Surgical-Pathology.com

               Labyrinthitis

 
 

                
Labyrinthitis is an inflammation of a structure in your inner ear called the labyrinth. 

Labyrinth is located inside the inner ear, deep in the bone at the base of the skull. It is made up of 3 semicircular canals that help in control of  hearing and balance.

The labyrinth consists of inter-connected channels filled with fluid and these channels are at different angles. When the head moves, the rolling of the fluid tells the brain how far, how fast and in what direction the head is moving. This information allows the body to balance properly. Part of the labyrinth, called the cochlea, also sends information about sounds to your brain .  

If the organs that control balance of a person's infected ear are inflamed, then the information they send to the brain will be different from the information sent from the unaffected ear.  

Serous Labyrinthitis is the mildest form due to local irritant, such as acute or chronic otitis media without bacterial invasion of inner ear, temporal bone or meningitis. Histological feature: Eosinophilic staining of the inner ear fluids with or without serofibrinous strands. Image Link 

Suppurative labyrinthitis is characterized by the presence of large numbers of  inflammatory cells.

Labyrinthitis Ossificans is end stage of labyrinthitis, with ossification of labyrinthian structures but no inflammatory infiltrate. The perilymphatic spaces are usually involved and the endolymphatic spaces are often spared. The region of the scala tympani, near the round window membrane, is the area most commonly affected. 

Image Link: Purulent labyrinthitis

Labyrinthitis is usually caused by a viral infection. There is a wide range of viruses that can cause an infection, but the condition often follows a common viral illness such as a cold, the flu, or mumps.  Viral labyrinthitis may also be due to measles and cytomegalovirus infection. Viral cytopathic changes are present in scala media.

Viral labyrinthitis: early pathology in the human. Laryngoscope.1983 Dec;93(12):1527-33.

Labyrinthitis can also be caused by a bacterial infection. Such cases are rare, but likely to be more serious. Bacteria can enter the labyrinth if the membranes (thin layers of tissue ) that separate the middle ear from the inner ear are broken. This can happen if the patients has middle ear infection (otitis media) or an infection of the brain lining (meningitis). Bacteria can also gain access to the inner ear as a result of an injury to your ear or head.

It is usually a mild condition that passes within a few weeks, although some cases are more serious and can do permanent damage to your hearing and balance. 

Labyrinthitis can affect people of any age, but it is rare in children.

The main symptom of labyrinthitis is vertigo, a spinning or whirling sensation which a person can feel although neither the person nor his surroundings are moving. 

With labyrinthitis, the vertigo begins suddenly, without warning, and often occurs 1 to 2 weeks after the person recovers from flu or a cold or other viral or bacterial infection. The sudden onset of vertigo may be severe enough to cause vomiting and nausea. The patient may also complain of tinnitus. Rarely only if the labyrinthitis is caused by a bacterial infection the hearing loss may be permanent.

                  

A case of tympanogenic labyrinthitis complicated by acute otitis media.Yonsei Med J. 2005 Feb 28;46(1):161-5.

Widespread use of antimicrobial drugs in the management of otitis media has significantly reduced the incidence of labyrinthitis nowadays. Cases of tympanogenic labyrinthitis following acute otitis media have rarely been reported in recent literature on otolaryngology. We report an unusual case of tympanogenic labyrinthitis that presented with sudden sensorineural hearing loss (SNHL) following acute otitis media in an adult who had no previous otological complaints. An audiogram revealed SNHL with pure tone threshold of 43.7 dB in the left ear. MRI was helpful to identify the inflammatory change of the membranous labyrinth. The patient's hearing returned to normal after treatment. The definite diagnosis of serous labyrinthitis was established retrospectively.

Temporal bone histopathology in a patient suspected of inner ear extension of otitis media. Nippon Jibiinkoka Gakkai Kaiho. 2005 May;108(5):533-6.

We report the histopathological findings in the temporal bone of a 30-year-old female who died of cervical esophageal carcinoma. The temporal bone sections revealed severe bilateral suppurative labyrinthitis and otitis media that presumably occurred immediately before her death. Many inflammatory cells were present in the middle ear, particularly around the stapes and the round window niche. They had also infiltrated the inner ear via the annular ligament of the stapes and the round window membrane. Inflammatory cell accumulation was also observed in the peri- and endolymphatic spaces, and it was most severe in the basal turn. Most of the inner and outer hair cells were preserved, but some had degenerated or were missing. Numerous round cells were observed in the modiolus, and some of the spiral ganglion cells had degenerated. On the basis of these findings, we concluded that bacterial otitis media had extended in to the inner ear via the oval window and round window membrane and had resulted in suppurative labyrinthitis. These findings are consistent with those of stage II suppurative labyrinthitis according to the classification of Schuknecht.

