Histopathology of transistory traumatic paraplegia in the monkey

1971 ◽  
Vol 35 (3) ◽  
pp. 272-276 ◽  
Author(s):  
Franklin C. Wagner ◽  
George J. Dohrmann ◽  
Paul C. Bucy
Keyword(s):  
Spinal Cord ◽  
Gray Matter ◽  
Internal Layers ◽  
Central Gray Matter ◽  
Microscopic Appearance ◽  
Content Type ◽  
Injured Area ◽  
Hemorrhagic Lesion ◽  
Central Gray ◽  
Fine Print

✓ The microscopic appearance of the primate spinal cord within a 4-hour interval following the delivery of a direct force sufficient to produce a transitory paraplegia was investigated by light microscopy. The resulting hemorrhagic lesion involved primarily the central gray matter and was attributed to the direct effect of the trauma on the vessels in the gray matter with a consequent impairment of blood supply to the injured area. Chromatolysis, vacuolation, and alterations in cytoplasmic density and stainability were observed within the neurons. The edematous changes in the white matter, which were more marked in the internal layers relative to the external layers, appeared minimal and explain in part why the paraplegia was transient.

The microvasculature in transitory traumatic paraplegia

1971 ◽  
Vol 35 (3) ◽  
pp. 263-271 ◽  
Author(s):  
George J. Dohrmann ◽  
Franklin C. Wagner ◽  
Paul C. Bucy
Keyword(s):  
Electron Microscopy ◽  
Spinal Cord ◽  
Gray Matter ◽  
Perivascular Spaces ◽  
Central Gray Matter ◽  
Content Type ◽  
Structural Alterations ◽  
Spinal Cord Contusion ◽  
Central Gray ◽  
Fine Print

✓ Fine structural alterations in the microvasculature, primarily of the gray matter, occur as one aspect of experimental spinal cord contusion. A force of 300 gm-cm, shown by the authors to produce a transitory paraplegia, was applied to the T-10 level of exposed primate spinal cord. At 5 min post-contusion, the muscular venules of the central gray matter were distended with erythrocytes. Erythrocytes were seen within the perivascular spaces of the post-capillary venules and muscular venules at 15 and 30 min post-contusion, and there was hemorrhage into the gray matter at 1 hour post-contusion. The appearance of erythrocytes within the perivenular spaces was apparently due to small ruptures in the walls of the muscular venules, which were first demonstrated by electron microscopy 15 min after contusion. Alterations in capillary and post-capillary venule endothelium of both gray and white matter were present at 4 hours post-contusion and consisted of vacuolation and endothelial swelling. In conclusion, following experimental contusion of the spinal cord sufficient to cause a transitory paraplegia, the principal changes were early perivascular and parenchymal hemorrhages followed by later evidence of ischemic endothelial injury in the microvasculature.

Luigi Rolando and his pioneering efforts to relate structure to function in the nervous system

1995 ◽  
Vol 83 (5) ◽  
pp. 933-937 ◽  
Author(s):  
Franco Caputi ◽  
Renato Spaziante ◽  
Enrico de Divitiis ◽  
Blaine S. Nashold
Keyword(s):  
Spinal Cord ◽  
Substantia Gelatinosa ◽  
Central Gray Matter ◽  
Content Type ◽  
Anatomical Dissection ◽  
Brain Functions ◽  
Central Gray ◽  
Electrical Impulses ◽  
Struggle For Recognition ◽  
Fine Print

✓ The fissure separating the motor from the sensory cortex and the substantia gelatinosa capping the posterior horn of the spinal cord are still known by the name of the Italian anatomist Rolando. Luigi Rolando was born in Turin, Italy, in 1773 and died in 1831. His life was not easy, the first of his problems being the death of his father when Rolando was still very young. Three people were to be influential in his life and career: Father Maffei, his maternal uncle who raised him; Dr. Cigna, the anatomy professor who discovered his talent; and Dr. Anformi, a general practitioner who introduced him to the practice of medicine and to the best circles of the city. Forced to leave Turin by the Napoleonic invasion of the country, Rolando first stopped in Florence, where he learned about anatomical dissection, drawing, and engraving and studied the appearance of nervous tissue under the microscope. Later he went to Sardinia where, although cut off from European cultural circles, he developed his major theories. Rolando pioneered the idea that brain functions could be differentiated and located in specific areas and discovered the fixed pattern of cerebral convolutions, highlighting motor and sensory gyri. He demonstrated the complexity of the central gray matter of the spinal cord, describing the “substantia gelatinosa,” and he deduced that nervous structures are connected in a network of nervous fibers linked by electrical impulses. Rolando had to struggle for recognition, however, as the priority of his discoveries was challenged by the almost contemporaneous work of Gall and Spurzheim on cerebral localization and of Flourens on cerebellar function. Nevertheless, his efforts contributed greatly to the clarification of brain function. His observations on nervous anatomy have been especially accurate, as shown by the nomenclature “fissure of Rolando” and “substantia gelatinosa of Rolando.”

