the cord. The division of the spinal cord into white and grey matter perturbed the bone fragment trajectory only marginally. In conclusion, the cerebrospinal fluid had a significant effect on the deformation pattern of the cord during impact and should be included in future models. The type of material models used for the spinal cord and the dura mater were found to be important to the stress and strain values within the components, but less important to the fragment trajectory.     

Effects of thoracic aortic occlusion and cerebrospinal fluid drainage on regional spinal cord blood flow in dogs: correlation with neurologic outcome

We studied the effect of thoracic aortic occlusion and cerebrospinal fluid (CSF) drainage on regional spinal cord blood flow and its correlation with neurologic outcome. Using isotope-tagged microspheres, we determined blood flow to the gray and white matter of five regions of the spinal cord in dogs: group I (control), group II (cross-clamp only), group III (cross-clamp plus CSF drainage). At 60 minutes after thoracic aortic occlusion in group II, median gray matter blood flow (GMBF) in the lower thoracic and lumbar cord decreased from 23.1 and 27.0 ml/100 gm/min at baseline to 4.0 and 2.5 ml/100 gm/min, respectively. The addition of CSF drainage improved GMBF during aortic cross-clamping in the lower thoracic and lumbar cord to 11.3 (p less than 0.05) and 15.1 ml/100 gm/min (p less than 0.03), respectively. After removal of the aortic cross-clamp, median blood flow more than tripled from baseline blood flow in group II, whereas CSF drainage prevented significant reperfusion hyperemia. Both low GMBF during cross-clamping and reperfusion hyperemia were associated with a worse neurologic outcome. In group II, no dog was neurologically normal, and more than 60% of the dogs had spastic paraplegia. In contrast, almost 60% of dogs in group III were normal, and none had spastic paraplegia (p less than 0.001). We conclude that CSF drainage in dogs during thoracic aortic occlusion maintained spinal cord perfusion above critical levels, diminished reperfusion hyperemia, and improved neurologic outcome.     

Finite element analysis of spinal cord injury in the rat

A three-dimensional (3D) finite element model (FEM) that simulates the Impactor weight-drop experimental model of traumatic spinal cord injury (SCI) was developed. The model consists of the rat spinal cord, with distinct element sets for the gray and white matter, the cerebrospinal fluid (CSF), the dura mater, a rigid rat spinal column, and a rigid impactor. Loading conditions were taken from the average impact velocities determined from previous parallel weight-drop experiments employing a 2.5-mm-diameter, 10-g rod dropped from either 12.5 or 25 mm. The mechanical properties were calibrated by comparing the predicted displacement of the spinal cord at the impact site to that measured experimentally. Parametric studies were performed to determine the sensitivity of the model to the relevant material properties, loading conditions, and essential boundary conditions, and it was determined that the shear modulus had the greatest influence on spinal cord displacement. Additional simulations were performed where gray and white matter were prescribed different material properties. These simulations generated similar drop trajectories to the homogeneous model, but the stress and strain distributions better matched patterns of acute albumin extravasation across the blood-spinal cord barrier following weight-drop SCI, as judged by a logit analysis. A final simulation was performed where the impact site was shifted laterally by 0.35 mm. The off-center impact had little effect on the rod trajectory, but caused marked shifts in the location of stress and strain contours. Different combinations of parameter values could reproduce the impactor trajectory, which suggests that another experimental measure of the tissue response is required for validation. The FEM can be a valuable tool for understanding the injury biomechanics associated with experimental SCI to identify areas for improvement in animal models and future research to identify thresholds for injury.     

Relation between spinal cord blood flow and functional recovery after blocking weight-induced spinal cord injury in rats

Spinal cord blood flow (SCBF) and motor performance on the inclined plane were measured up to 9 days after a reversible spinal cord compression injury in 49 Sprague-Dawley rats. A load of 35 g on 11 mm2 of the thoracic spinal cord for 5 minutes caused transient paraparesis with a decrease in the capacity angle on the inclined plane from 62 +/- 1 degree (mean +/- SEM) before injury to 33 +/- 1 degree on Day 1, 45 +/- 2 degrees on Day 4, d and 54 +/- 3 degrees on Day 9. SCBF was measured by the [14C]iodoantipyrine method, and in gray matter there was a decrease from 78.4 +/- 2.3 ml/min/100 g of tissue in uninjured animals to 33.7 +/- 1.5 ml/min/100 g of tissue on Day 1 after injury, increasing to 50.1 +/- 2.0 on Day 4 and to 70.5 +/- 2.7 ml/min/100 g of tissue on Day 9. At the corresponding times, the SCBF values in white matter were 14.5 +/- 0.5, 6.7 +/- 0.5, 10.2 +/- 0.6, and 13.4 +/- 0.6 ml/min/100 g of tissue, respectively. The animals in another group were loaded with 25 g for 5 minutes and on Day 1 exhibited a capacity angle of 43 +/- 2 degrees while the SCBF values for gray and white matter were 55.1 +/- 2.0 and 11.1 +/- 0.4 ml/min/100 g of tissue, respectively; thus, the results in this group were similar to the values on Day 4 in the animals loaded with 35 g.(ABSTRACT TRUNCATED AT 250 WORDS)     

