scholarly journals Unilateral loss of trigeminal nerve fibers at the ventral pons

2019 ◽  
Vol 12 (04) ◽  
Author(s):  
Tabinda Hasan
Author(s):  
Akiko Kato ◽  
Megumi Nakamura ◽  
Seishi Echigo ◽  
Yasuyuki Sasano

2001 ◽  
Vol 1 ◽  
pp. 20-20
Author(s):  
K. Messlinger

The mammalian dura mater encephali is richly supplied by trigeminal nerve fibers, a considerable proportion of which contains calcitonin gene-related peptide (CGRP). As plasma levels of CGRP are increased in some forms of headaches, the question is in which way CGRP is involved in nociceptive mechanisms within the peripheral and the central trigeminovascular system.


1986 ◽  
Vol 379 (2) ◽  
pp. 353-357 ◽  
Author(s):  
Sadao Kiyohara ◽  
Hiroshi Houman ◽  
Satoru Yamashita ◽  
John Caprio ◽  
Takayuki Marui

1996 ◽  
Vol 16 (6) ◽  
pp. 1319-1324 ◽  
Author(s):  
Joerg R. Weber ◽  
Klemens Angstwurm ◽  
Geoffrey M. Bove ◽  
Wolf Bürger ◽  
Karl M. Einhäupl ◽  
...  

We investigated whether trigeminal nerve fibers contribute to enhanced regional cerebral blood flow (rCBF) in a rat model of experimental bacterial meningitis. rCBF was measured continuously for 6 h by laser Doppler flowmetry through thinned bone over the frontal cortex. Meningitis was induced with pneumococcal cell wall components and confirmed by a significant increase of (a) leukocytes within the cerebrospinal fluid, (b) brain water content, (c) intracranial pressure and (d) rCBF. The increase of rCBF was significantly attenuated ( p < 0.05) at 3, 4, 5, and 6 h in animals after a chronic (200 ± 21% versus 138 ± 13% at 6 h on the intact and denervated sides, respectively) but not after an acute section of the nasociliary branch of the trigeminal nerve. We conclude that elevations in blood flow during the early phase of bacterial meningitis are mediated in part by the trigeminal nerve, probably by local perivascular release of neuropeptides from afferent axons innervating the meninges.


1971 ◽  
Vol 34 (5) ◽  
pp. 643-646 ◽  
Author(s):  
Kamal Mousa Mira ◽  
Ibrahiem Abou Elnaga ◽  
Hassanein El-Sherif

✓ Nerve cells histologically similar to the ganglionic cells of the trigeminal nerve were observed in the proximal part of the sensory root and in the motor root of the human trigeminal nerve. They were also seen in the sensory root of the trigeminal nerve of the dog. Counting of the nerve fibers showed doubling of the number of nerve fibers in the three divisions compared with the fibers in the sensory root adjacent to the trigeminal ganglion. There was also an increase in the number of fibers within the sensory root as it courses centrally, while a decrease was seen in the number of fibers in the proximal part of the motor root. Intermediate nerve bundles were seen leaving the motor root near the pons and joining the sensory root centrally. The fibers of the sensory root corresponding to each peripheral division maintained their specific location in the sensory root during the whole course centrally.


2018 ◽  
Vol 2018 ◽  
pp. 1-5
Author(s):  
Aya Kodama-Takahashi ◽  
Koji Sugioka ◽  
Tomoko Sato ◽  
Koichi Nishida ◽  
Keiichi Aomatsu ◽  
...  

Purpose. To report a case of persistent corneal epithelial defect that had occurred after a trigeminal nerve block. Case Presentation. A 75-year-old female had suffered from postherpetic neuralgia for 8 years. She underwent Gasserian ganglion block surgery and noticed declining visual acuity in the right eye on the following day. She presented with severe hyperemia and corneal epithelial defects in the right eye and experienced remarkable reduction of sensitivity in the right cornea. She was diagnosed with neurotrophic keratopathy. Ofloxacin eye ointment and rebamipide ophthalmic suspension ameliorated the corneal epithelial defects but superficial punctate keratopathy, corneal superficial neovascularization, and Descemet’s fold persisted. Although the epithelial defects occasionally recurred, the corneal sensation and epithelial defects, Descemet’s fold, and corneal superficial neovascularization all improved around 5 months after trigeminal nerve block. The HRT II Rostock Cornea Module (RCM) could not detect any corneal subbasal nerve fibers at postoperative 4 months; however, it could detect them at postoperative 6 months. Conclusions. As the nerve block effect wore off, the corneal subbasal nerve fibers slowly regenerated. As the corneal sensation improved, the corneal epithelial defects and superficial neovascularization also improved. The HRT II RCM appeared useful for observing loss and regeneration of the corneal subbasal nerve fibers.