Epidural perfusion cooling protection against protracted spinal cord ischemia in rabbits

1993 ◽  
Vol 79 (5) ◽  
pp. 736-741 ◽  
Author(s):  
Ivo Vanický ◽  
Martin Maršala ◽  
Ján Gálik ◽  
Jozef MarŠala
Keyword(s):  
Spinal Cord ◽  
Histopathological Examination ◽  
Spinal Cord Ischemia ◽  
Isotonic Saline ◽  
Central Gray Matter ◽  
Content Type ◽  
Ischemia Group ◽  
Group B ◽  
Central Gray ◽  
Fine Print

✓ The protective effect of a modified epidural cooling technique was assessed in a rabbit spinal cord ischemia model. The epidural space around the lumbar segments with induced ischemia was continually perfused with cold (5°C) isotonic saline via two communicating spinal canal openings. This procedure allowed the spinal cord to be kept deeply hypothermic (< 15°C within central gray matter) during the ischemic period. The animals were subjected to either normothermic ischemia (Group A) or hypothermic ischemia (Group B). Each group contained three subgroups of animals undergoing 20, 40, or 60 minutes of aortic ligation. Their neurological outcomes were evaluated up to 48 hours postischemia, and the intergroup differences were compared. Two days postischemia, all of the animals were sacrificed by transcardial perfusion-fixation and their lumbar segments were processed for histopathological examination. In addition, in animals with 60-minute ischemia, spinal somatosensory evoked potentials were recorded during surgical intervention and again after 48 hours. In the normothermic animals, a high incidence of paraplegia was detected: in 40% after 20 minutes of ischemia, in 75% after 40 minutes, and in 100% after 60 minutes. In contrast, all of the hypothermic animals exhibited full neurological recovery even after 60 minutes of ischemia. Both electrophysiological and histological observations clearly correlated with the neurological findings. The results suggest that deep spinal cord hypothermia produced by epidural perfusion cooling provides effective protection against protracted spinal cord ischemia in rabbits.

Pathological findings in acute experimental spinal cord trauma

1971 ◽  
Vol 35 (6) ◽  
pp. 700-708 ◽  
Author(s):  
Thomas B. Ducker ◽  
Glenn W. Kindt ◽  
Ludwig G. Kempe
Keyword(s):  
Spinal Cord ◽  
White Matter ◽  
Clinical Improvement ◽  
Spinal Cord Trauma ◽  
Pathological Findings ◽  
Pathological Changes ◽  
Content Type ◽  
Acute Trauma ◽  
Central Gray ◽  
Fine Print

✓ This study shows that spinal cord pathology secondary to acute trauma in monkeys evolves with stepwise sequential changes. The acute damage is more central than peripheral. Depending on the amount of trauma, the subacute damage may be limited to central gray necrosis or may progress or evolve to include the neighboring white matter. These pathological changes may be taking place even in the presence of clinical improvement.

Presence and significance of CD-95 (Fas/APO1) expression after spinal cord injury

2001 ◽  
Vol 94 (2) ◽  
pp. 257-264 ◽  
Author(s):  
Mercedes Zurita ◽  
Jesús Vaquero ◽  
Isabel Zurita
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
White Matter ◽  
Gray Matter ◽  
Spinal Cord Tissue ◽  
Injured Spinal Cord ◽  
Content Type ◽  
Cord Injury ◽  
Positive Immunostaining ◽  
Fine Print

Object. A glycoprotein, CD95 (Fas/APO1) is widely considered to be implicated in the development of apoptosis in a number of tissues. Based on the hypothesis that apoptosis is related to cell death after spinal cord injury (SCI), the authors studied the presence and distribution of CD95 (Fas/APO1)-positive cells in injured spinal cord tissue for the purpose of determining the significance of this protein during the early phases of SCI. Methods. The presence and distribution of cells showing positive immunostaining for CD95 (Fas/APO1) were studied 1, 4, 8, 24, 48, and 72 hours and 1, 2, and 4 weeks after induction of experimental SCI in rats. Studies were conducted using a monoclonal antibody to the CD95 (Fas/APO1) protein. Positivity for CD95 (Fas/APO1) was observed in apoptotic cells, mainly in the gray matter, 1 hour after trauma, and the number of immunostained cells increased for the first 8 hours, at which time the protein was expressed in both gray and white matter. From 24 to 72 hours postinjury, the number of immunostained cells decreased in the gray matter, but increased in the white matter. From then on, there were fewer CD95 (Fas/APO1)-positive cells, but some cells in the white matter still exhibited positive immunostaining 1 and 2 weeks after injury. At 4 weeks, there remained no CD95 (Fas/APO1)-positive cells in injured spinal cord. Conclusions. These findings indicate that CD95 (Fas/APO1) is expressed after SCI, suggesting a role for this protein in the development of apoptosis after trauma and the possibility of a new therapeutic approach to SCI based on blocking the CD95 (Fas/APO1) system.