Stress analysis of the cervical spinal cord: Impact of the morphology of spinal cord segments on stress

Objective: Although there are several classifications for cervical myelopathy, these do not take differences between spinal cord segments into account. Moreover, there has been no report of stress analyses for individual segments to date.

Methods: By using the finite element method, we constructed 3-dimensional spinal cord models comprised of gray matter, white matter, and pia mater of the second to eighth cervical vertebrae (C2–C8). We placed compression components (disc and yellow ligament) at the front and back of these models, and applied compression to the posterior section covering 10%, 20%, 30%, or 40% of the anteroposterior diameter of each cervical spinal cord segment.

Results: Our results revealed that, under compression applied to an area covering 10%, 20%, or 30% of the anteroposterior diameter of the cervical spinal cord segment, sites of increased stress varied depending on the morphology of each cervical spinal cord segment. Under 40% compression, stress was increased in the gray matter, lateral funiculus, and posterior funiculus of all spinal cord segments, and stress differences between the segments were smaller.

Conclusion: These results indicate that, under moderate compression, sites of increased stress vary depending on the morphology of each spinal cord segment or the shape of compression components, and also that the variability of symptoms may depend on the direction of compression. However, under severe compression, the differences among the cervical spinal segments are smaller, which may facilitate diagnosis.     

Indications and complications of omental transplantation to the spinal cord

From 1984 to 1986, 56 cases with traumatic paraplegia were treated by transplanting the intact omentum to the injured spinal cord. All patients were followed up 1 to 4 years. In these patients, the sensory level descended variously in 80.0%, muscular power increased in different degrees in 60.9% and sphincter function improved in 76.8%. The indications of this operation are incomplete paraplegia with EMG showing nervous activity. Satisfactory effects can be expected in injuries of the thoracolumbar segments and in mild contusion spinal cord. Fistula with of leak of cerebrospinal fluid, is a severe complication, it may be prevented by suturing the omentum to the dura, complete hemostasis, and tight muscular suturing. The absorb function of the omentum also helps in its prevention.     

Posterior longitudinal myelotomy as a surgical treatment of acute cervical spinal cord injury

Although it is of great tragedy to lose motor and sensory function of the spinal cord by spinal cord injury, there is no effective measure for complete cord lesions. In the central gray of the spinal cord at the region of injury, hemorrhagic necrosis and edema advance causing secondary damage to the spinal cord in rather early stage after injury. It has not been proved whether to remove necrotic tissue in the central gray matter can be effective to prevent secondary damage of the spinal cord or not. Operative result of six patients with acute physiologically complete cervical spinal cord lesion who have been subjected to posterior longitudinal myelotomy and removal of hematoma and necrotic tissue of the central gray of the spinal cord were evaluated. All of them admitted to Kitasato University Hospital within 24 hours after injury. They were five males and one female aged twenty to fifty-three. All the patients showed complete block of contrast medium on myelography at the level of one to two segments above the neurologically estimated level or injury of the spine, indicating marked swelling of the spinal cord. Average duration from injury to operation was sixteen hours ranging from six to thirty nine. Posterior longitudinal myelotomy was performed by using microsurgical technique. Skull traction was performed by using Crutchfield tongs for six weeks in five and twelve weeks in one of the patients. On admission forty mg of dexamethasone was used as steroid therapy followed gradual reduction.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of aminophylline and isoproterenol on spinal cord blood flow after impact injury

A study of the effects of spinal cord injury upon spinal cord blood flow was carried out in cats. A 400 mg-cm impact produced an overall reduction in spinal cord blood flow of 24% in the white matter and 30% in the gray matter, as determined by 14C-antipyrine autoradiography. At the level of the injury, white-matter flow was 8.1 ml/100 gm/min, a reduction of 49%, and in the gray matter, 12.5 ml/100 gm/min, a reduction of 76%. Treatment with aminophylline and isoproterenol improved the overall blood flow in the spinal cord. At the level of the injury, white-matter flow after this treatment was no longer significantly different from control values. The gray-matter flow remained decreased to 26.2 ml/100 gm/min, a reduction of only 47%. It is proposed that aminophylline and isoproterenol may increase cyclic adenosine monophosphate (AMP) and prevent platelet aggregation along the endothelial surfaces of the microcirculation, and may thereby help to maintain improved perfusion of the injured spinal cord.     

