Transitory traumatic paraplegia: electron microscopy of early alterations in myelinated nerve fibers

1972 ◽  
Vol 36 (4) ◽  
pp. 407-415 ◽  
Author(s):  
George J. Dohrmann ◽  
Franklin C. Wagner ◽  
Paul C. Bucy

✓ The white matter of the monkey spinal cord was examined by electron microscopy during the first 4 hours following a contusion sufficient to produce a transitory paraplegia. At 5 min after injury the myelinated nerve fibers resembled those of the control animals. By 15 and 30 min after contusion, selected fibers were noted to have moderately enlarged periaxonal spaces. Attenuated myelin sheaths, splaying of the myelin lamellae, and a marked increase in the periaxonal spaces were present in affected nerve fibers at 1 hr following trauma. By 4 hrs after contusion approximately one-fourth of the fibers showed breakage of the myelin sheaths and consequent denuding of axons or marked attenuation of the myelin sheaths, greatly enlarged periaxonal spaces, and degeneration of the associated axons.

1953 ◽  
Vol 98 (3) ◽  
pp. 269-276 ◽  
Author(s):  
E. De Robertis ◽  
C. M. Franchi

A technique has been developed for the extrusion of axon material from myelinated nerve fibers. This material is then compressed and prepared for observation with the electron microscope. All the stages of preparation and purification of the axon material can be checked microscopically and in the present paper they are illustrated with phase contrast photomicrographs. Observation with the electron microscope of the compressed axons showed the presence of the following components: granules, fibrils, and a membranous material. Only the larger granules could be seen with the ordinary microscope. A considerable number of dense granules were observed. Of these the largest resemble typical mitochondria of 250 mµ by 900 mµ. In addition rows or small clusters of dense granules ranging in diameter from 250 to 90 mµ were present. In several specimens fragments of a membrane 120 to 140 A thick and intimately connected with the axon were found. The entire axon appeared to be constituted of a large bundle of parallel tightly packed fibrils among which the granules are interspersed. The fibrils are of indefinite length and generally smooth. They are rather labile structures, less resistant in the rat than in the toad nerve. They varied between 100 and 400 A in diameter and in some cases disintegrated into very fine filaments (less than 100 A thick). The significance is discussed of the submicroscopic structures revealed by electron microscopy of the material prepared in the way described.


1971 ◽  
Vol 35 (6) ◽  
pp. 700-708 ◽  
Author(s):  
Thomas B. Ducker ◽  
Glenn W. Kindt ◽  
Ludwig G. Kempe

✓ 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.


2001 ◽  
Vol 94 (2) ◽  
pp. 257-264 ◽  
Author(s):  
Mercedes Zurita ◽  
Jesús Vaquero ◽  
Isabel Zurita

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.


2001 ◽  
Vol 94 (2) ◽  
pp. 310-312 ◽  
Author(s):  
Se Hoon Kim ◽  
Soya Paik ◽  
Do Heum Yoon ◽  
Tai Seung Kim

✓ The authors report a case of oncocytoma arising from the spinal cord in a 40-year-old woman who presented with the complaints of gradual difficulty in walking. The excised tumor was exclusively composed of polygonal cells with abundant homogeneous eosinophilic cytoplasms. Electron microscopy study showed densely packed swollen mitochondria and frequent desmosomes. The histological and ultrastructural findings were consistent with a diagnosis of oncocytoma. To the authors' knowledge, this represents the first reported case of oncocytoma of the spinal cord.


2011 ◽  
Vol 492 (2) ◽  
pp. 119-123 ◽  
Author(s):  
Xiao-yan Shi ◽  
Yuan-yu Zhao ◽  
Shu Yang ◽  
Chen Li ◽  
Lin Chen ◽  
...  

2001 ◽  
Vol 95 (2) ◽  
pp. 202-207 ◽  
Author(s):  
Henri-Dominique Fournier ◽  
Philippe Mercier ◽  
Philippe Menei

Object. Because central nervous system white matter exerts a powerful inhibitory effect on axonal growth, implantation of nerve grafts or rootlets into the cervical spinal cord following ventral root avulsion injury should, ideally, be performed directly through the ventral root exit zone (VRExZ), which is located near the anteromedial aspect of the anterior horn; the grafts/rootlets should not be implanted into the white matter of the lateral cord. This is not possible when using a conservative posterior approach. Therefore, the authors have studied the anatomy encountered when using the anterolateral approach and evaluated the technique in the particular case of avulsed ventral nerve roots. They also present a case illustration of the procedure, which is used currently in their department. Methods. Anterior access to the rootlets is obtained using a lateral interscalenic approach; the vertebral artery is exposed and mobilized, and oblique drilling of the vertebral bodies (VBs) is performed. Because the articular processes and half of the VBs are preserved, fusion is not required. The approach allows the surgeon to expose the anterior aspect of the cervical dura and the entire length of the emerging spinal nerves. The anterior aspect of the dura is opened at the desired levels for VRExZ exposure, and the position is ideal for implantation of the graft/rootlets. The interscalenic dissection is mandatory so that the lesions of the supraclavicular plexus can be evaluated and repaired. If necessary, the anterior approach allows for exploration of the infraclavicular plexus during the same procedure. Conclusions. The use of a true anterior approach to the ventral rootlets appears to be a valuable and appropriate approach that avoids extensive laminectomy/facetectomy while reimplantation is performed through the anterolateral sulcus itself. In this approach, however, reimplantation of dorsal roots into the spinal cord remains impossible.