Effects of Glycine Administration on Canine Experimental Spinal Spasticity and the Levels of Glycine, Glutamate, and Aspartate in the Lumbar Spinal Cord

Neurosurgery ◽  
1979 ◽  
Vol 4 (2) ◽  
pp. 152-156 ◽  
Author(s):  
J. E. Smith ◽  
P. V. Hall ◽  
M. R. Galvin ◽  
A. R. Jones ◽  
R. L. Campbell
Keyword(s):  
Spinal Cord ◽  
White Matter ◽  
Gray Matter ◽  
Clinical Signs ◽  
Spinal Cord Transection ◽  
Lumbar Spinal Cord ◽  
Central Gray Matter ◽  
Central Gray ◽  
Lumbar Spinal

Abstract Twelve female mongrel dogs were made paraplegic by midthoracic spinal cord transection. Beginning at 9 weeks posttransection, either glycine (50 mg/kg) or saline was injected intramuscularly each day and the signs of spinal spasticity were assessed clinically. After treating the dogs for 3 weeks, we removed the lumbar enlargement of each dog and microdissected it into gray and white areas which we assayed for glycine, glutamate, and aspartate content. Some of the clinical signs of spasticity improved in the animals injected with glycine compared to the saline-injected controls. The content of glycine was significantly elevated in the central gray matter and ventral medial white matter of the glycinetreated dogs. The levels of glutamate were also significantly elevated in the central, lateral ventral, and medial ventral gray matter and in the dorsal lateral and ventral medial white matter of the glycine-treated dogs. The possible role of these segmental putative neurotransmitters in spinal spasticity is discussed.

Effects of epidural hypothermic saline infusion on locomotor outcome and tissue preservation after moderate thoracic spinal cord contusion in rats

2005 ◽  
Vol 2 (3) ◽  
pp. 308-318 ◽  
Author(s):  
Carlos E. Casas ◽  
Loren P. Herrera ◽  
Chad Prusmack ◽  
Gladys Ruenes ◽  
Alexander Marcillo ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Gray Matter ◽  
Thoracic Spinal Cord ◽  
Content Type ◽  
Treatment Groups ◽  
Thoracic Spinal ◽  
Cord Injury ◽  
Spinal Cord Contusion ◽  
Tissue Sparing ◽  
Fine Print

Object. Regionally delivered hypothermia has advantages over systemic hypothermia for clinical application following spinal cord injury (SCI). The effects of local hypothermia on tissue sparing, neuronal preservation, and locomotor outcome were studied in a moderate thoracic spinal cord contusion model. Methods. Rats were randomized to four treatment groups and data were collected and analyzed in a blinded fashion. Chilled saline was perfused into the epidural space 30 minutes postcontusion to achieve the following epidural temperatures: 24 ± 2.3°C (16 rats), 30 ± 2.4°C (13 rats), and 35 ± 0.9°C (13 rats). Hypothermia was continued for 3 hours when a 45-minute period of rewarming was instituted. In a fourth group a moderate contusion only was induced in 14 animals. Rectal (core) and T9–10 (epidural) temperatures were measured continuously. Locomotor testing, using the Basso-Beattie-Bresnahan (Ba-Be-Br) scale, was performed for 6 weeks, and rats were videotaped for subsequent analysis. The lesion/preserved tissue ratio was calculated throughout the entire lesion cavity and the total lesion, spinal cord, and spared tissue volumes were determined. The rostral and caudal extent of gray matter loss was also measured. At 6 weeks locomotor recovery was similar in all groups (mean Ba-Be-Br Scale scores 14.88 ± 3.71, 14.83 ± 2.81, 14.50 ± 2.24, and 14.07 ± 2.39 [p = 0.77] for all four groups, respectively). No significant differences in spared tissue volumes were found when control and treatment groups were compared, but gray matter preservation was reduced in the infusion-treated groups. Conclusions. Regional cooling applied 30 minutes after a moderate contusive SCI was not beneficial in terms of tissue sparing, neuronal preservation, or locomotor outcome. This method of cooling may reduce blood flow in the injured spinal cord and exacerbate secondary injury.