Control of blood flow in the cat spinal cord

Spinal cord blood flow (SCBF) and the effect of end-tidal CO2 concentration (ETCO2) on SCBF (CO2 reactivity) were studied in the lumbar spinal cord of cats by means of the hydrogen-clearance technique Hydrogen gas was administered by inhalation, and its level in spinal cord tissue was estimated amperometrically with small (75 micrometers) platinum electrodes. The average SCBF's at normocapnia (ETCO2 = 4%) of the ventral horn gray matter and of the white matter at several locations were 43.2 and 16.2 ml . 100 gm-1 . min-1, respectively. For gray and white matter, the values of CO2 reactivity, estimated by the coefficient of the regression of SCBF (ml . 100 gm-1 . min-1) on ETCO2 (ml . 100 ml-1) were 11.6 and 2.1, respectively. No differences in SCBF or CO2 reactivity were observed between intact animals kept under N2O-O2 ventilation and decerebrated animals with no anesthesia. After an acute spinal section, ventral horn SCBF and CO2 reactivity (measured eight segments below the cordotomy) were not altered, in spite of the profound neural depression present (that is, spinal shock). Orthodromic (dorsal root) stimulation of the ventral horn neurons induced an average increase in blood flow of 128% above control values. Antidromic (ventral root) motoneuron activation failed to produce any significant changes in ventral horn blood flow.     

肿瘤压迫脊髓的实验研究

将１０６Ｗａｌｋｅｒ ２５６癌细胞经度注射到８０只Ｗｉｓｔａｒ鼠Ｔ１３椎体的前方， ５～ １０天后出现脊髓压迫损害。应用ＣＴ和ＭＲＩ扫描对椎旁肿瘤进行了测量。电镜检查发现受压段脊髓毛细血管扩张，以后塌瘪，渗透性高，常有红细胞溢出。脊髓微血管造影发现，肿瘤压迫早期为静脉回流障碍，晚期主要是白质和灰质的缺血。脊髓水分测定，证实局部存在脊髓水肿。实验结果表明：脊髓内血循环障碍和轴索破坏是造成截瘫的重要因素。     

Intrathecal administration of 4-aminopyridine in chronic spinal injured patients

STUDY DESIGN: Intrathecal administration of 4-aminopyridine (4-AP) in chronic spinal cord injured (SCI) patients. OBJECTIVE: To determine the safety and effects of intrathecal administration of 4-AP in a small population of chronic SCI patients. SETTING: The post anesthesia care unit of a tertiary care hospital. METHODS: Following animal mode studies to establish dosing safety, six subjects with chronic SCI were examined. In each subject, an intrathecal catheter was placed with the tip as close to the lesion level as possible. 4-AP was infused at 5 microg/h for a period of 4-5 h. Vital signs were recorded and sensory-motor physical examinations and pain questionnaires were administered for 24 h. In two patients, samples of cerebrospinal fluid for analysis were drawn from a second intrathecal catheter. RESULTS: No adverse systemic side effects were noted. One patient showed transient improvement in sensory function; two showed transient increases in spasticity; three showed transient increases in cutaneomuscular reflexes and two showed an apparent small increase in volitional motor control. The concentration of 4-aminopyridine in the cerebrospinal fluid reached a peak of 163 ng/ml at 4 h in one subject and 122 ng/ml at 5 h in the other subject examined. CONCLUSION: Intrathecal administration of 4-aminopyridine at a rate of 5 microg/h does not appear to cause adverse effects and may modify spinal cord function. This route of administration allows local cerebrospinal fluid concentrations equivalent to those produced by maximum tolerable systemic doses, which require 1000 times more drug substance to be delivered to the subject as a whole. Intrathecal administration offers the potential to focus therapeutic effects to the lesion site while minimizing systemic side effects.     

Effect of sodium nitroprusside on spinal cord perfusion and paraplegia during aortic cross-clamping

To evaluate the effects of sodium nitroprusside (SNP) on hemodynamics, cerebrospinal fluid dynamics, and neurological outcome after 30 minutes of thoracic aortic occlusion, we monitored proximal and distal blood pressure, cerebrospinal fluid pressure, spinal cord blood flow, and somatosensory evoked potentials. In group 1 (n = 6), no attempts were made to control proximal hypertension, whereas in group 2 (n = 6), proximal blood pressure was controlled with intravenous infusion of SNP. There was no significant difference in proximal or distal blood pressure or cerebrospinal fluid pressure between the two groups at baseline. During the crossclamp interval, the mean proximal aortic pressure rose from 108 +/- 21 to 146 +/- 14 mm Hg (p less than 0.001) in the control group, whereas the mean blood pressure in the SNP group was maintained at 99.8 +/- 12 mm Hg (p = not significant compared with baseline blood pressure). Mean distal aortic pressure decreased from systemic values to 23 +/- 7 mm Hg in control animals and to 11 +/- 5 mm Hg in the SNP group (p less than 0.005). In the latter group, cerebrospinal fluid pressure increased significantly from 10.6 +/- 1.9 to 20.1 +/- 5.5 mm Hg (p less than 0.005). In animals receiving SNP, spinal cord blood flow was decreased in the lower spinal cord segments and increased in the upper cord segments. When compared with controls, this difference did not reach significance.(ABSTRACT TRUNCATED AT 250 WORDS)     

