scholarly journals Origins of Vertigo

2021 ◽  
Vol 20 ◽  
Author(s):  
JMS Pearce ◽  
Keyword(s):  
Inner Ear ◽  
Cold Water ◽  
Semicircular Canals ◽  
Vital Role ◽  
Classical Period ◽  
Vestibular Apparatus ◽  
Excessive Heat ◽  
The Brain

The words for vertigo: ‘dinos’, ‘ilinggous’ ,‘skotomatikoi,’ date back to the classical period of Plato and Hippocrates. They were followed by the Latin ‘vertigine’ and ‘scotomia’. Excessive heat or blood in the brain was the original causes of vertigo, followed by Galen’s vaporous pneuma. Not until Flourens demonstration of circling movement in pigeons in which he had destroyed the semicircular canals, and Brown-Séquard’s observation of vertigo in man after syringing the ear with cold water, did the vital role of the vestibular apparatus appear. Subsequent syndromes described by Ménière and Bárány showed the role of the inner ear in causing vertigo in man.

scholarly journals The Dual Role of Microglia in Blood-Brain Barrier Dysfunction after Stroke

2020 ◽  
Vol 18 (12) ◽  
pp. 1237-1249 ◽  
Author(s):  
Ruiqing Kang ◽  
Marcin Gamdzyk ◽  
Cameron Lenahan ◽  
Jiping Tang ◽  
Sheng Tan ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Blood Brain Barrier ◽  
Vital Role ◽  
Dual Role ◽  
Brain Barrier ◽  
Barrier Dysfunction ◽  
Blood Brain ◽  
M2 Microglia ◽  
The Brain

It is well-known that stroke is one of the leading causes of death and disability all over the world. After a stroke, the blood-brain barrier subsequently breaks down. The BBB consists of endothelial cells surrounded by astrocytes. Microglia, considered the long-living resident immune cells of the brain, play a vital role in BBB function. M1 microglia worsen BBB disruption, while M2 microglia assist in repairing BBB damage. Microglia can also directly interact with endothelial cells and affect BBB permeability. In this review, we are going to discuss the mechanisms responsible for the dual role of microglia in BBB dysfunction after stroke.

Ménière Recognizes That Vertigo Can Originate from the Inner Ear

2016 ◽  
Author(s):  
Robert W. Baloh
Keyword(s):  
Hearing Loss ◽  
Inner Ear ◽  
Blood Vessels ◽  
Semicircular Canal ◽  
Semicircular Canals ◽  
Underlying Disease ◽  
The Brain ◽  
Benign Course

Prosper Ménière was the first clinician to conclude that vertigo can result from diseases of the inner ear. The symptom of vertigo originally fell under the rubric of apoplectiform cerebral congestion, a disorder thought to result from overfilling of blood vessels in the brain. Ménière noted that patients with vertigo and hearing loss associated with damage to the inner ear often have a benign course, and aggressive treatments such as bleeding can be more dangerous than the underlying disease. The first hint that the semicircular canals may be related to balance rather than hearing was provided by a Frenchman, Marie Jean Pierre Flourens. He systematically cut each semicircular canal in the pigeon and noted that the animal’s head and body tended to move in the plane of the damaged canal. The gyrations of the animals described by Flourens made Ménière think that vertigo in humans might be a similar phenomenon.

Introduction

2016 ◽  
Author(s):  
Robert W. Baloh
Keyword(s):  
Inner Ear ◽  
Angular Acceleration ◽  
Organ Of Corti ◽  
Semicircular Canals ◽  
Linear Acceleration ◽  
Positional Vertigo ◽  
Linear Movement ◽  
The Brain ◽  
Simple Bedside ◽  
Paroxysmal Positional Vertigo

The inner ear contains three major sensory receptors: the crista of the semicircular canals for sensing angular acceleration, the macule of the utricle and saccule for sensing linear acceleration, and the organ of Corti of the cochlea for sensing sound. Vertigo is an illusion of movement—usually spinning or turning but occasionally linear movement or tilt. Abnormalities of the inner ear or its connections in the brain cause an illusion of movement—vertigo. Benign paroxysmal positional vertigo (BPPV) is by far the most common cause of vertigo. Sudden violent spells of spinning are triggered by a change in position, such as turning over in bed, getting in and out of bed, and extending the head back to look up. This book tells the story of how the cause of BPPV was discovered and how a simple bedside cure was developed.

scholarly journals The Nuclear Receptor Nor-1 Is Essential for Proliferation of the Semicircular Canals of the Mouse Inner Ear

