The Iliolumbar Ligament Does Not Have a Direct Nerve Supply

2018 ◽  
Vol 2 (1) ◽  
pp. 1-5
Author(s):  
Joy MH Wang ◽  
Christie Kirkpatrick ◽  
Marios Loukas
1960 ◽  
Vol 1 (1) ◽  
pp. 12-18
Author(s):  
Lennart Nicander
Keyword(s):  

1987 ◽  
Vol 58 (2) ◽  
pp. 276-287 ◽  
Author(s):  
M. D. Womble ◽  
S. Roper

1. To study the retrograde effects of changes in target tissue upon the innervating nerve supply, we have examined the parasympathetic submandibular ganglion of the adult rat. Neurons of this ganglion innervate the submandibular and sublingual salivary glands. 2. Ligating the salivary ducts leads to rapid and prolonged salivary gland cell atrophy. 3. Duct ligations, without direct injury to the glandular nerve supply, initially produced few alterations in the ganglion. After 8 wk, however, neuron number was reduced by 50%. The numbers of presynaptic inputs/neuron and synapses/neuron perimeter were not affected by the cell loss. 4. After 1 wk of duct ligation in which the glandular nerve supply was intentionally damaged, some ganglionic neurons have lost all presynaptic inputs, suggesting synaptic disjunction. This is followed at 3 wk by a 40% decrease in neuron number and an increase in the number of inputs per (remaining) ganglion cell. However, the number of synapses/neuronal profile was unchanged. 5. Thus axotomy plus target atrophy causes synaptic disjunction, neuron cell death, and input rearrangement, presumably due to a combination of direct injury effects and an abrupt loss of peripheral trophic supplies. 6. In contrast, target atrophy alone produced more gradual changes in submandibular ganglion neurons. Only prolonged target atrophy leads to a decrease in the number of ganglionic neurons, perhaps due to the gradual loss of peripheral trophic supplies. However, other features, such as the number of inputs/cell and the number of synapses/neuron perimeter, remain unaltered. Evidently, the gradual loss of trophic support does not result in synaptic disjunction to the degree needed to produce presynaptic input rearrangement.


1950 ◽  
Vol 10 (1-2) ◽  
pp. 1-37 ◽  
Author(s):  
G.A.G. Mitchell
Keyword(s):  

1975 ◽  
Vol 79 (3-6) ◽  
pp. 276-276
Author(s):  
J. J. Grote ◽  
W. Kuijpers ◽  
P. L. M. Huygen

1989 ◽  
Vol 115 (2) ◽  
pp. 217-223 ◽  
Author(s):  
G. S. Goding ◽  
C. W. Cummings ◽  
D. A. Bright
Keyword(s):  

1954 ◽  
Vol 68 (8) ◽  
pp. 495-516 ◽  
Author(s):  
G. A. G. Mitchell
Keyword(s):  

1989 ◽  
Vol 98 (11) ◽  
pp. 907-909 ◽  
Author(s):  
Anthony J. Maniglia ◽  
Brian Dodds ◽  
M. B. Katirji ◽  
Kelly Sorensen ◽  
Mary L. Rosenbaum

This report analyzes the experience gained using two different techniques to reinnervate the paralyzed vocal cord. In the neurotization group, the superior laryngeal nerve (SLN) motor branch–cricothyroid muscle pedicle was used to reinnervate the posterior cricoarytenoid muscle. In the direct nerve anastomosis group, the SLN was anastomosed to the abductor branch of the recurrent laryngeal nerve (RLN), and the ansa hypoglossi (AH) to the adductor branch of the RLN. A third group of animals (control) had the right RLN sectioned without any anastomosis. About 5 to 6 months postoperatively the animals were killed painlessly and evaluated. The neurotization group revealed vocal fold mobilization on the right side to have an average of about half of the mobility of the left, normal side. After the RLN and SLN on the left were severed as well as the AH bilaterally, the vocal cord mobility was reduced to about one fourth. The direct nerve anastomosis group showed about fourfold less vocal cord mobility than the neurotization group. After the SLN, RLN, and AH were severed bilaterally, the control group showed no vocal cord mobility. The neurotization technique has been selected for further experimentation in human adults.


Spine ◽  
2000 ◽  
Vol 25 (9) ◽  
pp. 1098-1103 ◽  
Author(s):  
James M. Hartford ◽  
Geoffrey M. McCullen ◽  
Robert Harris ◽  
Cameron C. Brown
Keyword(s):  

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