Histopathology of labyrinthine fistulae in chronic otitis media with clinical implications. Am J Otol.1997 Jan;18(1):15-25.

The objective of this study was to describe the light microscopic pathology of labyrinthine fistulae in chronic otitis media (COM) in seven temporal bones and to discuss clinical and surgical implications. In COM, labyrinthine fistulae are usually caused by cholesteatoma, with the lateral semicircular canal being the most commonly affected site. Some fistulae are asymptomatic, whereas, others affect the auditory and vestibular systems to varying degrees. Surgical removal of cholesteatoma matrix over a fistula carries a risk of sensorineural hearing loss. Knowledge of the pathology of fistulae may provide a better understanding of their clinical manifestations and may allow a more rational approach to surgical management. The Massachusetts Eye and Ear Infirmary temporal bone collection contains 115 specimens with COM, of which seven specimens show pathologic fistulization of the bony labyrinth. Histologic sections from these seven bones were evaluated with respect to type of COM, location and size of fistula, changes in the inner ear adjacent to the fistula, middle ear and mastoid disease, and pathology in the vestibular and cochlear sense organs. The following conclusions are presented (a) Labyrinthine fistulae can be caused not only by cholesteatoma, but also by granulomatous COM without cholesteatoma and even by localized infection within a canal-down mastoid cavity. (b) Cholesteatoma matrix or inflammatory tissue usually becomes apposed to the endosteum or membranous labyrinth within the fistula. In most cases, reactive inner ear changes do not occur at the fistula site. Occasionally, there is thickening of the endosteum or chronic localized labyrinthitis. (c) Most bones do not show any alterations of the vestibular and cochlear sense organs. Occasionally, there is serous labyrinthitis, which might lead to partial sensorineural hearing loss. (d) A protective "walling-off" phenomenon in the labyrinth is not common. Therefore, if overwhelming infection or surgical trauma breaches the natural barriers of the endosteum/membranous labyrinth, then the fistula may allow rapid dissemination of infection throughout the inner ear.

A human temporal bone study of acute bacterial meningogenic labyrinthitis. Am J Otol. 1996 May;17(3):375-85.

It is well established that sensorineural hearing loss (SNHL) is an important sequela of acute bacterial meningitis. Previous human temporal bone histopathologic studies have suggested that such hearing loss is due to labyrinthitis. This study involved a detailed and systematic evaluation of the auditory and vestibular end-organs in 41 human temporal bones from patients with acute bacterial meningitis, aimed at describing the spectrum of histopathologic changes within the labyrinth, ascertaining likely routes for spread of infection from the meninges to the inner ear, and comparing the data from humans with those described in a rabbit model of meningogenic labyrinthitis. Our study revealed the following: (a) Suppurative labyrinthitis occurred in 20 (49%) bones. Of these 20 bones, the cochlea was affected in all, whereas the vestibular organs were involved in 10. Eosinophilic staining of inner ear fluids without the presence of inflammatory cells (so-called "serous" labyrinthitis) occurred in 14 of the remaining 21 bones. This staining occurred primarily within the vestibular system. Its significance and pathogenesis remains unknown; (b) Sensory and neural structures of the inner ear appeared intact in the majority of specimens, including bones with suppurative labyrinthitis and those with eosinophilic staining of inner ear fluids. This finding raises the possibility of preventing or reversing SNHL by therapeutic intervention. Spiral ganglion cells were severely degenerated in 12% of bones, indicating a retrocochlear site of hearing loss in addition to the cochlea. This subset of patients may perform poorly after cochlear implantation; (c) It has been traditionally assumed that irreversible and permanent SNHL is caused by suppurative labyrinthitis, whereas reversible SNHL is caused by serous labyrinthitis. Our findings question the validity of these assumptions; (d) The data were consistent with the hypothesis that both the cochlear modiolus and cochlear aqueduct can serve as potential pathways for spread of infection from the meninges to the inner ear; (e) There were many similarities in the histopathology of the inner ear in humans when compared with the rabbit model of meningogenic labyrinthitis. A notable difference was that the cochlear aqueduct appeared to be the sole pathway for spread of infection in the rabbit, whereas in the human, both the modiolus and aqueduct were possible pathways.

