Norepinephrine levels in experimental spinal cord trauma

1977 ◽  
Vol 46 (3) ◽  
pp. 342-349 ◽  
Author(s):  
Stephen E. Rawe ◽  
Robert H. Roth ◽  
Margaret Boadle-Biber ◽  
William F. Collins
Keyword(s):  
Spinal Cord ◽  
Tyrosine Hydroxylase ◽  
Concentration Gradient ◽  
Neurological Function ◽  
Spinal Cord Tissue ◽  
Spinal Cord Trauma ◽  
Content Type ◽  
Spinal Cord Segment ◽  
Fine Print

✓ Levels of norepinephrine (NE) in the spinal cord tissue of nontraumatized cats are highest in the cervical and lumbar enlargements. A rather uniform but slightly increasing concentration gradient from cephalad to caudad is observed in the thoracic segments. A 500 gm-cm trauma at the T-5 or C-7 spinal cord segment did not demonstrate any significant increase in NE levels measured sequentially over a 4-hour period after trauma. Dopamine levels could not be detected in the nontraumatized or traumatized cat spinal cords. Four traumatized cats treated with alpha methyl tyrosine, a tyrosine hydroxylase inhibitor, and followed clinically for 5 months showed no improvement in neurological function when compared to untreated traumatized cats. This study does not support the norepinephrine hypothesis of experimental spinal cord trauma.

Effect of anti—rat interleukin-6 antibody after spinal cord injury in the rat: inducible nitric oxide synthase expression, sodium- and potassium-activated, magnesium-dependent adenosine-5′-triphosphatase and superoxide dismutase activation, and ultrastructural changes

2001 ◽  
Vol 95 (1) ◽  
pp. 64-73 ◽  
Author(s):  
Metin Tuna ◽  
Sait Polat ◽  
Tahsin Erman ◽  
Faruk Ildan ◽  
A. Iskender Göçer ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Spinal Cord Tissue ◽  
Inos Activity ◽  
Content Type ◽  
Cord Injury ◽  
Oxide Synthase ◽  
Fine Print ◽  
Inducible Nitric Oxide

Object. The inflammatory cells that accumulate at the damaged site after spinal cord injury (SCI) may secrete interleukin-6 (IL-6), a mediator known to induce the expression of inducible nitric oxide synthase (iNOS). Any increased production of NO by iNOS activity would aggravate the primary neurological damage in SCI. If this mechanism does occur, the direct or indirect effects of IL-6 antagonists on iNOS activity should modulate this secondary injury. In this study, the authors produced spinal cord damage in rats and applied anti—rat IL-6 antibody to neutralize IL-6 bioactivity and to reduce iNOS. They determined the spinal cord tissue activities of Na+-K+/Mg++ adenosine-5′-triphosphatase (ATPase) and superoxide dismutase, evaluated iNOS immunoreactivity, and examined ultrastructural findings to assess the results of this treatment. Methods. Seventy rats were randomly allocated to four groups. Group I (10 rats) were killed to provide normal spinal cord tissue for testing. In Group II 20 rats underwent six-level laminectomy for the effects of total laminectomy alone to be determined. In Group III 20 rats underwent six-level T2–7 laminectomy and SCI was produced by extradural compression of the exposed cord. The same procedures were performed in the 20 Group IV rats, but these rats also received one (2 µg) intraperitoneal injection of anti—rat IL-6 antibody immediately after the injury and a second dose 24 hours posttrauma. Half of the rats from each of Groups II through IV were killed at 2 hours and the other half at 48 hours posttrauma. The exposed cord segments were immediately removed and processed for analysis. Conclusions. The results showed that neutralizing IL-6 bioactivity with anti—rat IL-6 antibody significantly attenuates iNOS activity and reduces secondary structural changes in damaged rat spinal cord tissue.

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.

Late neurological changes following traumatic spinal cord injury

1988 ◽  
Vol 69 (3) ◽  
pp. 399-402 ◽  
Author(s):  
Joseph M. Piepmeier ◽  
N. Ross Jenkins
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Spinal Cord Injuries ◽  
Neurological Status ◽  
Neurological Function ◽  
Traumatic Spinal Cord Injury ◽  
Content Type ◽  
Cord Injury ◽  
Fine Print

✓ Sixty-nine patients with traumatic spinal cord injuries were evaluated for changes in their functional neurological status at discharge from the hospital, and at 1 year, 3 years, and 5+ years following injury. The neurological examinations were used to classify patients' spinal cord injury according to the Frankel scale. This analysis revealed that the majority of improvement in neurological function occurred within the 1st year following injury; however, changes in the patients' status continued for many years. Follow-up examinations at an average of 3 years postinjury revealed that 23.3% of the patients continued to improve, whereas 7.1% had deteriorated compared to their status at 1 year. An examination at an average of 5+ years demonstrated further improvement in 12.5%, with 5.0% showing deterioration compared to the examinations at 3 years. These results demonstrate that, in patients with spinal trauma, significant changes in neurological function continue for many years.

