Neurotrophic Keratopathy after Trigeminal Nerve Block for Treatment of Postherpetic Neuralgia

Kodama-Takahashi, Aya; Sugioka, Koji; Sato, Tomoko; Nishida, Koichi; Aomatsu, Keiichi; Fukuda, Masahiko; Shimomura, Yoshikazu

doi:10.1155/2018/6815407

Cited by 4 publications

(4 citation statements)

References 11 publications

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“…Trigeminal nerve block is a surgical treatment for trigeminal neuralgia. Strategies include microwave coagulation and alcohol nerve injection, directly injuring the trigeminal ganglion 11 . While preganglionic trigeminal nerve root could be injured due to acoustic neurinoma operation 12 .…”

Section: Discussionmentioning

confidence: 99%

Treatment of Neurotrophic Keratopathy Associated with Central Nervous System Injury Using Cenegermin: A Case Series

et al. 2022

Preprint

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Background: Neurotrophic Keratopathy (NK) is an orphan disease caused by reduction or absence of corneal innervation. Among the numerous etiologies of NK, central nervous system injuries affecting normal trigeminal nerve function is especially rare and serious, making the management of thses cases very challenging. Cenegermin (Oxervate, Dompè Farmaceutici, Milan, Italy) is a new recombinant human nerve growth factor approved for the treatment of stage 2 or 3 NK. Here, we describe the long-term outcome of NK patients associated with central nervous system injury treated with cenegermin. Method: Retrospective, consecutive, observational case series study. Describe and compare three cases of neurotrophic keratopathy (NK) arisng after central nervous system injury in different regions and treated with cenegermin eye drops. Restoration of corneal epithelial defects, corneal sensation and reinnervation evaluated by IVCM were documented in this study. Results: After 1 to 2 course of cenegermin therapy, a successful epithelial restoration and an increase in corneal sensation were achieved in all patients. Regeneration of subbasal nerve plexus was maintained during and after 1 year of cenegermin therapy, demonstrated by in vivo confocal microscopy (IVCM). One patient underwent conjunctival flap surgery 12 months after cenegermin treatment due to recurrence of NK. Conclusion: Neurotrophic keratitis secondary to central nervous system injury deserves much more recognition and cenegermin represent valuable in the management of NK, especially in terms of subbasal corneal nerve regeneration.

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Section: Discussionmentioning

confidence: 99%

Treatment of Neurotrophic Keratopathy Associated with Central Nervous System Injury Using Cenegermin: A Case Series

et al. 2022

Preprint

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“…Even without direct involvement of the ophthalmic branch, the maxillary and mandibular trigeminal block can affect the adjacent ophthalmic branch, which leads to neurotrophic keratitis. Usually, a herpes zoster neurotrophic ulcer occurs in chronological order, but a surgically induced trigeminal nerve block-induced neurotrophic ulcer begins early [4]. …”

Section: Discussion/conclusionmentioning

confidence: 99%

“…One treatment of postherpetic neuralgia due to herpes zoster is trigeminal nerve block [4, 5]. However, contrastingly, nerve block can reactivate herpes zoster such as herpes zoster following axillary nerve block [6] and herpes zoster oticus following mandibular block [7].…”

Section: Introductionmentioning

confidence: 99%

Maxillary Zoster and Neurotrophic Keratitis following Trigeminal Block

Cho

Kwon

Pugazhendhi³

et al. 2019

Case Rep Ophthalmol

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Herpes zoster ophthalmicus is commonly used to describe viral reactivation from the trigeminal ganglia with ocular involvement. The ophthalmic branch is the most commonly involved, whereas the maxillary and mandibular dermatomes are less commonly affected. Neurotrophic ulcer may occur secondary to intentional or inadvertent damage to the trigeminal nucleus, root, ganglion, or any segment of the ophthalmic branch of this cranial nerve. We report a case of reactivated maxillary herpes zoster combined with neurotrophic keratitis due to percutaneous 2nd and 3rd branch of trigeminal nerve block with alcohol to treat trigeminal neuralgia. A 57-year-old female came to the ophthalmology department complaining of decreased visual acuity and skin vesicle over the right lower lid and cheek. She had undergone right trigeminal nerve block for treatment of trigeminal neuralgia. Clinical examination revealed neurotrophic keratitis and maxillary herpes zoster. She was treated with oral and topical antivirals and vigorous lubrication with eye drops. Her neurotrophic keratitis showed a slow recovery. Although a few cases of herpes zoster following nerve block have been described, it would appear that a case of simultaneous maxillary herpes zoster and neurotrophic keratitis following trigeminal block has not yet been documented. It is possible that trigeminal nerve block may cause reactivation of latent virus and refractory neurotrophic keratitis.

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“…Spontaneous corneal NV after trigeminal denervation has been reported in mice . This phenomenon is also observed clinically in a patient developing corneal NV after trigeminal nerve block for neuralgia . This circumstantial evidence indicates that neuronal support is needed to maintain corneal avascularity.…”

Section: Introductionmentioning

confidence: 99%

Sensory neurons directly promote angiogenesis in response to inflammation via substance P signaling

2020

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Blood vessels and nerves travel together to supply most tissues in the body. However, there is a knowledge gap in the mechanisms underlying the direct regulation of angiogenesis by nerves. In the current study, we examined the regulation of angiogenesis by sensory nerves in response to inflammation using the cornea, a normally avascular and densely innervated ocular tissue, as a model. We used desiccating stress as an inflammatory stimulus in vivo and found that sub‐basal and epithelial nerve densities in the cornea were reduced in dry eye disease (DED). We established a co‐culture system of trigeminal ganglion sensory neurons and vascular endothelial cells (VEC) and found that neurons isolated from mice with DED directly promoted VEC proliferation and tube formation compared with normal controls. In addition, these neurons expressed and secreted higher levels of substance P (SP), a proinflammatory neuropeptide. SP potently promoted VEC activation in vitro and blockade of SP signaling with spantide I, an antagonist of SP receptor Neurokinin‐1, significantly reduced corneal neovascularization in vivo. Spantide I and siRNA knockdown of SP abolished the promotion of VEC activation by DED neurons in vitro. Taken together, our data suggested that sensory neurons directly promote angiogenesis via SP signaling in response to inflammation in the cornea.

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Neurotrophic Keratopathy after Trigeminal Nerve Block for Treatment of Postherpetic Neuralgia

Cited by 4 publications

References 11 publications

Treatment of Neurotrophic Keratopathy Associated with Central Nervous System Injury Using Cenegermin: A Case Series

Treatment of Neurotrophic Keratopathy Associated with Central Nervous System Injury Using Cenegermin: A Case Series

Maxillary Zoster and Neurotrophic Keratitis following Trigeminal Block

Sensory neurons directly promote angiogenesis in response to inflammation via substance P signaling

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