Objective: To present the clinical, surgical and histopathological manifestations of meningioma intrinsic to the geniculate ganglion.
Study Design: Retrospective study of outcome.
Setting: Three private tertiary and one university (otology/neurotology) referral centers.
Patients: Six patients with cranial nerve VII paresis underwent magnetic resonance imaging and/or high-resolution computed tomography for subsequently histologically proven intrinsic meningioma of the geniculate ganglion. An additional six cases were identified in the literature. Most patients were female and ranged in age from 5 to 40 years.
Intervention: Total tumor removal via middle fossa and mastoid exposures followed by cable graft VII-VII neuroanastomosis.
Main Outcome Measure: Meningioma can occur intrinsic to the geniculate ganglion and produces gradual VIIth nerve paresis as its first symptom. Other sites of predilection may occur extrinsically within the temporal bone or along intracranial venous sinuses at sites of arachnoid villi.
Results: Hearing was maintained in each patient, and postoperative House-Brackmann grade III-V facial nerve function was achieved.
Conclusions: Intrinsic meningiomas of the geniculate ganglion rarely occur. However, this entity should be included in the differential diagnosis of a slowly progressive VIIth nerve paresis, especially in young females. Surgical removal and cable graft VII-VII neuroanastomosis is the treatment of choice. Long-term follow-up should be maintained because of the potential for von Recklinghausen's disease.
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PLoS One
December 2024
Department of Anatomical Sciences and Neurobiology, University of Louisville School of Medicine, Louisville, KY, United States of America.
Taste bud cells in the tongue transduce taste information from chemicals in food and transmit this information to gustatory neurons in the geniculate ganglion that innervate taste buds. The peripheral taste system is a dynamic environment where taste bud cells are continuously replaced, but further understanding of this phenomenon has been limited by the inability to directly observe this process. To overcome this challenge, we combined chronic in vivo two-photon laser scanning microscopy with genetic labeling of gustatory neurons and taste buds to observe how cells within the taste bud change over time.
View Article and Find Full Text PDFCurr Biol
November 2024
Deptartment of Psychological Sciences, University of Connecticut, Storrs, CT 06269, USA. Electronic address:
Motion perception is crucial to animal survival and effective environmental interactions. In mammals, detection of movement begins in the retina. Directionally selective (DS) retinal ganglion cells were first discovered in the rabbit eye, and they have since been found in mouse, cat, and monkey.
View Article and Find Full Text PDFTraumatic optic neuropathies cause the death of retinal ganglion cells (RGCs) and axon degeneration. This is a result of the blockage of neurotrophic factor (NTF) supply from the brain and a vicious cycle of neurotoxicity, possibly mediated by increased levels of retinal Zn . Ciliary neurotrophic factor (CNTF) and brain-derived neurotrophic factor (BDNF) are two NTFs that are known to support RGC survival and promote axon regeneration.
View Article and Find Full Text PDFNeural Regen Res
November 2024
State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, Guangdong Provincial Clinical Research Center for Ocular Diseases, Guangzhou, Guangdong Province, China.
Synaptic plasticity is essential for maintaining neuronal function in the central nervous system and serves as a critical indicator of the effects of neurodegenerative disease. Glaucoma directly impairs retinal ganglion cells and their axons, leading to axonal transport dysfuntion, subsequently causing secondary damage to anterior or posterior ends of the visual system. Accordingly, recent evidence indicates that glaucoma is a degenerative disease of the central nervous system that causes damage throughout the visual pathway.
View Article and Find Full Text PDFMult Scler
December 2024
Division of Neuroimmunology and Neurological Infections, Department of Neurology, Johns Hopkins University, Baltimore, MD, USA.
Background: Retrograde trans-synaptic degeneration (TSD) following retro-chiasmal pathology, typically retro-geniculate in multiple sclerosis (MS), may manifest as homonymous hemi-macular atrophy (HHMA) of the ganglion cell/inner plexiform layer (GCIPL).
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