Percutaneous cervical cordotomy: a review of 181 operations on 146 patients with a study on the location of “pain fibers” in the C-2 spinal cord segment of 29 cases

1994 ◽  
Vol 80 (6) ◽  
pp. 975-985 ◽  
Author(s):  
Juan Lahuerta ◽  
David Bowsher ◽  
Simpson Lipton ◽  
Peter H. Buxton
Keyword(s):  
Spinal Cord ◽  
Tissue Damage ◽  
Intractable Pain ◽  
Pain Sensation ◽  
Content Type ◽  
Somatotopic Organization ◽  
Current Series ◽  
Spinal Cord Segment ◽  
Pathological Pain ◽  
Fine Print

✓ The authors present a review of 146 patients who underwent 181 percutaneous cervical cordotomies for intractable pain. In addition, an anatomical-clinical correlation was carried out for 29 of these patients. It was found that the fibers subserving pain sensation in the C-2 segment lie in the anterolateral funiculus between the level of the denticulate ligament and a line drawn perpendicularly from the medial angle of the ventral gray-matter horn to the surface of the cord. The best analgesic results have been obtained by creating lesions that extend 5.0 mm deep to the surface of the cord and destroy about 20% of the hemicord. There is a somatotopic organization with sacral fibers running ventromedially and cervical fibers running dorsolaterally. The authors believe that the ascending fibers subserving the distinct sensations of pain induced by tissue damage and pinprick, although mixed (overlapping) in the anterolateral funiculus of the spinal cord, are physiologically distinct from one another. Whereas some cordotomies, both in the current series and as reported in the literature, may affect these functions differentially, optimum pain relief seems to be obtained only when pinprick sensation is also abolished in the affected segments. Evoked pain sensation is not abolished by cordotomy, but its threshold is greatly raised. When pathological pain is completely abolished, so is pinprick sensation. However, in a number of cases where pathological pain was only partially alleviated, pinprick sensation remained intact. The significance of these and other cases reported in the literature is discussed. The importance of clinically distinguishing between pain caused by tissue damage and pinprick sensation is emphasized, as well as that between return of pre-existing or new tissue-damage pain and painful dysesthesia.

Pathological basis of spinal cord cavitation in syringomyelia: analysis of 105 autopsy cases

1995 ◽  
Vol 82 (5) ◽  
pp. 802-812 ◽  
Author(s):  
Thomas H. Milhorat ◽  
Anthony L. Capocelli ◽  
Archinto P. Anzil ◽  
Rene M. Kotzen ◽  
Robert H. Milhorat
Keyword(s):  
Spinal Cord ◽  
Subarachnoid Space ◽  
Fourth Ventricle ◽  
Spastic Paraparesis ◽  
Central Canal ◽  
Spinal Cord Tissue ◽  
Content Type ◽  
Age Related ◽  
Spinal Subarachnoid Space ◽  
Fine Print