Cytomegalovirus endolabyrinthitis. Arch. Pathol Lab Med.1977 Mar;101 (3):118-21.

A premature male infant, who died 22 days after birth with hyaline membrane disease, was found to have had cytomegalic inclusion disease at autopsy. Histopathologic examination of the temporal bones showed cytomegalovirus (CMV) infection of the entire endolabyrinth without involvement of the neural and sensory structures. These findings support the thesis that late gestational or perinatal fetal CMV infection results in an endolymphatic labyrinthitis. We hypothesize that blood-borne virus passes from the stria vascularis into the endolymphatic spaces and infects the nonneurosensory epithelium. This pattern of infection differs from the perilabyrinthitis of human varicellazoster and experimentally produced mouse CMV.

 
Soft Tissue Pathology;

Myxoid Tumours of Soft Tissue Classification of Soft Tissue Tumour;  Gross examination of soft tissue specimen ;  A practical approach to histopathological reporting of soft tissue tumours Grading of soft tissue tumours ; Lipomatous tumours ;Neural tumours ; Myogenic tumours ;Vascular tumours ;Fibroblastic/Myofibroblastic tumours ; Myofibroblastic tumours ;  Fibrohistiocytic tumours ; ChondroOsseous tumours ; Soft TissueTumours of Uncertain Differentiation ; Notochordal Tumour -Chordoma ; Extra-adrenal Paraganglioma ; Gastrointestinal Stromal Tumour ;

 February 2008

Surgical-Pathology.com

Histopathology-India.net

Pathology-India.com

Pancreatic Pathology Online

Gall Bladder Pathology Online

Paediatric Pathology Online

Paraganglioma-Online

Endocrine Pathology Online

Eye Pathology Online

Ear Pathology Online

Cardiac Path Online

Lung Tumour-Online

Mesothelioma-Online

Pulmonary Pathology Online

Nutritional Pathology Online

Environmental Pathology Online

Pathology Quiz Online

Dermpath-India

GI Path Online

Soft Tissue Pathology

Case Index

Infectious Disease Online; INDEX: A-D ; INDEX: E-L ; INDEX: M-P INDEX: Q-Z ; FUNGAL DISEASE ; VIRAL DISEASE.

Accessory Tragus

First Branchial Cleft Anomalies

Salivary Gland Choristoma

Gout of Ear

Malakoplakia of Ear

Granuloma Inguinale of Ear

Idiopathic Auricular Ossificans

Idiopathic Cystic Chondromalacia of Auricular Cartilage

Inflammatory Aural Polyp

Angiolymphoid Hyperplasia with Eosinophilia of Ear

Kimura's Disease of Ear

Chondrodermatitis Nodularis Chronica Helicis

Necrotizing "Malignant" External Otitis

Relapsing Polychondritis

Wegener's Granulomatosis of Ear

Acquired Cholesteatoma

Congenital Cholesteatoma

Histopathology Image of Cholesteatoma

Neoplasms of the External Ear 

Squamous Cell Carcinoma of the External Ear 

Verrucous Carcinoma of the External Ear 

Basal cell carcinoma of the External Ear

Ceruminous Adenoma of the External Ear

Histopathology Images of Ceruminous Adenoma

Pleomorphic Adenoma of the External Ear 

Syringocystadenoma Papilliferum of the External Ear

Cylindroma of the External Ear

Ceruminous Adenocarcinoma of the External Ear

Adenoid Cystic Carcinoma of the External Ear 

Melanocytic Tumours of the External Ear 

Rhabdomyosarcoma of the External Ear

Benign Fibro-Osseous Lesion of the External Ear

Exostosis of the External Ear

Osteoma of the Ear (external auditory canal and middle ear)

Langerhans Cell Histiocytosis of the Ear

Primary Lymphoma of the Ear

Vestibular Schwannoma of the Ear

Middle Ear Adenoma

Meningioma of the Middle Ear

Histopathology Image of Meningioma of the Middle Ear

Jugulotympanic Paraganglioma

Histopathology Images of Jugulotympanic Paraganglioma