scholarly journals Untersuchungen zur Pathomorphologie und Pathogenese der Aujeszkyschen Krankheit

1967 ◽  
Vol 4 (2) ◽  
pp. 97-119 ◽  
Author(s):  
V. Bergmann ◽  
C.-H. Becker

Lumbo-intramuscular or naso-oral infection of 15 rabbits with Aujeszky's virus consistently produced alterations in the nerve cells of the spinal ganglia, the spinal nerve roots and the spinal cord, viz. nuclear inclusions of Cowdry types A and B. Lumbar infection produced neural lesions extending continuously from the site of infection via the spinal nerve roots and spinal ganglia as far as the dorsal and ventral nuclear regions of the spinal cord. The viral lesions following nasooral infection involved electively the sympathetic centers of the spinal cord with severe alterations of the sympathetic trunk ganglia. Despite this demonstration of viral propagation along neural routes, one should not disregard the possibility of hematogenous-lymphogenic propagation.

1892 ◽  
Vol 51 (308-314) ◽  
pp. 67-78 ◽  

At the commencement of some observations on the reflex mechanisms of the spinal cord in Macacus , difficulties were encountered which made it desirable to attempt for that animal a somewhat particular examination of the distribution of the efferent and afferent spinal nerve-roots belonging to the lumbo-sacral plexus. The present communication has reference to the distribution of the efferent fibres of the roots.


1980 ◽  
Vol 58 (2) ◽  
pp. 227-229 ◽  
Author(s):  
I. Bishai ◽  
F. Coceani

Catabolism of prostaglandin (PG) E2 was studied in homogenates of spinal cord and spinal nerve roots of the cat. Spinal roots enzymatically converted PGE2 to a product (metabolite I) with the chromatographic mobility of 15-keto-PGE2. Little metabolic degradation occurred in the spinal cord; however, incubation of PGE2 with combined spinal cord and nerve root tissue yielded a second metabolite (metabolite II) in addition to metabolite I. Metabolite II was identified as 15-keto-13,14-dihydro-PGE2. These results prove that spinal nerve roots, unlike the spinal cord, contain 15-hydroxyprostaglandin dehydrogenase (15-PGDH) which is the major and rate-limiting enzyme in the inactivation of prostaglandins. The location and functional significance of 15-PGDH in peripheral nerves remain to be elucidated.


The Lancet ◽  
1995 ◽  
Vol 346 (8986) ◽  
pp. 1323-1325 ◽  
Author(s):  
T Carlstedt ◽  
P Grane ◽  
R.G Hallin ◽  
G Norén

The following research was carried out in consequence of suggestions made to me by Professor Victor Horsley, to whom I wish to express my thanks for placing the facilities of his laboratory at my disposal, and for his advice and criticisms during the prosecution of the work and in the preparation of the paper. I also wish to return my best thanks to Professor Johannes Gad, in whose laboratory tire first part of the work was carried out, for his ever-ready and constant help and advice. I have further to thank my friend Dr. Risien Russell for his kindness in assisting me in some of my earlier experiments on the monkey. The researches were undertaken with the view of throwing light upon the degree to which certain movements or, speaking more precisely, sensori-motor (kinæsthetic) phenomena are represented in any given segment of the lumbo-sacral region of the mammalian spinal cord, and further what relationship exists between the representation of one movement and that of another. It is clear that at least three methods suggest themselves as means whereby this problem may be attacked, e. g. , (1) the excitation method, (2) the method of exclusion by ablation, and (3) the so-called degeneration method. Of these Nos. (2) and (3) have been already in part employed (No. (2) Sherrington, Risien Russell, No. (3) Grünbaum), but believing that with suitable precautions more exact localisation could be obtained by the excitation method, I have so far adopted that alone.


2020 ◽  
Vol 32 (6) ◽  
pp. 968-971
Author(s):  
Hayate Nishiura ◽  
Shino Jou ◽  
Toru Ogata ◽  
Hiroki Kondo ◽  
Toshihiro Ichijo ◽  
...  

Calving difficulty may lead to traumatic peripheral nerve injury. A male, 8-mo-old, Japanese Black calf with a history of secondary dystocia as a result of fetal gigantism had lameness and gait disturbance. At autopsy, multifocal dural thickening with adhesions to the adjacent spinal cord was observed at T12–13 and L4–5 vertebral levels. Microscopically, numerous traumatic neuroma-like fascicles of nerve twigs were embedded in the dura mater with abundant collagenous connective tissue. By immunohistochemistry, axons and Schwann cells were confirmed in each nerve fascicle. Our observations suggest that avulsion injuries in the preganglionic fibers of the spinal nerve roots, and secondary spinal cord compression, resulted in the development of neurologic signs.


1994 ◽  
Vol 6 (2) ◽  
pp. 230-237
Author(s):  
Donal O'Toole ◽  
Gerald Wells ◽  
James Ingram ◽  
William Cooley ◽  
Stephan Hawkins

The ultrastructural features of a recently described inherited lower motor neuron disease were studied in 5 affected pigs. Clinical signs comprised progressive ataxia and paresis of variable severity. Affected pigs, 6, 7, 15, 15, and 19 weeks of age, and 2 unrelated healthy pigs, 9 and 15 weeks of age, were anesthetized and their tissues were fixed by whole body perfusion with mixed aldehydes. From 1 or more affected pigs, samples of cervical and lumbar spinal ventral horn, lateral and ventral spinal columns, dorsal and ventral lumbar spinal nerve roots, 2 peripheral nerves (Nn. phrenicus and fibularis communis), and 2 skeletal muscles (Mm. diaphragma and tibialis cranialis) were examined ultrastructurally. There was widespread degeneration of myelinated axons in peripheral nerves and in lateral and ventral columns of lumbar and cervical segments of spinal cord. Axonal degeneration was present in ventral spinal nerve roots and was absent in dorsal spinal nerve roots sampled at the same lumbar levels. Unmyelinated axons in peripheral nerves and spinal nerve roots were unaffected. In 4 of 5 affected pigs, there were atrophic alpha motor neurons in cervical spinal cord that contained dense, round osmiophilic perikaryal inclusions up to 4 μm in diameter and round swollen mitochondria. Axonal regeneration was present in N. phrenicus of the 19-week-old affected pig that had clinical signs of longest duration (10 weeks). There was no morphologic evidence of axonal degeneration or spinal neuronal atrophy in either control pig. The ultrastructural features of this motor neuron disease distinguish it from other reported progressive spinal neuropathies of pigs.


1976 ◽  
Vol 13 (1) ◽  
pp. 47-58 ◽  
Author(s):  
M. Vandevelde ◽  
R. J. Higgins ◽  
C. E. Greene

Clinicopathological findings of three different neoplastic conditions involving the spinal cord and nerve roots in three dogs are described. One sarcomatous intramedullary tumor closely associated with the vasculature was classified as a reticulum cell sarcoma of the spinal cord. The second case had massive and widespread neoplastic proliferation of reticulohistiocytic cells around the perineurinal vessels of many spinal nerve roots. The process was classified as a primary neoplastic reticulosis of the spinal roots. Multiple highly malignant tumors, infiltrating the spinal cord were found in one thoracic and several lumbosacral spinal nerve roots in the third case. These were considered to be anaplastic neurofibrosarcomas because of high collagen content, intact nerve fibers, whorl formation, and the tendency to palisade in some areas.


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