✓ This report summarizes neuropathological, clinical, and general autopsy findings in 105 individuals with nonneoplastic syringomyelia. On the basis of detailed histological findings, three types of cavities were distinguished: 1) dilations of the central canal that communicated directly with the fourth ventricle (47 cases); 2) noncommunicating (isolated) dilations of the central canal that arose below a syrinx-free segment of spinal cord (23 cases); and 3) extracanalicular syrinxes that originated in the spinal cord parenchyma and did not communicate with the central canal (35 cases). The incidence of communicating syrinxes in this study reflects an autopsy bias of morbid conditions such as severe birth defects. Communicating central canal syrinxes were found in association with hydrocephalus. The cavities were lined wholly or partially by ependyma and their overall length was influenced by age-related stenosis of the central canal. Noncommunicating central canal syrinxes arose at a variable distance below the fourth ventricle and were associated with disorders that presumably affect cerebrospinal fluid dynamics in the spinal subarachnoid space, such as the Chiari I malformation, basilar impression, and arachnoiditis. These cavities were usually defined rostrally and caudally by stenosis of the central canal and were much more likely than communicating syrinxes to dissect paracentrally into the parenchymal tissues. The paracentral dissections of the central canal syrinxes occurred preferentially into the posterolateral quadrant of the spinal cord. Extracanalicular (parenchymal) syrinxes were found typically in the watershed area of the spinal cord and were associated with conditions that injure spinal cord tissue (for example, trauma, infarction, and hemorrhage). A distinguishing feature of this type of cavitation was its frequent association with myelomalacia. Extracanalicular syrinxes and the paracentral dissections of central canal syrinxes were lined by glial or fibroglial tissue, ruptured frequently into the spinal subarachnoid space, and were characterized by the presence of central chromatolysis, neuronophagia, and Wallerian degeneration. Some lesions extended rostrally into the medulla or pons (syringobulbia). Although clinical information was incomplete, simple dilations of the central canal tended to produce nonspecific neurological findings such as spastic paraparesis, whereas deficits associated with extracanalicular syrinxes and the paracentral dissections of central canal syrinxes included segmental signs that were referable to affected nuclei and tracts. It is concluded that syringomyelia has several distinct cavitary patterns with different mechanisms of pathogenesis that probably determine the clinical features of the condition.

Effects of multi-dose methylprednisolone sodium succinate administration on injured cat spinal cord neurofilament degradation and energy metabolism

1984 ◽  
Vol 61 (2) ◽  
pp. 290-295 ◽  
Author(s):  
J. Mark Braughler ◽  
Edward D. Hall
Keyword(s):  
Spinal Cord ◽  
Sodium Succinate ◽  
Energy Charge ◽  
Lumbar Spinal Cord ◽  
Spinal Cord Tissue ◽  
Injured Spinal Cord ◽  
Neurofilament Protein ◽  
Content Type ◽  
Methylprednisolone Sodium Succinate ◽  
Spinal Cord Segment

✓ Thirty minutes after experimental spinal cord contusion (500 gm-cm) injury, cats were treated with an initial intravenous dose of either vehicle (V) or 30 mg/kg of Solu-Medrol sterile powder (methylprednisolone sodium succinate; MPSS). Two hours later, cats received a second intravenous injection of either V or 15 mg/kg MPSS, giving three treatment groups: V/V; MPSS/V; MPSS/MPSS. At 4½ hours following injury of the cat lumbar spinal cord, the gray and white matter neurofilament protein content was reduced by over 70% within the injured segment of V/V-treated animals. The three major cat spinal cord neurofilament protein subunits of 200,000, 152,000, and 76,000 daltons were reduced in parallel by the injury. Treatment of cats with a single 30-mg/kg dose of MPSS (MPSS/V) provided a clear, although not significant, protection against neurofilament degradation compared with V/V-treated cats when measured at 4½ hours after injury. The lactic acid content of the injured spinal cord segment at 4½ hours after injury was significantly elevated in both V/V- and MPSS/V-treated cats, while the adenosine triphosphate (ATP) content, total adenylates, and energy charge were significantly reduced. The administration of a second intravenous 15-mg/kg dose of MPSS 2 hours after the initial 30-mg/kg dose (MPSS/MPSS) provided complete (p < 0.01) preservation of neurofilaments within the injured spinal cord segment measured at 4½ hours after injury. The levels of lactate, ATP, total adenylates, and tissue energy charge in MPSS/MPSS-treated cats were not different from those of uninjured spinal cords following laminectomy. The (Na+ + K+)-ATPase activity in the injured spinal segment was enhanced, although highly variable, in MPSS/V-treated animals. On the other hand, spinal cord enzyme activity was significantly and consistently elevated in the MPSS/MPSS-treated group. The results demonstrate that a 30-mg/kg dose of MPSS followed at 2 hours by a 15-mg/kg dose provides significantly better protection against injury-induced ischemia and Ca++-dependent neurofilament degradation than a single 30-mg/kg dose. These findings are in agreement with the spinal cord tissue pharmacokinetics and time-action characteristics of methylprednisolone observed in earlier studies.