2002 ◽  
Vol 22 (3) ◽  
pp. 935-945 ◽  
Author(s):  
Tiia Ponnio ◽  
Quiana Burton ◽  
Fred A. Pereira ◽  
Doris K. Wu ◽  
Orla M. Conneely
Keyword(s):  
Inner Ear ◽  
Nuclear Receptor ◽  
Semicircular Canals ◽  
Mammalian Development ◽  
Genomic Locus ◽  
Membranous Labyrinth ◽  
Spatiotemporal Expression ◽  
Proliferative Growth ◽  
Precise Role

ABSTRACT Nor-1 belongs to the nur subfamily of nuclear receptor transcription factors. The precise role of Nor-1 in mammalian development has not been established. However, recent studies indicate a function for this transcription factor in oncogenesis and apoptosis. To examine the spatiotemporal expression pattern of Nor-1 and the developmental and physiological consequences of Nor-1 ablation, Nor-1-null mice were generated by insertion of the lacZ gene into the Nor-1 genomic locus. Disruption of the Nor-1 gene results in inner ear defects and partial bidirectional circling behavior. During early otic development, Nor-1 is expressed exclusively in the semicircular canal forming fusion plates. After formation of the membranous labyrinth, Nor-1 expression in the vestibule is limited to nonsensory epithelial cells localized at the inner edge of the semicircular canals and to the ampullary and utricular walls. In the absence of Nor-1, the vestibular walls fuse together as normal; however, the endolymphatic fluid space in the semicircular canals is diminished and the roof of the ampulla appears flattened due to defective continual proliferative growth of the semicircular canals.

scholarly journals Experimental Fusion of Contrast Enhanced High-Field Magnetic Resonance Imaging and High-Resolution Micro-Computed Tomography in Imaging the Mouse Inner Ear

2015 ◽  
Vol 9 (1) ◽  
pp. 7-12 ◽  
Author(s):  
Allen Counter S ◽  
Peter Damberg ◽  
Sahar Nikkhou Aski ◽  
Kálmán Nagy ◽  
Cecilia Engmér Berglin ◽  
...  
Keyword(s):  
High Resolution ◽  
Inner Ear ◽  
High Field ◽  
Ex Vivo ◽  
Semicircular Canals ◽  
Vestibular Apparatus ◽  
Resonance Imaging ◽  
Micro Computed Tomography ◽  
Ultra High Field

Objective: Imaging cochlear, vestibular, and 8th cranial nerve abnormalities remains a challenge. In this study, the membranous and osseous labyrinths of the wild type mouse inner ear were examined using volumetric data from ultra high-field magnetic resonance imaging (MRI) with gadolinium contrast at 9.4 Tesla and high-resolution micro-computed tomography (µCT) to visualize the scalae and vestibular apparatus, and to establish imaging protocols and parameters for comparative analysis of the normal and mutant mouse inner ear. Methods: For in vivo MRI acquisition, animals were placed in a Milleped coil situated in the isocenter of a horizontal 9.4 T Varian magnet. For µCT examination, cone beam scans were performed ex vivo following MRI using the µCT component of a nanoScan PET/CT in vivo scanner. Results: The fusion of Gd enhanced high field MRI and high-resolution µCT scans revealed the dynamic membranous labyrinth of the perilymphatic fluid filled scala tympani and scala vestibule of the cochlea, and semicircular canals of the vestibular apparatus, within the µCT visualized contours of the contiguous osseous labyrinth. The ex vivo µCT segmentation revealed the surface contours and structural morphology of each cochlea turn and the semicircular canals in 3 planes. Conclusions: The fusion of ultra high-field MRI and high-resolution µCT imaging techniques were complementary, and provided high-resolution dynamic and static visualization of the complex morphological features of the normal mouse inner ear structures, which may offer a valuable approach for the investigation of cochlear and vestibular abnormalities that are associated with birth defects related to genetic inner ear disorders in humans.

Involvement of programmed cell death in morphogenesis of the vertebrate inner ear

Development ◽  
1997 ◽  
Vol 124 (12) ◽  
pp. 2451-2461 ◽  
Author(s):  
D.M. Fekete ◽  
S.A. Homburger ◽  
M.T. Waring ◽  
A.E. Riedl ◽  
L.F. Garcia
Keyword(s):  
Cell Death ◽  
Epithelial Cells ◽  
Programmed Cell Death ◽  
Inner Ear ◽  
Three Dimensional ◽  
Semicircular Canals ◽  
Otic Vesicle ◽  
New Evidence