1983 ◽  
Vol 42 (3) ◽  
pp. 239-242 ◽  
Author(s):  
Juha Lehtosalo ◽  
Hannu Uusitalo ◽  
Risto Uusitalo ◽  
Antti Poranen ◽  
Arto Palkama

2019 ◽  
Vol 48 ◽  
Author(s):  
Diego Matos Da Silva ◽  
Silvana Marques Caramalac ◽  
Thamara Matos De Andrade ◽  
Mariana Isa Poci Palumbo

Background: Idiopathic trigeminal neuropathy is a peripheral neuropathy whose clinical signs include inability to close the mouth. A neurological examination reveals mainly flaccid paralysis of the masticatory muscles, which may be accompanied by atony/hypotonia of the masseter and temporalis muscles. Altered sensitivity may also be present in very rare cases. This article reports a case of idiopathic trigeminal neuropathy with involvement of the motor and sensory nerve fibers in a dog, describing the clinical symptoms, neurological findings, exclusion of other diseases, and evolution of the condition.Case: A 5-year-old bitch showing signs of difficulty in picking up food, swallowing water, and hypersalivation was taken to a veterinary clinic. According to her owner, these signs had started spontaneously 2 days earlier. A physical examination of the animal revealed only a persistently open mouth, although the mouth opening and closing movements could be performed manually by manipulating the jaw. The patient showed swallowing ability, and her tongue movements were intact. The neurological examination revealed that the animal also presented bilateral absence of nasal sensitivity and absence of palpebral reflex. The animal’s blood test results showed changes only in the CK and AST levels, which were 1,182.60 U/L (reference: 1.5 to 28.4 U/L) and 87.1 IU/L (reference: 6.2 to 13 IU/L), respectively. The animal tested negative for distemper, leishmaniasis, toxoplasmosis and neosporosis. Abdominal ultrasound and thoracic radiography were performed to investigate neoplasia, as well as radiography of the temporomandibular joints, and none of these imaging tests revealed any alterations. A cerebrospinal fluid (CSF) analysis was also within the normal range of reference parameters. In view of the possibility of idiopathic trigeminal neuropathy, prednisolone (Prediderm® 10 mg) was prescribed, to be administered orally in a dose of 0.5 mg/kg at 12 h intervals for 2 days. In addition, the owner was told to provide supportive care by feeding the animal a pasty diet placed directly in the back of its mouth, using a syringe if necessary. An examination of the animal in a follow-up visit to the veterinary clinic 14 days later found that she had recovered completely from her initial condition.Discussion: Among the most common causes of neurogenic flaccid paralysis of the masticatory muscles is idiopathic trigeminal neuropathy, although trigeminal neuropathy secondary to neoplasms and infectious or parasitic diseases may also occur. Because its etiology is of unknown origin, it is essential to exclude other causes of peripheral neuropathies. Moreover, this disorder is characterized by its self-limiting evolution, with spontaneous cure of the clinical condition within two weeks, as was observed in the case reported here. The absence of nasal sensitivity is not usually found in dogs diagnosed with idiopathic trigeminal nerve paralysis. In this case, however, there was involvement of the motor and sensory fibers, since, in addition to flaccid paralysis of the masticatory muscles, nasal sensitivity was also found to be affected. The condition can be treated with corticosteroids when it first appears, simply in order to hasten the animal’s recovery from the disorder. In addition, given the animal’s inability to close its mouth, it is essential to provide supportive care by feeding it with pasty foods and water by hand to ensure it receives adequate nutrition during the course of the disorder.


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