Reversible spinal cord trauma: a model for electrical monitoring of spinal cord function

1972 ◽  
Vol 36 (4) ◽  
pp. 402-406 ◽  
Author(s):  
Thomas J. Croft ◽  
Jerald S. Brodkey ◽  
Frank E. Nulsen
Keyword(s):  
Spinal Cord ◽  
Evoked Potentials ◽  
Sensitive Indicator ◽  
Spinal Cord Trauma ◽  
Content Type ◽  
Cortical Evoked Potentials ◽  
Spinal Cord Damage ◽  
Sensory Transmission ◽  
Spinal Cord Function ◽  
Fine Print

✓ Cortical evoked potentials in anesthetized cats were recorded by a noninvasive averaging technique as a means of estimating spinal cord damage. Graded pressure on the spinal cord produced reversible blocking of these potentials. With this type of trauma, block of motor transmission through the cord paralleled the block of sensory transmission, and each seemed to be a sensitive indicator of spinal cord function. The possible use of such monitoring in anesthetized patients undergoing spinal operations is discussed.

The presence of 4-hydroxynonenal/protein complex as an indicator of oxidative stress after experimental spinal cord contusion in a rat model

1998 ◽  
Vol 88 (5) ◽  
pp. 874-883 ◽  
Author(s):  
Stanley A. Baldwin ◽  
Richard Broderick ◽  
David Osbourne ◽  
Georg Waeg ◽  
Deborah A. Blades ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Spinal Cord ◽  
Protein Complex ◽  
Synaptic Function ◽  
Motor Deficits ◽  
Spinal Cord Tissue ◽  
Injury Site ◽  
Content Type ◽  
Spinal Cord Contusion ◽  
Fine Print

Object. The authors tested the hypothesis that breach of the blood—spinal cord barrier (BSCB) will produce evidence of oxidative stress and that a similar staining pattern will be seen between 4-hydroxynonenal (HNE)/protein complexes and extravasated immunoglobulin G (IgG). Methods. Adult female Fischer 344 rats, each weighing 200 to 225 g, were subjected to a spinal cord contusion at T-10 by means of a weight-drop device. Spinal cord tissue was assessed for oxidative stress by localizing extravasated plasma contents with a monoclonal antibody for rat IgG and protein conjugation with HNE, which is an aldehyde byproduct of lipid peroxidation. The animals were killed at 1 and 6 hours, and 1, 2, and 7 days after surgery. Maximum HNE/protein staining was observed at 2 days postinjury, and HNE/protein and IgG manifested similar staining patterns. Analysis revealed a graduated but asymmetrical rostral—caudal response relative to the T-10 injury site. Both HNE/protein complex and IgG staining revealed that the caudal levels T-11 and T-12 stained significantly more intensely than the rostral levels T-9 and T-8, respectively. A higher percentage of neurons positive for HNE/protein immunostaining was observed in spinal cord levels caudal to the injury site compared with equidistant rostral regions. Protein dot-blot assays also revealed a similar asymmetrical rostral—caudal HNE/protein content. To analyze the timing of the BSCB breach, another group of animals received identical contusions, and horseradish peroxidase (HRP) was injected 10 minutes before or at various times after injury (1, 3, and 6 hours, and 1, 2, and 7 days). Maximum HRP permeability was seen immediately after injury, with a significant decrease occurring by 1 hour and a return to control levels by 2 days posttrauma. Conclusions. Data from this study indicate possible compromise of neuronal, axonal, glial, and synaptic function after trauma, which may be a factor in motor deficits seen in animals after spinal cord contusion. The colocalization of the IgG stain with the HNE/protein stain is consistent with the hypothesis of a mutual cause—effect relationship between BSCB and oxidative stress in central nervous system trauma.

Studies in experimental spinal cord trauma

1974 ◽  
Vol 40 (1) ◽  
pp. 37-43 ◽  
Author(s):  
Lynn S. Hedeman ◽  
M. Kent Shellenberger ◽  
J. H. Gordon
Keyword(s):  
Spinal Cord ◽  
Pilot Study ◽  
Spinal Cord Trauma ◽  
Significant Elevation ◽  
Small Pilot Study ◽  
Content Type ◽  
Essentially Normal ◽  
Before And After ◽  
Fine Print

✓ The authors report a study of levels of norepinephrine (NE), dopamine (DA), and 5-hydroxytryptamine (5-HT) in the traumatized spinal cords of dogs, and with alpha-mehtyltyrosine before and after injury. There was a significant elevation of DA 15 to 45 minutes after injury. NE was significantly reduced. Twenty-four hours of pretreatment with alpha-methyltyrosine depleted cord catecholamines and prevented trauma-induced DA elevation. Alpha-methyltyrosine given 15 minutes after the trauma did not prevent this trauma-related DA elevation. In a small pilot study in cats, DA was elevated and NE remained essentially normal.

Sign in / Sign up

Export Citation Format

Share Document