Experimental acute balloon compression of the spinal cord

1979 ◽  
Vol 51 (6) ◽  
pp. 841-845 ◽  
Author(s):  
Arthur I. Kobrine ◽  
Delbert E. Evans ◽  
Hugo V. Rizzoli

✓ Acute balloon compression of the thoracic spinal cord for 15, 7, 5, 3, and 1 minute in monkeys caused immediate disappearance of the spinal evoked response and complete focal ischemia of the compressed segment in all animals. Only the animals in the 1-minute group, however, demonstrated return of the evoked response. These data, coupled with data from previous experiments of slow balloon compression of the spinal cord and spinal cord ischemia, suggest that the major pathological substrate for neural dysfunction after balloon compression of the spinal cord, be it acute or slow, is physical injury of the neural membrane, irrespective of blood flow changes. These findings also suggest that the ability of that membrane to recover is related to rapidity and length of time of compression. Focal changes in blood flow do not appear to be significant in this mechanism.

1979 ◽  
Vol 50 (5) ◽  
pp. 639-644 ◽  
Author(s):  
Arthur I. Kobrine ◽  
Delbert E. Evans ◽  
Hugo V. Rizzoli

✓ In this experiment, the effects of ischemia on neural conduction in the monkey spinal cord were studied. In six monkeys generalized ischemia of the spinal cord was created by bleeding the animals to a hypotensive level below the lower limits of autoregulation in the spinal cord. The progressive development of spinal cord ischemia was documented by blood-flow measurement using the hydrogen clearance method. Physiological integrity of the spinal cord was monitored and recorded by the spinal evoked response. The spinal evoked response did not disappear until at least 10 minutes of profound ischemia. At levels of ischemia 20% to 25% of normal blood flow, the spinal evoked response was unchanged. It is concluded that long-tract neural conduction in the spinal cord is relatively resistant to the effects of ischemia.


1982 ◽  
Vol 57 (5) ◽  
pp. 651-659 ◽  
Author(s):  
Joseph F. Cusick ◽  
Joel Myklebust ◽  
Mark Zyvoloski ◽  
Anthony Sances ◽  
Chris Houterman ◽  
...  

✓ Experiments were performed to assess the effects of vertebral column distraction on evoked potential responses from multiple recording sites along the conducting pathway in the monkey, and on concurrent blood flows, measured with the radioactive microsphere technique, along the axis of the central nervous system. Linear distractive loads were applied until the amplitude of the evoked response was significantly reduced. In four monkeys, the loads (100 to 150 lb) were sustained, whereas in two monkeys the forces (80 to 110 lb) were relaxed. The earliest response changes were most marked in recordings dependent upon the integrity of the upper cervical dorsal columns or brain stem-lemniscal pathway. The responses returned to control levels with load relaxation, but maintenance of the tractive load produced generalized and progressive response attenuation. At selected periods of significant changes in the evoked potential response, blood flow remained stable except for the late onset of regional ischemia in the middle cervical through upper thoracic spinal cord levels in the animals undergoing sustained loads. These findings indicate that brain-stem or spinal cord dysfunction occurring with both acute and gradual elongation of the spinal canal are the result of excess tensile stress acting on fiber tracts, and the delayed onset of spinal cord ischemia is the probable result of a similar mechanical process acting upon intrinsic spinal cord blood vessels.


1979 ◽  
Vol 50 (2) ◽  
pp. 207-216 ◽  
Author(s):  
Howard J. Senter ◽  
Joan L. Venes ◽  
John S. Kauer

✓ Blood flow after severe experimental injury to the thoracic spinal cord was studied in cats, using a modification of the hydrogen clearance technique. Gamma hydroxybutyrate, a central nervous system depressant, was shown to markedly alter the ischemic response to injury if given during the early posttraumatic period. Other vasoactive drugs investigated had no effect on posttraumatic ischemia. Therapeutic intervention during the early posttraumatic period aimed at increasing blood flow while decreasing the metabolic requirements of the injured cord may prove of value in reversing or limiting some elements of long-tract dysfunction due to the secondary ischemic insult.


1976 ◽  
Vol 45 (6) ◽  
pp. 647-659 ◽  
Author(s):  
Alan N. Sandler ◽  
Charles H. Tator

✓ Spinal cord blood flow (SCBF) was measured in the primate thoracic spinal cord using the 14C-antipyrine autoradiographic technique that allowed clear differentiation between white and gray matter blood flow. Individual SCBF values were obtained for 0.1-sq mm areas of the thoracic cord cross section. White matter blood flow was homogeneous throughout with a mean value of 10.3 ± 0.2 ml/100 gm/min. Graymatter flow was more variable with lower values in the dorsal horns and higher values in the central gray and anterior horns. Mean gray-matter flow was 57.6 ± 2.3 ml/100 gm/min. Arterial pO2 was 123 ± 2 torr, pCO2 was 40.2 ± 0.5 torr and pH was 7.327 ± 0.010. Mean arterial blood pressure was 113 ± 3 mm Hg and core temperature was 36.4° ± 0.1° C.