Barbiturate protection in acute experimental spinal cord ischemia

1982 ◽  
Vol 56 (4) ◽  
pp. 511-516 ◽  
Author(s):  
Edward H. Oldfield ◽  
Robert J. Plunkett ◽  
William A. Nylander ◽  
William F. Meacham
Keyword(s):  
Spinal Cord ◽  
Histological Study ◽  
Spinal Cord Ischemia ◽  
Spinal Cord Infarction ◽  
Pathophysiological Mechanism ◽  
Microscopic Appearance ◽  
Content Type ◽  
Cord Injury ◽  
Barbiturate Protection ◽  
Fine Print

✓ Ischemia is the pathophysiological mechanism in many types of spinal cord injury. In the present study, the infrarenal segment of the aorta was occluded for 25 minutes to produce spinal cord infarction in rabbits. Paraplegia occurred in 100% of control animals. Thiopental administered before aortic occlusion resulted in paraplegia in only 40% of animals so treated (p < 0.01). Histological study of the spinal cord demonstrated infarction of the gray matter in all paraplegic animals, whereas the microscopic appearance was normal in animals without neurological deficit. The protective influence of thiopental therapy in spinal cord ischemia was demonstrated.

Promotion of regeneration of corticospinal tract axons in rats with recombinant vascular endothelial growth factor alone and combined with adenovirus coding for this factor

2002 ◽  
Vol 97 (1) ◽  
pp. 161-168 ◽  
Author(s):  
Francesco Facchiano ◽  
Eduardo Fernandez ◽  
Salvatore Mancarella ◽  
Giulio Maira ◽  
Massimo Miscusi ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Growth Factors ◽  
Corticospinal Tract ◽  
Vascular Endothelial ◽  
Adult Rats ◽  
Content Type ◽  
Injured Area ◽  
Cord Injury ◽  
Endothelial Growth Factor ◽  
Fine Print

Object. After spinal cord transection in adult rats, the axons of the corticospinal tract (CST) degenerate retrogradely and do not regenerate. This phenomenon is thought to be related to either secondary ischemia or deficiency of growth factors. To overcome the deficiency of both blood flow and growth factors, the authors added exogenous vascular endothelial growth factor (VEGF165) to the transected spinal cord either as recombinant protein alone or combined with an adenovirus coding for VEGF165. Because most growth factors are rapidly inactivated in the extracellular environment, the authors used an adenovirus coding for VEGF165 to maintain its activity for several days. Methods. In adult rats, the dorsal two thirds of the spinal cord were transected at the T-8 level. In experimental rats, either human recombinant VEGF165 or a combination of this factor and a replication-defective adenovirus coding for VEGF165 (Ad.CMV.VEGF165) was applied at the lesion site. Both recombinant VEGF165 alone and combined with Ad.CMV.VEGF165 were mixed with Matrigel, which is a reconstituted membrane basement protein extract. Control rats received Matrigel alone or Matrigel plus an adenoviral vector containing the LACZ gene (Ad.CMV.LACZ). Thirty days after spinal cord injury, the number of newly formed blood vessels was assessed in the injured area. In addition, the sensorimotor cortex was injected with anterogradely transported horseradish peroxidase (HRP) to label the CST axons in the spinal cord and to evaluate the extent of retrograde axonal degeneration and regeneration. Gene transfer was assessed using semiquantitative reverse transcription—polymerase chain reaction analysis, enzyme-linked immunosorbent assay for human VEGF and β-galactosidase expression in injured rats treated with Matrigel plus Ad.CMV.LACZ, Matrigel plus Ad.CMV.VEGF165, and untreated injured rats. A strong gene transfer in the spinal cord tissue of adenovirus-treated rats was found from Day 3 to Day 10 postinjury, confirming infection. In the injured spinal cord area, a significant increase of blood vessels (300% over control, p < 0.005) occurred both in rats treated with recombinant VEGF165 alone and in those treated with the combination of recombinant VEGF165 and Ad.CMV.VEGF165. Also, in both of these groups of animals the retrograde degeneration of CST axons was significantly reduced compared with rats treated with Matrigel alone or Matrigel plus Ad.CMV.LACZ. Furthermore, in rats treated with recombinant VEGF165 alone or combined with Ad.CMV.VEGF165, a few HRP-labeled CST axons, which were not detectable in control rats, were seen distal to the spinal cord injury, indicating some regeneration across the injured area. Conclusions. These results indicate that locally applied VEGF exerts angiogenic as well as neurotrophic effects in the injured spinal cord of rats.

Sign in / Sign up

Export Citation Format

Share Document