In vitro investigation of heat transfer in calf spinal cord during polymethylmethacrylate application for vertebral body reconstruction

The objective of this experimental study was to investigate the temperature variations within the spinal cord of calf cadavers during polymethlymethacrylate (PMMA) application for vertebral body reconstruction. Cervical spines including the cervical spinal cord of ten fresh cadavers were used. Corpectomy and laminectomy were performed and dura was exposed at the same level for proper placement of thermal sensors. Sensors were placed in multiple holes in the spinal cord at depths of 3, 6, 9 and 12 mm, respectively. Whether the thermal sensors were placed in the gray or white matter was determined by computerized tomography. The white and gray matters of the spinal cord exhibited different thermal properties. The white matter was more conductive and absorbed less heat than the gray matter. The heat sensor nearest to PMMA exhibited temperatures of 42–44°C. The second heat sensor placed at 9 mm depth within the gray matter showed 44°C. The third sensor, which was placed at 6 mm depth within the spinal cord recorded the same temperature as the first, i.e., nearest to PMMA sensor. The fourth heat sensor, which was at the farthest location from PMMA demonstrated 37–39°C. The temperature distribution within the gray matter was inversely proportional to the distance from the heat source. The temperature at the dorsal white matter, which was distant from the heating source, remained nearly constant and was not elevated. Our data suggest that thermal injury to the spinal cord during PMMA application may be expected to be more significant in the gray matter when compared with other neural tissues.     

Hemodynamic infarction of the spinal cord: involvement of the gray matter plus the border-zone between the central and peripheral arteries

OBJECTIVE: Hemodynamic infarction of the spinal cord that affected an 81-year-old female having a dissecting aortic aneurysm is presented. During the graft replacement operation, systemic hypotension occurred and the patient was subsequently complicated with paraplegia of the lower limbs. The patient died 2 weeks after the surgery due to gastrointestinal bleeding. An autopsy, which did not include the brain, was performed and the spinal cord was sampled. The aim of this report is to describe the pathologic profile of the spinal cord of the patient, and to gain insight into the pathogenesis of the lesion. METHODS: Histochemical and immunohistochemical methods were employed to study the spinal cord ranging from the lower thoracic to sacral segments. RESULTS: The whole central areas of the spinal cord showed coagulation and/or liquefaction necroses, while the white matter on the circumference of the cord remained unaffected, thus exhibiting a 'ring-like' appearance. CONCLUSION: This case is an example of hemodynamic infarction of the spinal cord involving the gray matter that is supplied by the central artery, plus the border-zone that is supplied by both the central and peripheral arteries. The former is probably associated with selective vulnerability of the gray matter to ischemia, while the latter is probably associated with intrinsic vulnerability of the border-zone to systemic hypotension or low blood-flow states.     

Morphologic change and astrocyte response to unilateral spinal cord compression in rabbits

In myelopathy, unilateral compression of the spinal cord in cases of disc herniation would be expected to produce Brown-Séquard syndrome. However, a transverse lesion syndrome occurs in most clinical cases. In order to reveal the mechanism by which unilateral compression induces transverse damage to the spinal cord, damage of the gray and white matter in each half of the spinal cord were evaluated quantitatively to determine the density of GFAP-positive astrocytes. The cervical spinal cord in rabbits was unilaterally compressed with a small screw. The area of each half of the damaged cord and the density of GFAP-positive astrocytes of the compressed and contralateral halves were investigated one week after the surgery. No apparent paralysis was observed during the period of observation. As the compression increased, the area of the compressed half of the spinal cord decreased significantly compared to the contralateral half. The densities of GFAP-positive astrocytes in the gray matter and the anterior funiculus increased significantly in the compressed half. There were no significant differences in the densities at the lateral and dorsal funiculi between the compressed and contralateral halves. The tissue damage in the gray matter of the compressed half was markedly higher. No significant difference between the two halves in damage was seen in the lateral funiculus, where in the lateral pyramidal and the dorsal spinocerebellar tracts are found. These findings provide evidence of the mechanistic basis for the spinal cord damage that leads to transverse lesion syndrome in unilateral compression myelopathy.