1992 ◽  
Vol 76 (5) ◽  
pp. 856-862 ◽  
Author(s):  
Haruyuki Yamada ◽  
Akira Yokota ◽  
Akiko Furuta ◽  
Akio Horie

✓ The morphological mechanism of the reconstitution of shunted mantle was studied histopathologically in 22 kaolin-treated hydrocephalic puppies. A remarkable attenuation of cerebral mantle to less than 1 cm in thickness was seen on computerized tomography (CT) scans of four animals sacrificed 1 to 2 months after kaolin treatment (preshunt group). Ventricular shunting resulted in successful recovery of the mantle on repeated CT scans obtained 1 to 2 months after shunting in seven animals (postshunt group). In the remaining 11 animals the cerebral mantle, which had been reduced to 4 mm in thickness prior to shunting, failed to recover even 2 months after the procedure (shunt-refractory group). On gross inspection, the preshunt specimens showed marked thinning of the white matter, with the cortical ribbon well preserved, while the postshunt specimens consisted predominantly of thickened white matter. Histopathological examination of the attenuated white matter of the preshunt specimens showed decreased nerve-fiber density, myelin destruction with myelin regeneration and/or repair of myelin sheaths, and reactive astrocytosis, which were prominent especially in the periventricular white matter. The main findings in the reconstituted white matter of the postshunt specimens were extensive myelin regeneration of residual axons and remarkable astroglial proliferation with mesenchymal reaction, particularly at capillaries. No clear evidence of increased numbers of nerve fibers or axonal regeneration was observed. The shunt-refractory specimens showed remarkable attenuation of cortex, in which reduced numbers of neurons and loss of cortical lamination were noted, with vestigial white matter. The results indicate that astroglial proliferation with mesenchymal reaction and myelin regeneration contribute to the reconstitution of the cerebral mantle volume following ventricular shunting in this model. It is suggested that the critical factor for mantle reconstitution in chronic hydrocephalus is whether cortex is preserved.


1980 ◽  
Vol 52 (3) ◽  
pp. 335-345 ◽  
Author(s):  
Dean C. Lohse ◽  
Howard J. Senter ◽  
John S. Kauer ◽  
Richard Wohns

✓ Blood flow in the lateral funiculus of the thoracic spinal cord was measured in 24 anesthetized cats using the hydrogen clearance method. In a control series of eight nontraumatized animals, blood flow measurements were taken from the T-5 and T-6 segments for 6 consecutive hours. The mean spinal cord blood flow (SCBF) in the control group was 12.8 ± 3.51 (SD) ml/min/100 gm on the basis of 107 measurements over 6 hours. In the experimental groups, 16 animals were similarly prepared. The spinal cords of these animals were then traumatized by dropping a 20-gm weight 5 cm (100 gm-cm trauma) or 13 cm (260 gm-cm trauma) onto the T-5 segment. Previous experiments have shown that these trauma levels lead to a transient paraplegia of less than 10 and 30 days' duration, respectively. Two hundred blood flow measurements from T-5 and T-6 were taken over the 6 hours following trauma. In the seven animals of the 100 gm-cm group, mean SCBF after trauma from the T-5 segment was 12.6 ± 3.45 (SD) ml/min/100 gm on the basis of 50 measurements taken over 6 hours; not significantly different from the controls (p > 0.70). In the 260 gm-cm group, mean SCBF from T-5 for 6 hours after trauma was 17.3 ± 6.60 (SD) ml/min/100 gm; significantly higher than controls (p < 0.001). Mean SCBF 3 to 6 hours after trauma was significantly elevated over controls (p < 0.05). The mean hyperemia in the 260 gm-cm group was found to be due to marked hyperemia in only four animals of the series, while five animals maintained blood flows in the normal range. This experiment provides quantitative evidence that white matter ischemia does not occur in spinal cord injuries that can be expected to produce only transient paraplegia. The data support the concept that white matter ischemia in the acute phase of severe spinal cord trauma may be related to secondary injury and subsequent permanent paraplegia.


1971 ◽  
Vol 35 (3) ◽  
pp. 263-271 ◽  
Author(s):  
George J. Dohrmann ◽  
Franklin C. Wagner ◽  
Paul C. Bucy

✓ 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.


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