1978 ◽  
Vol 49 (4) ◽  
pp. 569-578 ◽  
Author(s):  
Howard J. Senter ◽  
Joan L. Venes

✓ A modification of the hydrogen clearance technique was used to study blood flow in the dorsolateral funiculus of traumatized thoracic spinal cord in cats. The results of this study show that ischemia occurred in all animals both at the level of trauma, and 1 cm below the site of trauma. There was, however, a period of over 1 hour after trauma during which blood flow was maintained at both sites. This investigation not only confirms the presence of ischemia in the lateral funiculus of the injured spinal cord but suggests that a period of time exists in the posttraumatic period during which pharmacological intervention may alter the ischemic response and possibly prevent secondary injury resulting from the ischemia.


2004 ◽  
Vol 1 (2) ◽  
pp. 223-227 ◽  
Author(s):  
Ryder Gwinn ◽  
Fraser Henderson

✓ Anterior spinal cord herniation is a well-documented condition in which the thoracic cord becomes tethered within a defect in the anterior dura mater. Typical procedures have involved a posterior approach with direct manipulation of the thoracic cord to expose and blindly release its point of tethering. The authors report three cases in which a novel approach for the treatment of anterior thoracic cord herniation was performed, cord manipulation and traction are minimized, and direct dural repair of the defect is performed.


1991 ◽  
Vol 75 (6) ◽  
pp. 911-915 ◽  
Author(s):  
Thomas H. Milhorat ◽  
David E. Adler ◽  
Ian M. Heger ◽  
John I. Miller ◽  
Joanna R. Hollenberg-Sher

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


1978 ◽  
Vol 48 (6) ◽  
pp. 1002-1007 ◽  
Author(s):  
Stephen E. Rawe ◽  
William A. Lee ◽  
Phanor L. Perot

✓ The early sequential histopathological alterations following a concussive paraplegic injury to the posterior thoracic spinal cord in cats were studied. The lack of significant progression of hemorrhages over a 4-hour period after injury indicates that most hemorrhages probably occur within the first hour. The marked enhancement or retardation of hemorrhages in the post-injury period, when the blood pressure was increased or decreased, respectively, demonstrates the loss of autoregulation of spinal cord vasculature at the trauma site after a concussive paraplegic injury. Progressive edema formation was evident over a 4-hour period following injury, and it could be enhanced or retarded by elevation or reduction of the systemic blood pressure.


1984 ◽  
Vol 61 (4) ◽  
pp. 761-766 ◽  
Author(s):  
Michael Salcman ◽  
Ernesto Botero ◽  
Krishna C. V. Rao ◽  
Richard D. Broadwell ◽  
Eric Scott

✓ The development of a transplantable model brain tumor in the neonatal dog, the adaptation of the tumor to tissue culture, and the successful growth of the tumor in adult mongrel dogs has been adapted to producing similar tumors in the thoracic spinal cord of the adult dog. Ten adult dogs, weighing 4 to 25.4 kg each, were subjected to formal laminectomy. The tumor cell suspension was injected by hand with a Hamilton syringe at two or three sites over a distance of 1 cm; each site received an injection volume to 0.02 to 0.05 cc of the cell suspension after the dura had been opened. Immediately after injection the field was copiously irrigated and the puncture area sealed with a single drop of ethyl cyanoacrylate. Tumor cells for injection were obtained by thawing ampules stored at −195°C in a mixture of 10% dimethyl sulfoxide and RPMI 1640 culture medium. Cells were resuspended in Hank's balanced salt solution and 15% fetal calf serum on ice. Solutions had 90% cell viability, and animals received a dose in the range of 3 to 13 × 106 cells. Eight animals developed tumors and became paraparetic on the 9th to 14th postinjection day. Metrizamide myelography in three animals revealed complete blocks; two animals underwent spinal computerized tomography (CT) and demonstrated syringohydromyelia. Histology revealed the tumors to be highly vascular primitive neoplasms that invaded the surrounding cord. This spinal cord tumor model is large enough to be operated on, studied by CT and myelography, and subjected to pharmacological, electrophysiological, and blood flow study.


2000 ◽  
Vol 92 (2) ◽  
pp. 229-232 ◽  
Author(s):  
Federico Roncaroli ◽  
Bernd W. Scheithauer ◽  
H. Gordon Deen

✓ A case of multiple hemangiomas of the cauda equina nerve roots, conus medullaris, and lower spinal cord is described. The 74-year-old male patient presented with a 9-month history of progressive bilateral leg weakness. He had a history of lymphoma at the age of 39 years and renal cell carcinoma in his early 40s. Neither disease was evident at the time of this presentation. A magnetic resonance image revealed multiple enhancing nodules in the cauda equina region as well as on the pial surface of the lower thoracic spinal cord and conus medullaris. The patient underwent an L2–3 laminectomy. Cauda equina nerve roots were found to be studded with numerous purple nodules, the largest measuring 6 to 8 mm. The nodules were adherent to nerve roots from which they could not be resected. Two lesions were histologically examined and found to be capillary hemangiomas. Twelve months into an uneventful postoperative course, the patient is neurologically unchanged. This unique case might represent a distinct form of hemangiomatosis confined to the cauda equina nerve roots and spinal cord.


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