An outstanding challenge in developmental biology is to reveal the mechanisms underlying the morphogenesis of complex organs. A striking example is the developing inner ear of the vertebrate, which acquires a precise three-dimensional arrangement of its constituent epithelial cells to form three semicircular canals, a central vestibule and a coiled cochlea (in mammals). In generating a semicircular canal, epithelial cells seem to ‘disappear’ from the center of each canal. This phenomenon has been variously explained as (i) transdifferentiation of epithelium into mesenchyme, (ii) absorption of cells into the expanding canal or (iii) programmed cell death. In this study, an in situ DNA-end labeling technique (the TUNEL protocol) was used to map regions of cell death during inner ear morphogenesis in the chicken embryo from embryonic days 3.5-10. Regions of cell death previously identified in vertebrate ears have been confirmed, including the ventromedial otic vesicle, the base of the endolymphatic duct and the fusion plates of the semicircular canals. New regions of cell death are also described in and around the sensory organs. Reducing normal death using retrovirus-mediated overexpression of human bcl-2 causes abnormalities in ear morphogenesis: hollowing of the center of each canal is either delayed or fails entirely. These data provide new evidence to explain the role of cell death in morphogenesis of the semicircular canals.

Selective vulnerability of the inner ear to decompression sickness in divers with right-to-left shunt: the role of tissue gas supersaturation

2009 ◽  
Vol 106 (1) ◽  
pp. 298-301 ◽  
Author(s):  
Simon J. Mitchell ◽  
David J. Doolette
Keyword(s):  
Inner Ear ◽  
Decompression Sickness ◽  
Selective Vulnerability ◽  
Short Latency ◽  
Inert Gas ◽  
Nitrogen Washout ◽  
Frequent Absence ◽  
Inner Ear Decompression Sickness ◽  
The Brain

Inner ear decompression sickness has been strongly associated with the presence of right-to-left shunts. The implied involvement of intravascular bubbles shunted from venous to arterial circulations is inconsistent with the frequent absence of cerebral symptoms in these cases. If arterial bubbles reach the labyrinthine artery, they must also be distributing widely in the brain. This discrepancy could be explained by slower inert gas washout from the inner ear after diving and the consequent tendency for arterial bubbles entering this supersaturated territory to grow because of inward diffusion of gas. Published models for inner ear and brain inert gas kinetics were used to predict tissue gas tensions after an air dive to 4 atm absolute for 25 min. The models predict half-times for nitrogen washout of 8.8 min and 1.2 min for the inner ear and brain, respectively. The inner ear remains supersaturated with nitrogen for longer after diving than the brain, and in the simulated dive, for a period that corresponds with the latency of typical cases. It is therefore plausible that prolonged inner ear inert gas supersaturation contributes to the selective vulnerability of the inner ear to short latency decompression sickness in divers with right-to-left shunt.

scholarly journals Cadherin-12 Regulates Neurite Outgrowth Through the PKA/Rac1/Cdc42 Pathway in Cortical Neurons

2021 ◽  
Vol 9 ◽  
Author(s):  
Beibei Guo ◽  
Mengwei Qi ◽  
Shuai Huang ◽  
Run Zhuo ◽  
Wenxue Zhang ◽  
...  
Keyword(s):  
Neurite Outgrowth ◽  
Cortical Neurons ◽  
Vital Role ◽  
Dependent Manner ◽  
Zebrafish Model ◽  
Axon Extension ◽  
The Brain

Cadherins play an important role in tissue homeostasis, as they are responsible for cell-cell adhesion during embryogenesis, tissue morphogenesis, and differentiation. In this study, we identified Cadherin-12 (CDH12), which encodes a type II classical cadherin, as a gene that promotes neurite outgrowth in an in vitro model of neurons with differentiated intrinsic growth ability. First, the effects of CDH12 on neurons were evaluated via RNA interference, and the results indicated that the knockdown of CDH12 expression restrained the axon extension of E18 neurons. The transcriptome profile of neurons with or without siCDH12 treatment revealed a set of pathways positively correlated with the effect of CDH12 on neurite outgrowth. We further revealed that CDH12 affected Rac1/Cdc42 phosphorylation in a PKA-dependent manner after testing using H-89 and 8-Bromo-cAMP sodium salt. Moreover, we investigated the expression of CDH12 in the brain, spinal cord, and dorsal root ganglia (DRG) during development using immunofluorescence staining. After that, we explored the effects of CDH12 on neurite outgrowth in vivo. A zebrafish model of CDH12 knockdown was established using the NgAgo-gDNA system, and the vital role of CDH12 in peripheral neurogenesis was determined. In summary, our study is the first to report the effect of CDH12 on axonal extension in vitro and in vivo, and we provide a preliminary explanation for this mechanism.

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